Clinical Review

ABSTRACT

Upper limb injuries in soccer represent only a marginal portion of injuries, however this is mainly true for outfield players. Goalkeepers are reported to have up to 5 times more upper extremity injuries, many of them requiring substantial time-loss for treatment and rehabilitation. The most common upper extremity injury locations are the shoulder/clavicle followed by the hand/finger/thumb, elbow, wrist, forearm, and upper arm. The mechanism of injury, presentation, physical examination, and imaging features all play a significant role in reaching the correct diagnosis. Taking to consideration the position the player plays and his demands will also enable tailoring the optimal treatment plan that allows timely and safe return to play. This article discusses common upper extremity injuries observed in soccer players, focusing on proper diagnosis and optimal management.

Continue to: Upper limb injuries in association with soccer...

Upper limb injuries in association with soccer have been reported to represent only 3% of all time-loss injuries in professional soccer players¹. However, they are considered an increasing problem in recent years^2-4 and have been reported in high proportions in children under the age of 15 years.⁵ Some of the reasons for the increase in upper extremity injuries may be explained by modern soccer tactics that have been characterized by high speed, pressing, and marking.² Furthermore, upper extremity injuries may still be underestimated in soccer, mainly because outfield players are sometimes able to train and play even when they suffer from an upper extremity injury.

ABSTRACT

Upper limb injuries in soccer represent only a marginal portion of injuries, however this is mainly true for outfield players. Goalkeepers are reported to have up to 5 times more upper extremity injuries, many of them requiring substantial time-loss for treatment and rehabilitation. The most common upper extremity injury locations are the shoulder/clavicle followed by the hand/finger/thumb, elbow, wrist, forearm, and upper arm. The mechanism of injury, presentation, physical examination, and imaging features all play a significant role in reaching the correct diagnosis. Taking to consideration the position the player plays and his demands will also enable tailoring the optimal treatment plan that allows timely and safe return to play. This article discusses common upper extremity injuries observed in soccer players, focusing on proper diagnosis and optimal management.

Continue to: Upper limb injuries in association with soccer...

Upper limb injuries in association with soccer have been reported to represent only 3% of all time-loss injuries in professional soccer players¹. However, they are considered an increasing problem in recent years^2-4 and have been reported in high proportions in children under the age of 15 years.⁵ Some of the reasons for the increase in upper extremity injuries may be explained by modern soccer tactics that have been characterized by high speed, pressing, and marking.² Furthermore, upper extremity injuries may still be underestimated in soccer, mainly because outfield players are sometimes able to train and play even when they suffer from an upper extremity injury.

ABSTRACT

Upper limb injuries in soccer represent only a marginal portion of injuries, however this is mainly true for outfield players. Goalkeepers are reported to have up to 5 times more upper extremity injuries, many of them requiring substantial time-loss for treatment and rehabilitation. The most common upper extremity injury locations are the shoulder/clavicle followed by the hand/finger/thumb, elbow, wrist, forearm, and upper arm. The mechanism of injury, presentation, physical examination, and imaging features all play a significant role in reaching the correct diagnosis. Taking to consideration the position the player plays and his demands will also enable tailoring the optimal treatment plan that allows timely and safe return to play. This article discusses common upper extremity injuries observed in soccer players, focusing on proper diagnosis and optimal management.

Continue to: Upper limb injuries in association with soccer...

Upper limb injuries in association with soccer have been reported to represent only 3% of all time-loss injuries in professional soccer players¹. However, they are considered an increasing problem in recent years^2-4 and have been reported in high proportions in children under the age of 15 years.⁵ Some of the reasons for the increase in upper extremity injuries may be explained by modern soccer tactics that have been characterized by high speed, pressing, and marking.² Furthermore, upper extremity injuries may still be underestimated in soccer, mainly because outfield players are sometimes able to train and play even when they suffer from an upper extremity injury.

Schizophrenia has a heterogeneous presentation including both positive and negative symptoms. It is a relatively common disorder, affecting 0.7% of the world’s population.^1,2 Schizophrenia is defined by abnormalities in two or more of five domains:³

• Delusions,
• Hallucinations,
• Disorganized thinking/speech (eg, frequent derailment or incoherence),
• Grossly disorganized or abnormal motor behavior (including catatonia), or
• Negative symptoms (ie, diminished emotional expression or avolition).

Schizophrenia is defined as having two or more of the above domains. Each must present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these must be delusions, hallucinations, or disorganized speech. This must cause dysfunction in a major area, such as work, interpersonal relations, or self-care. Signs of the disturbance persist for at least 6 months. If mood symptoms exist, they may only be present for a minority of the total duration of symptoms. Symptoms are not attributable to the physiological effects of a substance (eg, a drug of abuse, a medication) or another medical condition.³

If symptoms are present for less than 1 month, then the diagnosis is brief psychotic disorder. If symptoms are present between 1 month and 6 months, then the diagnosis is schizophreniform disorder. If a patient has only delusions but does not hallucinate; possesses disorganized speech, grossly disorganized, or catatonic behavior; and negative symptoms, then the diagnosis is delusional disorder.

The exact pathophysiology of schizophrenia is not known at this time. However, it is theorized to be a mix of biological and environmental factors leading to dysfunction of the neurotransmitters dopamine and glutamate, as well as structural changes to the brain.²

Methods

There is an abundance of research on schizophrenia in the psychiatry literature; however, much of this deals with chronic management in patients with established diagnoses, thus this may be hard to translate into the realities of emergency practice. At the same time, although schizophrenia is discussed in the emergency medicine literature, most ED-based research is performed in patients with undifferentiated agitation and not specifically on one diagnostic subset. Therefore, a narrative review was utilized in order to focus in on studies that are relevant to emergency practice.

A narrative literature search was performed utilizing PubMed, the Cochrane database, and American Psychiatric Association Practice Alerts for the past 3 years; bibliographies of major psychiatric textbooks; and reviews and clinical policies in the National Guidelines Clearinghouse.

Epidemiology

The lifetime prevalence of schizophrenia is approximately 0.3% to 0.7%.² In addition, schizophrenia is a frequently deadly disease as one meta-analysis found lifetime suicide to be 4.9 %, which is far higher than the average risk in the United States,⁴ which is approximately 0.5%. From 1992 to 2000 there has been a 15% increase in ED visits for psychiatric problems.⁵ Patients with schizophrenia have been found to be significantly more likely to be “high utilizers” of ED services in comparison to those with other psychiatric diagnoses.⁶

The increase in psychiatric presentations to EDs is coupled with a lack of psychiatrists in many areas of the United States. The American Hospital Association has reported that 40% of American hospitals have difficulty maintaining adequate psychiatric coverage to meet patient demand in the ED, forcing many emergency medicine physicians to act as a primary psychiatrist.⁷

Differential Diagnosis

The characteristic symptoms of schizophrenia can be present in many other illnesses; therefore, the emergency clinician must be able to distinguish schizophrenia from other illnesses presenting with a psychotic component. Furthermore, schizophrenia is a diagnosis of exclusion as the diagnosis can only be made after all medical etiologies of the symptoms have been excluded.

Items on the differential include delirium, a substance induced psychosis,⁸ which can be caused by both substance intoxication and substance withdrawal; as well as psychosis caused by another medical condition.⁸ It should be stressed that a prior diagnosis of schizophrenia does not rule out a medical etiology of a patient’s current psychotic episode; therefore, a thorough history and examination is fundamental, even in patients with a known history of psychiatric illness. Moreover, many patients with schizophrenia present with a medical chief complaint, despite being symptomatic regarding their schizophrenia. In the latter case, providers must be vigilant regarding any medical comorbidities, particularly when patients are actively psychotic.

Finally, within the psychiatric disorders there are multiple disorders other than schizophrenia that may have psychotic features, including depression with psychotic features, bipolar disorder with psychotic features, and the other schizophrenia spectrum disorders; including brief psychotic disorder, schizophreniform disorder, schizoaffective disorder, and delusional disorder.

Emergency Department Evaluation

The process of evaluation of psychiatric patients who present to the ED should be directed towards a determination as to whether hospitalization is warranted, treatment of underlying medical condition is needed, or psychiatric care is indicated. New onset of psychiatric illness will commonly call for extensive evaluation, whereas patients with chronic schizophrenia may not need testing but may need psychiatric hospitalization.⁹ Additionally, emergency clinicians are frequently requested to preform “medical clearance” by their psychiatrist colleagues, before a patient can be transferred to a psychiatry department or psychiatric hospital. However, this is a poor term and a better nomenclature would be “assess for medical stability.”⁹ Emergency clinicians are, in essence, being asked whether the patient is medically stable enough for transfer to a unit or hospital where there is little or no medical support. Prior to transfer to a psychiatric unit, a patient’s non-psychiatric medical conditions should be stable enough for outpatient management.

Interacting with Patients Suffering from Psychosis

Although providers should not pretend to interact in the patient’s reality, they should express understanding in what the patient thinks or feels and kindly direct them back to the current situation.¹⁰ It is important for providers in the acute setting to be non-judgmental about reasons for relapse (in particular non-adherence to medication or substance misuse).¹⁰ Challenging the patient, while at times useful, is best done once the patient is stabilized and in a controlled environment.

History

The history should focus on age of onset; prior history of psychiatric symptoms; history of medical illness and use or abuse of illicit substances, as well as medications; the stability of psychotic symptoms; and if hallucinations are present, whether they are auditory or visual in nature.¹⁰ Table 1 highlights the differences between a patient presenting with a psychiatric complaint and the psychotic symptoms secondary to a medical illness. Table 2 provides salient differences between the examination of a patient with psychosis due to a psychiatric illness or another medical condition. Additionally, Table 3 lists various features, which differentiates schizophrenia from other psychiatric illnesses.

Additionally, patients with schizophrenia can become just as physically ill as anyone else; however, they may have difficulty expressing their specific physical complaints. Furthermore, patients with schizophrenia have a pronounced incidence of early death compared to the general population.¹¹ Therefore, performing a simple physical examination and paying attention to vital signs can rule out or detect a great deal of organic pathology.¹²Once a diagnosis of schizophrenia is made, the next priority is to determine whether the patient is a threat to themselves or others and whether this threat is imminent or not. Statements of suicidal or homicidal ideation, intent, and/or plan are the basic methods of screening for danger. However, physicians also need to screen for command auditory hallucinations, prior history of suicidal behavior, and violence. Finally, even in a patient with previously diagnosed schizophrenia, screening must also be done for substance intoxication and withdrawal.

Diagnostic Studies

The indications for diagnostic studies are influenced by whether the presentation is experiencing first break psychoses vs a presentation in a patient with known schizophrenia. In the former case there is a greater need for laboratory and other diagnostic tests. In the latter case minimal testing will likely be necessary. Patients with new onset psychiatric symptoms generally need extensive laboratory and radiographic evaluations, including a computed tomography scan of the head.⁹

For patients who have an established schizophrenia, extensive evidence supports that there is no need for testing and indeed more often results in false positives,^11,13and selective testing based on findings in the history and physical examination is the correct strategy.¹¹

Complicating the decision to obtain laboratory tests is the fact that many psychiatric facilities rely on referring hospitals to perform baseline testing, as they do not have the resources to perform the tests or to manage any identified abnormalities. Therefore, some tests are needed prior to transfer. In addition, at times, baseline laboratory tests are needed prior to starting antipsychotics.¹⁴

Additionally, some tests are unlikely to affect immediate disposition or treatment but may be useful to psychiatrists for long-term treatment planning.¹⁵ A common disagreement between psychiatrists and emergency providers is the urine toxicology screen or a blood alcohol level. Urine toxicology or a blood alcohol level does not usually affect initial treatment and disposition in the ED.^11,16 However, it may be invalid if collected subsequent to a transfer from the ED, and can determine whether a patient requires specific substance use disorder treatment or not.^16-18 Therefore, many psychiatric providers will request a urine toxicology screening or a blood alcohol level before accepting a transfer. Please note, urine toxicology screens only identify a small number of toxic ingestions. Therefore, a negative screen does not eliminate drug abuse or overdose.

Finally, in the case that a diagnostic examination is being done to satisfy a requirement for an institution to accept a patient or to assist in long-term treatment planning, disposition should not be delayed in order to wait for the result to return.¹¹

Treatment

Unfortunately, no level I or II studies have been found that examine the indications for treatment of the psychiatric patient in the ED.⁹ Additionally, in the ED, there is an ill-defined difference between the use of psychotropic medications as an intervention after patient assessment and plan of care, and the use of these medications to control behavior without an assessment and treatment plan.⁹ Therefore, many treatment recommendations have been made based on studies in other settings.

The first line treatment for a patient with schizophrenia is monotherapy with an antipsychotic agent other than clozapine.^19-21 (Clozapine is not used as a first line agent due to its high side effect burden and the testing necessary before starting.) This is supported by multiple randomized controlled trials and is the standard of care.^22-24 The response rates in treatment with antipsychotics in studies specifically designed to examine treatment of first-episode schizophrenia are high, ranging from 46% to 96%.²³ Therefore, the emergency medicine provider can confidently reassure patients and families that antipsychotic medications are effective in treating schizophrenia. Loading doses of antipsychotics should not be used.¹⁹

Although there are only small and inconsistent differences between different antipsychotics, other than clozapine, with respect to efficacy, there are large differences in adverse effect profiles.^25-30Therefore, the choice of antipsychotic medication is generally made based on previous response to individual antipsychotic medications and relative side effects.³¹

If extrapyramidal symptoms, including tardive dyskinesia, are of particular concern to a patient, then second generation or low potency first generation antipsychotics should be used.^25,32 If a patient complains of previous problems with sedation, then haloperidol or aripiprazole should be preferred.²⁵ Haloperidol, aripiprazole, or amisulpride should be considered for patients who are particularly concerned about weight gain, or who may be at the greatest risk of weight gain.²⁵

If there is no response to medication after 4 weeks,³² despite dose optimization, a change in antipsychotic should be considered.^33,34 Where there is partial response, the patient should be re-assessed after 8 weeks unless there are significant adverse effects.^14,19,20,34 A combination of different antipsychotic medications should not be used, except during transitional periods when patients are being switched from one antipsychotic to another, or when used for clozapine augmentation.¹⁴After an acute episode has passed, providers can consider offering depot/long-acting injectable antipsychotic medication to people with schizophrenia who would prefer such treatment; as long acting injectable antipsychotics have been shown to reduce medication non-adherence.^35,36 Long-acting depot antipsychotics should not be used for acute episodes because it may take 3 to 6 months for the medications to reach a stable state.¹⁴Once a patient achieves a remission of their symptoms, patients are recommended to stay on their antipsychotic medication for at least 2 years since their last acute exacerbation.^14,34 For maintenance therapy,the antipsychotic dose should be reduced gradually to the lowest possible effective dose, which should not be lower than half of the effective dose during the acute phase.³⁷

Clozapine should be offered to people with schizophrenia whose illness has not responded adequately to treatment with adequate doses of at least two different antipsychotic drugs.^38-41There is no indication to using dual antipsychotic agents on patients with schizophrenia prior to starting a clozapine trial.^42,43

Non-Pharmacological Intervention

There is strong evidence that people diagnosed with schizophrenia benefit from psychosocial treatments in addition to pharmacological treatment. Multiple randomized controlled studies, as well as national guidelines, have demonstrated cognitive behavioral therapy and family therapy to be effective for the treatment of schizophrenia.^44-51 Particular focuses of therapy include communication skills, problem solving, psychoeducation, and assisting with family conflict,^18,19 which are feasible in an emergency setting.⁵²

Recent studies have shown promise using a “crisis intervention” approach as an alternative option to the hospital or emergency medical services systems. Treatment usually involves a combination of medication as well as counseling (practical help with living skills and support for close family members). After the crisis has been stabilized, sufferers are carefully introduced to other models of care more suited for the chronic phases of psychiatric illnesses.⁵³ This is particularly important as psychosocial instability, such as changes in the psychosocial environment (ie, a primary caretaker going on vacation, or a patient being distanced from their family or support environment) have been associated with relapse.¹⁹

Acute Agitation

The vast majority of patients suffering from mental illness, including schizophrenia, are not violent and only a small proportion of the violence in our society can be attributed to persons who are mentally ill.⁵⁴ Furthermore, people with psychiatric disabilities are far more likely to be victims than perpetrators of violent crime.⁵⁵ However, schizophrenia and related disorders are associated with substantially increased rates of violence and violent offences compared to those who did not, independent of substance use.^56,57 Furthermore, the majority of acute hospital assaults occur in the ED.⁵⁸

Two emergency medicine evidence-based guidelines state a benzodiazepine (lorazepam or midazolam) or a conventional antipsychotic (droperidol or haloperidol) should be used as monotherapy for the treatment of acute undifferentiated agitation in the ED.^12,59 However, in cases of patients with a diagnosis or suspicion of schizophrenia, an antipsychotic should be used in order to start a “disease modifying agent” earlier in the course of treatment.^20,59,60Where possible, the same antipsychotic should be used as monotherapy for treatment of both acute agitation and standing antipsychotic medication.¹³The choice of medication for the treatment of acute agitation should be based on patient preference, past experience of antipsychotic treatment, the adverse effect profile, and concurrent medical history.^19,58 This is supported by a case controlled study, which showed patients’ subjective experiences in the acute phase of treatment affected their long-term adherence to medication.⁶¹

Haloperidol is the most commonly used medication for agitation in patients with schizophrenia.^59,62 When haloperidol is used to treat acute violence, it is almost always used in combination with a benzodiazepine unless medically compromised.^62,63 Intramuscular olanzapine has been shown to be effective in managing acute aggression or agitation in patients with schizophrenia, especially where it is necessary to avoid some of the older treatments. Olanzapine causes fewer movement disorders than halopridol.⁶⁴ Chlorpromazine is available in both per os and intramuscular formulations. However, chlorpromazine is associated with more side effects than other antipsychotics, including a higher incidence of prolonged QT and Torsades.⁶⁵ However, where choices are limited, chlorpromazine may be the only treatment available for acute agitation. If used, the close monitoring of blood pressure is indicated.⁶⁵ Inhaled loxapine received US Food and Drug Administration approval for treatment of acute agitation in 2012.⁶⁶ This is a useful option for an agitated patient who is calm enough to receive an inhaler, but is unable to take medication per os.

Restrictive intervention (restraints or seclusion) should only be used if de-escalation and other preventive strategies, including medication as needed, have failed and there is potential for harm to the patient or other people if no action is taken.⁵⁸

Telepsychiatry Consultation

Telepsychiatry is an approach, where by EDs that do not have access to psychiatrists can see patients in the ED itself, by forming a contract with either psychiatrists or companies to allow a psychiatrist at another location to perform an examination on a patient via video connection and advise the emergency room providers on treatment and intervention. There is very little data in the peer-reviewed literature on the use of telepsychiatry. The literature is limited to case reports, program descriptions, and randomized studies for reliability.^67,68 One randomized controlled trial showed that a telepsychiatry evaluation had a reliable diagnosis and disposition when compared to a face-to-face assessment.⁶⁹ One case control showed reduction in time-to-consult done in the ED, length of stay, and door-to-consult stay, once a telepsychiatry program was initiated.⁷⁰ A large case control study showed that telepsychiatry recipients were more likely to receive 30-day follow-up, 90-day follow-up, and total inpatient length of stay, totaling both initial admission and subsequent admissions.⁷¹ Therefore, it is reasonable for EDs to take advantage of telepsychiatry services if no immediate psychiatrist coverage is available.

Disposition

The primary disposition question regarding a patient presenting with a psychiatric chief complaint to the ED, including schizophrenia, is whether they require a psychiatric admission or not. If a patient requires hospitalization but refuses, the emergency clinician must decide if the patient meets criteria for involuntarily hospitalization. If a patient does not require an inpatient admission or would benefit from an inpatient admission but does not meet criteria for civil commitment, then the next major question is what type of outpatient treatment is sufficient for this particular patient (Figure).

For a patient with schizophrenia to require inpatient psychiatric admission he must be either a danger to himself or others or has failed outpatient treatment. In addition, the patient must currently have undergone a clinical evaluation of any suspected medical illness, and any medical problems the patient is experiencing must be sufficiently stable to allow safe transport and treatment at a psychiatric hospital unit.⁹ If a patient’s medical condition is not sufficiently stable for either transport or hospitalization at a psychiatric hospital but the patient still requires inpatient psychiatric treatment, the patient should be hospitalized on a standard medical ward and receive psychiatric care on that unit.

Patients with mental illness pose an additional challenge, in that their illness often time interferes with their judgment about whether they require treatment. Because of this possible lack of capacity and the potential danger of a patient with mental illness to self or others, most jurisdictions have a legal code that allows for involuntary hospitalization of the mentally ill. However, which patients qualify for involuntary hospitalizations vary by jurisdiction. Case law criteria for emergencies range from a risk of “imminent” harm to self or others to a deterioration in the patient’s mental condition if treatment is halted.⁷² Providers are recommended to familiarize themselves with laws regarding inpatient civil commitment in their particular jurisdiction.

When a patient is being discharged from the ED, either because they do not require a psychiatric inpatient admission or because they don’t meet criteria for involuntary commitment, there are various outpatient dispositions available. Any patient with a diagnosis of schizophrenia should have outpatient follow-up with a mental health provider upon discharge from the ED.

For patients who have a failed community treatment in the past, who do not have a significant support network, or whose disease is too severe for a regular outpatient clinic to handle would be better suited for a disposition to a transitional program over a standard outpatient appointment; such as partial hospitalization programs, intensive outpatient programs, and community mental health treatment teams (CMHT). Assertive community treatment (ACT) teams are a form of CMHT comprised of several disciplines, including nurses, occupational therapists, psychiatrists, psychologists, and social workers.⁷³ A large prospective cohort study found homeless patients to have made gains in multiple spheres of mental health while enrolled in ACT programs, and these benefits were retained after discharge from the ACT program.⁷⁴

Conclusion

Schizophrenia is characterized primarily by delusions, hallucinations, and disorganized thinking. Emergency medicine providers are frequently at the front lines of diagnosing, initiating treatment, and managing relapses for these individuals. As schizophrenia is an exclusion, the primary task of an emergency physician is to rule out all “organic”, for lack of a better term, causes of the psychosis or disordered thinking before making a definitive diagnosis of schizophrenia. As many EDs do not have sufficient psychiatry support and many patients with schizophrenia are using the ED as their location for primary mental health, many emergency physicians are finding themselves acting as the main providers for these individuals. The primary treatment for patients with schizophrenia remains monotherapy with antipsychotic medication. Although the highest-level disposition for a patient with schizophrenia remains the inpatient psychiatry department, there are many transitional dispositions that can bridge the gap between a discharge to standard community care and an inpatient admission.

Schizophrenia has a heterogeneous presentation including both positive and negative symptoms. It is a relatively common disorder, affecting 0.7% of the world’s population.^1,2 Schizophrenia is defined by abnormalities in two or more of five domains:³

• Delusions,
• Hallucinations,
• Disorganized thinking/speech (eg, frequent derailment or incoherence),
• Grossly disorganized or abnormal motor behavior (including catatonia), or
• Negative symptoms (ie, diminished emotional expression or avolition).

Schizophrenia is defined as having two or more of the above domains. Each must present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these must be delusions, hallucinations, or disorganized speech. This must cause dysfunction in a major area, such as work, interpersonal relations, or self-care. Signs of the disturbance persist for at least 6 months. If mood symptoms exist, they may only be present for a minority of the total duration of symptoms. Symptoms are not attributable to the physiological effects of a substance (eg, a drug of abuse, a medication) or another medical condition.³

If symptoms are present for less than 1 month, then the diagnosis is brief psychotic disorder. If symptoms are present between 1 month and 6 months, then the diagnosis is schizophreniform disorder. If a patient has only delusions but does not hallucinate; possesses disorganized speech, grossly disorganized, or catatonic behavior; and negative symptoms, then the diagnosis is delusional disorder.

The exact pathophysiology of schizophrenia is not known at this time. However, it is theorized to be a mix of biological and environmental factors leading to dysfunction of the neurotransmitters dopamine and glutamate, as well as structural changes to the brain.²

Methods

There is an abundance of research on schizophrenia in the psychiatry literature; however, much of this deals with chronic management in patients with established diagnoses, thus this may be hard to translate into the realities of emergency practice. At the same time, although schizophrenia is discussed in the emergency medicine literature, most ED-based research is performed in patients with undifferentiated agitation and not specifically on one diagnostic subset. Therefore, a narrative review was utilized in order to focus in on studies that are relevant to emergency practice.

A narrative literature search was performed utilizing PubMed, the Cochrane database, and American Psychiatric Association Practice Alerts for the past 3 years; bibliographies of major psychiatric textbooks; and reviews and clinical policies in the National Guidelines Clearinghouse.

Epidemiology

The lifetime prevalence of schizophrenia is approximately 0.3% to 0.7%.² In addition, schizophrenia is a frequently deadly disease as one meta-analysis found lifetime suicide to be 4.9 %, which is far higher than the average risk in the United States,⁴ which is approximately 0.5%. From 1992 to 2000 there has been a 15% increase in ED visits for psychiatric problems.⁵ Patients with schizophrenia have been found to be significantly more likely to be “high utilizers” of ED services in comparison to those with other psychiatric diagnoses.⁶

The increase in psychiatric presentations to EDs is coupled with a lack of psychiatrists in many areas of the United States. The American Hospital Association has reported that 40% of American hospitals have difficulty maintaining adequate psychiatric coverage to meet patient demand in the ED, forcing many emergency medicine physicians to act as a primary psychiatrist.⁷

Differential Diagnosis

The characteristic symptoms of schizophrenia can be present in many other illnesses; therefore, the emergency clinician must be able to distinguish schizophrenia from other illnesses presenting with a psychotic component. Furthermore, schizophrenia is a diagnosis of exclusion as the diagnosis can only be made after all medical etiologies of the symptoms have been excluded.

Items on the differential include delirium, a substance induced psychosis,⁸ which can be caused by both substance intoxication and substance withdrawal; as well as psychosis caused by another medical condition.⁸ It should be stressed that a prior diagnosis of schizophrenia does not rule out a medical etiology of a patient’s current psychotic episode; therefore, a thorough history and examination is fundamental, even in patients with a known history of psychiatric illness. Moreover, many patients with schizophrenia present with a medical chief complaint, despite being symptomatic regarding their schizophrenia. In the latter case, providers must be vigilant regarding any medical comorbidities, particularly when patients are actively psychotic.

Finally, within the psychiatric disorders there are multiple disorders other than schizophrenia that may have psychotic features, including depression with psychotic features, bipolar disorder with psychotic features, and the other schizophrenia spectrum disorders; including brief psychotic disorder, schizophreniform disorder, schizoaffective disorder, and delusional disorder.

Emergency Department Evaluation

The process of evaluation of psychiatric patients who present to the ED should be directed towards a determination as to whether hospitalization is warranted, treatment of underlying medical condition is needed, or psychiatric care is indicated. New onset of psychiatric illness will commonly call for extensive evaluation, whereas patients with chronic schizophrenia may not need testing but may need psychiatric hospitalization.⁹ Additionally, emergency clinicians are frequently requested to preform “medical clearance” by their psychiatrist colleagues, before a patient can be transferred to a psychiatry department or psychiatric hospital. However, this is a poor term and a better nomenclature would be “assess for medical stability.”⁹ Emergency clinicians are, in essence, being asked whether the patient is medically stable enough for transfer to a unit or hospital where there is little or no medical support. Prior to transfer to a psychiatric unit, a patient’s non-psychiatric medical conditions should be stable enough for outpatient management.

Interacting with Patients Suffering from Psychosis

Although providers should not pretend to interact in the patient’s reality, they should express understanding in what the patient thinks or feels and kindly direct them back to the current situation.¹⁰ It is important for providers in the acute setting to be non-judgmental about reasons for relapse (in particular non-adherence to medication or substance misuse).¹⁰ Challenging the patient, while at times useful, is best done once the patient is stabilized and in a controlled environment.

History

The history should focus on age of onset; prior history of psychiatric symptoms; history of medical illness and use or abuse of illicit substances, as well as medications; the stability of psychotic symptoms; and if hallucinations are present, whether they are auditory or visual in nature.¹⁰ Table 1 highlights the differences between a patient presenting with a psychiatric complaint and the psychotic symptoms secondary to a medical illness. Table 2 provides salient differences between the examination of a patient with psychosis due to a psychiatric illness or another medical condition. Additionally, Table 3 lists various features, which differentiates schizophrenia from other psychiatric illnesses.

Additionally, patients with schizophrenia can become just as physically ill as anyone else; however, they may have difficulty expressing their specific physical complaints. Furthermore, patients with schizophrenia have a pronounced incidence of early death compared to the general population.¹¹ Therefore, performing a simple physical examination and paying attention to vital signs can rule out or detect a great deal of organic pathology.¹²Once a diagnosis of schizophrenia is made, the next priority is to determine whether the patient is a threat to themselves or others and whether this threat is imminent or not. Statements of suicidal or homicidal ideation, intent, and/or plan are the basic methods of screening for danger. However, physicians also need to screen for command auditory hallucinations, prior history of suicidal behavior, and violence. Finally, even in a patient with previously diagnosed schizophrenia, screening must also be done for substance intoxication and withdrawal.

Diagnostic Studies

The indications for diagnostic studies are influenced by whether the presentation is experiencing first break psychoses vs a presentation in a patient with known schizophrenia. In the former case there is a greater need for laboratory and other diagnostic tests. In the latter case minimal testing will likely be necessary. Patients with new onset psychiatric symptoms generally need extensive laboratory and radiographic evaluations, including a computed tomography scan of the head.⁹

For patients who have an established schizophrenia, extensive evidence supports that there is no need for testing and indeed more often results in false positives,^11,13and selective testing based on findings in the history and physical examination is the correct strategy.¹¹

Complicating the decision to obtain laboratory tests is the fact that many psychiatric facilities rely on referring hospitals to perform baseline testing, as they do not have the resources to perform the tests or to manage any identified abnormalities. Therefore, some tests are needed prior to transfer. In addition, at times, baseline laboratory tests are needed prior to starting antipsychotics.¹⁴

Additionally, some tests are unlikely to affect immediate disposition or treatment but may be useful to psychiatrists for long-term treatment planning.¹⁵ A common disagreement between psychiatrists and emergency providers is the urine toxicology screen or a blood alcohol level. Urine toxicology or a blood alcohol level does not usually affect initial treatment and disposition in the ED.^11,16 However, it may be invalid if collected subsequent to a transfer from the ED, and can determine whether a patient requires specific substance use disorder treatment or not.^16-18 Therefore, many psychiatric providers will request a urine toxicology screening or a blood alcohol level before accepting a transfer. Please note, urine toxicology screens only identify a small number of toxic ingestions. Therefore, a negative screen does not eliminate drug abuse or overdose.

Finally, in the case that a diagnostic examination is being done to satisfy a requirement for an institution to accept a patient or to assist in long-term treatment planning, disposition should not be delayed in order to wait for the result to return.¹¹

Treatment

Unfortunately, no level I or II studies have been found that examine the indications for treatment of the psychiatric patient in the ED.⁹ Additionally, in the ED, there is an ill-defined difference between the use of psychotropic medications as an intervention after patient assessment and plan of care, and the use of these medications to control behavior without an assessment and treatment plan.⁹ Therefore, many treatment recommendations have been made based on studies in other settings.

The first line treatment for a patient with schizophrenia is monotherapy with an antipsychotic agent other than clozapine.^19-21 (Clozapine is not used as a first line agent due to its high side effect burden and the testing necessary before starting.) This is supported by multiple randomized controlled trials and is the standard of care.^22-24 The response rates in treatment with antipsychotics in studies specifically designed to examine treatment of first-episode schizophrenia are high, ranging from 46% to 96%.²³ Therefore, the emergency medicine provider can confidently reassure patients and families that antipsychotic medications are effective in treating schizophrenia. Loading doses of antipsychotics should not be used.¹⁹

Although there are only small and inconsistent differences between different antipsychotics, other than clozapine, with respect to efficacy, there are large differences in adverse effect profiles.^25-30Therefore, the choice of antipsychotic medication is generally made based on previous response to individual antipsychotic medications and relative side effects.³¹

If extrapyramidal symptoms, including tardive dyskinesia, are of particular concern to a patient, then second generation or low potency first generation antipsychotics should be used.^25,32 If a patient complains of previous problems with sedation, then haloperidol or aripiprazole should be preferred.²⁵ Haloperidol, aripiprazole, or amisulpride should be considered for patients who are particularly concerned about weight gain, or who may be at the greatest risk of weight gain.²⁵

If there is no response to medication after 4 weeks,³² despite dose optimization, a change in antipsychotic should be considered.^33,34 Where there is partial response, the patient should be re-assessed after 8 weeks unless there are significant adverse effects.^14,19,20,34 A combination of different antipsychotic medications should not be used, except during transitional periods when patients are being switched from one antipsychotic to another, or when used for clozapine augmentation.¹⁴After an acute episode has passed, providers can consider offering depot/long-acting injectable antipsychotic medication to people with schizophrenia who would prefer such treatment; as long acting injectable antipsychotics have been shown to reduce medication non-adherence.^35,36 Long-acting depot antipsychotics should not be used for acute episodes because it may take 3 to 6 months for the medications to reach a stable state.¹⁴Once a patient achieves a remission of their symptoms, patients are recommended to stay on their antipsychotic medication for at least 2 years since their last acute exacerbation.^14,34 For maintenance therapy,the antipsychotic dose should be reduced gradually to the lowest possible effective dose, which should not be lower than half of the effective dose during the acute phase.³⁷

Clozapine should be offered to people with schizophrenia whose illness has not responded adequately to treatment with adequate doses of at least two different antipsychotic drugs.^38-41There is no indication to using dual antipsychotic agents on patients with schizophrenia prior to starting a clozapine trial.^42,43

Non-Pharmacological Intervention

There is strong evidence that people diagnosed with schizophrenia benefit from psychosocial treatments in addition to pharmacological treatment. Multiple randomized controlled studies, as well as national guidelines, have demonstrated cognitive behavioral therapy and family therapy to be effective for the treatment of schizophrenia.^44-51 Particular focuses of therapy include communication skills, problem solving, psychoeducation, and assisting with family conflict,^18,19 which are feasible in an emergency setting.⁵²

Recent studies have shown promise using a “crisis intervention” approach as an alternative option to the hospital or emergency medical services systems. Treatment usually involves a combination of medication as well as counseling (practical help with living skills and support for close family members). After the crisis has been stabilized, sufferers are carefully introduced to other models of care more suited for the chronic phases of psychiatric illnesses.⁵³ This is particularly important as psychosocial instability, such as changes in the psychosocial environment (ie, a primary caretaker going on vacation, or a patient being distanced from their family or support environment) have been associated with relapse.¹⁹

Acute Agitation

The vast majority of patients suffering from mental illness, including schizophrenia, are not violent and only a small proportion of the violence in our society can be attributed to persons who are mentally ill.⁵⁴ Furthermore, people with psychiatric disabilities are far more likely to be victims than perpetrators of violent crime.⁵⁵ However, schizophrenia and related disorders are associated with substantially increased rates of violence and violent offences compared to those who did not, independent of substance use.^56,57 Furthermore, the majority of acute hospital assaults occur in the ED.⁵⁸

Two emergency medicine evidence-based guidelines state a benzodiazepine (lorazepam or midazolam) or a conventional antipsychotic (droperidol or haloperidol) should be used as monotherapy for the treatment of acute undifferentiated agitation in the ED.^12,59 However, in cases of patients with a diagnosis or suspicion of schizophrenia, an antipsychotic should be used in order to start a “disease modifying agent” earlier in the course of treatment.^20,59,60Where possible, the same antipsychotic should be used as monotherapy for treatment of both acute agitation and standing antipsychotic medication.¹³The choice of medication for the treatment of acute agitation should be based on patient preference, past experience of antipsychotic treatment, the adverse effect profile, and concurrent medical history.^19,58 This is supported by a case controlled study, which showed patients’ subjective experiences in the acute phase of treatment affected their long-term adherence to medication.⁶¹

Haloperidol is the most commonly used medication for agitation in patients with schizophrenia.^59,62 When haloperidol is used to treat acute violence, it is almost always used in combination with a benzodiazepine unless medically compromised.^62,63 Intramuscular olanzapine has been shown to be effective in managing acute aggression or agitation in patients with schizophrenia, especially where it is necessary to avoid some of the older treatments. Olanzapine causes fewer movement disorders than halopridol.⁶⁴ Chlorpromazine is available in both per os and intramuscular formulations. However, chlorpromazine is associated with more side effects than other antipsychotics, including a higher incidence of prolonged QT and Torsades.⁶⁵ However, where choices are limited, chlorpromazine may be the only treatment available for acute agitation. If used, the close monitoring of blood pressure is indicated.⁶⁵ Inhaled loxapine received US Food and Drug Administration approval for treatment of acute agitation in 2012.⁶⁶ This is a useful option for an agitated patient who is calm enough to receive an inhaler, but is unable to take medication per os.

Restrictive intervention (restraints or seclusion) should only be used if de-escalation and other preventive strategies, including medication as needed, have failed and there is potential for harm to the patient or other people if no action is taken.⁵⁸

Telepsychiatry Consultation

Telepsychiatry is an approach, where by EDs that do not have access to psychiatrists can see patients in the ED itself, by forming a contract with either psychiatrists or companies to allow a psychiatrist at another location to perform an examination on a patient via video connection and advise the emergency room providers on treatment and intervention. There is very little data in the peer-reviewed literature on the use of telepsychiatry. The literature is limited to case reports, program descriptions, and randomized studies for reliability.^67,68 One randomized controlled trial showed that a telepsychiatry evaluation had a reliable diagnosis and disposition when compared to a face-to-face assessment.⁶⁹ One case control showed reduction in time-to-consult done in the ED, length of stay, and door-to-consult stay, once a telepsychiatry program was initiated.⁷⁰ A large case control study showed that telepsychiatry recipients were more likely to receive 30-day follow-up, 90-day follow-up, and total inpatient length of stay, totaling both initial admission and subsequent admissions.⁷¹ Therefore, it is reasonable for EDs to take advantage of telepsychiatry services if no immediate psychiatrist coverage is available.

Disposition

The primary disposition question regarding a patient presenting with a psychiatric chief complaint to the ED, including schizophrenia, is whether they require a psychiatric admission or not. If a patient requires hospitalization but refuses, the emergency clinician must decide if the patient meets criteria for involuntarily hospitalization. If a patient does not require an inpatient admission or would benefit from an inpatient admission but does not meet criteria for civil commitment, then the next major question is what type of outpatient treatment is sufficient for this particular patient (Figure).

For a patient with schizophrenia to require inpatient psychiatric admission he must be either a danger to himself or others or has failed outpatient treatment. In addition, the patient must currently have undergone a clinical evaluation of any suspected medical illness, and any medical problems the patient is experiencing must be sufficiently stable to allow safe transport and treatment at a psychiatric hospital unit.⁹ If a patient’s medical condition is not sufficiently stable for either transport or hospitalization at a psychiatric hospital but the patient still requires inpatient psychiatric treatment, the patient should be hospitalized on a standard medical ward and receive psychiatric care on that unit.

Patients with mental illness pose an additional challenge, in that their illness often time interferes with their judgment about whether they require treatment. Because of this possible lack of capacity and the potential danger of a patient with mental illness to self or others, most jurisdictions have a legal code that allows for involuntary hospitalization of the mentally ill. However, which patients qualify for involuntary hospitalizations vary by jurisdiction. Case law criteria for emergencies range from a risk of “imminent” harm to self or others to a deterioration in the patient’s mental condition if treatment is halted.⁷² Providers are recommended to familiarize themselves with laws regarding inpatient civil commitment in their particular jurisdiction.

When a patient is being discharged from the ED, either because they do not require a psychiatric inpatient admission or because they don’t meet criteria for involuntary commitment, there are various outpatient dispositions available. Any patient with a diagnosis of schizophrenia should have outpatient follow-up with a mental health provider upon discharge from the ED.

For patients who have a failed community treatment in the past, who do not have a significant support network, or whose disease is too severe for a regular outpatient clinic to handle would be better suited for a disposition to a transitional program over a standard outpatient appointment; such as partial hospitalization programs, intensive outpatient programs, and community mental health treatment teams (CMHT). Assertive community treatment (ACT) teams are a form of CMHT comprised of several disciplines, including nurses, occupational therapists, psychiatrists, psychologists, and social workers.⁷³ A large prospective cohort study found homeless patients to have made gains in multiple spheres of mental health while enrolled in ACT programs, and these benefits were retained after discharge from the ACT program.⁷⁴

Conclusion

Schizophrenia is characterized primarily by delusions, hallucinations, and disorganized thinking. Emergency medicine providers are frequently at the front lines of diagnosing, initiating treatment, and managing relapses for these individuals. As schizophrenia is an exclusion, the primary task of an emergency physician is to rule out all “organic”, for lack of a better term, causes of the psychosis or disordered thinking before making a definitive diagnosis of schizophrenia. As many EDs do not have sufficient psychiatry support and many patients with schizophrenia are using the ED as their location for primary mental health, many emergency physicians are finding themselves acting as the main providers for these individuals. The primary treatment for patients with schizophrenia remains monotherapy with antipsychotic medication. Although the highest-level disposition for a patient with schizophrenia remains the inpatient psychiatry department, there are many transitional dispositions that can bridge the gap between a discharge to standard community care and an inpatient admission.

Schizophrenia has a heterogeneous presentation including both positive and negative symptoms. It is a relatively common disorder, affecting 0.7% of the world’s population.^1,2 Schizophrenia is defined by abnormalities in two or more of five domains:³

• Delusions,
• Hallucinations,
• Disorganized thinking/speech (eg, frequent derailment or incoherence),
• Grossly disorganized or abnormal motor behavior (including catatonia), or
• Negative symptoms (ie, diminished emotional expression or avolition).

Schizophrenia is defined as having two or more of the above domains. Each must present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these must be delusions, hallucinations, or disorganized speech. This must cause dysfunction in a major area, such as work, interpersonal relations, or self-care. Signs of the disturbance persist for at least 6 months. If mood symptoms exist, they may only be present for a minority of the total duration of symptoms. Symptoms are not attributable to the physiological effects of a substance (eg, a drug of abuse, a medication) or another medical condition.³

If symptoms are present for less than 1 month, then the diagnosis is brief psychotic disorder. If symptoms are present between 1 month and 6 months, then the diagnosis is schizophreniform disorder. If a patient has only delusions but does not hallucinate; possesses disorganized speech, grossly disorganized, or catatonic behavior; and negative symptoms, then the diagnosis is delusional disorder.

The exact pathophysiology of schizophrenia is not known at this time. However, it is theorized to be a mix of biological and environmental factors leading to dysfunction of the neurotransmitters dopamine and glutamate, as well as structural changes to the brain.²

Methods

There is an abundance of research on schizophrenia in the psychiatry literature; however, much of this deals with chronic management in patients with established diagnoses, thus this may be hard to translate into the realities of emergency practice. At the same time, although schizophrenia is discussed in the emergency medicine literature, most ED-based research is performed in patients with undifferentiated agitation and not specifically on one diagnostic subset. Therefore, a narrative review was utilized in order to focus in on studies that are relevant to emergency practice.

A narrative literature search was performed utilizing PubMed, the Cochrane database, and American Psychiatric Association Practice Alerts for the past 3 years; bibliographies of major psychiatric textbooks; and reviews and clinical policies in the National Guidelines Clearinghouse.

Epidemiology

The lifetime prevalence of schizophrenia is approximately 0.3% to 0.7%.² In addition, schizophrenia is a frequently deadly disease as one meta-analysis found lifetime suicide to be 4.9 %, which is far higher than the average risk in the United States,⁴ which is approximately 0.5%. From 1992 to 2000 there has been a 15% increase in ED visits for psychiatric problems.⁵ Patients with schizophrenia have been found to be significantly more likely to be “high utilizers” of ED services in comparison to those with other psychiatric diagnoses.⁶

The increase in psychiatric presentations to EDs is coupled with a lack of psychiatrists in many areas of the United States. The American Hospital Association has reported that 40% of American hospitals have difficulty maintaining adequate psychiatric coverage to meet patient demand in the ED, forcing many emergency medicine physicians to act as a primary psychiatrist.⁷

Differential Diagnosis

The characteristic symptoms of schizophrenia can be present in many other illnesses; therefore, the emergency clinician must be able to distinguish schizophrenia from other illnesses presenting with a psychotic component. Furthermore, schizophrenia is a diagnosis of exclusion as the diagnosis can only be made after all medical etiologies of the symptoms have been excluded.

Items on the differential include delirium, a substance induced psychosis,⁸ which can be caused by both substance intoxication and substance withdrawal; as well as psychosis caused by another medical condition.⁸ It should be stressed that a prior diagnosis of schizophrenia does not rule out a medical etiology of a patient’s current psychotic episode; therefore, a thorough history and examination is fundamental, even in patients with a known history of psychiatric illness. Moreover, many patients with schizophrenia present with a medical chief complaint, despite being symptomatic regarding their schizophrenia. In the latter case, providers must be vigilant regarding any medical comorbidities, particularly when patients are actively psychotic.

Finally, within the psychiatric disorders there are multiple disorders other than schizophrenia that may have psychotic features, including depression with psychotic features, bipolar disorder with psychotic features, and the other schizophrenia spectrum disorders; including brief psychotic disorder, schizophreniform disorder, schizoaffective disorder, and delusional disorder.

Emergency Department Evaluation

The process of evaluation of psychiatric patients who present to the ED should be directed towards a determination as to whether hospitalization is warranted, treatment of underlying medical condition is needed, or psychiatric care is indicated. New onset of psychiatric illness will commonly call for extensive evaluation, whereas patients with chronic schizophrenia may not need testing but may need psychiatric hospitalization.⁹ Additionally, emergency clinicians are frequently requested to preform “medical clearance” by their psychiatrist colleagues, before a patient can be transferred to a psychiatry department or psychiatric hospital. However, this is a poor term and a better nomenclature would be “assess for medical stability.”⁹ Emergency clinicians are, in essence, being asked whether the patient is medically stable enough for transfer to a unit or hospital where there is little or no medical support. Prior to transfer to a psychiatric unit, a patient’s non-psychiatric medical conditions should be stable enough for outpatient management.

Interacting with Patients Suffering from Psychosis

Although providers should not pretend to interact in the patient’s reality, they should express understanding in what the patient thinks or feels and kindly direct them back to the current situation.¹⁰ It is important for providers in the acute setting to be non-judgmental about reasons for relapse (in particular non-adherence to medication or substance misuse).¹⁰ Challenging the patient, while at times useful, is best done once the patient is stabilized and in a controlled environment.

History

The history should focus on age of onset; prior history of psychiatric symptoms; history of medical illness and use or abuse of illicit substances, as well as medications; the stability of psychotic symptoms; and if hallucinations are present, whether they are auditory or visual in nature.¹⁰ Table 1 highlights the differences between a patient presenting with a psychiatric complaint and the psychotic symptoms secondary to a medical illness. Table 2 provides salient differences between the examination of a patient with psychosis due to a psychiatric illness or another medical condition. Additionally, Table 3 lists various features, which differentiates schizophrenia from other psychiatric illnesses.

Additionally, patients with schizophrenia can become just as physically ill as anyone else; however, they may have difficulty expressing their specific physical complaints. Furthermore, patients with schizophrenia have a pronounced incidence of early death compared to the general population.¹¹ Therefore, performing a simple physical examination and paying attention to vital signs can rule out or detect a great deal of organic pathology.¹²Once a diagnosis of schizophrenia is made, the next priority is to determine whether the patient is a threat to themselves or others and whether this threat is imminent or not. Statements of suicidal or homicidal ideation, intent, and/or plan are the basic methods of screening for danger. However, physicians also need to screen for command auditory hallucinations, prior history of suicidal behavior, and violence. Finally, even in a patient with previously diagnosed schizophrenia, screening must also be done for substance intoxication and withdrawal.

Diagnostic Studies

The indications for diagnostic studies are influenced by whether the presentation is experiencing first break psychoses vs a presentation in a patient with known schizophrenia. In the former case there is a greater need for laboratory and other diagnostic tests. In the latter case minimal testing will likely be necessary. Patients with new onset psychiatric symptoms generally need extensive laboratory and radiographic evaluations, including a computed tomography scan of the head.⁹

For patients who have an established schizophrenia, extensive evidence supports that there is no need for testing and indeed more often results in false positives,^11,13and selective testing based on findings in the history and physical examination is the correct strategy.¹¹

Complicating the decision to obtain laboratory tests is the fact that many psychiatric facilities rely on referring hospitals to perform baseline testing, as they do not have the resources to perform the tests or to manage any identified abnormalities. Therefore, some tests are needed prior to transfer. In addition, at times, baseline laboratory tests are needed prior to starting antipsychotics.¹⁴

Additionally, some tests are unlikely to affect immediate disposition or treatment but may be useful to psychiatrists for long-term treatment planning.¹⁵ A common disagreement between psychiatrists and emergency providers is the urine toxicology screen or a blood alcohol level. Urine toxicology or a blood alcohol level does not usually affect initial treatment and disposition in the ED.^11,16 However, it may be invalid if collected subsequent to a transfer from the ED, and can determine whether a patient requires specific substance use disorder treatment or not.^16-18 Therefore, many psychiatric providers will request a urine toxicology screening or a blood alcohol level before accepting a transfer. Please note, urine toxicology screens only identify a small number of toxic ingestions. Therefore, a negative screen does not eliminate drug abuse or overdose.

Finally, in the case that a diagnostic examination is being done to satisfy a requirement for an institution to accept a patient or to assist in long-term treatment planning, disposition should not be delayed in order to wait for the result to return.¹¹

Treatment

Unfortunately, no level I or II studies have been found that examine the indications for treatment of the psychiatric patient in the ED.⁹ Additionally, in the ED, there is an ill-defined difference between the use of psychotropic medications as an intervention after patient assessment and plan of care, and the use of these medications to control behavior without an assessment and treatment plan.⁹ Therefore, many treatment recommendations have been made based on studies in other settings.

The first line treatment for a patient with schizophrenia is monotherapy with an antipsychotic agent other than clozapine.^19-21 (Clozapine is not used as a first line agent due to its high side effect burden and the testing necessary before starting.) This is supported by multiple randomized controlled trials and is the standard of care.^22-24 The response rates in treatment with antipsychotics in studies specifically designed to examine treatment of first-episode schizophrenia are high, ranging from 46% to 96%.²³ Therefore, the emergency medicine provider can confidently reassure patients and families that antipsychotic medications are effective in treating schizophrenia. Loading doses of antipsychotics should not be used.¹⁹

Although there are only small and inconsistent differences between different antipsychotics, other than clozapine, with respect to efficacy, there are large differences in adverse effect profiles.^25-30Therefore, the choice of antipsychotic medication is generally made based on previous response to individual antipsychotic medications and relative side effects.³¹

If extrapyramidal symptoms, including tardive dyskinesia, are of particular concern to a patient, then second generation or low potency first generation antipsychotics should be used.^25,32 If a patient complains of previous problems with sedation, then haloperidol or aripiprazole should be preferred.²⁵ Haloperidol, aripiprazole, or amisulpride should be considered for patients who are particularly concerned about weight gain, or who may be at the greatest risk of weight gain.²⁵

If there is no response to medication after 4 weeks,³² despite dose optimization, a change in antipsychotic should be considered.^33,34 Where there is partial response, the patient should be re-assessed after 8 weeks unless there are significant adverse effects.^14,19,20,34 A combination of different antipsychotic medications should not be used, except during transitional periods when patients are being switched from one antipsychotic to another, or when used for clozapine augmentation.¹⁴After an acute episode has passed, providers can consider offering depot/long-acting injectable antipsychotic medication to people with schizophrenia who would prefer such treatment; as long acting injectable antipsychotics have been shown to reduce medication non-adherence.^35,36 Long-acting depot antipsychotics should not be used for acute episodes because it may take 3 to 6 months for the medications to reach a stable state.¹⁴Once a patient achieves a remission of their symptoms, patients are recommended to stay on their antipsychotic medication for at least 2 years since their last acute exacerbation.^14,34 For maintenance therapy,the antipsychotic dose should be reduced gradually to the lowest possible effective dose, which should not be lower than half of the effective dose during the acute phase.³⁷

Clozapine should be offered to people with schizophrenia whose illness has not responded adequately to treatment with adequate doses of at least two different antipsychotic drugs.^38-41There is no indication to using dual antipsychotic agents on patients with schizophrenia prior to starting a clozapine trial.^42,43

Non-Pharmacological Intervention

There is strong evidence that people diagnosed with schizophrenia benefit from psychosocial treatments in addition to pharmacological treatment. Multiple randomized controlled studies, as well as national guidelines, have demonstrated cognitive behavioral therapy and family therapy to be effective for the treatment of schizophrenia.^44-51 Particular focuses of therapy include communication skills, problem solving, psychoeducation, and assisting with family conflict,^18,19 which are feasible in an emergency setting.⁵²

Recent studies have shown promise using a “crisis intervention” approach as an alternative option to the hospital or emergency medical services systems. Treatment usually involves a combination of medication as well as counseling (practical help with living skills and support for close family members). After the crisis has been stabilized, sufferers are carefully introduced to other models of care more suited for the chronic phases of psychiatric illnesses.⁵³ This is particularly important as psychosocial instability, such as changes in the psychosocial environment (ie, a primary caretaker going on vacation, or a patient being distanced from their family or support environment) have been associated with relapse.¹⁹

Acute Agitation

The vast majority of patients suffering from mental illness, including schizophrenia, are not violent and only a small proportion of the violence in our society can be attributed to persons who are mentally ill.⁵⁴ Furthermore, people with psychiatric disabilities are far more likely to be victims than perpetrators of violent crime.⁵⁵ However, schizophrenia and related disorders are associated with substantially increased rates of violence and violent offences compared to those who did not, independent of substance use.^56,57 Furthermore, the majority of acute hospital assaults occur in the ED.⁵⁸

Two emergency medicine evidence-based guidelines state a benzodiazepine (lorazepam or midazolam) or a conventional antipsychotic (droperidol or haloperidol) should be used as monotherapy for the treatment of acute undifferentiated agitation in the ED.^12,59 However, in cases of patients with a diagnosis or suspicion of schizophrenia, an antipsychotic should be used in order to start a “disease modifying agent” earlier in the course of treatment.^20,59,60Where possible, the same antipsychotic should be used as monotherapy for treatment of both acute agitation and standing antipsychotic medication.¹³The choice of medication for the treatment of acute agitation should be based on patient preference, past experience of antipsychotic treatment, the adverse effect profile, and concurrent medical history.^19,58 This is supported by a case controlled study, which showed patients’ subjective experiences in the acute phase of treatment affected their long-term adherence to medication.⁶¹

Haloperidol is the most commonly used medication for agitation in patients with schizophrenia.^59,62 When haloperidol is used to treat acute violence, it is almost always used in combination with a benzodiazepine unless medically compromised.^62,63 Intramuscular olanzapine has been shown to be effective in managing acute aggression or agitation in patients with schizophrenia, especially where it is necessary to avoid some of the older treatments. Olanzapine causes fewer movement disorders than halopridol.⁶⁴ Chlorpromazine is available in both per os and intramuscular formulations. However, chlorpromazine is associated with more side effects than other antipsychotics, including a higher incidence of prolonged QT and Torsades.⁶⁵ However, where choices are limited, chlorpromazine may be the only treatment available for acute agitation. If used, the close monitoring of blood pressure is indicated.⁶⁵ Inhaled loxapine received US Food and Drug Administration approval for treatment of acute agitation in 2012.⁶⁶ This is a useful option for an agitated patient who is calm enough to receive an inhaler, but is unable to take medication per os.

Restrictive intervention (restraints or seclusion) should only be used if de-escalation and other preventive strategies, including medication as needed, have failed and there is potential for harm to the patient or other people if no action is taken.⁵⁸

Telepsychiatry Consultation

Telepsychiatry is an approach, where by EDs that do not have access to psychiatrists can see patients in the ED itself, by forming a contract with either psychiatrists or companies to allow a psychiatrist at another location to perform an examination on a patient via video connection and advise the emergency room providers on treatment and intervention. There is very little data in the peer-reviewed literature on the use of telepsychiatry. The literature is limited to case reports, program descriptions, and randomized studies for reliability.^67,68 One randomized controlled trial showed that a telepsychiatry evaluation had a reliable diagnosis and disposition when compared to a face-to-face assessment.⁶⁹ One case control showed reduction in time-to-consult done in the ED, length of stay, and door-to-consult stay, once a telepsychiatry program was initiated.⁷⁰ A large case control study showed that telepsychiatry recipients were more likely to receive 30-day follow-up, 90-day follow-up, and total inpatient length of stay, totaling both initial admission and subsequent admissions.⁷¹ Therefore, it is reasonable for EDs to take advantage of telepsychiatry services if no immediate psychiatrist coverage is available.

Disposition

The primary disposition question regarding a patient presenting with a psychiatric chief complaint to the ED, including schizophrenia, is whether they require a psychiatric admission or not. If a patient requires hospitalization but refuses, the emergency clinician must decide if the patient meets criteria for involuntarily hospitalization. If a patient does not require an inpatient admission or would benefit from an inpatient admission but does not meet criteria for civil commitment, then the next major question is what type of outpatient treatment is sufficient for this particular patient (Figure).

For a patient with schizophrenia to require inpatient psychiatric admission he must be either a danger to himself or others or has failed outpatient treatment. In addition, the patient must currently have undergone a clinical evaluation of any suspected medical illness, and any medical problems the patient is experiencing must be sufficiently stable to allow safe transport and treatment at a psychiatric hospital unit.⁹ If a patient’s medical condition is not sufficiently stable for either transport or hospitalization at a psychiatric hospital but the patient still requires inpatient psychiatric treatment, the patient should be hospitalized on a standard medical ward and receive psychiatric care on that unit.

Patients with mental illness pose an additional challenge, in that their illness often time interferes with their judgment about whether they require treatment. Because of this possible lack of capacity and the potential danger of a patient with mental illness to self or others, most jurisdictions have a legal code that allows for involuntary hospitalization of the mentally ill. However, which patients qualify for involuntary hospitalizations vary by jurisdiction. Case law criteria for emergencies range from a risk of “imminent” harm to self or others to a deterioration in the patient’s mental condition if treatment is halted.⁷² Providers are recommended to familiarize themselves with laws regarding inpatient civil commitment in their particular jurisdiction.

When a patient is being discharged from the ED, either because they do not require a psychiatric inpatient admission or because they don’t meet criteria for involuntary commitment, there are various outpatient dispositions available. Any patient with a diagnosis of schizophrenia should have outpatient follow-up with a mental health provider upon discharge from the ED.

For patients who have a failed community treatment in the past, who do not have a significant support network, or whose disease is too severe for a regular outpatient clinic to handle would be better suited for a disposition to a transitional program over a standard outpatient appointment; such as partial hospitalization programs, intensive outpatient programs, and community mental health treatment teams (CMHT). Assertive community treatment (ACT) teams are a form of CMHT comprised of several disciplines, including nurses, occupational therapists, psychiatrists, psychologists, and social workers.⁷³ A large prospective cohort study found homeless patients to have made gains in multiple spheres of mental health while enrolled in ACT programs, and these benefits were retained after discharge from the ACT program.⁷⁴

Conclusion

Schizophrenia is characterized primarily by delusions, hallucinations, and disorganized thinking. Emergency medicine providers are frequently at the front lines of diagnosing, initiating treatment, and managing relapses for these individuals. As schizophrenia is an exclusion, the primary task of an emergency physician is to rule out all “organic”, for lack of a better term, causes of the psychosis or disordered thinking before making a definitive diagnosis of schizophrenia. As many EDs do not have sufficient psychiatry support and many patients with schizophrenia are using the ED as their location for primary mental health, many emergency physicians are finding themselves acting as the main providers for these individuals. The primary treatment for patients with schizophrenia remains monotherapy with antipsychotic medication. Although the highest-level disposition for a patient with schizophrenia remains the inpatient psychiatry department, there are many transitional dispositions that can bridge the gap between a discharge to standard community care and an inpatient admission.

ABSTRACT

Soccer requires significant physical conditioning and endurance, as well as the physicality required for contact play. In order to keep athletes safe, it is important that coaches, medical staff, and the players themselves are educated on the most common dangers to their health that they may encounter on a soccer pitch. This article aims to review the current literature and recommendations on concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer, with a goal of educating all those who help to keep athletes healthy and competing to their full potential.  

Continue to: Soccer is one of the most popular sports...

Soccer is one of the most popular sports in the modern world and requires significant physical conditioning and endurance, as well as the physicality required for contact play. This article covers the topics of concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer players. We provide a review of the prevention, recognition, and management required to keep athletes safe on the soccer pitch, both in practice and in competitive play.

HEAD

With an estimated 1.6 to 3.8 million sports-related mild traumatic brain injuries (ie, concussions) occurring annually in the United States,¹ there has been an appropriate increase in the focus on prevention and treatment of these injuries. For more than a decade the spotlight has been on concussions that occur in American football, but other sports have also had to examine the prevalence of concussions in their sport. This is certainly true for soccer.

There has been a steady increase in soccer participation in the United States. From 1973 to 2014 there was a 4-fold increase in high school boys and a 35-fold increase in high school girls playing soccer.² Currently, there are more than 3.7 million youth who play on teams under the supervision of the US Soccer Federation, the sport’s national governing body.³ With the growth of the sport, there has also been an intensified focus on injury prevention in soccer players, including concussive brain injuries.

A recent study examined injury rates in high school soccer players and noted that concussion is the second most common injury (17.9%), after ligament sprains (29.7%).⁴ The overall injury rate was 2.06 per 1000 athletic exposures (AEs [defined as participation in practice or game play]), but higher in games (4.42 per 1000 AEs) than during practices (1.05 per 1000 AEs). The overall concussion rate was 0.36 per 1000 AEs.⁴

Most concussions (54.8%) resulted in missing play between 1 to 3 weeks, but a sizeable portion of the athletes (14.9%) were out of play for more than 3 weeks. Additionally, 10.7% of all medical disqualifications were due to concussive injuries. Khodaee and colleagues⁴ found no statistically significant difference in concussion rates between male and female soccer players over the 9-year period of time that they examined, however previous studies have found higher rates in female athletes.⁵

In soccer, as in other sports, there is a concern about both the adequate recognition of concussions during practice and play and the underreporting of concussions by athletes. The US Soccer Federation has taken a proactive stance on addressing concussion in youth soccer by developing the “Recognize to Recover” program.⁶ Recognize to Recover is the US Soccer Federation’s “comprehensive player health and safety program aimed at promoting safe play and reducing injuries in soccer players of all ages.” The website provides an educational video geared toward players, along with links to concussion assessment tools, the US Soccer Federation Concussion Protocol, and US Soccer Federation-Centers for Disease Control fact sheets for athletes, parents, and coaches.⁶

Continue to: A challenge for all sports...

 

 

A challenge for all sports is allowing adequate evaluation of a suspected concussion by properly trained healthcare professionals. The 2017 Berlin Concussion in Sport Group position paper stated, “when a concussion is suspected, the athlete should be removed from the sporting environment and a multimodal assessment should be conducted in standardized fashion (eg, Sport Concussion Assessment Tool- 5th edition). Sporting bodies should allow adequate time to conduct this evaluation.”⁷ However, the International Federation of Football Association (FIFA) rules limit substitutions to 3 over the course of the game, which can make a thorough evaluation of players difficult as trainers and coaches are under increased pressure to quickly determine whether to use one of their valuable substitutions. Fortunately, the National Collegiate Athletic Association (NCAA) soccer has mitigated this issue by allowing unlimited substitutions during matches, and high school teams generally follow similar rules.

One of the goals of any safety education program is not only to raise the awareness of the signs and symptoms of concussion by all those involved in the sport, but also to increase the number of athletes who self-report their symptoms and decrease those who hide any possible concussions. A study found that a majority (58.6%) of middle school soccer players continued to play while experiencing concussion symptoms.⁵ However, in a very recent (not yet published) study, 92% of US Soccer Federation players reported that they did seek out a medical evaluation for their concussion.⁸ This is certainly a positive sign and further research needs to clarify what methods of education or training will maintain this level of self-reporting in soccer players.

There has also been an increased focus on understanding the mechanism of injury of concussions. In soccer, concussions can occur from player-to-player contact, contact with the player surface, contact with playing apparatus (eg, goal posts) and non-contact mechanisms. While there has been a focus on concussions from heading the ball, player-to-player contact is the most common cause of concussions. A 2017 study of 7- to 12-year-old soccer players in 4 European countries found that about 1 out of 10 concussions were caused by heading the ball.⁹ Comstock and colleageues¹⁰ found slightly higher numbers, roughly 25% to 30% (depending on gender), but 70% to 78% (again depending on gender) of those were caused by player-to-player contact rather than contact with the ball.

To date there has not been any meta-analytic review evaluating the cognitive and physical symptoms associated with heading in soccer. A recent review paper stated that the “current evidence seems insufficient to support a ban of heading in children’s football (soccer).”¹⁰ However, in December 2015 the US Soccer Federation included age-specific heading limitations. Players ages 10 years and under “shall not engage in heading, either in practices or in games” and players age 11 years and 12 years should have “limited heading in practice; maximum of 30 minutes of heading training per week, with no more than 15-20 headers per player, per week.”¹¹ US Soccer Federation officials acknowledged the limitations in the current science regarding heading in young soccer players but chose to err on the side of caution until further empirical evidence regarding the risks associated with repetitive heading is available.

The US Soccer Federation is also exploring other ways to reduce the incidence rate of concussions, including ensuring that the age-appropriate sized ball is used in practice and play, possible rule changes, evaluation of different playing surfaces, and equipment usage. To date, there is no strong evidence to support the use of mouth guards or helmets to reduce concussions in soccer. Additionally, the current data about the value of head impact sensors in soccer has not supported its widespread use.

Continue to: Finally, the issue of the prevalence...

 

 

Finally, the issue of the prevalence of chronic traumatic encephalopathy (CTE) in soccer players is beyond the scope of this article. The expert opinion from the 2017 US Soccer Federation, Major League Soccer (MLS), and National Women’s Soccer League (NWSL) conference concluded, “At present, no data exist that support that soccer participation is a risk factor for the development of neurodegenerative disease. Similarly, at this time, consistent with evidence discussed in the Berlin Concussion in Sport Group (CISG) Consensus Conference, our review suggests no causal relationship has been demonstrated between soccer and CTE pathology.”¹²

The more we know about concussions, both in general and those sustained during soccer play, the better we are able to diagnose and manage these injuries in our athletes. An important step is creating evidence-based protocols that evolve as our knowledge of concussions does as well. In April 2017, the US Soccer Federation, MLS, and the NWSL held a joint summit entitled, “Head Injury in Soccer: From Science to the Field” to address the current evidence-based science of concussions in soccer.⁸ An article discussing the findings of this meeting is forthcoming and will undoubtedly guide further development of concussion protocols for soccer players of all ages.

HEART

The physiologic demands of soccer place considerable stress on the cardiovascular system. Participation in training and competition is characterized by a combination of aerobic and anaerobic physiology with the typical athlete covering approximately 10 km over the course of the 90-minute match. The primary role of the heart and blood vessels is to supply the exercising skeletal muscle with oxygen and energy substrate and to clear the byproducts of metabolism. Among healthy athletes without cardiovascular disease, these processes are typically well tolerated and may be associated with beneficial cardiovascular adaptations over time. However, competitive soccer players are not completely immune to cardiovascular disease. Athletes across the age and competition spectrum may develop symptoms suggestive of underlying cardiovascular disease during play including exertional chest pain, inappropriate shortness of breath, palpitations, and syncope. These athletes require timely clinical evaluation. In extremely rare but high visibility cases, competitive soccer players may succumb to cardiac arrest on the pitch, underscoring the need for comprehensive emergency action plans (EAPs). We provide the practicing clinician with an overview of cardiovascular issues relevant to the competitive soccer athlete.

CARDIOVASCULAR ADAPTATIONS TO SPORT

The pressure (ie, repetitive surges in systemic blood pressure) and volume (ie, sustained increases in high cardiac output) challenges inherent in soccer participation place stress on the cardiovascular system. Healthy athletes across the age spectrum typically tolerate the hemodynamic stressors of participation without issues. Athletes that engage in training and competition over months to years often develop beneficial adaptations of the cardiovascular system that enhance on-field performance and contribute to optimal long-term health. Detailed discussion of how the heart and blood vessels respond to exercise training is beyond the scope of this article, but the interested reader is referred to several prior publications.^13,14 In brief, the heart of the healthy soccer athlete demonstrates the balanced mild chamber dilation and wall thickening characteristic of left ventricular eccentric remodeling. This form of exercise-induced cardiac remodeling facilitates maintenance of high stroke volume during exercise with minimal increases in cardiac work. In parallel, routine aerobic exercise training confers favorable changes in the systemic arterial system, which leads to reductions in age-associated ventricular stiffening and maintenance of healthy low blood pressure. It must be emphasized that the healthy heart muscle dilation and thickening that develop in response to sports participation, regardless of age, ethnicity, or gender, are relatively mild and should not be confused with common forms of heart muscle disease that may be seen in athletes at risk for adverse outcomes. In some situations, consultation with an extreme sports cardiologist may be required to differentiate exercise-induced remodeling from over heart muscle pathology.¹⁵

Continue to: THE SYMPTOMATIC ATHLETE...

 

 

THE SYMPTOMATIC ATHLETE

Any athlete presenting with symptoms suggestive of underlying cardiovascular disease should be withheld from training and competition until a comprehensive clinical evaluation has been completed. Common manifestations of underlying heart disease that occur in soccer players include exertional chest pain/pressure/tightness, shortness of breath that is out of proportion to workload, palpitations or the perception of irregular cardiac activity, and syncope. Chest discomfort, inappropriate shortness of breath, and palpitations that occur during training or competition should be managed with immediate removal from the playing field and prompt medical assessment. In many cases, thorough evaluation will involve collaboration between sports medicine and sports cardiology providers. Evaluations must be individualized on a case-by-case basis as tailored to the athlete’s presenting chief complaint and prior medical history. Most of these assessments will include a detailed medical history and physical examination, a 12-lead electrocardiogram (ECG), provocative exercise testing in a controlled environment, noninvasive cardiac imaging, and in some cases ambulatory rhythm monitoring. Uniformly, the athlete should be withheld from further training and competition until high-risk cardiovascular disease has been excluded. We refer the interested reader to a comprehensive discussion of symptom-based assessment of the athlete with suspected cardiovascular disease.¹⁶

Syncope (sudden and abrupt loss of consciousness with spontaneous neurologic recovery) is common among trained athletes. The vast majority of syncope is caused by “neurocardiogenic” mechanisms and carries a benign prognosis. Benign neurally-mediated syncope most often occurs outside of training and competition among athletes with heightened vagal tone and a predisposed susceptibility to triggers including pain, anxiety, emotional stimulation, and sudden postural change. Athletes who experience neurally-mediated syncope outside of training and competition routinely report a pre-event prodrome or aura that permits them to lower themselves to the ground, thereby avoiding injury. A distinct, but similarly benign and common, form of neurally-mediated fainting is post-exertional syncope. Here, fainting occurs within seconds of abrupt termination of exercise due to a rapid reduction cardiac preload and corollary cerebral blood supply. When either form of neurally-mediated syncope is suggested by a comprehensive medical history, normal physical examination, and a normal 12- lead ECG, further evaluation is unnecessary. However, the athlete and their coaching staff should be educated about avoidance tactics including hydration, dietary sodium supplementation, and avoidance of abrupt exercise termination as neutrally-mediated syncope tends to be recurrent without such measures. Fainting episodes that occur during training or competition that are not clearly post-exertional should be considered a medical emergency and should prompt comprehensive evaluation by a qualified cardiovascular specialist. Working closely with team physicians and athletic training staff, it is the responsibility of sports cardiologists to exclude potentially life-threatening forms of electrical, muscular, coronary, and valvular heart disease. Ideally, this evaluation should be conducted rapidly to avoid unnecessary delays in return to play.

CARDIAC ARREST AND SUDDEN DEATH

Numerous high-visibility cases of cardiac arrest on the soccer pitch have alerted the sporting community to the potential for these rare and potentially tragic events. Definitive incidence statistics defining the risk of cardiac arrest among soccer players are lacking. Data from the NCAA database suggest a sudden death incidence rate among collegiate male soccer athletes of approximately 1:24,000 athlete years.⁸ Similar data documenting incidence among female athletes and among those at lower (ie, youth level and high school) and higher (ie, professional) levels of play are unavailable. Underlying cardiovascular disease in the forms of heart muscle abnormalities (ie, genetic and acquired cardiomyopathy), coronary artery abnormalities (ie, genetic coronary anomalies and atherosclerotic coronary disease), valvular heart problems (ie, congenitally malformed aortic valves), and primary disturbances of the cardiac electrical system (ie, Wolf-Parkinson-White syndrome, long QT syndrome, etc.) explain a substantial percentage of on-pitch cardiac arrest. However, it is increasingly recognized that a significant minority of sudden cardiac deaths among athletes occur in the absence of attributable cardiovascular abnormality.¹⁷ Such cases, often referred to as “sudden unexplained death,” present unique challenges in the context of pre-participation screening, as they are undetectable and thus unpredictable.

Reduction of cardiac arrest and sudden death may best be accomplished through a combination of focused pre-participation screening and the development and implementation of a comprehensive EAP. Pre-participation involves the performance of a battery of tests prior to training and competition that are geared toward the detection of occult high-risk cardiovascular disease. Recommendations regarding pre-participation screening vary both across and within countries. Current US recommendations call for a focused medical history and physical examination prior to training and competition with consideration of the addition of a 12-lead ECG on a local level based on expertise and available resources.¹⁸ Conversely, current European guidelines including those endorsed by FIFA, suggest routine inclusion of a 12-lead ECG and in some cases, a transthoracic ECG.¹⁹ It must be emphasized that no screening approach has been confirmed to reduce the incidence of sudden death, and the decision to extend screening beyond the medical history and physical examination to include a 12-lead ECG or echocardiogram may come at the cost of increased false positive testing. In practice, decisions about how and when to screen are ideally made at a local level after consideration of medical and financial resources.²⁰

Continue to: Even the most comprehensive approach...

 

 

Even the most comprehensive approach to screening and evaluation of symptomatic athletes will not completely eliminate on-pitch cardiac arrest. Thus, all stakeholders that engage in the oversight of organized soccer must be committed to the development and implementation of an EAP.²¹ Key components of an effective EAP include the training of coaching staff, athletic trainers, and players in basic cardiopulmonary resuscitation, access to and training in the use of automated external defibrillators, and a triage/transport protocol that ensures timely access to advanced cardiac life support. Much like screening, emergency action planning involving these key core components must be developed and tailored locally. In the era of contemporary organized athletics, the absence of an EAP at any level of competition, from youth to professional leagues, is unacceptable. Effective EAPs must be developed, documented, and rehearsed at regular intervals. For the health and safety of competitive soccer players, as well as coaching staff and spectators, these steps are of critical importance.

HEAT

Heat-related illnesses can be serious and, at times, even life threatening. It is important for athletic staff and athletes to be well versed in the prevention, signs and symptoms, and treatment of heat-related illnesses in order to prevent serious and lasting injury. We aim to educate physicians about the prevention, recognition, and management of heat-related injury, and stress the importance of similarly educating athletes and coaching staff.

Exertional heat illnesses most often occur at temperatures >86°F, however they can occur at any temperature with heavy exertion.²² Signs and symptoms can be nonspecific early on, including weakness, fatigue, headache, nausea, and dizziness. Later signs can include imbalance, altered mentation, confusion, and behavior that is out of character such as irritability or aggression.²³ It is easy to see how the later signs can be confused for concussion in the right context. We cover the recognition and treatment of two common and serious heat-related illnesses: heat exhaustion and exertional heat stroke (EHS).

HEAT EXHAUSTION

Heat exhaustion occurs when an athlete cannot continue to exercise due to weakness and fatigue. While the exact mechanism is not well understood, it has been established that the combined effect of heat and dehydration have been proven to decrease exercise capacity and performance to a greater degree than either alone. The heat created by the body during exercise is 15 to 20 times greater than when at rest, and can increase core body temperature by 1°C every 5 minutes if no heat is lost, such as through sweating.²⁴ Additionally, when fluid deficits reach >3% to 5% of total body water, sweat production and skin blood flow decline, blunting the ability for the body to cool itself and causing progressive elevation of core body temperature if the athlete continues exerting him or herself. When fluid deficits reach 6% to 10%, cardiac output, sweat, and muscle blood flow decrease, likely leading to the symptoms seen with heat exhaustion: weakness, profound fatigue, and occasionally confusion and disorientation. Athletes with suspected heat exhaustion should be moved to a cooler area, laid down with legs elevated, and orally rehydrated. If they do not improve with oral rehydration, they may require intravenous fluids. The diagnosis of heat exhaustion hinges on a rectal temperature of <104°F; if >104°F the athlete should be presumed to have heat stroke, which will be addressed in the following paragraphs. Players can be cleared to return to play in mild cases within 24 to 48 hours with gradual increases in exercise intensity.²⁴

EXERTIONAL HEAT STROKE

EHS occurs when the body can no longer regulate the core body temperature and it rises to upwards of 104°F. In EHS, elevated core body temperature is associated with evidence of end organ dysfunction. The most easily identified on the playing field is likely central nervous system dysfunction, including irritability, confusion, irrational behavior, lethargy, dizziness, confusion, and even loss of consciousness. Temperature should be measured with rectal temperature only, as other methods of measurement have been shown to be consistently inaccurate.²² Heat stroke can be confused with exertional hyponatremia, heat exhaustion, or concussion, especially when core body temperature cannot be determined. However, EHS should always be the presumed cause of altered mentation when no rectal temperature is available because rapid cooling is critical to minimizing lasting effects. Morbidity and mortality are directly related to the length of time required to cool the athlete under 40°C (104°F).²⁴ Cooling should be completed on site prior to transport to a medical facility and is best achieved with submersion in an ice bath (ie, a kiddie pool or soaking tub full of ice and water).^22,25 If an ice bath is not available, ice bags should be applied to the neck axilla and groin and exchanged for fresh bags every 2 to 3 minutes.²² Ice bags have been shown to be inferior to whole body cooling, only cooling the athlete .04°C to .08°C/min compared to .15°C to .24°C/min with the ice bath.²⁴ All other tests should be delayed until cooling is achieved, unless they can be completed while cooling the athlete. The athlete can be removed from the ice bath once rectal temperatures reach <101°F to 102°F.²³ If the athlete returns to baseline after cooling, transportation to a medical facility may not be necessary. However, they should refrain from physical activity and heat exposure for at least 7 days and should be evaluated by a physician at that time. If all labs are normal and the athlete is asymptomatic, they can start progressive return to play under the direction of an athletic trainer or a sports medicine physician.²³

Continue to: HEAT-RELATED ILLNESS...

 

 

HEAT-RELATED ILLNESS

It is impossible to predict exactly which athletes will be most at risk for heat-related illness, so it is important to have a high degree of suspicion when environmental conditions are right. Athletes with recent illness, fever, or lack of sleep are at higher risk. Additional intrinsic risk factors include low fitness level, obesity, and inadequate hydration. Athletes who are highly competitive or motivated can be more likely to push through the early signs of illness or be reluctant to report symptoms.²³ Those with a history of exertional heat illness are more at risk for developing it again in the future.²³

The extrinsic risk factors for the development of heat-related illness are much easier to identify and modify in order to keep athletes safe. High temperature and high humidity conditions, heavy sun exposure, and exposure to similar conditions the preceding day put athletes at risk for exertional heat illness. Risks are even greater when the exercise is prolonged or intense with few breaks and access to hydration is limited.²³ Therefore, prevention of exertional heat illness is centered on these external risk factors.

Each team should have a heat policy as part of their EAP aimed at prevention and early recognition of heat-related illness. This policy should be shared with all athletes and coaches. The plan should be centered on acclimatization, activity modification, and early recognition and management as previously discussed. The US Soccer Federation “Recognize to Recover” Heat Guidelines suggest a 3-step process for appropriate activity modification:²²

1. Find the wet bulb globe temperature, either using a wet bulb globe thermometer or the temperature and humidity (Figure 1).

2. Find your regional weather category on the map (Figure 2).

3. Find your alert level and work to rest ratio recommendations (Figure 3).

Scheduled hydration breaks should be given as listed in Figure 3. Breaks of 4 minutes should be given for each 30 minutes of continuous practice or play. In a regulation 90-minute match, a hydration break should be given at 30 and 75 minutes (with half time at 45 minutes) at minimum. Athletes should be educated about where hydration can be accessed, and given unlimited access to hydration even outside of planned breaks.²²

Acclimatization to conditions is another integral part of preventing heat-related illness. It allows the body time to adapt to exercising in heat gradually, with a measured progression of exertion over the course of 10 to 14 days. The “Recognize to Recover” Heat Guidelines also provide guidance on acclimatization, and specifics can be found on the website.¹ Generally speaking, the warmest part of the day, usually between 11 AM and 4 PM, should be avoided for all training sessions, and length of practice and exertion should be gradually increased over 2 weeks.²²

In summary, appropriate acclimatization, hydration, activity modification, and education of athletes and staff are essential for the prevention of heat-related illness. Athletes and staff should understand the signs and symptoms of heat-related illness so that it can be recognized early and treated appropriately. If an athlete is altered in the heat and rectal temperature is >104°F or rectal temperature cannot be obtained, rapid cooling using an ice bath or ice bags is essential to prevent the morbidity and mortality associated with EHS. Above all, teams should have an explicit plan that includes protocols for acclimatization, activity modification, and all necessary equipment to prevent and treat heat-related illnesses should they occur, and ultimately keep athletes safe and healthy.

ABSTRACT

Soccer requires significant physical conditioning and endurance, as well as the physicality required for contact play. In order to keep athletes safe, it is important that coaches, medical staff, and the players themselves are educated on the most common dangers to their health that they may encounter on a soccer pitch. This article aims to review the current literature and recommendations on concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer, with a goal of educating all those who help to keep athletes healthy and competing to their full potential.  

Continue to: Soccer is one of the most popular sports...

Soccer is one of the most popular sports in the modern world and requires significant physical conditioning and endurance, as well as the physicality required for contact play. This article covers the topics of concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer players. We provide a review of the prevention, recognition, and management required to keep athletes safe on the soccer pitch, both in practice and in competitive play.

HEAD

With an estimated 1.6 to 3.8 million sports-related mild traumatic brain injuries (ie, concussions) occurring annually in the United States,¹ there has been an appropriate increase in the focus on prevention and treatment of these injuries. For more than a decade the spotlight has been on concussions that occur in American football, but other sports have also had to examine the prevalence of concussions in their sport. This is certainly true for soccer.

There has been a steady increase in soccer participation in the United States. From 1973 to 2014 there was a 4-fold increase in high school boys and a 35-fold increase in high school girls playing soccer.² Currently, there are more than 3.7 million youth who play on teams under the supervision of the US Soccer Federation, the sport’s national governing body.³ With the growth of the sport, there has also been an intensified focus on injury prevention in soccer players, including concussive brain injuries.

A recent study examined injury rates in high school soccer players and noted that concussion is the second most common injury (17.9%), after ligament sprains (29.7%).⁴ The overall injury rate was 2.06 per 1000 athletic exposures (AEs [defined as participation in practice or game play]), but higher in games (4.42 per 1000 AEs) than during practices (1.05 per 1000 AEs). The overall concussion rate was 0.36 per 1000 AEs.⁴

Most concussions (54.8%) resulted in missing play between 1 to 3 weeks, but a sizeable portion of the athletes (14.9%) were out of play for more than 3 weeks. Additionally, 10.7% of all medical disqualifications were due to concussive injuries. Khodaee and colleagues⁴ found no statistically significant difference in concussion rates between male and female soccer players over the 9-year period of time that they examined, however previous studies have found higher rates in female athletes.⁵

In soccer, as in other sports, there is a concern about both the adequate recognition of concussions during practice and play and the underreporting of concussions by athletes. The US Soccer Federation has taken a proactive stance on addressing concussion in youth soccer by developing the “Recognize to Recover” program.⁶ Recognize to Recover is the US Soccer Federation’s “comprehensive player health and safety program aimed at promoting safe play and reducing injuries in soccer players of all ages.” The website provides an educational video geared toward players, along with links to concussion assessment tools, the US Soccer Federation Concussion Protocol, and US Soccer Federation-Centers for Disease Control fact sheets for athletes, parents, and coaches.⁶

Continue to: A challenge for all sports...

 

 

A challenge for all sports is allowing adequate evaluation of a suspected concussion by properly trained healthcare professionals. The 2017 Berlin Concussion in Sport Group position paper stated, “when a concussion is suspected, the athlete should be removed from the sporting environment and a multimodal assessment should be conducted in standardized fashion (eg, Sport Concussion Assessment Tool- 5th edition). Sporting bodies should allow adequate time to conduct this evaluation.”⁷ However, the International Federation of Football Association (FIFA) rules limit substitutions to 3 over the course of the game, which can make a thorough evaluation of players difficult as trainers and coaches are under increased pressure to quickly determine whether to use one of their valuable substitutions. Fortunately, the National Collegiate Athletic Association (NCAA) soccer has mitigated this issue by allowing unlimited substitutions during matches, and high school teams generally follow similar rules.

One of the goals of any safety education program is not only to raise the awareness of the signs and symptoms of concussion by all those involved in the sport, but also to increase the number of athletes who self-report their symptoms and decrease those who hide any possible concussions. A study found that a majority (58.6%) of middle school soccer players continued to play while experiencing concussion symptoms.⁵ However, in a very recent (not yet published) study, 92% of US Soccer Federation players reported that they did seek out a medical evaluation for their concussion.⁸ This is certainly a positive sign and further research needs to clarify what methods of education or training will maintain this level of self-reporting in soccer players.

There has also been an increased focus on understanding the mechanism of injury of concussions. In soccer, concussions can occur from player-to-player contact, contact with the player surface, contact with playing apparatus (eg, goal posts) and non-contact mechanisms. While there has been a focus on concussions from heading the ball, player-to-player contact is the most common cause of concussions. A 2017 study of 7- to 12-year-old soccer players in 4 European countries found that about 1 out of 10 concussions were caused by heading the ball.⁹ Comstock and colleageues¹⁰ found slightly higher numbers, roughly 25% to 30% (depending on gender), but 70% to 78% (again depending on gender) of those were caused by player-to-player contact rather than contact with the ball.

To date there has not been any meta-analytic review evaluating the cognitive and physical symptoms associated with heading in soccer. A recent review paper stated that the “current evidence seems insufficient to support a ban of heading in children’s football (soccer).”¹⁰ However, in December 2015 the US Soccer Federation included age-specific heading limitations. Players ages 10 years and under “shall not engage in heading, either in practices or in games” and players age 11 years and 12 years should have “limited heading in practice; maximum of 30 minutes of heading training per week, with no more than 15-20 headers per player, per week.”¹¹ US Soccer Federation officials acknowledged the limitations in the current science regarding heading in young soccer players but chose to err on the side of caution until further empirical evidence regarding the risks associated with repetitive heading is available.

The US Soccer Federation is also exploring other ways to reduce the incidence rate of concussions, including ensuring that the age-appropriate sized ball is used in practice and play, possible rule changes, evaluation of different playing surfaces, and equipment usage. To date, there is no strong evidence to support the use of mouth guards or helmets to reduce concussions in soccer. Additionally, the current data about the value of head impact sensors in soccer has not supported its widespread use.

Continue to: Finally, the issue of the prevalence...

 

 

Finally, the issue of the prevalence of chronic traumatic encephalopathy (CTE) in soccer players is beyond the scope of this article. The expert opinion from the 2017 US Soccer Federation, Major League Soccer (MLS), and National Women’s Soccer League (NWSL) conference concluded, “At present, no data exist that support that soccer participation is a risk factor for the development of neurodegenerative disease. Similarly, at this time, consistent with evidence discussed in the Berlin Concussion in Sport Group (CISG) Consensus Conference, our review suggests no causal relationship has been demonstrated between soccer and CTE pathology.”¹²

The more we know about concussions, both in general and those sustained during soccer play, the better we are able to diagnose and manage these injuries in our athletes. An important step is creating evidence-based protocols that evolve as our knowledge of concussions does as well. In April 2017, the US Soccer Federation, MLS, and the NWSL held a joint summit entitled, “Head Injury in Soccer: From Science to the Field” to address the current evidence-based science of concussions in soccer.⁸ An article discussing the findings of this meeting is forthcoming and will undoubtedly guide further development of concussion protocols for soccer players of all ages.

HEART

The physiologic demands of soccer place considerable stress on the cardiovascular system. Participation in training and competition is characterized by a combination of aerobic and anaerobic physiology with the typical athlete covering approximately 10 km over the course of the 90-minute match. The primary role of the heart and blood vessels is to supply the exercising skeletal muscle with oxygen and energy substrate and to clear the byproducts of metabolism. Among healthy athletes without cardiovascular disease, these processes are typically well tolerated and may be associated with beneficial cardiovascular adaptations over time. However, competitive soccer players are not completely immune to cardiovascular disease. Athletes across the age and competition spectrum may develop symptoms suggestive of underlying cardiovascular disease during play including exertional chest pain, inappropriate shortness of breath, palpitations, and syncope. These athletes require timely clinical evaluation. In extremely rare but high visibility cases, competitive soccer players may succumb to cardiac arrest on the pitch, underscoring the need for comprehensive emergency action plans (EAPs). We provide the practicing clinician with an overview of cardiovascular issues relevant to the competitive soccer athlete.

CARDIOVASCULAR ADAPTATIONS TO SPORT

The pressure (ie, repetitive surges in systemic blood pressure) and volume (ie, sustained increases in high cardiac output) challenges inherent in soccer participation place stress on the cardiovascular system. Healthy athletes across the age spectrum typically tolerate the hemodynamic stressors of participation without issues. Athletes that engage in training and competition over months to years often develop beneficial adaptations of the cardiovascular system that enhance on-field performance and contribute to optimal long-term health. Detailed discussion of how the heart and blood vessels respond to exercise training is beyond the scope of this article, but the interested reader is referred to several prior publications.^13,14 In brief, the heart of the healthy soccer athlete demonstrates the balanced mild chamber dilation and wall thickening characteristic of left ventricular eccentric remodeling. This form of exercise-induced cardiac remodeling facilitates maintenance of high stroke volume during exercise with minimal increases in cardiac work. In parallel, routine aerobic exercise training confers favorable changes in the systemic arterial system, which leads to reductions in age-associated ventricular stiffening and maintenance of healthy low blood pressure. It must be emphasized that the healthy heart muscle dilation and thickening that develop in response to sports participation, regardless of age, ethnicity, or gender, are relatively mild and should not be confused with common forms of heart muscle disease that may be seen in athletes at risk for adverse outcomes. In some situations, consultation with an extreme sports cardiologist may be required to differentiate exercise-induced remodeling from over heart muscle pathology.¹⁵

Continue to: THE SYMPTOMATIC ATHLETE...

 

 

THE SYMPTOMATIC ATHLETE

Any athlete presenting with symptoms suggestive of underlying cardiovascular disease should be withheld from training and competition until a comprehensive clinical evaluation has been completed. Common manifestations of underlying heart disease that occur in soccer players include exertional chest pain/pressure/tightness, shortness of breath that is out of proportion to workload, palpitations or the perception of irregular cardiac activity, and syncope. Chest discomfort, inappropriate shortness of breath, and palpitations that occur during training or competition should be managed with immediate removal from the playing field and prompt medical assessment. In many cases, thorough evaluation will involve collaboration between sports medicine and sports cardiology providers. Evaluations must be individualized on a case-by-case basis as tailored to the athlete’s presenting chief complaint and prior medical history. Most of these assessments will include a detailed medical history and physical examination, a 12-lead electrocardiogram (ECG), provocative exercise testing in a controlled environment, noninvasive cardiac imaging, and in some cases ambulatory rhythm monitoring. Uniformly, the athlete should be withheld from further training and competition until high-risk cardiovascular disease has been excluded. We refer the interested reader to a comprehensive discussion of symptom-based assessment of the athlete with suspected cardiovascular disease.¹⁶

Syncope (sudden and abrupt loss of consciousness with spontaneous neurologic recovery) is common among trained athletes. The vast majority of syncope is caused by “neurocardiogenic” mechanisms and carries a benign prognosis. Benign neurally-mediated syncope most often occurs outside of training and competition among athletes with heightened vagal tone and a predisposed susceptibility to triggers including pain, anxiety, emotional stimulation, and sudden postural change. Athletes who experience neurally-mediated syncope outside of training and competition routinely report a pre-event prodrome or aura that permits them to lower themselves to the ground, thereby avoiding injury. A distinct, but similarly benign and common, form of neurally-mediated fainting is post-exertional syncope. Here, fainting occurs within seconds of abrupt termination of exercise due to a rapid reduction cardiac preload and corollary cerebral blood supply. When either form of neurally-mediated syncope is suggested by a comprehensive medical history, normal physical examination, and a normal 12- lead ECG, further evaluation is unnecessary. However, the athlete and their coaching staff should be educated about avoidance tactics including hydration, dietary sodium supplementation, and avoidance of abrupt exercise termination as neutrally-mediated syncope tends to be recurrent without such measures. Fainting episodes that occur during training or competition that are not clearly post-exertional should be considered a medical emergency and should prompt comprehensive evaluation by a qualified cardiovascular specialist. Working closely with team physicians and athletic training staff, it is the responsibility of sports cardiologists to exclude potentially life-threatening forms of electrical, muscular, coronary, and valvular heart disease. Ideally, this evaluation should be conducted rapidly to avoid unnecessary delays in return to play.

CARDIAC ARREST AND SUDDEN DEATH

Numerous high-visibility cases of cardiac arrest on the soccer pitch have alerted the sporting community to the potential for these rare and potentially tragic events. Definitive incidence statistics defining the risk of cardiac arrest among soccer players are lacking. Data from the NCAA database suggest a sudden death incidence rate among collegiate male soccer athletes of approximately 1:24,000 athlete years.⁸ Similar data documenting incidence among female athletes and among those at lower (ie, youth level and high school) and higher (ie, professional) levels of play are unavailable. Underlying cardiovascular disease in the forms of heart muscle abnormalities (ie, genetic and acquired cardiomyopathy), coronary artery abnormalities (ie, genetic coronary anomalies and atherosclerotic coronary disease), valvular heart problems (ie, congenitally malformed aortic valves), and primary disturbances of the cardiac electrical system (ie, Wolf-Parkinson-White syndrome, long QT syndrome, etc.) explain a substantial percentage of on-pitch cardiac arrest. However, it is increasingly recognized that a significant minority of sudden cardiac deaths among athletes occur in the absence of attributable cardiovascular abnormality.¹⁷ Such cases, often referred to as “sudden unexplained death,” present unique challenges in the context of pre-participation screening, as they are undetectable and thus unpredictable.

Reduction of cardiac arrest and sudden death may best be accomplished through a combination of focused pre-participation screening and the development and implementation of a comprehensive EAP. Pre-participation involves the performance of a battery of tests prior to training and competition that are geared toward the detection of occult high-risk cardiovascular disease. Recommendations regarding pre-participation screening vary both across and within countries. Current US recommendations call for a focused medical history and physical examination prior to training and competition with consideration of the addition of a 12-lead ECG on a local level based on expertise and available resources.¹⁸ Conversely, current European guidelines including those endorsed by FIFA, suggest routine inclusion of a 12-lead ECG and in some cases, a transthoracic ECG.¹⁹ It must be emphasized that no screening approach has been confirmed to reduce the incidence of sudden death, and the decision to extend screening beyond the medical history and physical examination to include a 12-lead ECG or echocardiogram may come at the cost of increased false positive testing. In practice, decisions about how and when to screen are ideally made at a local level after consideration of medical and financial resources.²⁰

Continue to: Even the most comprehensive approach...

 

 

Even the most comprehensive approach to screening and evaluation of symptomatic athletes will not completely eliminate on-pitch cardiac arrest. Thus, all stakeholders that engage in the oversight of organized soccer must be committed to the development and implementation of an EAP.²¹ Key components of an effective EAP include the training of coaching staff, athletic trainers, and players in basic cardiopulmonary resuscitation, access to and training in the use of automated external defibrillators, and a triage/transport protocol that ensures timely access to advanced cardiac life support. Much like screening, emergency action planning involving these key core components must be developed and tailored locally. In the era of contemporary organized athletics, the absence of an EAP at any level of competition, from youth to professional leagues, is unacceptable. Effective EAPs must be developed, documented, and rehearsed at regular intervals. For the health and safety of competitive soccer players, as well as coaching staff and spectators, these steps are of critical importance.

HEAT

Heat-related illnesses can be serious and, at times, even life threatening. It is important for athletic staff and athletes to be well versed in the prevention, signs and symptoms, and treatment of heat-related illnesses in order to prevent serious and lasting injury. We aim to educate physicians about the prevention, recognition, and management of heat-related injury, and stress the importance of similarly educating athletes and coaching staff.

Exertional heat illnesses most often occur at temperatures >86°F, however they can occur at any temperature with heavy exertion.²² Signs and symptoms can be nonspecific early on, including weakness, fatigue, headache, nausea, and dizziness. Later signs can include imbalance, altered mentation, confusion, and behavior that is out of character such as irritability or aggression.²³ It is easy to see how the later signs can be confused for concussion in the right context. We cover the recognition and treatment of two common and serious heat-related illnesses: heat exhaustion and exertional heat stroke (EHS).

HEAT EXHAUSTION

Heat exhaustion occurs when an athlete cannot continue to exercise due to weakness and fatigue. While the exact mechanism is not well understood, it has been established that the combined effect of heat and dehydration have been proven to decrease exercise capacity and performance to a greater degree than either alone. The heat created by the body during exercise is 15 to 20 times greater than when at rest, and can increase core body temperature by 1°C every 5 minutes if no heat is lost, such as through sweating.²⁴ Additionally, when fluid deficits reach >3% to 5% of total body water, sweat production and skin blood flow decline, blunting the ability for the body to cool itself and causing progressive elevation of core body temperature if the athlete continues exerting him or herself. When fluid deficits reach 6% to 10%, cardiac output, sweat, and muscle blood flow decrease, likely leading to the symptoms seen with heat exhaustion: weakness, profound fatigue, and occasionally confusion and disorientation. Athletes with suspected heat exhaustion should be moved to a cooler area, laid down with legs elevated, and orally rehydrated. If they do not improve with oral rehydration, they may require intravenous fluids. The diagnosis of heat exhaustion hinges on a rectal temperature of <104°F; if >104°F the athlete should be presumed to have heat stroke, which will be addressed in the following paragraphs. Players can be cleared to return to play in mild cases within 24 to 48 hours with gradual increases in exercise intensity.²⁴

EXERTIONAL HEAT STROKE

EHS occurs when the body can no longer regulate the core body temperature and it rises to upwards of 104°F. In EHS, elevated core body temperature is associated with evidence of end organ dysfunction. The most easily identified on the playing field is likely central nervous system dysfunction, including irritability, confusion, irrational behavior, lethargy, dizziness, confusion, and even loss of consciousness. Temperature should be measured with rectal temperature only, as other methods of measurement have been shown to be consistently inaccurate.²² Heat stroke can be confused with exertional hyponatremia, heat exhaustion, or concussion, especially when core body temperature cannot be determined. However, EHS should always be the presumed cause of altered mentation when no rectal temperature is available because rapid cooling is critical to minimizing lasting effects. Morbidity and mortality are directly related to the length of time required to cool the athlete under 40°C (104°F).²⁴ Cooling should be completed on site prior to transport to a medical facility and is best achieved with submersion in an ice bath (ie, a kiddie pool or soaking tub full of ice and water).^22,25 If an ice bath is not available, ice bags should be applied to the neck axilla and groin and exchanged for fresh bags every 2 to 3 minutes.²² Ice bags have been shown to be inferior to whole body cooling, only cooling the athlete .04°C to .08°C/min compared to .15°C to .24°C/min with the ice bath.²⁴ All other tests should be delayed until cooling is achieved, unless they can be completed while cooling the athlete. The athlete can be removed from the ice bath once rectal temperatures reach <101°F to 102°F.²³ If the athlete returns to baseline after cooling, transportation to a medical facility may not be necessary. However, they should refrain from physical activity and heat exposure for at least 7 days and should be evaluated by a physician at that time. If all labs are normal and the athlete is asymptomatic, they can start progressive return to play under the direction of an athletic trainer or a sports medicine physician.²³

Continue to: HEAT-RELATED ILLNESS...

 

 

HEAT-RELATED ILLNESS

It is impossible to predict exactly which athletes will be most at risk for heat-related illness, so it is important to have a high degree of suspicion when environmental conditions are right. Athletes with recent illness, fever, or lack of sleep are at higher risk. Additional intrinsic risk factors include low fitness level, obesity, and inadequate hydration. Athletes who are highly competitive or motivated can be more likely to push through the early signs of illness or be reluctant to report symptoms.²³ Those with a history of exertional heat illness are more at risk for developing it again in the future.²³

The extrinsic risk factors for the development of heat-related illness are much easier to identify and modify in order to keep athletes safe. High temperature and high humidity conditions, heavy sun exposure, and exposure to similar conditions the preceding day put athletes at risk for exertional heat illness. Risks are even greater when the exercise is prolonged or intense with few breaks and access to hydration is limited.²³ Therefore, prevention of exertional heat illness is centered on these external risk factors.

Each team should have a heat policy as part of their EAP aimed at prevention and early recognition of heat-related illness. This policy should be shared with all athletes and coaches. The plan should be centered on acclimatization, activity modification, and early recognition and management as previously discussed. The US Soccer Federation “Recognize to Recover” Heat Guidelines suggest a 3-step process for appropriate activity modification:²²

1. Find the wet bulb globe temperature, either using a wet bulb globe thermometer or the temperature and humidity (Figure 1).

2. Find your regional weather category on the map (Figure 2).

3. Find your alert level and work to rest ratio recommendations (Figure 3).

Scheduled hydration breaks should be given as listed in Figure 3. Breaks of 4 minutes should be given for each 30 minutes of continuous practice or play. In a regulation 90-minute match, a hydration break should be given at 30 and 75 minutes (with half time at 45 minutes) at minimum. Athletes should be educated about where hydration can be accessed, and given unlimited access to hydration even outside of planned breaks.²²

Acclimatization to conditions is another integral part of preventing heat-related illness. It allows the body time to adapt to exercising in heat gradually, with a measured progression of exertion over the course of 10 to 14 days. The “Recognize to Recover” Heat Guidelines also provide guidance on acclimatization, and specifics can be found on the website.¹ Generally speaking, the warmest part of the day, usually between 11 AM and 4 PM, should be avoided for all training sessions, and length of practice and exertion should be gradually increased over 2 weeks.²²

In summary, appropriate acclimatization, hydration, activity modification, and education of athletes and staff are essential for the prevention of heat-related illness. Athletes and staff should understand the signs and symptoms of heat-related illness so that it can be recognized early and treated appropriately. If an athlete is altered in the heat and rectal temperature is >104°F or rectal temperature cannot be obtained, rapid cooling using an ice bath or ice bags is essential to prevent the morbidity and mortality associated with EHS. Above all, teams should have an explicit plan that includes protocols for acclimatization, activity modification, and all necessary equipment to prevent and treat heat-related illnesses should they occur, and ultimately keep athletes safe and healthy.

ABSTRACT

Soccer requires significant physical conditioning and endurance, as well as the physicality required for contact play. In order to keep athletes safe, it is important that coaches, medical staff, and the players themselves are educated on the most common dangers to their health that they may encounter on a soccer pitch. This article aims to review the current literature and recommendations on concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer, with a goal of educating all those who help to keep athletes healthy and competing to their full potential.  

Continue to: Soccer is one of the most popular sports...

Soccer is one of the most popular sports in the modern world and requires significant physical conditioning and endurance, as well as the physicality required for contact play. This article covers the topics of concussion, cardiovascular considerations, and heat-related illness as they relate to competitive soccer players. We provide a review of the prevention, recognition, and management required to keep athletes safe on the soccer pitch, both in practice and in competitive play.

HEAD

With an estimated 1.6 to 3.8 million sports-related mild traumatic brain injuries (ie, concussions) occurring annually in the United States,¹ there has been an appropriate increase in the focus on prevention and treatment of these injuries. For more than a decade the spotlight has been on concussions that occur in American football, but other sports have also had to examine the prevalence of concussions in their sport. This is certainly true for soccer.

There has been a steady increase in soccer participation in the United States. From 1973 to 2014 there was a 4-fold increase in high school boys and a 35-fold increase in high school girls playing soccer.² Currently, there are more than 3.7 million youth who play on teams under the supervision of the US Soccer Federation, the sport’s national governing body.³ With the growth of the sport, there has also been an intensified focus on injury prevention in soccer players, including concussive brain injuries.

A recent study examined injury rates in high school soccer players and noted that concussion is the second most common injury (17.9%), after ligament sprains (29.7%).⁴ The overall injury rate was 2.06 per 1000 athletic exposures (AEs [defined as participation in practice or game play]), but higher in games (4.42 per 1000 AEs) than during practices (1.05 per 1000 AEs). The overall concussion rate was 0.36 per 1000 AEs.⁴

Most concussions (54.8%) resulted in missing play between 1 to 3 weeks, but a sizeable portion of the athletes (14.9%) were out of play for more than 3 weeks. Additionally, 10.7% of all medical disqualifications were due to concussive injuries. Khodaee and colleagues⁴ found no statistically significant difference in concussion rates between male and female soccer players over the 9-year period of time that they examined, however previous studies have found higher rates in female athletes.⁵

In soccer, as in other sports, there is a concern about both the adequate recognition of concussions during practice and play and the underreporting of concussions by athletes. The US Soccer Federation has taken a proactive stance on addressing concussion in youth soccer by developing the “Recognize to Recover” program.⁶ Recognize to Recover is the US Soccer Federation’s “comprehensive player health and safety program aimed at promoting safe play and reducing injuries in soccer players of all ages.” The website provides an educational video geared toward players, along with links to concussion assessment tools, the US Soccer Federation Concussion Protocol, and US Soccer Federation-Centers for Disease Control fact sheets for athletes, parents, and coaches.⁶

Continue to: A challenge for all sports...

 

 

A challenge for all sports is allowing adequate evaluation of a suspected concussion by properly trained healthcare professionals. The 2017 Berlin Concussion in Sport Group position paper stated, “when a concussion is suspected, the athlete should be removed from the sporting environment and a multimodal assessment should be conducted in standardized fashion (eg, Sport Concussion Assessment Tool- 5th edition). Sporting bodies should allow adequate time to conduct this evaluation.”⁷ However, the International Federation of Football Association (FIFA) rules limit substitutions to 3 over the course of the game, which can make a thorough evaluation of players difficult as trainers and coaches are under increased pressure to quickly determine whether to use one of their valuable substitutions. Fortunately, the National Collegiate Athletic Association (NCAA) soccer has mitigated this issue by allowing unlimited substitutions during matches, and high school teams generally follow similar rules.

One of the goals of any safety education program is not only to raise the awareness of the signs and symptoms of concussion by all those involved in the sport, but also to increase the number of athletes who self-report their symptoms and decrease those who hide any possible concussions. A study found that a majority (58.6%) of middle school soccer players continued to play while experiencing concussion symptoms.⁵ However, in a very recent (not yet published) study, 92% of US Soccer Federation players reported that they did seek out a medical evaluation for their concussion.⁸ This is certainly a positive sign and further research needs to clarify what methods of education or training will maintain this level of self-reporting in soccer players.

There has also been an increased focus on understanding the mechanism of injury of concussions. In soccer, concussions can occur from player-to-player contact, contact with the player surface, contact with playing apparatus (eg, goal posts) and non-contact mechanisms. While there has been a focus on concussions from heading the ball, player-to-player contact is the most common cause of concussions. A 2017 study of 7- to 12-year-old soccer players in 4 European countries found that about 1 out of 10 concussions were caused by heading the ball.⁹ Comstock and colleageues¹⁰ found slightly higher numbers, roughly 25% to 30% (depending on gender), but 70% to 78% (again depending on gender) of those were caused by player-to-player contact rather than contact with the ball.

To date there has not been any meta-analytic review evaluating the cognitive and physical symptoms associated with heading in soccer. A recent review paper stated that the “current evidence seems insufficient to support a ban of heading in children’s football (soccer).”¹⁰ However, in December 2015 the US Soccer Federation included age-specific heading limitations. Players ages 10 years and under “shall not engage in heading, either in practices or in games” and players age 11 years and 12 years should have “limited heading in practice; maximum of 30 minutes of heading training per week, with no more than 15-20 headers per player, per week.”¹¹ US Soccer Federation officials acknowledged the limitations in the current science regarding heading in young soccer players but chose to err on the side of caution until further empirical evidence regarding the risks associated with repetitive heading is available.

The US Soccer Federation is also exploring other ways to reduce the incidence rate of concussions, including ensuring that the age-appropriate sized ball is used in practice and play, possible rule changes, evaluation of different playing surfaces, and equipment usage. To date, there is no strong evidence to support the use of mouth guards or helmets to reduce concussions in soccer. Additionally, the current data about the value of head impact sensors in soccer has not supported its widespread use.

Continue to: Finally, the issue of the prevalence...

 

 

Finally, the issue of the prevalence of chronic traumatic encephalopathy (CTE) in soccer players is beyond the scope of this article. The expert opinion from the 2017 US Soccer Federation, Major League Soccer (MLS), and National Women’s Soccer League (NWSL) conference concluded, “At present, no data exist that support that soccer participation is a risk factor for the development of neurodegenerative disease. Similarly, at this time, consistent with evidence discussed in the Berlin Concussion in Sport Group (CISG) Consensus Conference, our review suggests no causal relationship has been demonstrated between soccer and CTE pathology.”¹²

The more we know about concussions, both in general and those sustained during soccer play, the better we are able to diagnose and manage these injuries in our athletes. An important step is creating evidence-based protocols that evolve as our knowledge of concussions does as well. In April 2017, the US Soccer Federation, MLS, and the NWSL held a joint summit entitled, “Head Injury in Soccer: From Science to the Field” to address the current evidence-based science of concussions in soccer.⁸ An article discussing the findings of this meeting is forthcoming and will undoubtedly guide further development of concussion protocols for soccer players of all ages.

HEART

The physiologic demands of soccer place considerable stress on the cardiovascular system. Participation in training and competition is characterized by a combination of aerobic and anaerobic physiology with the typical athlete covering approximately 10 km over the course of the 90-minute match. The primary role of the heart and blood vessels is to supply the exercising skeletal muscle with oxygen and energy substrate and to clear the byproducts of metabolism. Among healthy athletes without cardiovascular disease, these processes are typically well tolerated and may be associated with beneficial cardiovascular adaptations over time. However, competitive soccer players are not completely immune to cardiovascular disease. Athletes across the age and competition spectrum may develop symptoms suggestive of underlying cardiovascular disease during play including exertional chest pain, inappropriate shortness of breath, palpitations, and syncope. These athletes require timely clinical evaluation. In extremely rare but high visibility cases, competitive soccer players may succumb to cardiac arrest on the pitch, underscoring the need for comprehensive emergency action plans (EAPs). We provide the practicing clinician with an overview of cardiovascular issues relevant to the competitive soccer athlete.

CARDIOVASCULAR ADAPTATIONS TO SPORT

The pressure (ie, repetitive surges in systemic blood pressure) and volume (ie, sustained increases in high cardiac output) challenges inherent in soccer participation place stress on the cardiovascular system. Healthy athletes across the age spectrum typically tolerate the hemodynamic stressors of participation without issues. Athletes that engage in training and competition over months to years often develop beneficial adaptations of the cardiovascular system that enhance on-field performance and contribute to optimal long-term health. Detailed discussion of how the heart and blood vessels respond to exercise training is beyond the scope of this article, but the interested reader is referred to several prior publications.^13,14 In brief, the heart of the healthy soccer athlete demonstrates the balanced mild chamber dilation and wall thickening characteristic of left ventricular eccentric remodeling. This form of exercise-induced cardiac remodeling facilitates maintenance of high stroke volume during exercise with minimal increases in cardiac work. In parallel, routine aerobic exercise training confers favorable changes in the systemic arterial system, which leads to reductions in age-associated ventricular stiffening and maintenance of healthy low blood pressure. It must be emphasized that the healthy heart muscle dilation and thickening that develop in response to sports participation, regardless of age, ethnicity, or gender, are relatively mild and should not be confused with common forms of heart muscle disease that may be seen in athletes at risk for adverse outcomes. In some situations, consultation with an extreme sports cardiologist may be required to differentiate exercise-induced remodeling from over heart muscle pathology.¹⁵

Continue to: THE SYMPTOMATIC ATHLETE...

 

 

THE SYMPTOMATIC ATHLETE

Any athlete presenting with symptoms suggestive of underlying cardiovascular disease should be withheld from training and competition until a comprehensive clinical evaluation has been completed. Common manifestations of underlying heart disease that occur in soccer players include exertional chest pain/pressure/tightness, shortness of breath that is out of proportion to workload, palpitations or the perception of irregular cardiac activity, and syncope. Chest discomfort, inappropriate shortness of breath, and palpitations that occur during training or competition should be managed with immediate removal from the playing field and prompt medical assessment. In many cases, thorough evaluation will involve collaboration between sports medicine and sports cardiology providers. Evaluations must be individualized on a case-by-case basis as tailored to the athlete’s presenting chief complaint and prior medical history. Most of these assessments will include a detailed medical history and physical examination, a 12-lead electrocardiogram (ECG), provocative exercise testing in a controlled environment, noninvasive cardiac imaging, and in some cases ambulatory rhythm monitoring. Uniformly, the athlete should be withheld from further training and competition until high-risk cardiovascular disease has been excluded. We refer the interested reader to a comprehensive discussion of symptom-based assessment of the athlete with suspected cardiovascular disease.¹⁶

Syncope (sudden and abrupt loss of consciousness with spontaneous neurologic recovery) is common among trained athletes. The vast majority of syncope is caused by “neurocardiogenic” mechanisms and carries a benign prognosis. Benign neurally-mediated syncope most often occurs outside of training and competition among athletes with heightened vagal tone and a predisposed susceptibility to triggers including pain, anxiety, emotional stimulation, and sudden postural change. Athletes who experience neurally-mediated syncope outside of training and competition routinely report a pre-event prodrome or aura that permits them to lower themselves to the ground, thereby avoiding injury. A distinct, but similarly benign and common, form of neurally-mediated fainting is post-exertional syncope. Here, fainting occurs within seconds of abrupt termination of exercise due to a rapid reduction cardiac preload and corollary cerebral blood supply. When either form of neurally-mediated syncope is suggested by a comprehensive medical history, normal physical examination, and a normal 12- lead ECG, further evaluation is unnecessary. However, the athlete and their coaching staff should be educated about avoidance tactics including hydration, dietary sodium supplementation, and avoidance of abrupt exercise termination as neutrally-mediated syncope tends to be recurrent without such measures. Fainting episodes that occur during training or competition that are not clearly post-exertional should be considered a medical emergency and should prompt comprehensive evaluation by a qualified cardiovascular specialist. Working closely with team physicians and athletic training staff, it is the responsibility of sports cardiologists to exclude potentially life-threatening forms of electrical, muscular, coronary, and valvular heart disease. Ideally, this evaluation should be conducted rapidly to avoid unnecessary delays in return to play.

CARDIAC ARREST AND SUDDEN DEATH

Numerous high-visibility cases of cardiac arrest on the soccer pitch have alerted the sporting community to the potential for these rare and potentially tragic events. Definitive incidence statistics defining the risk of cardiac arrest among soccer players are lacking. Data from the NCAA database suggest a sudden death incidence rate among collegiate male soccer athletes of approximately 1:24,000 athlete years.⁸ Similar data documenting incidence among female athletes and among those at lower (ie, youth level and high school) and higher (ie, professional) levels of play are unavailable. Underlying cardiovascular disease in the forms of heart muscle abnormalities (ie, genetic and acquired cardiomyopathy), coronary artery abnormalities (ie, genetic coronary anomalies and atherosclerotic coronary disease), valvular heart problems (ie, congenitally malformed aortic valves), and primary disturbances of the cardiac electrical system (ie, Wolf-Parkinson-White syndrome, long QT syndrome, etc.) explain a substantial percentage of on-pitch cardiac arrest. However, it is increasingly recognized that a significant minority of sudden cardiac deaths among athletes occur in the absence of attributable cardiovascular abnormality.¹⁷ Such cases, often referred to as “sudden unexplained death,” present unique challenges in the context of pre-participation screening, as they are undetectable and thus unpredictable.

Reduction of cardiac arrest and sudden death may best be accomplished through a combination of focused pre-participation screening and the development and implementation of a comprehensive EAP. Pre-participation involves the performance of a battery of tests prior to training and competition that are geared toward the detection of occult high-risk cardiovascular disease. Recommendations regarding pre-participation screening vary both across and within countries. Current US recommendations call for a focused medical history and physical examination prior to training and competition with consideration of the addition of a 12-lead ECG on a local level based on expertise and available resources.¹⁸ Conversely, current European guidelines including those endorsed by FIFA, suggest routine inclusion of a 12-lead ECG and in some cases, a transthoracic ECG.¹⁹ It must be emphasized that no screening approach has been confirmed to reduce the incidence of sudden death, and the decision to extend screening beyond the medical history and physical examination to include a 12-lead ECG or echocardiogram may come at the cost of increased false positive testing. In practice, decisions about how and when to screen are ideally made at a local level after consideration of medical and financial resources.²⁰

Continue to: Even the most comprehensive approach...

 

 

Even the most comprehensive approach to screening and evaluation of symptomatic athletes will not completely eliminate on-pitch cardiac arrest. Thus, all stakeholders that engage in the oversight of organized soccer must be committed to the development and implementation of an EAP.²¹ Key components of an effective EAP include the training of coaching staff, athletic trainers, and players in basic cardiopulmonary resuscitation, access to and training in the use of automated external defibrillators, and a triage/transport protocol that ensures timely access to advanced cardiac life support. Much like screening, emergency action planning involving these key core components must be developed and tailored locally. In the era of contemporary organized athletics, the absence of an EAP at any level of competition, from youth to professional leagues, is unacceptable. Effective EAPs must be developed, documented, and rehearsed at regular intervals. For the health and safety of competitive soccer players, as well as coaching staff and spectators, these steps are of critical importance.

HEAT

Heat-related illnesses can be serious and, at times, even life threatening. It is important for athletic staff and athletes to be well versed in the prevention, signs and symptoms, and treatment of heat-related illnesses in order to prevent serious and lasting injury. We aim to educate physicians about the prevention, recognition, and management of heat-related injury, and stress the importance of similarly educating athletes and coaching staff.

Exertional heat illnesses most often occur at temperatures >86°F, however they can occur at any temperature with heavy exertion.²² Signs and symptoms can be nonspecific early on, including weakness, fatigue, headache, nausea, and dizziness. Later signs can include imbalance, altered mentation, confusion, and behavior that is out of character such as irritability or aggression.²³ It is easy to see how the later signs can be confused for concussion in the right context. We cover the recognition and treatment of two common and serious heat-related illnesses: heat exhaustion and exertional heat stroke (EHS).

HEAT EXHAUSTION

Heat exhaustion occurs when an athlete cannot continue to exercise due to weakness and fatigue. While the exact mechanism is not well understood, it has been established that the combined effect of heat and dehydration have been proven to decrease exercise capacity and performance to a greater degree than either alone. The heat created by the body during exercise is 15 to 20 times greater than when at rest, and can increase core body temperature by 1°C every 5 minutes if no heat is lost, such as through sweating.²⁴ Additionally, when fluid deficits reach >3% to 5% of total body water, sweat production and skin blood flow decline, blunting the ability for the body to cool itself and causing progressive elevation of core body temperature if the athlete continues exerting him or herself. When fluid deficits reach 6% to 10%, cardiac output, sweat, and muscle blood flow decrease, likely leading to the symptoms seen with heat exhaustion: weakness, profound fatigue, and occasionally confusion and disorientation. Athletes with suspected heat exhaustion should be moved to a cooler area, laid down with legs elevated, and orally rehydrated. If they do not improve with oral rehydration, they may require intravenous fluids. The diagnosis of heat exhaustion hinges on a rectal temperature of <104°F; if >104°F the athlete should be presumed to have heat stroke, which will be addressed in the following paragraphs. Players can be cleared to return to play in mild cases within 24 to 48 hours with gradual increases in exercise intensity.²⁴

EXERTIONAL HEAT STROKE

EHS occurs when the body can no longer regulate the core body temperature and it rises to upwards of 104°F. In EHS, elevated core body temperature is associated with evidence of end organ dysfunction. The most easily identified on the playing field is likely central nervous system dysfunction, including irritability, confusion, irrational behavior, lethargy, dizziness, confusion, and even loss of consciousness. Temperature should be measured with rectal temperature only, as other methods of measurement have been shown to be consistently inaccurate.²² Heat stroke can be confused with exertional hyponatremia, heat exhaustion, or concussion, especially when core body temperature cannot be determined. However, EHS should always be the presumed cause of altered mentation when no rectal temperature is available because rapid cooling is critical to minimizing lasting effects. Morbidity and mortality are directly related to the length of time required to cool the athlete under 40°C (104°F).²⁴ Cooling should be completed on site prior to transport to a medical facility and is best achieved with submersion in an ice bath (ie, a kiddie pool or soaking tub full of ice and water).^22,25 If an ice bath is not available, ice bags should be applied to the neck axilla and groin and exchanged for fresh bags every 2 to 3 minutes.²² Ice bags have been shown to be inferior to whole body cooling, only cooling the athlete .04°C to .08°C/min compared to .15°C to .24°C/min with the ice bath.²⁴ All other tests should be delayed until cooling is achieved, unless they can be completed while cooling the athlete. The athlete can be removed from the ice bath once rectal temperatures reach <101°F to 102°F.²³ If the athlete returns to baseline after cooling, transportation to a medical facility may not be necessary. However, they should refrain from physical activity and heat exposure for at least 7 days and should be evaluated by a physician at that time. If all labs are normal and the athlete is asymptomatic, they can start progressive return to play under the direction of an athletic trainer or a sports medicine physician.²³

Continue to: HEAT-RELATED ILLNESS...

 

 

HEAT-RELATED ILLNESS

It is impossible to predict exactly which athletes will be most at risk for heat-related illness, so it is important to have a high degree of suspicion when environmental conditions are right. Athletes with recent illness, fever, or lack of sleep are at higher risk. Additional intrinsic risk factors include low fitness level, obesity, and inadequate hydration. Athletes who are highly competitive or motivated can be more likely to push through the early signs of illness or be reluctant to report symptoms.²³ Those with a history of exertional heat illness are more at risk for developing it again in the future.²³

The extrinsic risk factors for the development of heat-related illness are much easier to identify and modify in order to keep athletes safe. High temperature and high humidity conditions, heavy sun exposure, and exposure to similar conditions the preceding day put athletes at risk for exertional heat illness. Risks are even greater when the exercise is prolonged or intense with few breaks and access to hydration is limited.²³ Therefore, prevention of exertional heat illness is centered on these external risk factors.

Each team should have a heat policy as part of their EAP aimed at prevention and early recognition of heat-related illness. This policy should be shared with all athletes and coaches. The plan should be centered on acclimatization, activity modification, and early recognition and management as previously discussed. The US Soccer Federation “Recognize to Recover” Heat Guidelines suggest a 3-step process for appropriate activity modification:²²

1. Find the wet bulb globe temperature, either using a wet bulb globe thermometer or the temperature and humidity (Figure 1).

2. Find your regional weather category on the map (Figure 2).

3. Find your alert level and work to rest ratio recommendations (Figure 3).

Scheduled hydration breaks should be given as listed in Figure 3. Breaks of 4 minutes should be given for each 30 minutes of continuous practice or play. In a regulation 90-minute match, a hydration break should be given at 30 and 75 minutes (with half time at 45 minutes) at minimum. Athletes should be educated about where hydration can be accessed, and given unlimited access to hydration even outside of planned breaks.²²

Acclimatization to conditions is another integral part of preventing heat-related illness. It allows the body time to adapt to exercising in heat gradually, with a measured progression of exertion over the course of 10 to 14 days. The “Recognize to Recover” Heat Guidelines also provide guidance on acclimatization, and specifics can be found on the website.¹ Generally speaking, the warmest part of the day, usually between 11 AM and 4 PM, should be avoided for all training sessions, and length of practice and exertion should be gradually increased over 2 weeks.²²

In summary, appropriate acclimatization, hydration, activity modification, and education of athletes and staff are essential for the prevention of heat-related illness. Athletes and staff should understand the signs and symptoms of heat-related illness so that it can be recognized early and treated appropriately. If an athlete is altered in the heat and rectal temperature is >104°F or rectal temperature cannot be obtained, rapid cooling using an ice bath or ice bags is essential to prevent the morbidity and mortality associated with EHS. Above all, teams should have an explicit plan that includes protocols for acclimatization, activity modification, and all necessary equipment to prevent and treat heat-related illnesses should they occur, and ultimately keep athletes safe and healthy.

ABSTRACT

As one of the most popular sports in the world, soccer injury rates involving the knee continue to rise. An alarming trend of knee injuries, including increased anterior cruciate ligament ruptures, underscores the need to review our current understanding of these injuries in soccer players. This article includes a critical review of the epidemiology of knee injuries in soccer, anterior cruciate ligament and other ligamentous injuries, cartilage and meniscal injury, post-traumatic osteoarthritis, as well as current prevention initiatives.

Continue to: EPIDEMIOLOGY...

EPIDEMIOLOGY

There are currently 28 players on each of the Major League Soccer (MLS) teams, and during the 2013 to 2014 academic year, the National Federation of State High School Associations (NFHS) reported that 417,419 boys and 374,564 girls played high school soccer and the National Collegiate Athletic Association (NCAA) reported that 23,602 males and 26,358 females played collegiate soccer.⁵ As such, knee injuries in this population are a major concern for those involved in sports medicine. Several injuries occurring during soccer involve the lower extremity, particularly the knee.¹ In fact, multiple reports estimate that up to 17.6% of soccer-related injuries presenting to the emergency room involved the knee.^1,6-9 The majority of these injuries are noncontact injuries, although contact injuries do still occur.^10,11

Risk factors for injuries in soccer may be non-modifiable (such as age and gender) and modifiable (such as level of conditioning, force, balance, and flexibility). Inadequate lower motor coordination may result in injury in the adolescent population, and advanced age >28 years in males and >25 years in females is considered as a high-risk factor for injury.^12,13 Importantly, gender and age have been reported to play a significant role as risk factors for ACL injury.⁶ In fact, female players have a 3 to 5 times higher risk of significant knee injury, including ACL injuries, than male players.^4,14-16 Preventative programs such as the FIFA 11+ program have been set forth to augment conditioning as part of managing the modifiable risk factors.

Like American football, playing on artificial turf has been questioned as a contributor to injury compared to playing on natural grass.^17,18 In recent years, newer generations of artificial turf have been developed to more closely replicate the characteristics of natural grass. Meyers¹⁹ compared the incidence, mechanisms, and severity of match-related collegiate men’s soccer injuries on artificial turf and those on natural grass and demonstrated no significant difference in knee injuries between the 2 surfaces. This finding was consistent with previous studies that reported no difference in the incidence of knee injuries on either surface in women’s collegiate and elite-level soccer.^15,20,21

Continue to: ACL INJURIES...

ACL INJURIES

ACL injuries are life-changing events that can significantly affect the career of a soccer athlete. As a major stabilizer of the knee, the ACL primarily prevents anterior tibial translation with the anteromedial bundle and secondarily resists tibial rotation with the posterolateral bundle. The ligament takes origin from the posteromedial aspect of the lateral femoral condyle and inserts anterior to the tibial intercondylar eminence. Grading of ACL injuries is based on the Lachman test, which is performed between 20°and 30° of knee flexion and measures the amount of anterior tibial translation relative to the femur (A = firm endpoint, B = no endpoint; grade I: 3-5 mm, grade II (A/B): 5-10 mm, grade III (A/B): >10 mm).

ACL injury may occur via contact or noncontact mechanisms. Noncontact mechanisms of ACL injury in soccer athletes contribute to about 85% of injuries.^6,22-25 Typical noncontact mechanism of injury involves a forceful valgus collapse with the knee near full extension and combined external or internal rotation of the tibia^23,26 (Figure 1). This on-field scenario generally involves cutting and torsional movement, as well as landing after a jump, particularly in 1-legged stance. Similarly, a disturbance in balance caused by the opponent may incite a noncontact mechanism resulting in ACL rupture.^6,27 Video analyses of professional soccer players have also demonstrated a higher risk of noncontact ACL injury within the first 9 minutes of the match, with the most common playing situation resulting in injury being pressing, followed by kicking and heading.^24,25,28 Contact mechanisms resulting in ACL injury, however, are not an uncommon occurrence in soccer players with higher risk for certain positions. Brophy and colleagues²⁹ reviewed ACL injuries in professional and collegiate soccer players and reported a higher risk of ACL injury during defending and tackling. Similarly, Faude and colleagues³⁰ found the risk of injury to be higher in defenders and strikers than in goalkeepers and midfielders.

Female athletes participating in elite-level athletics, especially soccer, represent a high-risk group for ACL injury. In fact, these soccer athletes experience ACL injury at an incidence 3 times higher than that in male athletes.^31-35 Female soccer athletes may also be at risk for reinjury to the ACL and contralateral ACL injury. Female gender, in combination with participation in soccer, thus represents a high-risk group for ACL tear in athletics. Allen and colleagues³⁶ retrospectively reviewed 180 female patients who had undergone ACL reconstruction (ACLR) (90 soccer players and 90 non-soccer players) over a mean period of 68.8 months. In their series, soccer players sustained significantly more ACL injuries than non-soccer players, including graft failures (11% vs 1%) and contralateral ACL tears (17% vs 4%).

ACLR is the gold standard treatment for elite soccer athletes. A recent survey of MLS team orthopedic surgeons revealed several important details regarding decision-making in ACLR in this population. From a technical standpoint, the vast majority of surgeons used a single incision, arthroscopically assisted, single-bundle reconstruction (91%). Femoral tunnel drilling was almost equally split between transtibial (51%) and use of an accessory medial portal (46%). Bone-patella-tendon-bone (BPTB) autograft was the most preferred graft choice (68%), and quadriceps tendon autograft was the least preferred. The majority of surgeons preformed ACLR within 4 weeks and permitted return to sport (RTS) without restrictions at 6 to 8 months.³⁷

Continue to: There is a scarcity of literature regarding...

There is a scarcity of literature regarding the use of soft tissue and BPTB allografts in soccer athletes. However, one study reported no difference in patient-reported outcomes and return to preinjury level of activity (including soccer) with the use of either autograft or allograft BPTB in ACLR.³⁸ The authors’ preference was to avoid the use of allograft in elite-level soccer athletes as the reported rate of ACL re-tear was 4 to 8 times higher than that with autograft reconstruction, as shown in athletes and military personnel.^39,40 BPTB autograft and hamstring autograft (semitendinosus and/or gracilis) are common graft choices for soccer athletes. Gifstad and colleagues⁴¹ compared BPTB autograft and hamstring autograft in 45,998 primary ACLRs performed in Scandinavia. Although the cohort included, but was not limited to, soccer players, the authors reported an overall risk of revision that was significantly lower in the BPTB autograft group than in the hamstring autograft group (hazard ratio, 0.63; 95% confidence interval, 0.53-0.74).⁴¹ Mohammadi and colleagues⁴² prospectively compared the functional outcomes of 42 competitive soccer players who underwent ACLR with BPTB autograft vs those who underwent ACLR with hamstring autograft at the time of RTS. Players who had undergone ACLR with hamstring autograft demonstrated greater quadriceps torque, as well as better performance with triple-hop, crossover-hop, and jump-landing tests; however, both groups demonstrated similar hamstring torque and performance in 2 other hop tests.⁴² In the authors’ opinion, there may be a concern regarding the use of hamstring autograft in elite soccer players considering that hamstring strains are extremely common in this athletic population; however, further research would be necessary to elucidate whether this is an actual or a theoretical risk. Although not yet studied in elite-level athletes, early clinical results of ACL repair with suture augmentation show promise for certain injury patterns. These include proximal femoral ACL avulsion injuries (Sherman type 1) of excellent tissue quality that have the ability to be reapproximated to the femoral origin⁴³ (Figures 2A, 2B). In a recent series,^43-45 early clinical outcomes were found to be excellent and maintained at midterm follow-up.

In the NCAA soccer athletes, an overall RTS rate of 85% has been reported in those undergoing ACLR, with a significantly higher rate observed in scholarship versus non-scholarship athletes.⁴⁶ Howard and colleagues⁴⁶ reported median time to unrestricted game play of 6.1 months, with 75% returning to the same or higher level position on the depth chart. Among their studied collegiate soccer athletes, 32% reported continued participation in soccer on some level after college (recreational, semiprofessional, or professional).⁴⁶ RTS rates for MLS soccer players have also been reported to be high, ranging from 74% to 77%, most of them returning within the following season at 10 ± 2.8 months.^47,48 These findings were consistent with the RTS rate of 72% reported by the Multicenter Orthopaedic Outcomes Network (MOON) group, which analyzed 100 female and male soccer players undergoing ACLR at a minimum 7-year follow-up. In this series, Brophy and colleagues^29,49 reported an RTS at 12 ± 14.3 months, with 85% returning to the same or a higher level of play prior to their injury. Erickson and colleagues⁴⁷ analyzed a series of 57 ACLRs performed in MLS athletes and reported no significant difference in preinjury or postoperative performance, or between cases and uninjured controls. Arundale and colleagues⁴⁸ demonstrated no significantly increased risk of lower extremity injury in MLS athletes after ACLR, but the athletes had significantly shorter careers than their uninjured counterparts. Curiously, RTS rates for European professional soccer athletes have been reported to be substantially higher at 95% to 97%.^50,51 Although we can only speculate the reasons for such a discrepancy, the difference in RTS rates for similar athletes highlights a need for objective criteria to determine and report RTS rates, while also providing guidelines to prevent reinjury. Such a consensus among orthopedists is not yet present in the literature.

Soccer players and adolescent age in combination have been shown to portend a 3-fold increased risk of revision surgery for ACL failure in a cohort of 16,930 patients from the Swedish National Knee Ligament Register.⁵² Published data regarding ACL failure and management of revision ACLR in elite-level soccer athletes are currently lacking. However, low failure rates of 3% to 10% requiring revision reconstruction have been reported.^47,49 Arundale and colleagues⁴⁸ reported 2 incidences of players with ACL graft failures, 1 BPTB autograft and 1 BPTB allograft, both of whom were able to return to MLS after revision ACLR. It is the authors’ preference to use ipsilateral hamstring autograft or contralateral BPTB autograft when an ACL revision reconstruction is required.

Continue to: OTHER LIGAMENTOUS INJURIES...

OTHER LIGAMENTOUS INJURIES

The majority of research efforts regarding knee injuries in this population are focused on the ACL. Correspondingly, literature regarding injury to the collateral ligaments and the posterior cruciate ligament (PCL) in soccer players is sparse. The lateral collateral ligament (LCL) and the medial collateral ligament (MCL) play important roles as primary stabilizers to varus and valgus forces, respectively. The PCL is the primary posterior stabilizer of the knee, preventing posterior translation of the tibia. Injury to these structures may result in significant time lost from soccer and risk of reinjury.^53,54

The MCL is the one of the most commonly injured ligaments in sports, including soccer.^53,55 The injury mechanism generally involves contact with a resulting valgus force applied to the knee.⁵⁵ Grading of MCL injuries is based on the amount of medial joint gapping with applied valgus force during examination (grade I: <5 mm, grade II: 5-10 mm, grade III: >10 mm). Kramer and colleagues⁵³ reviewed collateral ligament injuries in the adolescent population and found that MCL injuries occurred 4 times more often than LCL injuries and about 25% were grade III injuries, most commonly occurring in American football and soccer players. Soccer also touts the highest sport-specific MCL injury rate for high school and collegiate athletics, particularly for female NCAA soccer players.⁵⁶ At the professional level, Lundblad and colleagues⁵⁵ reported 346 MCL injuries in 27 European teams over an 11-year period, of which 70% were contact-related, and the average time-off from soccer was 28 days.

Most surgeons treat isolated MCL injuries nonoperatively, regardless of grade.^57,58 This includes activity modification, use of a hinged knee brace, quadriceps strengthening, and progressive return to play. The literature currently lacks substantial data to guide MCL injury management, specifically in elite soccer athletes. In our experience, grade I injuries are managed nonoperatively and RTS is allowed at 4 to 6 weeks. Grade II injuries are also managed nonoperatively and RTS is allowed at 6 to 8 weeks. Grade III injuries are generally allowed RTS at 8 to 12 weeks and may be considered for surgery in the context of concomitant injuries (eg, posteromedial capsular injury, multiligamentous knee injuries, and meniscal injuries). In some athletes, we consider using a varus unloader brace to help maximize decreased stress on the MCL while still allowing the athlete to be fully weight-bearing. We have found it less ideal to limit weight-bearing in elite athletes, which may negatively affect overall lower extremity neuromuscular proprioception and potentially prolong a safe return to play. Some athletes may experience prolonged soreness at the MCL femoral or tibial attachment despite being able to return to play. It is important to counsel athletes about these prolonged symptoms to set expectations, as this may even occur with grade I MCL injuries. Other rare instances where surgical management may be indicated include persistent pain and instability following nonoperative treatment of grade III injuries and highly displaced tibial avulsions of the ligament resulting in poor healing.^59,60

Data regarding LCL injuries in soccer are extremely sparse. In our experience, treatment and RTS rates for isolated LCL injuries are similar to those for MCL injuries. However, it is worth noting that one-quarter of LCL injuries may occur in combination with injury to other posterolateral corner structures.⁵³

PCL injuries are more commonly associated with vehicular trauma but have also been reported to occur in sports at a rate of 33% to 40%.^61,62 The mechanism of injury in athletes generally involves a fall onto the hyperflexed knee with the foot in plantarflexion or a direct blow to the anterior tibia in a flexed knee.^62,63 Classification of PCL injuries is based on posterior translation of the tibia relative to the femur with the knee flexed to 90°(grade I: 1-5 mm, grade II: 6-10 mm, grade III: >10 mm). In one cohort of 62 patients with isolated PCL injuries, soccer was found to be among the top 5 causes of injury.⁶⁴ A Scandinavian review of 1287 patients who underwent PCL reconstruction found soccer to be the sport with the highest number of injuries (13.1%).⁶⁵ The goalkeeper was most commonly subjected to this injury.⁶² Krutsch and colleagues⁵⁴ compared PCL injuries in new, professional soccer players to those in players at the closest amateur level of play. In their series, 90% of PCL injuries occurred during preseason in players who were at a lower level of play in the previous season. This finding suggested that a rapid increase in training and playing intensity may have been a significant risk factor for PCL injury. Substantial literature supporting nonoperative or operative management of PCL injuries in soccer athletes is currently lacking. Historically, nonoperative treatment has been the initial management for isolated PCL injuries; however, surgical intervention has become increasingly used for both isolated and combined PCL injuries.⁶⁶

Continue to: CARTILAGE AND MENISCAL INJURIES...

CARTILAGE AND MENISCAL INJURIES

The prevalence of osteoarthritis (OA) in retired soccer players is high.^67,68 Articular cartilage degeneration with subsequent OA occurs in up to 32% of soccer players and ultimately leads to significant disability and retirement from the sport. High physical demands and concomitant knee injuries probably predispose to the development of posttraumatic OA.^69-71

Several techniques addressing cartilage débridement or restoration have been reported, with successful RTS but with variable durability.^72-75 Recently, Andrade and colleagues⁷⁶ performed a systematic review of 217 articular cartilage defects in soccer players that were treated using restoration techniques, including chondroplasty, microfracture, autologous chondrocyte implantation (ACI), and osteochondral autograft. Although no superior technique could be ascertained, microfracture and osteochondral autograft procedures led to the quickest return to play, and ACI techniques enhanced long-standing clinical and functional results.⁷⁶ More recently, osteochondral allograft transplantation has also been described with an 84% return to some level of activity (including soccer) and 60% of athletes returning to high-level sports participation at a mean follow-up of 4.5 years⁷⁷ (Figures 3A-3C). Although chondroplasty may be successful and allow for a quicker return to play in some soccer players (return to play from 6-12 weeks), the authors believe that a strong cartilage scaffold repair strategy with early weight-bearing, including osteochondral autograft and allograft procedures (return to play from 6-9 months), must also be considered in focal chondral defects to optimize both short-term and potential long-term success.

Meniscal injuries are also prevalent in the soccer population, and consistent with ACL injuries, female players are at least twice as likely to sustain a meniscal tear.^78,79 Meniscal damage can occur in isolation or in association with ACL rupture. Repair techniques should be strongly considered as chondral changes in the setting of meniscal deficiency are a significant short- and long-term concern for elite athletes. However, due to intrinsically poor healing potential, partial meniscectomy is unfortunately more often performed.^79,80 In either case, meniscal deficiency is recognized as a precursor to the development of OA as meniscal functionality is lost and the articular cartilage is subjected to increased biomechanical loading.^81,82 Nawabi and colleagues⁸³ analyzed RTS in 90 professional soccer players following partial meniscectomy. Median RTS was at 7 weeks for lateral meniscectomies and at 5 weeks for medial meniscectomies. RTS probability was 5.99 times greater after medial meniscectomy at all time points. Lateral meniscectomies were associated with an increased risk of postoperative adverse events, reoperation, and a significantly lower rate of return to play.⁸³ In the case of severe meniscal deficiency, particularly post-meniscectomy, meniscal allograft transplantation (MAT) may be considered. In a series of MATs in lower division Spanish players, 12/14 (85.7%) returned to play at an average of 7.6 months.⁸⁴ A more recent series of professional players reported 9/12 (75%) RTS as professionals and 2/12 (17%) as semiprofessionals at an average of 10.5 months.⁸⁵ The authors’ strong preference is to perform meniscus-saving procedures whenever possible. Due to the longer recovery and return to play associated with meniscus repair than partial meniscectomy, most of the soccer players will often prefer to proceed with partial meniscectomy. Despite the ultimate treatment, it is critical that the surgeon and the soccer player have an in-depth conversation concerning the risks and benefits for each procedure and individualize treatment to the individual soccer player accordingly.

Continue to: INJURY PREVENTION...

INJURY PREVENTION

Given the breadth and the prevalence of soccer-related injuries, the FIFA11+ program was developed in 2006 as an injury prevention measure (Figure 4). The warm-up program includes 15 structured exercises emphasizing core stabilization, thigh muscle training, proprioception, dynamic stabilization, and plyometric exercises. The routine is believed to be easily executed and effective at preventing the incidence of noncontact injuries.^86,87 Recently, Sadigursky and colleagues¹ performed a systematic review of randomized clinical trials examining the efficacy of FIFA11+. The authors reported a reduction in injuries by 30% and a relative risk of 0.70 for lower limb injuries, highlighting the significant preventative importance of the program.¹ Post-training programs may also be beneficial as it has been shown that performing FIFA11+ both before and after training reduced overall injury rates in male, amateur soccer players.⁸⁸ Regardless of the prevention program, it is critical that every league, team, medical team, and athlete have a thorough injury prevention strategy to help keep players healthy and not wait until they have instead sustained a significant injury.

CONCLUSION

Knee injuries are common in soccer, with an alarming number of ACL injuries, as well as other significant pathology. Understanding the unique epidemiology, risk factors, treatment, and injury prevention strategies is critically important in helping medical professionals provide care for all levels of elite soccer players.

ABSTRACT

As one of the most popular sports in the world, soccer injury rates involving the knee continue to rise. An alarming trend of knee injuries, including increased anterior cruciate ligament ruptures, underscores the need to review our current understanding of these injuries in soccer players. This article includes a critical review of the epidemiology of knee injuries in soccer, anterior cruciate ligament and other ligamentous injuries, cartilage and meniscal injury, post-traumatic osteoarthritis, as well as current prevention initiatives.

Continue to: EPIDEMIOLOGY...

EPIDEMIOLOGY

There are currently 28 players on each of the Major League Soccer (MLS) teams, and during the 2013 to 2014 academic year, the National Federation of State High School Associations (NFHS) reported that 417,419 boys and 374,564 girls played high school soccer and the National Collegiate Athletic Association (NCAA) reported that 23,602 males and 26,358 females played collegiate soccer.⁵ As such, knee injuries in this population are a major concern for those involved in sports medicine. Several injuries occurring during soccer involve the lower extremity, particularly the knee.¹ In fact, multiple reports estimate that up to 17.6% of soccer-related injuries presenting to the emergency room involved the knee.^1,6-9 The majority of these injuries are noncontact injuries, although contact injuries do still occur.^10,11

Risk factors for injuries in soccer may be non-modifiable (such as age and gender) and modifiable (such as level of conditioning, force, balance, and flexibility). Inadequate lower motor coordination may result in injury in the adolescent population, and advanced age >28 years in males and >25 years in females is considered as a high-risk factor for injury.^12,13 Importantly, gender and age have been reported to play a significant role as risk factors for ACL injury.⁶ In fact, female players have a 3 to 5 times higher risk of significant knee injury, including ACL injuries, than male players.^4,14-16 Preventative programs such as the FIFA 11+ program have been set forth to augment conditioning as part of managing the modifiable risk factors.

Like American football, playing on artificial turf has been questioned as a contributor to injury compared to playing on natural grass.^17,18 In recent years, newer generations of artificial turf have been developed to more closely replicate the characteristics of natural grass. Meyers¹⁹ compared the incidence, mechanisms, and severity of match-related collegiate men’s soccer injuries on artificial turf and those on natural grass and demonstrated no significant difference in knee injuries between the 2 surfaces. This finding was consistent with previous studies that reported no difference in the incidence of knee injuries on either surface in women’s collegiate and elite-level soccer.^15,20,21

Continue to: ACL INJURIES...

ACL INJURIES

ACL injuries are life-changing events that can significantly affect the career of a soccer athlete. As a major stabilizer of the knee, the ACL primarily prevents anterior tibial translation with the anteromedial bundle and secondarily resists tibial rotation with the posterolateral bundle. The ligament takes origin from the posteromedial aspect of the lateral femoral condyle and inserts anterior to the tibial intercondylar eminence. Grading of ACL injuries is based on the Lachman test, which is performed between 20°and 30° of knee flexion and measures the amount of anterior tibial translation relative to the femur (A = firm endpoint, B = no endpoint; grade I: 3-5 mm, grade II (A/B): 5-10 mm, grade III (A/B): >10 mm).

ACL injury may occur via contact or noncontact mechanisms. Noncontact mechanisms of ACL injury in soccer athletes contribute to about 85% of injuries.^6,22-25 Typical noncontact mechanism of injury involves a forceful valgus collapse with the knee near full extension and combined external or internal rotation of the tibia^23,26 (Figure 1). This on-field scenario generally involves cutting and torsional movement, as well as landing after a jump, particularly in 1-legged stance. Similarly, a disturbance in balance caused by the opponent may incite a noncontact mechanism resulting in ACL rupture.^6,27 Video analyses of professional soccer players have also demonstrated a higher risk of noncontact ACL injury within the first 9 minutes of the match, with the most common playing situation resulting in injury being pressing, followed by kicking and heading.^24,25,28 Contact mechanisms resulting in ACL injury, however, are not an uncommon occurrence in soccer players with higher risk for certain positions. Brophy and colleagues²⁹ reviewed ACL injuries in professional and collegiate soccer players and reported a higher risk of ACL injury during defending and tackling. Similarly, Faude and colleagues³⁰ found the risk of injury to be higher in defenders and strikers than in goalkeepers and midfielders.

Female athletes participating in elite-level athletics, especially soccer, represent a high-risk group for ACL injury. In fact, these soccer athletes experience ACL injury at an incidence 3 times higher than that in male athletes.^31-35 Female soccer athletes may also be at risk for reinjury to the ACL and contralateral ACL injury. Female gender, in combination with participation in soccer, thus represents a high-risk group for ACL tear in athletics. Allen and colleagues³⁶ retrospectively reviewed 180 female patients who had undergone ACL reconstruction (ACLR) (90 soccer players and 90 non-soccer players) over a mean period of 68.8 months. In their series, soccer players sustained significantly more ACL injuries than non-soccer players, including graft failures (11% vs 1%) and contralateral ACL tears (17% vs 4%).

ACLR is the gold standard treatment for elite soccer athletes. A recent survey of MLS team orthopedic surgeons revealed several important details regarding decision-making in ACLR in this population. From a technical standpoint, the vast majority of surgeons used a single incision, arthroscopically assisted, single-bundle reconstruction (91%). Femoral tunnel drilling was almost equally split between transtibial (51%) and use of an accessory medial portal (46%). Bone-patella-tendon-bone (BPTB) autograft was the most preferred graft choice (68%), and quadriceps tendon autograft was the least preferred. The majority of surgeons preformed ACLR within 4 weeks and permitted return to sport (RTS) without restrictions at 6 to 8 months.³⁷

Continue to: There is a scarcity of literature regarding...

There is a scarcity of literature regarding the use of soft tissue and BPTB allografts in soccer athletes. However, one study reported no difference in patient-reported outcomes and return to preinjury level of activity (including soccer) with the use of either autograft or allograft BPTB in ACLR.³⁸ The authors’ preference was to avoid the use of allograft in elite-level soccer athletes as the reported rate of ACL re-tear was 4 to 8 times higher than that with autograft reconstruction, as shown in athletes and military personnel.^39,40 BPTB autograft and hamstring autograft (semitendinosus and/or gracilis) are common graft choices for soccer athletes. Gifstad and colleagues⁴¹ compared BPTB autograft and hamstring autograft in 45,998 primary ACLRs performed in Scandinavia. Although the cohort included, but was not limited to, soccer players, the authors reported an overall risk of revision that was significantly lower in the BPTB autograft group than in the hamstring autograft group (hazard ratio, 0.63; 95% confidence interval, 0.53-0.74).⁴¹ Mohammadi and colleagues⁴² prospectively compared the functional outcomes of 42 competitive soccer players who underwent ACLR with BPTB autograft vs those who underwent ACLR with hamstring autograft at the time of RTS. Players who had undergone ACLR with hamstring autograft demonstrated greater quadriceps torque, as well as better performance with triple-hop, crossover-hop, and jump-landing tests; however, both groups demonstrated similar hamstring torque and performance in 2 other hop tests.⁴² In the authors’ opinion, there may be a concern regarding the use of hamstring autograft in elite soccer players considering that hamstring strains are extremely common in this athletic population; however, further research would be necessary to elucidate whether this is an actual or a theoretical risk. Although not yet studied in elite-level athletes, early clinical results of ACL repair with suture augmentation show promise for certain injury patterns. These include proximal femoral ACL avulsion injuries (Sherman type 1) of excellent tissue quality that have the ability to be reapproximated to the femoral origin⁴³ (Figures 2A, 2B). In a recent series,^43-45 early clinical outcomes were found to be excellent and maintained at midterm follow-up.

In the NCAA soccer athletes, an overall RTS rate of 85% has been reported in those undergoing ACLR, with a significantly higher rate observed in scholarship versus non-scholarship athletes.⁴⁶ Howard and colleagues⁴⁶ reported median time to unrestricted game play of 6.1 months, with 75% returning to the same or higher level position on the depth chart. Among their studied collegiate soccer athletes, 32% reported continued participation in soccer on some level after college (recreational, semiprofessional, or professional).⁴⁶ RTS rates for MLS soccer players have also been reported to be high, ranging from 74% to 77%, most of them returning within the following season at 10 ± 2.8 months.^47,48 These findings were consistent with the RTS rate of 72% reported by the Multicenter Orthopaedic Outcomes Network (MOON) group, which analyzed 100 female and male soccer players undergoing ACLR at a minimum 7-year follow-up. In this series, Brophy and colleagues^29,49 reported an RTS at 12 ± 14.3 months, with 85% returning to the same or a higher level of play prior to their injury. Erickson and colleagues⁴⁷ analyzed a series of 57 ACLRs performed in MLS athletes and reported no significant difference in preinjury or postoperative performance, or between cases and uninjured controls. Arundale and colleagues⁴⁸ demonstrated no significantly increased risk of lower extremity injury in MLS athletes after ACLR, but the athletes had significantly shorter careers than their uninjured counterparts. Curiously, RTS rates for European professional soccer athletes have been reported to be substantially higher at 95% to 97%.^50,51 Although we can only speculate the reasons for such a discrepancy, the difference in RTS rates for similar athletes highlights a need for objective criteria to determine and report RTS rates, while also providing guidelines to prevent reinjury. Such a consensus among orthopedists is not yet present in the literature.

Soccer players and adolescent age in combination have been shown to portend a 3-fold increased risk of revision surgery for ACL failure in a cohort of 16,930 patients from the Swedish National Knee Ligament Register.⁵² Published data regarding ACL failure and management of revision ACLR in elite-level soccer athletes are currently lacking. However, low failure rates of 3% to 10% requiring revision reconstruction have been reported.^47,49 Arundale and colleagues⁴⁸ reported 2 incidences of players with ACL graft failures, 1 BPTB autograft and 1 BPTB allograft, both of whom were able to return to MLS after revision ACLR. It is the authors’ preference to use ipsilateral hamstring autograft or contralateral BPTB autograft when an ACL revision reconstruction is required.

Continue to: OTHER LIGAMENTOUS INJURIES...

OTHER LIGAMENTOUS INJURIES

The majority of research efforts regarding knee injuries in this population are focused on the ACL. Correspondingly, literature regarding injury to the collateral ligaments and the posterior cruciate ligament (PCL) in soccer players is sparse. The lateral collateral ligament (LCL) and the medial collateral ligament (MCL) play important roles as primary stabilizers to varus and valgus forces, respectively. The PCL is the primary posterior stabilizer of the knee, preventing posterior translation of the tibia. Injury to these structures may result in significant time lost from soccer and risk of reinjury.^53,54

The MCL is the one of the most commonly injured ligaments in sports, including soccer.^53,55 The injury mechanism generally involves contact with a resulting valgus force applied to the knee.⁵⁵ Grading of MCL injuries is based on the amount of medial joint gapping with applied valgus force during examination (grade I: <5 mm, grade II: 5-10 mm, grade III: >10 mm). Kramer and colleagues⁵³ reviewed collateral ligament injuries in the adolescent population and found that MCL injuries occurred 4 times more often than LCL injuries and about 25% were grade III injuries, most commonly occurring in American football and soccer players. Soccer also touts the highest sport-specific MCL injury rate for high school and collegiate athletics, particularly for female NCAA soccer players.⁵⁶ At the professional level, Lundblad and colleagues⁵⁵ reported 346 MCL injuries in 27 European teams over an 11-year period, of which 70% were contact-related, and the average time-off from soccer was 28 days.

Most surgeons treat isolated MCL injuries nonoperatively, regardless of grade.^57,58 This includes activity modification, use of a hinged knee brace, quadriceps strengthening, and progressive return to play. The literature currently lacks substantial data to guide MCL injury management, specifically in elite soccer athletes. In our experience, grade I injuries are managed nonoperatively and RTS is allowed at 4 to 6 weeks. Grade II injuries are also managed nonoperatively and RTS is allowed at 6 to 8 weeks. Grade III injuries are generally allowed RTS at 8 to 12 weeks and may be considered for surgery in the context of concomitant injuries (eg, posteromedial capsular injury, multiligamentous knee injuries, and meniscal injuries). In some athletes, we consider using a varus unloader brace to help maximize decreased stress on the MCL while still allowing the athlete to be fully weight-bearing. We have found it less ideal to limit weight-bearing in elite athletes, which may negatively affect overall lower extremity neuromuscular proprioception and potentially prolong a safe return to play. Some athletes may experience prolonged soreness at the MCL femoral or tibial attachment despite being able to return to play. It is important to counsel athletes about these prolonged symptoms to set expectations, as this may even occur with grade I MCL injuries. Other rare instances where surgical management may be indicated include persistent pain and instability following nonoperative treatment of grade III injuries and highly displaced tibial avulsions of the ligament resulting in poor healing.^59,60

Data regarding LCL injuries in soccer are extremely sparse. In our experience, treatment and RTS rates for isolated LCL injuries are similar to those for MCL injuries. However, it is worth noting that one-quarter of LCL injuries may occur in combination with injury to other posterolateral corner structures.⁵³

PCL injuries are more commonly associated with vehicular trauma but have also been reported to occur in sports at a rate of 33% to 40%.^61,62 The mechanism of injury in athletes generally involves a fall onto the hyperflexed knee with the foot in plantarflexion or a direct blow to the anterior tibia in a flexed knee.^62,63 Classification of PCL injuries is based on posterior translation of the tibia relative to the femur with the knee flexed to 90°(grade I: 1-5 mm, grade II: 6-10 mm, grade III: >10 mm). In one cohort of 62 patients with isolated PCL injuries, soccer was found to be among the top 5 causes of injury.⁶⁴ A Scandinavian review of 1287 patients who underwent PCL reconstruction found soccer to be the sport with the highest number of injuries (13.1%).⁶⁵ The goalkeeper was most commonly subjected to this injury.⁶² Krutsch and colleagues⁵⁴ compared PCL injuries in new, professional soccer players to those in players at the closest amateur level of play. In their series, 90% of PCL injuries occurred during preseason in players who were at a lower level of play in the previous season. This finding suggested that a rapid increase in training and playing intensity may have been a significant risk factor for PCL injury. Substantial literature supporting nonoperative or operative management of PCL injuries in soccer athletes is currently lacking. Historically, nonoperative treatment has been the initial management for isolated PCL injuries; however, surgical intervention has become increasingly used for both isolated and combined PCL injuries.⁶⁶

Continue to: CARTILAGE AND MENISCAL INJURIES...

CARTILAGE AND MENISCAL INJURIES

The prevalence of osteoarthritis (OA) in retired soccer players is high.^67,68 Articular cartilage degeneration with subsequent OA occurs in up to 32% of soccer players and ultimately leads to significant disability and retirement from the sport. High physical demands and concomitant knee injuries probably predispose to the development of posttraumatic OA.^69-71

Several techniques addressing cartilage débridement or restoration have been reported, with successful RTS but with variable durability.^72-75 Recently, Andrade and colleagues⁷⁶ performed a systematic review of 217 articular cartilage defects in soccer players that were treated using restoration techniques, including chondroplasty, microfracture, autologous chondrocyte implantation (ACI), and osteochondral autograft. Although no superior technique could be ascertained, microfracture and osteochondral autograft procedures led to the quickest return to play, and ACI techniques enhanced long-standing clinical and functional results.⁷⁶ More recently, osteochondral allograft transplantation has also been described with an 84% return to some level of activity (including soccer) and 60% of athletes returning to high-level sports participation at a mean follow-up of 4.5 years⁷⁷ (Figures 3A-3C). Although chondroplasty may be successful and allow for a quicker return to play in some soccer players (return to play from 6-12 weeks), the authors believe that a strong cartilage scaffold repair strategy with early weight-bearing, including osteochondral autograft and allograft procedures (return to play from 6-9 months), must also be considered in focal chondral defects to optimize both short-term and potential long-term success.

Meniscal injuries are also prevalent in the soccer population, and consistent with ACL injuries, female players are at least twice as likely to sustain a meniscal tear.^78,79 Meniscal damage can occur in isolation or in association with ACL rupture. Repair techniques should be strongly considered as chondral changes in the setting of meniscal deficiency are a significant short- and long-term concern for elite athletes. However, due to intrinsically poor healing potential, partial meniscectomy is unfortunately more often performed.^79,80 In either case, meniscal deficiency is recognized as a precursor to the development of OA as meniscal functionality is lost and the articular cartilage is subjected to increased biomechanical loading.^81,82 Nawabi and colleagues⁸³ analyzed RTS in 90 professional soccer players following partial meniscectomy. Median RTS was at 7 weeks for lateral meniscectomies and at 5 weeks for medial meniscectomies. RTS probability was 5.99 times greater after medial meniscectomy at all time points. Lateral meniscectomies were associated with an increased risk of postoperative adverse events, reoperation, and a significantly lower rate of return to play.⁸³ In the case of severe meniscal deficiency, particularly post-meniscectomy, meniscal allograft transplantation (MAT) may be considered. In a series of MATs in lower division Spanish players, 12/14 (85.7%) returned to play at an average of 7.6 months.⁸⁴ A more recent series of professional players reported 9/12 (75%) RTS as professionals and 2/12 (17%) as semiprofessionals at an average of 10.5 months.⁸⁵ The authors’ strong preference is to perform meniscus-saving procedures whenever possible. Due to the longer recovery and return to play associated with meniscus repair than partial meniscectomy, most of the soccer players will often prefer to proceed with partial meniscectomy. Despite the ultimate treatment, it is critical that the surgeon and the soccer player have an in-depth conversation concerning the risks and benefits for each procedure and individualize treatment to the individual soccer player accordingly.

Continue to: INJURY PREVENTION...

INJURY PREVENTION

Given the breadth and the prevalence of soccer-related injuries, the FIFA11+ program was developed in 2006 as an injury prevention measure (Figure 4). The warm-up program includes 15 structured exercises emphasizing core stabilization, thigh muscle training, proprioception, dynamic stabilization, and plyometric exercises. The routine is believed to be easily executed and effective at preventing the incidence of noncontact injuries.^86,87 Recently, Sadigursky and colleagues¹ performed a systematic review of randomized clinical trials examining the efficacy of FIFA11+. The authors reported a reduction in injuries by 30% and a relative risk of 0.70 for lower limb injuries, highlighting the significant preventative importance of the program.¹ Post-training programs may also be beneficial as it has been shown that performing FIFA11+ both before and after training reduced overall injury rates in male, amateur soccer players.⁸⁸ Regardless of the prevention program, it is critical that every league, team, medical team, and athlete have a thorough injury prevention strategy to help keep players healthy and not wait until they have instead sustained a significant injury.

CONCLUSION

Knee injuries are common in soccer, with an alarming number of ACL injuries, as well as other significant pathology. Understanding the unique epidemiology, risk factors, treatment, and injury prevention strategies is critically important in helping medical professionals provide care for all levels of elite soccer players.

ABSTRACT

As one of the most popular sports in the world, soccer injury rates involving the knee continue to rise. An alarming trend of knee injuries, including increased anterior cruciate ligament ruptures, underscores the need to review our current understanding of these injuries in soccer players. This article includes a critical review of the epidemiology of knee injuries in soccer, anterior cruciate ligament and other ligamentous injuries, cartilage and meniscal injury, post-traumatic osteoarthritis, as well as current prevention initiatives.

Continue to: EPIDEMIOLOGY...

EPIDEMIOLOGY

There are currently 28 players on each of the Major League Soccer (MLS) teams, and during the 2013 to 2014 academic year, the National Federation of State High School Associations (NFHS) reported that 417,419 boys and 374,564 girls played high school soccer and the National Collegiate Athletic Association (NCAA) reported that 23,602 males and 26,358 females played collegiate soccer.⁵ As such, knee injuries in this population are a major concern for those involved in sports medicine. Several injuries occurring during soccer involve the lower extremity, particularly the knee.¹ In fact, multiple reports estimate that up to 17.6% of soccer-related injuries presenting to the emergency room involved the knee.^1,6-9 The majority of these injuries are noncontact injuries, although contact injuries do still occur.^10,11

Risk factors for injuries in soccer may be non-modifiable (such as age and gender) and modifiable (such as level of conditioning, force, balance, and flexibility). Inadequate lower motor coordination may result in injury in the adolescent population, and advanced age >28 years in males and >25 years in females is considered as a high-risk factor for injury.^12,13 Importantly, gender and age have been reported to play a significant role as risk factors for ACL injury.⁶ In fact, female players have a 3 to 5 times higher risk of significant knee injury, including ACL injuries, than male players.^4,14-16 Preventative programs such as the FIFA 11+ program have been set forth to augment conditioning as part of managing the modifiable risk factors.

Like American football, playing on artificial turf has been questioned as a contributor to injury compared to playing on natural grass.^17,18 In recent years, newer generations of artificial turf have been developed to more closely replicate the characteristics of natural grass. Meyers¹⁹ compared the incidence, mechanisms, and severity of match-related collegiate men’s soccer injuries on artificial turf and those on natural grass and demonstrated no significant difference in knee injuries between the 2 surfaces. This finding was consistent with previous studies that reported no difference in the incidence of knee injuries on either surface in women’s collegiate and elite-level soccer.^15,20,21

Continue to: ACL INJURIES...

ACL INJURIES

ACL injuries are life-changing events that can significantly affect the career of a soccer athlete. As a major stabilizer of the knee, the ACL primarily prevents anterior tibial translation with the anteromedial bundle and secondarily resists tibial rotation with the posterolateral bundle. The ligament takes origin from the posteromedial aspect of the lateral femoral condyle and inserts anterior to the tibial intercondylar eminence. Grading of ACL injuries is based on the Lachman test, which is performed between 20°and 30° of knee flexion and measures the amount of anterior tibial translation relative to the femur (A = firm endpoint, B = no endpoint; grade I: 3-5 mm, grade II (A/B): 5-10 mm, grade III (A/B): >10 mm).

ACL injury may occur via contact or noncontact mechanisms. Noncontact mechanisms of ACL injury in soccer athletes contribute to about 85% of injuries.^6,22-25 Typical noncontact mechanism of injury involves a forceful valgus collapse with the knee near full extension and combined external or internal rotation of the tibia^23,26 (Figure 1). This on-field scenario generally involves cutting and torsional movement, as well as landing after a jump, particularly in 1-legged stance. Similarly, a disturbance in balance caused by the opponent may incite a noncontact mechanism resulting in ACL rupture.^6,27 Video analyses of professional soccer players have also demonstrated a higher risk of noncontact ACL injury within the first 9 minutes of the match, with the most common playing situation resulting in injury being pressing, followed by kicking and heading.^24,25,28 Contact mechanisms resulting in ACL injury, however, are not an uncommon occurrence in soccer players with higher risk for certain positions. Brophy and colleagues²⁹ reviewed ACL injuries in professional and collegiate soccer players and reported a higher risk of ACL injury during defending and tackling. Similarly, Faude and colleagues³⁰ found the risk of injury to be higher in defenders and strikers than in goalkeepers and midfielders.

Female athletes participating in elite-level athletics, especially soccer, represent a high-risk group for ACL injury. In fact, these soccer athletes experience ACL injury at an incidence 3 times higher than that in male athletes.^31-35 Female soccer athletes may also be at risk for reinjury to the ACL and contralateral ACL injury. Female gender, in combination with participation in soccer, thus represents a high-risk group for ACL tear in athletics. Allen and colleagues³⁶ retrospectively reviewed 180 female patients who had undergone ACL reconstruction (ACLR) (90 soccer players and 90 non-soccer players) over a mean period of 68.8 months. In their series, soccer players sustained significantly more ACL injuries than non-soccer players, including graft failures (11% vs 1%) and contralateral ACL tears (17% vs 4%).

ACLR is the gold standard treatment for elite soccer athletes. A recent survey of MLS team orthopedic surgeons revealed several important details regarding decision-making in ACLR in this population. From a technical standpoint, the vast majority of surgeons used a single incision, arthroscopically assisted, single-bundle reconstruction (91%). Femoral tunnel drilling was almost equally split between transtibial (51%) and use of an accessory medial portal (46%). Bone-patella-tendon-bone (BPTB) autograft was the most preferred graft choice (68%), and quadriceps tendon autograft was the least preferred. The majority of surgeons preformed ACLR within 4 weeks and permitted return to sport (RTS) without restrictions at 6 to 8 months.³⁷

Continue to: There is a scarcity of literature regarding...

There is a scarcity of literature regarding the use of soft tissue and BPTB allografts in soccer athletes. However, one study reported no difference in patient-reported outcomes and return to preinjury level of activity (including soccer) with the use of either autograft or allograft BPTB in ACLR.³⁸ The authors’ preference was to avoid the use of allograft in elite-level soccer athletes as the reported rate of ACL re-tear was 4 to 8 times higher than that with autograft reconstruction, as shown in athletes and military personnel.^39,40 BPTB autograft and hamstring autograft (semitendinosus and/or gracilis) are common graft choices for soccer athletes. Gifstad and colleagues⁴¹ compared BPTB autograft and hamstring autograft in 45,998 primary ACLRs performed in Scandinavia. Although the cohort included, but was not limited to, soccer players, the authors reported an overall risk of revision that was significantly lower in the BPTB autograft group than in the hamstring autograft group (hazard ratio, 0.63; 95% confidence interval, 0.53-0.74).⁴¹ Mohammadi and colleagues⁴² prospectively compared the functional outcomes of 42 competitive soccer players who underwent ACLR with BPTB autograft vs those who underwent ACLR with hamstring autograft at the time of RTS. Players who had undergone ACLR with hamstring autograft demonstrated greater quadriceps torque, as well as better performance with triple-hop, crossover-hop, and jump-landing tests; however, both groups demonstrated similar hamstring torque and performance in 2 other hop tests.⁴² In the authors’ opinion, there may be a concern regarding the use of hamstring autograft in elite soccer players considering that hamstring strains are extremely common in this athletic population; however, further research would be necessary to elucidate whether this is an actual or a theoretical risk. Although not yet studied in elite-level athletes, early clinical results of ACL repair with suture augmentation show promise for certain injury patterns. These include proximal femoral ACL avulsion injuries (Sherman type 1) of excellent tissue quality that have the ability to be reapproximated to the femoral origin⁴³ (Figures 2A, 2B). In a recent series,^43-45 early clinical outcomes were found to be excellent and maintained at midterm follow-up.

In the NCAA soccer athletes, an overall RTS rate of 85% has been reported in those undergoing ACLR, with a significantly higher rate observed in scholarship versus non-scholarship athletes.⁴⁶ Howard and colleagues⁴⁶ reported median time to unrestricted game play of 6.1 months, with 75% returning to the same or higher level position on the depth chart. Among their studied collegiate soccer athletes, 32% reported continued participation in soccer on some level after college (recreational, semiprofessional, or professional).⁴⁶ RTS rates for MLS soccer players have also been reported to be high, ranging from 74% to 77%, most of them returning within the following season at 10 ± 2.8 months.^47,48 These findings were consistent with the RTS rate of 72% reported by the Multicenter Orthopaedic Outcomes Network (MOON) group, which analyzed 100 female and male soccer players undergoing ACLR at a minimum 7-year follow-up. In this series, Brophy and colleagues^29,49 reported an RTS at 12 ± 14.3 months, with 85% returning to the same or a higher level of play prior to their injury. Erickson and colleagues⁴⁷ analyzed a series of 57 ACLRs performed in MLS athletes and reported no significant difference in preinjury or postoperative performance, or between cases and uninjured controls. Arundale and colleagues⁴⁸ demonstrated no significantly increased risk of lower extremity injury in MLS athletes after ACLR, but the athletes had significantly shorter careers than their uninjured counterparts. Curiously, RTS rates for European professional soccer athletes have been reported to be substantially higher at 95% to 97%.^50,51 Although we can only speculate the reasons for such a discrepancy, the difference in RTS rates for similar athletes highlights a need for objective criteria to determine and report RTS rates, while also providing guidelines to prevent reinjury. Such a consensus among orthopedists is not yet present in the literature.

Soccer players and adolescent age in combination have been shown to portend a 3-fold increased risk of revision surgery for ACL failure in a cohort of 16,930 patients from the Swedish National Knee Ligament Register.⁵² Published data regarding ACL failure and management of revision ACLR in elite-level soccer athletes are currently lacking. However, low failure rates of 3% to 10% requiring revision reconstruction have been reported.^47,49 Arundale and colleagues⁴⁸ reported 2 incidences of players with ACL graft failures, 1 BPTB autograft and 1 BPTB allograft, both of whom were able to return to MLS after revision ACLR. It is the authors’ preference to use ipsilateral hamstring autograft or contralateral BPTB autograft when an ACL revision reconstruction is required.

Continue to: OTHER LIGAMENTOUS INJURIES...

OTHER LIGAMENTOUS INJURIES

The majority of research efforts regarding knee injuries in this population are focused on the ACL. Correspondingly, literature regarding injury to the collateral ligaments and the posterior cruciate ligament (PCL) in soccer players is sparse. The lateral collateral ligament (LCL) and the medial collateral ligament (MCL) play important roles as primary stabilizers to varus and valgus forces, respectively. The PCL is the primary posterior stabilizer of the knee, preventing posterior translation of the tibia. Injury to these structures may result in significant time lost from soccer and risk of reinjury.^53,54

The MCL is the one of the most commonly injured ligaments in sports, including soccer.^53,55 The injury mechanism generally involves contact with a resulting valgus force applied to the knee.⁵⁵ Grading of MCL injuries is based on the amount of medial joint gapping with applied valgus force during examination (grade I: <5 mm, grade II: 5-10 mm, grade III: >10 mm). Kramer and colleagues⁵³ reviewed collateral ligament injuries in the adolescent population and found that MCL injuries occurred 4 times more often than LCL injuries and about 25% were grade III injuries, most commonly occurring in American football and soccer players. Soccer also touts the highest sport-specific MCL injury rate for high school and collegiate athletics, particularly for female NCAA soccer players.⁵⁶ At the professional level, Lundblad and colleagues⁵⁵ reported 346 MCL injuries in 27 European teams over an 11-year period, of which 70% were contact-related, and the average time-off from soccer was 28 days.

Most surgeons treat isolated MCL injuries nonoperatively, regardless of grade.^57,58 This includes activity modification, use of a hinged knee brace, quadriceps strengthening, and progressive return to play. The literature currently lacks substantial data to guide MCL injury management, specifically in elite soccer athletes. In our experience, grade I injuries are managed nonoperatively and RTS is allowed at 4 to 6 weeks. Grade II injuries are also managed nonoperatively and RTS is allowed at 6 to 8 weeks. Grade III injuries are generally allowed RTS at 8 to 12 weeks and may be considered for surgery in the context of concomitant injuries (eg, posteromedial capsular injury, multiligamentous knee injuries, and meniscal injuries). In some athletes, we consider using a varus unloader brace to help maximize decreased stress on the MCL while still allowing the athlete to be fully weight-bearing. We have found it less ideal to limit weight-bearing in elite athletes, which may negatively affect overall lower extremity neuromuscular proprioception and potentially prolong a safe return to play. Some athletes may experience prolonged soreness at the MCL femoral or tibial attachment despite being able to return to play. It is important to counsel athletes about these prolonged symptoms to set expectations, as this may even occur with grade I MCL injuries. Other rare instances where surgical management may be indicated include persistent pain and instability following nonoperative treatment of grade III injuries and highly displaced tibial avulsions of the ligament resulting in poor healing.^59,60

Data regarding LCL injuries in soccer are extremely sparse. In our experience, treatment and RTS rates for isolated LCL injuries are similar to those for MCL injuries. However, it is worth noting that one-quarter of LCL injuries may occur in combination with injury to other posterolateral corner structures.⁵³

PCL injuries are more commonly associated with vehicular trauma but have also been reported to occur in sports at a rate of 33% to 40%.^61,62 The mechanism of injury in athletes generally involves a fall onto the hyperflexed knee with the foot in plantarflexion or a direct blow to the anterior tibia in a flexed knee.^62,63 Classification of PCL injuries is based on posterior translation of the tibia relative to the femur with the knee flexed to 90°(grade I: 1-5 mm, grade II: 6-10 mm, grade III: >10 mm). In one cohort of 62 patients with isolated PCL injuries, soccer was found to be among the top 5 causes of injury.⁶⁴ A Scandinavian review of 1287 patients who underwent PCL reconstruction found soccer to be the sport with the highest number of injuries (13.1%).⁶⁵ The goalkeeper was most commonly subjected to this injury.⁶² Krutsch and colleagues⁵⁴ compared PCL injuries in new, professional soccer players to those in players at the closest amateur level of play. In their series, 90% of PCL injuries occurred during preseason in players who were at a lower level of play in the previous season. This finding suggested that a rapid increase in training and playing intensity may have been a significant risk factor for PCL injury. Substantial literature supporting nonoperative or operative management of PCL injuries in soccer athletes is currently lacking. Historically, nonoperative treatment has been the initial management for isolated PCL injuries; however, surgical intervention has become increasingly used for both isolated and combined PCL injuries.⁶⁶

Continue to: CARTILAGE AND MENISCAL INJURIES...

CARTILAGE AND MENISCAL INJURIES

The prevalence of osteoarthritis (OA) in retired soccer players is high.^67,68 Articular cartilage degeneration with subsequent OA occurs in up to 32% of soccer players and ultimately leads to significant disability and retirement from the sport. High physical demands and concomitant knee injuries probably predispose to the development of posttraumatic OA.^69-71

Several techniques addressing cartilage débridement or restoration have been reported, with successful RTS but with variable durability.^72-75 Recently, Andrade and colleagues⁷⁶ performed a systematic review of 217 articular cartilage defects in soccer players that were treated using restoration techniques, including chondroplasty, microfracture, autologous chondrocyte implantation (ACI), and osteochondral autograft. Although no superior technique could be ascertained, microfracture and osteochondral autograft procedures led to the quickest return to play, and ACI techniques enhanced long-standing clinical and functional results.⁷⁶ More recently, osteochondral allograft transplantation has also been described with an 84% return to some level of activity (including soccer) and 60% of athletes returning to high-level sports participation at a mean follow-up of 4.5 years⁷⁷ (Figures 3A-3C). Although chondroplasty may be successful and allow for a quicker return to play in some soccer players (return to play from 6-12 weeks), the authors believe that a strong cartilage scaffold repair strategy with early weight-bearing, including osteochondral autograft and allograft procedures (return to play from 6-9 months), must also be considered in focal chondral defects to optimize both short-term and potential long-term success.

Meniscal injuries are also prevalent in the soccer population, and consistent with ACL injuries, female players are at least twice as likely to sustain a meniscal tear.^78,79 Meniscal damage can occur in isolation or in association with ACL rupture. Repair techniques should be strongly considered as chondral changes in the setting of meniscal deficiency are a significant short- and long-term concern for elite athletes. However, due to intrinsically poor healing potential, partial meniscectomy is unfortunately more often performed.^79,80 In either case, meniscal deficiency is recognized as a precursor to the development of OA as meniscal functionality is lost and the articular cartilage is subjected to increased biomechanical loading.^81,82 Nawabi and colleagues⁸³ analyzed RTS in 90 professional soccer players following partial meniscectomy. Median RTS was at 7 weeks for lateral meniscectomies and at 5 weeks for medial meniscectomies. RTS probability was 5.99 times greater after medial meniscectomy at all time points. Lateral meniscectomies were associated with an increased risk of postoperative adverse events, reoperation, and a significantly lower rate of return to play.⁸³ In the case of severe meniscal deficiency, particularly post-meniscectomy, meniscal allograft transplantation (MAT) may be considered. In a series of MATs in lower division Spanish players, 12/14 (85.7%) returned to play at an average of 7.6 months.⁸⁴ A more recent series of professional players reported 9/12 (75%) RTS as professionals and 2/12 (17%) as semiprofessionals at an average of 10.5 months.⁸⁵ The authors’ strong preference is to perform meniscus-saving procedures whenever possible. Due to the longer recovery and return to play associated with meniscus repair than partial meniscectomy, most of the soccer players will often prefer to proceed with partial meniscectomy. Despite the ultimate treatment, it is critical that the surgeon and the soccer player have an in-depth conversation concerning the risks and benefits for each procedure and individualize treatment to the individual soccer player accordingly.

Continue to: INJURY PREVENTION...

INJURY PREVENTION

Given the breadth and the prevalence of soccer-related injuries, the FIFA11+ program was developed in 2006 as an injury prevention measure (Figure 4). The warm-up program includes 15 structured exercises emphasizing core stabilization, thigh muscle training, proprioception, dynamic stabilization, and plyometric exercises. The routine is believed to be easily executed and effective at preventing the incidence of noncontact injuries.^86,87 Recently, Sadigursky and colleagues¹ performed a systematic review of randomized clinical trials examining the efficacy of FIFA11+. The authors reported a reduction in injuries by 30% and a relative risk of 0.70 for lower limb injuries, highlighting the significant preventative importance of the program.¹ Post-training programs may also be beneficial as it has been shown that performing FIFA11+ both before and after training reduced overall injury rates in male, amateur soccer players.⁸⁸ Regardless of the prevention program, it is critical that every league, team, medical team, and athlete have a thorough injury prevention strategy to help keep players healthy and not wait until they have instead sustained a significant injury.

CONCLUSION

Knee injuries are common in soccer, with an alarming number of ACL injuries, as well as other significant pathology. Understanding the unique epidemiology, risk factors, treatment, and injury prevention strategies is critically important in helping medical professionals provide care for all levels of elite soccer players.

Placenta accreta spectrum (PAS) describes abnormal invasion of placental tissue into or through the myometrium, comprising 3 distinct conditions: placenta accreta, placenta increta, and placenta percreta. This complication is relatively new to obstetrics, first described in 1937.¹

The overall incidence of PAS has been increasing over several decades, in parallel to an increasing rate of cesarean delivery (CD), with an incidence from 1982 through 2002 of 1 in 533 pregnancies, representing a 5-fold increase since the 1980s.² PAS is associated with significant morbidity and mortality, including fetal growth restriction, preterm delivery, placental abruption antenatally, and hemorrhage during delivery or postpartum.

Prenatal diagnosis of PAS and planned delivery at an experienced center are associated with significant reduction in maternal and fetal morbidity.³ In an era of advanced imaging modalities, prenatal detection of PAS regrettably remains variable and largely subjective: As many as 20% to 50% of cases of PAS escape prenatal diagnosis.^3,4

In this article, we review the sonographic markers of PAS, including diagnostic accuracy, and propose a standardized approach to prenatal diagnosis. Throughout our discussion, we describe protocols for detection of PAS practiced at our Maternal-Fetal Medicine Program in the Department of Obstetrics and Gynecology, Eastern Virginia Medical School (also see “US evaluation of PAS risk: The authors’ recommended approach”).

Numerous risk factors

There are many risk factors for PAS, including prior uterine surgery or instrumentation, such as CD, uterine curettage, myomectomy, pelvic radiation, and endometrial ablation. Other risk factors include smoking, in vitro fertilization, advanced maternal age, multiparity, and a brief interval between prior CD and subsequent pregnancy.⁵ Of major significance is the increased risk of PAS in the presence of placenta previa with prior CD.⁶ Knowledge of clinical risk factors by the interpreting physician appears to be associated with improved detection of PAS on ultrasonography (US).⁴

Ultrasonographic markers of PAS

First-trimester markers

Sonographic markers of PAS in the first trimester include:

• a gestational sac implanted in the lower uterine segment or in a CD scar
• multiple hypoechoic spaces within the placenta (lacunae).⁷

Lower uterine-segment implantation has been defined by Ballas and colleagues as 1) a gestational sac implanted in the lower one-third of the uterus between 8 and 10 weeks’ gestation or 2) a gestational sac occupying primarily the lower uterine segment from 10 weeks’ gestation onward (FIGURE 1).⁸ Our experience is that it is difficult to accurately assess lower uterine-segment implantation beyond 13 weeks of gestation because the sac typically expands to fill the upper uterine cavity.

Continue to: Color Doppler US...

Color Doppler US can help differentiate lower uterine-segment implantation from a gestational sac of a failed pregnancy in the process of expulsion by demonstrating loss of circumferential blood flow in the failed pregnancy. Furthermore, applying pressure to the anterior surface of the uterus will result in downward movement of the gestational sac of a failed pregnancy.⁹

Not all gestational sacs that implant in the lower uterine segment lead to PAS: Subsequent normal pregnancies have been reported in this circumstance. In such cases, a normal thick myometrium is noted anterior to the gestational sac.⁷ A patient with lower uterine-segment implantation without evidence of anterior myometrial thinning remains at risk for third-trimester placenta previa.⁷

Cesarean scar pregnancy carries significant risk of PAS. In these cases, the gestational sac is typically implanted within the scar, resulting in a thin anterior myometrium and significantly increased vascularity of the placental–myometrial and bladder–uterine wall interfaces (FIGURE 2).⁹ Differentiating cesarean scar pregnancy from a lower uterine-segment implantation is easier to perform before the eighth week of gestation but becomes more difficult as pregnancy advances. Although it might be useful to distinguish between true cesarean scar pregnancy and lower uterine-segment implantation adjacent to or involving the scar, both carry considerable risk of PAS and excessive hemorrhage, and the approach to treating both conditions is quite similar.

Lacunae, with or without documented blood flow on color Doppler US, are the third marker of PAS in the first trimester.⁸ Although some retrospective series and case reports describe the finding of lacunae in the first trimester of patients with diagnosed PAS, more recent literature suggests that these spaces are seen infrequently and at a similar frequency in women with and without PAS at delivery.⁷

Second- and third-trimester markers

Multiple diagnostic sonographic markers of PAS have been described in the second and third trimesters.

Placental location is a significant risk factor for PAS. Placenta previa in the setting of prior CD carries the highest risk of PAS—as high as 61% in women with both placenta previa and a history of 3 CDs.¹⁰ An anterior placenta appears to be a stronger risk factor for PAS than a posterior placenta in women with prior CD; the location of the placenta should therefore be evaluated in all women in the second trimester.

Continue to: Lacunae

Lacunae. The finding of multiple hypoechoic vascular spaces within the placental parenchyma has been associated with PAS (FIGURES 3 and 4). The pathogenesis of this finding is probably related to alterations in placental tissue resulting from long-term exposure to pulsatile blood flow.¹¹

Finberg and colleagues introduced a grading system for placental lacunae in 1992 that is still used:

• Grade 0: no lacunae seen
• Grade 1: 1 to 3 lacunae seen
• Grade 2: 4 to 6 lacunae seen
• Grade 3: multiple lacunae seen throughout the placenta.¹²

The sensitivity and specificity of lacunae as an independent marker for PAS have been reported to be 77% and 95%, respectively.¹³ Despite these findings, several studies report a range of sensitivity (73% to 100%) and negative predictive value (88% to 100%).¹⁴ Even in Finberg’s original work, 27% of cases of confirmed PAS had Grade 0 or Grade 1 placental lacunae and 11% of cases of placenta previa, without PAS, demonstrated Grade 2 lacunae.¹² There is agreement, however, that, the more lacunae, the higher the risk of PAS.

Continue to: Other US markers for PAS

Retroplacental–myometrial interface

Loss of the normal hypoechoic (clear) retroplacental zone, also referred to as loss of the clear space between placenta and uterus, is another marker of PAS (FIGURE 5). This finding corresponds to pathologic loss of the decidua basalis as trophoblastic tissue invades directly through the myometrium.¹⁵ This sonographic finding has been reported to have a detection rate of approximately 93%, with sensitivity of 52% and specificity of 57%, for PAS; the false-positive rate, however, has been in the range of 21% or higher. This marker should not be used alone because it is angle-dependent and can be found (as an absent clear zone) in normal anterior placentas.¹⁶

The strength of this US marker is in its negative predictive value, which ranges from 96% to 100%. The presence of a hypoechoic retroplacental clear space that extends the length of the placenta makes PAS unlikely.¹⁷ Of note, the clear zone may appear falsely absent as a result of increased pressure from the US probe.

Retroplacental myometrial thickness

Retroplacental myometrial thickness is difficult to assess because the lower uterine-segment myometrium thins in normal pregnancy as term approaches. This measurement also can be influenced by direct pressure of the US probe and fullness of the maternal bladder.¹⁸ In patients who have had a CD but who do not have PAS, the median myometrial thickness of the lower uterine segment in the third trimester is 2.4 mm.¹⁹

Thinning of the myometrium in the upper uterine segment always should be of concern. Studies of this marker have reported sensitivity of US ranging from 22% to 100% and specificity from 72% to 100%.^9,20 Given such variability, it is important to standardize the gestational age and sonographic approach for this marker.

Continue to: Uterovesical interface

Studies also have reported that abnormalities of the uterovesical interface are predictive of PAS. The uterovesical interface is best evaluated in a sagittal plane containing the lower uterine segment and a partially full bladder in gray-scale and color Doppler US.¹⁵ The normal uterovesical interface appears as a smooth line, without irregularities or increased vascularity on sagittal imaging.

Abnormalities include focal interruption of the hyperechoic bladder wall, bulging of the bladder wall, and increased vascularity, such as varicosities (FIGURES 5, 6, and 7).¹⁵ These findings may be seen as early as the first trimester but are more commonly noted in the second and third trimesters.⁷ The authors of a recent meta-analysis concluded that irregularity of the uterovesical interface is the most specific marker for invasive placentation (99.75% confidence interval; range, 99.5% to 99.9%).¹³

Other US markers and modalities

Three-dimensional US. Studies have evaluated the role of 3-dimensional (3D) US for predicting PAS. Application of 3D US in vascular mode has shown promise because it allows for semiquantitative assessment of placental vasculature.²² Using 3D US to screen for PAS presents drawbacks, however: The technology is not well-standardized and requires significant operator expertise for volume acquisition and manipulation. Prospective studies are needed before 3D US can be applied routinely to screen for and diagnose PAS.

Color Doppler US. As an adjunct to gray-scale US, color Doppler US can be used for making a diagnosis of PAS. Color Doppler US helps differentiate a normal subplacental venous complex with nonpulsatile, low-velocity venous blood flow waveforms from markedly dilated peripheral subplacental vascular channels with pulsatile venous-type flow, which suggests PAS. These vascular channels are often located directly over the cervix. In addition, the observation of bridging vessels linking the placenta and bladder with high diastolic arterial blood flow also suggests invasion.²¹ In a meta-analysis, overall sensitivity of color Doppler US for the diagnosis of PAS was 91%, with specificity of 87%.¹³

The value of utilizing multiple markers

The accuracy of US diagnosis of PAS is likely improved by using more than 1 sonographic marker. Pilloni and colleagues,²⁰ in a prospective analysis, found that 81% of cases of confirmed PAS had ≥2 markers and 51% of cases had ≥3 markers.

Several scoring systems have been proposed for making the diagnosis of PAS using combinations of sonographic markers, placental location, and clinical history.^19,24,25 In 2016, Tovbin and colleagues,²⁵ in a prospective study, evaluated a scoring system that included:

• number of previous CDs
• number of, maximum dimension of, and presence of blood flow in lacunae
• loss of uteroplacental clear zone
• placental location
• hypervascularity of the uterovesical or uteroplacental interface.

Tovbin assigned 1 or 2 points to each criterion. Each sonographic marker was found to be significantly associated with PAS when compared to a high-risk control group. A score of ≥8 was considered “at high risk” and predicted 69% of PAS cases.

Regrettably, no combination of US markers reliably predicts the depth of invasion of the placenta.²⁶

Continue to: A standardized approach is needed

To decrease variability and improve the US diagnosis of PAS, it is important to define and standardize the diagnosis of each sonographic marker for PAS.⁴ In 2016, the European Working Group on Abnormally Invasive Placenta (EW-AIP) proposed a set of US markers that always should be reported when performing an US examination for suspected abnormal placentation (TABLE).²³ Despite this effort by the EW-AIP, ambiguity remains over sonographic definitions of several PAS markers. For example, what determines a placental lacuna on US? And what constitutes an abnormal uterovesical interface? There is a need for a more objective definition of US markers of PAS and a standardized approach to the US examination in at-risk pregnancies.

The Society for Maternal-Fetal Medicine is coordinating a multi-society task force to address the need to define and standardize the US diagnosis of PAS.

Observations on other PAS diagnostic modalities

Magnetic resonance imaging

Adjunctive role. Magnetic resonance imaging (MRI) is often used as an adjunctive diagnostic modality in cases of suspected PAS. Several markers for PAS have been described on MRI, including¹⁵:

• intraplacental T2-weighted dark bands
• abnormal intraplacental vascularity
• heterogeneous intraplacental signal intensity
• focal interruption of the myometrium by the placenta
• uterine bulging.

Based on a recent meta-analysis, overall sensitivity of MRI for detecting PAS is 86% to 95%, with specificity of 80% to 95%. Although this is comparable to the sensitivity and specificity of US,²⁷ studies of MRI in PAS are smaller and more prone to bias than in studies of US, because MRI typically is used only in patients at highest risk for PAS. Few studies comparing US to MRI for PAS have been performed; all are small and lack statistical power.

Complementary role. MRI can be complementary to US in cases in which the placenta is posterior or located laterally²⁸ but, importantly, rarely changes decisions about surgical management when used in conjunction with US to assess patients for the diagnosis of PAS. (An exception might lie in the ability of MRI to assess the degree or depth of invasion of the placenta and discerning placenta percreta from placenta accreta.¹⁵)

Enhancement with contrast. Addition of gadolinium-based contrast might improve the ability of MRI to make a diagnosis of PAS, but gadolinium crosses the placenta barrier. Although fetal effects of gadolinium have not been observed, American College of Radiology guidelines recommend avoiding this contrast agent during pregnancy unless absolutely essential.²⁹

Specific indications. MRI without contrast should be considered 1) when US is inconclusive and 2) to further evaluate a posterior placenta suspicious for invasion, to define the precise topography of extrauterine placental invasion. The additional information offered by MRI might alter surgical planning.¹⁵

Biomarkers

Multiple serum biomarkers have been proposed to predict PAS in high-risk women. PAS might be associated with increased levels of first-trimester pregnancy-associated plasma protein A, second-trimester maternal serum alpha fetoprotein, and human chorionic gonadotropin, but studies of the utility of these biomarkers have yielded contradictory results.^30,31 Biomarkers are of interest and have significant clinical applicability, but none of the ones identified to date have high sensitivity or specificity for predicting PAS prenatally. Research is ongoing to identify markers of PAS that have sufficient predictive power.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Placenta accreta spectrum (PAS) describes abnormal invasion of placental tissue into or through the myometrium, comprising 3 distinct conditions: placenta accreta, placenta increta, and placenta percreta. This complication is relatively new to obstetrics, first described in 1937.¹

The overall incidence of PAS has been increasing over several decades, in parallel to an increasing rate of cesarean delivery (CD), with an incidence from 1982 through 2002 of 1 in 533 pregnancies, representing a 5-fold increase since the 1980s.² PAS is associated with significant morbidity and mortality, including fetal growth restriction, preterm delivery, placental abruption antenatally, and hemorrhage during delivery or postpartum.

Prenatal diagnosis of PAS and planned delivery at an experienced center are associated with significant reduction in maternal and fetal morbidity.³ In an era of advanced imaging modalities, prenatal detection of PAS regrettably remains variable and largely subjective: As many as 20% to 50% of cases of PAS escape prenatal diagnosis.^3,4

In this article, we review the sonographic markers of PAS, including diagnostic accuracy, and propose a standardized approach to prenatal diagnosis. Throughout our discussion, we describe protocols for detection of PAS practiced at our Maternal-Fetal Medicine Program in the Department of Obstetrics and Gynecology, Eastern Virginia Medical School (also see “US evaluation of PAS risk: The authors’ recommended approach”).

Numerous risk factors

There are many risk factors for PAS, including prior uterine surgery or instrumentation, such as CD, uterine curettage, myomectomy, pelvic radiation, and endometrial ablation. Other risk factors include smoking, in vitro fertilization, advanced maternal age, multiparity, and a brief interval between prior CD and subsequent pregnancy.⁵ Of major significance is the increased risk of PAS in the presence of placenta previa with prior CD.⁶ Knowledge of clinical risk factors by the interpreting physician appears to be associated with improved detection of PAS on ultrasonography (US).⁴

Ultrasonographic markers of PAS

First-trimester markers

Sonographic markers of PAS in the first trimester include:

• a gestational sac implanted in the lower uterine segment or in a CD scar
• multiple hypoechoic spaces within the placenta (lacunae).⁷

Lower uterine-segment implantation has been defined by Ballas and colleagues as 1) a gestational sac implanted in the lower one-third of the uterus between 8 and 10 weeks’ gestation or 2) a gestational sac occupying primarily the lower uterine segment from 10 weeks’ gestation onward (FIGURE 1).⁸ Our experience is that it is difficult to accurately assess lower uterine-segment implantation beyond 13 weeks of gestation because the sac typically expands to fill the upper uterine cavity.

Continue to: Color Doppler US...

Color Doppler US can help differentiate lower uterine-segment implantation from a gestational sac of a failed pregnancy in the process of expulsion by demonstrating loss of circumferential blood flow in the failed pregnancy. Furthermore, applying pressure to the anterior surface of the uterus will result in downward movement of the gestational sac of a failed pregnancy.⁹

Not all gestational sacs that implant in the lower uterine segment lead to PAS: Subsequent normal pregnancies have been reported in this circumstance. In such cases, a normal thick myometrium is noted anterior to the gestational sac.⁷ A patient with lower uterine-segment implantation without evidence of anterior myometrial thinning remains at risk for third-trimester placenta previa.⁷

Cesarean scar pregnancy carries significant risk of PAS. In these cases, the gestational sac is typically implanted within the scar, resulting in a thin anterior myometrium and significantly increased vascularity of the placental–myometrial and bladder–uterine wall interfaces (FIGURE 2).⁹ Differentiating cesarean scar pregnancy from a lower uterine-segment implantation is easier to perform before the eighth week of gestation but becomes more difficult as pregnancy advances. Although it might be useful to distinguish between true cesarean scar pregnancy and lower uterine-segment implantation adjacent to or involving the scar, both carry considerable risk of PAS and excessive hemorrhage, and the approach to treating both conditions is quite similar.

Lacunae, with or without documented blood flow on color Doppler US, are the third marker of PAS in the first trimester.⁸ Although some retrospective series and case reports describe the finding of lacunae in the first trimester of patients with diagnosed PAS, more recent literature suggests that these spaces are seen infrequently and at a similar frequency in women with and without PAS at delivery.⁷

Second- and third-trimester markers

Multiple diagnostic sonographic markers of PAS have been described in the second and third trimesters.

Placental location is a significant risk factor for PAS. Placenta previa in the setting of prior CD carries the highest risk of PAS—as high as 61% in women with both placenta previa and a history of 3 CDs.¹⁰ An anterior placenta appears to be a stronger risk factor for PAS than a posterior placenta in women with prior CD; the location of the placenta should therefore be evaluated in all women in the second trimester.

Continue to: Lacunae

Lacunae. The finding of multiple hypoechoic vascular spaces within the placental parenchyma has been associated with PAS (FIGURES 3 and 4). The pathogenesis of this finding is probably related to alterations in placental tissue resulting from long-term exposure to pulsatile blood flow.¹¹

Finberg and colleagues introduced a grading system for placental lacunae in 1992 that is still used:

• Grade 0: no lacunae seen
• Grade 1: 1 to 3 lacunae seen
• Grade 2: 4 to 6 lacunae seen
• Grade 3: multiple lacunae seen throughout the placenta.¹²

The sensitivity and specificity of lacunae as an independent marker for PAS have been reported to be 77% and 95%, respectively.¹³ Despite these findings, several studies report a range of sensitivity (73% to 100%) and negative predictive value (88% to 100%).¹⁴ Even in Finberg’s original work, 27% of cases of confirmed PAS had Grade 0 or Grade 1 placental lacunae and 11% of cases of placenta previa, without PAS, demonstrated Grade 2 lacunae.¹² There is agreement, however, that, the more lacunae, the higher the risk of PAS.

Continue to: Other US markers for PAS

Retroplacental–myometrial interface

Loss of the normal hypoechoic (clear) retroplacental zone, also referred to as loss of the clear space between placenta and uterus, is another marker of PAS (FIGURE 5). This finding corresponds to pathologic loss of the decidua basalis as trophoblastic tissue invades directly through the myometrium.¹⁵ This sonographic finding has been reported to have a detection rate of approximately 93%, with sensitivity of 52% and specificity of 57%, for PAS; the false-positive rate, however, has been in the range of 21% or higher. This marker should not be used alone because it is angle-dependent and can be found (as an absent clear zone) in normal anterior placentas.¹⁶

The strength of this US marker is in its negative predictive value, which ranges from 96% to 100%. The presence of a hypoechoic retroplacental clear space that extends the length of the placenta makes PAS unlikely.¹⁷ Of note, the clear zone may appear falsely absent as a result of increased pressure from the US probe.

Retroplacental myometrial thickness

Retroplacental myometrial thickness is difficult to assess because the lower uterine-segment myometrium thins in normal pregnancy as term approaches. This measurement also can be influenced by direct pressure of the US probe and fullness of the maternal bladder.¹⁸ In patients who have had a CD but who do not have PAS, the median myometrial thickness of the lower uterine segment in the third trimester is 2.4 mm.¹⁹

Thinning of the myometrium in the upper uterine segment always should be of concern. Studies of this marker have reported sensitivity of US ranging from 22% to 100% and specificity from 72% to 100%.^9,20 Given such variability, it is important to standardize the gestational age and sonographic approach for this marker.

Continue to: Uterovesical interface

Studies also have reported that abnormalities of the uterovesical interface are predictive of PAS. The uterovesical interface is best evaluated in a sagittal plane containing the lower uterine segment and a partially full bladder in gray-scale and color Doppler US.¹⁵ The normal uterovesical interface appears as a smooth line, without irregularities or increased vascularity on sagittal imaging.

Abnormalities include focal interruption of the hyperechoic bladder wall, bulging of the bladder wall, and increased vascularity, such as varicosities (FIGURES 5, 6, and 7).¹⁵ These findings may be seen as early as the first trimester but are more commonly noted in the second and third trimesters.⁷ The authors of a recent meta-analysis concluded that irregularity of the uterovesical interface is the most specific marker for invasive placentation (99.75% confidence interval; range, 99.5% to 99.9%).¹³

Other US markers and modalities

Three-dimensional US. Studies have evaluated the role of 3-dimensional (3D) US for predicting PAS. Application of 3D US in vascular mode has shown promise because it allows for semiquantitative assessment of placental vasculature.²² Using 3D US to screen for PAS presents drawbacks, however: The technology is not well-standardized and requires significant operator expertise for volume acquisition and manipulation. Prospective studies are needed before 3D US can be applied routinely to screen for and diagnose PAS.

Color Doppler US. As an adjunct to gray-scale US, color Doppler US can be used for making a diagnosis of PAS. Color Doppler US helps differentiate a normal subplacental venous complex with nonpulsatile, low-velocity venous blood flow waveforms from markedly dilated peripheral subplacental vascular channels with pulsatile venous-type flow, which suggests PAS. These vascular channels are often located directly over the cervix. In addition, the observation of bridging vessels linking the placenta and bladder with high diastolic arterial blood flow also suggests invasion.²¹ In a meta-analysis, overall sensitivity of color Doppler US for the diagnosis of PAS was 91%, with specificity of 87%.¹³

The value of utilizing multiple markers

The accuracy of US diagnosis of PAS is likely improved by using more than 1 sonographic marker. Pilloni and colleagues,²⁰ in a prospective analysis, found that 81% of cases of confirmed PAS had ≥2 markers and 51% of cases had ≥3 markers.

Several scoring systems have been proposed for making the diagnosis of PAS using combinations of sonographic markers, placental location, and clinical history.^19,24,25 In 2016, Tovbin and colleagues,²⁵ in a prospective study, evaluated a scoring system that included:

• number of previous CDs
• number of, maximum dimension of, and presence of blood flow in lacunae
• loss of uteroplacental clear zone
• placental location
• hypervascularity of the uterovesical or uteroplacental interface.

Tovbin assigned 1 or 2 points to each criterion. Each sonographic marker was found to be significantly associated with PAS when compared to a high-risk control group. A score of ≥8 was considered “at high risk” and predicted 69% of PAS cases.

Regrettably, no combination of US markers reliably predicts the depth of invasion of the placenta.²⁶

Continue to: A standardized approach is needed

To decrease variability and improve the US diagnosis of PAS, it is important to define and standardize the diagnosis of each sonographic marker for PAS.⁴ In 2016, the European Working Group on Abnormally Invasive Placenta (EW-AIP) proposed a set of US markers that always should be reported when performing an US examination for suspected abnormal placentation (TABLE).²³ Despite this effort by the EW-AIP, ambiguity remains over sonographic definitions of several PAS markers. For example, what determines a placental lacuna on US? And what constitutes an abnormal uterovesical interface? There is a need for a more objective definition of US markers of PAS and a standardized approach to the US examination in at-risk pregnancies.

The Society for Maternal-Fetal Medicine is coordinating a multi-society task force to address the need to define and standardize the US diagnosis of PAS.

Observations on other PAS diagnostic modalities

Magnetic resonance imaging

Adjunctive role. Magnetic resonance imaging (MRI) is often used as an adjunctive diagnostic modality in cases of suspected PAS. Several markers for PAS have been described on MRI, including¹⁵:

• intraplacental T2-weighted dark bands
• abnormal intraplacental vascularity
• heterogeneous intraplacental signal intensity
• focal interruption of the myometrium by the placenta
• uterine bulging.

Based on a recent meta-analysis, overall sensitivity of MRI for detecting PAS is 86% to 95%, with specificity of 80% to 95%. Although this is comparable to the sensitivity and specificity of US,²⁷ studies of MRI in PAS are smaller and more prone to bias than in studies of US, because MRI typically is used only in patients at highest risk for PAS. Few studies comparing US to MRI for PAS have been performed; all are small and lack statistical power.

Complementary role. MRI can be complementary to US in cases in which the placenta is posterior or located laterally²⁸ but, importantly, rarely changes decisions about surgical management when used in conjunction with US to assess patients for the diagnosis of PAS. (An exception might lie in the ability of MRI to assess the degree or depth of invasion of the placenta and discerning placenta percreta from placenta accreta.¹⁵)

Enhancement with contrast. Addition of gadolinium-based contrast might improve the ability of MRI to make a diagnosis of PAS, but gadolinium crosses the placenta barrier. Although fetal effects of gadolinium have not been observed, American College of Radiology guidelines recommend avoiding this contrast agent during pregnancy unless absolutely essential.²⁹

Specific indications. MRI without contrast should be considered 1) when US is inconclusive and 2) to further evaluate a posterior placenta suspicious for invasion, to define the precise topography of extrauterine placental invasion. The additional information offered by MRI might alter surgical planning.¹⁵

Biomarkers

Multiple serum biomarkers have been proposed to predict PAS in high-risk women. PAS might be associated with increased levels of first-trimester pregnancy-associated plasma protein A, second-trimester maternal serum alpha fetoprotein, and human chorionic gonadotropin, but studies of the utility of these biomarkers have yielded contradictory results.^30,31 Biomarkers are of interest and have significant clinical applicability, but none of the ones identified to date have high sensitivity or specificity for predicting PAS prenatally. Research is ongoing to identify markers of PAS that have sufficient predictive power.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Placenta accreta spectrum (PAS) describes abnormal invasion of placental tissue into or through the myometrium, comprising 3 distinct conditions: placenta accreta, placenta increta, and placenta percreta. This complication is relatively new to obstetrics, first described in 1937.¹

The overall incidence of PAS has been increasing over several decades, in parallel to an increasing rate of cesarean delivery (CD), with an incidence from 1982 through 2002 of 1 in 533 pregnancies, representing a 5-fold increase since the 1980s.² PAS is associated with significant morbidity and mortality, including fetal growth restriction, preterm delivery, placental abruption antenatally, and hemorrhage during delivery or postpartum.

Prenatal diagnosis of PAS and planned delivery at an experienced center are associated with significant reduction in maternal and fetal morbidity.³ In an era of advanced imaging modalities, prenatal detection of PAS regrettably remains variable and largely subjective: As many as 20% to 50% of cases of PAS escape prenatal diagnosis.^3,4

In this article, we review the sonographic markers of PAS, including diagnostic accuracy, and propose a standardized approach to prenatal diagnosis. Throughout our discussion, we describe protocols for detection of PAS practiced at our Maternal-Fetal Medicine Program in the Department of Obstetrics and Gynecology, Eastern Virginia Medical School (also see “US evaluation of PAS risk: The authors’ recommended approach”).

Numerous risk factors

There are many risk factors for PAS, including prior uterine surgery or instrumentation, such as CD, uterine curettage, myomectomy, pelvic radiation, and endometrial ablation. Other risk factors include smoking, in vitro fertilization, advanced maternal age, multiparity, and a brief interval between prior CD and subsequent pregnancy.⁵ Of major significance is the increased risk of PAS in the presence of placenta previa with prior CD.⁶ Knowledge of clinical risk factors by the interpreting physician appears to be associated with improved detection of PAS on ultrasonography (US).⁴

Ultrasonographic markers of PAS

First-trimester markers

Sonographic markers of PAS in the first trimester include:

• a gestational sac implanted in the lower uterine segment or in a CD scar
• multiple hypoechoic spaces within the placenta (lacunae).⁷

Lower uterine-segment implantation has been defined by Ballas and colleagues as 1) a gestational sac implanted in the lower one-third of the uterus between 8 and 10 weeks’ gestation or 2) a gestational sac occupying primarily the lower uterine segment from 10 weeks’ gestation onward (FIGURE 1).⁸ Our experience is that it is difficult to accurately assess lower uterine-segment implantation beyond 13 weeks of gestation because the sac typically expands to fill the upper uterine cavity.

Continue to: Color Doppler US...

Color Doppler US can help differentiate lower uterine-segment implantation from a gestational sac of a failed pregnancy in the process of expulsion by demonstrating loss of circumferential blood flow in the failed pregnancy. Furthermore, applying pressure to the anterior surface of the uterus will result in downward movement of the gestational sac of a failed pregnancy.⁹

Not all gestational sacs that implant in the lower uterine segment lead to PAS: Subsequent normal pregnancies have been reported in this circumstance. In such cases, a normal thick myometrium is noted anterior to the gestational sac.⁷ A patient with lower uterine-segment implantation without evidence of anterior myometrial thinning remains at risk for third-trimester placenta previa.⁷

Cesarean scar pregnancy carries significant risk of PAS. In these cases, the gestational sac is typically implanted within the scar, resulting in a thin anterior myometrium and significantly increased vascularity of the placental–myometrial and bladder–uterine wall interfaces (FIGURE 2).⁹ Differentiating cesarean scar pregnancy from a lower uterine-segment implantation is easier to perform before the eighth week of gestation but becomes more difficult as pregnancy advances. Although it might be useful to distinguish between true cesarean scar pregnancy and lower uterine-segment implantation adjacent to or involving the scar, both carry considerable risk of PAS and excessive hemorrhage, and the approach to treating both conditions is quite similar.

Lacunae, with or without documented blood flow on color Doppler US, are the third marker of PAS in the first trimester.⁸ Although some retrospective series and case reports describe the finding of lacunae in the first trimester of patients with diagnosed PAS, more recent literature suggests that these spaces are seen infrequently and at a similar frequency in women with and without PAS at delivery.⁷

Second- and third-trimester markers

Multiple diagnostic sonographic markers of PAS have been described in the second and third trimesters.

Placental location is a significant risk factor for PAS. Placenta previa in the setting of prior CD carries the highest risk of PAS—as high as 61% in women with both placenta previa and a history of 3 CDs.¹⁰ An anterior placenta appears to be a stronger risk factor for PAS than a posterior placenta in women with prior CD; the location of the placenta should therefore be evaluated in all women in the second trimester.

Continue to: Lacunae

Lacunae. The finding of multiple hypoechoic vascular spaces within the placental parenchyma has been associated with PAS (FIGURES 3 and 4). The pathogenesis of this finding is probably related to alterations in placental tissue resulting from long-term exposure to pulsatile blood flow.¹¹

Finberg and colleagues introduced a grading system for placental lacunae in 1992 that is still used:

• Grade 0: no lacunae seen
• Grade 1: 1 to 3 lacunae seen
• Grade 2: 4 to 6 lacunae seen
• Grade 3: multiple lacunae seen throughout the placenta.¹²

The sensitivity and specificity of lacunae as an independent marker for PAS have been reported to be 77% and 95%, respectively.¹³ Despite these findings, several studies report a range of sensitivity (73% to 100%) and negative predictive value (88% to 100%).¹⁴ Even in Finberg’s original work, 27% of cases of confirmed PAS had Grade 0 or Grade 1 placental lacunae and 11% of cases of placenta previa, without PAS, demonstrated Grade 2 lacunae.¹² There is agreement, however, that, the more lacunae, the higher the risk of PAS.

Continue to: Other US markers for PAS

Retroplacental–myometrial interface

Loss of the normal hypoechoic (clear) retroplacental zone, also referred to as loss of the clear space between placenta and uterus, is another marker of PAS (FIGURE 5). This finding corresponds to pathologic loss of the decidua basalis as trophoblastic tissue invades directly through the myometrium.¹⁵ This sonographic finding has been reported to have a detection rate of approximately 93%, with sensitivity of 52% and specificity of 57%, for PAS; the false-positive rate, however, has been in the range of 21% or higher. This marker should not be used alone because it is angle-dependent and can be found (as an absent clear zone) in normal anterior placentas.¹⁶

The strength of this US marker is in its negative predictive value, which ranges from 96% to 100%. The presence of a hypoechoic retroplacental clear space that extends the length of the placenta makes PAS unlikely.¹⁷ Of note, the clear zone may appear falsely absent as a result of increased pressure from the US probe.

Retroplacental myometrial thickness

Retroplacental myometrial thickness is difficult to assess because the lower uterine-segment myometrium thins in normal pregnancy as term approaches. This measurement also can be influenced by direct pressure of the US probe and fullness of the maternal bladder.¹⁸ In patients who have had a CD but who do not have PAS, the median myometrial thickness of the lower uterine segment in the third trimester is 2.4 mm.¹⁹

Thinning of the myometrium in the upper uterine segment always should be of concern. Studies of this marker have reported sensitivity of US ranging from 22% to 100% and specificity from 72% to 100%.^9,20 Given such variability, it is important to standardize the gestational age and sonographic approach for this marker.

Continue to: Uterovesical interface

Studies also have reported that abnormalities of the uterovesical interface are predictive of PAS. The uterovesical interface is best evaluated in a sagittal plane containing the lower uterine segment and a partially full bladder in gray-scale and color Doppler US.¹⁵ The normal uterovesical interface appears as a smooth line, without irregularities or increased vascularity on sagittal imaging.

Abnormalities include focal interruption of the hyperechoic bladder wall, bulging of the bladder wall, and increased vascularity, such as varicosities (FIGURES 5, 6, and 7).¹⁵ These findings may be seen as early as the first trimester but are more commonly noted in the second and third trimesters.⁷ The authors of a recent meta-analysis concluded that irregularity of the uterovesical interface is the most specific marker for invasive placentation (99.75% confidence interval; range, 99.5% to 99.9%).¹³

Other US markers and modalities

Three-dimensional US. Studies have evaluated the role of 3-dimensional (3D) US for predicting PAS. Application of 3D US in vascular mode has shown promise because it allows for semiquantitative assessment of placental vasculature.²² Using 3D US to screen for PAS presents drawbacks, however: The technology is not well-standardized and requires significant operator expertise for volume acquisition and manipulation. Prospective studies are needed before 3D US can be applied routinely to screen for and diagnose PAS.

Color Doppler US. As an adjunct to gray-scale US, color Doppler US can be used for making a diagnosis of PAS. Color Doppler US helps differentiate a normal subplacental venous complex with nonpulsatile, low-velocity venous blood flow waveforms from markedly dilated peripheral subplacental vascular channels with pulsatile venous-type flow, which suggests PAS. These vascular channels are often located directly over the cervix. In addition, the observation of bridging vessels linking the placenta and bladder with high diastolic arterial blood flow also suggests invasion.²¹ In a meta-analysis, overall sensitivity of color Doppler US for the diagnosis of PAS was 91%, with specificity of 87%.¹³

The value of utilizing multiple markers

The accuracy of US diagnosis of PAS is likely improved by using more than 1 sonographic marker. Pilloni and colleagues,²⁰ in a prospective analysis, found that 81% of cases of confirmed PAS had ≥2 markers and 51% of cases had ≥3 markers.

Several scoring systems have been proposed for making the diagnosis of PAS using combinations of sonographic markers, placental location, and clinical history.^19,24,25 In 2016, Tovbin and colleagues,²⁵ in a prospective study, evaluated a scoring system that included:

• number of previous CDs
• number of, maximum dimension of, and presence of blood flow in lacunae
• loss of uteroplacental clear zone
• placental location
• hypervascularity of the uterovesical or uteroplacental interface.

Tovbin assigned 1 or 2 points to each criterion. Each sonographic marker was found to be significantly associated with PAS when compared to a high-risk control group. A score of ≥8 was considered “at high risk” and predicted 69% of PAS cases.

Regrettably, no combination of US markers reliably predicts the depth of invasion of the placenta.²⁶

Continue to: A standardized approach is needed

To decrease variability and improve the US diagnosis of PAS, it is important to define and standardize the diagnosis of each sonographic marker for PAS.⁴ In 2016, the European Working Group on Abnormally Invasive Placenta (EW-AIP) proposed a set of US markers that always should be reported when performing an US examination for suspected abnormal placentation (TABLE).²³ Despite this effort by the EW-AIP, ambiguity remains over sonographic definitions of several PAS markers. For example, what determines a placental lacuna on US? And what constitutes an abnormal uterovesical interface? There is a need for a more objective definition of US markers of PAS and a standardized approach to the US examination in at-risk pregnancies.

The Society for Maternal-Fetal Medicine is coordinating a multi-society task force to address the need to define and standardize the US diagnosis of PAS.

Observations on other PAS diagnostic modalities

Magnetic resonance imaging

Adjunctive role. Magnetic resonance imaging (MRI) is often used as an adjunctive diagnostic modality in cases of suspected PAS. Several markers for PAS have been described on MRI, including¹⁵:

• intraplacental T2-weighted dark bands
• abnormal intraplacental vascularity
• heterogeneous intraplacental signal intensity
• focal interruption of the myometrium by the placenta
• uterine bulging.

Based on a recent meta-analysis, overall sensitivity of MRI for detecting PAS is 86% to 95%, with specificity of 80% to 95%. Although this is comparable to the sensitivity and specificity of US,²⁷ studies of MRI in PAS are smaller and more prone to bias than in studies of US, because MRI typically is used only in patients at highest risk for PAS. Few studies comparing US to MRI for PAS have been performed; all are small and lack statistical power.

Complementary role. MRI can be complementary to US in cases in which the placenta is posterior or located laterally²⁸ but, importantly, rarely changes decisions about surgical management when used in conjunction with US to assess patients for the diagnosis of PAS. (An exception might lie in the ability of MRI to assess the degree or depth of invasion of the placenta and discerning placenta percreta from placenta accreta.¹⁵)

Enhancement with contrast. Addition of gadolinium-based contrast might improve the ability of MRI to make a diagnosis of PAS, but gadolinium crosses the placenta barrier. Although fetal effects of gadolinium have not been observed, American College of Radiology guidelines recommend avoiding this contrast agent during pregnancy unless absolutely essential.²⁹

Specific indications. MRI without contrast should be considered 1) when US is inconclusive and 2) to further evaluate a posterior placenta suspicious for invasion, to define the precise topography of extrauterine placental invasion. The additional information offered by MRI might alter surgical planning.¹⁵

Biomarkers

Multiple serum biomarkers have been proposed to predict PAS in high-risk women. PAS might be associated with increased levels of first-trimester pregnancy-associated plasma protein A, second-trimester maternal serum alpha fetoprotein, and human chorionic gonadotropin, but studies of the utility of these biomarkers have yielded contradictory results.^30,31 Biomarkers are of interest and have significant clinical applicability, but none of the ones identified to date have high sensitivity or specificity for predicting PAS prenatally. Research is ongoing to identify markers of PAS that have sufficient predictive power.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Using cystoscopy to evaluate ureteral efflux and bladder integrity following benign gynecologic surgery increases the detection rate of urinary tract injuries.¹ Currently, it is standard of care to perform a cystoscopy following anti-incontinence procedures, but there is no consensus among ObGyns regarding the use of universal cystoscopy following benign gynecologic surgery.² A number of studies, however, have suggested potential best practices for evaluating urinary tract injury during pelvic surgery for benign gynecologic conditions.

Pelvic surgeries for benign gynecologic conditions, including fibroids, menorrhagia, and pelvic organ prolapse (POP), are common. More than 500,000 hysterectomies are performed annually in the United States, and up to 11% of women will undergo at least one surgery for POP or urinary incontinence in their lifetime.^3,4 During gynecologic surgery, the urinary tract is at risk, and the injury rate ranges from 0.02% to 2% for ureteral injury and from 1% to 5% for bladder injury.^5,6

In a recent large randomized controlled trial, the rate of intraoperative ureteral obstruction following uterosacral ligament suspension (USLS) was 3.2%.⁷ Vaginal vault suspensions, as well as other vaginal cuff closure techniques, are common procedures associated with urinary tract injury.⁸ Additionally, ureteral injury during surgery for POP occurs in as many as 2% of anterior vaginal wall repairs.⁹

It is well documented that a delay in diagnosis of ureteral and/or bladder injuries is associated with increased morbidity, including the need for additional surgery to repair the injury; in addition, significant delay in identifying an injury may lead to subsequent sequela, such as renal injury and fistula formation.⁸

A large study in California found that 36.5% of hysterectomies performed for POP were performed by general gynecologists.¹⁰ General ObGyns performing these surgeries therefore must understand the risk of urinary tract injury during hysterectomy and reconstructive pelvic procedures so that they can appropriately identify, evaluate, and repair injuries in a timely fashion.

The best way to identify urinary tract injury at the time of gynecologic surgery is by cystoscopy, including a bladder survey and ureteral efflux evaluation. When should a cystoscopy be performed, and what is the best method for visualizing ureteral efflux? Can instituting universal cystoscopy for all gynecologic procedures make a difference in the rate of injury detection? In this Update, we summarize the data from 4 studies that help to answer these questions.

Continue to: About 30% of urinary tract injuries...

About 30% of urinary tract injuries identified prior to cystoscopy at hysterectomy (which detected 5 of 6 injuries)

Vakili B, Chesson RR, Kyle BL, et al. The incidence of urinary tract injury during hysterectomy: a prospective analysis based on universal cystoscopy. Am J Obstet Gynecol. 2005;192(5):1599–1604.

Vakili and colleagues conducted a multicenter prospective cohort study of women undergoing hysterectomy for benign indications; cystoscopy was performed in all cases. The 3 hospitals involved were all part of the Louisiana State University Health system. The investigators’ goal was to determine the rate of urinary tract injury in this patient population at the time of intraoperative cystoscopy.

Intraoperative cystoscopy beats visual evaluation

Four hundred and seventy-one women underwent hysterectomy and had intraoperative cystoscopy, including evaluation of ureteral patency with administration of intravenous (IV) indigo carmine. Patients underwent abdominal, vaginal, or laparoscopic hysterectomy, and 54 (11.4%) had concurrent POP or anti-incontinence procedures. The majority underwent an abdominal hysterectomy (59%), 31% had a vaginal hysterectomy, and 10% had a laparoscopic-assisted vaginal hysterectomy or total laparoscopic hysterectomy.

Rate of urinary tract injuries. The total urinary tract injury rate detected by cystoscopy was 4.8%. The ureteral injury rate was 1.7%, and the bladder injury rate was 3.6%. A combined ureteral and bladder injury occurred in 2 women.

Surgery for POP significantly increased the risk of ureteral injury (7.3% vs 1.2%; P = .025). All cases of ureteral injury during POP surgery occurred during USLS. There was a trend toward a higher rate of bladder injury in the group with concurrent anti-incontinence surgery (12.5% vs 3.1%; P = .049). Regarding the route of hysterectomy, the vaginal approach had the highest rate of ureteral injury; however, when prolapse cases were removed from the analysis, there were no differences between the abdominal, vaginal, and laparoscopic approaches for ureteral or bladder injuries.

Injury detection with cystoscopy. Importantly, the authors found that only 30% of injuries were identified prior to performing intraoperative cystoscopy. The majority of these were bladder injuries. In addition, despite visual confirmation of ureteral peristalsis during abdominal hysterectomy, when intraoperative cystoscopy was performed with evaluation for ureteral efflux, 5 of 6 ureteral injury cases were identified. The authors reported 1 postoperative vesicovaginal fistula and concluded that it was likely due to an unrecognized bladder injury. No other undetected injuries were identified.

Notably, no complications occurred as a result of cystoscopy.

Multiple surgical indications reflect real-world scenario

The study included physicians from 3 different hospitals and all routes of hysterectomy for multiple benign gynecologic indications as well as concomitant pelvic reconstructive procedures. While this enhances the generalizability of the study results, all study sites were located in Louisiana at hospitals with resident trainee involvement. Additionally, this study confirms previous retrospective studies that reported higher rates of injury with pelvic reconstructive procedures.

The study is limited by the inability to blind surgeons, which may have resulted in the surgeons altering their techniques and/or having a heightened awareness of the urinary tract. However, their rates of ureteral and bladder injuries were slightly higher than previously reported rates, suggesting that the procedures inherently carry risk. The study is further limited by the lack of a retrospective comparison group of hysterectomy without routine cystoscopy and a longer follow-up period that may have revealed additional missed delayed urologic injuries.

Continue to: Universal cystoscopy policy...

Chi AM, Curran DS, Morgan DM, Fenner DE, Swenson CW. Universal cystoscopy after benign hysterectomy: examining the effects of an institutional policy. Obstet Gynecol. 2016;127(2):369–375.

In a retrospective cohort study, Chi and colleagues evaluated urinary tract injuries at the time of hysterectomy before and after the institution of a universal cystoscopy policy. At the time of policy implementation at the University of Michigan, all faculty who performed hysterectomies attended a cystoscopy workshop. Attending physicians without prior cystoscopy training also were proctored in the operating room for 3 sessions and were required to demonstrate competency with bladder survey, visualizing ureteral efflux, and urethral assessment. Indigo carmine was used to visualize ureteral efflux.

Detection of urologic injury almost doubled with cystoscopy

A total of 2,822 hysterectomies were included in the study, with 973 in the pre–universal cystoscopy group and 1,849 in the post–universal cystoscopy group. The study period was 7 years, and data on complications were abstracted for 1 year after the completion of the study period.

The primary outcome had 3 components:

• the rate of urologic injury before and after the policy
• the cystoscopy detection rate of urologic injury
• the adherence rate to the policy.

The overall rate of bladder and ureteral injury was 2.1%; the rate of injury during pre–universal screening was 2.6%, and during post–universal screening was 1.8%. The intraoperative detection rate of injury nearly doubled, from 24% to 47%, when intraoperative cystoscopy was utilized. In addition, the percentage of delayed urologic complications decreased from 28% to 5.9% (P = .03) following implementation of the universal cystoscopy policy. With regard to surgeon adherence, cystoscopy was documented in 86.1% of the hysterectomy cases after the policy was implemented compared with 35.7% of cases before the policy.

The investigators performed a cost analysis and found that hospital costs were nearly twice as much if a delayed urologic injury was diagnosed. 
 

Study had many strengths

This study evaluated aspects of implementing quality initiatives after proper training and proctoring of a procedure. The authors compared very large cohorts from a busy academic medical center in which surgeon adherence with routine cystoscopy was high. The majority of patient outcomes were tracked for an extended period following surgery, thereby minimizing the risk of missing delayed urologic injuries. Notably, however, there was shorter follow-up time for the post–universal cystoscopy group, which could result in underestimating the rate of delayed urologic injuries in this cohort.

Continue to: Cystoscopy reveals ureteral obstruction...

Gustilo-Ashby AM, Jelovsek JE, Barber MD, Yoo EH, Paraiso MF, Walters MD. The incidence of ureteral obstruction and the value of intraoperative cystoscopy during vaginal surgery for pelvic organ prolapse. Am J Obstet Gynecol. 2006;194(5):1478–1485.

To determine the rate of ureteral obstruction and ureteral injury during vaginal surgery for POP and the accuracy of using intraoperative cystoscopy to prevent upper urinary tract morbidity, Gustilo-Ashby and colleagues performed a retrospective review study of a large patient cohort.

Cystoscopy with indigo carmine is highly sensitive
 

The study included 700 patients who underwent vaginal surgery for anterior and/or apical POP. Patients had 1 or more of the following anterior and apical prolapse repair procedures: USLS (51%), distal McCall culdeplasty (26%), proximal McCall culdeplasty (29%), anterior colporrhaphy (82%), and colpocleisis (1.4%). Of note, distal McCall culdeplasty was defined as incorporation of the “vaginal epithelium into the uterosacral plication,” while proximal McCall culdeplasty involved plication of “the uterosacral ligaments in the midline proximal to the vaginal cuff.” All patients were given IV indigo carmine to aid in visualizing ureteral efflux.

The majority of patients had a hysterectomy (56%). When accounting for rare false-positive and negative cystoscopy results, the overall ureteral obstruction rate was 5.1% and the ureteral injury rate was 0.9%. The majority of obstructions occurred with USLS (5.9%), proximal McCall culdeplasty (4.4%), and colpocleisis (4.2%). Ureteral injuries occurred only in 6 cases: 3 USLS and 3 proximal McCall culdeplasty procedures.

Based on these findings, the authors calculated that cystoscopy at the time of vaginal surgery for anterior and/or apical prolapse has a sensitivity of 94.4% and a specificity of 99.5% for detecting ureteral obstruction. The positive predictive value of cystoscopy with the use of indigo carmine for detection of ureteral obstruction is 91.9% and the negative predictive value is 99.7%.

Impact of indigo carmine’s unavailability 

This study’s strengths include its large sample size and the variety of surgical approaches used for repair of anterior vaginal wall and apical prolapse. Its retrospective design, however, is a limitation; this could result in underreporting of ureteral injuries if patients received care at another institution after surgery. Furthermore, it is unclear if cystoscopy would be as predictive of ureteral injury without the use of indigo carmine, which is no longer available at most institutions.
 

Continue to: Sodium fluorescein and 10% dextrose...

Espaillat-Rijo L, Siff L, Alas AN, et al. Intraoperative cystoscopic evaluation of ureteral patency: a randomized controlled trial. Obstet Gynecol. 2016;128(6):1378–1383.

In a multicenter randomized controlled trial, Espaillat-Rijo and colleagues compared various methods for visualizing ureteral efflux in participants who underwent gynecologic or urogynecologic procedures in which cystoscopy was performed.

Study compared 4 media

The investigators enrolled 176 participants (174 completed the trial) and randomly assigned them to receive 1 of 4 modalities: 1) normal saline as a bladder distention medium (control), 2) 10% dextrose as a bladder distention medium, 3) 200 mg oral phenazopyridine given 30 minutes prior to cystoscopy, or 4) 50 mg IV sodium fluorescein at the start of cystoscopy. Indigo carmine was not included in this study because it has not been routinely available since 2014.

Surgeons were asked to categorize the ureteral jets as “clearly visible,” “somewhat visible,” or “not visible.”

The primary outcome was subjective visibility of the ureteral jet with each modality during cystoscopy. Secondary outcomes included surgeon satisfaction, adverse reactions to the modality used, postoperative urinary tract infection, postoperative urinary retention, and delayed diagnosis of ureteral injury.

Visibility assessment results. Overall, ureteral jets were “clearly visible” in 125 cases (71%) compared with “somewhat visible” in 45 (25.6%) and “not visible” in 4 (2.3%) cases. There was a statistically significant difference between the 4 groups. Use of sodium fluorescein and 10% dextrose resulted in significantly better visualization of ureteral jets (P < .001 and P = .004, respectively) compared with the control group. Visibility with phenazopyridine was not significantly different from that in the control group or in the 10% dextrose group (FIGURE).

Surgeon satisfaction was highest with 10% dextrose and sodium fluorescein. In 6 cases, the surgeon was not satisfied with visualization of the ureteral jets and relied on fluorescein (5 times) or 10% dextrose (1 time) to ultimately see efflux. No significant adverse events occurred; the rate of urinary tract infection was 24.1% and did not differ between groups.

Results are widely generalizable

This was a well-designed randomized multicenter trial that included both benign gynecologic and urogynecologic procedures, thus strengthening the generalizability of the study. The study was timely since proven methods for visualization of ureteral patency became limited with the withdrawal of commercially available indigo carmine, the previous gold standard.

Continue to: The cost-effectiveness consideration

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Using cystoscopy to evaluate ureteral efflux and bladder integrity following benign gynecologic surgery increases the detection rate of urinary tract injuries.¹ Currently, it is standard of care to perform a cystoscopy following anti-incontinence procedures, but there is no consensus among ObGyns regarding the use of universal cystoscopy following benign gynecologic surgery.² A number of studies, however, have suggested potential best practices for evaluating urinary tract injury during pelvic surgery for benign gynecologic conditions.

Pelvic surgeries for benign gynecologic conditions, including fibroids, menorrhagia, and pelvic organ prolapse (POP), are common. More than 500,000 hysterectomies are performed annually in the United States, and up to 11% of women will undergo at least one surgery for POP or urinary incontinence in their lifetime.^3,4 During gynecologic surgery, the urinary tract is at risk, and the injury rate ranges from 0.02% to 2% for ureteral injury and from 1% to 5% for bladder injury.^5,6

In a recent large randomized controlled trial, the rate of intraoperative ureteral obstruction following uterosacral ligament suspension (USLS) was 3.2%.⁷ Vaginal vault suspensions, as well as other vaginal cuff closure techniques, are common procedures associated with urinary tract injury.⁸ Additionally, ureteral injury during surgery for POP occurs in as many as 2% of anterior vaginal wall repairs.⁹

It is well documented that a delay in diagnosis of ureteral and/or bladder injuries is associated with increased morbidity, including the need for additional surgery to repair the injury; in addition, significant delay in identifying an injury may lead to subsequent sequela, such as renal injury and fistula formation.⁸

A large study in California found that 36.5% of hysterectomies performed for POP were performed by general gynecologists.¹⁰ General ObGyns performing these surgeries therefore must understand the risk of urinary tract injury during hysterectomy and reconstructive pelvic procedures so that they can appropriately identify, evaluate, and repair injuries in a timely fashion.

The best way to identify urinary tract injury at the time of gynecologic surgery is by cystoscopy, including a bladder survey and ureteral efflux evaluation. When should a cystoscopy be performed, and what is the best method for visualizing ureteral efflux? Can instituting universal cystoscopy for all gynecologic procedures make a difference in the rate of injury detection? In this Update, we summarize the data from 4 studies that help to answer these questions.

Continue to: About 30% of urinary tract injuries...

About 30% of urinary tract injuries identified prior to cystoscopy at hysterectomy (which detected 5 of 6 injuries)

Vakili B, Chesson RR, Kyle BL, et al. The incidence of urinary tract injury during hysterectomy: a prospective analysis based on universal cystoscopy. Am J Obstet Gynecol. 2005;192(5):1599–1604.

Vakili and colleagues conducted a multicenter prospective cohort study of women undergoing hysterectomy for benign indications; cystoscopy was performed in all cases. The 3 hospitals involved were all part of the Louisiana State University Health system. The investigators’ goal was to determine the rate of urinary tract injury in this patient population at the time of intraoperative cystoscopy.

Intraoperative cystoscopy beats visual evaluation

Four hundred and seventy-one women underwent hysterectomy and had intraoperative cystoscopy, including evaluation of ureteral patency with administration of intravenous (IV) indigo carmine. Patients underwent abdominal, vaginal, or laparoscopic hysterectomy, and 54 (11.4%) had concurrent POP or anti-incontinence procedures. The majority underwent an abdominal hysterectomy (59%), 31% had a vaginal hysterectomy, and 10% had a laparoscopic-assisted vaginal hysterectomy or total laparoscopic hysterectomy.

Rate of urinary tract injuries. The total urinary tract injury rate detected by cystoscopy was 4.8%. The ureteral injury rate was 1.7%, and the bladder injury rate was 3.6%. A combined ureteral and bladder injury occurred in 2 women.

Surgery for POP significantly increased the risk of ureteral injury (7.3% vs 1.2%; P = .025). All cases of ureteral injury during POP surgery occurred during USLS. There was a trend toward a higher rate of bladder injury in the group with concurrent anti-incontinence surgery (12.5% vs 3.1%; P = .049). Regarding the route of hysterectomy, the vaginal approach had the highest rate of ureteral injury; however, when prolapse cases were removed from the analysis, there were no differences between the abdominal, vaginal, and laparoscopic approaches for ureteral or bladder injuries.

Injury detection with cystoscopy. Importantly, the authors found that only 30% of injuries were identified prior to performing intraoperative cystoscopy. The majority of these were bladder injuries. In addition, despite visual confirmation of ureteral peristalsis during abdominal hysterectomy, when intraoperative cystoscopy was performed with evaluation for ureteral efflux, 5 of 6 ureteral injury cases were identified. The authors reported 1 postoperative vesicovaginal fistula and concluded that it was likely due to an unrecognized bladder injury. No other undetected injuries were identified.

Notably, no complications occurred as a result of cystoscopy.

Multiple surgical indications reflect real-world scenario

The study included physicians from 3 different hospitals and all routes of hysterectomy for multiple benign gynecologic indications as well as concomitant pelvic reconstructive procedures. While this enhances the generalizability of the study results, all study sites were located in Louisiana at hospitals with resident trainee involvement. Additionally, this study confirms previous retrospective studies that reported higher rates of injury with pelvic reconstructive procedures.

The study is limited by the inability to blind surgeons, which may have resulted in the surgeons altering their techniques and/or having a heightened awareness of the urinary tract. However, their rates of ureteral and bladder injuries were slightly higher than previously reported rates, suggesting that the procedures inherently carry risk. The study is further limited by the lack of a retrospective comparison group of hysterectomy without routine cystoscopy and a longer follow-up period that may have revealed additional missed delayed urologic injuries.

Continue to: Universal cystoscopy policy...

Chi AM, Curran DS, Morgan DM, Fenner DE, Swenson CW. Universal cystoscopy after benign hysterectomy: examining the effects of an institutional policy. Obstet Gynecol. 2016;127(2):369–375.

In a retrospective cohort study, Chi and colleagues evaluated urinary tract injuries at the time of hysterectomy before and after the institution of a universal cystoscopy policy. At the time of policy implementation at the University of Michigan, all faculty who performed hysterectomies attended a cystoscopy workshop. Attending physicians without prior cystoscopy training also were proctored in the operating room for 3 sessions and were required to demonstrate competency with bladder survey, visualizing ureteral efflux, and urethral assessment. Indigo carmine was used to visualize ureteral efflux.

Detection of urologic injury almost doubled with cystoscopy

A total of 2,822 hysterectomies were included in the study, with 973 in the pre–universal cystoscopy group and 1,849 in the post–universal cystoscopy group. The study period was 7 years, and data on complications were abstracted for 1 year after the completion of the study period.

The primary outcome had 3 components:

• the rate of urologic injury before and after the policy
• the cystoscopy detection rate of urologic injury
• the adherence rate to the policy.

The overall rate of bladder and ureteral injury was 2.1%; the rate of injury during pre–universal screening was 2.6%, and during post–universal screening was 1.8%. The intraoperative detection rate of injury nearly doubled, from 24% to 47%, when intraoperative cystoscopy was utilized. In addition, the percentage of delayed urologic complications decreased from 28% to 5.9% (P = .03) following implementation of the universal cystoscopy policy. With regard to surgeon adherence, cystoscopy was documented in 86.1% of the hysterectomy cases after the policy was implemented compared with 35.7% of cases before the policy.

The investigators performed a cost analysis and found that hospital costs were nearly twice as much if a delayed urologic injury was diagnosed. 
 

Study had many strengths

This study evaluated aspects of implementing quality initiatives after proper training and proctoring of a procedure. The authors compared very large cohorts from a busy academic medical center in which surgeon adherence with routine cystoscopy was high. The majority of patient outcomes were tracked for an extended period following surgery, thereby minimizing the risk of missing delayed urologic injuries. Notably, however, there was shorter follow-up time for the post–universal cystoscopy group, which could result in underestimating the rate of delayed urologic injuries in this cohort.

Continue to: Cystoscopy reveals ureteral obstruction...

Gustilo-Ashby AM, Jelovsek JE, Barber MD, Yoo EH, Paraiso MF, Walters MD. The incidence of ureteral obstruction and the value of intraoperative cystoscopy during vaginal surgery for pelvic organ prolapse. Am J Obstet Gynecol. 2006;194(5):1478–1485.

To determine the rate of ureteral obstruction and ureteral injury during vaginal surgery for POP and the accuracy of using intraoperative cystoscopy to prevent upper urinary tract morbidity, Gustilo-Ashby and colleagues performed a retrospective review study of a large patient cohort.

Cystoscopy with indigo carmine is highly sensitive
 

The study included 700 patients who underwent vaginal surgery for anterior and/or apical POP. Patients had 1 or more of the following anterior and apical prolapse repair procedures: USLS (51%), distal McCall culdeplasty (26%), proximal McCall culdeplasty (29%), anterior colporrhaphy (82%), and colpocleisis (1.4%). Of note, distal McCall culdeplasty was defined as incorporation of the “vaginal epithelium into the uterosacral plication,” while proximal McCall culdeplasty involved plication of “the uterosacral ligaments in the midline proximal to the vaginal cuff.” All patients were given IV indigo carmine to aid in visualizing ureteral efflux.

The majority of patients had a hysterectomy (56%). When accounting for rare false-positive and negative cystoscopy results, the overall ureteral obstruction rate was 5.1% and the ureteral injury rate was 0.9%. The majority of obstructions occurred with USLS (5.9%), proximal McCall culdeplasty (4.4%), and colpocleisis (4.2%). Ureteral injuries occurred only in 6 cases: 3 USLS and 3 proximal McCall culdeplasty procedures.

Based on these findings, the authors calculated that cystoscopy at the time of vaginal surgery for anterior and/or apical prolapse has a sensitivity of 94.4% and a specificity of 99.5% for detecting ureteral obstruction. The positive predictive value of cystoscopy with the use of indigo carmine for detection of ureteral obstruction is 91.9% and the negative predictive value is 99.7%.

Impact of indigo carmine’s unavailability 

This study’s strengths include its large sample size and the variety of surgical approaches used for repair of anterior vaginal wall and apical prolapse. Its retrospective design, however, is a limitation; this could result in underreporting of ureteral injuries if patients received care at another institution after surgery. Furthermore, it is unclear if cystoscopy would be as predictive of ureteral injury without the use of indigo carmine, which is no longer available at most institutions.
 

Continue to: Sodium fluorescein and 10% dextrose...

Espaillat-Rijo L, Siff L, Alas AN, et al. Intraoperative cystoscopic evaluation of ureteral patency: a randomized controlled trial. Obstet Gynecol. 2016;128(6):1378–1383.

In a multicenter randomized controlled trial, Espaillat-Rijo and colleagues compared various methods for visualizing ureteral efflux in participants who underwent gynecologic or urogynecologic procedures in which cystoscopy was performed.

Study compared 4 media

The investigators enrolled 176 participants (174 completed the trial) and randomly assigned them to receive 1 of 4 modalities: 1) normal saline as a bladder distention medium (control), 2) 10% dextrose as a bladder distention medium, 3) 200 mg oral phenazopyridine given 30 minutes prior to cystoscopy, or 4) 50 mg IV sodium fluorescein at the start of cystoscopy. Indigo carmine was not included in this study because it has not been routinely available since 2014.

Surgeons were asked to categorize the ureteral jets as “clearly visible,” “somewhat visible,” or “not visible.”

The primary outcome was subjective visibility of the ureteral jet with each modality during cystoscopy. Secondary outcomes included surgeon satisfaction, adverse reactions to the modality used, postoperative urinary tract infection, postoperative urinary retention, and delayed diagnosis of ureteral injury.

Visibility assessment results. Overall, ureteral jets were “clearly visible” in 125 cases (71%) compared with “somewhat visible” in 45 (25.6%) and “not visible” in 4 (2.3%) cases. There was a statistically significant difference between the 4 groups. Use of sodium fluorescein and 10% dextrose resulted in significantly better visualization of ureteral jets (P < .001 and P = .004, respectively) compared with the control group. Visibility with phenazopyridine was not significantly different from that in the control group or in the 10% dextrose group (FIGURE).

Surgeon satisfaction was highest with 10% dextrose and sodium fluorescein. In 6 cases, the surgeon was not satisfied with visualization of the ureteral jets and relied on fluorescein (5 times) or 10% dextrose (1 time) to ultimately see efflux. No significant adverse events occurred; the rate of urinary tract infection was 24.1% and did not differ between groups.

Results are widely generalizable

This was a well-designed randomized multicenter trial that included both benign gynecologic and urogynecologic procedures, thus strengthening the generalizability of the study. The study was timely since proven methods for visualization of ureteral patency became limited with the withdrawal of commercially available indigo carmine, the previous gold standard.

Continue to: The cost-effectiveness consideration

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Using cystoscopy to evaluate ureteral efflux and bladder integrity following benign gynecologic surgery increases the detection rate of urinary tract injuries.¹ Currently, it is standard of care to perform a cystoscopy following anti-incontinence procedures, but there is no consensus among ObGyns regarding the use of universal cystoscopy following benign gynecologic surgery.² A number of studies, however, have suggested potential best practices for evaluating urinary tract injury during pelvic surgery for benign gynecologic conditions.

Pelvic surgeries for benign gynecologic conditions, including fibroids, menorrhagia, and pelvic organ prolapse (POP), are common. More than 500,000 hysterectomies are performed annually in the United States, and up to 11% of women will undergo at least one surgery for POP or urinary incontinence in their lifetime.^3,4 During gynecologic surgery, the urinary tract is at risk, and the injury rate ranges from 0.02% to 2% for ureteral injury and from 1% to 5% for bladder injury.^5,6

In a recent large randomized controlled trial, the rate of intraoperative ureteral obstruction following uterosacral ligament suspension (USLS) was 3.2%.⁷ Vaginal vault suspensions, as well as other vaginal cuff closure techniques, are common procedures associated with urinary tract injury.⁸ Additionally, ureteral injury during surgery for POP occurs in as many as 2% of anterior vaginal wall repairs.⁹

It is well documented that a delay in diagnosis of ureteral and/or bladder injuries is associated with increased morbidity, including the need for additional surgery to repair the injury; in addition, significant delay in identifying an injury may lead to subsequent sequela, such as renal injury and fistula formation.⁸

A large study in California found that 36.5% of hysterectomies performed for POP were performed by general gynecologists.¹⁰ General ObGyns performing these surgeries therefore must understand the risk of urinary tract injury during hysterectomy and reconstructive pelvic procedures so that they can appropriately identify, evaluate, and repair injuries in a timely fashion.

The best way to identify urinary tract injury at the time of gynecologic surgery is by cystoscopy, including a bladder survey and ureteral efflux evaluation. When should a cystoscopy be performed, and what is the best method for visualizing ureteral efflux? Can instituting universal cystoscopy for all gynecologic procedures make a difference in the rate of injury detection? In this Update, we summarize the data from 4 studies that help to answer these questions.

Continue to: About 30% of urinary tract injuries...

About 30% of urinary tract injuries identified prior to cystoscopy at hysterectomy (which detected 5 of 6 injuries)

Vakili B, Chesson RR, Kyle BL, et al. The incidence of urinary tract injury during hysterectomy: a prospective analysis based on universal cystoscopy. Am J Obstet Gynecol. 2005;192(5):1599–1604.

Vakili and colleagues conducted a multicenter prospective cohort study of women undergoing hysterectomy for benign indications; cystoscopy was performed in all cases. The 3 hospitals involved were all part of the Louisiana State University Health system. The investigators’ goal was to determine the rate of urinary tract injury in this patient population at the time of intraoperative cystoscopy.

Intraoperative cystoscopy beats visual evaluation

Four hundred and seventy-one women underwent hysterectomy and had intraoperative cystoscopy, including evaluation of ureteral patency with administration of intravenous (IV) indigo carmine. Patients underwent abdominal, vaginal, or laparoscopic hysterectomy, and 54 (11.4%) had concurrent POP or anti-incontinence procedures. The majority underwent an abdominal hysterectomy (59%), 31% had a vaginal hysterectomy, and 10% had a laparoscopic-assisted vaginal hysterectomy or total laparoscopic hysterectomy.

Rate of urinary tract injuries. The total urinary tract injury rate detected by cystoscopy was 4.8%. The ureteral injury rate was 1.7%, and the bladder injury rate was 3.6%. A combined ureteral and bladder injury occurred in 2 women.

Surgery for POP significantly increased the risk of ureteral injury (7.3% vs 1.2%; P = .025). All cases of ureteral injury during POP surgery occurred during USLS. There was a trend toward a higher rate of bladder injury in the group with concurrent anti-incontinence surgery (12.5% vs 3.1%; P = .049). Regarding the route of hysterectomy, the vaginal approach had the highest rate of ureteral injury; however, when prolapse cases were removed from the analysis, there were no differences between the abdominal, vaginal, and laparoscopic approaches for ureteral or bladder injuries.

Injury detection with cystoscopy. Importantly, the authors found that only 30% of injuries were identified prior to performing intraoperative cystoscopy. The majority of these were bladder injuries. In addition, despite visual confirmation of ureteral peristalsis during abdominal hysterectomy, when intraoperative cystoscopy was performed with evaluation for ureteral efflux, 5 of 6 ureteral injury cases were identified. The authors reported 1 postoperative vesicovaginal fistula and concluded that it was likely due to an unrecognized bladder injury. No other undetected injuries were identified.

Notably, no complications occurred as a result of cystoscopy.

Multiple surgical indications reflect real-world scenario

The study included physicians from 3 different hospitals and all routes of hysterectomy for multiple benign gynecologic indications as well as concomitant pelvic reconstructive procedures. While this enhances the generalizability of the study results, all study sites were located in Louisiana at hospitals with resident trainee involvement. Additionally, this study confirms previous retrospective studies that reported higher rates of injury with pelvic reconstructive procedures.

The study is limited by the inability to blind surgeons, which may have resulted in the surgeons altering their techniques and/or having a heightened awareness of the urinary tract. However, their rates of ureteral and bladder injuries were slightly higher than previously reported rates, suggesting that the procedures inherently carry risk. The study is further limited by the lack of a retrospective comparison group of hysterectomy without routine cystoscopy and a longer follow-up period that may have revealed additional missed delayed urologic injuries.

Continue to: Universal cystoscopy policy...

Chi AM, Curran DS, Morgan DM, Fenner DE, Swenson CW. Universal cystoscopy after benign hysterectomy: examining the effects of an institutional policy. Obstet Gynecol. 2016;127(2):369–375.

In a retrospective cohort study, Chi and colleagues evaluated urinary tract injuries at the time of hysterectomy before and after the institution of a universal cystoscopy policy. At the time of policy implementation at the University of Michigan, all faculty who performed hysterectomies attended a cystoscopy workshop. Attending physicians without prior cystoscopy training also were proctored in the operating room for 3 sessions and were required to demonstrate competency with bladder survey, visualizing ureteral efflux, and urethral assessment. Indigo carmine was used to visualize ureteral efflux.

Detection of urologic injury almost doubled with cystoscopy

A total of 2,822 hysterectomies were included in the study, with 973 in the pre–universal cystoscopy group and 1,849 in the post–universal cystoscopy group. The study period was 7 years, and data on complications were abstracted for 1 year after the completion of the study period.

The primary outcome had 3 components:

• the rate of urologic injury before and after the policy
• the cystoscopy detection rate of urologic injury
• the adherence rate to the policy.

The overall rate of bladder and ureteral injury was 2.1%; the rate of injury during pre–universal screening was 2.6%, and during post–universal screening was 1.8%. The intraoperative detection rate of injury nearly doubled, from 24% to 47%, when intraoperative cystoscopy was utilized. In addition, the percentage of delayed urologic complications decreased from 28% to 5.9% (P = .03) following implementation of the universal cystoscopy policy. With regard to surgeon adherence, cystoscopy was documented in 86.1% of the hysterectomy cases after the policy was implemented compared with 35.7% of cases before the policy.

The investigators performed a cost analysis and found that hospital costs were nearly twice as much if a delayed urologic injury was diagnosed. 
 

Study had many strengths

This study evaluated aspects of implementing quality initiatives after proper training and proctoring of a procedure. The authors compared very large cohorts from a busy academic medical center in which surgeon adherence with routine cystoscopy was high. The majority of patient outcomes were tracked for an extended period following surgery, thereby minimizing the risk of missing delayed urologic injuries. Notably, however, there was shorter follow-up time for the post–universal cystoscopy group, which could result in underestimating the rate of delayed urologic injuries in this cohort.

Continue to: Cystoscopy reveals ureteral obstruction...

Gustilo-Ashby AM, Jelovsek JE, Barber MD, Yoo EH, Paraiso MF, Walters MD. The incidence of ureteral obstruction and the value of intraoperative cystoscopy during vaginal surgery for pelvic organ prolapse. Am J Obstet Gynecol. 2006;194(5):1478–1485.

To determine the rate of ureteral obstruction and ureteral injury during vaginal surgery for POP and the accuracy of using intraoperative cystoscopy to prevent upper urinary tract morbidity, Gustilo-Ashby and colleagues performed a retrospective review study of a large patient cohort.

Cystoscopy with indigo carmine is highly sensitive
 

The study included 700 patients who underwent vaginal surgery for anterior and/or apical POP. Patients had 1 or more of the following anterior and apical prolapse repair procedures: USLS (51%), distal McCall culdeplasty (26%), proximal McCall culdeplasty (29%), anterior colporrhaphy (82%), and colpocleisis (1.4%). Of note, distal McCall culdeplasty was defined as incorporation of the “vaginal epithelium into the uterosacral plication,” while proximal McCall culdeplasty involved plication of “the uterosacral ligaments in the midline proximal to the vaginal cuff.” All patients were given IV indigo carmine to aid in visualizing ureteral efflux.

The majority of patients had a hysterectomy (56%). When accounting for rare false-positive and negative cystoscopy results, the overall ureteral obstruction rate was 5.1% and the ureteral injury rate was 0.9%. The majority of obstructions occurred with USLS (5.9%), proximal McCall culdeplasty (4.4%), and colpocleisis (4.2%). Ureteral injuries occurred only in 6 cases: 3 USLS and 3 proximal McCall culdeplasty procedures.

Based on these findings, the authors calculated that cystoscopy at the time of vaginal surgery for anterior and/or apical prolapse has a sensitivity of 94.4% and a specificity of 99.5% for detecting ureteral obstruction. The positive predictive value of cystoscopy with the use of indigo carmine for detection of ureteral obstruction is 91.9% and the negative predictive value is 99.7%.

Impact of indigo carmine’s unavailability 

This study’s strengths include its large sample size and the variety of surgical approaches used for repair of anterior vaginal wall and apical prolapse. Its retrospective design, however, is a limitation; this could result in underreporting of ureteral injuries if patients received care at another institution after surgery. Furthermore, it is unclear if cystoscopy would be as predictive of ureteral injury without the use of indigo carmine, which is no longer available at most institutions.
 

Continue to: Sodium fluorescein and 10% dextrose...

Espaillat-Rijo L, Siff L, Alas AN, et al. Intraoperative cystoscopic evaluation of ureteral patency: a randomized controlled trial. Obstet Gynecol. 2016;128(6):1378–1383.

In a multicenter randomized controlled trial, Espaillat-Rijo and colleagues compared various methods for visualizing ureteral efflux in participants who underwent gynecologic or urogynecologic procedures in which cystoscopy was performed.

Study compared 4 media

The investigators enrolled 176 participants (174 completed the trial) and randomly assigned them to receive 1 of 4 modalities: 1) normal saline as a bladder distention medium (control), 2) 10% dextrose as a bladder distention medium, 3) 200 mg oral phenazopyridine given 30 minutes prior to cystoscopy, or 4) 50 mg IV sodium fluorescein at the start of cystoscopy. Indigo carmine was not included in this study because it has not been routinely available since 2014.

Surgeons were asked to categorize the ureteral jets as “clearly visible,” “somewhat visible,” or “not visible.”

The primary outcome was subjective visibility of the ureteral jet with each modality during cystoscopy. Secondary outcomes included surgeon satisfaction, adverse reactions to the modality used, postoperative urinary tract infection, postoperative urinary retention, and delayed diagnosis of ureteral injury.

Visibility assessment results. Overall, ureteral jets were “clearly visible” in 125 cases (71%) compared with “somewhat visible” in 45 (25.6%) and “not visible” in 4 (2.3%) cases. There was a statistically significant difference between the 4 groups. Use of sodium fluorescein and 10% dextrose resulted in significantly better visualization of ureteral jets (P < .001 and P = .004, respectively) compared with the control group. Visibility with phenazopyridine was not significantly different from that in the control group or in the 10% dextrose group (FIGURE).

Surgeon satisfaction was highest with 10% dextrose and sodium fluorescein. In 6 cases, the surgeon was not satisfied with visualization of the ureteral jets and relied on fluorescein (5 times) or 10% dextrose (1 time) to ultimately see efflux. No significant adverse events occurred; the rate of urinary tract infection was 24.1% and did not differ between groups.

Results are widely generalizable

This was a well-designed randomized multicenter trial that included both benign gynecologic and urogynecologic procedures, thus strengthening the generalizability of the study. The study was timely since proven methods for visualization of ureteral patency became limited with the withdrawal of commercially available indigo carmine, the previous gold standard.

Continue to: The cost-effectiveness consideration

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Last year’s influenza season was severe enough that hospitals around the United States set up special evaluation areas beyond their emergency departments, at times spilling over to tents or other temporary structures in what otherwise would be parking lots. The scale and potential severity of the annual epidemic can be difficult to convey to our patients, who sometimes say “just the flu” to refer to an illness responsible for more than 170 pediatric deaths in the United States this past year.¹ The Centers for Disease Control and Prevention (CDC) recently updated its 5-year estimates of influenza-related deaths in the United States; influenza mortality ranges from about 12,000 deaths in a mild season (such as 2011-2012) to 56,000 in a more severe season (eg, 2012-2013).²

Although influenza cannot be completely prevented, the following strategies can help reduce the risk for the illness and limit its severity if contracted.

Prevention

Strategy 1: Vaccinate against influenza

While the efficacy of vaccines varies from year to year, vaccination remains the core of influenza prevention efforts. In this decade, vaccine effectiveness has ranged from 19% to 60%.³ However, models suggest that even when the vaccine is only 20% effective, vaccinating 140 million people (the average number of doses delivered annually in the United States over the past 5 seasons) prevents 21 million infections, 130,000 hospitalizations, and more than 61,000 deaths.⁴ In a case-control study, Flannery et al found that vaccination was 65% effective in preventing laboratory-confirmed influenza-associated death in children over 4 seasons (July 2010 through June 2014).⁵

Deciding who should be vaccinated is simpler than in prior years: Rather than targeting people who are at higher risk (those ages 65 and older, or those with comorbidities), the current CDC recommendation is to vaccinate nearly everyone ages 6 months or older, with limited exceptions.^6,7 (See Table 1⁸).

Formulations. Many types of influenza vaccine are approved for use in the United States; these differ in the number of strains included (3 or 4), the amount of antigen present for each strain, the presence of an adjuvant, the growth medium used for the virus, and the route of administration (see Table 2⁹). The relative merits of each type are a matter of some debate. There is ongoing research into the comparative efficacy of vaccines comprised of egg- vs cell-based cultures, as well as studies comparing high-dose or adjuvant vaccines to standard-dose inactivated vaccines.

Previously, the CDC has recommended preferential use (or avoidance) of some vaccine types, based on their efficacy. For the 2018-2019 flu season, however, the CDC has rescinded its recommendation against vaccine containing live attenuated virus (LAIV; FluMist brand) and expresses no preference for any vaccine formulation for patients of appropriate age and health status.¹⁰ The American Academy of Pediatrics (AAP), however, is recommends that LAIV be used only if patients and their families decline injectable vaccines.¹¹

Timing. Influenza vaccines are now distributed as early as July to some locations, raising concerns about waning immunity from early vaccination (July/August) if the influenza season does not peak until February or March.^8,12,13 Currently, the CDC recommends balancing the possible benefit of delayed vaccination against the risks of missed opportunities to vaccinate, a possible early season, and logistical problems related to vaccinating the same number of people in a smaller time interval. Offering vaccination by the end of October, if possible, is recommended in order for immunity to develop by mid-November.⁸ Note: Children ages 6 months to 8 years will need to receive their initial vaccination in 2 half-doses administered at least 28 days apart; completing their vaccination by the end of October would require starting the process weeks earlier.

[polldaddy:10124269]

Continue to: Strategy 2

Strategy 2: Make use of chemoprophylaxis

Preventive use of antiviral medication (chemoprophylaxis) may be a useful adjunct or alternative to vaccination in certain circumstances: if the patient is at high risk for complications, has been exposed to someone with influenza, has contraindications to vaccination, or received the vaccine within the past 2 weeks. The CDC also suggests that chemoprophylaxis be considered for those with immune deficiencies or who are otherwise immunosuppressed after exposure.¹⁴ Antivirals can also be used to control outbreaks in long-term care facilities; in these cases, the recommendedregimen is daily administration for at least 2 weeks, continuing until at least 7 days after the identification of the last case.¹⁴ Oseltamivir (Tamiflu) and zanamivir (Relenza) are the recommended prophylactic agents; a related intravenous medication, peramivir (Rapivab), is recommend for treatment only (see Table 3¹⁴).

Strategy 3: Prevent comorbidities and opportunistic infections

Morbidity associated with influenza often comes from secondary infection. Pneumonia is among the most common complications, so influenza season is a good time to ensure that patients are appropriately vaccinated against pneumococcus, as well. Pneumococcal conjugate vaccine (Prevnar or PCV13) is recommended for children younger than 2 years of age, to be administered in a series of 4 doses: at 2, 4, 6, and 12-15 months. Vaccination with PCV13 is also recommended for those ages 65 or older, to be followed at least one year later with pneumococcal polysaccharide vaccine (Pneumovax or PPSV23).¹⁵ Additional doses of PCV13, PPSV23, or both may be indicated, depending on health status.

Strategy 4: Encourage good hygiene

The availability of immunizations and anti­virals does not replace good hygiene. Frequent handwashing reduces the transmission of respiratory viruses, including influenza.¹⁶ Few studies have evaluated the use of alcohol-based hand sanitizers, but available evidence suggests they are effective in lowering viral transmission.¹⁶

Barriers, such as masks, gloves, and gowns, are helpful for health care workers.¹⁶ Surgical masks are often considered more comfortable to wear than N95 respirators. It may therefore be welcome news that when a 2009 randomized study assessed their use by hospital-based nurses, masks were non-inferior in protecting these health care workers against influenza.¹⁷

Presenteeism, the practice of going to work while sick, should be discouraged. People at risk for influenza may wish to avoid crowds during flu season; those with symptoms should be encouraged to stay home and limit contact with others.

Continue to: Treatment

Strategy 1: Make prompt use of antivirals

Despite available preventive measures, tens of millions of people in the United States develop influenza every year. Use of antiviral medication, begun early in the course of illness, can reduce the duration of symptoms and may reduce the risk for complications.

The neuraminidase inhibitor (NI) group of antivirals—oseltamivir, zanamivir, and peramivir—is effective against influenza types A and B and current resistance rates are low.

The adamantine family of antivirals, amantadine and rimantadine, treat type A only. Since the circulating influenza strains in the past several seasons have demonstrated resistance >99%, these medications are not currently recommended.¹⁴

NIs reduce the duration of influenza symptoms by 10% to 20%, shortening the illness by 6 to 24 hours.^18,19 In otherwise healthy patients, this benefit must be balanced against the increased risk for nausea and vomiting (oseltamivir), bronchospasm and sinusitis (zanamivir), and diarrhea (peramivir). In adults, NIs reduce the risk for lower respiratory tract complications and hospitalization. A 2015 meta-analysis by Dobson et al found a relative risk for hospitalization among those prescribed oseltamivir vs placebo of 37%.¹⁸

In the past, antivirals were used only in high-risk patients, such as children younger than 2 years, adults older than 65 years, and those with chronic health conditions.¹⁴ Now, antivirals are recommended for those who are at higher risk for complications (see Table 4), those with “severe, complicated, or progressive illness,” and hospitalized patients.¹⁴

Continue to: Antiviral treatment may have some value...

Antiviral treatment may have some value for hospitalized patients when started even 5 days after symptom onset. Treatment may be extended beyond the usual recommendations (5 days for oseltamivir or zanamivir) in immunosuppressed patients or the critically ill. Additionally, recent guidelines include consideration of antiviral treatment in outpatients who are at normal risk if treatment can be started within 48 hours of symptom onset.¹⁴

The CDC currently recommends use of oseltamivir rather than other antivirals for most hospitalized patients, based on the availability of data on its use in this setting.¹⁴ Intravenous peramivir is recommended for patients who cannot tolerate or absorb oral medication; inhaled zanamivir or IV peramivir are preferred for patients with end-stage renal disease who are not undergoing dialysis (see Table 3).¹⁴

Strategy 2: Exercise caution when it comes to supportive care

There are other medications that may offer symptom relief or prevent complications, especially when antivirals are contraindicated or unavailable.

Corticosteroids are recommended as part of the treatment of community-acquired pneumonia,²⁰ but their role in influenza is controversial. A 2016 Cochrane review²¹ found no randomized controlled trials on the topic. Although the balance of available data from observational studies indicated that use of corticosteroids was associated with increased mortality, the authors also noted that all the studies included in their meta-analysis were of “very low quality.” They concluded that “the use of steroids in influenza remains a clinical judgement call.”

Offering vaccination by the end of October, if possible, is recommended in order for immunity to develop by mid-November.

Statins may be associated with improved outcomes in influenza and pneumonia. Studies thus far have given contradictory results,^22,23 and a planned Cochrane review of the question has been withdrawn.²⁴

Continue to: Over-the-counter medications...

Over-the-counter medications, such as aspirin, acetaminophen, and ibuprofen are often used to manage the fever and myalgia associated with influenza. Patients should be cautioned against using the same ingredient in multiple different branded medications. Acetaminophen, for example, is not limited to Tylenol-branded products. To avoid Reye’s syndrome, children and teens with febrile illness, such as influenza, should not use aspirin.

CORRESPONDENCE
Jennifer L. Hamilton, MD, PhD, Drexel Family Medicine, 10 Shurs Lane, Suite 301, Philadelphia, PA 19127; [email protected].

Last year’s influenza season was severe enough that hospitals around the United States set up special evaluation areas beyond their emergency departments, at times spilling over to tents or other temporary structures in what otherwise would be parking lots. The scale and potential severity of the annual epidemic can be difficult to convey to our patients, who sometimes say “just the flu” to refer to an illness responsible for more than 170 pediatric deaths in the United States this past year.¹ The Centers for Disease Control and Prevention (CDC) recently updated its 5-year estimates of influenza-related deaths in the United States; influenza mortality ranges from about 12,000 deaths in a mild season (such as 2011-2012) to 56,000 in a more severe season (eg, 2012-2013).²

Although influenza cannot be completely prevented, the following strategies can help reduce the risk for the illness and limit its severity if contracted.

Prevention

Strategy 1: Vaccinate against influenza

While the efficacy of vaccines varies from year to year, vaccination remains the core of influenza prevention efforts. In this decade, vaccine effectiveness has ranged from 19% to 60%.³ However, models suggest that even when the vaccine is only 20% effective, vaccinating 140 million people (the average number of doses delivered annually in the United States over the past 5 seasons) prevents 21 million infections, 130,000 hospitalizations, and more than 61,000 deaths.⁴ In a case-control study, Flannery et al found that vaccination was 65% effective in preventing laboratory-confirmed influenza-associated death in children over 4 seasons (July 2010 through June 2014).⁵

Deciding who should be vaccinated is simpler than in prior years: Rather than targeting people who are at higher risk (those ages 65 and older, or those with comorbidities), the current CDC recommendation is to vaccinate nearly everyone ages 6 months or older, with limited exceptions.^6,7 (See Table 1⁸).

Formulations. Many types of influenza vaccine are approved for use in the United States; these differ in the number of strains included (3 or 4), the amount of antigen present for each strain, the presence of an adjuvant, the growth medium used for the virus, and the route of administration (see Table 2⁹). The relative merits of each type are a matter of some debate. There is ongoing research into the comparative efficacy of vaccines comprised of egg- vs cell-based cultures, as well as studies comparing high-dose or adjuvant vaccines to standard-dose inactivated vaccines.

Previously, the CDC has recommended preferential use (or avoidance) of some vaccine types, based on their efficacy. For the 2018-2019 flu season, however, the CDC has rescinded its recommendation against vaccine containing live attenuated virus (LAIV; FluMist brand) and expresses no preference for any vaccine formulation for patients of appropriate age and health status.¹⁰ The American Academy of Pediatrics (AAP), however, is recommends that LAIV be used only if patients and their families decline injectable vaccines.¹¹

Timing. Influenza vaccines are now distributed as early as July to some locations, raising concerns about waning immunity from early vaccination (July/August) if the influenza season does not peak until February or March.^8,12,13 Currently, the CDC recommends balancing the possible benefit of delayed vaccination against the risks of missed opportunities to vaccinate, a possible early season, and logistical problems related to vaccinating the same number of people in a smaller time interval. Offering vaccination by the end of October, if possible, is recommended in order for immunity to develop by mid-November.⁸ Note: Children ages 6 months to 8 years will need to receive their initial vaccination in 2 half-doses administered at least 28 days apart; completing their vaccination by the end of October would require starting the process weeks earlier.

[polldaddy:10124269]

Continue to: Strategy 2

Strategy 2: Make use of chemoprophylaxis

Preventive use of antiviral medication (chemoprophylaxis) may be a useful adjunct or alternative to vaccination in certain circumstances: if the patient is at high risk for complications, has been exposed to someone with influenza, has contraindications to vaccination, or received the vaccine within the past 2 weeks. The CDC also suggests that chemoprophylaxis be considered for those with immune deficiencies or who are otherwise immunosuppressed after exposure.¹⁴ Antivirals can also be used to control outbreaks in long-term care facilities; in these cases, the recommendedregimen is daily administration for at least 2 weeks, continuing until at least 7 days after the identification of the last case.¹⁴ Oseltamivir (Tamiflu) and zanamivir (Relenza) are the recommended prophylactic agents; a related intravenous medication, peramivir (Rapivab), is recommend for treatment only (see Table 3¹⁴).

Strategy 3: Prevent comorbidities and opportunistic infections

Morbidity associated with influenza often comes from secondary infection. Pneumonia is among the most common complications, so influenza season is a good time to ensure that patients are appropriately vaccinated against pneumococcus, as well. Pneumococcal conjugate vaccine (Prevnar or PCV13) is recommended for children younger than 2 years of age, to be administered in a series of 4 doses: at 2, 4, 6, and 12-15 months. Vaccination with PCV13 is also recommended for those ages 65 or older, to be followed at least one year later with pneumococcal polysaccharide vaccine (Pneumovax or PPSV23).¹⁵ Additional doses of PCV13, PPSV23, or both may be indicated, depending on health status.

Strategy 4: Encourage good hygiene

The availability of immunizations and anti­virals does not replace good hygiene. Frequent handwashing reduces the transmission of respiratory viruses, including influenza.¹⁶ Few studies have evaluated the use of alcohol-based hand sanitizers, but available evidence suggests they are effective in lowering viral transmission.¹⁶

Barriers, such as masks, gloves, and gowns, are helpful for health care workers.¹⁶ Surgical masks are often considered more comfortable to wear than N95 respirators. It may therefore be welcome news that when a 2009 randomized study assessed their use by hospital-based nurses, masks were non-inferior in protecting these health care workers against influenza.¹⁷

Presenteeism, the practice of going to work while sick, should be discouraged. People at risk for influenza may wish to avoid crowds during flu season; those with symptoms should be encouraged to stay home and limit contact with others.

Continue to: Treatment

Strategy 1: Make prompt use of antivirals

Despite available preventive measures, tens of millions of people in the United States develop influenza every year. Use of antiviral medication, begun early in the course of illness, can reduce the duration of symptoms and may reduce the risk for complications.

The neuraminidase inhibitor (NI) group of antivirals—oseltamivir, zanamivir, and peramivir—is effective against influenza types A and B and current resistance rates are low.

The adamantine family of antivirals, amantadine and rimantadine, treat type A only. Since the circulating influenza strains in the past several seasons have demonstrated resistance >99%, these medications are not currently recommended.¹⁴

NIs reduce the duration of influenza symptoms by 10% to 20%, shortening the illness by 6 to 24 hours.^18,19 In otherwise healthy patients, this benefit must be balanced against the increased risk for nausea and vomiting (oseltamivir), bronchospasm and sinusitis (zanamivir), and diarrhea (peramivir). In adults, NIs reduce the risk for lower respiratory tract complications and hospitalization. A 2015 meta-analysis by Dobson et al found a relative risk for hospitalization among those prescribed oseltamivir vs placebo of 37%.¹⁸

In the past, antivirals were used only in high-risk patients, such as children younger than 2 years, adults older than 65 years, and those with chronic health conditions.¹⁴ Now, antivirals are recommended for those who are at higher risk for complications (see Table 4), those with “severe, complicated, or progressive illness,” and hospitalized patients.¹⁴

Continue to: Antiviral treatment may have some value...

Antiviral treatment may have some value for hospitalized patients when started even 5 days after symptom onset. Treatment may be extended beyond the usual recommendations (5 days for oseltamivir or zanamivir) in immunosuppressed patients or the critically ill. Additionally, recent guidelines include consideration of antiviral treatment in outpatients who are at normal risk if treatment can be started within 48 hours of symptom onset.¹⁴

The CDC currently recommends use of oseltamivir rather than other antivirals for most hospitalized patients, based on the availability of data on its use in this setting.¹⁴ Intravenous peramivir is recommended for patients who cannot tolerate or absorb oral medication; inhaled zanamivir or IV peramivir are preferred for patients with end-stage renal disease who are not undergoing dialysis (see Table 3).¹⁴

Strategy 2: Exercise caution when it comes to supportive care

There are other medications that may offer symptom relief or prevent complications, especially when antivirals are contraindicated or unavailable.

Corticosteroids are recommended as part of the treatment of community-acquired pneumonia,²⁰ but their role in influenza is controversial. A 2016 Cochrane review²¹ found no randomized controlled trials on the topic. Although the balance of available data from observational studies indicated that use of corticosteroids was associated with increased mortality, the authors also noted that all the studies included in their meta-analysis were of “very low quality.” They concluded that “the use of steroids in influenza remains a clinical judgement call.”

Offering vaccination by the end of October, if possible, is recommended in order for immunity to develop by mid-November.

Statins may be associated with improved outcomes in influenza and pneumonia. Studies thus far have given contradictory results,^22,23 and a planned Cochrane review of the question has been withdrawn.²⁴

Continue to: Over-the-counter medications...

Over-the-counter medications, such as aspirin, acetaminophen, and ibuprofen are often used to manage the fever and myalgia associated with influenza. Patients should be cautioned against using the same ingredient in multiple different branded medications. Acetaminophen, for example, is not limited to Tylenol-branded products. To avoid Reye’s syndrome, children and teens with febrile illness, such as influenza, should not use aspirin.

CORRESPONDENCE
Jennifer L. Hamilton, MD, PhD, Drexel Family Medicine, 10 Shurs Lane, Suite 301, Philadelphia, PA 19127; [email protected].

Last year’s influenza season was severe enough that hospitals around the United States set up special evaluation areas beyond their emergency departments, at times spilling over to tents or other temporary structures in what otherwise would be parking lots. The scale and potential severity of the annual epidemic can be difficult to convey to our patients, who sometimes say “just the flu” to refer to an illness responsible for more than 170 pediatric deaths in the United States this past year.¹ The Centers for Disease Control and Prevention (CDC) recently updated its 5-year estimates of influenza-related deaths in the United States; influenza mortality ranges from about 12,000 deaths in a mild season (such as 2011-2012) to 56,000 in a more severe season (eg, 2012-2013).²

Although influenza cannot be completely prevented, the following strategies can help reduce the risk for the illness and limit its severity if contracted.

Prevention

Strategy 1: Vaccinate against influenza

While the efficacy of vaccines varies from year to year, vaccination remains the core of influenza prevention efforts. In this decade, vaccine effectiveness has ranged from 19% to 60%.³ However, models suggest that even when the vaccine is only 20% effective, vaccinating 140 million people (the average number of doses delivered annually in the United States over the past 5 seasons) prevents 21 million infections, 130,000 hospitalizations, and more than 61,000 deaths.⁴ In a case-control study, Flannery et al found that vaccination was 65% effective in preventing laboratory-confirmed influenza-associated death in children over 4 seasons (July 2010 through June 2014).⁵

Deciding who should be vaccinated is simpler than in prior years: Rather than targeting people who are at higher risk (those ages 65 and older, or those with comorbidities), the current CDC recommendation is to vaccinate nearly everyone ages 6 months or older, with limited exceptions.^6,7 (See Table 1⁸).

Formulations. Many types of influenza vaccine are approved for use in the United States; these differ in the number of strains included (3 or 4), the amount of antigen present for each strain, the presence of an adjuvant, the growth medium used for the virus, and the route of administration (see Table 2⁹). The relative merits of each type are a matter of some debate. There is ongoing research into the comparative efficacy of vaccines comprised of egg- vs cell-based cultures, as well as studies comparing high-dose or adjuvant vaccines to standard-dose inactivated vaccines.

Previously, the CDC has recommended preferential use (or avoidance) of some vaccine types, based on their efficacy. For the 2018-2019 flu season, however, the CDC has rescinded its recommendation against vaccine containing live attenuated virus (LAIV; FluMist brand) and expresses no preference for any vaccine formulation for patients of appropriate age and health status.¹⁰ The American Academy of Pediatrics (AAP), however, is recommends that LAIV be used only if patients and their families decline injectable vaccines.¹¹

Timing. Influenza vaccines are now distributed as early as July to some locations, raising concerns about waning immunity from early vaccination (July/August) if the influenza season does not peak until February or March.^8,12,13 Currently, the CDC recommends balancing the possible benefit of delayed vaccination against the risks of missed opportunities to vaccinate, a possible early season, and logistical problems related to vaccinating the same number of people in a smaller time interval. Offering vaccination by the end of October, if possible, is recommended in order for immunity to develop by mid-November.⁸ Note: Children ages 6 months to 8 years will need to receive their initial vaccination in 2 half-doses administered at least 28 days apart; completing their vaccination by the end of October would require starting the process weeks earlier.

[polldaddy:10124269]

Continue to: Strategy 2

Strategy 2: Make use of chemoprophylaxis

Preventive use of antiviral medication (chemoprophylaxis) may be a useful adjunct or alternative to vaccination in certain circumstances: if the patient is at high risk for complications, has been exposed to someone with influenza, has contraindications to vaccination, or received the vaccine within the past 2 weeks. The CDC also suggests that chemoprophylaxis be considered for those with immune deficiencies or who are otherwise immunosuppressed after exposure.¹⁴ Antivirals can also be used to control outbreaks in long-term care facilities; in these cases, the recommendedregimen is daily administration for at least 2 weeks, continuing until at least 7 days after the identification of the last case.¹⁴ Oseltamivir (Tamiflu) and zanamivir (Relenza) are the recommended prophylactic agents; a related intravenous medication, peramivir (Rapivab), is recommend for treatment only (see Table 3¹⁴).

Strategy 3: Prevent comorbidities and opportunistic infections

Morbidity associated with influenza often comes from secondary infection. Pneumonia is among the most common complications, so influenza season is a good time to ensure that patients are appropriately vaccinated against pneumococcus, as well. Pneumococcal conjugate vaccine (Prevnar or PCV13) is recommended for children younger than 2 years of age, to be administered in a series of 4 doses: at 2, 4, 6, and 12-15 months. Vaccination with PCV13 is also recommended for those ages 65 or older, to be followed at least one year later with pneumococcal polysaccharide vaccine (Pneumovax or PPSV23).¹⁵ Additional doses of PCV13, PPSV23, or both may be indicated, depending on health status.

Strategy 4: Encourage good hygiene

The availability of immunizations and anti­virals does not replace good hygiene. Frequent handwashing reduces the transmission of respiratory viruses, including influenza.¹⁶ Few studies have evaluated the use of alcohol-based hand sanitizers, but available evidence suggests they are effective in lowering viral transmission.¹⁶

Barriers, such as masks, gloves, and gowns, are helpful for health care workers.¹⁶ Surgical masks are often considered more comfortable to wear than N95 respirators. It may therefore be welcome news that when a 2009 randomized study assessed their use by hospital-based nurses, masks were non-inferior in protecting these health care workers against influenza.¹⁷

Presenteeism, the practice of going to work while sick, should be discouraged. People at risk for influenza may wish to avoid crowds during flu season; those with symptoms should be encouraged to stay home and limit contact with others.

Continue to: Treatment

Strategy 1: Make prompt use of antivirals

Despite available preventive measures, tens of millions of people in the United States develop influenza every year. Use of antiviral medication, begun early in the course of illness, can reduce the duration of symptoms and may reduce the risk for complications.

The neuraminidase inhibitor (NI) group of antivirals—oseltamivir, zanamivir, and peramivir—is effective against influenza types A and B and current resistance rates are low.

The adamantine family of antivirals, amantadine and rimantadine, treat type A only. Since the circulating influenza strains in the past several seasons have demonstrated resistance >99%, these medications are not currently recommended.¹⁴

NIs reduce the duration of influenza symptoms by 10% to 20%, shortening the illness by 6 to 24 hours.^18,19 In otherwise healthy patients, this benefit must be balanced against the increased risk for nausea and vomiting (oseltamivir), bronchospasm and sinusitis (zanamivir), and diarrhea (peramivir). In adults, NIs reduce the risk for lower respiratory tract complications and hospitalization. A 2015 meta-analysis by Dobson et al found a relative risk for hospitalization among those prescribed oseltamivir vs placebo of 37%.¹⁸

In the past, antivirals were used only in high-risk patients, such as children younger than 2 years, adults older than 65 years, and those with chronic health conditions.¹⁴ Now, antivirals are recommended for those who are at higher risk for complications (see Table 4), those with “severe, complicated, or progressive illness,” and hospitalized patients.¹⁴

Continue to: Antiviral treatment may have some value...

Antiviral treatment may have some value for hospitalized patients when started even 5 days after symptom onset. Treatment may be extended beyond the usual recommendations (5 days for oseltamivir or zanamivir) in immunosuppressed patients or the critically ill. Additionally, recent guidelines include consideration of antiviral treatment in outpatients who are at normal risk if treatment can be started within 48 hours of symptom onset.¹⁴

The CDC currently recommends use of oseltamivir rather than other antivirals for most hospitalized patients, based on the availability of data on its use in this setting.¹⁴ Intravenous peramivir is recommended for patients who cannot tolerate or absorb oral medication; inhaled zanamivir or IV peramivir are preferred for patients with end-stage renal disease who are not undergoing dialysis (see Table 3).¹⁴

Strategy 2: Exercise caution when it comes to supportive care

There are other medications that may offer symptom relief or prevent complications, especially when antivirals are contraindicated or unavailable.

Corticosteroids are recommended as part of the treatment of community-acquired pneumonia,²⁰ but their role in influenza is controversial. A 2016 Cochrane review²¹ found no randomized controlled trials on the topic. Although the balance of available data from observational studies indicated that use of corticosteroids was associated with increased mortality, the authors also noted that all the studies included in their meta-analysis were of “very low quality.” They concluded that “the use of steroids in influenza remains a clinical judgement call.”

Offering vaccination by the end of October, if possible, is recommended in order for immunity to develop by mid-November.

Statins may be associated with improved outcomes in influenza and pneumonia. Studies thus far have given contradictory results,^22,23 and a planned Cochrane review of the question has been withdrawn.²⁴

Continue to: Over-the-counter medications...

Over-the-counter medications, such as aspirin, acetaminophen, and ibuprofen are often used to manage the fever and myalgia associated with influenza. Patients should be cautioned against using the same ingredient in multiple different branded medications. Acetaminophen, for example, is not limited to Tylenol-branded products. To avoid Reye’s syndrome, children and teens with febrile illness, such as influenza, should not use aspirin.

CORRESPONDENCE
Jennifer L. Hamilton, MD, PhD, Drexel Family Medicine, 10 Shurs Lane, Suite 301, Philadelphia, PA 19127; [email protected].