Case

A 29-year-old man presented to the ED several hours after ingesting what he described as a “hefty” bottle of hand sanitizer. The patient stated that he ingested such a considerable quantity of liquid hand sanitizer because he was unable to obtain beer or liquor. He further admitted to drinking two 40-ounce beers daily for the past several years, noting that he last consumed drinking alcohol the preceding day.

The patient denied any other coingestants. He also denied nausea, vomiting, abdominal pain, or other somatic complaints. The patient’s medical history was significant for hypertension and hepatitis C, and his social history was significant for daily alcohol consumption, tobacco abuse, and former benzodiazepine, marijuana, and intravenous heroin abuse. His psychiatric history was significant for borderline personality disorder, major depression, and bulimia. The patient’s home medications included a daily multivitamin, folate, thiamine, sertraline, mirtazapine, and prazosin.

Initial vital signs at presentation were: blood pressure, 124/77 mm Hg; heart rate, 86 beats/min; respiratory rate, 15 breaths/min; and temperature, 98.0°F. On physical examination, he was noted to have slurred speech and nystagmus. His pupils were equal and reactive, without scleral icterus. The abdomen was nontender and nondistended, with regular bowel sounds, and without ascites or varicosities visualized. The rest of the examination was unremarkable. The patient did express thoughts of suicidality, but denied any homicidal ideation.

Laboratory studies revealed a serum ethanol concentration of 446 mg/dL. The patient’s basic metabolic panel was unremarkable, and liver function test results showed mildly elevated enzymes. The coagulation panel was within normal limits.

Is alcohol-based hand sanitizer consumption an emerging public health concern?

Excessive alcohol consumption is a recognized public health problem in the United States and is associated with an average of 88,000 deaths per year.¹ In a select population of patients, an untoward effect has developed from another public health target—that of hand hygiene.

Alcohol-based liquid hand sanitizers have become ubiquitous as a weapon in the antimicrobial arsenal with recommendations for its use as an alternative to soap and water in certain clinical settings. Liquid hand sanitizers are ideal for hospital or community use as they are faster, more effective, and less irritating to the skin than traditional hand-washing techniques.²

The downside to the widespread availability of hand sanitizers is that they offer easy access to individuals in search of clandestine sources of alcohol. Prior case reports have discussed the practice of consuming alcohol-based hand sanitizers for the purpose of intoxication in institutionalized persons, such as prisoners or patients in psychiatric facilities who are restricted to conventional sources of alcohol.

Children and confused elderly patients are also at risk for unintentional ingestions.^3,4 An article reviewed exposures reported to the American Association of Poison Control Center’s National Poison Data System over a 5-year period from 2005 to 2009.³ Of the 68,712 reported cases in this cohort, 80.5% were in children younger than 6 years of age. The investigators also noted an increased incidence of exposure over this period with an average of 1,894 additional cases per year.³There were 17,154 children aged 12 years and younger reported in 2017 to poison centers with exposures to hand sanitizers. Young children may be enticed by the bright colorful packaging and similarity to food and candy smells.⁵

What are the clinical manifestations of alcohol-based hand sanitizer ingestion?

Significant hazards exist from ingesting liquid hand sanitizer, including the high alcohol content, which varies from 40% to 85%.² Because isopropanol is commonly one of the components (if not the sole component) of many hand-sanitizer preparations, isopropanol toxicity may occur when ingested. The effects of isopropanol are similar to those of ethanol, with clinical effects reported after ingestion of as little as 100 mL of 70% isopropanol solution.⁴

Hand sanitizer formulations vary by manufacturer and contain different concentrations of ethanol and/or isopropanol, as well as additional potential inactive ingredients such as acetone, 1-propanol, 2-propanol, benzyl alcohol, hydrogen peroxide, glycerin, water, and different perfumes.^3,4

Persons who consume hand sanitizers recreationally are often unaware of the large alcohol content by volume that they are consuming. Recreational ingestion of hand sanitizer is believed to be the cause of at least one case of lethal ethanol intoxication. An articlereported a case of a male patient who suffered respiratory arrest after consuming an ethanol-based hand sanitizer.⁶ This patient was noted to have a serum ethanol of 536 mg/dL after consuming an unknown quantity of a 354 mL container of a 62% ethanol by volume hand sanitizer.⁶

Institutionalized individuals seeking alcohol through this source have discovered novel ways to yield a stronger product. Through the use of table salt and a cotton sock, it is possible to extract a liquid from a gel hand sanitizer preparation, yielding an alcohol context 30% higher by volume than the parent mixture.⁷

Alcohol intoxication poses a host of health effects. In nonhabituated individuals, a lethal load of alcohol can be achieved by consuming a volume of as little as 400 mL of an 80% alcohol-based solution.⁴ Symptoms from ingestion of an alcohol-based liquid hand sanitizer typically appear 1 to 2 hours after ingestion and mirror that of the alcohol toxidrome. Most commonly, this includes nausea, vomiting, epigastric pain, and varying degrees of central nervous system (CNS) depression.⁴ The life-threatening clinical manifestation of alcohol intoxication includes severe CNS and respiratory depression resulting in respiratory arrest, hypothermia, cardiac dysrhythmias with possible cardiac arrest, hypoglycemia, ketoacidosis, and hypotension.³

How is alcohol-based hand sanitizer ingestion managed?

The management of patients with alcohol-based hand sanitizer ingestion is the same as the management of alcohol ingestion from more socially acceptable sources and is mainly supportive.^3,4 These measures are directed at managing the patient’s airway with intubation and mechanical ventilation when appropriate, as well as supportive measures to address any underlying metabolic derangement or hypotension.² While hemodialysis has been used in some patients who had severe organ dysfunction and did not respond to supportive measures, it is usually not necessary.^1,3

Case Conclusion

The patient in this case was subsequently admitted to an intermediate level of care. He did not require intubation or further hemodynamic support during his initial acute intoxication. Later in the patient’s hospital course, he was noted to be in alcohol withdrawal, and proper management was initiated. He also required therapeutic one-to-one supervision after members of the nursing staff observed the patient consuming the hand sanitizer gel present in patient-care areas. He was later seen by psychiatry services. The psychiatrist recommended transfer to an inpatient psychiatric facility upon medical clearance for treatment of his psychiatric illness as well as alcohol dependence.

Case

A 29-year-old man presented to the ED several hours after ingesting what he described as a “hefty” bottle of hand sanitizer. The patient stated that he ingested such a considerable quantity of liquid hand sanitizer because he was unable to obtain beer or liquor. He further admitted to drinking two 40-ounce beers daily for the past several years, noting that he last consumed drinking alcohol the preceding day.

The patient denied any other coingestants. He also denied nausea, vomiting, abdominal pain, or other somatic complaints. The patient’s medical history was significant for hypertension and hepatitis C, and his social history was significant for daily alcohol consumption, tobacco abuse, and former benzodiazepine, marijuana, and intravenous heroin abuse. His psychiatric history was significant for borderline personality disorder, major depression, and bulimia. The patient’s home medications included a daily multivitamin, folate, thiamine, sertraline, mirtazapine, and prazosin.

Initial vital signs at presentation were: blood pressure, 124/77 mm Hg; heart rate, 86 beats/min; respiratory rate, 15 breaths/min; and temperature, 98.0°F. On physical examination, he was noted to have slurred speech and nystagmus. His pupils were equal and reactive, without scleral icterus. The abdomen was nontender and nondistended, with regular bowel sounds, and without ascites or varicosities visualized. The rest of the examination was unremarkable. The patient did express thoughts of suicidality, but denied any homicidal ideation.

Laboratory studies revealed a serum ethanol concentration of 446 mg/dL. The patient’s basic metabolic panel was unremarkable, and liver function test results showed mildly elevated enzymes. The coagulation panel was within normal limits.

Is alcohol-based hand sanitizer consumption an emerging public health concern?

Excessive alcohol consumption is a recognized public health problem in the United States and is associated with an average of 88,000 deaths per year.¹ In a select population of patients, an untoward effect has developed from another public health target—that of hand hygiene.

Alcohol-based liquid hand sanitizers have become ubiquitous as a weapon in the antimicrobial arsenal with recommendations for its use as an alternative to soap and water in certain clinical settings. Liquid hand sanitizers are ideal for hospital or community use as they are faster, more effective, and less irritating to the skin than traditional hand-washing techniques.²

The downside to the widespread availability of hand sanitizers is that they offer easy access to individuals in search of clandestine sources of alcohol. Prior case reports have discussed the practice of consuming alcohol-based hand sanitizers for the purpose of intoxication in institutionalized persons, such as prisoners or patients in psychiatric facilities who are restricted to conventional sources of alcohol.

Children and confused elderly patients are also at risk for unintentional ingestions.^3,4 An article reviewed exposures reported to the American Association of Poison Control Center’s National Poison Data System over a 5-year period from 2005 to 2009.³ Of the 68,712 reported cases in this cohort, 80.5% were in children younger than 6 years of age. The investigators also noted an increased incidence of exposure over this period with an average of 1,894 additional cases per year.³There were 17,154 children aged 12 years and younger reported in 2017 to poison centers with exposures to hand sanitizers. Young children may be enticed by the bright colorful packaging and similarity to food and candy smells.⁵

What are the clinical manifestations of alcohol-based hand sanitizer ingestion?

Significant hazards exist from ingesting liquid hand sanitizer, including the high alcohol content, which varies from 40% to 85%.² Because isopropanol is commonly one of the components (if not the sole component) of many hand-sanitizer preparations, isopropanol toxicity may occur when ingested. The effects of isopropanol are similar to those of ethanol, with clinical effects reported after ingestion of as little as 100 mL of 70% isopropanol solution.⁴

Hand sanitizer formulations vary by manufacturer and contain different concentrations of ethanol and/or isopropanol, as well as additional potential inactive ingredients such as acetone, 1-propanol, 2-propanol, benzyl alcohol, hydrogen peroxide, glycerin, water, and different perfumes.^3,4

Persons who consume hand sanitizers recreationally are often unaware of the large alcohol content by volume that they are consuming. Recreational ingestion of hand sanitizer is believed to be the cause of at least one case of lethal ethanol intoxication. An articlereported a case of a male patient who suffered respiratory arrest after consuming an ethanol-based hand sanitizer.⁶ This patient was noted to have a serum ethanol of 536 mg/dL after consuming an unknown quantity of a 354 mL container of a 62% ethanol by volume hand sanitizer.⁶

Institutionalized individuals seeking alcohol through this source have discovered novel ways to yield a stronger product. Through the use of table salt and a cotton sock, it is possible to extract a liquid from a gel hand sanitizer preparation, yielding an alcohol context 30% higher by volume than the parent mixture.⁷

Alcohol intoxication poses a host of health effects. In nonhabituated individuals, a lethal load of alcohol can be achieved by consuming a volume of as little as 400 mL of an 80% alcohol-based solution.⁴ Symptoms from ingestion of an alcohol-based liquid hand sanitizer typically appear 1 to 2 hours after ingestion and mirror that of the alcohol toxidrome. Most commonly, this includes nausea, vomiting, epigastric pain, and varying degrees of central nervous system (CNS) depression.⁴ The life-threatening clinical manifestation of alcohol intoxication includes severe CNS and respiratory depression resulting in respiratory arrest, hypothermia, cardiac dysrhythmias with possible cardiac arrest, hypoglycemia, ketoacidosis, and hypotension.³

How is alcohol-based hand sanitizer ingestion managed?

The management of patients with alcohol-based hand sanitizer ingestion is the same as the management of alcohol ingestion from more socially acceptable sources and is mainly supportive.^3,4 These measures are directed at managing the patient’s airway with intubation and mechanical ventilation when appropriate, as well as supportive measures to address any underlying metabolic derangement or hypotension.² While hemodialysis has been used in some patients who had severe organ dysfunction and did not respond to supportive measures, it is usually not necessary.^1,3

Case Conclusion

The patient in this case was subsequently admitted to an intermediate level of care. He did not require intubation or further hemodynamic support during his initial acute intoxication. Later in the patient’s hospital course, he was noted to be in alcohol withdrawal, and proper management was initiated. He also required therapeutic one-to-one supervision after members of the nursing staff observed the patient consuming the hand sanitizer gel present in patient-care areas. He was later seen by psychiatry services. The psychiatrist recommended transfer to an inpatient psychiatric facility upon medical clearance for treatment of his psychiatric illness as well as alcohol dependence.

Case

A 29-year-old man presented to the ED several hours after ingesting what he described as a “hefty” bottle of hand sanitizer. The patient stated that he ingested such a considerable quantity of liquid hand sanitizer because he was unable to obtain beer or liquor. He further admitted to drinking two 40-ounce beers daily for the past several years, noting that he last consumed drinking alcohol the preceding day.

The patient denied any other coingestants. He also denied nausea, vomiting, abdominal pain, or other somatic complaints. The patient’s medical history was significant for hypertension and hepatitis C, and his social history was significant for daily alcohol consumption, tobacco abuse, and former benzodiazepine, marijuana, and intravenous heroin abuse. His psychiatric history was significant for borderline personality disorder, major depression, and bulimia. The patient’s home medications included a daily multivitamin, folate, thiamine, sertraline, mirtazapine, and prazosin.

Initial vital signs at presentation were: blood pressure, 124/77 mm Hg; heart rate, 86 beats/min; respiratory rate, 15 breaths/min; and temperature, 98.0°F. On physical examination, he was noted to have slurred speech and nystagmus. His pupils were equal and reactive, without scleral icterus. The abdomen was nontender and nondistended, with regular bowel sounds, and without ascites or varicosities visualized. The rest of the examination was unremarkable. The patient did express thoughts of suicidality, but denied any homicidal ideation.

Laboratory studies revealed a serum ethanol concentration of 446 mg/dL. The patient’s basic metabolic panel was unremarkable, and liver function test results showed mildly elevated enzymes. The coagulation panel was within normal limits.

Is alcohol-based hand sanitizer consumption an emerging public health concern?

Excessive alcohol consumption is a recognized public health problem in the United States and is associated with an average of 88,000 deaths per year.¹ In a select population of patients, an untoward effect has developed from another public health target—that of hand hygiene.

Alcohol-based liquid hand sanitizers have become ubiquitous as a weapon in the antimicrobial arsenal with recommendations for its use as an alternative to soap and water in certain clinical settings. Liquid hand sanitizers are ideal for hospital or community use as they are faster, more effective, and less irritating to the skin than traditional hand-washing techniques.²

The downside to the widespread availability of hand sanitizers is that they offer easy access to individuals in search of clandestine sources of alcohol. Prior case reports have discussed the practice of consuming alcohol-based hand sanitizers for the purpose of intoxication in institutionalized persons, such as prisoners or patients in psychiatric facilities who are restricted to conventional sources of alcohol.

Children and confused elderly patients are also at risk for unintentional ingestions.^3,4 An article reviewed exposures reported to the American Association of Poison Control Center’s National Poison Data System over a 5-year period from 2005 to 2009.³ Of the 68,712 reported cases in this cohort, 80.5% were in children younger than 6 years of age. The investigators also noted an increased incidence of exposure over this period with an average of 1,894 additional cases per year.³There were 17,154 children aged 12 years and younger reported in 2017 to poison centers with exposures to hand sanitizers. Young children may be enticed by the bright colorful packaging and similarity to food and candy smells.⁵

What are the clinical manifestations of alcohol-based hand sanitizer ingestion?

Significant hazards exist from ingesting liquid hand sanitizer, including the high alcohol content, which varies from 40% to 85%.² Because isopropanol is commonly one of the components (if not the sole component) of many hand-sanitizer preparations, isopropanol toxicity may occur when ingested. The effects of isopropanol are similar to those of ethanol, with clinical effects reported after ingestion of as little as 100 mL of 70% isopropanol solution.⁴

Hand sanitizer formulations vary by manufacturer and contain different concentrations of ethanol and/or isopropanol, as well as additional potential inactive ingredients such as acetone, 1-propanol, 2-propanol, benzyl alcohol, hydrogen peroxide, glycerin, water, and different perfumes.^3,4

Persons who consume hand sanitizers recreationally are often unaware of the large alcohol content by volume that they are consuming. Recreational ingestion of hand sanitizer is believed to be the cause of at least one case of lethal ethanol intoxication. An articlereported a case of a male patient who suffered respiratory arrest after consuming an ethanol-based hand sanitizer.⁶ This patient was noted to have a serum ethanol of 536 mg/dL after consuming an unknown quantity of a 354 mL container of a 62% ethanol by volume hand sanitizer.⁶

Institutionalized individuals seeking alcohol through this source have discovered novel ways to yield a stronger product. Through the use of table salt and a cotton sock, it is possible to extract a liquid from a gel hand sanitizer preparation, yielding an alcohol context 30% higher by volume than the parent mixture.⁷

Alcohol intoxication poses a host of health effects. In nonhabituated individuals, a lethal load of alcohol can be achieved by consuming a volume of as little as 400 mL of an 80% alcohol-based solution.⁴ Symptoms from ingestion of an alcohol-based liquid hand sanitizer typically appear 1 to 2 hours after ingestion and mirror that of the alcohol toxidrome. Most commonly, this includes nausea, vomiting, epigastric pain, and varying degrees of central nervous system (CNS) depression.⁴ The life-threatening clinical manifestation of alcohol intoxication includes severe CNS and respiratory depression resulting in respiratory arrest, hypothermia, cardiac dysrhythmias with possible cardiac arrest, hypoglycemia, ketoacidosis, and hypotension.³

How is alcohol-based hand sanitizer ingestion managed?

The management of patients with alcohol-based hand sanitizer ingestion is the same as the management of alcohol ingestion from more socially acceptable sources and is mainly supportive.^3,4 These measures are directed at managing the patient’s airway with intubation and mechanical ventilation when appropriate, as well as supportive measures to address any underlying metabolic derangement or hypotension.² While hemodialysis has been used in some patients who had severe organ dysfunction and did not respond to supportive measures, it is usually not necessary.^1,3

Case Conclusion

The patient in this case was subsequently admitted to an intermediate level of care. He did not require intubation or further hemodynamic support during his initial acute intoxication. Later in the patient’s hospital course, he was noted to be in alcohol withdrawal, and proper management was initiated. He also required therapeutic one-to-one supervision after members of the nursing staff observed the patient consuming the hand sanitizer gel present in patient-care areas. He was later seen by psychiatry services. The psychiatrist recommended transfer to an inpatient psychiatric facility upon medical clearance for treatment of his psychiatric illness as well as alcohol dependence.

Critically ill patients presenting to the ED represent the most time-sensitive patient encounter for the emergency physician (EP), as delays in restoring physiological homeostasis increase the risks of organ dysfunction and death. Management and treatment strategies in critically ill patients have evolved from the routine use of invasive catheters and radiography for cardiopulmonary evaluation to a variety of noninvasive devices and pathways. The widespread adoption of point-of-care ultrasound (POCUS) in EDs provides the opportunity to rapidly obtain invaluable information about the diagnosis and etiology to guide resuscitation in critically ill patients—particularly those in shock and acute dyspnea. 

Over the last two decades, EPs and critical care physicians have employed POCUS to assist in identifying emergent reversible causes of shock and cardiac arrest, including cardiac tamponade, massive pulmonary embolism (PE), and hemoperitoneum. Recent advances in hemodynamic and cardiopulmonary POCUS allow for a nuanced approach to hemodynamic evaluation.¹ In addition, the use of ultrasound “first” in the critical care setting may reduce the dependence on radiographic-based management, catheter-based protocols, and the need for invasive procedures. 

Bedside cardiopulmonary ultrasound to evaluate the hemodynamic status of hypotensive patients can help determine the etiology of shock, provide evidence of fluid-volume responsiveness, visualize hemodynamic abnormalities that would alter fluid resuscitation strategies, and assess patient response to an intervention. The use of ultrasound can also identify the etiology of acute respiratory failure—providing the opportunity to initiate the appropriate interventions prior to patient decompensation. Findings such as pneumothorax or pleural effusion may require immediate procedural intervention, while other findings may only require noninvasive positive pressure ventilation and diuresis. 

The tools to implement these concepts include basic POCUS education common to emergency medicine and critical care (American College of Emergency Physicians Guidelines and American College of Chest Physicians/Society of Critical Care Medicine guidelines); ultrasound machines with phased array, linear, and curvilinear probes; and ultrasonographic instrumentation such as M-Mode, color Doppler, and spectral Doppler. An understanding of common Doppler imaging techniques optimizes the examination, and the use of presets common to cardiac packages may further assist the provider with adoption. 

When evaluating critically ill patients, we recommend the following step-wise approach: 

• Identify a clinical question to be answered prior to doing the examination; 
• Determine the hemodynamic profile of the patient to guide therapeutic maneuvers; and 
• Monitor the response to any therapeutic maneuver and adjust accordingly. (In these complicated patients, repeat examinations are invaluable, as the hemodynamic profile can change rapidly.)

Emergency physicians are increasingly utilizing POCUS to rapidly evaluate the thoracic cavity in critically ill patients. This modality is an appealing alternative to formal chest radiography because of the ease of rapid image acquisition, lack of ionizing radiation, and the ability to repeat the examination in real-time. 

When critically ill patients present in respiratory distress, POCUS allows the EP to rapidly diagnose potential etiologies, such as pleural effusion, pneumothorax, or pulmonary edema, and employ emergent intervention, which can greatly alter the patient’s clinical course. Additionally, the rapid diagnosis of consolidation permits earlier appropriate management of sepsis and respiratory failure when the clinical setting is consistent with pneumonia. 

In many cases, ultrasound has been shown to be superior to traditional chest radiography to assess critically ill patients.^2-8 Although there are several protocols that utilize thoracic ultrasound in evaluating the critical patient, this review focuses solely on the components of thoracic ultrasound, rather than specific protocols.  

Pneumothorax 

Ultrasound imaging with a high-frequency probe is highly sensitive and specific in assessing for pneumothorax in a supine patient.⁹ In the normal lung, the visceral and parietal pleura are visualized as sliding with each breath. In this examination, the transducer is placed on the chest wall to visualize two ribs and the pleura between them (Figures 2a and 2b).

When lung sliding is present, the appearance in M-mode is that of the “seashore” or “sandy beach.” The hyperechoic white pleura is seen as moving with the respiratory cycle. Additionally, lung artifacts such as A-lines, horizontal reverberation artifacts; and B-lines (also referred to as “comet-tails”), vertical lines arising from distended subpleural alveoli, will be seen in a normal lung. If pneumothorax is present, no sliding or comet-tail artifacts will be present at the pleural surface. Although A-lines may also be absent in pneumothorax, studies have shown that the absence of lung sliding and the presence of A-lines are associated with increased specificity (94% vs 78% with absent lung sliding alone) for diagnosing occult pneumothorax.⁹

While the lack of pleural sliding is highly sensitive for pneumothorax, the clinician must place this finding within the clinical context of the patient. For example, an intubated patient may not have left-sided sliding in the case of a right main-stem intubation. Moreover, patients who have an underlying obstructive lung disease (eg, chronic obstructive pulmonary disease [COPD]) and/or emphysema may present a more challenging examination because pleural sliding is often absent, especially in the apical segments, and can mimic pneumothorax in these patients.¹⁰ 

In addition to pleural sliding, presence or absence of a lung pulse also assists in assessing patients for pneumothorax. The detection of a lung pulse on M-mode ultrasound indicates subtle cardiac pulsation at the periphery of the lung; this finding only appears in the nonventilated lung in the absence of a pneumothorax. The presence of lung pulse is therefore useful in distinguishing other causes of nonventilated lung from pneumothorax.¹¹

Pleural Fluid

The low-frequency curvilinear or phased array probes are used to assess for pleural fluid. In this study, the clinician fans the probe cephalad from Morison’s pouch on the patient’s right side, or from the splenorenal recess on the left side, to visualize the bright, hyperechoic diaphragm. If pleural fluid is present, there will be loss of the mirroring artifact, and the fluid will appear as an anechoic collection cephalad to the diaphragm. In addition, when fluid is present, the normal lung may be visualized moving within the effusion, evoking a quad or sinusoid sign with M-mode imaging.^12,13 In the setting of complicated parapneumonic effusion, the echogenicity may be mixed or difficult to detect.  

Visualization of the thoracic spine above the diaphragm may serve as a surrogate marker for the presence of fluid. Typically, the thoracic spine is not visualized on ultrasound due to the scatter caused by the air-filled lungs.

Ultrasound has been shown to be superior to routine chest radiograph for the identification of small pleural effusions.⁷ Given that both critically ill medical and injured patients can present with pleural fluid, the use of POCUS to rapidly determine the presence or absence of fluid is an adjunct in the evaluation of these patients. 

Interstitial Fluid

Evaluation of the thoracic cavity for interstitial fluid in the setting of acute pulmonary edema, acute respiratory distress syndrome (ARDS), or interstitial pneumonia is best accomplished using either the curvilinear low-frequency probe or the phased array probe. The visualization of vertically oriented B-lines in the upper lung fields is very sensitive for interstitial fluid or edema of the interlobular septa (Figures 2a and 2b).^13,15 In this study, B-lines originate at the pleural line, move with the pleura, and extend off the bottom of the monitor without obliteration (in contrast to A-lines). An isolated B-line may be physiological; however, the presence of several B-lines is consistent with an interstitial pathology. On imaging, the presence of three or more B-lines in a single rib space with a convex probe, or more than six B-lines when utilizing the curvilinear, is considered pathological and referred to as “lung rockets.” B-lines may be focal or diffuse, as seen respectively in cases of pneumonia or acute pulmonary edema.¹⁶ 

Pulmonary Assessment for Fluid Resuscitation

Fluid Resuscitation 

Lung ultrasound studies have been proposed as a means of determining adequate fluid resuscitation and preventing complications associated with excessive fluid. The appearance of diffuse B-lines of acute interstitial syndrome on lung ultrasound can uncover the first signs of extravascular lung water and prevent pulmonary alveolar edema and associated morbidity and mortality.¹⁷ The appearance of an A-line predominance throughout the lung does not predict fluid responsiveness, but rather potential fluid tolerance. 

A benefit of lung ultrasound is that it provides information more rapidly than many of the dynamic measures of fluid responsiveness and cardiac output variability. In addition, lung ultrasound studies are much more easily reproduced than repeating a velocity time integral (VTI) measurements.

Lichtenstein’s FALLS Protocol

Lichtenstein’s FALLS (Fluid Administration Limited by Lung Sonography) protocol provides an approach to performing lung ultrasound on patients presenting in shock.¹² In this approach, lung ultrasound studies are performed after echocardiography to evaluate the patient for causes of obstructive shock. The predominance of B-lines on lung ultrasound suggests cardiogenic shock and, by definition, fluid intolerance. The predominance of A-lines on ultrasound may be present in patients in hypovolemic or septic shock. 

In hypovolemic shock, continued fluid boluses will improve hemodynamics with preserved A-line predominance. In septic shock, B-lines will begin to appear, suggesting that other means of improving forward flow should be initiated.

Consolidation

Chest radiography is known to have variable test characteristics for the detection of pneumonia. Consolidation may not be detected in profoundly immunocompromised or dehydrated patients. Additionally, in critically ill patients, it is often challenging to obtain a posteroanterior and lateral chest X-ray, given the patient’s hemodynamic status and stability for transport, and a single portable anteroposterior film will often miss retrocardiac infiltrates. In both of these clinical settings, POCUS can provide a rapid diagnosis, expediting the care of these septic patients. 

In the presence of a dense consolidation, there may be hepatization of the lung parenchyma (Figure 4b). Additionally, hyperechoic air bronchograms are often visualized. Pneumonia is often associated with pleural effusion and localized B-lines. Using lung ultrasound, rapid bedside detection of these pulmonary findings in clinical presentations suggestive of pneumonia can accelerate appropriate antibiotic and respiratory supportive treatment.  

Left Ventricular Systolic Assessment 

Critically ill patients commonly present with a mixed shock picture, and it is rare for a patient to have solely cardiogenic shock, hemorrhagic shock, etc. Rather, a patient who presents in septic shock may have an underlying cardiomyopathy for which she or he is being treated with a beta-blocker. 

Cardiomyopathy associated with sepsis is common¹⁸ and, at least in the case of diastolic dysfunction, it is underdiagnosed and associated with a higher mortality rate.¹⁹ It is therefore essential that the EP evaluate left ventricular (LV) systolic function rapidly and reliably—particularly in critically ill patients whose disease process may be undifferentiated and whose hemodynamic status is unclear.^20-22 Bedside echocardiography by the EP is invaluable in identifying the LV contribution to the hemodynamic profile and tailoring resuscitation to optimize patient outcomes. 

Although gross visual assessment is the most widely used method by which EPs estimate LV systolic function, this strategy is subjective, operator-dependent, and requires at least two quality views to understand the heart’s three-dimensional movement. However, when faced with a rapid diagnostic dilemma, a global visual estimate of the overall contractility (hyperdynamic, normal, depressed, severely depressed) may be more useful than estimating the ejection fraction (EF), especially when the patient’s baseline EF is unknown. 

Regional wall-motion abnormalities can be evaluated by considering  and correlating the coronary artery distributions with the electrocardiographic findings and the clinical scenario (Figure 5).

Simpson’s Rule

Although no one parameter can quantitatively assess LV function, the EF is the one most commonly used. The Simpson’s Rule or the “method of disks” estimates EF by changes in calculated ventricular volumes. The endocardial border is outlined in end-diastole and end-systole (ES) in both the apical four- (AP4) and two-chamber views. The cardiac package on the ultrasound system can divide the selected area into a series of disks, calculate the volume of each disk, and then add these figures to estimate the ventricular volume (Figure 6a). Limitations of this study include potentially difficult visualization of the endocardial border, and the length of time to conduct this study. 

Fractional Shortening

M-mode ultrasound can be used in several ways to estimate LV EF. Fractional shortening (FS) estimates the size reduction of the LV during systole. In the parasternal long axis (PLAX) view, the M-mode cursor is placed over the walls of the LV, just apical to the tips of the mitral valve (MV) leaflets (Figure 6b). Maximal (end-diastolic diameter [EDD]) and minimal (end-systolic diameter [ESD]) dimensions of the LV are measured and FS is calculated as (LVEDD – LVESD)/ LVEDD. A normal value is more than 25%, and a rough estimate of EF is FS x 2.²⁴ Limitations to this study include nonplacement of the M-mode cursor perpendicular to the LV walls, and inaccuracy in patients with regional wall abnormalities. 

E-Point Septal Separation

Another way to assess EF with POCUS is through E-point septal separation (EPSS), which uses the movement of the MV during diastole to estimate the EF during systole. In the PLAX view, the M-mode cursor is placed over the apical tip of the anterior leaflet of the MV to visualize the movement of the leaflet in relation to the interventricular septum (Figure 6c). Two characteristic waves are created during each diastole—the larger first wave representing early filling (the E-wave) and the smaller second wave representing the atrial kick (the A-wave). The E-point is the tallest point of the E-wave, and the EPSS is measured as the distance in millimeters between the E-point and the interventricular septum.²¹ 

The opening of the anterior leaflet of the MV toward the interventricular septum in diastole requires a pressure difference between the left atrium (LA) and LV. In a patient with poor LV systolic function, the LV is still full at the end of systole, the pressure difference is not as great, and the mitral leaflets will not snap open vigorously. The EPSS should be at or less than 6 mm in patients with normal LV systolic function. An EPSS of 6 to 12 mm suggests moderately depressed LV systolic function, and over 12 mm signifies severely decreased LV systolic function.²⁵ Limitations include inaccuracy in patients with valvular abnormalities, such as mitral stenosis or aortic regurgitation, severe LV or septal hypertrophy, regional wall abnormalities or severe LV dilation, limited data, and a wide margin of error when comparing to magnetic resonance imaging measurement of EF.

Cardiac Output 

Left Ventricular Diastolic Assessment

In an aging population of patients who have longstanding, undiagnosed, or untreated hypertension, LV hypertrophy leads to impaired relaxation and diastolic filling, eventually causing elevated LA pressure and, in extreme cases, restrictive cardiomyopathy. It has been reported that approximately half of all symptomatic patients with heart failure have a preserved EF.²⁷ 

Determination of LV pressures allows for the distinction between hydrostatic pulmonary edema and ARDS. Diagnosing elevated LA pressure is not inconsequential, as diastolic dysfunction in septic patients has been associated with increased mortality, likely due to increased pulmonary edema from fluid resuscitation.¹⁹ An invasive method of using a pulmonary artery catheter and measuring the pulmonary artery occlusion pressure to estimate the LA pressure is the gold standard, but is no longer routinely performed. 

Echocardiography is a noninvasive surrogate to estimating LA and LV filling pressures. Two different echocardiographic measurements can be used in conjunction to estimate LV filling pressures: MV inflow velocity and tissue Doppler imaging. 

Mitral Valve Inflow Velocity

Assessment of the MV inflow is performed by placing the pulse-wave Doppler gate between the tips of the MV leaflets in the AP4 view. Early diastolic filling produces the E-wave, and LA contraction produces the late diastolic A-wave (Figure 8a).

Tissue Doppler Imaging

Tissue Doppler imaging enables the clinician to measure myocardial velocities such as the speed of relaxation to evaluate if LV relaxation is due to a drop in LV pressure below LA pressure after systole, pulling the MV open; or if increased LA pressure is required to push open the MV and fill the LV. 

For this study, the tissue Doppler sampling gate is placed at the septal or lateral annulus of the MV in the AP4 view to visualize early diastolic mitral annulus velocity (e’) (Figure 8b). The E/e’ ratio can be helpful for estimating LV filling pressures. An E/e’ of less than 8 is associated with normal LV filling pressure whereas an E/e’ >15 is associated with an elevated LV filling pressure.28,29 When the E/e’ is 8 to 10, other indices such as the E/A ratio and deceleration time, as well as the clinical picture, can provide insight into the presence of hemodynamically significant diastolic dysfunction.

Learning and applying the assessment of diastolic parameters can be challenging; however, these parameters can be used to help predict LV filling pressures in patients with findings of pulmonary edema on chest radiograph. Limitations of these techniques are inter-rater variability, as well as the ability of the operator to acquire the required AP4 view. In addition, these techniques are unreliable in patients with irregular cardiac rhythms, severe mitral disease, and in hypertrophic cardiomyopathy. 

Right Ventricular Assessment

The right ventricle (RV) is a small, thin-walled ventricle with only two layers of muscle, as opposed to the three layers of the LV. In contrast to the rocking motion of LV contraction, the orientation of the two muscle layers of the RV permits mostly longitudinal contraction. The circumferential muscle fibers are shared at the base and apex with the LV, which can provide some of the contractile strength of the RV.³⁰ Because of this orientation, RV strain, which can manifest as decreased longitudinal contraction, speed of contraction, septal movement, and tethering abnormalities through ventricular interdependence, can be measured easily using bedside echocardiography. 

In healthy individuals, the RV is a low-pressure chamber that acts as a conduit for propelling venous return into the pulmonary circulation without much effect on systemic hemodynamics. However, in critical illness, RV abnormalities can have profound effects on hemodynamics, and  the efforts typically used to improve LV performance will worsen a failing RV. 

While RV dysfunction is most commonly due to chronic LV disease, acute RV dysfunction is commonly encountered in critical illness,³¹ including many septic patients with ARDS,^32,33 PE, or decompensated chronic pulmonary hypertension.³⁴ The examinations that follow, allow the EP to assess for the presence of RV dysfunction and to guide resuscitation appropriately to avoid the untoward hemodynamic effects of conventional resuscitation strategies in these patients. 

When evaluating the RV, the clinician must determine (1) if the patient’s RV strain is due to pressure or volume overload; and (2) if the patient’s RV is responsive or nonresponsive to a preload challenge, prompting an alteration in the resuscitation plan in nonresponsive cases. 

Right Ventricular Pressure/Volume Overload

While inferior vena cava (IVC) ultrasound has been shown to be a pre-heart/lung assessment of cardiopulmonary interactions that predicts volume responsiveness, the IVC is also a good predictor of right atrial (RA) pressure.³⁵ If the IVC is dilated and lacks respiratory variation, the patient likely has an elevated RA pressure, which is most likely transmitted from an elevated RV pressure (Figure 9a). However, compliance of the RA, RA pressure and, by extension, IVC prediction of that RA pressure, may underestimate the degree of RV pressure or afterload. 

Right Ventricular Strain and Contractile Reserve 

From the same apical view, tissue Doppler at the lateral tricuspid annulus will give a tricuspid annular peak velocity, a measure of the isovolumetric contraction velocity. This measurement will provide a measure of the contractile reserve of the RV (Figure 10b). A measure of less than 10 cm/sec indicates that further volume and inotropic challenges to the RV will not be effective, and the focus should be to decrease RV afterload with pulmonary vasodilators.^34,39,40 

Fluid Resuscitation Assessment 

Restoring circulating volume to increase cardiac output and improve oxygen delivery is the primary objective when managing patients in shock. Patient outcomes improve dramatically with early aggressive fluid resuscitation.^41-44 However, many critically ill patients do not respond to fluid resuscitation, which is generally defined as the rise of cardiac output of more than 15% in response to volume expansion. Not all patients found to be fluid responsive will require volume expansion.^45,46 

Excessive fluid resuscitation has been shown to increase intensive care unit length of stay, morbidity, and mortality.^47,48 Further, pathophysiological processes such as RV dysfunction and severe diastolic dysfunction can significantly alter the hemodynamic profile such that fluid management can be quite challenging in critically ill patients.

Distinguishing responders from nonresponders prior to fluid administration is the goal of early resuscitation. Unfortunately, this distinction cannot be made based on the patient’s vital signs or the physical examination.⁴⁹ Static filling pressures and volumetric measures are unreliable markers of fluid responsiveness.^50,51 The practice of administering a fluid challenge and observing the clinical effect on cardiac output is undesirable because it requires, by definition, on administering fluids, which ultimately may be harmful to the patient. 

Dynamic measures of fluid responsiveness that reliably predict cardiac response to a preload challenge are proven to be of greater utility.^52,53 These assessments determine volume responsiveness by evaluating the change in LV output with intrathoracic pressure changes due to the respiratory cycle, (ie, cardiopulmonary interaction). Ultrasound studies to assess cardiopulmonary interactions include IVC variability, arterial flow variability, brachial artery peak velocity variability, and common carotid artery (CCA) flow. In addition to echocardiography, lung ultrasound may be used to determine the endpoint of fluid resuscitation by monitoring for the appearance of extravascular lung water. 

Inferior Vena Cava Variability 

The IVC is a large extrathoracic vein which is easily insonated and accessible, even to a clinician with basic bedside ultrasound competency. Static IVC measures, such as diameter alone, correlate with central venous pressure but do not predict fluid responsiveness.^54-56 Dynamic IVC evaluation provides an upstream assessment of cardiopulmonary interactions. 

In the spontaneously breathing patient, the IVC collapses with inspiration as the RA pressure falls below atmospheric pressure, collapsing the intrathoracic veins for a short period until the intravascular pressure at the entry to the thorax exceeds atmospheric pressure, causing a bolus of venous return to the right heart. The overall effect is an increase in venous return⁵⁹. Conversely, in the mechanically ventilated patient, the IVC will distend with insufflation as increased intrathoracic pressure results in increased RV afterload and a transient increase in pulmonary artery pressure with an overall net decrease in venous return.⁶⁰

This IVC variability, termed the caval index, quantifies the degree of change in size of the IVC between end-inspiration and end-expiration. An M-mode imaging evaluation of the IVC allows for measurement of the maximal and minimal diameters for this calculation (Figure 11). Passively mechanically ventilated patients, with tidal volumes (TV) of 8 to 10 cc/kg in sinus rhythm, are predictably volume-responsive when the IVC distends by 12% to 18%.^54,61,62 However, there is considerable debate as to whether evaluating the degree of IVC collapse is of value in spontaneously breathing patients.⁶³ Cardiopulmonary interactions that drive IVC variability are affected by variable TV, intrathoracic pressure changes, etc. Nonetheless, two studies have shown that IVC collapse reliably predicts fluid responsiveness in spontaneously breathing patients.^64,65 

Stroke Volume/Arterial Flow Variability

Intrathoracic pressure changes induce dynamic changes in venous return that ultimately result in alterations in LV stroke volume (LVSV) when the blood volume traverses pulmonary circulation.⁶⁶ This variability in LVSV is the basis for all dynamic assessments of cardiopulmonary interactions, whether by arterial pressure waveform analysis or echocardiographic assessment of arterial flow. 

The LVSV variability reliably predicts fluid responsiveness and may be assessed by esophageal Doppler echocardiography of the ascending aorta.^67,68 Transesophageal echocardiography has also been used to assess SV variability at the LVOT.⁶⁹ Both of these measures require equipment and skill that may not be available in every clinical setting. Fortunately, LVOT SV is easily obtained through transthoracic echocardiography (TTE) (Figures 7a and 7b) using LVOT Doppler velocities as a surrogate for SV variations. A small study of TTE in mechanically ventilated children found that aortic flow variability predicted fluid responsiveness.⁷⁰ Therefore, transthoracic echocardiography provides a well-established alternative to thermodilution in determining cardiac output. Multiplication of the HR by an estimate of the column of blood flowing through the LVOT with each systolic contraction gives the cardiac output.⁷¹ 

Using TTE measurement of SV and cardiac output, the clinician can assess the effect of small fluid challenges on cardiac output.⁷² Cardiac output can be augmented with the passive leg raise (PLR), which is an entirely reversible preload challenge maneuver thought to increase preload by 300 to 500 mL. To assess volume responsiveness using this technique, LVOT cardiac output must first be determined. With the transducer in place, the patient’s legs are lifted to a 45° angle. After a minute of equilibration, the LVOT VTI is repeated and cardiac output recalculated. An increase in VTI of more than 12.5% predicts an increase in cardiac output with volume expansion.^73,74 This procedure requires proficiency with pulsed-wave Doppler and the ability to obtain the apical five-chamber view while a patient’s legs are being manipulated. In addition, the angle of insonation and location of measurement of LVOT and VTI must not vary for this measure to be valid. 

Alternatively, respiratory variation in LVOT peak velocities has been shown to reliably predict volume responsiveness when variability is more than 12% (Figure 7c).⁶⁹ This measurement is easier to obtain in that it does not require multiple views or complex calculations, and can be easily augmented with a passive leg raise maneuver. 

In the search for easily accessible alternatives to cardiac and aortic flow, brachial artery peak velocity variation (BAPVV) was found to be useful for predicting volume responsiveness.⁷⁵ To perform this study, the brachial artery is imaged in the long axis view using a linear transducer. Doppler gating should be adjusted to ensure an angle of less than 60°. The patient’s BAPVV is calculated as the difference between maximum and minimum peak velocity divided by the mean peak velocity. A variability in peak velocity of more than 10% predicts volume responsiveness.⁷⁵ 

Common Carotid Artery Flow

Similarly, CCA flow has attracted attention as a potential surrogate to assess SV response to preload challenge.^76,77 The CCA is large, easily accessible and does not require specialized training to assess (Figure 12).⁷⁸

Even though cardiopulmonary interaction assessment has excellent performance for predicting volume responsiveness, limitations do exist. For example, cardiopulmonary interactions may be exaggerated or diminished—thus decreasing the reliability of this assessment—in patients on mechanical ventilation who have spontaneous breathing, high positive end-expiratory pressures or a high minute ventilation, low TV, dysrhythmias, external compression of extra- or intrathoracic vessels (eg, intra-abdominal hypertension, pericardial tamponade, COPD/asthma exacerbations); and in patients who have decreased arterial elastance, or high RV afterload causing RV dysfunction or failure.

Conclusion

The advanced ultrasound techniques described in this review provide several useful tools to rapidly evaluate and manage cardiopulmonary interactions and assess the hemodynamic profile of critically ill patients. With these bedside techniques added to basic POCUS examinations, a new era in noninvasive critical care management is now available. 

As we enter the days of precision medicine, these examinations will enable EPs to optimize the care of this high-risk patient population. Moreover, future research by the emergency ultrasound and critical care communities on morbidity and mortality associated with resuscitation strategies in the ED will undoubtedly incorporate cardiopulmonary and hemodynamic ultrasound. 

Critically ill patients presenting to the ED represent the most time-sensitive patient encounter for the emergency physician (EP), as delays in restoring physiological homeostasis increase the risks of organ dysfunction and death. Management and treatment strategies in critically ill patients have evolved from the routine use of invasive catheters and radiography for cardiopulmonary evaluation to a variety of noninvasive devices and pathways. The widespread adoption of point-of-care ultrasound (POCUS) in EDs provides the opportunity to rapidly obtain invaluable information about the diagnosis and etiology to guide resuscitation in critically ill patients—particularly those in shock and acute dyspnea. 

Over the last two decades, EPs and critical care physicians have employed POCUS to assist in identifying emergent reversible causes of shock and cardiac arrest, including cardiac tamponade, massive pulmonary embolism (PE), and hemoperitoneum. Recent advances in hemodynamic and cardiopulmonary POCUS allow for a nuanced approach to hemodynamic evaluation.¹ In addition, the use of ultrasound “first” in the critical care setting may reduce the dependence on radiographic-based management, catheter-based protocols, and the need for invasive procedures. 

Bedside cardiopulmonary ultrasound to evaluate the hemodynamic status of hypotensive patients can help determine the etiology of shock, provide evidence of fluid-volume responsiveness, visualize hemodynamic abnormalities that would alter fluid resuscitation strategies, and assess patient response to an intervention. The use of ultrasound can also identify the etiology of acute respiratory failure—providing the opportunity to initiate the appropriate interventions prior to patient decompensation. Findings such as pneumothorax or pleural effusion may require immediate procedural intervention, while other findings may only require noninvasive positive pressure ventilation and diuresis. 

The tools to implement these concepts include basic POCUS education common to emergency medicine and critical care (American College of Emergency Physicians Guidelines and American College of Chest Physicians/Society of Critical Care Medicine guidelines); ultrasound machines with phased array, linear, and curvilinear probes; and ultrasonographic instrumentation such as M-Mode, color Doppler, and spectral Doppler. An understanding of common Doppler imaging techniques optimizes the examination, and the use of presets common to cardiac packages may further assist the provider with adoption. 

When evaluating critically ill patients, we recommend the following step-wise approach: 

• Identify a clinical question to be answered prior to doing the examination; 
• Determine the hemodynamic profile of the patient to guide therapeutic maneuvers; and 
• Monitor the response to any therapeutic maneuver and adjust accordingly. (In these complicated patients, repeat examinations are invaluable, as the hemodynamic profile can change rapidly.)

Emergency physicians are increasingly utilizing POCUS to rapidly evaluate the thoracic cavity in critically ill patients. This modality is an appealing alternative to formal chest radiography because of the ease of rapid image acquisition, lack of ionizing radiation, and the ability to repeat the examination in real-time. 

When critically ill patients present in respiratory distress, POCUS allows the EP to rapidly diagnose potential etiologies, such as pleural effusion, pneumothorax, or pulmonary edema, and employ emergent intervention, which can greatly alter the patient’s clinical course. Additionally, the rapid diagnosis of consolidation permits earlier appropriate management of sepsis and respiratory failure when the clinical setting is consistent with pneumonia. 

In many cases, ultrasound has been shown to be superior to traditional chest radiography to assess critically ill patients.^2-8 Although there are several protocols that utilize thoracic ultrasound in evaluating the critical patient, this review focuses solely on the components of thoracic ultrasound, rather than specific protocols.  

Pneumothorax 

Ultrasound imaging with a high-frequency probe is highly sensitive and specific in assessing for pneumothorax in a supine patient.⁹ In the normal lung, the visceral and parietal pleura are visualized as sliding with each breath. In this examination, the transducer is placed on the chest wall to visualize two ribs and the pleura between them (Figures 2a and 2b).

When lung sliding is present, the appearance in M-mode is that of the “seashore” or “sandy beach.” The hyperechoic white pleura is seen as moving with the respiratory cycle. Additionally, lung artifacts such as A-lines, horizontal reverberation artifacts; and B-lines (also referred to as “comet-tails”), vertical lines arising from distended subpleural alveoli, will be seen in a normal lung. If pneumothorax is present, no sliding or comet-tail artifacts will be present at the pleural surface. Although A-lines may also be absent in pneumothorax, studies have shown that the absence of lung sliding and the presence of A-lines are associated with increased specificity (94% vs 78% with absent lung sliding alone) for diagnosing occult pneumothorax.⁹

While the lack of pleural sliding is highly sensitive for pneumothorax, the clinician must place this finding within the clinical context of the patient. For example, an intubated patient may not have left-sided sliding in the case of a right main-stem intubation. Moreover, patients who have an underlying obstructive lung disease (eg, chronic obstructive pulmonary disease [COPD]) and/or emphysema may present a more challenging examination because pleural sliding is often absent, especially in the apical segments, and can mimic pneumothorax in these patients.¹⁰ 

In addition to pleural sliding, presence or absence of a lung pulse also assists in assessing patients for pneumothorax. The detection of a lung pulse on M-mode ultrasound indicates subtle cardiac pulsation at the periphery of the lung; this finding only appears in the nonventilated lung in the absence of a pneumothorax. The presence of lung pulse is therefore useful in distinguishing other causes of nonventilated lung from pneumothorax.¹¹

Pleural Fluid

The low-frequency curvilinear or phased array probes are used to assess for pleural fluid. In this study, the clinician fans the probe cephalad from Morison’s pouch on the patient’s right side, or from the splenorenal recess on the left side, to visualize the bright, hyperechoic diaphragm. If pleural fluid is present, there will be loss of the mirroring artifact, and the fluid will appear as an anechoic collection cephalad to the diaphragm. In addition, when fluid is present, the normal lung may be visualized moving within the effusion, evoking a quad or sinusoid sign with M-mode imaging.^12,13 In the setting of complicated parapneumonic effusion, the echogenicity may be mixed or difficult to detect.  

Visualization of the thoracic spine above the diaphragm may serve as a surrogate marker for the presence of fluid. Typically, the thoracic spine is not visualized on ultrasound due to the scatter caused by the air-filled lungs.

Ultrasound has been shown to be superior to routine chest radiograph for the identification of small pleural effusions.⁷ Given that both critically ill medical and injured patients can present with pleural fluid, the use of POCUS to rapidly determine the presence or absence of fluid is an adjunct in the evaluation of these patients. 

Interstitial Fluid

Evaluation of the thoracic cavity for interstitial fluid in the setting of acute pulmonary edema, acute respiratory distress syndrome (ARDS), or interstitial pneumonia is best accomplished using either the curvilinear low-frequency probe or the phased array probe. The visualization of vertically oriented B-lines in the upper lung fields is very sensitive for interstitial fluid or edema of the interlobular septa (Figures 2a and 2b).^13,15 In this study, B-lines originate at the pleural line, move with the pleura, and extend off the bottom of the monitor without obliteration (in contrast to A-lines). An isolated B-line may be physiological; however, the presence of several B-lines is consistent with an interstitial pathology. On imaging, the presence of three or more B-lines in a single rib space with a convex probe, or more than six B-lines when utilizing the curvilinear, is considered pathological and referred to as “lung rockets.” B-lines may be focal or diffuse, as seen respectively in cases of pneumonia or acute pulmonary edema.¹⁶ 

Pulmonary Assessment for Fluid Resuscitation

Fluid Resuscitation 

Lung ultrasound studies have been proposed as a means of determining adequate fluid resuscitation and preventing complications associated with excessive fluid. The appearance of diffuse B-lines of acute interstitial syndrome on lung ultrasound can uncover the first signs of extravascular lung water and prevent pulmonary alveolar edema and associated morbidity and mortality.¹⁷ The appearance of an A-line predominance throughout the lung does not predict fluid responsiveness, but rather potential fluid tolerance. 

A benefit of lung ultrasound is that it provides information more rapidly than many of the dynamic measures of fluid responsiveness and cardiac output variability. In addition, lung ultrasound studies are much more easily reproduced than repeating a velocity time integral (VTI) measurements.

Lichtenstein’s FALLS Protocol

Lichtenstein’s FALLS (Fluid Administration Limited by Lung Sonography) protocol provides an approach to performing lung ultrasound on patients presenting in shock.¹² In this approach, lung ultrasound studies are performed after echocardiography to evaluate the patient for causes of obstructive shock. The predominance of B-lines on lung ultrasound suggests cardiogenic shock and, by definition, fluid intolerance. The predominance of A-lines on ultrasound may be present in patients in hypovolemic or septic shock. 

In hypovolemic shock, continued fluid boluses will improve hemodynamics with preserved A-line predominance. In septic shock, B-lines will begin to appear, suggesting that other means of improving forward flow should be initiated.

Consolidation

Chest radiography is known to have variable test characteristics for the detection of pneumonia. Consolidation may not be detected in profoundly immunocompromised or dehydrated patients. Additionally, in critically ill patients, it is often challenging to obtain a posteroanterior and lateral chest X-ray, given the patient’s hemodynamic status and stability for transport, and a single portable anteroposterior film will often miss retrocardiac infiltrates. In both of these clinical settings, POCUS can provide a rapid diagnosis, expediting the care of these septic patients. 

In the presence of a dense consolidation, there may be hepatization of the lung parenchyma (Figure 4b). Additionally, hyperechoic air bronchograms are often visualized. Pneumonia is often associated with pleural effusion and localized B-lines. Using lung ultrasound, rapid bedside detection of these pulmonary findings in clinical presentations suggestive of pneumonia can accelerate appropriate antibiotic and respiratory supportive treatment.  

Left Ventricular Systolic Assessment 

Critically ill patients commonly present with a mixed shock picture, and it is rare for a patient to have solely cardiogenic shock, hemorrhagic shock, etc. Rather, a patient who presents in septic shock may have an underlying cardiomyopathy for which she or he is being treated with a beta-blocker. 

Cardiomyopathy associated with sepsis is common¹⁸ and, at least in the case of diastolic dysfunction, it is underdiagnosed and associated with a higher mortality rate.¹⁹ It is therefore essential that the EP evaluate left ventricular (LV) systolic function rapidly and reliably—particularly in critically ill patients whose disease process may be undifferentiated and whose hemodynamic status is unclear.^20-22 Bedside echocardiography by the EP is invaluable in identifying the LV contribution to the hemodynamic profile and tailoring resuscitation to optimize patient outcomes. 

Although gross visual assessment is the most widely used method by which EPs estimate LV systolic function, this strategy is subjective, operator-dependent, and requires at least two quality views to understand the heart’s three-dimensional movement. However, when faced with a rapid diagnostic dilemma, a global visual estimate of the overall contractility (hyperdynamic, normal, depressed, severely depressed) may be more useful than estimating the ejection fraction (EF), especially when the patient’s baseline EF is unknown. 

Regional wall-motion abnormalities can be evaluated by considering  and correlating the coronary artery distributions with the electrocardiographic findings and the clinical scenario (Figure 5).

Simpson’s Rule

Although no one parameter can quantitatively assess LV function, the EF is the one most commonly used. The Simpson’s Rule or the “method of disks” estimates EF by changes in calculated ventricular volumes. The endocardial border is outlined in end-diastole and end-systole (ES) in both the apical four- (AP4) and two-chamber views. The cardiac package on the ultrasound system can divide the selected area into a series of disks, calculate the volume of each disk, and then add these figures to estimate the ventricular volume (Figure 6a). Limitations of this study include potentially difficult visualization of the endocardial border, and the length of time to conduct this study. 

Fractional Shortening

M-mode ultrasound can be used in several ways to estimate LV EF. Fractional shortening (FS) estimates the size reduction of the LV during systole. In the parasternal long axis (PLAX) view, the M-mode cursor is placed over the walls of the LV, just apical to the tips of the mitral valve (MV) leaflets (Figure 6b). Maximal (end-diastolic diameter [EDD]) and minimal (end-systolic diameter [ESD]) dimensions of the LV are measured and FS is calculated as (LVEDD – LVESD)/ LVEDD. A normal value is more than 25%, and a rough estimate of EF is FS x 2.²⁴ Limitations to this study include nonplacement of the M-mode cursor perpendicular to the LV walls, and inaccuracy in patients with regional wall abnormalities. 

E-Point Septal Separation

Another way to assess EF with POCUS is through E-point septal separation (EPSS), which uses the movement of the MV during diastole to estimate the EF during systole. In the PLAX view, the M-mode cursor is placed over the apical tip of the anterior leaflet of the MV to visualize the movement of the leaflet in relation to the interventricular septum (Figure 6c). Two characteristic waves are created during each diastole—the larger first wave representing early filling (the E-wave) and the smaller second wave representing the atrial kick (the A-wave). The E-point is the tallest point of the E-wave, and the EPSS is measured as the distance in millimeters between the E-point and the interventricular septum.²¹ 

The opening of the anterior leaflet of the MV toward the interventricular septum in diastole requires a pressure difference between the left atrium (LA) and LV. In a patient with poor LV systolic function, the LV is still full at the end of systole, the pressure difference is not as great, and the mitral leaflets will not snap open vigorously. The EPSS should be at or less than 6 mm in patients with normal LV systolic function. An EPSS of 6 to 12 mm suggests moderately depressed LV systolic function, and over 12 mm signifies severely decreased LV systolic function.²⁵ Limitations include inaccuracy in patients with valvular abnormalities, such as mitral stenosis or aortic regurgitation, severe LV or septal hypertrophy, regional wall abnormalities or severe LV dilation, limited data, and a wide margin of error when comparing to magnetic resonance imaging measurement of EF.

Cardiac Output 

Left Ventricular Diastolic Assessment

In an aging population of patients who have longstanding, undiagnosed, or untreated hypertension, LV hypertrophy leads to impaired relaxation and diastolic filling, eventually causing elevated LA pressure and, in extreme cases, restrictive cardiomyopathy. It has been reported that approximately half of all symptomatic patients with heart failure have a preserved EF.²⁷ 

Determination of LV pressures allows for the distinction between hydrostatic pulmonary edema and ARDS. Diagnosing elevated LA pressure is not inconsequential, as diastolic dysfunction in septic patients has been associated with increased mortality, likely due to increased pulmonary edema from fluid resuscitation.¹⁹ An invasive method of using a pulmonary artery catheter and measuring the pulmonary artery occlusion pressure to estimate the LA pressure is the gold standard, but is no longer routinely performed. 

Echocardiography is a noninvasive surrogate to estimating LA and LV filling pressures. Two different echocardiographic measurements can be used in conjunction to estimate LV filling pressures: MV inflow velocity and tissue Doppler imaging. 

Mitral Valve Inflow Velocity

Assessment of the MV inflow is performed by placing the pulse-wave Doppler gate between the tips of the MV leaflets in the AP4 view. Early diastolic filling produces the E-wave, and LA contraction produces the late diastolic A-wave (Figure 8a).

Tissue Doppler Imaging

Tissue Doppler imaging enables the clinician to measure myocardial velocities such as the speed of relaxation to evaluate if LV relaxation is due to a drop in LV pressure below LA pressure after systole, pulling the MV open; or if increased LA pressure is required to push open the MV and fill the LV. 

For this study, the tissue Doppler sampling gate is placed at the septal or lateral annulus of the MV in the AP4 view to visualize early diastolic mitral annulus velocity (e’) (Figure 8b). The E/e’ ratio can be helpful for estimating LV filling pressures. An E/e’ of less than 8 is associated with normal LV filling pressure whereas an E/e’ >15 is associated with an elevated LV filling pressure.28,29 When the E/e’ is 8 to 10, other indices such as the E/A ratio and deceleration time, as well as the clinical picture, can provide insight into the presence of hemodynamically significant diastolic dysfunction.

Learning and applying the assessment of diastolic parameters can be challenging; however, these parameters can be used to help predict LV filling pressures in patients with findings of pulmonary edema on chest radiograph. Limitations of these techniques are inter-rater variability, as well as the ability of the operator to acquire the required AP4 view. In addition, these techniques are unreliable in patients with irregular cardiac rhythms, severe mitral disease, and in hypertrophic cardiomyopathy. 

Right Ventricular Assessment

The right ventricle (RV) is a small, thin-walled ventricle with only two layers of muscle, as opposed to the three layers of the LV. In contrast to the rocking motion of LV contraction, the orientation of the two muscle layers of the RV permits mostly longitudinal contraction. The circumferential muscle fibers are shared at the base and apex with the LV, which can provide some of the contractile strength of the RV.³⁰ Because of this orientation, RV strain, which can manifest as decreased longitudinal contraction, speed of contraction, septal movement, and tethering abnormalities through ventricular interdependence, can be measured easily using bedside echocardiography. 

In healthy individuals, the RV is a low-pressure chamber that acts as a conduit for propelling venous return into the pulmonary circulation without much effect on systemic hemodynamics. However, in critical illness, RV abnormalities can have profound effects on hemodynamics, and  the efforts typically used to improve LV performance will worsen a failing RV. 

While RV dysfunction is most commonly due to chronic LV disease, acute RV dysfunction is commonly encountered in critical illness,³¹ including many septic patients with ARDS,^32,33 PE, or decompensated chronic pulmonary hypertension.³⁴ The examinations that follow, allow the EP to assess for the presence of RV dysfunction and to guide resuscitation appropriately to avoid the untoward hemodynamic effects of conventional resuscitation strategies in these patients. 

When evaluating the RV, the clinician must determine (1) if the patient’s RV strain is due to pressure or volume overload; and (2) if the patient’s RV is responsive or nonresponsive to a preload challenge, prompting an alteration in the resuscitation plan in nonresponsive cases. 

Right Ventricular Pressure/Volume Overload

While inferior vena cava (IVC) ultrasound has been shown to be a pre-heart/lung assessment of cardiopulmonary interactions that predicts volume responsiveness, the IVC is also a good predictor of right atrial (RA) pressure.³⁵ If the IVC is dilated and lacks respiratory variation, the patient likely has an elevated RA pressure, which is most likely transmitted from an elevated RV pressure (Figure 9a). However, compliance of the RA, RA pressure and, by extension, IVC prediction of that RA pressure, may underestimate the degree of RV pressure or afterload. 

Right Ventricular Strain and Contractile Reserve 

From the same apical view, tissue Doppler at the lateral tricuspid annulus will give a tricuspid annular peak velocity, a measure of the isovolumetric contraction velocity. This measurement will provide a measure of the contractile reserve of the RV (Figure 10b). A measure of less than 10 cm/sec indicates that further volume and inotropic challenges to the RV will not be effective, and the focus should be to decrease RV afterload with pulmonary vasodilators.^34,39,40 

Fluid Resuscitation Assessment 

Restoring circulating volume to increase cardiac output and improve oxygen delivery is the primary objective when managing patients in shock. Patient outcomes improve dramatically with early aggressive fluid resuscitation.^41-44 However, many critically ill patients do not respond to fluid resuscitation, which is generally defined as the rise of cardiac output of more than 15% in response to volume expansion. Not all patients found to be fluid responsive will require volume expansion.^45,46 

Excessive fluid resuscitation has been shown to increase intensive care unit length of stay, morbidity, and mortality.^47,48 Further, pathophysiological processes such as RV dysfunction and severe diastolic dysfunction can significantly alter the hemodynamic profile such that fluid management can be quite challenging in critically ill patients.

Distinguishing responders from nonresponders prior to fluid administration is the goal of early resuscitation. Unfortunately, this distinction cannot be made based on the patient’s vital signs or the physical examination.⁴⁹ Static filling pressures and volumetric measures are unreliable markers of fluid responsiveness.^50,51 The practice of administering a fluid challenge and observing the clinical effect on cardiac output is undesirable because it requires, by definition, on administering fluids, which ultimately may be harmful to the patient. 

Dynamic measures of fluid responsiveness that reliably predict cardiac response to a preload challenge are proven to be of greater utility.^52,53 These assessments determine volume responsiveness by evaluating the change in LV output with intrathoracic pressure changes due to the respiratory cycle, (ie, cardiopulmonary interaction). Ultrasound studies to assess cardiopulmonary interactions include IVC variability, arterial flow variability, brachial artery peak velocity variability, and common carotid artery (CCA) flow. In addition to echocardiography, lung ultrasound may be used to determine the endpoint of fluid resuscitation by monitoring for the appearance of extravascular lung water. 

Inferior Vena Cava Variability 

The IVC is a large extrathoracic vein which is easily insonated and accessible, even to a clinician with basic bedside ultrasound competency. Static IVC measures, such as diameter alone, correlate with central venous pressure but do not predict fluid responsiveness.^54-56 Dynamic IVC evaluation provides an upstream assessment of cardiopulmonary interactions. 

In the spontaneously breathing patient, the IVC collapses with inspiration as the RA pressure falls below atmospheric pressure, collapsing the intrathoracic veins for a short period until the intravascular pressure at the entry to the thorax exceeds atmospheric pressure, causing a bolus of venous return to the right heart. The overall effect is an increase in venous return⁵⁹. Conversely, in the mechanically ventilated patient, the IVC will distend with insufflation as increased intrathoracic pressure results in increased RV afterload and a transient increase in pulmonary artery pressure with an overall net decrease in venous return.⁶⁰

This IVC variability, termed the caval index, quantifies the degree of change in size of the IVC between end-inspiration and end-expiration. An M-mode imaging evaluation of the IVC allows for measurement of the maximal and minimal diameters for this calculation (Figure 11). Passively mechanically ventilated patients, with tidal volumes (TV) of 8 to 10 cc/kg in sinus rhythm, are predictably volume-responsive when the IVC distends by 12% to 18%.^54,61,62 However, there is considerable debate as to whether evaluating the degree of IVC collapse is of value in spontaneously breathing patients.⁶³ Cardiopulmonary interactions that drive IVC variability are affected by variable TV, intrathoracic pressure changes, etc. Nonetheless, two studies have shown that IVC collapse reliably predicts fluid responsiveness in spontaneously breathing patients.^64,65 

Stroke Volume/Arterial Flow Variability

Intrathoracic pressure changes induce dynamic changes in venous return that ultimately result in alterations in LV stroke volume (LVSV) when the blood volume traverses pulmonary circulation.⁶⁶ This variability in LVSV is the basis for all dynamic assessments of cardiopulmonary interactions, whether by arterial pressure waveform analysis or echocardiographic assessment of arterial flow. 

The LVSV variability reliably predicts fluid responsiveness and may be assessed by esophageal Doppler echocardiography of the ascending aorta.^67,68 Transesophageal echocardiography has also been used to assess SV variability at the LVOT.⁶⁹ Both of these measures require equipment and skill that may not be available in every clinical setting. Fortunately, LVOT SV is easily obtained through transthoracic echocardiography (TTE) (Figures 7a and 7b) using LVOT Doppler velocities as a surrogate for SV variations. A small study of TTE in mechanically ventilated children found that aortic flow variability predicted fluid responsiveness.⁷⁰ Therefore, transthoracic echocardiography provides a well-established alternative to thermodilution in determining cardiac output. Multiplication of the HR by an estimate of the column of blood flowing through the LVOT with each systolic contraction gives the cardiac output.⁷¹ 

Using TTE measurement of SV and cardiac output, the clinician can assess the effect of small fluid challenges on cardiac output.⁷² Cardiac output can be augmented with the passive leg raise (PLR), which is an entirely reversible preload challenge maneuver thought to increase preload by 300 to 500 mL. To assess volume responsiveness using this technique, LVOT cardiac output must first be determined. With the transducer in place, the patient’s legs are lifted to a 45° angle. After a minute of equilibration, the LVOT VTI is repeated and cardiac output recalculated. An increase in VTI of more than 12.5% predicts an increase in cardiac output with volume expansion.^73,74 This procedure requires proficiency with pulsed-wave Doppler and the ability to obtain the apical five-chamber view while a patient’s legs are being manipulated. In addition, the angle of insonation and location of measurement of LVOT and VTI must not vary for this measure to be valid. 

Alternatively, respiratory variation in LVOT peak velocities has been shown to reliably predict volume responsiveness when variability is more than 12% (Figure 7c).⁶⁹ This measurement is easier to obtain in that it does not require multiple views or complex calculations, and can be easily augmented with a passive leg raise maneuver. 

In the search for easily accessible alternatives to cardiac and aortic flow, brachial artery peak velocity variation (BAPVV) was found to be useful for predicting volume responsiveness.⁷⁵ To perform this study, the brachial artery is imaged in the long axis view using a linear transducer. Doppler gating should be adjusted to ensure an angle of less than 60°. The patient’s BAPVV is calculated as the difference between maximum and minimum peak velocity divided by the mean peak velocity. A variability in peak velocity of more than 10% predicts volume responsiveness.⁷⁵ 

Common Carotid Artery Flow

Similarly, CCA flow has attracted attention as a potential surrogate to assess SV response to preload challenge.^76,77 The CCA is large, easily accessible and does not require specialized training to assess (Figure 12).⁷⁸

Even though cardiopulmonary interaction assessment has excellent performance for predicting volume responsiveness, limitations do exist. For example, cardiopulmonary interactions may be exaggerated or diminished—thus decreasing the reliability of this assessment—in patients on mechanical ventilation who have spontaneous breathing, high positive end-expiratory pressures or a high minute ventilation, low TV, dysrhythmias, external compression of extra- or intrathoracic vessels (eg, intra-abdominal hypertension, pericardial tamponade, COPD/asthma exacerbations); and in patients who have decreased arterial elastance, or high RV afterload causing RV dysfunction or failure.

Conclusion

The advanced ultrasound techniques described in this review provide several useful tools to rapidly evaluate and manage cardiopulmonary interactions and assess the hemodynamic profile of critically ill patients. With these bedside techniques added to basic POCUS examinations, a new era in noninvasive critical care management is now available. 

As we enter the days of precision medicine, these examinations will enable EPs to optimize the care of this high-risk patient population. Moreover, future research by the emergency ultrasound and critical care communities on morbidity and mortality associated with resuscitation strategies in the ED will undoubtedly incorporate cardiopulmonary and hemodynamic ultrasound. 

Critically ill patients presenting to the ED represent the most time-sensitive patient encounter for the emergency physician (EP), as delays in restoring physiological homeostasis increase the risks of organ dysfunction and death. Management and treatment strategies in critically ill patients have evolved from the routine use of invasive catheters and radiography for cardiopulmonary evaluation to a variety of noninvasive devices and pathways. The widespread adoption of point-of-care ultrasound (POCUS) in EDs provides the opportunity to rapidly obtain invaluable information about the diagnosis and etiology to guide resuscitation in critically ill patients—particularly those in shock and acute dyspnea. 

Over the last two decades, EPs and critical care physicians have employed POCUS to assist in identifying emergent reversible causes of shock and cardiac arrest, including cardiac tamponade, massive pulmonary embolism (PE), and hemoperitoneum. Recent advances in hemodynamic and cardiopulmonary POCUS allow for a nuanced approach to hemodynamic evaluation.¹ In addition, the use of ultrasound “first” in the critical care setting may reduce the dependence on radiographic-based management, catheter-based protocols, and the need for invasive procedures. 

Bedside cardiopulmonary ultrasound to evaluate the hemodynamic status of hypotensive patients can help determine the etiology of shock, provide evidence of fluid-volume responsiveness, visualize hemodynamic abnormalities that would alter fluid resuscitation strategies, and assess patient response to an intervention. The use of ultrasound can also identify the etiology of acute respiratory failure—providing the opportunity to initiate the appropriate interventions prior to patient decompensation. Findings such as pneumothorax or pleural effusion may require immediate procedural intervention, while other findings may only require noninvasive positive pressure ventilation and diuresis. 

The tools to implement these concepts include basic POCUS education common to emergency medicine and critical care (American College of Emergency Physicians Guidelines and American College of Chest Physicians/Society of Critical Care Medicine guidelines); ultrasound machines with phased array, linear, and curvilinear probes; and ultrasonographic instrumentation such as M-Mode, color Doppler, and spectral Doppler. An understanding of common Doppler imaging techniques optimizes the examination, and the use of presets common to cardiac packages may further assist the provider with adoption. 

When evaluating critically ill patients, we recommend the following step-wise approach: 

• Identify a clinical question to be answered prior to doing the examination; 
• Determine the hemodynamic profile of the patient to guide therapeutic maneuvers; and 
• Monitor the response to any therapeutic maneuver and adjust accordingly. (In these complicated patients, repeat examinations are invaluable, as the hemodynamic profile can change rapidly.)

Emergency physicians are increasingly utilizing POCUS to rapidly evaluate the thoracic cavity in critically ill patients. This modality is an appealing alternative to formal chest radiography because of the ease of rapid image acquisition, lack of ionizing radiation, and the ability to repeat the examination in real-time. 

When critically ill patients present in respiratory distress, POCUS allows the EP to rapidly diagnose potential etiologies, such as pleural effusion, pneumothorax, or pulmonary edema, and employ emergent intervention, which can greatly alter the patient’s clinical course. Additionally, the rapid diagnosis of consolidation permits earlier appropriate management of sepsis and respiratory failure when the clinical setting is consistent with pneumonia. 

In many cases, ultrasound has been shown to be superior to traditional chest radiography to assess critically ill patients.^2-8 Although there are several protocols that utilize thoracic ultrasound in evaluating the critical patient, this review focuses solely on the components of thoracic ultrasound, rather than specific protocols.  

Pneumothorax 

Ultrasound imaging with a high-frequency probe is highly sensitive and specific in assessing for pneumothorax in a supine patient.⁹ In the normal lung, the visceral and parietal pleura are visualized as sliding with each breath. In this examination, the transducer is placed on the chest wall to visualize two ribs and the pleura between them (Figures 2a and 2b).

When lung sliding is present, the appearance in M-mode is that of the “seashore” or “sandy beach.” The hyperechoic white pleura is seen as moving with the respiratory cycle. Additionally, lung artifacts such as A-lines, horizontal reverberation artifacts; and B-lines (also referred to as “comet-tails”), vertical lines arising from distended subpleural alveoli, will be seen in a normal lung. If pneumothorax is present, no sliding or comet-tail artifacts will be present at the pleural surface. Although A-lines may also be absent in pneumothorax, studies have shown that the absence of lung sliding and the presence of A-lines are associated with increased specificity (94% vs 78% with absent lung sliding alone) for diagnosing occult pneumothorax.⁹

While the lack of pleural sliding is highly sensitive for pneumothorax, the clinician must place this finding within the clinical context of the patient. For example, an intubated patient may not have left-sided sliding in the case of a right main-stem intubation. Moreover, patients who have an underlying obstructive lung disease (eg, chronic obstructive pulmonary disease [COPD]) and/or emphysema may present a more challenging examination because pleural sliding is often absent, especially in the apical segments, and can mimic pneumothorax in these patients.¹⁰ 

In addition to pleural sliding, presence or absence of a lung pulse also assists in assessing patients for pneumothorax. The detection of a lung pulse on M-mode ultrasound indicates subtle cardiac pulsation at the periphery of the lung; this finding only appears in the nonventilated lung in the absence of a pneumothorax. The presence of lung pulse is therefore useful in distinguishing other causes of nonventilated lung from pneumothorax.¹¹

Pleural Fluid

The low-frequency curvilinear or phased array probes are used to assess for pleural fluid. In this study, the clinician fans the probe cephalad from Morison’s pouch on the patient’s right side, or from the splenorenal recess on the left side, to visualize the bright, hyperechoic diaphragm. If pleural fluid is present, there will be loss of the mirroring artifact, and the fluid will appear as an anechoic collection cephalad to the diaphragm. In addition, when fluid is present, the normal lung may be visualized moving within the effusion, evoking a quad or sinusoid sign with M-mode imaging.^12,13 In the setting of complicated parapneumonic effusion, the echogenicity may be mixed or difficult to detect.  

Visualization of the thoracic spine above the diaphragm may serve as a surrogate marker for the presence of fluid. Typically, the thoracic spine is not visualized on ultrasound due to the scatter caused by the air-filled lungs.

Ultrasound has been shown to be superior to routine chest radiograph for the identification of small pleural effusions.⁷ Given that both critically ill medical and injured patients can present with pleural fluid, the use of POCUS to rapidly determine the presence or absence of fluid is an adjunct in the evaluation of these patients. 

Interstitial Fluid

Evaluation of the thoracic cavity for interstitial fluid in the setting of acute pulmonary edema, acute respiratory distress syndrome (ARDS), or interstitial pneumonia is best accomplished using either the curvilinear low-frequency probe or the phased array probe. The visualization of vertically oriented B-lines in the upper lung fields is very sensitive for interstitial fluid or edema of the interlobular septa (Figures 2a and 2b).^13,15 In this study, B-lines originate at the pleural line, move with the pleura, and extend off the bottom of the monitor without obliteration (in contrast to A-lines). An isolated B-line may be physiological; however, the presence of several B-lines is consistent with an interstitial pathology. On imaging, the presence of three or more B-lines in a single rib space with a convex probe, or more than six B-lines when utilizing the curvilinear, is considered pathological and referred to as “lung rockets.” B-lines may be focal or diffuse, as seen respectively in cases of pneumonia or acute pulmonary edema.¹⁶ 

Pulmonary Assessment for Fluid Resuscitation

Fluid Resuscitation 

Lung ultrasound studies have been proposed as a means of determining adequate fluid resuscitation and preventing complications associated with excessive fluid. The appearance of diffuse B-lines of acute interstitial syndrome on lung ultrasound can uncover the first signs of extravascular lung water and prevent pulmonary alveolar edema and associated morbidity and mortality.¹⁷ The appearance of an A-line predominance throughout the lung does not predict fluid responsiveness, but rather potential fluid tolerance. 

A benefit of lung ultrasound is that it provides information more rapidly than many of the dynamic measures of fluid responsiveness and cardiac output variability. In addition, lung ultrasound studies are much more easily reproduced than repeating a velocity time integral (VTI) measurements.

Lichtenstein’s FALLS Protocol

Lichtenstein’s FALLS (Fluid Administration Limited by Lung Sonography) protocol provides an approach to performing lung ultrasound on patients presenting in shock.¹² In this approach, lung ultrasound studies are performed after echocardiography to evaluate the patient for causes of obstructive shock. The predominance of B-lines on lung ultrasound suggests cardiogenic shock and, by definition, fluid intolerance. The predominance of A-lines on ultrasound may be present in patients in hypovolemic or septic shock. 

In hypovolemic shock, continued fluid boluses will improve hemodynamics with preserved A-line predominance. In septic shock, B-lines will begin to appear, suggesting that other means of improving forward flow should be initiated.

Consolidation

Chest radiography is known to have variable test characteristics for the detection of pneumonia. Consolidation may not be detected in profoundly immunocompromised or dehydrated patients. Additionally, in critically ill patients, it is often challenging to obtain a posteroanterior and lateral chest X-ray, given the patient’s hemodynamic status and stability for transport, and a single portable anteroposterior film will often miss retrocardiac infiltrates. In both of these clinical settings, POCUS can provide a rapid diagnosis, expediting the care of these septic patients. 

In the presence of a dense consolidation, there may be hepatization of the lung parenchyma (Figure 4b). Additionally, hyperechoic air bronchograms are often visualized. Pneumonia is often associated with pleural effusion and localized B-lines. Using lung ultrasound, rapid bedside detection of these pulmonary findings in clinical presentations suggestive of pneumonia can accelerate appropriate antibiotic and respiratory supportive treatment.  

Left Ventricular Systolic Assessment 

Critically ill patients commonly present with a mixed shock picture, and it is rare for a patient to have solely cardiogenic shock, hemorrhagic shock, etc. Rather, a patient who presents in septic shock may have an underlying cardiomyopathy for which she or he is being treated with a beta-blocker. 

Cardiomyopathy associated with sepsis is common¹⁸ and, at least in the case of diastolic dysfunction, it is underdiagnosed and associated with a higher mortality rate.¹⁹ It is therefore essential that the EP evaluate left ventricular (LV) systolic function rapidly and reliably—particularly in critically ill patients whose disease process may be undifferentiated and whose hemodynamic status is unclear.^20-22 Bedside echocardiography by the EP is invaluable in identifying the LV contribution to the hemodynamic profile and tailoring resuscitation to optimize patient outcomes. 

Although gross visual assessment is the most widely used method by which EPs estimate LV systolic function, this strategy is subjective, operator-dependent, and requires at least two quality views to understand the heart’s three-dimensional movement. However, when faced with a rapid diagnostic dilemma, a global visual estimate of the overall contractility (hyperdynamic, normal, depressed, severely depressed) may be more useful than estimating the ejection fraction (EF), especially when the patient’s baseline EF is unknown. 

Regional wall-motion abnormalities can be evaluated by considering  and correlating the coronary artery distributions with the electrocardiographic findings and the clinical scenario (Figure 5).

Simpson’s Rule

Although no one parameter can quantitatively assess LV function, the EF is the one most commonly used. The Simpson’s Rule or the “method of disks” estimates EF by changes in calculated ventricular volumes. The endocardial border is outlined in end-diastole and end-systole (ES) in both the apical four- (AP4) and two-chamber views. The cardiac package on the ultrasound system can divide the selected area into a series of disks, calculate the volume of each disk, and then add these figures to estimate the ventricular volume (Figure 6a). Limitations of this study include potentially difficult visualization of the endocardial border, and the length of time to conduct this study. 

Fractional Shortening

M-mode ultrasound can be used in several ways to estimate LV EF. Fractional shortening (FS) estimates the size reduction of the LV during systole. In the parasternal long axis (PLAX) view, the M-mode cursor is placed over the walls of the LV, just apical to the tips of the mitral valve (MV) leaflets (Figure 6b). Maximal (end-diastolic diameter [EDD]) and minimal (end-systolic diameter [ESD]) dimensions of the LV are measured and FS is calculated as (LVEDD – LVESD)/ LVEDD. A normal value is more than 25%, and a rough estimate of EF is FS x 2.²⁴ Limitations to this study include nonplacement of the M-mode cursor perpendicular to the LV walls, and inaccuracy in patients with regional wall abnormalities. 

E-Point Septal Separation

Another way to assess EF with POCUS is through E-point septal separation (EPSS), which uses the movement of the MV during diastole to estimate the EF during systole. In the PLAX view, the M-mode cursor is placed over the apical tip of the anterior leaflet of the MV to visualize the movement of the leaflet in relation to the interventricular septum (Figure 6c). Two characteristic waves are created during each diastole—the larger first wave representing early filling (the E-wave) and the smaller second wave representing the atrial kick (the A-wave). The E-point is the tallest point of the E-wave, and the EPSS is measured as the distance in millimeters between the E-point and the interventricular septum.²¹ 

The opening of the anterior leaflet of the MV toward the interventricular septum in diastole requires a pressure difference between the left atrium (LA) and LV. In a patient with poor LV systolic function, the LV is still full at the end of systole, the pressure difference is not as great, and the mitral leaflets will not snap open vigorously. The EPSS should be at or less than 6 mm in patients with normal LV systolic function. An EPSS of 6 to 12 mm suggests moderately depressed LV systolic function, and over 12 mm signifies severely decreased LV systolic function.²⁵ Limitations include inaccuracy in patients with valvular abnormalities, such as mitral stenosis or aortic regurgitation, severe LV or septal hypertrophy, regional wall abnormalities or severe LV dilation, limited data, and a wide margin of error when comparing to magnetic resonance imaging measurement of EF.

Cardiac Output 

Left Ventricular Diastolic Assessment

In an aging population of patients who have longstanding, undiagnosed, or untreated hypertension, LV hypertrophy leads to impaired relaxation and diastolic filling, eventually causing elevated LA pressure and, in extreme cases, restrictive cardiomyopathy. It has been reported that approximately half of all symptomatic patients with heart failure have a preserved EF.²⁷ 

Determination of LV pressures allows for the distinction between hydrostatic pulmonary edema and ARDS. Diagnosing elevated LA pressure is not inconsequential, as diastolic dysfunction in septic patients has been associated with increased mortality, likely due to increased pulmonary edema from fluid resuscitation.¹⁹ An invasive method of using a pulmonary artery catheter and measuring the pulmonary artery occlusion pressure to estimate the LA pressure is the gold standard, but is no longer routinely performed. 

Echocardiography is a noninvasive surrogate to estimating LA and LV filling pressures. Two different echocardiographic measurements can be used in conjunction to estimate LV filling pressures: MV inflow velocity and tissue Doppler imaging. 

Mitral Valve Inflow Velocity

Assessment of the MV inflow is performed by placing the pulse-wave Doppler gate between the tips of the MV leaflets in the AP4 view. Early diastolic filling produces the E-wave, and LA contraction produces the late diastolic A-wave (Figure 8a).

Tissue Doppler Imaging

Tissue Doppler imaging enables the clinician to measure myocardial velocities such as the speed of relaxation to evaluate if LV relaxation is due to a drop in LV pressure below LA pressure after systole, pulling the MV open; or if increased LA pressure is required to push open the MV and fill the LV. 

For this study, the tissue Doppler sampling gate is placed at the septal or lateral annulus of the MV in the AP4 view to visualize early diastolic mitral annulus velocity (e’) (Figure 8b). The E/e’ ratio can be helpful for estimating LV filling pressures. An E/e’ of less than 8 is associated with normal LV filling pressure whereas an E/e’ >15 is associated with an elevated LV filling pressure.28,29 When the E/e’ is 8 to 10, other indices such as the E/A ratio and deceleration time, as well as the clinical picture, can provide insight into the presence of hemodynamically significant diastolic dysfunction.

Learning and applying the assessment of diastolic parameters can be challenging; however, these parameters can be used to help predict LV filling pressures in patients with findings of pulmonary edema on chest radiograph. Limitations of these techniques are inter-rater variability, as well as the ability of the operator to acquire the required AP4 view. In addition, these techniques are unreliable in patients with irregular cardiac rhythms, severe mitral disease, and in hypertrophic cardiomyopathy. 

Right Ventricular Assessment

The right ventricle (RV) is a small, thin-walled ventricle with only two layers of muscle, as opposed to the three layers of the LV. In contrast to the rocking motion of LV contraction, the orientation of the two muscle layers of the RV permits mostly longitudinal contraction. The circumferential muscle fibers are shared at the base and apex with the LV, which can provide some of the contractile strength of the RV.³⁰ Because of this orientation, RV strain, which can manifest as decreased longitudinal contraction, speed of contraction, septal movement, and tethering abnormalities through ventricular interdependence, can be measured easily using bedside echocardiography. 

In healthy individuals, the RV is a low-pressure chamber that acts as a conduit for propelling venous return into the pulmonary circulation without much effect on systemic hemodynamics. However, in critical illness, RV abnormalities can have profound effects on hemodynamics, and  the efforts typically used to improve LV performance will worsen a failing RV. 

While RV dysfunction is most commonly due to chronic LV disease, acute RV dysfunction is commonly encountered in critical illness,³¹ including many septic patients with ARDS,^32,33 PE, or decompensated chronic pulmonary hypertension.³⁴ The examinations that follow, allow the EP to assess for the presence of RV dysfunction and to guide resuscitation appropriately to avoid the untoward hemodynamic effects of conventional resuscitation strategies in these patients. 

When evaluating the RV, the clinician must determine (1) if the patient’s RV strain is due to pressure or volume overload; and (2) if the patient’s RV is responsive or nonresponsive to a preload challenge, prompting an alteration in the resuscitation plan in nonresponsive cases. 

Right Ventricular Pressure/Volume Overload

While inferior vena cava (IVC) ultrasound has been shown to be a pre-heart/lung assessment of cardiopulmonary interactions that predicts volume responsiveness, the IVC is also a good predictor of right atrial (RA) pressure.³⁵ If the IVC is dilated and lacks respiratory variation, the patient likely has an elevated RA pressure, which is most likely transmitted from an elevated RV pressure (Figure 9a). However, compliance of the RA, RA pressure and, by extension, IVC prediction of that RA pressure, may underestimate the degree of RV pressure or afterload. 

Right Ventricular Strain and Contractile Reserve 

From the same apical view, tissue Doppler at the lateral tricuspid annulus will give a tricuspid annular peak velocity, a measure of the isovolumetric contraction velocity. This measurement will provide a measure of the contractile reserve of the RV (Figure 10b). A measure of less than 10 cm/sec indicates that further volume and inotropic challenges to the RV will not be effective, and the focus should be to decrease RV afterload with pulmonary vasodilators.^34,39,40 

Fluid Resuscitation Assessment 

Restoring circulating volume to increase cardiac output and improve oxygen delivery is the primary objective when managing patients in shock. Patient outcomes improve dramatically with early aggressive fluid resuscitation.^41-44 However, many critically ill patients do not respond to fluid resuscitation, which is generally defined as the rise of cardiac output of more than 15% in response to volume expansion. Not all patients found to be fluid responsive will require volume expansion.^45,46 

Excessive fluid resuscitation has been shown to increase intensive care unit length of stay, morbidity, and mortality.^47,48 Further, pathophysiological processes such as RV dysfunction and severe diastolic dysfunction can significantly alter the hemodynamic profile such that fluid management can be quite challenging in critically ill patients.

Distinguishing responders from nonresponders prior to fluid administration is the goal of early resuscitation. Unfortunately, this distinction cannot be made based on the patient’s vital signs or the physical examination.⁴⁹ Static filling pressures and volumetric measures are unreliable markers of fluid responsiveness.^50,51 The practice of administering a fluid challenge and observing the clinical effect on cardiac output is undesirable because it requires, by definition, on administering fluids, which ultimately may be harmful to the patient. 

Dynamic measures of fluid responsiveness that reliably predict cardiac response to a preload challenge are proven to be of greater utility.^52,53 These assessments determine volume responsiveness by evaluating the change in LV output with intrathoracic pressure changes due to the respiratory cycle, (ie, cardiopulmonary interaction). Ultrasound studies to assess cardiopulmonary interactions include IVC variability, arterial flow variability, brachial artery peak velocity variability, and common carotid artery (CCA) flow. In addition to echocardiography, lung ultrasound may be used to determine the endpoint of fluid resuscitation by monitoring for the appearance of extravascular lung water. 

Inferior Vena Cava Variability 

The IVC is a large extrathoracic vein which is easily insonated and accessible, even to a clinician with basic bedside ultrasound competency. Static IVC measures, such as diameter alone, correlate with central venous pressure but do not predict fluid responsiveness.^54-56 Dynamic IVC evaluation provides an upstream assessment of cardiopulmonary interactions. 

In the spontaneously breathing patient, the IVC collapses with inspiration as the RA pressure falls below atmospheric pressure, collapsing the intrathoracic veins for a short period until the intravascular pressure at the entry to the thorax exceeds atmospheric pressure, causing a bolus of venous return to the right heart. The overall effect is an increase in venous return⁵⁹. Conversely, in the mechanically ventilated patient, the IVC will distend with insufflation as increased intrathoracic pressure results in increased RV afterload and a transient increase in pulmonary artery pressure with an overall net decrease in venous return.⁶⁰

This IVC variability, termed the caval index, quantifies the degree of change in size of the IVC between end-inspiration and end-expiration. An M-mode imaging evaluation of the IVC allows for measurement of the maximal and minimal diameters for this calculation (Figure 11). Passively mechanically ventilated patients, with tidal volumes (TV) of 8 to 10 cc/kg in sinus rhythm, are predictably volume-responsive when the IVC distends by 12% to 18%.^54,61,62 However, there is considerable debate as to whether evaluating the degree of IVC collapse is of value in spontaneously breathing patients.⁶³ Cardiopulmonary interactions that drive IVC variability are affected by variable TV, intrathoracic pressure changes, etc. Nonetheless, two studies have shown that IVC collapse reliably predicts fluid responsiveness in spontaneously breathing patients.^64,65 

Stroke Volume/Arterial Flow Variability

Intrathoracic pressure changes induce dynamic changes in venous return that ultimately result in alterations in LV stroke volume (LVSV) when the blood volume traverses pulmonary circulation.⁶⁶ This variability in LVSV is the basis for all dynamic assessments of cardiopulmonary interactions, whether by arterial pressure waveform analysis or echocardiographic assessment of arterial flow. 

The LVSV variability reliably predicts fluid responsiveness and may be assessed by esophageal Doppler echocardiography of the ascending aorta.^67,68 Transesophageal echocardiography has also been used to assess SV variability at the LVOT.⁶⁹ Both of these measures require equipment and skill that may not be available in every clinical setting. Fortunately, LVOT SV is easily obtained through transthoracic echocardiography (TTE) (Figures 7a and 7b) using LVOT Doppler velocities as a surrogate for SV variations. A small study of TTE in mechanically ventilated children found that aortic flow variability predicted fluid responsiveness.⁷⁰ Therefore, transthoracic echocardiography provides a well-established alternative to thermodilution in determining cardiac output. Multiplication of the HR by an estimate of the column of blood flowing through the LVOT with each systolic contraction gives the cardiac output.⁷¹ 

Using TTE measurement of SV and cardiac output, the clinician can assess the effect of small fluid challenges on cardiac output.⁷² Cardiac output can be augmented with the passive leg raise (PLR), which is an entirely reversible preload challenge maneuver thought to increase preload by 300 to 500 mL. To assess volume responsiveness using this technique, LVOT cardiac output must first be determined. With the transducer in place, the patient’s legs are lifted to a 45° angle. After a minute of equilibration, the LVOT VTI is repeated and cardiac output recalculated. An increase in VTI of more than 12.5% predicts an increase in cardiac output with volume expansion.^73,74 This procedure requires proficiency with pulsed-wave Doppler and the ability to obtain the apical five-chamber view while a patient’s legs are being manipulated. In addition, the angle of insonation and location of measurement of LVOT and VTI must not vary for this measure to be valid. 

Alternatively, respiratory variation in LVOT peak velocities has been shown to reliably predict volume responsiveness when variability is more than 12% (Figure 7c).⁶⁹ This measurement is easier to obtain in that it does not require multiple views or complex calculations, and can be easily augmented with a passive leg raise maneuver. 

In the search for easily accessible alternatives to cardiac and aortic flow, brachial artery peak velocity variation (BAPVV) was found to be useful for predicting volume responsiveness.⁷⁵ To perform this study, the brachial artery is imaged in the long axis view using a linear transducer. Doppler gating should be adjusted to ensure an angle of less than 60°. The patient’s BAPVV is calculated as the difference between maximum and minimum peak velocity divided by the mean peak velocity. A variability in peak velocity of more than 10% predicts volume responsiveness.⁷⁵ 

Common Carotid Artery Flow

Similarly, CCA flow has attracted attention as a potential surrogate to assess SV response to preload challenge.^76,77 The CCA is large, easily accessible and does not require specialized training to assess (Figure 12).⁷⁸

Even though cardiopulmonary interaction assessment has excellent performance for predicting volume responsiveness, limitations do exist. For example, cardiopulmonary interactions may be exaggerated or diminished—thus decreasing the reliability of this assessment—in patients on mechanical ventilation who have spontaneous breathing, high positive end-expiratory pressures or a high minute ventilation, low TV, dysrhythmias, external compression of extra- or intrathoracic vessels (eg, intra-abdominal hypertension, pericardial tamponade, COPD/asthma exacerbations); and in patients who have decreased arterial elastance, or high RV afterload causing RV dysfunction or failure.

Conclusion

The advanced ultrasound techniques described in this review provide several useful tools to rapidly evaluate and manage cardiopulmonary interactions and assess the hemodynamic profile of critically ill patients. With these bedside techniques added to basic POCUS examinations, a new era in noninvasive critical care management is now available. 

As we enter the days of precision medicine, these examinations will enable EPs to optimize the care of this high-risk patient population. Moreover, future research by the emergency ultrasound and critical care communities on morbidity and mortality associated with resuscitation strategies in the ED will undoubtedly incorporate cardiopulmonary and hemodynamic ultrasound. 

The beginning of a new year is always associated with changes, accompanied by new challenges and opportunities. This year is no different and, in fact, begins with some significant changes. First, I am incredibly honored, and humbled, to be named your new editor-in-chief. By way of background and introduction, I am residency-trained and board-certified in emergency medicine (EM). I founded the first academic department of EM in Virginia in 1992, and continue to serve in the role of chair. From 1990 to 2010, I served as the program director of our 3-year EM residency program, which I still consider the best job in EM. Most importantly, I continue to see and care for patients in the ED primarily, in addition to supervising and teaching EM residents and fellows in the delivery of care in the clinical arena. I know first-hand the needs of practicing emergency physicians (EPs).

I feel very fortunate to have been associated with Emergency Medicine (EM) since 1988, the year the journal published my very first manuscript. I served on the editorial board from 1999 to 2006, and for the past 11 years, have served as the associate editor-in-chief. I hold a very special regard and respect for this journal, and its role in our specialty. My goal is to continue to publish high-quality content and ensure we consistently provide timely and clinically useful information to the practicing EP. We will invite the very best in our specialty to share their knowledge and clinical tips. We will of course continue some of your favorite sections, like “Emergency Ultrasound,” “Diagnosis at a Glance,” and “Case Studies in Toxicology.” We will also encourage our readers to submit interesting and informative case reports, review articles, and interesting images. While I plan to write a few editorials each year, I will invite thought leaders in EM to write on their area(s) of expertise.

Come writers and critics who prophesize with your pen.

Another major change has to do with the journal itself. This will be the last paper copy of EM (so think about keeping this one for posterity, or eBay). Starting with the February issue, all future issues will be digital and online-only. This decision was not an easy one, and has been in the making for some time. Thanks to the growth in our Web site traffic, it is clear that many of you have already become “digital-first” readers. This fact, combined with the added financial challenge of publishing a large-circulation journal within an environment of declining print advertising, convinced us that this is the right time to make the leap to the digital-only format. While some of you (including myself), will miss physically holding and reading a hard copy of EM, you may simply continue to access the journal as you have for years, on your desktop, laptop, or iPad, and never further away than your cell phone. This change has the advantage of providing opportunities to deliver valuable clinical content in new ways, through increased use of audio and video, as well as text. To ensure that you receive your copy, please e-mail our Editor, Kellie DeSantis ([email protected]) to make sure we have your correct and preferred e-mail address. While our goal is to push each issue out to you via e-mail, you will always be able to access the most recent articles by going to our Web site, www.emed-journal.com.

And don’t criticize

What you can’t understand.

Finally, 2018 promises to be a very interesting year, with the unknown implications of tax reform, the repeal of the individual mandate for health insurance, the opioid crisis, and the curious mergers within the health insurance industry (ie, CVS and Aetna). It is too soon for anyone to say how these changes will affect EM on the national stage. What will not change however, is that EPs will continue to provide outstanding care to any and every patient who presents to the ED. Emergency physicians will ensure that all patients receive the care they need (but not necessarily the care they want) and will do so without regard to gender, religion, national origin, race, age, sexual preference, or insurance status.

I wish each and every one of you a happy and healthy 2018.

The beginning of a new year is always associated with changes, accompanied by new challenges and opportunities. This year is no different and, in fact, begins with some significant changes. First, I am incredibly honored, and humbled, to be named your new editor-in-chief. By way of background and introduction, I am residency-trained and board-certified in emergency medicine (EM). I founded the first academic department of EM in Virginia in 1992, and continue to serve in the role of chair. From 1990 to 2010, I served as the program director of our 3-year EM residency program, which I still consider the best job in EM. Most importantly, I continue to see and care for patients in the ED primarily, in addition to supervising and teaching EM residents and fellows in the delivery of care in the clinical arena. I know first-hand the needs of practicing emergency physicians (EPs).

I feel very fortunate to have been associated with Emergency Medicine (EM) since 1988, the year the journal published my very first manuscript. I served on the editorial board from 1999 to 2006, and for the past 11 years, have served as the associate editor-in-chief. I hold a very special regard and respect for this journal, and its role in our specialty. My goal is to continue to publish high-quality content and ensure we consistently provide timely and clinically useful information to the practicing EP. We will invite the very best in our specialty to share their knowledge and clinical tips. We will of course continue some of your favorite sections, like “Emergency Ultrasound,” “Diagnosis at a Glance,” and “Case Studies in Toxicology.” We will also encourage our readers to submit interesting and informative case reports, review articles, and interesting images. While I plan to write a few editorials each year, I will invite thought leaders in EM to write on their area(s) of expertise.

Come writers and critics who prophesize with your pen.

Another major change has to do with the journal itself. This will be the last paper copy of EM (so think about keeping this one for posterity, or eBay). Starting with the February issue, all future issues will be digital and online-only. This decision was not an easy one, and has been in the making for some time. Thanks to the growth in our Web site traffic, it is clear that many of you have already become “digital-first” readers. This fact, combined with the added financial challenge of publishing a large-circulation journal within an environment of declining print advertising, convinced us that this is the right time to make the leap to the digital-only format. While some of you (including myself), will miss physically holding and reading a hard copy of EM, you may simply continue to access the journal as you have for years, on your desktop, laptop, or iPad, and never further away than your cell phone. This change has the advantage of providing opportunities to deliver valuable clinical content in new ways, through increased use of audio and video, as well as text. To ensure that you receive your copy, please e-mail our Editor, Kellie DeSantis ([email protected]) to make sure we have your correct and preferred e-mail address. While our goal is to push each issue out to you via e-mail, you will always be able to access the most recent articles by going to our Web site, www.emed-journal.com.

And don’t criticize

What you can’t understand.

Finally, 2018 promises to be a very interesting year, with the unknown implications of tax reform, the repeal of the individual mandate for health insurance, the opioid crisis, and the curious mergers within the health insurance industry (ie, CVS and Aetna). It is too soon for anyone to say how these changes will affect EM on the national stage. What will not change however, is that EPs will continue to provide outstanding care to any and every patient who presents to the ED. Emergency physicians will ensure that all patients receive the care they need (but not necessarily the care they want) and will do so without regard to gender, religion, national origin, race, age, sexual preference, or insurance status.

I wish each and every one of you a happy and healthy 2018.

The beginning of a new year is always associated with changes, accompanied by new challenges and opportunities. This year is no different and, in fact, begins with some significant changes. First, I am incredibly honored, and humbled, to be named your new editor-in-chief. By way of background and introduction, I am residency-trained and board-certified in emergency medicine (EM). I founded the first academic department of EM in Virginia in 1992, and continue to serve in the role of chair. From 1990 to 2010, I served as the program director of our 3-year EM residency program, which I still consider the best job in EM. Most importantly, I continue to see and care for patients in the ED primarily, in addition to supervising and teaching EM residents and fellows in the delivery of care in the clinical arena. I know first-hand the needs of practicing emergency physicians (EPs).

I feel very fortunate to have been associated with Emergency Medicine (EM) since 1988, the year the journal published my very first manuscript. I served on the editorial board from 1999 to 2006, and for the past 11 years, have served as the associate editor-in-chief. I hold a very special regard and respect for this journal, and its role in our specialty. My goal is to continue to publish high-quality content and ensure we consistently provide timely and clinically useful information to the practicing EP. We will invite the very best in our specialty to share their knowledge and clinical tips. We will of course continue some of your favorite sections, like “Emergency Ultrasound,” “Diagnosis at a Glance,” and “Case Studies in Toxicology.” We will also encourage our readers to submit interesting and informative case reports, review articles, and interesting images. While I plan to write a few editorials each year, I will invite thought leaders in EM to write on their area(s) of expertise.

Come writers and critics who prophesize with your pen.

Another major change has to do with the journal itself. This will be the last paper copy of EM (so think about keeping this one for posterity, or eBay). Starting with the February issue, all future issues will be digital and online-only. This decision was not an easy one, and has been in the making for some time. Thanks to the growth in our Web site traffic, it is clear that many of you have already become “digital-first” readers. This fact, combined with the added financial challenge of publishing a large-circulation journal within an environment of declining print advertising, convinced us that this is the right time to make the leap to the digital-only format. While some of you (including myself), will miss physically holding and reading a hard copy of EM, you may simply continue to access the journal as you have for years, on your desktop, laptop, or iPad, and never further away than your cell phone. This change has the advantage of providing opportunities to deliver valuable clinical content in new ways, through increased use of audio and video, as well as text. To ensure that you receive your copy, please e-mail our Editor, Kellie DeSantis ([email protected]) to make sure we have your correct and preferred e-mail address. While our goal is to push each issue out to you via e-mail, you will always be able to access the most recent articles by going to our Web site, www.emed-journal.com.

And don’t criticize

What you can’t understand.

Finally, 2018 promises to be a very interesting year, with the unknown implications of tax reform, the repeal of the individual mandate for health insurance, the opioid crisis, and the curious mergers within the health insurance industry (ie, CVS and Aetna). It is too soon for anyone to say how these changes will affect EM on the national stage. What will not change however, is that EPs will continue to provide outstanding care to any and every patient who presents to the ED. Emergency physicians will ensure that all patients receive the care they need (but not necessarily the care they want) and will do so without regard to gender, religion, national origin, race, age, sexual preference, or insurance status.

I wish each and every one of you a happy and healthy 2018.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the chronic activation of the immune system, leading to the formation of autoantibodies and multi-organ damage. The prevalence of SLE in the United States is 20 to 150 per 100,000 persons.¹ Ninety percent of patients with SLE are women, and the condition is more common and often more severe among patients of black African or of Asian descent.

General Acute-Care Management

While a patient’s presentation could be secondary to a lupus-related complication, consideration must always be given to common conditions that are not related to SLE. Biomarkers such as erythrocyte sedimentation rate, C-reactive protein, C3 and C4 complement, and double-stranded DNA levels can be helpful in assessing lupus disease activity and differentiating a lupus-related complication from an unrelated event. Comparing these biomarkers to the patient’s baseline values can be informative; however, depending on the laboratory facilities, test results may not be available during an ED visit. Lastly, infections should be considered more strongly than usual in the differential diagnosis due to the immunocompromised status of a substantial proportion of these patients, by virtue of their disease or the cytotoxic medications used for treatment.

Musculoskeletal Complications

Common Complications

Polyarthralgias and Polymyalgias. More than 90% of SLE patients experience polyarthralgias and polymyalgias. Physical examination findings may be normal, even when joint pain is present, which is often due to mild synovitis. In some cases, Jaccoud arthropathy is seen, which presents as deformities such as swan neck deformities and ulnar deviations that are characteristically reducible on manipulation (Figures 1a and 1b). These deformities are not caused by direct joint damage, but by chronic tenosynovitis and the resulting laxity of tendons and ligaments.¹ Classically, plain radiographic imaging reveals nonerosive joint changes. Muscle and joint pains may worsen with disease progression or flare.

Avascular Necrosis. Avascular necrosis affects 5% to 12% of SLE patients.² Most commonly, this involves the femoral head, but it may also involve the femoral condyle or tibial plateau. Patients may present with acute or subacute onset of pain in the groin or buttocks when the femoral head is involved, or in the knee when the femoral condyle or tibial plateau is involved. Plain radiographs may reveal joint-space narrowing and other evidence of degenerative joint disease. Magnetic resonance imaging (MRI) is more sensitive in diagnosing avascular necrosis, and may be indicated when clinical suspicion is high despite negative plain radiographs, although this would not typically need to be performed urgently in the ED.² While analgesics and physical therapy may provide some pain relief to patients with avascular necrosis, this condition generally requires nonemergent operative intervention.

Emergent Complications

Septic Arthritis. When a patient with SLE presents with an isolated swollen joint, septic arthritis should be suspected, and diagnosis should be confirmed by arthrocentesis. Synovial fluid samples showing a white blood cell count greater than 50 × 10⁹/Lsuggest infection, which can be confirmed by gram stain and cultures.

For reasons that remain unclear, but may involve primary immune defects and the use of immunosuppressant medications, patients with SLE are predisposed to Salmonella joint infections. In one study, 59% of septic arthritis cases in patients with SLE were due to Salmonella species; therefore, treatment for septic arthritis in this population should include ceftriaxone in addition to vancomycin for typical organisms, such as Staphylococcus and Streptococcus species.³

Cutaneous Manifestations

Common Complications

Malar Rash. Eighty percent to 90% of patients with SLE have dermatological involvement,¹ the most common finding of which is the malar or butterfly facial rash, which appears as raised erythema over the bridge of the nose and cheeks while sparing the nasolabial folds (Figure 2).

Discoid Lupus. Chronic discoid lupus appears as a scarring rash often found on the face, ears, and scalp. These patients may also exhibit a photosensitive rash, which consists of an erythematous eruption if acute, or annular scaly lesions if subacute.

Oral and Nasal Ulcerations. Common mucous membrane findings include oral or nasal ulcers, which are typically painless.

Worsening of any of these skin findings may be associated with disease flare. Secondary bacterial infection of lupus rashes or ulcerations is uncommon, although cellulitis should be considered when a rash is unilateral, not in a sun-exposed area, or is otherwise different from the patient’s typical lupus rash. Sun avoidance and topical corticosteroids are the mainstays of treatment of dermatological disease in SLE.

Emergent Complications

Systemic Vasculitis. Patients with SLE are susceptible to vasculitis. Although isolated cutaneous vasculitis is not typically an emergent condition, it may portend systemic vasculitis. Any palpable purpura or other evidence of cutaneous vasculitis should prompt a careful review of systems and basic laboratory workup for systemic vasculitis, which can involve the kidneys, lungs, central or peripheral nervous system, or gastrointestinal tract.

Symptoms of systemic vasculitis may include fevers, chills, chest pain, cough, hemoptysis, abdominal pain, and changes in color or amount of urine. Laboratory workup should be tailored to symptoms, and may include basic metabolic panel, liver function tests, complete blood count, and urinalysis.⁴

Digital Gangrene. Patients with SLE may also develop digital gangrene related to severe Raynaud phenomenon, vasculitis, or thromboembolism. Pharmacological treatment with vasodilators such as sildenafil, endothelin receptor antagonists, or intravenous prostacyclins may be needed.⁵ To save the involved digit, vascular surgery services should be consulted urgently.⁶

Renal Complications

Common Complications

Chronic Kidney Disease. Chronic kidney disease (CKD) is common among SLE patients, especially among those with a history of lupus nephritis.⁷ Patients with CKD may have persistently elevated serum creatinine, chronic hypertension, and/or chronic peripheral edema. Patients presenting with new development of hypertension, peripheral edema, hematuria, or polyuria should be screened for lupus nephritis with urinalysis and serum creatinine. Elevated creatinine or new or worsening proteinuria or hematuria should prompt consultation with nephrology services.

Emergent Complications

Lupus Nephritis. About 50% of SLE patients will develop lupus nephritis during the course of their lives,¹ which may present as nephrotic disease with significant proteinuria, peripheral edema, and low serum albumin, or as nephritic disease, with increased serum creatinine and hematuria. Acute kidney injury in SLE patients should generally prompt admission for workup of reversible causes and evaluation for lupus nephritis, which often includes renal biopsy.⁸

Neuropsychiatric Complications

Common Complications

Neuropsychiatric lupus is a broad category that includes 19 manifestations of SLE in the central and peripheral nervous systems.⁹ Conditions range from depression or chronic headaches to seizures or psychosis.

Mood and Anxiety Disorders. Anxiety and depression have been observed in up to 75% of SLE patients.¹ Mood and anxiety disorders are likely influenced by the psychosocial elements of this chronic disease, as well as by direct effects of SLE on the brain.¹

Peripheral Neuropathy. Approximately 10% of SLE patients have a peripheral neuropathy, which generally presents as a mononeuritis (either single or multiplex), rather than the stocking-glove distribution seen in other systemic causes of neuropathy.¹⁰

Headache. Headache disorders may also develop in SLE patients, and tend to have similar patterns to primary headache disorders in the general population. In most cases, treatment for headache in SLE patients is similar to that of the general population.¹¹ However, if a patient presents with concerning findings, such as focal neurological deficit, meningismus, or fever, or if the headache is new-onset or different from previous headaches, further investigation should be considered, including a head computed tomography (CT) scan and lumbar puncture (LP).

Emergent Complications

In general, due to the variety of neurological emergencies that may present with SLE, and the subtlety with which true emergencies may present in this population, the threshold to obtain imaging on SLE patients with any new neurological complaints should be low.

Cerebrovascular Accidents. Patients with SLE are susceptible to cerebrovascular accidents (CVAs), typically from occlusive or embolic causes. Etiologies may include primary central nervous system (CNS) vasculitis, embolic disease from antiphospholipid syndrome (APS), or embolic disease from a Libman-Sacks endocarditis.¹²

Successful thrombolysis has been reported in SLE patients presenting with stroke, but it remains controversial due to risk of hemorrhagic conversion if CNS vasculitis, rather than embolism, is the cause.¹³ Proper imaging and consultation with a neurologist familiar with the disease is critical for early treatment decisions.

Seizures. Fifteen percent to 35% of SLE patients may develop seizures. These may be focal or generalized, but generalized tonic-clonic seizures tend to be more common in SLE patients.² Workup and management of seizures in SLE patients is the same as in the general population.

Sinus Thrombosis. Dural sinus thrombosis often presents as a new-onset headache, sometimes with focal neurological deficits. The diagnosis of dural sinus thrombosis can be challenging, as CT imaging studies may be falsely negative. There should be a low threshold for obtaining MRI/magnetic resonance angiography (MRA) in SLE patients presenting with a new-onset headache.¹⁴

CNS Vasculitis. Patients with SLE are also susceptible to CNS vasculitis, which can manifest as seizures, psychosis, cognitive decline, altered mental status, or coma. Magnetic resonance imaging/MRA studies may suggest the diagnosis, but if this is equivocal, angiography or even brain biopsy may be needed to make the diagnosis. Unless the patient’s symptoms are very mild (eg, mild cognitive decline), she or he should be admitted for diagnostic workup and consideration of aggressive immunosuppressive therapy.²

Transverse Myelitis and Spinal Artery Thrombosis. Acute loss of lower limb sensation or motor function in SLE patients may be caused by transverse myelitis or spinal artery thrombosis. Epidural abscess should also be considered, especially if the patient is immunocompromised.²

Infection. A CNS infection should be considered in any SLE patient presenting with new neurological complaints. Fever or meningismus, especially in conjunction with headache or focal neurological deficits, should prompt an LP and consideration for imaging. Immunocompromised patients are at increased risk for common organisms as well as atypical organisms, such as fungus or mycobacteria.¹⁵

Pulmonary Complications

Common Complications

Pleuritis. Many patients with SLE develop pleuritis, with or without effusion. This may be treated with nonsteroidal anti-inflammatory drugs, or corticosteroids if symptoms are more severe. Pleuritis is the most common respiratory complication of SLE, but due to the number of serious cardiopulmonary complications associated with SLE, pleuritis should be a diagnosis of exclusion.

Interstitial Lung Disease. Interstitial lung disease may be caused by SLE or may be medication-induced. This commonly presents as subacute or chronic dyspnea and/or cough. Patient workup may be done on an outpatient basis with high resolution chest CT and pulmonary function testing.

Pulmonary Hypertension. Patients with SLE may develop pulmonary hypertension, either directly due to SLE or from chronic thromboembolic disease. In general, pulmonary hypertension is managed as an outpatient, but may require emergent inpatient treatment if the condition is rapidly progressive or associated with right heart failure.

Shrinking Lung Syndrome. This condition may cause subacute or chronic dyspnea and pleuritic chest pain. Shrinking lung syndrome is caused by diaphragmatic dysfunction rather than from a primary disease of the lungs, and it is characterized by a restrictive pattern on pulmonary function testing and an elevated hemidiaphragm. Shrinking lung syndrome typically responds well to immunosuppressive therapy.¹⁶

Emergent Conditions

Pulmonary Embolism. A pulmonary embolism should be strongly considered in any patient with SLE presenting with the appropri ate clinical picture. Patients with APS are at particularly high risk for thromboembolic disease. However, even SLE patients without this APS are known to be at an increased risk of developing thromboembolism compared to the general public.¹⁷ Pulmonary embolism in SLE patients should be diagnosed and treated in the usual manner.

Pneumonia. Immunosuppressed patients are susceptible to opportunistic pulmonary infections as well as typical community pathogens. Fungal or mycobacterial infections may be suspected with a more subacute onset of symptoms.

Acute Lupus Pneumonitis. This serious condition may present with severe pneumonia-like signs and symptoms, including fever, cough, dyspnea, hypoxia, and infiltrates on chest radiograph (Figure 3).

Diffuse Alveolar Hemorrhage. A rare complication with a mortality rate of 50% to 90%, SLE patients who develop diffuse alveolar hemorrhage may present with fever, cough, dyspnea, and hypoxia.¹⁸ The condition may be suggested by infiltrates on chest radiograph, a drop in hemoglobin representing bleeding into the lungs, and/or hemoptysis. However, the absence of hemoptysis does not rule out diffuse alveolar hemorrhage, so clinical suspicion should remain high, even in the absence of this symptom.

Because emergent pulmonary conditions often present with similar symptoms, most patients with acute or new-onset symptoms will require admission for diagnostic workup (likely to include chest CT scan and/or bronchoscopy with bronchoalveolar lavage), as well as for close monitoring and initiation of treatment. If hypoxia or respiratory distress is severe, or if diffuse alveolar hemorrhage is suspected, admission to the intensive care unit (ICU) should be considered. We suggest that antibiotics be started in the ED when pneumonia is part of the differential diagnosis. As in the general population, coverage should be chosen based on the patient’s risk factors for antibiotic-resistant organisms. Initiation of corticosteroid therapy or other changes in immune therapy can be delayed until the EP consults with rheumatology and/or pulmonology services.

Cardiac Complications

Common Complications

Pericarditis. Pericarditis with or without pericardial effusion is very common in SLE patients and is usually related to lupus itself, rather than an infectious etiology. Patients may present with substernal, positional chest pain, tachycardia, and diffuse ST-segment elevation on electrocardiogram. Most effusions are small, asymptomatic, and discovered incidentally. However, among patients with symptomatic pericardial effusions, tamponade can be present in 21%.¹⁹ Corticosteroid therapy is often required to treat SLE-associated pericarditis, but colchicine is being explored as a possible steroid-sparing agent in this patient population.^20,21

Valvular Abnormalities. Approximately 60% of SLE patients have valvular abnormalities detectable by echocardiography. The most common abnormalities in one study were valvular thickening or regurgitation.²² Many of these abnormalities occurred in asymptomatic patients and never progressed to clinical disease in a 5-year follow-up. However, patients with any valvular abnormality were more likely to develop complications, including stroke, peripheral embolism, infective endocarditis, need for valve replacement, congestive heart failure, or death.²²

Emergent Complications

Acute Coronary Syndrome. Even in relatively young patients, acute coronary syndrome (ACS) should be considered in SLE patients presenting with chest pain, as this patient population has a 10-fold higher risk of developing coronary artery disease (CAD) than the general population, and SLE patients with CAD often lack traditional risk factors, such as advanced age, family history, or metabolic syndrome.¹

A high clinical suspicion should be maintained even in patients who would traditionally be considered low-risk. The EP should have a low-threshold for ECG, cardiac biomarker testing, and stress testing for SLE patients presenting with chest pain. The treatment of ACS in SLE patients is the same as in the general population.

Libman-Sacks Endocarditis. A sterile, fibrinous valvular vegetation, Libman-Sacks endocarditis is unique to patients with SLE. When present, patients usually develop a subacute or chronic onset of dyspnea or chest pain. However, patients may become acutely ill if they develop severe valvular regurgitation. Additionally, the valve damage from Libman-Sacks endocarditis can predispose patients to developing infective endocarditis.²⁰

Hematological Complications

Common Complications

Patients with SLE commonly have mild-to-moderate leukopenia (especially lymphopenia), anemia, and thrombocytopenia. This may be related to the disease process or may be secondary to prescribed medications. A comparison to recent baseline laboratory studies should be sought if there is suspicion for new or worsening cytopenia.

Antiphospholipid Syndrome. Nearly 40% of SLE patients also have APS, which is defined by a clinical history of thrombosis in conjunction with one of the antiphospholipid antibodies (anticardiolipin, anti-beta-2-glycoprotein, lupus anticoagulant). Antiphospholipid syndrome causes both venous and arterial thrombosis and may be associated with recurrent miscarriage. Acute thrombotic events should be treated with heparin or enoxaparin and transitioned to warfarin. The new generation of direct oral anticoagulants have not been well studied in APS, though, multiple small case series suggest a higher thrombotic risk with these drugs than with warfarin.²³Patients who have recurrent venous thromboembolism, or who have any arterial thromboembolism should be on lifelong anticoagulation therapy.²

Emergent Complications

Thrombocytopenia. Severe thrombocytopenia or hemolytic anemia can be life-threatening, and often requires inpatient admission for immunosuppressive therapy, monitoring, and supportive care.

Catastrophic Antiphospholipid Syndrome. This condition should be suspected in patients with SLE who present with multiple sites of thrombosis or new multi-organ damage. Catastrophic APS (CAPS) may occur in SLE patients who have no prior history of APS. Since the mortality rate for CAPS approaches 50%, these patients require anticoagulation, immunosuppressant therapy (high-dose corticosteroids, cyclophosphamide, and/or plasma exchange), and admission to the ICU.²⁴

Gastrointestinal Complications

Common Complications

Intestinal Pseudo-obstruction. Dysphagia related to esophageal dysmotility is present in up to 13% of SLE patients.²⁵ Intestinal pseudo-obstruction may be seen in SLE patients, and is characterized by symptoms of intestinal obstruction caused by decreased intestinal motility, rather than from mechanical obstruction. Presenting symptoms may be acute or chronic, and include nausea, vomiting, and abdominal distension. Abdominal CT studies will show dilated bowel loops without evidence of mechanical obstruction. Manometry reveals widespread hypomotility. Intestinal pseudo-obstruction typically responds well to corticosteroids and other immunosuppressant therapies.²⁶

Emergent Conditions

Acute Abdominal Pain. Approximately half of SLE patients who present to the ED with acute abdominal pain are found to have either mesenteric vasculitis or pancreatitis, both of which are thought to be related to SLE disease activity.²⁷ Other causes of acute abdominal pain that are common in the general population remain common in SLE patients, including gallbladder disease, gastroenteritis, appendicitis, and peptic ulcer disease.

Mesenteric Vasculitis. Also known as lupus enteritis, mesenteric vasculitis is a unique cause of acute abdominal pain in SLE patients. The condition presents with acute, diffuse abdominal pain and may be associated with nausea and vomiting, diarrhea, or hematochezia. Abdominal CT findings suggestive of diffuse enteritis support the diagnosis. Medical management with pulse-dose corticosteroids and supportive care is generally sufficient, but if bowel necrosis or intestinal perforation is present or suspected, surgical consultation should be obtained immediately.¹⁵

Conclusion

Complications of SLE are diverse and may be difficult to diagnose. Understanding the common and emergent complications of SLE will help the EP to recognize severe illness and make appropriate treatment decisions in this complex patient population.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the chronic activation of the immune system, leading to the formation of autoantibodies and multi-organ damage. The prevalence of SLE in the United States is 20 to 150 per 100,000 persons.¹ Ninety percent of patients with SLE are women, and the condition is more common and often more severe among patients of black African or of Asian descent.

General Acute-Care Management

While a patient’s presentation could be secondary to a lupus-related complication, consideration must always be given to common conditions that are not related to SLE. Biomarkers such as erythrocyte sedimentation rate, C-reactive protein, C3 and C4 complement, and double-stranded DNA levels can be helpful in assessing lupus disease activity and differentiating a lupus-related complication from an unrelated event. Comparing these biomarkers to the patient’s baseline values can be informative; however, depending on the laboratory facilities, test results may not be available during an ED visit. Lastly, infections should be considered more strongly than usual in the differential diagnosis due to the immunocompromised status of a substantial proportion of these patients, by virtue of their disease or the cytotoxic medications used for treatment.

Musculoskeletal Complications

Common Complications

Polyarthralgias and Polymyalgias. More than 90% of SLE patients experience polyarthralgias and polymyalgias. Physical examination findings may be normal, even when joint pain is present, which is often due to mild synovitis. In some cases, Jaccoud arthropathy is seen, which presents as deformities such as swan neck deformities and ulnar deviations that are characteristically reducible on manipulation (Figures 1a and 1b). These deformities are not caused by direct joint damage, but by chronic tenosynovitis and the resulting laxity of tendons and ligaments.¹ Classically, plain radiographic imaging reveals nonerosive joint changes. Muscle and joint pains may worsen with disease progression or flare.

Avascular Necrosis. Avascular necrosis affects 5% to 12% of SLE patients.² Most commonly, this involves the femoral head, but it may also involve the femoral condyle or tibial plateau. Patients may present with acute or subacute onset of pain in the groin or buttocks when the femoral head is involved, or in the knee when the femoral condyle or tibial plateau is involved. Plain radiographs may reveal joint-space narrowing and other evidence of degenerative joint disease. Magnetic resonance imaging (MRI) is more sensitive in diagnosing avascular necrosis, and may be indicated when clinical suspicion is high despite negative plain radiographs, although this would not typically need to be performed urgently in the ED.² While analgesics and physical therapy may provide some pain relief to patients with avascular necrosis, this condition generally requires nonemergent operative intervention.

Emergent Complications

Septic Arthritis. When a patient with SLE presents with an isolated swollen joint, septic arthritis should be suspected, and diagnosis should be confirmed by arthrocentesis. Synovial fluid samples showing a white blood cell count greater than 50 × 10⁹/Lsuggest infection, which can be confirmed by gram stain and cultures.

For reasons that remain unclear, but may involve primary immune defects and the use of immunosuppressant medications, patients with SLE are predisposed to Salmonella joint infections. In one study, 59% of septic arthritis cases in patients with SLE were due to Salmonella species; therefore, treatment for septic arthritis in this population should include ceftriaxone in addition to vancomycin for typical organisms, such as Staphylococcus and Streptococcus species.³

Cutaneous Manifestations

Common Complications

Malar Rash. Eighty percent to 90% of patients with SLE have dermatological involvement,¹ the most common finding of which is the malar or butterfly facial rash, which appears as raised erythema over the bridge of the nose and cheeks while sparing the nasolabial folds (Figure 2).

Discoid Lupus. Chronic discoid lupus appears as a scarring rash often found on the face, ears, and scalp. These patients may also exhibit a photosensitive rash, which consists of an erythematous eruption if acute, or annular scaly lesions if subacute.

Oral and Nasal Ulcerations. Common mucous membrane findings include oral or nasal ulcers, which are typically painless.

Worsening of any of these skin findings may be associated with disease flare. Secondary bacterial infection of lupus rashes or ulcerations is uncommon, although cellulitis should be considered when a rash is unilateral, not in a sun-exposed area, or is otherwise different from the patient’s typical lupus rash. Sun avoidance and topical corticosteroids are the mainstays of treatment of dermatological disease in SLE.

Emergent Complications

Systemic Vasculitis. Patients with SLE are susceptible to vasculitis. Although isolated cutaneous vasculitis is not typically an emergent condition, it may portend systemic vasculitis. Any palpable purpura or other evidence of cutaneous vasculitis should prompt a careful review of systems and basic laboratory workup for systemic vasculitis, which can involve the kidneys, lungs, central or peripheral nervous system, or gastrointestinal tract.

Symptoms of systemic vasculitis may include fevers, chills, chest pain, cough, hemoptysis, abdominal pain, and changes in color or amount of urine. Laboratory workup should be tailored to symptoms, and may include basic metabolic panel, liver function tests, complete blood count, and urinalysis.⁴

Digital Gangrene. Patients with SLE may also develop digital gangrene related to severe Raynaud phenomenon, vasculitis, or thromboembolism. Pharmacological treatment with vasodilators such as sildenafil, endothelin receptor antagonists, or intravenous prostacyclins may be needed.⁵ To save the involved digit, vascular surgery services should be consulted urgently.⁶

Renal Complications

Common Complications

Chronic Kidney Disease. Chronic kidney disease (CKD) is common among SLE patients, especially among those with a history of lupus nephritis.⁷ Patients with CKD may have persistently elevated serum creatinine, chronic hypertension, and/or chronic peripheral edema. Patients presenting with new development of hypertension, peripheral edema, hematuria, or polyuria should be screened for lupus nephritis with urinalysis and serum creatinine. Elevated creatinine or new or worsening proteinuria or hematuria should prompt consultation with nephrology services.

Emergent Complications

Lupus Nephritis. About 50% of SLE patients will develop lupus nephritis during the course of their lives,¹ which may present as nephrotic disease with significant proteinuria, peripheral edema, and low serum albumin, or as nephritic disease, with increased serum creatinine and hematuria. Acute kidney injury in SLE patients should generally prompt admission for workup of reversible causes and evaluation for lupus nephritis, which often includes renal biopsy.⁸

Neuropsychiatric Complications

Common Complications

Neuropsychiatric lupus is a broad category that includes 19 manifestations of SLE in the central and peripheral nervous systems.⁹ Conditions range from depression or chronic headaches to seizures or psychosis.

Mood and Anxiety Disorders. Anxiety and depression have been observed in up to 75% of SLE patients.¹ Mood and anxiety disorders are likely influenced by the psychosocial elements of this chronic disease, as well as by direct effects of SLE on the brain.¹

Peripheral Neuropathy. Approximately 10% of SLE patients have a peripheral neuropathy, which generally presents as a mononeuritis (either single or multiplex), rather than the stocking-glove distribution seen in other systemic causes of neuropathy.¹⁰

Headache. Headache disorders may also develop in SLE patients, and tend to have similar patterns to primary headache disorders in the general population. In most cases, treatment for headache in SLE patients is similar to that of the general population.¹¹ However, if a patient presents with concerning findings, such as focal neurological deficit, meningismus, or fever, or if the headache is new-onset or different from previous headaches, further investigation should be considered, including a head computed tomography (CT) scan and lumbar puncture (LP).

Emergent Complications

In general, due to the variety of neurological emergencies that may present with SLE, and the subtlety with which true emergencies may present in this population, the threshold to obtain imaging on SLE patients with any new neurological complaints should be low.

Cerebrovascular Accidents. Patients with SLE are susceptible to cerebrovascular accidents (CVAs), typically from occlusive or embolic causes. Etiologies may include primary central nervous system (CNS) vasculitis, embolic disease from antiphospholipid syndrome (APS), or embolic disease from a Libman-Sacks endocarditis.¹²

Successful thrombolysis has been reported in SLE patients presenting with stroke, but it remains controversial due to risk of hemorrhagic conversion if CNS vasculitis, rather than embolism, is the cause.¹³ Proper imaging and consultation with a neurologist familiar with the disease is critical for early treatment decisions.

Seizures. Fifteen percent to 35% of SLE patients may develop seizures. These may be focal or generalized, but generalized tonic-clonic seizures tend to be more common in SLE patients.² Workup and management of seizures in SLE patients is the same as in the general population.

Sinus Thrombosis. Dural sinus thrombosis often presents as a new-onset headache, sometimes with focal neurological deficits. The diagnosis of dural sinus thrombosis can be challenging, as CT imaging studies may be falsely negative. There should be a low threshold for obtaining MRI/magnetic resonance angiography (MRA) in SLE patients presenting with a new-onset headache.¹⁴

CNS Vasculitis. Patients with SLE are also susceptible to CNS vasculitis, which can manifest as seizures, psychosis, cognitive decline, altered mental status, or coma. Magnetic resonance imaging/MRA studies may suggest the diagnosis, but if this is equivocal, angiography or even brain biopsy may be needed to make the diagnosis. Unless the patient’s symptoms are very mild (eg, mild cognitive decline), she or he should be admitted for diagnostic workup and consideration of aggressive immunosuppressive therapy.²

Transverse Myelitis and Spinal Artery Thrombosis. Acute loss of lower limb sensation or motor function in SLE patients may be caused by transverse myelitis or spinal artery thrombosis. Epidural abscess should also be considered, especially if the patient is immunocompromised.²

Infection. A CNS infection should be considered in any SLE patient presenting with new neurological complaints. Fever or meningismus, especially in conjunction with headache or focal neurological deficits, should prompt an LP and consideration for imaging. Immunocompromised patients are at increased risk for common organisms as well as atypical organisms, such as fungus or mycobacteria.¹⁵

Pulmonary Complications

Common Complications

Pleuritis. Many patients with SLE develop pleuritis, with or without effusion. This may be treated with nonsteroidal anti-inflammatory drugs, or corticosteroids if symptoms are more severe. Pleuritis is the most common respiratory complication of SLE, but due to the number of serious cardiopulmonary complications associated with SLE, pleuritis should be a diagnosis of exclusion.

Interstitial Lung Disease. Interstitial lung disease may be caused by SLE or may be medication-induced. This commonly presents as subacute or chronic dyspnea and/or cough. Patient workup may be done on an outpatient basis with high resolution chest CT and pulmonary function testing.

Pulmonary Hypertension. Patients with SLE may develop pulmonary hypertension, either directly due to SLE or from chronic thromboembolic disease. In general, pulmonary hypertension is managed as an outpatient, but may require emergent inpatient treatment if the condition is rapidly progressive or associated with right heart failure.

Shrinking Lung Syndrome. This condition may cause subacute or chronic dyspnea and pleuritic chest pain. Shrinking lung syndrome is caused by diaphragmatic dysfunction rather than from a primary disease of the lungs, and it is characterized by a restrictive pattern on pulmonary function testing and an elevated hemidiaphragm. Shrinking lung syndrome typically responds well to immunosuppressive therapy.¹⁶

Emergent Conditions

Pulmonary Embolism. A pulmonary embolism should be strongly considered in any patient with SLE presenting with the appropri ate clinical picture. Patients with APS are at particularly high risk for thromboembolic disease. However, even SLE patients without this APS are known to be at an increased risk of developing thromboembolism compared to the general public.¹⁷ Pulmonary embolism in SLE patients should be diagnosed and treated in the usual manner.

Pneumonia. Immunosuppressed patients are susceptible to opportunistic pulmonary infections as well as typical community pathogens. Fungal or mycobacterial infections may be suspected with a more subacute onset of symptoms.

Acute Lupus Pneumonitis. This serious condition may present with severe pneumonia-like signs and symptoms, including fever, cough, dyspnea, hypoxia, and infiltrates on chest radiograph (Figure 3).

Diffuse Alveolar Hemorrhage. A rare complication with a mortality rate of 50% to 90%, SLE patients who develop diffuse alveolar hemorrhage may present with fever, cough, dyspnea, and hypoxia.¹⁸ The condition may be suggested by infiltrates on chest radiograph, a drop in hemoglobin representing bleeding into the lungs, and/or hemoptysis. However, the absence of hemoptysis does not rule out diffuse alveolar hemorrhage, so clinical suspicion should remain high, even in the absence of this symptom.

Because emergent pulmonary conditions often present with similar symptoms, most patients with acute or new-onset symptoms will require admission for diagnostic workup (likely to include chest CT scan and/or bronchoscopy with bronchoalveolar lavage), as well as for close monitoring and initiation of treatment. If hypoxia or respiratory distress is severe, or if diffuse alveolar hemorrhage is suspected, admission to the intensive care unit (ICU) should be considered. We suggest that antibiotics be started in the ED when pneumonia is part of the differential diagnosis. As in the general population, coverage should be chosen based on the patient’s risk factors for antibiotic-resistant organisms. Initiation of corticosteroid therapy or other changes in immune therapy can be delayed until the EP consults with rheumatology and/or pulmonology services.

Cardiac Complications

Common Complications

Pericarditis. Pericarditis with or without pericardial effusion is very common in SLE patients and is usually related to lupus itself, rather than an infectious etiology. Patients may present with substernal, positional chest pain, tachycardia, and diffuse ST-segment elevation on electrocardiogram. Most effusions are small, asymptomatic, and discovered incidentally. However, among patients with symptomatic pericardial effusions, tamponade can be present in 21%.¹⁹ Corticosteroid therapy is often required to treat SLE-associated pericarditis, but colchicine is being explored as a possible steroid-sparing agent in this patient population.^20,21

Valvular Abnormalities. Approximately 60% of SLE patients have valvular abnormalities detectable by echocardiography. The most common abnormalities in one study were valvular thickening or regurgitation.²² Many of these abnormalities occurred in asymptomatic patients and never progressed to clinical disease in a 5-year follow-up. However, patients with any valvular abnormality were more likely to develop complications, including stroke, peripheral embolism, infective endocarditis, need for valve replacement, congestive heart failure, or death.²²

Emergent Complications

Acute Coronary Syndrome. Even in relatively young patients, acute coronary syndrome (ACS) should be considered in SLE patients presenting with chest pain, as this patient population has a 10-fold higher risk of developing coronary artery disease (CAD) than the general population, and SLE patients with CAD often lack traditional risk factors, such as advanced age, family history, or metabolic syndrome.¹

A high clinical suspicion should be maintained even in patients who would traditionally be considered low-risk. The EP should have a low-threshold for ECG, cardiac biomarker testing, and stress testing for SLE patients presenting with chest pain. The treatment of ACS in SLE patients is the same as in the general population.

Libman-Sacks Endocarditis. A sterile, fibrinous valvular vegetation, Libman-Sacks endocarditis is unique to patients with SLE. When present, patients usually develop a subacute or chronic onset of dyspnea or chest pain. However, patients may become acutely ill if they develop severe valvular regurgitation. Additionally, the valve damage from Libman-Sacks endocarditis can predispose patients to developing infective endocarditis.²⁰

Hematological Complications

Common Complications

Patients with SLE commonly have mild-to-moderate leukopenia (especially lymphopenia), anemia, and thrombocytopenia. This may be related to the disease process or may be secondary to prescribed medications. A comparison to recent baseline laboratory studies should be sought if there is suspicion for new or worsening cytopenia.

Antiphospholipid Syndrome. Nearly 40% of SLE patients also have APS, which is defined by a clinical history of thrombosis in conjunction with one of the antiphospholipid antibodies (anticardiolipin, anti-beta-2-glycoprotein, lupus anticoagulant). Antiphospholipid syndrome causes both venous and arterial thrombosis and may be associated with recurrent miscarriage. Acute thrombotic events should be treated with heparin or enoxaparin and transitioned to warfarin. The new generation of direct oral anticoagulants have not been well studied in APS, though, multiple small case series suggest a higher thrombotic risk with these drugs than with warfarin.²³Patients who have recurrent venous thromboembolism, or who have any arterial thromboembolism should be on lifelong anticoagulation therapy.²

Emergent Complications

Thrombocytopenia. Severe thrombocytopenia or hemolytic anemia can be life-threatening, and often requires inpatient admission for immunosuppressive therapy, monitoring, and supportive care.

Catastrophic Antiphospholipid Syndrome. This condition should be suspected in patients with SLE who present with multiple sites of thrombosis or new multi-organ damage. Catastrophic APS (CAPS) may occur in SLE patients who have no prior history of APS. Since the mortality rate for CAPS approaches 50%, these patients require anticoagulation, immunosuppressant therapy (high-dose corticosteroids, cyclophosphamide, and/or plasma exchange), and admission to the ICU.²⁴

Gastrointestinal Complications

Common Complications

Intestinal Pseudo-obstruction. Dysphagia related to esophageal dysmotility is present in up to 13% of SLE patients.²⁵ Intestinal pseudo-obstruction may be seen in SLE patients, and is characterized by symptoms of intestinal obstruction caused by decreased intestinal motility, rather than from mechanical obstruction. Presenting symptoms may be acute or chronic, and include nausea, vomiting, and abdominal distension. Abdominal CT studies will show dilated bowel loops without evidence of mechanical obstruction. Manometry reveals widespread hypomotility. Intestinal pseudo-obstruction typically responds well to corticosteroids and other immunosuppressant therapies.²⁶

Emergent Conditions

Acute Abdominal Pain. Approximately half of SLE patients who present to the ED with acute abdominal pain are found to have either mesenteric vasculitis or pancreatitis, both of which are thought to be related to SLE disease activity.²⁷ Other causes of acute abdominal pain that are common in the general population remain common in SLE patients, including gallbladder disease, gastroenteritis, appendicitis, and peptic ulcer disease.

Mesenteric Vasculitis. Also known as lupus enteritis, mesenteric vasculitis is a unique cause of acute abdominal pain in SLE patients. The condition presents with acute, diffuse abdominal pain and may be associated with nausea and vomiting, diarrhea, or hematochezia. Abdominal CT findings suggestive of diffuse enteritis support the diagnosis. Medical management with pulse-dose corticosteroids and supportive care is generally sufficient, but if bowel necrosis or intestinal perforation is present or suspected, surgical consultation should be obtained immediately.¹⁵

Conclusion

Complications of SLE are diverse and may be difficult to diagnose. Understanding the common and emergent complications of SLE will help the EP to recognize severe illness and make appropriate treatment decisions in this complex patient population.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the chronic activation of the immune system, leading to the formation of autoantibodies and multi-organ damage. The prevalence of SLE in the United States is 20 to 150 per 100,000 persons.¹ Ninety percent of patients with SLE are women, and the condition is more common and often more severe among patients of black African or of Asian descent.

General Acute-Care Management

While a patient’s presentation could be secondary to a lupus-related complication, consideration must always be given to common conditions that are not related to SLE. Biomarkers such as erythrocyte sedimentation rate, C-reactive protein, C3 and C4 complement, and double-stranded DNA levels can be helpful in assessing lupus disease activity and differentiating a lupus-related complication from an unrelated event. Comparing these biomarkers to the patient’s baseline values can be informative; however, depending on the laboratory facilities, test results may not be available during an ED visit. Lastly, infections should be considered more strongly than usual in the differential diagnosis due to the immunocompromised status of a substantial proportion of these patients, by virtue of their disease or the cytotoxic medications used for treatment.

Musculoskeletal Complications

Common Complications

Polyarthralgias and Polymyalgias. More than 90% of SLE patients experience polyarthralgias and polymyalgias. Physical examination findings may be normal, even when joint pain is present, which is often due to mild synovitis. In some cases, Jaccoud arthropathy is seen, which presents as deformities such as swan neck deformities and ulnar deviations that are characteristically reducible on manipulation (Figures 1a and 1b). These deformities are not caused by direct joint damage, but by chronic tenosynovitis and the resulting laxity of tendons and ligaments.¹ Classically, plain radiographic imaging reveals nonerosive joint changes. Muscle and joint pains may worsen with disease progression or flare.

Avascular Necrosis. Avascular necrosis affects 5% to 12% of SLE patients.² Most commonly, this involves the femoral head, but it may also involve the femoral condyle or tibial plateau. Patients may present with acute or subacute onset of pain in the groin or buttocks when the femoral head is involved, or in the knee when the femoral condyle or tibial plateau is involved. Plain radiographs may reveal joint-space narrowing and other evidence of degenerative joint disease. Magnetic resonance imaging (MRI) is more sensitive in diagnosing avascular necrosis, and may be indicated when clinical suspicion is high despite negative plain radiographs, although this would not typically need to be performed urgently in the ED.² While analgesics and physical therapy may provide some pain relief to patients with avascular necrosis, this condition generally requires nonemergent operative intervention.

Emergent Complications

Septic Arthritis. When a patient with SLE presents with an isolated swollen joint, septic arthritis should be suspected, and diagnosis should be confirmed by arthrocentesis. Synovial fluid samples showing a white blood cell count greater than 50 × 10⁹/Lsuggest infection, which can be confirmed by gram stain and cultures.

For reasons that remain unclear, but may involve primary immune defects and the use of immunosuppressant medications, patients with SLE are predisposed to Salmonella joint infections. In one study, 59% of septic arthritis cases in patients with SLE were due to Salmonella species; therefore, treatment for septic arthritis in this population should include ceftriaxone in addition to vancomycin for typical organisms, such as Staphylococcus and Streptococcus species.³

Cutaneous Manifestations

Common Complications

Malar Rash. Eighty percent to 90% of patients with SLE have dermatological involvement,¹ the most common finding of which is the malar or butterfly facial rash, which appears as raised erythema over the bridge of the nose and cheeks while sparing the nasolabial folds (Figure 2).

Discoid Lupus. Chronic discoid lupus appears as a scarring rash often found on the face, ears, and scalp. These patients may also exhibit a photosensitive rash, which consists of an erythematous eruption if acute, or annular scaly lesions if subacute.

Oral and Nasal Ulcerations. Common mucous membrane findings include oral or nasal ulcers, which are typically painless.

Worsening of any of these skin findings may be associated with disease flare. Secondary bacterial infection of lupus rashes or ulcerations is uncommon, although cellulitis should be considered when a rash is unilateral, not in a sun-exposed area, or is otherwise different from the patient’s typical lupus rash. Sun avoidance and topical corticosteroids are the mainstays of treatment of dermatological disease in SLE.

Emergent Complications

Systemic Vasculitis. Patients with SLE are susceptible to vasculitis. Although isolated cutaneous vasculitis is not typically an emergent condition, it may portend systemic vasculitis. Any palpable purpura or other evidence of cutaneous vasculitis should prompt a careful review of systems and basic laboratory workup for systemic vasculitis, which can involve the kidneys, lungs, central or peripheral nervous system, or gastrointestinal tract.

Symptoms of systemic vasculitis may include fevers, chills, chest pain, cough, hemoptysis, abdominal pain, and changes in color or amount of urine. Laboratory workup should be tailored to symptoms, and may include basic metabolic panel, liver function tests, complete blood count, and urinalysis.⁴

Digital Gangrene. Patients with SLE may also develop digital gangrene related to severe Raynaud phenomenon, vasculitis, or thromboembolism. Pharmacological treatment with vasodilators such as sildenafil, endothelin receptor antagonists, or intravenous prostacyclins may be needed.⁵ To save the involved digit, vascular surgery services should be consulted urgently.⁶

Renal Complications

Common Complications

Chronic Kidney Disease. Chronic kidney disease (CKD) is common among SLE patients, especially among those with a history of lupus nephritis.⁷ Patients with CKD may have persistently elevated serum creatinine, chronic hypertension, and/or chronic peripheral edema. Patients presenting with new development of hypertension, peripheral edema, hematuria, or polyuria should be screened for lupus nephritis with urinalysis and serum creatinine. Elevated creatinine or new or worsening proteinuria or hematuria should prompt consultation with nephrology services.

Emergent Complications

Lupus Nephritis. About 50% of SLE patients will develop lupus nephritis during the course of their lives,¹ which may present as nephrotic disease with significant proteinuria, peripheral edema, and low serum albumin, or as nephritic disease, with increased serum creatinine and hematuria. Acute kidney injury in SLE patients should generally prompt admission for workup of reversible causes and evaluation for lupus nephritis, which often includes renal biopsy.⁸

Neuropsychiatric Complications

Common Complications

Neuropsychiatric lupus is a broad category that includes 19 manifestations of SLE in the central and peripheral nervous systems.⁹ Conditions range from depression or chronic headaches to seizures or psychosis.

Mood and Anxiety Disorders. Anxiety and depression have been observed in up to 75% of SLE patients.¹ Mood and anxiety disorders are likely influenced by the psychosocial elements of this chronic disease, as well as by direct effects of SLE on the brain.¹

Peripheral Neuropathy. Approximately 10% of SLE patients have a peripheral neuropathy, which generally presents as a mononeuritis (either single or multiplex), rather than the stocking-glove distribution seen in other systemic causes of neuropathy.¹⁰

Headache. Headache disorders may also develop in SLE patients, and tend to have similar patterns to primary headache disorders in the general population. In most cases, treatment for headache in SLE patients is similar to that of the general population.¹¹ However, if a patient presents with concerning findings, such as focal neurological deficit, meningismus, or fever, or if the headache is new-onset or different from previous headaches, further investigation should be considered, including a head computed tomography (CT) scan and lumbar puncture (LP).

Emergent Complications

In general, due to the variety of neurological emergencies that may present with SLE, and the subtlety with which true emergencies may present in this population, the threshold to obtain imaging on SLE patients with any new neurological complaints should be low.

Cerebrovascular Accidents. Patients with SLE are susceptible to cerebrovascular accidents (CVAs), typically from occlusive or embolic causes. Etiologies may include primary central nervous system (CNS) vasculitis, embolic disease from antiphospholipid syndrome (APS), or embolic disease from a Libman-Sacks endocarditis.¹²

Successful thrombolysis has been reported in SLE patients presenting with stroke, but it remains controversial due to risk of hemorrhagic conversion if CNS vasculitis, rather than embolism, is the cause.¹³ Proper imaging and consultation with a neurologist familiar with the disease is critical for early treatment decisions.

Seizures. Fifteen percent to 35% of SLE patients may develop seizures. These may be focal or generalized, but generalized tonic-clonic seizures tend to be more common in SLE patients.² Workup and management of seizures in SLE patients is the same as in the general population.

Sinus Thrombosis. Dural sinus thrombosis often presents as a new-onset headache, sometimes with focal neurological deficits. The diagnosis of dural sinus thrombosis can be challenging, as CT imaging studies may be falsely negative. There should be a low threshold for obtaining MRI/magnetic resonance angiography (MRA) in SLE patients presenting with a new-onset headache.¹⁴

CNS Vasculitis. Patients with SLE are also susceptible to CNS vasculitis, which can manifest as seizures, psychosis, cognitive decline, altered mental status, or coma. Magnetic resonance imaging/MRA studies may suggest the diagnosis, but if this is equivocal, angiography or even brain biopsy may be needed to make the diagnosis. Unless the patient’s symptoms are very mild (eg, mild cognitive decline), she or he should be admitted for diagnostic workup and consideration of aggressive immunosuppressive therapy.²

Transverse Myelitis and Spinal Artery Thrombosis. Acute loss of lower limb sensation or motor function in SLE patients may be caused by transverse myelitis or spinal artery thrombosis. Epidural abscess should also be considered, especially if the patient is immunocompromised.²

Infection. A CNS infection should be considered in any SLE patient presenting with new neurological complaints. Fever or meningismus, especially in conjunction with headache or focal neurological deficits, should prompt an LP and consideration for imaging. Immunocompromised patients are at increased risk for common organisms as well as atypical organisms, such as fungus or mycobacteria.¹⁵

Pulmonary Complications

Common Complications

Pleuritis. Many patients with SLE develop pleuritis, with or without effusion. This may be treated with nonsteroidal anti-inflammatory drugs, or corticosteroids if symptoms are more severe. Pleuritis is the most common respiratory complication of SLE, but due to the number of serious cardiopulmonary complications associated with SLE, pleuritis should be a diagnosis of exclusion.

Interstitial Lung Disease. Interstitial lung disease may be caused by SLE or may be medication-induced. This commonly presents as subacute or chronic dyspnea and/or cough. Patient workup may be done on an outpatient basis with high resolution chest CT and pulmonary function testing.

Pulmonary Hypertension. Patients with SLE may develop pulmonary hypertension, either directly due to SLE or from chronic thromboembolic disease. In general, pulmonary hypertension is managed as an outpatient, but may require emergent inpatient treatment if the condition is rapidly progressive or associated with right heart failure.

Shrinking Lung Syndrome. This condition may cause subacute or chronic dyspnea and pleuritic chest pain. Shrinking lung syndrome is caused by diaphragmatic dysfunction rather than from a primary disease of the lungs, and it is characterized by a restrictive pattern on pulmonary function testing and an elevated hemidiaphragm. Shrinking lung syndrome typically responds well to immunosuppressive therapy.¹⁶

Emergent Conditions

Pulmonary Embolism. A pulmonary embolism should be strongly considered in any patient with SLE presenting with the appropri ate clinical picture. Patients with APS are at particularly high risk for thromboembolic disease. However, even SLE patients without this APS are known to be at an increased risk of developing thromboembolism compared to the general public.¹⁷ Pulmonary embolism in SLE patients should be diagnosed and treated in the usual manner.

Pneumonia. Immunosuppressed patients are susceptible to opportunistic pulmonary infections as well as typical community pathogens. Fungal or mycobacterial infections may be suspected with a more subacute onset of symptoms.

Acute Lupus Pneumonitis. This serious condition may present with severe pneumonia-like signs and symptoms, including fever, cough, dyspnea, hypoxia, and infiltrates on chest radiograph (Figure 3).

Diffuse Alveolar Hemorrhage. A rare complication with a mortality rate of 50% to 90%, SLE patients who develop diffuse alveolar hemorrhage may present with fever, cough, dyspnea, and hypoxia.¹⁸ The condition may be suggested by infiltrates on chest radiograph, a drop in hemoglobin representing bleeding into the lungs, and/or hemoptysis. However, the absence of hemoptysis does not rule out diffuse alveolar hemorrhage, so clinical suspicion should remain high, even in the absence of this symptom.

Because emergent pulmonary conditions often present with similar symptoms, most patients with acute or new-onset symptoms will require admission for diagnostic workup (likely to include chest CT scan and/or bronchoscopy with bronchoalveolar lavage), as well as for close monitoring and initiation of treatment. If hypoxia or respiratory distress is severe, or if diffuse alveolar hemorrhage is suspected, admission to the intensive care unit (ICU) should be considered. We suggest that antibiotics be started in the ED when pneumonia is part of the differential diagnosis. As in the general population, coverage should be chosen based on the patient’s risk factors for antibiotic-resistant organisms. Initiation of corticosteroid therapy or other changes in immune therapy can be delayed until the EP consults with rheumatology and/or pulmonology services.

Cardiac Complications

Common Complications

Pericarditis. Pericarditis with or without pericardial effusion is very common in SLE patients and is usually related to lupus itself, rather than an infectious etiology. Patients may present with substernal, positional chest pain, tachycardia, and diffuse ST-segment elevation on electrocardiogram. Most effusions are small, asymptomatic, and discovered incidentally. However, among patients with symptomatic pericardial effusions, tamponade can be present in 21%.¹⁹ Corticosteroid therapy is often required to treat SLE-associated pericarditis, but colchicine is being explored as a possible steroid-sparing agent in this patient population.^20,21

Valvular Abnormalities. Approximately 60% of SLE patients have valvular abnormalities detectable by echocardiography. The most common abnormalities in one study were valvular thickening or regurgitation.²² Many of these abnormalities occurred in asymptomatic patients and never progressed to clinical disease in a 5-year follow-up. However, patients with any valvular abnormality were more likely to develop complications, including stroke, peripheral embolism, infective endocarditis, need for valve replacement, congestive heart failure, or death.²²

Emergent Complications

Acute Coronary Syndrome. Even in relatively young patients, acute coronary syndrome (ACS) should be considered in SLE patients presenting with chest pain, as this patient population has a 10-fold higher risk of developing coronary artery disease (CAD) than the general population, and SLE patients with CAD often lack traditional risk factors, such as advanced age, family history, or metabolic syndrome.¹

A high clinical suspicion should be maintained even in patients who would traditionally be considered low-risk. The EP should have a low-threshold for ECG, cardiac biomarker testing, and stress testing for SLE patients presenting with chest pain. The treatment of ACS in SLE patients is the same as in the general population.

Libman-Sacks Endocarditis. A sterile, fibrinous valvular vegetation, Libman-Sacks endocarditis is unique to patients with SLE. When present, patients usually develop a subacute or chronic onset of dyspnea or chest pain. However, patients may become acutely ill if they develop severe valvular regurgitation. Additionally, the valve damage from Libman-Sacks endocarditis can predispose patients to developing infective endocarditis.²⁰

Hematological Complications

Common Complications

Patients with SLE commonly have mild-to-moderate leukopenia (especially lymphopenia), anemia, and thrombocytopenia. This may be related to the disease process or may be secondary to prescribed medications. A comparison to recent baseline laboratory studies should be sought if there is suspicion for new or worsening cytopenia.

Antiphospholipid Syndrome. Nearly 40% of SLE patients also have APS, which is defined by a clinical history of thrombosis in conjunction with one of the antiphospholipid antibodies (anticardiolipin, anti-beta-2-glycoprotein, lupus anticoagulant). Antiphospholipid syndrome causes both venous and arterial thrombosis and may be associated with recurrent miscarriage. Acute thrombotic events should be treated with heparin or enoxaparin and transitioned to warfarin. The new generation of direct oral anticoagulants have not been well studied in APS, though, multiple small case series suggest a higher thrombotic risk with these drugs than with warfarin.²³Patients who have recurrent venous thromboembolism, or who have any arterial thromboembolism should be on lifelong anticoagulation therapy.²

Emergent Complications

Thrombocytopenia. Severe thrombocytopenia or hemolytic anemia can be life-threatening, and often requires inpatient admission for immunosuppressive therapy, monitoring, and supportive care.

Catastrophic Antiphospholipid Syndrome. This condition should be suspected in patients with SLE who present with multiple sites of thrombosis or new multi-organ damage. Catastrophic APS (CAPS) may occur in SLE patients who have no prior history of APS. Since the mortality rate for CAPS approaches 50%, these patients require anticoagulation, immunosuppressant therapy (high-dose corticosteroids, cyclophosphamide, and/or plasma exchange), and admission to the ICU.²⁴

Gastrointestinal Complications

Common Complications

Intestinal Pseudo-obstruction. Dysphagia related to esophageal dysmotility is present in up to 13% of SLE patients.²⁵ Intestinal pseudo-obstruction may be seen in SLE patients, and is characterized by symptoms of intestinal obstruction caused by decreased intestinal motility, rather than from mechanical obstruction. Presenting symptoms may be acute or chronic, and include nausea, vomiting, and abdominal distension. Abdominal CT studies will show dilated bowel loops without evidence of mechanical obstruction. Manometry reveals widespread hypomotility. Intestinal pseudo-obstruction typically responds well to corticosteroids and other immunosuppressant therapies.²⁶

Emergent Conditions

Acute Abdominal Pain. Approximately half of SLE patients who present to the ED with acute abdominal pain are found to have either mesenteric vasculitis or pancreatitis, both of which are thought to be related to SLE disease activity.²⁷ Other causes of acute abdominal pain that are common in the general population remain common in SLE patients, including gallbladder disease, gastroenteritis, appendicitis, and peptic ulcer disease.

Mesenteric Vasculitis. Also known as lupus enteritis, mesenteric vasculitis is a unique cause of acute abdominal pain in SLE patients. The condition presents with acute, diffuse abdominal pain and may be associated with nausea and vomiting, diarrhea, or hematochezia. Abdominal CT findings suggestive of diffuse enteritis support the diagnosis. Medical management with pulse-dose corticosteroids and supportive care is generally sufficient, but if bowel necrosis or intestinal perforation is present or suspected, surgical consultation should be obtained immediately.¹⁵

Conclusion

Complications of SLE are diverse and may be difficult to diagnose. Understanding the common and emergent complications of SLE will help the EP to recognize severe illness and make appropriate treatment decisions in this complex patient population.

“Enhanced Recovery After Surgery” (ERAS) practices and protocols have been increasingly refined and adopted for the field of gynecology, and there is hope among gynecologic surgeons – and some recent evidence – that, with the ERAS movement, we are improving patient recoveries and outcomes and minimizing the need for opioids.

This applies not only to open surgeries but also to the minimally invasive procedures that already are prized for significant reductions in morbidity and length of stay. The overarching and guiding principle of ERAS is that any surgery – whether open or minimally invasive, major or minor – places stress on the body and is associated with risks and morbidity.

Improved Outcomes

The ERAS mindset notably intersected gynecology with the publication in 2016 of a two-part series of guidelines for gynecology/oncology surgery from the ERAS Society. The 8-year-old society has its roots in a study group of European surgeons and others who decided to examine surgical practices and the concept of multimodal surgical care put forth in the 1990s by Henrik Kehlet, MD, PhD, then a professor at the University of Copenhagen.

The first set of recommendations addressed pre- and intraoperative care (Gynecol Oncol. 2016 Feb;140[2]:313-22), and the second set addressed postoperative care (Gynecol Oncol. 2016 Feb;140[2]:323-32). Similar evidence-based recommendations were previously written for colonic resections, rectal and pelvic surgery, and other surgical specialties.

Most of the published outcomes of enhanced recovery protocols come from colorectal surgery. As noted in the ERAS Society gynecology/oncology guidelines, the benefits include an average reduction in length of stay of 2.5 days and a decrease in complications by as much as 50%.

There is growing evidence, however, that ERAS programs are also beneficial for patients undergoing laparoscopic surgery, and outcomes from gynecology – including minimally invasive surgery – are also being reported.

For instance, a retrospective case-control study of 55 consecutive gynecologic oncology patients treated at the University of California, San Francisco, with laparoscopic or robotic surgery and an enhanced recovery pathway – and 110 historical control patients matched on the basis of age and surgery type – found significant improvements in recovery time, decreased pain despite reduced opioid use, and overall lower hospital costs (Obstet Gynecol. 2016 Jul;128[1]:138-44).

The enhanced recovery pathway included patient education, multimodal antiemetics, multimodal analgesia, and balanced fluid administration. Early catheter removal, ambulation, and feeding were also components. Analgesia included routine preoperative gabapentin, diclofenac, and acetaminophen; routine postoperative gabapentin, NSAIDs, and acetaminophen; and transversus abdominis plane blocks in 32 of the ERAS patients.

ERAS patients were significantly more likely to be discharged on day 1 (91%, compared with 60% in the control group). Opioid use decreased by 30%, and pain scores on postoperative day 1 were significantly lower.

Another study looking at the effect of enhanced recovery implementation in gynecologic surgeries at the University of Virginia, Charlottesville, (gynecologic oncology, urogynecology, and general gynecology) similarly reported benefits for vaginal and minimally invasive procedures, as well as for open procedures (Obstet Gynecol. 2016 Sep;128[3]:457-66).

In the minimally invasive group, investigators compared 324 patients before ERAS implementation with 249 patients afterward and found that the median length of stay was unchanged (1 day). However, intraoperative and postoperative opioid consumption decreased significantly and – even though actual pain scores improved only slightly – patient satisfaction scores improved markedly among post-ERAS patients. Patients gave higher marks, for instance, to questions regarding pain control (“how well your pain was controlled”) and teamwork (“staff worked together to care for you”).

Reducing Opioids

New opioid use that persists after a surgical procedure is a postsurgical complication that we all should be working to prevent. It has been estimated that 6% of surgical patients – even those who’ve had relatively minor surgical procedures – will become long-term opioid users, developing a dependence on the drugs prescribed to them for postsurgical pain.

This was shown last year in a national study of insurance claims data from between 2013 and 2014; investigators identified adults without opioid use in the year prior to surgery (including hysterectomy) and found that 5.9%-6.5% were filling opioid prescriptions 90-180 days after their surgical procedure. The incidence in a nonoperative control cohort was 0.4% (JAMA Surg. 2017 Jun 21;152[6]:e170504). Notably, this prolonged use was greatest in patients with prior pain conditions, substance abuse, and mental health disorders – a finding that may have implications for the counseling we provide prior to surgery.

It’s not clear what the optimal analgesic regimen is for minimally invasive or other gynecologic surgeries. What is clearly recommended, however, is that the approach be multifaceted. In our practice, we believe that the preoperative use of acetaminophen, pregabalin, and celecoxib plays an important role in reducing postoperative pain and opioid use. But we also have striven to create a practice-wide culture shift (throughout the operating and recovery rooms), for instance, that encourages using the least amounts of narcotics possible and using the shortest-acting formulations possible.

Transversus abdominis plane (TAP) blocks are also often part of ERAS protocols; they have been shown in at least two randomized controlled trials of abdominal hysterectomy to reduce intraoperative fentanyl requirements and to reduce immediate postoperative pain scores and postoperative morphine requirements (Anesth Analg. 2008 Dec;107[6]:2056-60; J Anaesthesiol Clin Pharmacol. 2014 Jul-Sep;30[3]:391-6).

More recently, liposomal bupivacaine, which is slowly released over several days, has gained traction as a substitute for standard bupivacaine and other agents in TAP blocks. In one recent retrospective study, abdominal incision infiltration with liposomal bupivacaine was associated with less opioid use (with no change in pain scores), compared with bupivacaine hydrochloride after laparotomy for gynecologic malignancies (Obstet Gynecol. 2016 Nov;128[5]:1009-17). It’s significantly more expensive, however, making it likely that the formulation is being used more judiciously in minimally invasive gynecologic surgery than in open surgeries.

Because of costs, we currently are restricted to using liposomal bupivacaine in our robotic surgeries only. In our practice, the single 20 mL vial (266 mg of liposomal bupivacaine) is diluted with 20 mL of normal saline, but it can be further diluted without loss of efficacy. With a 16-gauge needle, the liposomal bupivacaine is distributed across the incisions (usually 20 mL in the umbilicus with a larger incision and 10 mL in each of the two lateral incisions). Patients are counseled that they may have more discomfort after 3 days, but by this point most are mobile and feeling relatively well with a combination of NSAIDs and acetaminophen.

With growing visibility of the problem of narcotic dependence in the United States, patients seem increasingly receptive and even eager to limit or avoid the use of opioids. Patients should be counseled that minimizing or avoiding opioids may also speed recovery. Narcotics cause gut motility to slow down, which may hinder mobilization. Early mobilization (within 24 hours) is among the enhanced recovery elements that the ERAS Society guidelines say is “of particular value” for minimally invasive surgery, along with maintenance of normothermia and normovolemia with maintenance of adequate cardiac output.
 

Selecting Steps

Our practice is also trying to reduce preoperative bowel preparation and preoperative fasting, both of which have been found to be stressful for the body without evidence of benefit. These practices can lead to insulin resistance and hyperglycemia, which are associated with increased morbidity and length of stay.

It is now recommended that clear fluids be allowed up to 2 hours before surgery and solids up to 6 hours before. Some health systems and practices also recommend presurgical carbohydrate loading (for example, 10 ounces of apple juice 2 hours before surgery) – another small change on the ERAS menu – to further reduce postoperative insulin resistance and help the body cope with its stress response to surgery.

Along with nutritional changes are also various measures aimed at optimizing the body’s functionality before surgery (“prehabilitation”), from walking 30 minutes a day to abstaining from alcohol for patients who drink heavily.

Throughout the country, enhanced recovery protocols are taking shape in gynecologic surgery. ERAS was featured in an aptly titled panel session at the 2017 annual meeting of the American Association of Gynecologic Laparoscopists: “Outpatient Hysterectomy, ERAS, and Same-Day Discharge: The Next Big Thing in Gyn Surgery.” Others are applying ERAS to scheduled cesarean sections. And in our practice, I believe that if we continue making small changes, we will reach our goal of opioid-free recoveries and a better surgical experience for our patients.
 

Kirsten Sasaki, MD, is an associate of the Advanced Gynecologic Surgery Institute. She reported that she has no disclosures relevant to this Master Class.

“Enhanced Recovery After Surgery” (ERAS) practices and protocols have been increasingly refined and adopted for the field of gynecology, and there is hope among gynecologic surgeons – and some recent evidence – that, with the ERAS movement, we are improving patient recoveries and outcomes and minimizing the need for opioids.

This applies not only to open surgeries but also to the minimally invasive procedures that already are prized for significant reductions in morbidity and length of stay. The overarching and guiding principle of ERAS is that any surgery – whether open or minimally invasive, major or minor – places stress on the body and is associated with risks and morbidity.

Improved Outcomes

The ERAS mindset notably intersected gynecology with the publication in 2016 of a two-part series of guidelines for gynecology/oncology surgery from the ERAS Society. The 8-year-old society has its roots in a study group of European surgeons and others who decided to examine surgical practices and the concept of multimodal surgical care put forth in the 1990s by Henrik Kehlet, MD, PhD, then a professor at the University of Copenhagen.

The first set of recommendations addressed pre- and intraoperative care (Gynecol Oncol. 2016 Feb;140[2]:313-22), and the second set addressed postoperative care (Gynecol Oncol. 2016 Feb;140[2]:323-32). Similar evidence-based recommendations were previously written for colonic resections, rectal and pelvic surgery, and other surgical specialties.

Most of the published outcomes of enhanced recovery protocols come from colorectal surgery. As noted in the ERAS Society gynecology/oncology guidelines, the benefits include an average reduction in length of stay of 2.5 days and a decrease in complications by as much as 50%.

There is growing evidence, however, that ERAS programs are also beneficial for patients undergoing laparoscopic surgery, and outcomes from gynecology – including minimally invasive surgery – are also being reported.

For instance, a retrospective case-control study of 55 consecutive gynecologic oncology patients treated at the University of California, San Francisco, with laparoscopic or robotic surgery and an enhanced recovery pathway – and 110 historical control patients matched on the basis of age and surgery type – found significant improvements in recovery time, decreased pain despite reduced opioid use, and overall lower hospital costs (Obstet Gynecol. 2016 Jul;128[1]:138-44).

The enhanced recovery pathway included patient education, multimodal antiemetics, multimodal analgesia, and balanced fluid administration. Early catheter removal, ambulation, and feeding were also components. Analgesia included routine preoperative gabapentin, diclofenac, and acetaminophen; routine postoperative gabapentin, NSAIDs, and acetaminophen; and transversus abdominis plane blocks in 32 of the ERAS patients.

ERAS patients were significantly more likely to be discharged on day 1 (91%, compared with 60% in the control group). Opioid use decreased by 30%, and pain scores on postoperative day 1 were significantly lower.

Another study looking at the effect of enhanced recovery implementation in gynecologic surgeries at the University of Virginia, Charlottesville, (gynecologic oncology, urogynecology, and general gynecology) similarly reported benefits for vaginal and minimally invasive procedures, as well as for open procedures (Obstet Gynecol. 2016 Sep;128[3]:457-66).

In the minimally invasive group, investigators compared 324 patients before ERAS implementation with 249 patients afterward and found that the median length of stay was unchanged (1 day). However, intraoperative and postoperative opioid consumption decreased significantly and – even though actual pain scores improved only slightly – patient satisfaction scores improved markedly among post-ERAS patients. Patients gave higher marks, for instance, to questions regarding pain control (“how well your pain was controlled”) and teamwork (“staff worked together to care for you”).

Reducing Opioids

New opioid use that persists after a surgical procedure is a postsurgical complication that we all should be working to prevent. It has been estimated that 6% of surgical patients – even those who’ve had relatively minor surgical procedures – will become long-term opioid users, developing a dependence on the drugs prescribed to them for postsurgical pain.

This was shown last year in a national study of insurance claims data from between 2013 and 2014; investigators identified adults without opioid use in the year prior to surgery (including hysterectomy) and found that 5.9%-6.5% were filling opioid prescriptions 90-180 days after their surgical procedure. The incidence in a nonoperative control cohort was 0.4% (JAMA Surg. 2017 Jun 21;152[6]:e170504). Notably, this prolonged use was greatest in patients with prior pain conditions, substance abuse, and mental health disorders – a finding that may have implications for the counseling we provide prior to surgery.

It’s not clear what the optimal analgesic regimen is for minimally invasive or other gynecologic surgeries. What is clearly recommended, however, is that the approach be multifaceted. In our practice, we believe that the preoperative use of acetaminophen, pregabalin, and celecoxib plays an important role in reducing postoperative pain and opioid use. But we also have striven to create a practice-wide culture shift (throughout the operating and recovery rooms), for instance, that encourages using the least amounts of narcotics possible and using the shortest-acting formulations possible.

Transversus abdominis plane (TAP) blocks are also often part of ERAS protocols; they have been shown in at least two randomized controlled trials of abdominal hysterectomy to reduce intraoperative fentanyl requirements and to reduce immediate postoperative pain scores and postoperative morphine requirements (Anesth Analg. 2008 Dec;107[6]:2056-60; J Anaesthesiol Clin Pharmacol. 2014 Jul-Sep;30[3]:391-6).

More recently, liposomal bupivacaine, which is slowly released over several days, has gained traction as a substitute for standard bupivacaine and other agents in TAP blocks. In one recent retrospective study, abdominal incision infiltration with liposomal bupivacaine was associated with less opioid use (with no change in pain scores), compared with bupivacaine hydrochloride after laparotomy for gynecologic malignancies (Obstet Gynecol. 2016 Nov;128[5]:1009-17). It’s significantly more expensive, however, making it likely that the formulation is being used more judiciously in minimally invasive gynecologic surgery than in open surgeries.

Because of costs, we currently are restricted to using liposomal bupivacaine in our robotic surgeries only. In our practice, the single 20 mL vial (266 mg of liposomal bupivacaine) is diluted with 20 mL of normal saline, but it can be further diluted without loss of efficacy. With a 16-gauge needle, the liposomal bupivacaine is distributed across the incisions (usually 20 mL in the umbilicus with a larger incision and 10 mL in each of the two lateral incisions). Patients are counseled that they may have more discomfort after 3 days, but by this point most are mobile and feeling relatively well with a combination of NSAIDs and acetaminophen.

With growing visibility of the problem of narcotic dependence in the United States, patients seem increasingly receptive and even eager to limit or avoid the use of opioids. Patients should be counseled that minimizing or avoiding opioids may also speed recovery. Narcotics cause gut motility to slow down, which may hinder mobilization. Early mobilization (within 24 hours) is among the enhanced recovery elements that the ERAS Society guidelines say is “of particular value” for minimally invasive surgery, along with maintenance of normothermia and normovolemia with maintenance of adequate cardiac output.
 

Selecting Steps

Our practice is also trying to reduce preoperative bowel preparation and preoperative fasting, both of which have been found to be stressful for the body without evidence of benefit. These practices can lead to insulin resistance and hyperglycemia, which are associated with increased morbidity and length of stay.

It is now recommended that clear fluids be allowed up to 2 hours before surgery and solids up to 6 hours before. Some health systems and practices also recommend presurgical carbohydrate loading (for example, 10 ounces of apple juice 2 hours before surgery) – another small change on the ERAS menu – to further reduce postoperative insulin resistance and help the body cope with its stress response to surgery.

Along with nutritional changes are also various measures aimed at optimizing the body’s functionality before surgery (“prehabilitation”), from walking 30 minutes a day to abstaining from alcohol for patients who drink heavily.

Throughout the country, enhanced recovery protocols are taking shape in gynecologic surgery. ERAS was featured in an aptly titled panel session at the 2017 annual meeting of the American Association of Gynecologic Laparoscopists: “Outpatient Hysterectomy, ERAS, and Same-Day Discharge: The Next Big Thing in Gyn Surgery.” Others are applying ERAS to scheduled cesarean sections. And in our practice, I believe that if we continue making small changes, we will reach our goal of opioid-free recoveries and a better surgical experience for our patients.
 

Kirsten Sasaki, MD, is an associate of the Advanced Gynecologic Surgery Institute. She reported that she has no disclosures relevant to this Master Class.

“Enhanced Recovery After Surgery” (ERAS) practices and protocols have been increasingly refined and adopted for the field of gynecology, and there is hope among gynecologic surgeons – and some recent evidence – that, with the ERAS movement, we are improving patient recoveries and outcomes and minimizing the need for opioids.

This applies not only to open surgeries but also to the minimally invasive procedures that already are prized for significant reductions in morbidity and length of stay. The overarching and guiding principle of ERAS is that any surgery – whether open or minimally invasive, major or minor – places stress on the body and is associated with risks and morbidity.

Improved Outcomes

The ERAS mindset notably intersected gynecology with the publication in 2016 of a two-part series of guidelines for gynecology/oncology surgery from the ERAS Society. The 8-year-old society has its roots in a study group of European surgeons and others who decided to examine surgical practices and the concept of multimodal surgical care put forth in the 1990s by Henrik Kehlet, MD, PhD, then a professor at the University of Copenhagen.

The first set of recommendations addressed pre- and intraoperative care (Gynecol Oncol. 2016 Feb;140[2]:313-22), and the second set addressed postoperative care (Gynecol Oncol. 2016 Feb;140[2]:323-32). Similar evidence-based recommendations were previously written for colonic resections, rectal and pelvic surgery, and other surgical specialties.

Most of the published outcomes of enhanced recovery protocols come from colorectal surgery. As noted in the ERAS Society gynecology/oncology guidelines, the benefits include an average reduction in length of stay of 2.5 days and a decrease in complications by as much as 50%.

There is growing evidence, however, that ERAS programs are also beneficial for patients undergoing laparoscopic surgery, and outcomes from gynecology – including minimally invasive surgery – are also being reported.

For instance, a retrospective case-control study of 55 consecutive gynecologic oncology patients treated at the University of California, San Francisco, with laparoscopic or robotic surgery and an enhanced recovery pathway – and 110 historical control patients matched on the basis of age and surgery type – found significant improvements in recovery time, decreased pain despite reduced opioid use, and overall lower hospital costs (Obstet Gynecol. 2016 Jul;128[1]:138-44).

The enhanced recovery pathway included patient education, multimodal antiemetics, multimodal analgesia, and balanced fluid administration. Early catheter removal, ambulation, and feeding were also components. Analgesia included routine preoperative gabapentin, diclofenac, and acetaminophen; routine postoperative gabapentin, NSAIDs, and acetaminophen; and transversus abdominis plane blocks in 32 of the ERAS patients.

ERAS patients were significantly more likely to be discharged on day 1 (91%, compared with 60% in the control group). Opioid use decreased by 30%, and pain scores on postoperative day 1 were significantly lower.

Another study looking at the effect of enhanced recovery implementation in gynecologic surgeries at the University of Virginia, Charlottesville, (gynecologic oncology, urogynecology, and general gynecology) similarly reported benefits for vaginal and minimally invasive procedures, as well as for open procedures (Obstet Gynecol. 2016 Sep;128[3]:457-66).

In the minimally invasive group, investigators compared 324 patients before ERAS implementation with 249 patients afterward and found that the median length of stay was unchanged (1 day). However, intraoperative and postoperative opioid consumption decreased significantly and – even though actual pain scores improved only slightly – patient satisfaction scores improved markedly among post-ERAS patients. Patients gave higher marks, for instance, to questions regarding pain control (“how well your pain was controlled”) and teamwork (“staff worked together to care for you”).

Reducing Opioids

New opioid use that persists after a surgical procedure is a postsurgical complication that we all should be working to prevent. It has been estimated that 6% of surgical patients – even those who’ve had relatively minor surgical procedures – will become long-term opioid users, developing a dependence on the drugs prescribed to them for postsurgical pain.

This was shown last year in a national study of insurance claims data from between 2013 and 2014; investigators identified adults without opioid use in the year prior to surgery (including hysterectomy) and found that 5.9%-6.5% were filling opioid prescriptions 90-180 days after their surgical procedure. The incidence in a nonoperative control cohort was 0.4% (JAMA Surg. 2017 Jun 21;152[6]:e170504). Notably, this prolonged use was greatest in patients with prior pain conditions, substance abuse, and mental health disorders – a finding that may have implications for the counseling we provide prior to surgery.

It’s not clear what the optimal analgesic regimen is for minimally invasive or other gynecologic surgeries. What is clearly recommended, however, is that the approach be multifaceted. In our practice, we believe that the preoperative use of acetaminophen, pregabalin, and celecoxib plays an important role in reducing postoperative pain and opioid use. But we also have striven to create a practice-wide culture shift (throughout the operating and recovery rooms), for instance, that encourages using the least amounts of narcotics possible and using the shortest-acting formulations possible.

Transversus abdominis plane (TAP) blocks are also often part of ERAS protocols; they have been shown in at least two randomized controlled trials of abdominal hysterectomy to reduce intraoperative fentanyl requirements and to reduce immediate postoperative pain scores and postoperative morphine requirements (Anesth Analg. 2008 Dec;107[6]:2056-60; J Anaesthesiol Clin Pharmacol. 2014 Jul-Sep;30[3]:391-6).

More recently, liposomal bupivacaine, which is slowly released over several days, has gained traction as a substitute for standard bupivacaine and other agents in TAP blocks. In one recent retrospective study, abdominal incision infiltration with liposomal bupivacaine was associated with less opioid use (with no change in pain scores), compared with bupivacaine hydrochloride after laparotomy for gynecologic malignancies (Obstet Gynecol. 2016 Nov;128[5]:1009-17). It’s significantly more expensive, however, making it likely that the formulation is being used more judiciously in minimally invasive gynecologic surgery than in open surgeries.

Because of costs, we currently are restricted to using liposomal bupivacaine in our robotic surgeries only. In our practice, the single 20 mL vial (266 mg of liposomal bupivacaine) is diluted with 20 mL of normal saline, but it can be further diluted without loss of efficacy. With a 16-gauge needle, the liposomal bupivacaine is distributed across the incisions (usually 20 mL in the umbilicus with a larger incision and 10 mL in each of the two lateral incisions). Patients are counseled that they may have more discomfort after 3 days, but by this point most are mobile and feeling relatively well with a combination of NSAIDs and acetaminophen.

With growing visibility of the problem of narcotic dependence in the United States, patients seem increasingly receptive and even eager to limit or avoid the use of opioids. Patients should be counseled that minimizing or avoiding opioids may also speed recovery. Narcotics cause gut motility to slow down, which may hinder mobilization. Early mobilization (within 24 hours) is among the enhanced recovery elements that the ERAS Society guidelines say is “of particular value” for minimally invasive surgery, along with maintenance of normothermia and normovolemia with maintenance of adequate cardiac output.
 

Selecting Steps

Our practice is also trying to reduce preoperative bowel preparation and preoperative fasting, both of which have been found to be stressful for the body without evidence of benefit. These practices can lead to insulin resistance and hyperglycemia, which are associated with increased morbidity and length of stay.

It is now recommended that clear fluids be allowed up to 2 hours before surgery and solids up to 6 hours before. Some health systems and practices also recommend presurgical carbohydrate loading (for example, 10 ounces of apple juice 2 hours before surgery) – another small change on the ERAS menu – to further reduce postoperative insulin resistance and help the body cope with its stress response to surgery.

Along with nutritional changes are also various measures aimed at optimizing the body’s functionality before surgery (“prehabilitation”), from walking 30 minutes a day to abstaining from alcohol for patients who drink heavily.

Throughout the country, enhanced recovery protocols are taking shape in gynecologic surgery. ERAS was featured in an aptly titled panel session at the 2017 annual meeting of the American Association of Gynecologic Laparoscopists: “Outpatient Hysterectomy, ERAS, and Same-Day Discharge: The Next Big Thing in Gyn Surgery.” Others are applying ERAS to scheduled cesarean sections. And in our practice, I believe that if we continue making small changes, we will reach our goal of opioid-free recoveries and a better surgical experience for our patients.
 

Kirsten Sasaki, MD, is an associate of the Advanced Gynecologic Surgery Institute. She reported that she has no disclosures relevant to this Master Class.

Click Here to Read the Supplement

Topics include:

• BV terminology and treatment over time
• Current understanding of BV etiology
• BV consequences
• BV treatments
• Future research needs in BV

Author:
Steven E. Chavoustie, MD, FACOG, CCRP

University of Miami

Miller School of Medicine

Miami, Florida

Click Here to Read the Supplement

Click Here to Read the Supplement

Topics include:

• BV terminology and treatment over time
• Current understanding of BV etiology
• BV consequences
• BV treatments
• Future research needs in BV

Author:
Steven E. Chavoustie, MD, FACOG, CCRP

University of Miami

Miller School of Medicine

Miami, Florida

Click Here to Read the Supplement

Click Here to Read the Supplement

Topics include:

• BV terminology and treatment over time
• Current understanding of BV etiology
• BV consequences
• BV treatments
• Future research needs in BV

Author:
Steven E. Chavoustie, MD, FACOG, CCRP

University of Miami

Miller School of Medicine

Miami, Florida

Click Here to Read the Supplement

MIAMI – Pearls for providers of photodynamic therapy (PDT) include tips on skin preparation, eye protection, and use of three new codes to maximize reimbursement. Also trending in medical dermatology are best practices for intralesional injections of 5-FU to treat the often challenging isomorphic squamous cell carcinomas (SCCs) or keratoacanthomas on the lower leg, as well as use of neoadjuvant hedgehog inhibitors to shrink large skin cancer lesions, according to Glenn David Goldman, MD.

“This talk is about what you can do medically as a dermatologic surgeon,” Dr. Goldman said at the Orlando Dermatology Aesthetic and Clinical Conference.
 

Use new billing codes for photodynamic therapy

There are now three new PDT billing codes. “Make sure your coders are using these properly. They are active now, and if you don’t use them, you won’t get paid properly,” said Dr. Goldman, professor and medical director of dermatology at the University of Vermont, Burlington. Specifically, 96567 is for standard PDT applied by staff; 96573 is for PDT applied by a physician; and 96574 is for PDT and curettage performed by a physician.

“Be involved, don’t delegate,” Dr. Goldman added. “If you do, you will get paid half as much as you used to, which means you will lose money on every single patient you treat.”

What type of PDT physicians choose to use in their practice remains controversial. “Do you do short-contact PDT, do you do daylight PDT? We’ve gone back and forth in our practice,” Dr. Goldman said. “I’m not impressed with daylight PDT. I know this is at odds with some of the people here, but at least in Vermont, it doesn’t work very well.”

The way PDT was described in the original trials (a photosensitizer applied in the office followed by PDT) “works the best, with one caveat,” Dr. Goldman said. The caveat is that dermatologists should aim for a PDT clearance that approaches the efficacy of 5-fluorouracil (5-FU). “If you can get to that – which is difficult by the way – I think your patients will really appreciate this.”

An additional PDT pearl Dr. Goldman shared involves skin preparation: the use of acetone to defat the skin, even in patients with very thick lesions. Apply acetone with gauze to the site for 5 minutes and “all of that hyperkeratosis just wipes away,” curette off any residual hyperkeratosis – and consider a ring anesthetic block to control pain for the patient with severe disease, he advised.

Another tip is to forgo the goggles that come with most PDT kits. Instead, purchase smaller, disposable laser eye shields for PDT patients, Dr. Goldman said. “They work better. You can get closer to the eye … and they are more comfortable for the patient.”

Dr. Goldman’s practice is providing more PDT and much less 5-FU for patient convenience. “I believe if someone is willing to go through 3 weeks of 5-FU or 12-16 weeks of imiquimod, they get the best results. However, most people don’t want to do that if they can sit in front of a light for 15 minutes.”
 

Consider intralesional injections for SCCs and KAs on the legs

An ongoing challenge in medical dermatology is preventing rapid recurrence of SCCs and/or keratoacanthomas (KAs) near sites of previous excision on the legs. “We all see this quite a bit. Often you get lesions on the leg, you cut them out, and they come right back” close to the excision site, Dr. Goldman said.

He does not recommend methotrexate injections for these lesions. “Methotrexate does not work. It doesn’t hurt, but I’ve injected methotrexate into squamous cell carcinomas many times and they’ve never gone away.” In contrast, 5-FU “works incredibly well. They go away, I’ve had tremendous success. This has changed the way we treat these lesions.” 5-FU is inexpensive and can be obtained from oncology pharmacies. One caveat is 5-FU injections can be painful and patients require anesthesia prior to injection.

Using a 25-gauge or 27-gauge needle, Dr. Goldman injects 5-FU “exactly as I would a hypertrophic scar. I inject a squamous cell carcinoma carefully and ‘expand’ the tumor.” He typically injects a lesion every 2 weeks until it resolves completely, which typically takes two or three sessions.

“I want to emphasize that that’s really true about intralesional 5-FU for those KAs and scars on the legs,” said session moderator James Spencer, MD, a dermatologist in private practice in St. Petersburg, Florida. “Otherwise, you’re just chasing your tail trying to cut them out. You’ll do much better with the intralesional 5-FU; it’s easy to get, it’s affordable, it comes as 50 mg/mL … just keep it in the office.”
 

A recommended role for hedgehog inhibitors

Hedgehog inhibitors work best as neoadjuvant therapy to shrink large skin cancer tumors prior to excision, Dr. Goldman said. “Hedgehog inhibitors don’t cure anything … except for rare cases of small basal cell carcinomas.” For most lesions, however, the strategy is not curative.

“I don’t believe in hedgehog inhibitors for things that are readily resectable. We use them to shrink things down,” he added.

Dr. Goldman recommended treating patients with neoadjuvant hedgehog inhibitors to achieve the maximum tumor shrinking effect. Adverse effects tend to develop slowly over time, typically after a 6-week “grace period.” Nighttime leg muscle cramps, loss of taste, hair loss, and weight loss can occur. Also, electrolyte imbalances can occur, particularly in older patients with renal clearance issues. When the patient can no longer reasonably tolerate the adverse effects, which is usually the case, “then you do the surgery,” Dr. Goldman said.

“The benefits of neoadjuvant hedgehog inhibitors include predictable shrinkage of tumors,” and manufacturers have been helpful with financial issues, he noted.

Dr. Goldman had no relevant financial disclosures. Dr. Spencer has served on the speakers bureau for Genentech and Leo Pharma.

MIAMI – Pearls for providers of photodynamic therapy (PDT) include tips on skin preparation, eye protection, and use of three new codes to maximize reimbursement. Also trending in medical dermatology are best practices for intralesional injections of 5-FU to treat the often challenging isomorphic squamous cell carcinomas (SCCs) or keratoacanthomas on the lower leg, as well as use of neoadjuvant hedgehog inhibitors to shrink large skin cancer lesions, according to Glenn David Goldman, MD.

“This talk is about what you can do medically as a dermatologic surgeon,” Dr. Goldman said at the Orlando Dermatology Aesthetic and Clinical Conference.
 

Use new billing codes for photodynamic therapy

There are now three new PDT billing codes. “Make sure your coders are using these properly. They are active now, and if you don’t use them, you won’t get paid properly,” said Dr. Goldman, professor and medical director of dermatology at the University of Vermont, Burlington. Specifically, 96567 is for standard PDT applied by staff; 96573 is for PDT applied by a physician; and 96574 is for PDT and curettage performed by a physician.

“Be involved, don’t delegate,” Dr. Goldman added. “If you do, you will get paid half as much as you used to, which means you will lose money on every single patient you treat.”

What type of PDT physicians choose to use in their practice remains controversial. “Do you do short-contact PDT, do you do daylight PDT? We’ve gone back and forth in our practice,” Dr. Goldman said. “I’m not impressed with daylight PDT. I know this is at odds with some of the people here, but at least in Vermont, it doesn’t work very well.”

The way PDT was described in the original trials (a photosensitizer applied in the office followed by PDT) “works the best, with one caveat,” Dr. Goldman said. The caveat is that dermatologists should aim for a PDT clearance that approaches the efficacy of 5-fluorouracil (5-FU). “If you can get to that – which is difficult by the way – I think your patients will really appreciate this.”

An additional PDT pearl Dr. Goldman shared involves skin preparation: the use of acetone to defat the skin, even in patients with very thick lesions. Apply acetone with gauze to the site for 5 minutes and “all of that hyperkeratosis just wipes away,” curette off any residual hyperkeratosis – and consider a ring anesthetic block to control pain for the patient with severe disease, he advised.

Another tip is to forgo the goggles that come with most PDT kits. Instead, purchase smaller, disposable laser eye shields for PDT patients, Dr. Goldman said. “They work better. You can get closer to the eye … and they are more comfortable for the patient.”

Dr. Goldman’s practice is providing more PDT and much less 5-FU for patient convenience. “I believe if someone is willing to go through 3 weeks of 5-FU or 12-16 weeks of imiquimod, they get the best results. However, most people don’t want to do that if they can sit in front of a light for 15 minutes.”
 

Consider intralesional injections for SCCs and KAs on the legs

An ongoing challenge in medical dermatology is preventing rapid recurrence of SCCs and/or keratoacanthomas (KAs) near sites of previous excision on the legs. “We all see this quite a bit. Often you get lesions on the leg, you cut them out, and they come right back” close to the excision site, Dr. Goldman said.

He does not recommend methotrexate injections for these lesions. “Methotrexate does not work. It doesn’t hurt, but I’ve injected methotrexate into squamous cell carcinomas many times and they’ve never gone away.” In contrast, 5-FU “works incredibly well. They go away, I’ve had tremendous success. This has changed the way we treat these lesions.” 5-FU is inexpensive and can be obtained from oncology pharmacies. One caveat is 5-FU injections can be painful and patients require anesthesia prior to injection.

Using a 25-gauge or 27-gauge needle, Dr. Goldman injects 5-FU “exactly as I would a hypertrophic scar. I inject a squamous cell carcinoma carefully and ‘expand’ the tumor.” He typically injects a lesion every 2 weeks until it resolves completely, which typically takes two or three sessions.

“I want to emphasize that that’s really true about intralesional 5-FU for those KAs and scars on the legs,” said session moderator James Spencer, MD, a dermatologist in private practice in St. Petersburg, Florida. “Otherwise, you’re just chasing your tail trying to cut them out. You’ll do much better with the intralesional 5-FU; it’s easy to get, it’s affordable, it comes as 50 mg/mL … just keep it in the office.”
 

A recommended role for hedgehog inhibitors

Hedgehog inhibitors work best as neoadjuvant therapy to shrink large skin cancer tumors prior to excision, Dr. Goldman said. “Hedgehog inhibitors don’t cure anything … except for rare cases of small basal cell carcinomas.” For most lesions, however, the strategy is not curative.

“I don’t believe in hedgehog inhibitors for things that are readily resectable. We use them to shrink things down,” he added.

Dr. Goldman recommended treating patients with neoadjuvant hedgehog inhibitors to achieve the maximum tumor shrinking effect. Adverse effects tend to develop slowly over time, typically after a 6-week “grace period.” Nighttime leg muscle cramps, loss of taste, hair loss, and weight loss can occur. Also, electrolyte imbalances can occur, particularly in older patients with renal clearance issues. When the patient can no longer reasonably tolerate the adverse effects, which is usually the case, “then you do the surgery,” Dr. Goldman said.

“The benefits of neoadjuvant hedgehog inhibitors include predictable shrinkage of tumors,” and manufacturers have been helpful with financial issues, he noted.

Dr. Goldman had no relevant financial disclosures. Dr. Spencer has served on the speakers bureau for Genentech and Leo Pharma.

MIAMI – Pearls for providers of photodynamic therapy (PDT) include tips on skin preparation, eye protection, and use of three new codes to maximize reimbursement. Also trending in medical dermatology are best practices for intralesional injections of 5-FU to treat the often challenging isomorphic squamous cell carcinomas (SCCs) or keratoacanthomas on the lower leg, as well as use of neoadjuvant hedgehog inhibitors to shrink large skin cancer lesions, according to Glenn David Goldman, MD.

“This talk is about what you can do medically as a dermatologic surgeon,” Dr. Goldman said at the Orlando Dermatology Aesthetic and Clinical Conference.
 

Use new billing codes for photodynamic therapy

There are now three new PDT billing codes. “Make sure your coders are using these properly. They are active now, and if you don’t use them, you won’t get paid properly,” said Dr. Goldman, professor and medical director of dermatology at the University of Vermont, Burlington. Specifically, 96567 is for standard PDT applied by staff; 96573 is for PDT applied by a physician; and 96574 is for PDT and curettage performed by a physician.

“Be involved, don’t delegate,” Dr. Goldman added. “If you do, you will get paid half as much as you used to, which means you will lose money on every single patient you treat.”

What type of PDT physicians choose to use in their practice remains controversial. “Do you do short-contact PDT, do you do daylight PDT? We’ve gone back and forth in our practice,” Dr. Goldman said. “I’m not impressed with daylight PDT. I know this is at odds with some of the people here, but at least in Vermont, it doesn’t work very well.”

The way PDT was described in the original trials (a photosensitizer applied in the office followed by PDT) “works the best, with one caveat,” Dr. Goldman said. The caveat is that dermatologists should aim for a PDT clearance that approaches the efficacy of 5-fluorouracil (5-FU). “If you can get to that – which is difficult by the way – I think your patients will really appreciate this.”

An additional PDT pearl Dr. Goldman shared involves skin preparation: the use of acetone to defat the skin, even in patients with very thick lesions. Apply acetone with gauze to the site for 5 minutes and “all of that hyperkeratosis just wipes away,” curette off any residual hyperkeratosis – and consider a ring anesthetic block to control pain for the patient with severe disease, he advised.

Another tip is to forgo the goggles that come with most PDT kits. Instead, purchase smaller, disposable laser eye shields for PDT patients, Dr. Goldman said. “They work better. You can get closer to the eye … and they are more comfortable for the patient.”

Dr. Goldman’s practice is providing more PDT and much less 5-FU for patient convenience. “I believe if someone is willing to go through 3 weeks of 5-FU or 12-16 weeks of imiquimod, they get the best results. However, most people don’t want to do that if they can sit in front of a light for 15 minutes.”
 

Consider intralesional injections for SCCs and KAs on the legs

An ongoing challenge in medical dermatology is preventing rapid recurrence of SCCs and/or keratoacanthomas (KAs) near sites of previous excision on the legs. “We all see this quite a bit. Often you get lesions on the leg, you cut them out, and they come right back” close to the excision site, Dr. Goldman said.

He does not recommend methotrexate injections for these lesions. “Methotrexate does not work. It doesn’t hurt, but I’ve injected methotrexate into squamous cell carcinomas many times and they’ve never gone away.” In contrast, 5-FU “works incredibly well. They go away, I’ve had tremendous success. This has changed the way we treat these lesions.” 5-FU is inexpensive and can be obtained from oncology pharmacies. One caveat is 5-FU injections can be painful and patients require anesthesia prior to injection.

Using a 25-gauge or 27-gauge needle, Dr. Goldman injects 5-FU “exactly as I would a hypertrophic scar. I inject a squamous cell carcinoma carefully and ‘expand’ the tumor.” He typically injects a lesion every 2 weeks until it resolves completely, which typically takes two or three sessions.

“I want to emphasize that that’s really true about intralesional 5-FU for those KAs and scars on the legs,” said session moderator James Spencer, MD, a dermatologist in private practice in St. Petersburg, Florida. “Otherwise, you’re just chasing your tail trying to cut them out. You’ll do much better with the intralesional 5-FU; it’s easy to get, it’s affordable, it comes as 50 mg/mL … just keep it in the office.”
 

A recommended role for hedgehog inhibitors

Hedgehog inhibitors work best as neoadjuvant therapy to shrink large skin cancer tumors prior to excision, Dr. Goldman said. “Hedgehog inhibitors don’t cure anything … except for rare cases of small basal cell carcinomas.” For most lesions, however, the strategy is not curative.

“I don’t believe in hedgehog inhibitors for things that are readily resectable. We use them to shrink things down,” he added.

Dr. Goldman recommended treating patients with neoadjuvant hedgehog inhibitors to achieve the maximum tumor shrinking effect. Adverse effects tend to develop slowly over time, typically after a 6-week “grace period.” Nighttime leg muscle cramps, loss of taste, hair loss, and weight loss can occur. Also, electrolyte imbalances can occur, particularly in older patients with renal clearance issues. When the patient can no longer reasonably tolerate the adverse effects, which is usually the case, “then you do the surgery,” Dr. Goldman said.

“The benefits of neoadjuvant hedgehog inhibitors include predictable shrinkage of tumors,” and manufacturers have been helpful with financial issues, he noted.

Dr. Goldman had no relevant financial disclosures. Dr. Spencer has served on the speakers bureau for Genentech and Leo Pharma.

A randomized clinical trial will compare two techniques for achieving extraperitoneal space during hernia surgery.

The Telescopic Dissection vs. Balloon Dissection During Laparoscopic TEP Inguinal Hernia Repair trial aims to determine whether these techniques are comparable in operative times, early postoperative pain scores, surgical complications, and rate of hernia recurrence. The Spacemaker Balloon Dissector will be used for the trial.

[email protected]

SOURCE: Clinical Trial NCT03276871.

A randomized clinical trial will compare two techniques for achieving extraperitoneal space during hernia surgery.

The Telescopic Dissection vs. Balloon Dissection During Laparoscopic TEP Inguinal Hernia Repair trial aims to determine whether these techniques are comparable in operative times, early postoperative pain scores, surgical complications, and rate of hernia recurrence. The Spacemaker Balloon Dissector will be used for the trial.

[email protected]

SOURCE: Clinical Trial NCT03276871.

A randomized clinical trial will compare two techniques for achieving extraperitoneal space during hernia surgery.

The Telescopic Dissection vs. Balloon Dissection During Laparoscopic TEP Inguinal Hernia Repair trial aims to determine whether these techniques are comparable in operative times, early postoperative pain scores, surgical complications, and rate of hernia recurrence. The Spacemaker Balloon Dissector will be used for the trial.

[email protected]

SOURCE: Clinical Trial NCT03276871.

ATLANTA – An intriguing link between the sex steroid hormonal milieu and platelet mitochondria has potential implications for reducing thrombosis risk.

The link, which involves a mitochondrial protein known as optic atrophy 1 (OPA1), appears to play a role in the regulation of thrombosis, and provides a possible explanation for the marked differences in cardiovascular risks between men and women, according to E. Dale Abel, MD, chair of the department of internal medicine, and director of the Fraternal Order of Eagles Diabetes Research Center at the University of Iowa, Iowa City.

The findings could lead to risk-stratification strategies and the identification of therapeutic targets, Dr. Abel said in an interview.

Courtesy Dr. E. Dale Abel

“If we understand that, we may be in a position to stratify these women based on thrombosis risk in the setting of estrogen exposure. I think the other thing that will come out of the work, as we begin to understand the mechanisms for this relationship, is the identification of targets that we could therapeutically modulate to reduce this risk,” he added.

Eventually, as more is learned about the mechanisms that underlie the relationship between OPA1 and platelet activation, the findings might also lead to new approaches for reducing the risk of thrombosis in men, he noted.

Dr. Abel and Dr. Weyrich reported having no relevant financial disclosures.

[email protected]

ATLANTA – An intriguing link between the sex steroid hormonal milieu and platelet mitochondria has potential implications for reducing thrombosis risk.

The link, which involves a mitochondrial protein known as optic atrophy 1 (OPA1), appears to play a role in the regulation of thrombosis, and provides a possible explanation for the marked differences in cardiovascular risks between men and women, according to E. Dale Abel, MD, chair of the department of internal medicine, and director of the Fraternal Order of Eagles Diabetes Research Center at the University of Iowa, Iowa City.

The findings could lead to risk-stratification strategies and the identification of therapeutic targets, Dr. Abel said in an interview.

Courtesy Dr. E. Dale Abel

“If we understand that, we may be in a position to stratify these women based on thrombosis risk in the setting of estrogen exposure. I think the other thing that will come out of the work, as we begin to understand the mechanisms for this relationship, is the identification of targets that we could therapeutically modulate to reduce this risk,” he added.

Eventually, as more is learned about the mechanisms that underlie the relationship between OPA1 and platelet activation, the findings might also lead to new approaches for reducing the risk of thrombosis in men, he noted.

Dr. Abel and Dr. Weyrich reported having no relevant financial disclosures.

[email protected]

ATLANTA – An intriguing link between the sex steroid hormonal milieu and platelet mitochondria has potential implications for reducing thrombosis risk.

The link, which involves a mitochondrial protein known as optic atrophy 1 (OPA1), appears to play a role in the regulation of thrombosis, and provides a possible explanation for the marked differences in cardiovascular risks between men and women, according to E. Dale Abel, MD, chair of the department of internal medicine, and director of the Fraternal Order of Eagles Diabetes Research Center at the University of Iowa, Iowa City.

The findings could lead to risk-stratification strategies and the identification of therapeutic targets, Dr. Abel said in an interview.

Courtesy Dr. E. Dale Abel

“If we understand that, we may be in a position to stratify these women based on thrombosis risk in the setting of estrogen exposure. I think the other thing that will come out of the work, as we begin to understand the mechanisms for this relationship, is the identification of targets that we could therapeutically modulate to reduce this risk,” he added.

Eventually, as more is learned about the mechanisms that underlie the relationship between OPA1 and platelet activation, the findings might also lead to new approaches for reducing the risk of thrombosis in men, he noted.

Dr. Abel and Dr. Weyrich reported having no relevant financial disclosures.

[email protected]

LAS VEGAS – Male gender and white race rank among epidemiologic risk factors that predict which inflammatory bowel disease (IBD) patients go on to develop nonmelanoma skin cancer, a large national analysis showed.

“Some studies have shown that patients with IBD may be at increased risk for nonmelanoma skin cancer (NMSC) because of the immunomodulators that they take for the management of their disease,” Zubair Khan, MD, said in an interview at the Crohn’s & Colitis Congress, a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association. “But these are mostly small, single-center studies.” In an effort to determine the epidemiology of NMSC in patients hospitalized with IBD, Dr. Khan, associate chief resident in the internal medicine department at the University of Toledo (Ohio) Medical Center and his associates analyzed the National Inpatient Sample (NIS) database for all subjects who had a primary or secondary discharge diagnosis of IBD during 2002-2014. Next, they used ICD-9 codes to identify the rate of NMSC in this population.

Doug Brunk/Frontline Medical News

*This story was updated on 3/26.

[email protected]

SOURCE: Khan Z et al. Crohn’s & Colitis Congress, Poster 209.

LAS VEGAS – Male gender and white race rank among epidemiologic risk factors that predict which inflammatory bowel disease (IBD) patients go on to develop nonmelanoma skin cancer, a large national analysis showed.

“Some studies have shown that patients with IBD may be at increased risk for nonmelanoma skin cancer (NMSC) because of the immunomodulators that they take for the management of their disease,” Zubair Khan, MD, said in an interview at the Crohn’s & Colitis Congress, a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association. “But these are mostly small, single-center studies.” In an effort to determine the epidemiology of NMSC in patients hospitalized with IBD, Dr. Khan, associate chief resident in the internal medicine department at the University of Toledo (Ohio) Medical Center and his associates analyzed the National Inpatient Sample (NIS) database for all subjects who had a primary or secondary discharge diagnosis of IBD during 2002-2014. Next, they used ICD-9 codes to identify the rate of NMSC in this population.

Doug Brunk/Frontline Medical News

*This story was updated on 3/26.

[email protected]

SOURCE: Khan Z et al. Crohn’s & Colitis Congress, Poster 209.

LAS VEGAS – Male gender and white race rank among epidemiologic risk factors that predict which inflammatory bowel disease (IBD) patients go on to develop nonmelanoma skin cancer, a large national analysis showed.

“Some studies have shown that patients with IBD may be at increased risk for nonmelanoma skin cancer (NMSC) because of the immunomodulators that they take for the management of their disease,” Zubair Khan, MD, said in an interview at the Crohn’s & Colitis Congress, a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association. “But these are mostly small, single-center studies.” In an effort to determine the epidemiology of NMSC in patients hospitalized with IBD, Dr. Khan, associate chief resident in the internal medicine department at the University of Toledo (Ohio) Medical Center and his associates analyzed the National Inpatient Sample (NIS) database for all subjects who had a primary or secondary discharge diagnosis of IBD during 2002-2014. Next, they used ICD-9 codes to identify the rate of NMSC in this population.

Doug Brunk/Frontline Medical News

*This story was updated on 3/26.

[email protected]

SOURCE: Khan Z et al. Crohn’s & Colitis Congress, Poster 209.