Applied Evidence

A 42-year-old man has chronic fatigue and fibromyalgia that has led to a 13-month disability leave from work. The reason for his current office visit is longstanding pain in his shoulders. As you take his history, he is sitting with hands clenched and he generally appears tense.

A 38-year-old woman with severe incapacitating gastroesophageal reflux disease, irritable bowel syndrome, and depression has been too disabled to work for 2 years. At the time of your interview, her posture is relaxed and she shows no signs of anxiety.

These 2 very different patients (whose cases I will review in detail) share a common problem: somatization, the translation of emotions into somatic problems or complaints. It is well documented—though still largely unrecognized in practice—that somatization accounts for a large proportion of office visits to primary care physicians as well as specialists,^1,2 leading to unnecessary testing, treatment, and hospitalization, disability and corporate financial loss,³ likely earlier mortality,⁴ and frustration for patients and physicians.⁵

No longer a diagnosis of exclusion

Despite the burden somatization places on the medical system, the diagnosis is often made by indirect methods such as checklist, speculation, or exclusion when other problems are ruled out.⁶ The common position, even in recent reviews, is that somatization should be treated by nonspecific measures, such as frequent office visits to increase the patient’s and physician’s ability to cope with what is often seen to be a chronic and incurable disorder.^7-11 Such a position is no longer warranted.

Based on recent quantitative and extensive case-based research, specific emotion-focused brief therapies and videotape-based research have clarified how emotions are experienced in the body and how somatization of emotions occurs (see The physiology of emotions). These methods, including short-term dynamic psychotherapy (STDP) have been used to diagnose and treat somatization effectively since the 1980s. Somatization, with its morbidity and chronicity, need no longer be diagnosed by exclusion nor treated palliatively without specific diagnostic testing.

FIGURE
The 4 patterns of somatization

Videotaped case-series research shows 4 main patterns of somatization: 1) striated muscle unconscious anxiety, 2) smooth muscle tension 3) cognitive-perceptual disruption, and 4) conversion.¹⁸

Striated muscle tension due to unconscious anxiety manifests through hand clenching, sighing, and even hyperventilation that the patient is not aware of. These patients may report panic attacks, chest pain, headache, fibromyalgia, and other musculoskeletal complaints. These conditions are often frustrating to family, employers, and physicians since conditions like chronic pain respond to treatment slowly or not at all.

Smooth muscle tension due to unconscious anxiety causes acute or chronic spasm of blood vessels, GI tract, airways, and the bladder. Patients exhibiting smooth muscle tension may present with GI symptoms, migraine, hypertension, urinary frequency, and upper airway constriction mimicking asthma. They often report histories of depression, panic, substance abuse, personality disorders, and past sexual or physical abuse.

Cognitive perceptual disruption due to unconscious anxiety typically involves visual blurring, tunnel vision, loss of train of thought, and “drifting,” wherein the patient is temporarily mentally absent from the room. These patients have chronically poor memories and concentration. They are commonly victims or perpetrators of partner abuse, have frequent accidents, and have transient paranoia. They often end up seeing neurologists and undergoing expensive testing. Most have histories of dissociative disorders, personality disorders, or childhood abuse. In the family doctor’s office they frequently forget what was said and call back after the appointment. They appear confused and easily flustered and either avoid physical examinations entirely or endure them with great anxiety.

Conversion manifests as muscle weakness or paralysis in any voluntary muscle. Patients with acute conversion describe dropping items or even dropping to the floor as muscles give way without explanation. They will often report histories of witnessing or experiencing violent abuse.

One pattern usually predominates

The total amount of somatized emotion is distributed over the 4 pathways ( Table 1 ). One pathway generally prevails at any given time, though different pathways may come into play as anxiety waxes or wanes. When anxiety is expressed primarily through smooth muscle tension, cognitive perceptual disruption, or conversion, the striated muscles are relatively relaxed.

This finding of apparent calm while somatizing has been noted elsewhere in research of patients with hypertension. This is the “belle indifference” a patient expresses as they are temporarily relieved of muscle tension through somatization elsewhere.¹⁹

TABLE 1
Examples of diagnosable somatization patterns

Major types of defense

Two important categories of defense include isolation of affect and repression.

Isolation of affect is awareness of emotions in one’s head without experiencing them in the body. Intellectualization is a form of isolation of affect.

Repression is the unconscious process by which emotions are shunted into the body rather than reaching consciousness at all. For example, strong emotions, including rage, may directly cause sighing and a panic attack without the person being aware of either the emotion or the sighing.²⁰

Experiencing the emotions overcomes somatization

Videotaped research also shows that if a person can experience true feelings in the moment, somatization of these feelings is weakened and overcome. The feelings being experienced push out the anxiety and somatization ( Figure ). Thus, somatization can be reduced or removed by helping a patient feel emotions being stirred by recent events or from past events. Through this process one may diagnose somatization and also produce a therapeutic effect for a patient.

Direct diagnosis of somatization

An objective assessment

Because the process of somatization is unconscious to the patient, diagnosis is based on objective findings during examination rather than on a patient’s report. This is similar to evaluating a patient with abdominal pathology: we would not expect the patient to report an abdominal mass, even though we could detect it and train the patient to palpate it. The somatizing patient believes the problem is physical, so the history reported is more likely to lead to physical testing and medical treatments than to a direct examination of the emotional system. Although clues in the history may suggest a patient is somatizing,²⁰ the definitive test, like that of an abdominal examination, is “hands on,” observing the patient’s direct response to an emotion-focused interview.

Actively exploring emotions

Examination of the emotional system is analogous to a physical examination of other systems, and progresses from observation to “palpation” or “percussion” ( Table 2 ).

Observe the patient for visible unconscious anxiety. Then, in the context of a supportive patient-doctor relationship, explore emotionally charged situations that generate symptoms.

Alternatively, one may ask in what way strong emotions like anger affect the patient’s physical problems. Asking about specific recent events and feelings that were triggered usually mobilizes emotions, giving you and the patient a direct look at how emotions affect them physically.

If a patient is anxious in the office, it will be most meaningful to examine the feelings they experience during the interview.

TABLE 2
Exploring emotions in a patient-centered interview

Managing defenses

At times, the defenses used to avoid feelings must be pointed out before the patient can see and interrupt these behaviors. If the process is too detached or intellectual, then feelings will not be activated and the system cannot be assessed. The physician’s rapport allows him or her to clarify the process and the need for the patient to try to approach and experience feelings when speaking about them. This is analogous to the process of examining a sore abdomen when a patient is guarding: the patient must relax for examination to take place, and we help them do this by explaining the process.

Patients who are defensive and insist the problem is not related to emotions are managed differently. These patients usually are quite tense and already emotionally activated. An open examination of feelings the patient has about coming to see you that day is a good way to begin. Through this focus one can see the patient’s somatizing patterns directly as well as develop a working rapport.

Managing anxiety

If the patient becomes anxious when asked about emotions, introduce a calming step by asking the patient to intellectualize about the specific bodily anxiety symptoms. This reduces the anxiety by using the defense of intellectualization.

Recap and planning

The interview is concluded by reviewing the findings with the patient in the same way one would share findings of a blood test. Management options would depend on the findings and may include another interview, further medical investigations, referral for treatment, or follow-up to gauge the patient’s response to the interview itself.

Interpreting the patient’s responses

With the focused assessment, the somatic symptoms will transiently increase or decrease, disappear, or not change at all ( Table 3 ).

An increase in symptoms with emotional focus suggests that emotions aggravate or directly cause the problems. A decrease in symptoms during the test also suggests a linkage to emotions. Disappearance of the symptoms by bringing emotional experiences to awareness is the best direct evidence that somatization of these emotions was causing the patient’s symptoms.

No change in a patient’s symptoms or signs—provided there was adequate emotional activation—suggests no somatization of emotions. In these cases, other physical factors must be sought. For example, a woman with chronic left leg weakness and numbness had no shift in symptoms with this test: she was found to have neuropathy due to multiple sclerosis. We have found that 5% to 10% of patients referred to our diagnostic clinic have physical problems that were mistaken for somatization.

TABLE 3
Interpretation of responses to emotionally focused assessment

False negatives

False negatives occur when the test does not detect the process of somatization when it is present. This will occur if the level of emotion mobilized was too low, if the patient is too sedated, if the defenses the patient used were not sufficiently interrupted, or when the patient is not working collaboratively with the doctor during the test. In each case the patient must allow emotions to be mobilized and the doctor must focus adequately on the emotional experiences to yield an interpretable response.

False positives

False positives occur when the patient has a rise or fall in symptoms during the test for other reasons—eg, coincidental shifts in episodic conditions like muscle spasm or symptom reduction due to distraction during the test itself. It is important in these cases to repeat the test more than once and see if the results are reproducible.

Treatment: short-term dynamic psychotherapy

STDP is clinically effective for patients with somatization

Short-term dynamic psychotherapy (STDP) formats specifically help a patient to examine trauma and loss-related emotions that result in somatization, depression, anxiety, and self-defeating behaviors. Case-series videotaped research over the past 30 years has established the effectiveness of the methods in both short and long term follow-up.²¹

STDP is efficacious in controlled trials and meta-analyses

In 1995, Anderson and Lambert²² conducted a meta-analysis of 26 controlled studies and found STDP to be superior to minimal treatment controls and wait lists including in samples with somatization. It was found to be as effective in removing anxiety and depressive symptoms as cognitive behavioral therapy. A recent meta-analysis,²³ using more strict inclusion criteria, yielded the same findings. In a recent randomized controlled trial of symptomatic patients with personality disorders, STDP brought significant symptom reduction while cognitive therapy did not, suggesting that STDP may have added benefits in more resistant and complex symptomatic patients.²⁴

In our current Cochrane review search,²⁵ we have found 40 published randomized controlled trials supporting its efficacy with a range of disorders including ulcer disease, irritable bowel syndrome, dyspepsia, and urethral syndrome.^26-29 Our review has likewise found STDP to be superior to minimal treatment or waitlist controls and that the gains are maintained in follow-up averaging over 1 year.

STDP is cost-effective and reduces health care utilization

STDP has been shown to reduce healthcare utilization and to be cost-effective in treating patients with dyspepsia, irritable bowel syndrome, depression, and self-harm and treatment-resistant conditions.³⁰ Of specific cost figures cited in reviewed papers, 27 out of 34 showed cost savings with STDP including reduction in total costs, medication costs, disability, hospital, and physician use.

Case Illustrations

Case 1: Striated muscle anxiety

This 42-year-old man had chronic fatigue and fibromyalgia which lead to a 13 month disability up to the time of consultation. He came to the office with longstanding pain in his shoulders. His hands were clenched during the interview, and he appeared tense while giving his history.

• DOCTOR: Can you tell about a specific time when you had an emotional upset so we can understand how exactly it affects you?
• PATIENT: Yeah, problems at home with my wife…. Saturday she wanted me to do some work on the garage. She started to yell. Every day it’s the same thing and I’m getting tired of it.… DOCTOR: So how do you feel toward her?
• PATIENT: [Takes a deep sigh, hands become clenched] Mad.
• DOCTOR: You mean mad … angry?
• PATIENT: Yeah.
• DOCTOR: How do you experience the anger inside physically?
• PATIENT: Very, very… tense
• DOCTOR: That is tension…anxiety?
• PATIENT: Yeah.
• DOCTOR: How did you experience the anger?
• PATIENT: I start to ignore her.
• DOCTOR: Is that a mechanism to deal with anger?
• PATIENT: It’s really hard to put a word on it…. I get really mad…it’s like a rage.
• DOCTOR: So how do you experience the rage?
• PATIENT: [Patient takes a big sigh and clenches his hands tightly]
• DOCTOR: Do you notice you sigh and become tense when you talk about the rage.
• PATIENT: No, I didn’t. I don’t feel anxious.
• DOCTOR: But, do you notice the sigh and your hands?
• PATIENT: I do now, but didn’t see it before.
• DOCTOR: Is this what is happening to you … that you are getting all tensed up about these feelings?
• PATIENT: Yeah, it must be.

At a later point in the 1-hour session, the patient was able to feel the visceral emotions of rage, guilt about the rage, and sadness over several years of conflict. When the feelings were experienced in the office, he had an abrupt drop in muscle tension and bodily pain: this was further evidence he had been somatizing, or as he said, “bottling up” these complex feelings.

As is typical of patients with primarily striated muscle anxiety, he denies being nervous despite showing obvious anxiety in the interview. He denies anxiety because it has been unconscious to him, thus free to create fibromyalgia pain. Through this single interview a link is made for both patient and doctor between blocked feelings and body pain. With 10 treatment sessions focused on this process, his fibromyalgia resolved; he returned to work and no longer needed antidepressants.

Case 2: Smooth muscle anxiety

This patient is a 38 year-old woman with severe incapacitating GERD, irritable bowel syndrome, and depression who was disabled from work for 2 years at the time of consultation. This woman had a very relaxed posture with relaxed hands and an absence of obvious anxiety. After 10 minutes of exploring situations and events that make her stomach worse, we arrive at the following point.

• DOCTOR: Can you tell me about another time when your stomach felt worse?
• PATIENT: Yes. There was once when my sister-inlaw did something and it made me angry. Yeah, when people make me angry I don’t tell them, I just avoid them.
• DOCTOR: Can you describe one of those times, so we can see how that affects you.
• PATIENT: Once she was arguing with my brother, like they usually do….
• DOCTOR: How did you feel then?
• PATIENT: … Now I just got that again [pointing to her stomach and chest with upward motion and burps]
• DOCTOR: Heartburn? Just came on?
• PATIENT: Yeah, heartburn, just came on.
• DOCTOR: Is there anything else you notice? Like in your stomach?
• PATIENT: No, just that … but I can hear my stomach churning.
• DOCTOR: So is it when you have anger your stomach churns and you get this acid?
• PATIENT: Must be….
• DOCTOR: …because in your approach to talk about anger you got cramps and acid. So is that one way the anger goes?
• PATIENT: Yes it must be, but I never thought of that part. [Stomach stops churning and heartburn stops as we talk about it for few minutes.] You know, this all started to get worse when my fiancé dumped me. [She goes onto describe a story of being not only rejected but also feeling humiliated by how it was done. She never felt emotional about it but just got severe diarrhea and was confined to her room for 3 weeks.]
• DOCTOR: How did you feel toward your fiancé when he dumped you that way?
• PATIENT: I was just so sick and depressed. I didn’t feel any anger. [Patient burps again this time rubs abdomen due to some discomfort.]
• DOCTOR: Did you get the stomach upset just now again?
• PATIENT: My stomach is upset again. Just the noise and acid again.
• DOCTOR: So again, when we focus on the feelings, the cramps and acid come back.
• PATIENT: For sure. What can we do about that?
• DOCTOR: Can we try to help you identify these feelings before they go to your stomach, to try to interrupt that process. Can you tell me about another incident like that?

The patient required 3 one-hour sessions to improve her tolerance of anxiety, so she could intellectualize about feelings rather than have them directly affect her stomach. The feelings of rejection had triggered rage and guilt about rage associated with sexual abuse by her brother and the abandonment she felt from her mother when she told her mother about it. With 12 sessions of therapy, she was able to stop her IBS medication, anxiolytic, and antidepressant.

This vignette is typical for patients with primarily smooth muscle unconscious anxiety. The patient had no visible anxiety but had GI symptoms when focusing on emotions about recent trauma. The symptoms were mobilized and reduced repeatedly, confirming a link with emotions. Note that outwardly she looked calm, but the emotions mobilized were being shunted to her GI tract.

Incorporating emotion diagnostics into practice

To perform these interview procedures, the physician must understand emotion physiology and the patterns of somatization as outlined above. This is entirely intuitive to many physicians the first time seeing this material: they can readily employ that which they already know. In general, though, physicians reading this will want to ponder it and see how it may apply case by case as they develop skills with it over time. Senior clinicians have usually done these assessments by default, by pressure from patients, or because they learned elements of this over time from various experiences.

Helpful short-cuts

Family physicians trained in emotion assessment note that abbreviated elements can easily be incorporated into a patient-centered assessment process. For example, one may ask how “stress,” “emotions,” or “anger” affects the person and their body or ask how the person handles anger in specific incidents.

In an initial patient questionnaire, one can include a few questions that encourage the patient to think about how stress affects them and to describe their body’s tendency to experience anxiety. When they later present with symptoms, one can use these baseline data to aid in the new assessment. Thus, a culture of considering emotional factors can be woven into practice, weakening any resistance to the idea that emotions and health, mind and body, are tightly bound.

Time factors

Based on our experience, family physicians can perform two thirds of these diagnostic assessments during 15 minutes of focused interviewing. More complex cases, such as patients with cognitive disruption or multiple manifestations of anxiety, may take longer to diagnose and generally need more specialized care or referral. If required, a patient could be asked back for a 1 half-hour session later in the day or week.

Taking care of ourselves

Despite the importance of the emotional system in medicine, medical curricula generally fail to provide sufficient education in this area. At the same time, up to half of our own ranks report emotional burnout.³¹ Even with the lack of mainstream medical teaching about emotions and health, it behooves us to learn what we can about the emotional system as it applies to the patient and to ourselves in relation to these most challenging problems. Focused seminars, peer case review, select reading, and videotape training can all help in this educational process.³²

Acknowledgments

The author wishes to thank the many colleagues who reviewed and commented on this manuscript. This work is supported by Dalhousie University, Capital Health and the Nova Scotia Department of Health.

Correspondence
Allan Abbass, MD, FRCPC, Associate Professor and Director of Education, Psychiatry, Director, Center for Emotions and Health, 8th Floor, Abbie J. Lane Memorial Building, Halifax, NS B3H 2E2, Canada. E-mail: [email protected].

A 42-year-old man has chronic fatigue and fibromyalgia that has led to a 13-month disability leave from work. The reason for his current office visit is longstanding pain in his shoulders. As you take his history, he is sitting with hands clenched and he generally appears tense.

A 38-year-old woman with severe incapacitating gastroesophageal reflux disease, irritable bowel syndrome, and depression has been too disabled to work for 2 years. At the time of your interview, her posture is relaxed and she shows no signs of anxiety.

These 2 very different patients (whose cases I will review in detail) share a common problem: somatization, the translation of emotions into somatic problems or complaints. It is well documented—though still largely unrecognized in practice—that somatization accounts for a large proportion of office visits to primary care physicians as well as specialists,^1,2 leading to unnecessary testing, treatment, and hospitalization, disability and corporate financial loss,³ likely earlier mortality,⁴ and frustration for patients and physicians.⁵

No longer a diagnosis of exclusion

Despite the burden somatization places on the medical system, the diagnosis is often made by indirect methods such as checklist, speculation, or exclusion when other problems are ruled out.⁶ The common position, even in recent reviews, is that somatization should be treated by nonspecific measures, such as frequent office visits to increase the patient’s and physician’s ability to cope with what is often seen to be a chronic and incurable disorder.^7-11 Such a position is no longer warranted.

Based on recent quantitative and extensive case-based research, specific emotion-focused brief therapies and videotape-based research have clarified how emotions are experienced in the body and how somatization of emotions occurs (see The physiology of emotions). These methods, including short-term dynamic psychotherapy (STDP) have been used to diagnose and treat somatization effectively since the 1980s. Somatization, with its morbidity and chronicity, need no longer be diagnosed by exclusion nor treated palliatively without specific diagnostic testing.

FIGURE
The 4 patterns of somatization

Videotaped case-series research shows 4 main patterns of somatization: 1) striated muscle unconscious anxiety, 2) smooth muscle tension 3) cognitive-perceptual disruption, and 4) conversion.¹⁸

Striated muscle tension due to unconscious anxiety manifests through hand clenching, sighing, and even hyperventilation that the patient is not aware of. These patients may report panic attacks, chest pain, headache, fibromyalgia, and other musculoskeletal complaints. These conditions are often frustrating to family, employers, and physicians since conditions like chronic pain respond to treatment slowly or not at all.

Smooth muscle tension due to unconscious anxiety causes acute or chronic spasm of blood vessels, GI tract, airways, and the bladder. Patients exhibiting smooth muscle tension may present with GI symptoms, migraine, hypertension, urinary frequency, and upper airway constriction mimicking asthma. They often report histories of depression, panic, substance abuse, personality disorders, and past sexual or physical abuse.

Cognitive perceptual disruption due to unconscious anxiety typically involves visual blurring, tunnel vision, loss of train of thought, and “drifting,” wherein the patient is temporarily mentally absent from the room. These patients have chronically poor memories and concentration. They are commonly victims or perpetrators of partner abuse, have frequent accidents, and have transient paranoia. They often end up seeing neurologists and undergoing expensive testing. Most have histories of dissociative disorders, personality disorders, or childhood abuse. In the family doctor’s office they frequently forget what was said and call back after the appointment. They appear confused and easily flustered and either avoid physical examinations entirely or endure them with great anxiety.

Conversion manifests as muscle weakness or paralysis in any voluntary muscle. Patients with acute conversion describe dropping items or even dropping to the floor as muscles give way without explanation. They will often report histories of witnessing or experiencing violent abuse.

One pattern usually predominates

The total amount of somatized emotion is distributed over the 4 pathways ( Table 1 ). One pathway generally prevails at any given time, though different pathways may come into play as anxiety waxes or wanes. When anxiety is expressed primarily through smooth muscle tension, cognitive perceptual disruption, or conversion, the striated muscles are relatively relaxed.

This finding of apparent calm while somatizing has been noted elsewhere in research of patients with hypertension. This is the “belle indifference” a patient expresses as they are temporarily relieved of muscle tension through somatization elsewhere.¹⁹

TABLE 1
Examples of diagnosable somatization patterns

Major types of defense

Two important categories of defense include isolation of affect and repression.

Isolation of affect is awareness of emotions in one’s head without experiencing them in the body. Intellectualization is a form of isolation of affect.

Repression is the unconscious process by which emotions are shunted into the body rather than reaching consciousness at all. For example, strong emotions, including rage, may directly cause sighing and a panic attack without the person being aware of either the emotion or the sighing.²⁰

Experiencing the emotions overcomes somatization

Videotaped research also shows that if a person can experience true feelings in the moment, somatization of these feelings is weakened and overcome. The feelings being experienced push out the anxiety and somatization ( Figure ). Thus, somatization can be reduced or removed by helping a patient feel emotions being stirred by recent events or from past events. Through this process one may diagnose somatization and also produce a therapeutic effect for a patient.

Direct diagnosis of somatization

An objective assessment

Because the process of somatization is unconscious to the patient, diagnosis is based on objective findings during examination rather than on a patient’s report. This is similar to evaluating a patient with abdominal pathology: we would not expect the patient to report an abdominal mass, even though we could detect it and train the patient to palpate it. The somatizing patient believes the problem is physical, so the history reported is more likely to lead to physical testing and medical treatments than to a direct examination of the emotional system. Although clues in the history may suggest a patient is somatizing,²⁰ the definitive test, like that of an abdominal examination, is “hands on,” observing the patient’s direct response to an emotion-focused interview.

Actively exploring emotions

Examination of the emotional system is analogous to a physical examination of other systems, and progresses from observation to “palpation” or “percussion” ( Table 2 ).

Observe the patient for visible unconscious anxiety. Then, in the context of a supportive patient-doctor relationship, explore emotionally charged situations that generate symptoms.

Alternatively, one may ask in what way strong emotions like anger affect the patient’s physical problems. Asking about specific recent events and feelings that were triggered usually mobilizes emotions, giving you and the patient a direct look at how emotions affect them physically.

If a patient is anxious in the office, it will be most meaningful to examine the feelings they experience during the interview.

TABLE 2
Exploring emotions in a patient-centered interview

Managing defenses

At times, the defenses used to avoid feelings must be pointed out before the patient can see and interrupt these behaviors. If the process is too detached or intellectual, then feelings will not be activated and the system cannot be assessed. The physician’s rapport allows him or her to clarify the process and the need for the patient to try to approach and experience feelings when speaking about them. This is analogous to the process of examining a sore abdomen when a patient is guarding: the patient must relax for examination to take place, and we help them do this by explaining the process.

Patients who are defensive and insist the problem is not related to emotions are managed differently. These patients usually are quite tense and already emotionally activated. An open examination of feelings the patient has about coming to see you that day is a good way to begin. Through this focus one can see the patient’s somatizing patterns directly as well as develop a working rapport.

Managing anxiety

If the patient becomes anxious when asked about emotions, introduce a calming step by asking the patient to intellectualize about the specific bodily anxiety symptoms. This reduces the anxiety by using the defense of intellectualization.

Recap and planning

The interview is concluded by reviewing the findings with the patient in the same way one would share findings of a blood test. Management options would depend on the findings and may include another interview, further medical investigations, referral for treatment, or follow-up to gauge the patient’s response to the interview itself.

Interpreting the patient’s responses

With the focused assessment, the somatic symptoms will transiently increase or decrease, disappear, or not change at all ( Table 3 ).

An increase in symptoms with emotional focus suggests that emotions aggravate or directly cause the problems. A decrease in symptoms during the test also suggests a linkage to emotions. Disappearance of the symptoms by bringing emotional experiences to awareness is the best direct evidence that somatization of these emotions was causing the patient’s symptoms.

No change in a patient’s symptoms or signs—provided there was adequate emotional activation—suggests no somatization of emotions. In these cases, other physical factors must be sought. For example, a woman with chronic left leg weakness and numbness had no shift in symptoms with this test: she was found to have neuropathy due to multiple sclerosis. We have found that 5% to 10% of patients referred to our diagnostic clinic have physical problems that were mistaken for somatization.

TABLE 3
Interpretation of responses to emotionally focused assessment

False negatives

False negatives occur when the test does not detect the process of somatization when it is present. This will occur if the level of emotion mobilized was too low, if the patient is too sedated, if the defenses the patient used were not sufficiently interrupted, or when the patient is not working collaboratively with the doctor during the test. In each case the patient must allow emotions to be mobilized and the doctor must focus adequately on the emotional experiences to yield an interpretable response.

False positives

False positives occur when the patient has a rise or fall in symptoms during the test for other reasons—eg, coincidental shifts in episodic conditions like muscle spasm or symptom reduction due to distraction during the test itself. It is important in these cases to repeat the test more than once and see if the results are reproducible.

Treatment: short-term dynamic psychotherapy

STDP is clinically effective for patients with somatization

Short-term dynamic psychotherapy (STDP) formats specifically help a patient to examine trauma and loss-related emotions that result in somatization, depression, anxiety, and self-defeating behaviors. Case-series videotaped research over the past 30 years has established the effectiveness of the methods in both short and long term follow-up.²¹

STDP is efficacious in controlled trials and meta-analyses

In 1995, Anderson and Lambert²² conducted a meta-analysis of 26 controlled studies and found STDP to be superior to minimal treatment controls and wait lists including in samples with somatization. It was found to be as effective in removing anxiety and depressive symptoms as cognitive behavioral therapy. A recent meta-analysis,²³ using more strict inclusion criteria, yielded the same findings. In a recent randomized controlled trial of symptomatic patients with personality disorders, STDP brought significant symptom reduction while cognitive therapy did not, suggesting that STDP may have added benefits in more resistant and complex symptomatic patients.²⁴

In our current Cochrane review search,²⁵ we have found 40 published randomized controlled trials supporting its efficacy with a range of disorders including ulcer disease, irritable bowel syndrome, dyspepsia, and urethral syndrome.^26-29 Our review has likewise found STDP to be superior to minimal treatment or waitlist controls and that the gains are maintained in follow-up averaging over 1 year.

STDP is cost-effective and reduces health care utilization

STDP has been shown to reduce healthcare utilization and to be cost-effective in treating patients with dyspepsia, irritable bowel syndrome, depression, and self-harm and treatment-resistant conditions.³⁰ Of specific cost figures cited in reviewed papers, 27 out of 34 showed cost savings with STDP including reduction in total costs, medication costs, disability, hospital, and physician use.

Case Illustrations

Case 1: Striated muscle anxiety

This 42-year-old man had chronic fatigue and fibromyalgia which lead to a 13 month disability up to the time of consultation. He came to the office with longstanding pain in his shoulders. His hands were clenched during the interview, and he appeared tense while giving his history.

• DOCTOR: Can you tell about a specific time when you had an emotional upset so we can understand how exactly it affects you?
• PATIENT: Yeah, problems at home with my wife…. Saturday she wanted me to do some work on the garage. She started to yell. Every day it’s the same thing and I’m getting tired of it.… DOCTOR: So how do you feel toward her?
• PATIENT: [Takes a deep sigh, hands become clenched] Mad.
• DOCTOR: You mean mad … angry?
• PATIENT: Yeah.
• DOCTOR: How do you experience the anger inside physically?
• PATIENT: Very, very… tense
• DOCTOR: That is tension…anxiety?
• PATIENT: Yeah.
• DOCTOR: How did you experience the anger?
• PATIENT: I start to ignore her.
• DOCTOR: Is that a mechanism to deal with anger?
• PATIENT: It’s really hard to put a word on it…. I get really mad…it’s like a rage.
• DOCTOR: So how do you experience the rage?
• PATIENT: [Patient takes a big sigh and clenches his hands tightly]
• DOCTOR: Do you notice you sigh and become tense when you talk about the rage.
• PATIENT: No, I didn’t. I don’t feel anxious.
• DOCTOR: But, do you notice the sigh and your hands?
• PATIENT: I do now, but didn’t see it before.
• DOCTOR: Is this what is happening to you … that you are getting all tensed up about these feelings?
• PATIENT: Yeah, it must be.

At a later point in the 1-hour session, the patient was able to feel the visceral emotions of rage, guilt about the rage, and sadness over several years of conflict. When the feelings were experienced in the office, he had an abrupt drop in muscle tension and bodily pain: this was further evidence he had been somatizing, or as he said, “bottling up” these complex feelings.

As is typical of patients with primarily striated muscle anxiety, he denies being nervous despite showing obvious anxiety in the interview. He denies anxiety because it has been unconscious to him, thus free to create fibromyalgia pain. Through this single interview a link is made for both patient and doctor between blocked feelings and body pain. With 10 treatment sessions focused on this process, his fibromyalgia resolved; he returned to work and no longer needed antidepressants.

Case 2: Smooth muscle anxiety

This patient is a 38 year-old woman with severe incapacitating GERD, irritable bowel syndrome, and depression who was disabled from work for 2 years at the time of consultation. This woman had a very relaxed posture with relaxed hands and an absence of obvious anxiety. After 10 minutes of exploring situations and events that make her stomach worse, we arrive at the following point.

• DOCTOR: Can you tell me about another time when your stomach felt worse?
• PATIENT: Yes. There was once when my sister-inlaw did something and it made me angry. Yeah, when people make me angry I don’t tell them, I just avoid them.
• DOCTOR: Can you describe one of those times, so we can see how that affects you.
• PATIENT: Once she was arguing with my brother, like they usually do….
• DOCTOR: How did you feel then?
• PATIENT: … Now I just got that again [pointing to her stomach and chest with upward motion and burps]
• DOCTOR: Heartburn? Just came on?
• PATIENT: Yeah, heartburn, just came on.
• DOCTOR: Is there anything else you notice? Like in your stomach?
• PATIENT: No, just that … but I can hear my stomach churning.
• DOCTOR: So is it when you have anger your stomach churns and you get this acid?
• PATIENT: Must be….
• DOCTOR: …because in your approach to talk about anger you got cramps and acid. So is that one way the anger goes?
• PATIENT: Yes it must be, but I never thought of that part. [Stomach stops churning and heartburn stops as we talk about it for few minutes.] You know, this all started to get worse when my fiancé dumped me. [She goes onto describe a story of being not only rejected but also feeling humiliated by how it was done. She never felt emotional about it but just got severe diarrhea and was confined to her room for 3 weeks.]
• DOCTOR: How did you feel toward your fiancé when he dumped you that way?
• PATIENT: I was just so sick and depressed. I didn’t feel any anger. [Patient burps again this time rubs abdomen due to some discomfort.]
• DOCTOR: Did you get the stomach upset just now again?
• PATIENT: My stomach is upset again. Just the noise and acid again.
• DOCTOR: So again, when we focus on the feelings, the cramps and acid come back.
• PATIENT: For sure. What can we do about that?
• DOCTOR: Can we try to help you identify these feelings before they go to your stomach, to try to interrupt that process. Can you tell me about another incident like that?

The patient required 3 one-hour sessions to improve her tolerance of anxiety, so she could intellectualize about feelings rather than have them directly affect her stomach. The feelings of rejection had triggered rage and guilt about rage associated with sexual abuse by her brother and the abandonment she felt from her mother when she told her mother about it. With 12 sessions of therapy, she was able to stop her IBS medication, anxiolytic, and antidepressant.

This vignette is typical for patients with primarily smooth muscle unconscious anxiety. The patient had no visible anxiety but had GI symptoms when focusing on emotions about recent trauma. The symptoms were mobilized and reduced repeatedly, confirming a link with emotions. Note that outwardly she looked calm, but the emotions mobilized were being shunted to her GI tract.

Incorporating emotion diagnostics into practice

To perform these interview procedures, the physician must understand emotion physiology and the patterns of somatization as outlined above. This is entirely intuitive to many physicians the first time seeing this material: they can readily employ that which they already know. In general, though, physicians reading this will want to ponder it and see how it may apply case by case as they develop skills with it over time. Senior clinicians have usually done these assessments by default, by pressure from patients, or because they learned elements of this over time from various experiences.

Helpful short-cuts

Family physicians trained in emotion assessment note that abbreviated elements can easily be incorporated into a patient-centered assessment process. For example, one may ask how “stress,” “emotions,” or “anger” affects the person and their body or ask how the person handles anger in specific incidents.

In an initial patient questionnaire, one can include a few questions that encourage the patient to think about how stress affects them and to describe their body’s tendency to experience anxiety. When they later present with symptoms, one can use these baseline data to aid in the new assessment. Thus, a culture of considering emotional factors can be woven into practice, weakening any resistance to the idea that emotions and health, mind and body, are tightly bound.

Time factors

Based on our experience, family physicians can perform two thirds of these diagnostic assessments during 15 minutes of focused interviewing. More complex cases, such as patients with cognitive disruption or multiple manifestations of anxiety, may take longer to diagnose and generally need more specialized care or referral. If required, a patient could be asked back for a 1 half-hour session later in the day or week.

Taking care of ourselves

Despite the importance of the emotional system in medicine, medical curricula generally fail to provide sufficient education in this area. At the same time, up to half of our own ranks report emotional burnout.³¹ Even with the lack of mainstream medical teaching about emotions and health, it behooves us to learn what we can about the emotional system as it applies to the patient and to ourselves in relation to these most challenging problems. Focused seminars, peer case review, select reading, and videotape training can all help in this educational process.³²

Acknowledgments

The author wishes to thank the many colleagues who reviewed and commented on this manuscript. This work is supported by Dalhousie University, Capital Health and the Nova Scotia Department of Health.

Correspondence
Allan Abbass, MD, FRCPC, Associate Professor and Director of Education, Psychiatry, Director, Center for Emotions and Health, 8th Floor, Abbie J. Lane Memorial Building, Halifax, NS B3H 2E2, Canada. E-mail: [email protected].

A 42-year-old man has chronic fatigue and fibromyalgia that has led to a 13-month disability leave from work. The reason for his current office visit is longstanding pain in his shoulders. As you take his history, he is sitting with hands clenched and he generally appears tense.

A 38-year-old woman with severe incapacitating gastroesophageal reflux disease, irritable bowel syndrome, and depression has been too disabled to work for 2 years. At the time of your interview, her posture is relaxed and she shows no signs of anxiety.

These 2 very different patients (whose cases I will review in detail) share a common problem: somatization, the translation of emotions into somatic problems or complaints. It is well documented—though still largely unrecognized in practice—that somatization accounts for a large proportion of office visits to primary care physicians as well as specialists,^1,2 leading to unnecessary testing, treatment, and hospitalization, disability and corporate financial loss,³ likely earlier mortality,⁴ and frustration for patients and physicians.⁵

No longer a diagnosis of exclusion

Despite the burden somatization places on the medical system, the diagnosis is often made by indirect methods such as checklist, speculation, or exclusion when other problems are ruled out.⁶ The common position, even in recent reviews, is that somatization should be treated by nonspecific measures, such as frequent office visits to increase the patient’s and physician’s ability to cope with what is often seen to be a chronic and incurable disorder.^7-11 Such a position is no longer warranted.

Based on recent quantitative and extensive case-based research, specific emotion-focused brief therapies and videotape-based research have clarified how emotions are experienced in the body and how somatization of emotions occurs (see The physiology of emotions). These methods, including short-term dynamic psychotherapy (STDP) have been used to diagnose and treat somatization effectively since the 1980s. Somatization, with its morbidity and chronicity, need no longer be diagnosed by exclusion nor treated palliatively without specific diagnostic testing.

FIGURE
The 4 patterns of somatization

Videotaped case-series research shows 4 main patterns of somatization: 1) striated muscle unconscious anxiety, 2) smooth muscle tension 3) cognitive-perceptual disruption, and 4) conversion.¹⁸

Striated muscle tension due to unconscious anxiety manifests through hand clenching, sighing, and even hyperventilation that the patient is not aware of. These patients may report panic attacks, chest pain, headache, fibromyalgia, and other musculoskeletal complaints. These conditions are often frustrating to family, employers, and physicians since conditions like chronic pain respond to treatment slowly or not at all.

Smooth muscle tension due to unconscious anxiety causes acute or chronic spasm of blood vessels, GI tract, airways, and the bladder. Patients exhibiting smooth muscle tension may present with GI symptoms, migraine, hypertension, urinary frequency, and upper airway constriction mimicking asthma. They often report histories of depression, panic, substance abuse, personality disorders, and past sexual or physical abuse.

Cognitive perceptual disruption due to unconscious anxiety typically involves visual blurring, tunnel vision, loss of train of thought, and “drifting,” wherein the patient is temporarily mentally absent from the room. These patients have chronically poor memories and concentration. They are commonly victims or perpetrators of partner abuse, have frequent accidents, and have transient paranoia. They often end up seeing neurologists and undergoing expensive testing. Most have histories of dissociative disorders, personality disorders, or childhood abuse. In the family doctor’s office they frequently forget what was said and call back after the appointment. They appear confused and easily flustered and either avoid physical examinations entirely or endure them with great anxiety.

Conversion manifests as muscle weakness or paralysis in any voluntary muscle. Patients with acute conversion describe dropping items or even dropping to the floor as muscles give way without explanation. They will often report histories of witnessing or experiencing violent abuse.

One pattern usually predominates

The total amount of somatized emotion is distributed over the 4 pathways ( Table 1 ). One pathway generally prevails at any given time, though different pathways may come into play as anxiety waxes or wanes. When anxiety is expressed primarily through smooth muscle tension, cognitive perceptual disruption, or conversion, the striated muscles are relatively relaxed.

This finding of apparent calm while somatizing has been noted elsewhere in research of patients with hypertension. This is the “belle indifference” a patient expresses as they are temporarily relieved of muscle tension through somatization elsewhere.¹⁹

TABLE 1
Examples of diagnosable somatization patterns

Major types of defense

Two important categories of defense include isolation of affect and repression.

Isolation of affect is awareness of emotions in one’s head without experiencing them in the body. Intellectualization is a form of isolation of affect.

Repression is the unconscious process by which emotions are shunted into the body rather than reaching consciousness at all. For example, strong emotions, including rage, may directly cause sighing and a panic attack without the person being aware of either the emotion or the sighing.²⁰

Experiencing the emotions overcomes somatization

Videotaped research also shows that if a person can experience true feelings in the moment, somatization of these feelings is weakened and overcome. The feelings being experienced push out the anxiety and somatization ( Figure ). Thus, somatization can be reduced or removed by helping a patient feel emotions being stirred by recent events or from past events. Through this process one may diagnose somatization and also produce a therapeutic effect for a patient.

Direct diagnosis of somatization

An objective assessment

Because the process of somatization is unconscious to the patient, diagnosis is based on objective findings during examination rather than on a patient’s report. This is similar to evaluating a patient with abdominal pathology: we would not expect the patient to report an abdominal mass, even though we could detect it and train the patient to palpate it. The somatizing patient believes the problem is physical, so the history reported is more likely to lead to physical testing and medical treatments than to a direct examination of the emotional system. Although clues in the history may suggest a patient is somatizing,²⁰ the definitive test, like that of an abdominal examination, is “hands on,” observing the patient’s direct response to an emotion-focused interview.

Actively exploring emotions

Examination of the emotional system is analogous to a physical examination of other systems, and progresses from observation to “palpation” or “percussion” ( Table 2 ).

Observe the patient for visible unconscious anxiety. Then, in the context of a supportive patient-doctor relationship, explore emotionally charged situations that generate symptoms.

Alternatively, one may ask in what way strong emotions like anger affect the patient’s physical problems. Asking about specific recent events and feelings that were triggered usually mobilizes emotions, giving you and the patient a direct look at how emotions affect them physically.

If a patient is anxious in the office, it will be most meaningful to examine the feelings they experience during the interview.

TABLE 2
Exploring emotions in a patient-centered interview

Managing defenses

At times, the defenses used to avoid feelings must be pointed out before the patient can see and interrupt these behaviors. If the process is too detached or intellectual, then feelings will not be activated and the system cannot be assessed. The physician’s rapport allows him or her to clarify the process and the need for the patient to try to approach and experience feelings when speaking about them. This is analogous to the process of examining a sore abdomen when a patient is guarding: the patient must relax for examination to take place, and we help them do this by explaining the process.

Patients who are defensive and insist the problem is not related to emotions are managed differently. These patients usually are quite tense and already emotionally activated. An open examination of feelings the patient has about coming to see you that day is a good way to begin. Through this focus one can see the patient’s somatizing patterns directly as well as develop a working rapport.

Managing anxiety

If the patient becomes anxious when asked about emotions, introduce a calming step by asking the patient to intellectualize about the specific bodily anxiety symptoms. This reduces the anxiety by using the defense of intellectualization.

Recap and planning

The interview is concluded by reviewing the findings with the patient in the same way one would share findings of a blood test. Management options would depend on the findings and may include another interview, further medical investigations, referral for treatment, or follow-up to gauge the patient’s response to the interview itself.

Interpreting the patient’s responses

With the focused assessment, the somatic symptoms will transiently increase or decrease, disappear, or not change at all ( Table 3 ).

An increase in symptoms with emotional focus suggests that emotions aggravate or directly cause the problems. A decrease in symptoms during the test also suggests a linkage to emotions. Disappearance of the symptoms by bringing emotional experiences to awareness is the best direct evidence that somatization of these emotions was causing the patient’s symptoms.

No change in a patient’s symptoms or signs—provided there was adequate emotional activation—suggests no somatization of emotions. In these cases, other physical factors must be sought. For example, a woman with chronic left leg weakness and numbness had no shift in symptoms with this test: she was found to have neuropathy due to multiple sclerosis. We have found that 5% to 10% of patients referred to our diagnostic clinic have physical problems that were mistaken for somatization.

TABLE 3
Interpretation of responses to emotionally focused assessment

False negatives

False negatives occur when the test does not detect the process of somatization when it is present. This will occur if the level of emotion mobilized was too low, if the patient is too sedated, if the defenses the patient used were not sufficiently interrupted, or when the patient is not working collaboratively with the doctor during the test. In each case the patient must allow emotions to be mobilized and the doctor must focus adequately on the emotional experiences to yield an interpretable response.

False positives

False positives occur when the patient has a rise or fall in symptoms during the test for other reasons—eg, coincidental shifts in episodic conditions like muscle spasm or symptom reduction due to distraction during the test itself. It is important in these cases to repeat the test more than once and see if the results are reproducible.

Treatment: short-term dynamic psychotherapy

STDP is clinically effective for patients with somatization

Short-term dynamic psychotherapy (STDP) formats specifically help a patient to examine trauma and loss-related emotions that result in somatization, depression, anxiety, and self-defeating behaviors. Case-series videotaped research over the past 30 years has established the effectiveness of the methods in both short and long term follow-up.²¹

STDP is efficacious in controlled trials and meta-analyses

In 1995, Anderson and Lambert²² conducted a meta-analysis of 26 controlled studies and found STDP to be superior to minimal treatment controls and wait lists including in samples with somatization. It was found to be as effective in removing anxiety and depressive symptoms as cognitive behavioral therapy. A recent meta-analysis,²³ using more strict inclusion criteria, yielded the same findings. In a recent randomized controlled trial of symptomatic patients with personality disorders, STDP brought significant symptom reduction while cognitive therapy did not, suggesting that STDP may have added benefits in more resistant and complex symptomatic patients.²⁴

In our current Cochrane review search,²⁵ we have found 40 published randomized controlled trials supporting its efficacy with a range of disorders including ulcer disease, irritable bowel syndrome, dyspepsia, and urethral syndrome.^26-29 Our review has likewise found STDP to be superior to minimal treatment or waitlist controls and that the gains are maintained in follow-up averaging over 1 year.

STDP is cost-effective and reduces health care utilization

STDP has been shown to reduce healthcare utilization and to be cost-effective in treating patients with dyspepsia, irritable bowel syndrome, depression, and self-harm and treatment-resistant conditions.³⁰ Of specific cost figures cited in reviewed papers, 27 out of 34 showed cost savings with STDP including reduction in total costs, medication costs, disability, hospital, and physician use.

Case Illustrations

Case 1: Striated muscle anxiety

This 42-year-old man had chronic fatigue and fibromyalgia which lead to a 13 month disability up to the time of consultation. He came to the office with longstanding pain in his shoulders. His hands were clenched during the interview, and he appeared tense while giving his history.

• DOCTOR: Can you tell about a specific time when you had an emotional upset so we can understand how exactly it affects you?
• PATIENT: Yeah, problems at home with my wife…. Saturday she wanted me to do some work on the garage. She started to yell. Every day it’s the same thing and I’m getting tired of it.… DOCTOR: So how do you feel toward her?
• PATIENT: [Takes a deep sigh, hands become clenched] Mad.
• DOCTOR: You mean mad … angry?
• PATIENT: Yeah.
• DOCTOR: How do you experience the anger inside physically?
• PATIENT: Very, very… tense
• DOCTOR: That is tension…anxiety?
• PATIENT: Yeah.
• DOCTOR: How did you experience the anger?
• PATIENT: I start to ignore her.
• DOCTOR: Is that a mechanism to deal with anger?
• PATIENT: It’s really hard to put a word on it…. I get really mad…it’s like a rage.
• DOCTOR: So how do you experience the rage?
• PATIENT: [Patient takes a big sigh and clenches his hands tightly]
• DOCTOR: Do you notice you sigh and become tense when you talk about the rage.
• PATIENT: No, I didn’t. I don’t feel anxious.
• DOCTOR: But, do you notice the sigh and your hands?
• PATIENT: I do now, but didn’t see it before.
• DOCTOR: Is this what is happening to you … that you are getting all tensed up about these feelings?
• PATIENT: Yeah, it must be.

At a later point in the 1-hour session, the patient was able to feel the visceral emotions of rage, guilt about the rage, and sadness over several years of conflict. When the feelings were experienced in the office, he had an abrupt drop in muscle tension and bodily pain: this was further evidence he had been somatizing, or as he said, “bottling up” these complex feelings.

As is typical of patients with primarily striated muscle anxiety, he denies being nervous despite showing obvious anxiety in the interview. He denies anxiety because it has been unconscious to him, thus free to create fibromyalgia pain. Through this single interview a link is made for both patient and doctor between blocked feelings and body pain. With 10 treatment sessions focused on this process, his fibromyalgia resolved; he returned to work and no longer needed antidepressants.

Case 2: Smooth muscle anxiety

This patient is a 38 year-old woman with severe incapacitating GERD, irritable bowel syndrome, and depression who was disabled from work for 2 years at the time of consultation. This woman had a very relaxed posture with relaxed hands and an absence of obvious anxiety. After 10 minutes of exploring situations and events that make her stomach worse, we arrive at the following point.

• DOCTOR: Can you tell me about another time when your stomach felt worse?
• PATIENT: Yes. There was once when my sister-inlaw did something and it made me angry. Yeah, when people make me angry I don’t tell them, I just avoid them.
• DOCTOR: Can you describe one of those times, so we can see how that affects you.
• PATIENT: Once she was arguing with my brother, like they usually do….
• DOCTOR: How did you feel then?
• PATIENT: … Now I just got that again [pointing to her stomach and chest with upward motion and burps]
• DOCTOR: Heartburn? Just came on?
• PATIENT: Yeah, heartburn, just came on.
• DOCTOR: Is there anything else you notice? Like in your stomach?
• PATIENT: No, just that … but I can hear my stomach churning.
• DOCTOR: So is it when you have anger your stomach churns and you get this acid?
• PATIENT: Must be….
• DOCTOR: …because in your approach to talk about anger you got cramps and acid. So is that one way the anger goes?
• PATIENT: Yes it must be, but I never thought of that part. [Stomach stops churning and heartburn stops as we talk about it for few minutes.] You know, this all started to get worse when my fiancé dumped me. [She goes onto describe a story of being not only rejected but also feeling humiliated by how it was done. She never felt emotional about it but just got severe diarrhea and was confined to her room for 3 weeks.]
• DOCTOR: How did you feel toward your fiancé when he dumped you that way?
• PATIENT: I was just so sick and depressed. I didn’t feel any anger. [Patient burps again this time rubs abdomen due to some discomfort.]
• DOCTOR: Did you get the stomach upset just now again?
• PATIENT: My stomach is upset again. Just the noise and acid again.
• DOCTOR: So again, when we focus on the feelings, the cramps and acid come back.
• PATIENT: For sure. What can we do about that?
• DOCTOR: Can we try to help you identify these feelings before they go to your stomach, to try to interrupt that process. Can you tell me about another incident like that?

The patient required 3 one-hour sessions to improve her tolerance of anxiety, so she could intellectualize about feelings rather than have them directly affect her stomach. The feelings of rejection had triggered rage and guilt about rage associated with sexual abuse by her brother and the abandonment she felt from her mother when she told her mother about it. With 12 sessions of therapy, she was able to stop her IBS medication, anxiolytic, and antidepressant.

This vignette is typical for patients with primarily smooth muscle unconscious anxiety. The patient had no visible anxiety but had GI symptoms when focusing on emotions about recent trauma. The symptoms were mobilized and reduced repeatedly, confirming a link with emotions. Note that outwardly she looked calm, but the emotions mobilized were being shunted to her GI tract.

Incorporating emotion diagnostics into practice

To perform these interview procedures, the physician must understand emotion physiology and the patterns of somatization as outlined above. This is entirely intuitive to many physicians the first time seeing this material: they can readily employ that which they already know. In general, though, physicians reading this will want to ponder it and see how it may apply case by case as they develop skills with it over time. Senior clinicians have usually done these assessments by default, by pressure from patients, or because they learned elements of this over time from various experiences.

Helpful short-cuts

Family physicians trained in emotion assessment note that abbreviated elements can easily be incorporated into a patient-centered assessment process. For example, one may ask how “stress,” “emotions,” or “anger” affects the person and their body or ask how the person handles anger in specific incidents.

In an initial patient questionnaire, one can include a few questions that encourage the patient to think about how stress affects them and to describe their body’s tendency to experience anxiety. When they later present with symptoms, one can use these baseline data to aid in the new assessment. Thus, a culture of considering emotional factors can be woven into practice, weakening any resistance to the idea that emotions and health, mind and body, are tightly bound.

Time factors

Based on our experience, family physicians can perform two thirds of these diagnostic assessments during 15 minutes of focused interviewing. More complex cases, such as patients with cognitive disruption or multiple manifestations of anxiety, may take longer to diagnose and generally need more specialized care or referral. If required, a patient could be asked back for a 1 half-hour session later in the day or week.

Taking care of ourselves

Despite the importance of the emotional system in medicine, medical curricula generally fail to provide sufficient education in this area. At the same time, up to half of our own ranks report emotional burnout.³¹ Even with the lack of mainstream medical teaching about emotions and health, it behooves us to learn what we can about the emotional system as it applies to the patient and to ourselves in relation to these most challenging problems. Focused seminars, peer case review, select reading, and videotape training can all help in this educational process.³²

Acknowledgments

The author wishes to thank the many colleagues who reviewed and commented on this manuscript. This work is supported by Dalhousie University, Capital Health and the Nova Scotia Department of Health.

Correspondence
Allan Abbass, MD, FRCPC, Associate Professor and Director of Education, Psychiatry, Director, Center for Emotions and Health, 8th Floor, Abbie J. Lane Memorial Building, Halifax, NS B3H 2E2, Canada. E-mail: [email protected].

Most shoulder pain responds best to NSAIDs or subacromial corticosteroid injections followed by a home exercise program or formal physical therapy exercises. Accumulating evidence is making it clearer what works and what doesn’t for specific diagnoses.

Time to healing varies greatly among persons with shoulder pain, and specific prognostic indicators may help you and your patients know what to expect.

Quick diagnostic review

Consider the patient’s age, history of trauma, details of injury, and previous shoulder problems. Observe the patient’s general movements, assess range of motion, and use provocative testing to form a differential diagnosis ( Figure 1 ).

If the diagnosis is unclear, arrange for imaging studies ( Table 1 ). A more thorough review for diagnosing shoulder pain may be found in the article “Approach to the patient with shoulder pain” (J Fam Pract 2002; 7:605–611). The conditions causing shoulder pain (in order of frequency, as seen by primary care physicians) are subacromial impingement syndrome (SIS), adhesive capsulitis, acute bursitis, calcific tendinitis, glenohumeral arthrosis, biceps tendinitis, and labral tear.^1,2

TABLE 1
Value of imaging tests for shoulder injuries

FIGURE 1
Evaluating shoulder pain for possible rotator cuff tear

Subacromial impingement syndrome

This condition was first described by Neer, who estimated it leads to 95% of rotator cuff tears.³

Impingement occurs from repetitive overhead activities, acute trauma, or instability of the glenohumeral joint (subtle or overt). Current theory holds that degeneration of the rotator cuff tendons or inflammation of the subacromial bursa—caused by irritation against the coracoacromial arch—can progress to degeneration and a complete rotator cuff tear. So-called rotator cuff tendinitis is better described as a tendinopathy with mucoid degeneration of the tendon. SIS stage I involves edema and hemorrhage, as would be seen with rotator cuff tendinopathy or bursitis.

Progressive feedback loop of subacromial impingement syndrome. Acute bursitis involves the subacromial bursa and typically is secondary to subacromial impingement. As underlying tendinopathy, instability, or heterotrophic bone irritates the bursa, it will become inflamed and irritated. Inflammation exacerbates the impingement and that in turn causes worsening of the bursitis.

Stage II and III impingement syndrome. SIS stage II is a progression to fibrosis and partial tear of the rotator cuff. Stage III is a full-thickness tear of the rotator cuff. These stages of SIS are seen predominantly in patients over the age of 40 years, and they become more common with increasing age. The tear—partial or complete— usually occurs in the supraspinatus tendon. Tears of other rotator cuff muscles are less common.

Magnetic resonance imaging (MRI), with or without arthrography, is used in clinical practice and in research to diagnose rotator cuff tears. Growing evidence indicates that ultrasound is a less expensive and equally effective way to diagnose stage II or III impingement. In the United States, however, the option of ultrasound is limited by scarce availability and inadequate operator skill.

The subacromial injection test is useful in clinical practice. Local anesthetic is injected into the subacromial space. Persisting loss of strength despite pain relief is a positive sign of impairment of the rotator cuff.

MRI or ultrasound must be done in conjunction with history taking and physical examination. As the age of a person increases, the amount of asymptomatic rotator cuff tendon injury will also increase. The incidence of rotator cuff tears has been found to be between 50% to 60% in cadavers of deceased elderly. Thirty percent were found to be stage III impingement; 20% to 30% were partial stage II impingement.⁴

Adhesive capsulitis

Also known as frozen shoulder, adhesive capsulitis may begin with any inflammatory condition, but it is most commonly idiopathic. It characteristically progresses through 3 stages.

The hallmark of adhesive capsulitis is a progressive lack of range of motion with both passive and active movement.

The first stage involves progressive pain and decreased range of motion as the capsule scars.

The second stage involves maturation of capsule scaring, resulting in decreased pain and increased restriction of movement.

The third stage is resolution of the condition, leading to a gradual increase in range of motion.

Full range of motion may or may not return, and the time to resolution is typically 1 to 2 years. Adhesive capsulitis is most common in older persons, especially women in the fourth and fifth decades.⁵

Comparing nonoperative treatments

Nonoperative treatment modalities include protection, relative rest, and ice (PRI); anti-inflammatory medications; physical therapy (supervised or home exercise program); acupuncture; and steroid injection.

Operative treatments, depending on the particular disorder, include rotator cuff repair, subacromial decompression, capsular tightening, or manipulation under anesthesia.

The efficacy of nonoperative treatments for shoulder pain is not well known. Studies of treatment modalities have been numerous but generally of poor quality due to a lack of uniformity in how shoulder disorders are defined and in the variability of outcome measures used. Several recent systematic reviews have tried to identify which interventions are efficacious ( Table 2 ).^6-11

Overall, NSAIDs and subacromial steroid injections are effective in the short-term treatment of shoulder pain.^26-28 However, only nonselective NSAIDs have been studied. Evidence is insufficient to recommend use of cyclooxygenase-2 (COX-2) medications for shoulder pain.

Steroid injections may not confer extra benefit when added to NSAIDs, but they appear superior to NSAIDs in improving shoulder abduction. This is particularly true for the painful stiff shoulder, as seen with impingement or rotator cuff disease.^26,28

Two recent randomized control trials showed corticosteroid injections to be superior to physical therapy for treatment of shoulder complaints.^12,13

Shoulder instability may be treated nonoperatively at first with PRI, NSAIDs, and strengthening and proprioceptive exercises for the rotator cuff. If 3 to 6 months of nonoperative treatment fails, the patient should be referred for surgical evaluation, especially in cases of full-thickness rotator cuff tears.¹⁴

TABLE 2
Nonoperative treatment options for shoulder pain

Treatment of specific shoulder disorders

Subacromial impingement syndrome stage I

A recommendation (SOR: B) can be made for the use of NSAIDs in the treatment of stage I impingement ( Table 3 ). This is based on level 2 evidence that NSAIDs are beneficial for rotator cuff tendinopathy and bicipital tendinitis, compared with placebo in a 1 to 2 week follow-up.^15,17 No specific NSAID has proved better than another.^18,19

Steroid injection ( Figure 2 ) is beneficial for the acute treatment of SIS I reflected by improvement in pain (SOR: A).^20-23 This is particularly evident during the first 1 to 2 weeks following injections.³⁸ At 4 to 6 weeks, there appears to be no difference in the efficacy of steroid injection compared with NSAIDs,^24,25 but they are both better than placebo.⁴³

Physical therapy, specifically rotator cuff strengthening and range of motion, is as beneficial as surgery for SIS I at 6 month and 2¹/2-year follow-up, and both were better than placebo (SOR: B).^26,27

TABLE 3
Treatments for SIS I impingement (rotator cuff tendinitis/tendinosis)

FIGURE 2
Steroid injection in the subacromial space

SIS stages II and III

There is very good evidence (SOR: B) regarding the efficacy of nonoperative treatment of SIS II and III, based on level 2 cohort studies that suggest nonoperative care leads to improvements in patient satisfaction, pain, and daily activities.^28,29 Similar outcomes are reported for patients undergoing physical therapy alone.^30,31 Weiss reported that corticosteroid injections for stage III/full-thickness rotator cuff tears resulted in an 86% improvement as measured by return to previous activities and less or no pain with motion ( Table 4 ).³²

The most constant outcome measure was report of a reduction in pain. Younger patients or those with higher functional demands will likely consider surgical repair if nonoperative measures fail, particularly for full-thickness tears.

TABLE 4
Nonoperative treatments for SIS III (full-thickness rotator cuff tears)

Adhesive capsulitis

There is no consistent evidence that treatment of any one form reduces the pain or improves range of motion in frozen shoulders. Various treatments that have been tried include, though are not limited to, steroid injection, NSAIDs, and physical therapy.^33-37 Studies on treatment efficacy are complicated by inherent discrepancy between patient and observer opinions of limitations in this condition, with objective range of motion findings often not being consistent with patient reported limitations.³⁸

Indicators of quicker or slower recovery

Studies of prognosis following treatment have been difficult to assess due the heterogeneity of the underlying conditions and variability of treatments. A follow-up questionnaire in one instance found no difference between treatment groups. Complaints of pain or impaired mobility 2 to 3 years after treatment were similar among patients treated with steroid injection and physical therapy and with physical therapy alone.³⁰ Overall, 76% of respondents were symptom free at 2 to 3 years.

Two prospective studies confirm that speed of recovery is slow, with complete recovery 23% at 1 month, 21% to 51% at 6 months, 59% at 1 year, and 69% at 18 months.^39,40

Prognostic indicators of quicker recovery were preceding overuse or slight trauma and early presentation to the physician.⁵⁸ Protracted recovery occurred more often with high pain levels during the day or associated neck pain.⁵⁸ These results suggest that patients with subacromial impingement stage I respond better to nonoperative treatment than those patients with underlying degenerative changes or referred pain from the neck.

Finally, specialty surgical referral may be necessary in cases of failed nonoperative therapy or persistent diagnostic and therapeutic challenges.

Corresponding author
Thomas H. Trojian, MD, 99 Woodland Street, Hartford, CT 06105. E-mail: [email protected].

Most shoulder pain responds best to NSAIDs or subacromial corticosteroid injections followed by a home exercise program or formal physical therapy exercises. Accumulating evidence is making it clearer what works and what doesn’t for specific diagnoses.

Time to healing varies greatly among persons with shoulder pain, and specific prognostic indicators may help you and your patients know what to expect.

Quick diagnostic review

Consider the patient’s age, history of trauma, details of injury, and previous shoulder problems. Observe the patient’s general movements, assess range of motion, and use provocative testing to form a differential diagnosis ( Figure 1 ).

If the diagnosis is unclear, arrange for imaging studies ( Table 1 ). A more thorough review for diagnosing shoulder pain may be found in the article “Approach to the patient with shoulder pain” (J Fam Pract 2002; 7:605–611). The conditions causing shoulder pain (in order of frequency, as seen by primary care physicians) are subacromial impingement syndrome (SIS), adhesive capsulitis, acute bursitis, calcific tendinitis, glenohumeral arthrosis, biceps tendinitis, and labral tear.^1,2

TABLE 1
Value of imaging tests for shoulder injuries

FIGURE 1
Evaluating shoulder pain for possible rotator cuff tear

Subacromial impingement syndrome

This condition was first described by Neer, who estimated it leads to 95% of rotator cuff tears.³

Impingement occurs from repetitive overhead activities, acute trauma, or instability of the glenohumeral joint (subtle or overt). Current theory holds that degeneration of the rotator cuff tendons or inflammation of the subacromial bursa—caused by irritation against the coracoacromial arch—can progress to degeneration and a complete rotator cuff tear. So-called rotator cuff tendinitis is better described as a tendinopathy with mucoid degeneration of the tendon. SIS stage I involves edema and hemorrhage, as would be seen with rotator cuff tendinopathy or bursitis.

Progressive feedback loop of subacromial impingement syndrome. Acute bursitis involves the subacromial bursa and typically is secondary to subacromial impingement. As underlying tendinopathy, instability, or heterotrophic bone irritates the bursa, it will become inflamed and irritated. Inflammation exacerbates the impingement and that in turn causes worsening of the bursitis.

Stage II and III impingement syndrome. SIS stage II is a progression to fibrosis and partial tear of the rotator cuff. Stage III is a full-thickness tear of the rotator cuff. These stages of SIS are seen predominantly in patients over the age of 40 years, and they become more common with increasing age. The tear—partial or complete— usually occurs in the supraspinatus tendon. Tears of other rotator cuff muscles are less common.

Magnetic resonance imaging (MRI), with or without arthrography, is used in clinical practice and in research to diagnose rotator cuff tears. Growing evidence indicates that ultrasound is a less expensive and equally effective way to diagnose stage II or III impingement. In the United States, however, the option of ultrasound is limited by scarce availability and inadequate operator skill.

The subacromial injection test is useful in clinical practice. Local anesthetic is injected into the subacromial space. Persisting loss of strength despite pain relief is a positive sign of impairment of the rotator cuff.

MRI or ultrasound must be done in conjunction with history taking and physical examination. As the age of a person increases, the amount of asymptomatic rotator cuff tendon injury will also increase. The incidence of rotator cuff tears has been found to be between 50% to 60% in cadavers of deceased elderly. Thirty percent were found to be stage III impingement; 20% to 30% were partial stage II impingement.⁴

Adhesive capsulitis

Also known as frozen shoulder, adhesive capsulitis may begin with any inflammatory condition, but it is most commonly idiopathic. It characteristically progresses through 3 stages.

The hallmark of adhesive capsulitis is a progressive lack of range of motion with both passive and active movement.

The first stage involves progressive pain and decreased range of motion as the capsule scars.

The second stage involves maturation of capsule scaring, resulting in decreased pain and increased restriction of movement.

The third stage is resolution of the condition, leading to a gradual increase in range of motion.

Full range of motion may or may not return, and the time to resolution is typically 1 to 2 years. Adhesive capsulitis is most common in older persons, especially women in the fourth and fifth decades.⁵

Comparing nonoperative treatments

Nonoperative treatment modalities include protection, relative rest, and ice (PRI); anti-inflammatory medications; physical therapy (supervised or home exercise program); acupuncture; and steroid injection.

Operative treatments, depending on the particular disorder, include rotator cuff repair, subacromial decompression, capsular tightening, or manipulation under anesthesia.

The efficacy of nonoperative treatments for shoulder pain is not well known. Studies of treatment modalities have been numerous but generally of poor quality due to a lack of uniformity in how shoulder disorders are defined and in the variability of outcome measures used. Several recent systematic reviews have tried to identify which interventions are efficacious ( Table 2 ).^6-11

Overall, NSAIDs and subacromial steroid injections are effective in the short-term treatment of shoulder pain.^26-28 However, only nonselective NSAIDs have been studied. Evidence is insufficient to recommend use of cyclooxygenase-2 (COX-2) medications for shoulder pain.

Steroid injections may not confer extra benefit when added to NSAIDs, but they appear superior to NSAIDs in improving shoulder abduction. This is particularly true for the painful stiff shoulder, as seen with impingement or rotator cuff disease.^26,28

Two recent randomized control trials showed corticosteroid injections to be superior to physical therapy for treatment of shoulder complaints.^12,13

Shoulder instability may be treated nonoperatively at first with PRI, NSAIDs, and strengthening and proprioceptive exercises for the rotator cuff. If 3 to 6 months of nonoperative treatment fails, the patient should be referred for surgical evaluation, especially in cases of full-thickness rotator cuff tears.¹⁴

TABLE 2
Nonoperative treatment options for shoulder pain

Treatment of specific shoulder disorders

Subacromial impingement syndrome stage I

A recommendation (SOR: B) can be made for the use of NSAIDs in the treatment of stage I impingement ( Table 3 ). This is based on level 2 evidence that NSAIDs are beneficial for rotator cuff tendinopathy and bicipital tendinitis, compared with placebo in a 1 to 2 week follow-up.^15,17 No specific NSAID has proved better than another.^18,19

Steroid injection ( Figure 2 ) is beneficial for the acute treatment of SIS I reflected by improvement in pain (SOR: A).^20-23 This is particularly evident during the first 1 to 2 weeks following injections.³⁸ At 4 to 6 weeks, there appears to be no difference in the efficacy of steroid injection compared with NSAIDs,^24,25 but they are both better than placebo.⁴³

Physical therapy, specifically rotator cuff strengthening and range of motion, is as beneficial as surgery for SIS I at 6 month and 2¹/2-year follow-up, and both were better than placebo (SOR: B).^26,27

TABLE 3
Treatments for SIS I impingement (rotator cuff tendinitis/tendinosis)

FIGURE 2
Steroid injection in the subacromial space

SIS stages II and III

There is very good evidence (SOR: B) regarding the efficacy of nonoperative treatment of SIS II and III, based on level 2 cohort studies that suggest nonoperative care leads to improvements in patient satisfaction, pain, and daily activities.^28,29 Similar outcomes are reported for patients undergoing physical therapy alone.^30,31 Weiss reported that corticosteroid injections for stage III/full-thickness rotator cuff tears resulted in an 86% improvement as measured by return to previous activities and less or no pain with motion ( Table 4 ).³²

The most constant outcome measure was report of a reduction in pain. Younger patients or those with higher functional demands will likely consider surgical repair if nonoperative measures fail, particularly for full-thickness tears.

TABLE 4
Nonoperative treatments for SIS III (full-thickness rotator cuff tears)

Adhesive capsulitis

There is no consistent evidence that treatment of any one form reduces the pain or improves range of motion in frozen shoulders. Various treatments that have been tried include, though are not limited to, steroid injection, NSAIDs, and physical therapy.^33-37 Studies on treatment efficacy are complicated by inherent discrepancy between patient and observer opinions of limitations in this condition, with objective range of motion findings often not being consistent with patient reported limitations.³⁸

Indicators of quicker or slower recovery

Studies of prognosis following treatment have been difficult to assess due the heterogeneity of the underlying conditions and variability of treatments. A follow-up questionnaire in one instance found no difference between treatment groups. Complaints of pain or impaired mobility 2 to 3 years after treatment were similar among patients treated with steroid injection and physical therapy and with physical therapy alone.³⁰ Overall, 76% of respondents were symptom free at 2 to 3 years.

Two prospective studies confirm that speed of recovery is slow, with complete recovery 23% at 1 month, 21% to 51% at 6 months, 59% at 1 year, and 69% at 18 months.^39,40

Prognostic indicators of quicker recovery were preceding overuse or slight trauma and early presentation to the physician.⁵⁸ Protracted recovery occurred more often with high pain levels during the day or associated neck pain.⁵⁸ These results suggest that patients with subacromial impingement stage I respond better to nonoperative treatment than those patients with underlying degenerative changes or referred pain from the neck.

Finally, specialty surgical referral may be necessary in cases of failed nonoperative therapy or persistent diagnostic and therapeutic challenges.

Corresponding author
Thomas H. Trojian, MD, 99 Woodland Street, Hartford, CT 06105. E-mail: [email protected].

Most shoulder pain responds best to NSAIDs or subacromial corticosteroid injections followed by a home exercise program or formal physical therapy exercises. Accumulating evidence is making it clearer what works and what doesn’t for specific diagnoses.

Time to healing varies greatly among persons with shoulder pain, and specific prognostic indicators may help you and your patients know what to expect.

Quick diagnostic review

Consider the patient’s age, history of trauma, details of injury, and previous shoulder problems. Observe the patient’s general movements, assess range of motion, and use provocative testing to form a differential diagnosis ( Figure 1 ).

If the diagnosis is unclear, arrange for imaging studies ( Table 1 ). A more thorough review for diagnosing shoulder pain may be found in the article “Approach to the patient with shoulder pain” (J Fam Pract 2002; 7:605–611). The conditions causing shoulder pain (in order of frequency, as seen by primary care physicians) are subacromial impingement syndrome (SIS), adhesive capsulitis, acute bursitis, calcific tendinitis, glenohumeral arthrosis, biceps tendinitis, and labral tear.^1,2

TABLE 1
Value of imaging tests for shoulder injuries

FIGURE 1
Evaluating shoulder pain for possible rotator cuff tear

Subacromial impingement syndrome

This condition was first described by Neer, who estimated it leads to 95% of rotator cuff tears.³

Impingement occurs from repetitive overhead activities, acute trauma, or instability of the glenohumeral joint (subtle or overt). Current theory holds that degeneration of the rotator cuff tendons or inflammation of the subacromial bursa—caused by irritation against the coracoacromial arch—can progress to degeneration and a complete rotator cuff tear. So-called rotator cuff tendinitis is better described as a tendinopathy with mucoid degeneration of the tendon. SIS stage I involves edema and hemorrhage, as would be seen with rotator cuff tendinopathy or bursitis.

Progressive feedback loop of subacromial impingement syndrome. Acute bursitis involves the subacromial bursa and typically is secondary to subacromial impingement. As underlying tendinopathy, instability, or heterotrophic bone irritates the bursa, it will become inflamed and irritated. Inflammation exacerbates the impingement and that in turn causes worsening of the bursitis.

Stage II and III impingement syndrome. SIS stage II is a progression to fibrosis and partial tear of the rotator cuff. Stage III is a full-thickness tear of the rotator cuff. These stages of SIS are seen predominantly in patients over the age of 40 years, and they become more common with increasing age. The tear—partial or complete— usually occurs in the supraspinatus tendon. Tears of other rotator cuff muscles are less common.

Magnetic resonance imaging (MRI), with or without arthrography, is used in clinical practice and in research to diagnose rotator cuff tears. Growing evidence indicates that ultrasound is a less expensive and equally effective way to diagnose stage II or III impingement. In the United States, however, the option of ultrasound is limited by scarce availability and inadequate operator skill.

The subacromial injection test is useful in clinical practice. Local anesthetic is injected into the subacromial space. Persisting loss of strength despite pain relief is a positive sign of impairment of the rotator cuff.

MRI or ultrasound must be done in conjunction with history taking and physical examination. As the age of a person increases, the amount of asymptomatic rotator cuff tendon injury will also increase. The incidence of rotator cuff tears has been found to be between 50% to 60% in cadavers of deceased elderly. Thirty percent were found to be stage III impingement; 20% to 30% were partial stage II impingement.⁴

Adhesive capsulitis

Also known as frozen shoulder, adhesive capsulitis may begin with any inflammatory condition, but it is most commonly idiopathic. It characteristically progresses through 3 stages.

The hallmark of adhesive capsulitis is a progressive lack of range of motion with both passive and active movement.

The first stage involves progressive pain and decreased range of motion as the capsule scars.

The second stage involves maturation of capsule scaring, resulting in decreased pain and increased restriction of movement.

The third stage is resolution of the condition, leading to a gradual increase in range of motion.

Full range of motion may or may not return, and the time to resolution is typically 1 to 2 years. Adhesive capsulitis is most common in older persons, especially women in the fourth and fifth decades.⁵

Comparing nonoperative treatments

Nonoperative treatment modalities include protection, relative rest, and ice (PRI); anti-inflammatory medications; physical therapy (supervised or home exercise program); acupuncture; and steroid injection.

Operative treatments, depending on the particular disorder, include rotator cuff repair, subacromial decompression, capsular tightening, or manipulation under anesthesia.

The efficacy of nonoperative treatments for shoulder pain is not well known. Studies of treatment modalities have been numerous but generally of poor quality due to a lack of uniformity in how shoulder disorders are defined and in the variability of outcome measures used. Several recent systematic reviews have tried to identify which interventions are efficacious ( Table 2 ).^6-11

Overall, NSAIDs and subacromial steroid injections are effective in the short-term treatment of shoulder pain.^26-28 However, only nonselective NSAIDs have been studied. Evidence is insufficient to recommend use of cyclooxygenase-2 (COX-2) medications for shoulder pain.

Steroid injections may not confer extra benefit when added to NSAIDs, but they appear superior to NSAIDs in improving shoulder abduction. This is particularly true for the painful stiff shoulder, as seen with impingement or rotator cuff disease.^26,28

Two recent randomized control trials showed corticosteroid injections to be superior to physical therapy for treatment of shoulder complaints.^12,13

Shoulder instability may be treated nonoperatively at first with PRI, NSAIDs, and strengthening and proprioceptive exercises for the rotator cuff. If 3 to 6 months of nonoperative treatment fails, the patient should be referred for surgical evaluation, especially in cases of full-thickness rotator cuff tears.¹⁴

TABLE 2
Nonoperative treatment options for shoulder pain

Treatment of specific shoulder disorders

Subacromial impingement syndrome stage I

A recommendation (SOR: B) can be made for the use of NSAIDs in the treatment of stage I impingement ( Table 3 ). This is based on level 2 evidence that NSAIDs are beneficial for rotator cuff tendinopathy and bicipital tendinitis, compared with placebo in a 1 to 2 week follow-up.^15,17 No specific NSAID has proved better than another.^18,19

Steroid injection ( Figure 2 ) is beneficial for the acute treatment of SIS I reflected by improvement in pain (SOR: A).^20-23 This is particularly evident during the first 1 to 2 weeks following injections.³⁸ At 4 to 6 weeks, there appears to be no difference in the efficacy of steroid injection compared with NSAIDs,^24,25 but they are both better than placebo.⁴³

Physical therapy, specifically rotator cuff strengthening and range of motion, is as beneficial as surgery for SIS I at 6 month and 2¹/2-year follow-up, and both were better than placebo (SOR: B).^26,27

TABLE 3
Treatments for SIS I impingement (rotator cuff tendinitis/tendinosis)

FIGURE 2
Steroid injection in the subacromial space

SIS stages II and III

There is very good evidence (SOR: B) regarding the efficacy of nonoperative treatment of SIS II and III, based on level 2 cohort studies that suggest nonoperative care leads to improvements in patient satisfaction, pain, and daily activities.^28,29 Similar outcomes are reported for patients undergoing physical therapy alone.^30,31 Weiss reported that corticosteroid injections for stage III/full-thickness rotator cuff tears resulted in an 86% improvement as measured by return to previous activities and less or no pain with motion ( Table 4 ).³²

The most constant outcome measure was report of a reduction in pain. Younger patients or those with higher functional demands will likely consider surgical repair if nonoperative measures fail, particularly for full-thickness tears.

TABLE 4
Nonoperative treatments for SIS III (full-thickness rotator cuff tears)

Adhesive capsulitis

There is no consistent evidence that treatment of any one form reduces the pain or improves range of motion in frozen shoulders. Various treatments that have been tried include, though are not limited to, steroid injection, NSAIDs, and physical therapy.^33-37 Studies on treatment efficacy are complicated by inherent discrepancy between patient and observer opinions of limitations in this condition, with objective range of motion findings often not being consistent with patient reported limitations.³⁸

Indicators of quicker or slower recovery

Studies of prognosis following treatment have been difficult to assess due the heterogeneity of the underlying conditions and variability of treatments. A follow-up questionnaire in one instance found no difference between treatment groups. Complaints of pain or impaired mobility 2 to 3 years after treatment were similar among patients treated with steroid injection and physical therapy and with physical therapy alone.³⁰ Overall, 76% of respondents were symptom free at 2 to 3 years.

Two prospective studies confirm that speed of recovery is slow, with complete recovery 23% at 1 month, 21% to 51% at 6 months, 59% at 1 year, and 69% at 18 months.^39,40

Prognostic indicators of quicker recovery were preceding overuse or slight trauma and early presentation to the physician.⁵⁸ Protracted recovery occurred more often with high pain levels during the day or associated neck pain.⁵⁸ These results suggest that patients with subacromial impingement stage I respond better to nonoperative treatment than those patients with underlying degenerative changes or referred pain from the neck.

Finally, specialty surgical referral may be necessary in cases of failed nonoperative therapy or persistent diagnostic and therapeutic challenges.

Corresponding author
Thomas H. Trojian, MD, 99 Woodland Street, Hartford, CT 06105. E-mail: [email protected].

Evaluate for open-angle glaucoma (OAG) when a patient reports decreased vision, or when a patient even with good eyesight is found to be at high risk for the disease. Most patients with early glaucoma are unaware of the initial decrease in peripheral vision.¹

A relatively new diagnostic technique can detect even moderate damage to the optic nerve, and the procedure is brief. Ophthalmologists can choose from among several topical medications to reduce intraocular pressure. Your knowledge of the patient’s medical history is critical to avoiding potential drug-drug interactions.

Laser surgery and trabeculectomy may be indicated as first-line therapy for select patients.

Whom to screen

Persons aged older than 60 years, African Americans of any age, and those with a family history of OAG are at particularly high risk, and all risk factors should be fully assessed (SOR: B).² (See Open-angle glaucoma: The scope of the problem.)

In the Caucasian population aged 40 to 49 years with no family history of OAG, disease prevalence is just 0.18%. Prevalence is 4 times greater in African Americans of the same age range. Caucasians aged 60 to 69 years have a prevalence of OAG 4 times greater than patients aged 40 to 49. For African Americans older than 80 years, prevalence exceeds 11%.³

For persons with a first-degree relative with OAG, risk was found to be 9.2 times greater than for those without such a history.⁸

Ask specifically about decreased vision, loss of peripheral vision, difficulty seeing in the dark, and difficulty reading (SOR: B).

Before referring high-risk patients for a full ophthalmologic examination, examine the optic nerve with direct ophthalmoscopy (SOR: B).

Determining optic nerve status

Examination of the optic nerve head provides clues as to whether structural damage has occurred. Cup-disc ratio is used to assess risk of glaucoma development. The probability of abnormality increases dramatically for values above 0.5.⁹

The standard clinical technique used by primary care clinicians is with the direct ophthalmoscope. Sensitivity and specificity for a cup-disc ratio greater than 0.6 have been reported to be 64% and 96%, respectively, using direct ophthalmoscopy.¹⁰

Ophthalmologists use stereoscopic fundus photography to visualize the optic nerve. With this technique, sensitivity and specificity for a cup-disc ratio greater than 0.5 have been found to be 48% and 89%, respectively.¹¹ Studies, however, have reported a high interobserver variation in measurement of the cup-disc ratio even among experts in the field.¹²

What to look for. Characteristic changes include narrowing or notching of the neuroretinal rim, or characteristic visual field loss, such as arcuate defects and nasal loss.¹³ Describe an abnormal optic disc in terms of its cup-disc ratio, and report visual loss to the ophthalmologist as a defect in a respective field quadrant as detected on confrontational visual field testing or as an afferent pupillary defect in a given eye.

Referral. A final diagnosis of open-angle glaucoma can be made only after characteristic damage to the optic nerve has been confirmed by an ophthalmologist (SOR: B). Therefore, patients at high risk of developing OAG (age >60 years, African American race, positive family history) should be referred for an eye examination.

Other key diagnostic tests include measurement of intraocular pressure and visual field testing.² The accuracy of these tests is outlined in Table 1.

TABLE 1
Characteristics of diagnostic tests for open-angle glaucoma

Intraocular pressure: Caveats

Intraocular pressure (IOP) is measured by a tonometer. The eye is subjected to a force that flattens the cornea. This force is then related to the pressure in the eye, or IOP. The standard instrument for measuring IOP is the Goldman applanation tonometer. Handheld versions (tonopen) are useful for screening by the primary care clinician.¹¹ Studies of IOP distribution show the normal range of IOP values to be less than 21 mm Hg with a slight skew towards higher values.¹⁶

The altering effect of corneal thickness. IOP measurement may vary with the thickness of one’s cornea. A corneal thickness greater than 555 μm can produce falsely high readings, and a corneal thickness less than 540 μm can produce falsely low readings.^2,17,18 Thus, central corneal thickness (CCT) is a factor that may affect the accuracy of an IOP reading. Central corneal thickness is measured with a pachymeter, and an ophthalmologist must take this measurement into account when assessing a patient’s IOP.

Pressure may not be elevated in OAG. A number of population-based studies have documented an increase in the prevalence of OAG with an increase in IOP.^7,19,20 However, these same studies have also concluded that many patients with OAG have IOP levels in the normal range. These patients are deemed to have normal pressure glaucoma (NPG), a subtype of OAG.²¹

Likewise, many patients with elevated IOP have no demonstrable optic nerve damage;^19,20 this condition has been termed ocular hypertension (OHT).

A proper perspective. So, although an elevated IOP is associated with glaucoma, it is important to note that OAG is not defined by the presence of an elevated IOP. Optic nerve atrophy can occur in the absence of an increased IOP. ²¹ These findings, taken together with the variance of IOP with CCT, are reflected in the modest sensitivity and specificity for IOP readings greater than 21 mm Hg—47.1% and 92.4%, respectively. ¹⁴ Patients with a high IOP (>21 mm Hg) are at higher risk for developing OAG, but further ancillary studies and tests are necessary to confirm the diagnosis. ¹³

Evaluating the visual field

Visual field deterioration is the final manifestation of glaucoma. Vision is first lost peripherally. Central vision loss occurs at the end stage of the disease.

An ophthalmologist will use automated static threshold perimetry to evaluate the visual field. With this technique, the patient must identify white target lights of variable brightness in different locations of a dim 1-m bowl. Various data algorithms are then employed to compare any abnormality in the visual field with patterns that are characteristic of glaucoma.⁹ One study reported a 97% sensitivity and 84% specificity using a certain algorithm to recognize field abnormalities due to glaucoma.¹⁵ However, automated perimetry requires 10 to 20 minutes per eye, and patient fatigue often reduces reliability of the test. Also, an optic nerve head has typically undergone considerable damage before visual field changes are detected.²

An improved test. Frequency doubling technology promises to detect glaucomatous visual defects when there has been only moderate damage to the optic nerve. With frequency doubling technology, patients must recognize patterns of alternating light and dark bars. An abnormality in recognition is thought to be indicative of the pattern of field loss in glaucoma. One study found a sensitivity and specificity each greater than 90% for identifying patients thought to have glaucoma. Another benefit is that the exam takes an average of only 6 minutes to complete in both eyes. ²²

No single test result is enough

Successful screening for glaucoma should not rely solely on measuring IOP, assessment of the optic nerve, or visual field testing. These diagnostic clues are complementary and must be taken together to evaluate high-risk populations, including African Americans, those with a family history of glaucoma, and the elderly (SOR: C).

Regular follow-up

Regardless of findings, patients aged 40 to 60 years should be encouraged to have eye exams every other year, and those over age 60 should have annual eye exams (SOR: B).¹³ Regular ocular exams including vision check, extraocular muscle exam, papillary exam, and confrontational visual fields should be performed in these patients as well (SOR: C).

Treatment

IOP is the only risk factor for glaucoma that can be treated. Lowering IOP in randomized control trials has reduced the progression of visual field loss in OAG patients with abnormally high pressures²³ as well as in NPG patients with pressures in the normal range.²⁴

In the Early Manifest Glaucoma Trial, a 30% reduction in IOP reduced the rate of progression in the treatment group (45%) compared with the control group (62%; P=.007).²⁵ Progression risk decreased by approximately 10% per mm Hg of IOP reduction.

Setting a target pressure. Before beginning therapy, an ophthalmologist sets a target pressure that should halt further optic nerve damage. The initial target pressure is usually 20% to 30% lower than the pretreatment pressure. If damage to the optic nerve is already substantial, the target pressure may be set even lower.²

Stepwise therapy. Topical medications are usually given first, as eye drops. A comparison of these medications is outlined in Table 2. If IOP cannot be lowered pharmacologically, argon laser trabeculoplasty (ALT) is the next step. If the pressure still cannot be lowered, filtering surgery is the final alternative (SOR: C).²

TABLE 2
Pharmacologic options for patients with open-angle glaucoma

Pharmacologic options

Medical agents work in 1 of 2 ways to lower IOP: by decreasing production of aqueous humor, or by increasing drainage of aqueous humor out of the eye. Though most glaucoma medications are given topically, severe systemic side effects can occur.² Because the consulting ophthalmologist may not be aware of a patient’s other medical conditions, inquire about the topical ocular drops being recommended to make certain they are not contraindicated and to be alert to the potential for adverse effects (SOR: C).¹³

Beta-adrenergic antagonists can lower IOP by up to 31% ²⁵ and are often used as first-line treatment (SOR: A).²¹ However, nonselective beta-blockers (timolol, carteolol, levobunolol, metipranolol) are associated with a number of adverse effects including bronchospasm,³³ bradycardia, and hypotension. ³⁴

Betaxolol is a selective beta-blocker with less tendency to cause pulmonary side effects,³⁴ but it may still do so in patients with severe pulmonary disease.³⁵ Selective beta-blockers lower IOP to a lesser degree than nonselective drugs³⁶ and can cause the same cardiac effects of bradycardia and hypotension.³⁸

Prostaglandin analogs (latanoprost, travoprost, unoprostone) increase drainage of the aqueous humor. Prostaglandins are clinically and statistically superior to beta-blockers, having lowered IOP by up to 40% in randomized controlled trials.³⁷ Side effects include increased eyelash growth and iris pigmentation,²⁶ and muscle and joint pain.³⁸

Alpha-adrenergic drugs (apraclonidine, brimonidine) lower aqueous humor production. Apraclonidine administered topically does not cross the blood-brain barrier, effectively lowering IOP without causing cardiovascular side effects.²⁸ The most common side effects are dry nose, dry mouth,²⁸ and follicular conjunctivitis.²⁹ Unlike apraclonidine, brimonidine crosses the blood-brain barrier and can cause mild hypotension.³⁰ One randomized controlled trial found no statistical difference in efficacy between brimonidine and apraclonidine, both lowering IOP by up to 23%.³⁹

Carbonic anhydrase inhibitors block water flow into the eye, preventing aqueous humor formation. Until recently, carbonic anhydrase inhibitors such as acetazolamide were administered only orally and adverse effects were therefore common.²⁷ Topical carbonic anhydrase inhibitors (brinzolamide, dorzolamide), recently introduced, lower IOP by up to 26% and with few side effects.³¹

Cholinergic agonists (pilocarpine, carbachol) increase aqueous outflow from the eye by stimulating contraction of the ciliary body, which opens the trabecular meshwork to allow further drainage.⁴⁰ Because of its ocular side effects including small, fixed pupils, induced myopia, and cataracts, pilocarpine is reserved for second-or third-line therapy (SOR: A). ^9,27,32

Medicinal marijuana used to lower IOP in glaucoma patients is controversial. The primary active ingredient in marijuana, tetrahydrocannabinol (THC), lowers IOP when inhaled. However, it lowers IOP for only 3 hours, and glaucoma management requires a constant reduction in IOP. Due to its intense side effects of altered mental status, tachycardia, and systemic hypotension, medicinal marijuana is not desirable for the treatment of glaucoma.⁴¹

Benefit in combining regimens. Using different classes of drugs produces an additive effect in lowering IOP, so the ophthalmologist may use up to 3 drugs simultaneously. When therapy is begun, a topical drug is often applied to only 1 eye, letting the opposite eye serve as a control. If IOP is not lowered in the treated eye when compared with the control eye, the drug is discontinued (SOR: A).²⁷

Dealing with noncompliance. More than one third of patients exhibit poor compliance with therapy,⁹ and strict adherence to the regimen is necessary to lower IOP. Instruct patients in proper techniques for taking and using medications, and record dosage and frequency at each physician visit.

Advise patients that glaucoma can progress, but that blindness is not inevitable. Stress the importance of adhering to the prescribed treatment regimen (SOR: C). ¹³ If poor compliance remains an issue, let the patient know that therapeutic alternatives may be possible (SOR: C). ²

Argon laser trabeculoplasty

Argon laser trabeculoplasty (ALT) is an outpatient procedure. Laser energy is directed at the trabecular meshwork to facilitate aqueous humor outflow. In a large clinical trial with long-term follow-up, initial ALT therapy was found to be at least as effective as initial pharmacological treatment.⁴²

Medical treatment is often continued after ALT.⁴³ In the Early Manifest Glaucoma Trial,²⁵ glaucoma patients randomized to receive ALT therapy plus a topical beta-blocker (betaxolol) had a 30% reduction in IOP. Compared with the control group, patients treated with ALT and beta-blocker exhibited half the risk of visual field deterioration, with a number needed to treat of 2.24 to prevent field loss in a patient with a baseline IOP of 24 mm Hg.

Surgery

Although surgical treatment is generally considered a final alternative in management, it may be an appropriate first-line therapy for patients with cardiovascular or pulmonary conditions contraindicating use of medical therapy. ¹³

Filtering surgery (trabeculectomy) (Figure) is an outpatient procedure wherein IOP is lowered by creating a fistula in the globe of the eye to drain aqueous humor into the sub-conjunctival space.²¹ In a randomized controlled trial, trabeculectomy used alone or with medical therapy in a previously unoperated eye successfully lowered IOP by a rate of 85% to 95% at 2 years.⁴⁴ At 5 years, the success rate in Caucasians is 90%; in African Americans, 80%.⁴⁴ However, a recent meta-analysis suggests that glaucoma surgery is associated with accelerated progression of cataract.⁴⁵ The Collaborative Initial Glaucoma Treatment Study (CIGTS) found 3 times the incidence of cataract surgery among subjects randomized to initial filtration surgery as opposed to medical management (P=.0001).⁴⁶

FIGURE
Filtering surgery for glaucoma

Prognosis

Glaucoma progresses insidiously. Peripheral vision is lost first in early stages of the disease and may not even be noticed by the patient. Central vision is spared until late stages of the disease.

Blindness can usually be prevented if glaucoma is detected early and IOP is lowered sufficiently.⁴⁷ Unfortunately a small number of patients may suffer irreversible vision loss even with adequate treatment; they should be referred for low-vision rehabilitation and social services (SOR: C).² In May 2002, the Centers for Medicare and Medicaid Services approved Medicare coverage for these services.⁴⁸ Services offering rehabilitation for those with low-vision: Prevent Blindness America (preventblindness.org), National Federation of the Blind (www.nfb.org), National Library Service for the Blind and Physically Handicapped (www.loc.gov/nls), and the Foundation Fighting Blindness (www.blindness.org).

Corresponding author
Ahmad A. Aref, BS, 401 East Ontario St, Suite 710, Chicago, IL 60611. E-mail:[email protected].

Evaluate for open-angle glaucoma (OAG) when a patient reports decreased vision, or when a patient even with good eyesight is found to be at high risk for the disease. Most patients with early glaucoma are unaware of the initial decrease in peripheral vision.¹

A relatively new diagnostic technique can detect even moderate damage to the optic nerve, and the procedure is brief. Ophthalmologists can choose from among several topical medications to reduce intraocular pressure. Your knowledge of the patient’s medical history is critical to avoiding potential drug-drug interactions.

Laser surgery and trabeculectomy may be indicated as first-line therapy for select patients.

Whom to screen

Persons aged older than 60 years, African Americans of any age, and those with a family history of OAG are at particularly high risk, and all risk factors should be fully assessed (SOR: B).² (See Open-angle glaucoma: The scope of the problem.)

In the Caucasian population aged 40 to 49 years with no family history of OAG, disease prevalence is just 0.18%. Prevalence is 4 times greater in African Americans of the same age range. Caucasians aged 60 to 69 years have a prevalence of OAG 4 times greater than patients aged 40 to 49. For African Americans older than 80 years, prevalence exceeds 11%.³

For persons with a first-degree relative with OAG, risk was found to be 9.2 times greater than for those without such a history.⁸

Ask specifically about decreased vision, loss of peripheral vision, difficulty seeing in the dark, and difficulty reading (SOR: B).

Before referring high-risk patients for a full ophthalmologic examination, examine the optic nerve with direct ophthalmoscopy (SOR: B).

Determining optic nerve status

Examination of the optic nerve head provides clues as to whether structural damage has occurred. Cup-disc ratio is used to assess risk of glaucoma development. The probability of abnormality increases dramatically for values above 0.5.⁹

The standard clinical technique used by primary care clinicians is with the direct ophthalmoscope. Sensitivity and specificity for a cup-disc ratio greater than 0.6 have been reported to be 64% and 96%, respectively, using direct ophthalmoscopy.¹⁰

Ophthalmologists use stereoscopic fundus photography to visualize the optic nerve. With this technique, sensitivity and specificity for a cup-disc ratio greater than 0.5 have been found to be 48% and 89%, respectively.¹¹ Studies, however, have reported a high interobserver variation in measurement of the cup-disc ratio even among experts in the field.¹²

What to look for. Characteristic changes include narrowing or notching of the neuroretinal rim, or characteristic visual field loss, such as arcuate defects and nasal loss.¹³ Describe an abnormal optic disc in terms of its cup-disc ratio, and report visual loss to the ophthalmologist as a defect in a respective field quadrant as detected on confrontational visual field testing or as an afferent pupillary defect in a given eye.

Referral. A final diagnosis of open-angle glaucoma can be made only after characteristic damage to the optic nerve has been confirmed by an ophthalmologist (SOR: B). Therefore, patients at high risk of developing OAG (age >60 years, African American race, positive family history) should be referred for an eye examination.

Other key diagnostic tests include measurement of intraocular pressure and visual field testing.² The accuracy of these tests is outlined in Table 1.

TABLE 1
Characteristics of diagnostic tests for open-angle glaucoma

Intraocular pressure: Caveats

Intraocular pressure (IOP) is measured by a tonometer. The eye is subjected to a force that flattens the cornea. This force is then related to the pressure in the eye, or IOP. The standard instrument for measuring IOP is the Goldman applanation tonometer. Handheld versions (tonopen) are useful for screening by the primary care clinician.¹¹ Studies of IOP distribution show the normal range of IOP values to be less than 21 mm Hg with a slight skew towards higher values.¹⁶

The altering effect of corneal thickness. IOP measurement may vary with the thickness of one’s cornea. A corneal thickness greater than 555 μm can produce falsely high readings, and a corneal thickness less than 540 μm can produce falsely low readings.^2,17,18 Thus, central corneal thickness (CCT) is a factor that may affect the accuracy of an IOP reading. Central corneal thickness is measured with a pachymeter, and an ophthalmologist must take this measurement into account when assessing a patient’s IOP.

Pressure may not be elevated in OAG. A number of population-based studies have documented an increase in the prevalence of OAG with an increase in IOP.^7,19,20 However, these same studies have also concluded that many patients with OAG have IOP levels in the normal range. These patients are deemed to have normal pressure glaucoma (NPG), a subtype of OAG.²¹

Likewise, many patients with elevated IOP have no demonstrable optic nerve damage;^19,20 this condition has been termed ocular hypertension (OHT).

A proper perspective. So, although an elevated IOP is associated with glaucoma, it is important to note that OAG is not defined by the presence of an elevated IOP. Optic nerve atrophy can occur in the absence of an increased IOP. ²¹ These findings, taken together with the variance of IOP with CCT, are reflected in the modest sensitivity and specificity for IOP readings greater than 21 mm Hg—47.1% and 92.4%, respectively. ¹⁴ Patients with a high IOP (>21 mm Hg) are at higher risk for developing OAG, but further ancillary studies and tests are necessary to confirm the diagnosis. ¹³

Evaluating the visual field

Visual field deterioration is the final manifestation of glaucoma. Vision is first lost peripherally. Central vision loss occurs at the end stage of the disease.

An ophthalmologist will use automated static threshold perimetry to evaluate the visual field. With this technique, the patient must identify white target lights of variable brightness in different locations of a dim 1-m bowl. Various data algorithms are then employed to compare any abnormality in the visual field with patterns that are characteristic of glaucoma.⁹ One study reported a 97% sensitivity and 84% specificity using a certain algorithm to recognize field abnormalities due to glaucoma.¹⁵ However, automated perimetry requires 10 to 20 minutes per eye, and patient fatigue often reduces reliability of the test. Also, an optic nerve head has typically undergone considerable damage before visual field changes are detected.²

An improved test. Frequency doubling technology promises to detect glaucomatous visual defects when there has been only moderate damage to the optic nerve. With frequency doubling technology, patients must recognize patterns of alternating light and dark bars. An abnormality in recognition is thought to be indicative of the pattern of field loss in glaucoma. One study found a sensitivity and specificity each greater than 90% for identifying patients thought to have glaucoma. Another benefit is that the exam takes an average of only 6 minutes to complete in both eyes. ²²

No single test result is enough

Successful screening for glaucoma should not rely solely on measuring IOP, assessment of the optic nerve, or visual field testing. These diagnostic clues are complementary and must be taken together to evaluate high-risk populations, including African Americans, those with a family history of glaucoma, and the elderly (SOR: C).

Regular follow-up

Regardless of findings, patients aged 40 to 60 years should be encouraged to have eye exams every other year, and those over age 60 should have annual eye exams (SOR: B).¹³ Regular ocular exams including vision check, extraocular muscle exam, papillary exam, and confrontational visual fields should be performed in these patients as well (SOR: C).

Treatment

IOP is the only risk factor for glaucoma that can be treated. Lowering IOP in randomized control trials has reduced the progression of visual field loss in OAG patients with abnormally high pressures²³ as well as in NPG patients with pressures in the normal range.²⁴

In the Early Manifest Glaucoma Trial, a 30% reduction in IOP reduced the rate of progression in the treatment group (45%) compared with the control group (62%; P=.007).²⁵ Progression risk decreased by approximately 10% per mm Hg of IOP reduction.

Setting a target pressure. Before beginning therapy, an ophthalmologist sets a target pressure that should halt further optic nerve damage. The initial target pressure is usually 20% to 30% lower than the pretreatment pressure. If damage to the optic nerve is already substantial, the target pressure may be set even lower.²

Stepwise therapy. Topical medications are usually given first, as eye drops. A comparison of these medications is outlined in Table 2. If IOP cannot be lowered pharmacologically, argon laser trabeculoplasty (ALT) is the next step. If the pressure still cannot be lowered, filtering surgery is the final alternative (SOR: C).²

TABLE 2
Pharmacologic options for patients with open-angle glaucoma

Pharmacologic options

Medical agents work in 1 of 2 ways to lower IOP: by decreasing production of aqueous humor, or by increasing drainage of aqueous humor out of the eye. Though most glaucoma medications are given topically, severe systemic side effects can occur.² Because the consulting ophthalmologist may not be aware of a patient’s other medical conditions, inquire about the topical ocular drops being recommended to make certain they are not contraindicated and to be alert to the potential for adverse effects (SOR: C).¹³

Beta-adrenergic antagonists can lower IOP by up to 31% ²⁵ and are often used as first-line treatment (SOR: A).²¹ However, nonselective beta-blockers (timolol, carteolol, levobunolol, metipranolol) are associated with a number of adverse effects including bronchospasm,³³ bradycardia, and hypotension. ³⁴

Betaxolol is a selective beta-blocker with less tendency to cause pulmonary side effects,³⁴ but it may still do so in patients with severe pulmonary disease.³⁵ Selective beta-blockers lower IOP to a lesser degree than nonselective drugs³⁶ and can cause the same cardiac effects of bradycardia and hypotension.³⁸

Prostaglandin analogs (latanoprost, travoprost, unoprostone) increase drainage of the aqueous humor. Prostaglandins are clinically and statistically superior to beta-blockers, having lowered IOP by up to 40% in randomized controlled trials.³⁷ Side effects include increased eyelash growth and iris pigmentation,²⁶ and muscle and joint pain.³⁸

Alpha-adrenergic drugs (apraclonidine, brimonidine) lower aqueous humor production. Apraclonidine administered topically does not cross the blood-brain barrier, effectively lowering IOP without causing cardiovascular side effects.²⁸ The most common side effects are dry nose, dry mouth,²⁸ and follicular conjunctivitis.²⁹ Unlike apraclonidine, brimonidine crosses the blood-brain barrier and can cause mild hypotension.³⁰ One randomized controlled trial found no statistical difference in efficacy between brimonidine and apraclonidine, both lowering IOP by up to 23%.³⁹

Carbonic anhydrase inhibitors block water flow into the eye, preventing aqueous humor formation. Until recently, carbonic anhydrase inhibitors such as acetazolamide were administered only orally and adverse effects were therefore common.²⁷ Topical carbonic anhydrase inhibitors (brinzolamide, dorzolamide), recently introduced, lower IOP by up to 26% and with few side effects.³¹

Cholinergic agonists (pilocarpine, carbachol) increase aqueous outflow from the eye by stimulating contraction of the ciliary body, which opens the trabecular meshwork to allow further drainage.⁴⁰ Because of its ocular side effects including small, fixed pupils, induced myopia, and cataracts, pilocarpine is reserved for second-or third-line therapy (SOR: A). ^9,27,32

Medicinal marijuana used to lower IOP in glaucoma patients is controversial. The primary active ingredient in marijuana, tetrahydrocannabinol (THC), lowers IOP when inhaled. However, it lowers IOP for only 3 hours, and glaucoma management requires a constant reduction in IOP. Due to its intense side effects of altered mental status, tachycardia, and systemic hypotension, medicinal marijuana is not desirable for the treatment of glaucoma.⁴¹

Benefit in combining regimens. Using different classes of drugs produces an additive effect in lowering IOP, so the ophthalmologist may use up to 3 drugs simultaneously. When therapy is begun, a topical drug is often applied to only 1 eye, letting the opposite eye serve as a control. If IOP is not lowered in the treated eye when compared with the control eye, the drug is discontinued (SOR: A).²⁷

Dealing with noncompliance. More than one third of patients exhibit poor compliance with therapy,⁹ and strict adherence to the regimen is necessary to lower IOP. Instruct patients in proper techniques for taking and using medications, and record dosage and frequency at each physician visit.

Advise patients that glaucoma can progress, but that blindness is not inevitable. Stress the importance of adhering to the prescribed treatment regimen (SOR: C). ¹³ If poor compliance remains an issue, let the patient know that therapeutic alternatives may be possible (SOR: C). ²

Argon laser trabeculoplasty

Argon laser trabeculoplasty (ALT) is an outpatient procedure. Laser energy is directed at the trabecular meshwork to facilitate aqueous humor outflow. In a large clinical trial with long-term follow-up, initial ALT therapy was found to be at least as effective as initial pharmacological treatment.⁴²

Medical treatment is often continued after ALT.⁴³ In the Early Manifest Glaucoma Trial,²⁵ glaucoma patients randomized to receive ALT therapy plus a topical beta-blocker (betaxolol) had a 30% reduction in IOP. Compared with the control group, patients treated with ALT and beta-blocker exhibited half the risk of visual field deterioration, with a number needed to treat of 2.24 to prevent field loss in a patient with a baseline IOP of 24 mm Hg.

Surgery

Although surgical treatment is generally considered a final alternative in management, it may be an appropriate first-line therapy for patients with cardiovascular or pulmonary conditions contraindicating use of medical therapy. ¹³

Filtering surgery (trabeculectomy) (Figure) is an outpatient procedure wherein IOP is lowered by creating a fistula in the globe of the eye to drain aqueous humor into the sub-conjunctival space.²¹ In a randomized controlled trial, trabeculectomy used alone or with medical therapy in a previously unoperated eye successfully lowered IOP by a rate of 85% to 95% at 2 years.⁴⁴ At 5 years, the success rate in Caucasians is 90%; in African Americans, 80%.⁴⁴ However, a recent meta-analysis suggests that glaucoma surgery is associated with accelerated progression of cataract.⁴⁵ The Collaborative Initial Glaucoma Treatment Study (CIGTS) found 3 times the incidence of cataract surgery among subjects randomized to initial filtration surgery as opposed to medical management (P=.0001).⁴⁶

FIGURE
Filtering surgery for glaucoma

Prognosis

Glaucoma progresses insidiously. Peripheral vision is lost first in early stages of the disease and may not even be noticed by the patient. Central vision is spared until late stages of the disease.

Blindness can usually be prevented if glaucoma is detected early and IOP is lowered sufficiently.⁴⁷ Unfortunately a small number of patients may suffer irreversible vision loss even with adequate treatment; they should be referred for low-vision rehabilitation and social services (SOR: C).² In May 2002, the Centers for Medicare and Medicaid Services approved Medicare coverage for these services.⁴⁸ Services offering rehabilitation for those with low-vision: Prevent Blindness America (preventblindness.org), National Federation of the Blind (www.nfb.org), National Library Service for the Blind and Physically Handicapped (www.loc.gov/nls), and the Foundation Fighting Blindness (www.blindness.org).

Corresponding author
Ahmad A. Aref, BS, 401 East Ontario St, Suite 710, Chicago, IL 60611. E-mail:[email protected].

Evaluate for open-angle glaucoma (OAG) when a patient reports decreased vision, or when a patient even with good eyesight is found to be at high risk for the disease. Most patients with early glaucoma are unaware of the initial decrease in peripheral vision.¹

A relatively new diagnostic technique can detect even moderate damage to the optic nerve, and the procedure is brief. Ophthalmologists can choose from among several topical medications to reduce intraocular pressure. Your knowledge of the patient’s medical history is critical to avoiding potential drug-drug interactions.

Laser surgery and trabeculectomy may be indicated as first-line therapy for select patients.

Whom to screen

Persons aged older than 60 years, African Americans of any age, and those with a family history of OAG are at particularly high risk, and all risk factors should be fully assessed (SOR: B).² (See Open-angle glaucoma: The scope of the problem.)

In the Caucasian population aged 40 to 49 years with no family history of OAG, disease prevalence is just 0.18%. Prevalence is 4 times greater in African Americans of the same age range. Caucasians aged 60 to 69 years have a prevalence of OAG 4 times greater than patients aged 40 to 49. For African Americans older than 80 years, prevalence exceeds 11%.³

For persons with a first-degree relative with OAG, risk was found to be 9.2 times greater than for those without such a history.⁸

Ask specifically about decreased vision, loss of peripheral vision, difficulty seeing in the dark, and difficulty reading (SOR: B).

Before referring high-risk patients for a full ophthalmologic examination, examine the optic nerve with direct ophthalmoscopy (SOR: B).

Determining optic nerve status

Examination of the optic nerve head provides clues as to whether structural damage has occurred. Cup-disc ratio is used to assess risk of glaucoma development. The probability of abnormality increases dramatically for values above 0.5.⁹

The standard clinical technique used by primary care clinicians is with the direct ophthalmoscope. Sensitivity and specificity for a cup-disc ratio greater than 0.6 have been reported to be 64% and 96%, respectively, using direct ophthalmoscopy.¹⁰

Ophthalmologists use stereoscopic fundus photography to visualize the optic nerve. With this technique, sensitivity and specificity for a cup-disc ratio greater than 0.5 have been found to be 48% and 89%, respectively.¹¹ Studies, however, have reported a high interobserver variation in measurement of the cup-disc ratio even among experts in the field.¹²

What to look for. Characteristic changes include narrowing or notching of the neuroretinal rim, or characteristic visual field loss, such as arcuate defects and nasal loss.¹³ Describe an abnormal optic disc in terms of its cup-disc ratio, and report visual loss to the ophthalmologist as a defect in a respective field quadrant as detected on confrontational visual field testing or as an afferent pupillary defect in a given eye.

Referral. A final diagnosis of open-angle glaucoma can be made only after characteristic damage to the optic nerve has been confirmed by an ophthalmologist (SOR: B). Therefore, patients at high risk of developing OAG (age >60 years, African American race, positive family history) should be referred for an eye examination.

Other key diagnostic tests include measurement of intraocular pressure and visual field testing.² The accuracy of these tests is outlined in Table 1.

TABLE 1
Characteristics of diagnostic tests for open-angle glaucoma

Intraocular pressure: Caveats

Intraocular pressure (IOP) is measured by a tonometer. The eye is subjected to a force that flattens the cornea. This force is then related to the pressure in the eye, or IOP. The standard instrument for measuring IOP is the Goldman applanation tonometer. Handheld versions (tonopen) are useful for screening by the primary care clinician.¹¹ Studies of IOP distribution show the normal range of IOP values to be less than 21 mm Hg with a slight skew towards higher values.¹⁶

The altering effect of corneal thickness. IOP measurement may vary with the thickness of one’s cornea. A corneal thickness greater than 555 μm can produce falsely high readings, and a corneal thickness less than 540 μm can produce falsely low readings.^2,17,18 Thus, central corneal thickness (CCT) is a factor that may affect the accuracy of an IOP reading. Central corneal thickness is measured with a pachymeter, and an ophthalmologist must take this measurement into account when assessing a patient’s IOP.

Pressure may not be elevated in OAG. A number of population-based studies have documented an increase in the prevalence of OAG with an increase in IOP.^7,19,20 However, these same studies have also concluded that many patients with OAG have IOP levels in the normal range. These patients are deemed to have normal pressure glaucoma (NPG), a subtype of OAG.²¹

Likewise, many patients with elevated IOP have no demonstrable optic nerve damage;^19,20 this condition has been termed ocular hypertension (OHT).

A proper perspective. So, although an elevated IOP is associated with glaucoma, it is important to note that OAG is not defined by the presence of an elevated IOP. Optic nerve atrophy can occur in the absence of an increased IOP. ²¹ These findings, taken together with the variance of IOP with CCT, are reflected in the modest sensitivity and specificity for IOP readings greater than 21 mm Hg—47.1% and 92.4%, respectively. ¹⁴ Patients with a high IOP (>21 mm Hg) are at higher risk for developing OAG, but further ancillary studies and tests are necessary to confirm the diagnosis. ¹³

Evaluating the visual field

Visual field deterioration is the final manifestation of glaucoma. Vision is first lost peripherally. Central vision loss occurs at the end stage of the disease.

An ophthalmologist will use automated static threshold perimetry to evaluate the visual field. With this technique, the patient must identify white target lights of variable brightness in different locations of a dim 1-m bowl. Various data algorithms are then employed to compare any abnormality in the visual field with patterns that are characteristic of glaucoma.⁹ One study reported a 97% sensitivity and 84% specificity using a certain algorithm to recognize field abnormalities due to glaucoma.¹⁵ However, automated perimetry requires 10 to 20 minutes per eye, and patient fatigue often reduces reliability of the test. Also, an optic nerve head has typically undergone considerable damage before visual field changes are detected.²

An improved test. Frequency doubling technology promises to detect glaucomatous visual defects when there has been only moderate damage to the optic nerve. With frequency doubling technology, patients must recognize patterns of alternating light and dark bars. An abnormality in recognition is thought to be indicative of the pattern of field loss in glaucoma. One study found a sensitivity and specificity each greater than 90% for identifying patients thought to have glaucoma. Another benefit is that the exam takes an average of only 6 minutes to complete in both eyes. ²²

No single test result is enough

Successful screening for glaucoma should not rely solely on measuring IOP, assessment of the optic nerve, or visual field testing. These diagnostic clues are complementary and must be taken together to evaluate high-risk populations, including African Americans, those with a family history of glaucoma, and the elderly (SOR: C).

Regular follow-up

Regardless of findings, patients aged 40 to 60 years should be encouraged to have eye exams every other year, and those over age 60 should have annual eye exams (SOR: B).¹³ Regular ocular exams including vision check, extraocular muscle exam, papillary exam, and confrontational visual fields should be performed in these patients as well (SOR: C).

Treatment

IOP is the only risk factor for glaucoma that can be treated. Lowering IOP in randomized control trials has reduced the progression of visual field loss in OAG patients with abnormally high pressures²³ as well as in NPG patients with pressures in the normal range.²⁴

In the Early Manifest Glaucoma Trial, a 30% reduction in IOP reduced the rate of progression in the treatment group (45%) compared with the control group (62%; P=.007).²⁵ Progression risk decreased by approximately 10% per mm Hg of IOP reduction.

Setting a target pressure. Before beginning therapy, an ophthalmologist sets a target pressure that should halt further optic nerve damage. The initial target pressure is usually 20% to 30% lower than the pretreatment pressure. If damage to the optic nerve is already substantial, the target pressure may be set even lower.²

Stepwise therapy. Topical medications are usually given first, as eye drops. A comparison of these medications is outlined in Table 2. If IOP cannot be lowered pharmacologically, argon laser trabeculoplasty (ALT) is the next step. If the pressure still cannot be lowered, filtering surgery is the final alternative (SOR: C).²

TABLE 2
Pharmacologic options for patients with open-angle glaucoma

Pharmacologic options

Medical agents work in 1 of 2 ways to lower IOP: by decreasing production of aqueous humor, or by increasing drainage of aqueous humor out of the eye. Though most glaucoma medications are given topically, severe systemic side effects can occur.² Because the consulting ophthalmologist may not be aware of a patient’s other medical conditions, inquire about the topical ocular drops being recommended to make certain they are not contraindicated and to be alert to the potential for adverse effects (SOR: C).¹³

Beta-adrenergic antagonists can lower IOP by up to 31% ²⁵ and are often used as first-line treatment (SOR: A).²¹ However, nonselective beta-blockers (timolol, carteolol, levobunolol, metipranolol) are associated with a number of adverse effects including bronchospasm,³³ bradycardia, and hypotension. ³⁴

Betaxolol is a selective beta-blocker with less tendency to cause pulmonary side effects,³⁴ but it may still do so in patients with severe pulmonary disease.³⁵ Selective beta-blockers lower IOP to a lesser degree than nonselective drugs³⁶ and can cause the same cardiac effects of bradycardia and hypotension.³⁸

Prostaglandin analogs (latanoprost, travoprost, unoprostone) increase drainage of the aqueous humor. Prostaglandins are clinically and statistically superior to beta-blockers, having lowered IOP by up to 40% in randomized controlled trials.³⁷ Side effects include increased eyelash growth and iris pigmentation,²⁶ and muscle and joint pain.³⁸

Alpha-adrenergic drugs (apraclonidine, brimonidine) lower aqueous humor production. Apraclonidine administered topically does not cross the blood-brain barrier, effectively lowering IOP without causing cardiovascular side effects.²⁸ The most common side effects are dry nose, dry mouth,²⁸ and follicular conjunctivitis.²⁹ Unlike apraclonidine, brimonidine crosses the blood-brain barrier and can cause mild hypotension.³⁰ One randomized controlled trial found no statistical difference in efficacy between brimonidine and apraclonidine, both lowering IOP by up to 23%.³⁹

Carbonic anhydrase inhibitors block water flow into the eye, preventing aqueous humor formation. Until recently, carbonic anhydrase inhibitors such as acetazolamide were administered only orally and adverse effects were therefore common.²⁷ Topical carbonic anhydrase inhibitors (brinzolamide, dorzolamide), recently introduced, lower IOP by up to 26% and with few side effects.³¹

Cholinergic agonists (pilocarpine, carbachol) increase aqueous outflow from the eye by stimulating contraction of the ciliary body, which opens the trabecular meshwork to allow further drainage.⁴⁰ Because of its ocular side effects including small, fixed pupils, induced myopia, and cataracts, pilocarpine is reserved for second-or third-line therapy (SOR: A). ^9,27,32

Medicinal marijuana used to lower IOP in glaucoma patients is controversial. The primary active ingredient in marijuana, tetrahydrocannabinol (THC), lowers IOP when inhaled. However, it lowers IOP for only 3 hours, and glaucoma management requires a constant reduction in IOP. Due to its intense side effects of altered mental status, tachycardia, and systemic hypotension, medicinal marijuana is not desirable for the treatment of glaucoma.⁴¹

Benefit in combining regimens. Using different classes of drugs produces an additive effect in lowering IOP, so the ophthalmologist may use up to 3 drugs simultaneously. When therapy is begun, a topical drug is often applied to only 1 eye, letting the opposite eye serve as a control. If IOP is not lowered in the treated eye when compared with the control eye, the drug is discontinued (SOR: A).²⁷

Dealing with noncompliance. More than one third of patients exhibit poor compliance with therapy,⁹ and strict adherence to the regimen is necessary to lower IOP. Instruct patients in proper techniques for taking and using medications, and record dosage and frequency at each physician visit.

Advise patients that glaucoma can progress, but that blindness is not inevitable. Stress the importance of adhering to the prescribed treatment regimen (SOR: C). ¹³ If poor compliance remains an issue, let the patient know that therapeutic alternatives may be possible (SOR: C). ²

Argon laser trabeculoplasty

Argon laser trabeculoplasty (ALT) is an outpatient procedure. Laser energy is directed at the trabecular meshwork to facilitate aqueous humor outflow. In a large clinical trial with long-term follow-up, initial ALT therapy was found to be at least as effective as initial pharmacological treatment.⁴²

Medical treatment is often continued after ALT.⁴³ In the Early Manifest Glaucoma Trial,²⁵ glaucoma patients randomized to receive ALT therapy plus a topical beta-blocker (betaxolol) had a 30% reduction in IOP. Compared with the control group, patients treated with ALT and beta-blocker exhibited half the risk of visual field deterioration, with a number needed to treat of 2.24 to prevent field loss in a patient with a baseline IOP of 24 mm Hg.

Surgery

Although surgical treatment is generally considered a final alternative in management, it may be an appropriate first-line therapy for patients with cardiovascular or pulmonary conditions contraindicating use of medical therapy. ¹³

Filtering surgery (trabeculectomy) (Figure) is an outpatient procedure wherein IOP is lowered by creating a fistula in the globe of the eye to drain aqueous humor into the sub-conjunctival space.²¹ In a randomized controlled trial, trabeculectomy used alone or with medical therapy in a previously unoperated eye successfully lowered IOP by a rate of 85% to 95% at 2 years.⁴⁴ At 5 years, the success rate in Caucasians is 90%; in African Americans, 80%.⁴⁴ However, a recent meta-analysis suggests that glaucoma surgery is associated with accelerated progression of cataract.⁴⁵ The Collaborative Initial Glaucoma Treatment Study (CIGTS) found 3 times the incidence of cataract surgery among subjects randomized to initial filtration surgery as opposed to medical management (P=.0001).⁴⁶

FIGURE
Filtering surgery for glaucoma

Prognosis

Glaucoma progresses insidiously. Peripheral vision is lost first in early stages of the disease and may not even be noticed by the patient. Central vision is spared until late stages of the disease.

Blindness can usually be prevented if glaucoma is detected early and IOP is lowered sufficiently.⁴⁷ Unfortunately a small number of patients may suffer irreversible vision loss even with adequate treatment; they should be referred for low-vision rehabilitation and social services (SOR: C).² In May 2002, the Centers for Medicare and Medicaid Services approved Medicare coverage for these services.⁴⁸ Services offering rehabilitation for those with low-vision: Prevent Blindness America (preventblindness.org), National Federation of the Blind (www.nfb.org), National Library Service for the Blind and Physically Handicapped (www.loc.gov/nls), and the Foundation Fighting Blindness (www.blindness.org).

Corresponding author
Ahmad A. Aref, BS, 401 East Ontario St, Suite 710, Chicago, IL 60611. E-mail:[email protected].

Family physicians providing maternity care often face a scenario in which an otherwise low-risk, term patient is incidentally noted to have a low amniotic fluid index (AFI). Common reasons for obtaining an AFI in a woman with a low-risk pregnancy include evaluation of decreased fetal movement, spontaneous variable decelerations during monitoring to evaluate for labor, or an ultrasound evaluation for fundal height measurements discordant with gestational age. How should “isolated” oligohydramnios—an AFI <5 cm—be interpreted, and should immediate induction be recommended for such patients?

Oligohydramnios occurs in about 1% to 5% of pregnancies at term.^1,2 Because adverse outcomes occur in high-risk pregnancies complicated by low amniotic fluid volume, oligohydramnios commonly prompts labor induction.^1,3,4 At one university center, oligohydramnios is now the leading indication for labor induction.⁵ Many centers may even induce labor when the AFI is between 5 cm and 8 cm, the so-called borderline AFI.³

Labor induction increases the use of cesarean delivery, particularly for the primiparous woman with an unripe cervix.⁶ Recent studies questioning the safety of labor induction in women who have had a cesarean may increase the number of elective repeat cesarean procedures when delivery is believed indicated for oligohydramnios.⁷ (See Underlying causes of oligohydramnios.)

Oligohydramnios is difficult to assess

True oligohydramnios can be difficult to confirm due to the questionable accuracy of amniotic fluid measurement by ultrasound. There is controversy, for example, about whether (and how) to include pockets of amniotic fluid containing umbilical cord.¹⁵ The AFI was introduced in 1987² to replace the 2 cm “pocket technique” of fluid assessment, and studies continue to question to what extent the AFI reflects actual amniotic fluid volume.

AFI measurements may vary with the amount of pressure applied to the abdomen and with fetal position or movement.¹⁶

Serial measurements taken by the same ultrasound operator have been shown to differ from the true volume by 1 cm, or 10.8%; serial measurements taken by multiple operators have differed by as much as 2 cm, or 15.4%.^17,18

O’Reilly-Green compared the diagnosis of oligohydramnios in 449 post-term patients with actual amniotic fluid volume measured at rupture of membranes.¹⁹ They found a positive predictive value of 50% for oligohydramnios at an AFI of 5 cm as the lower limit of normal. A study of 144 third trimester patients using the dye-dilution technique found that, to achieve 95% confidence for ruling out oligohydramnios, a cutoff AFI of 30 cm would need to be used, a value consistent with polyhydramnios.²⁰

What is the association between oligohydramnios and poor fetal outcomes?

A number of studies over the past 15 years have shown an association between oligohydramnios and poor fetal outcomes. These were predominantly retrospective studies, which failed to control for the presence of factors known to be associated with oligohydramnios such as intrauterine growth restriction (IUGR) and urogenital malformations.

No studies have directly addressed whether labor induction improves outcomes. A meta-analysis of 18 studies examining outcomes of pregnancies with AFI <5 cm found an increased risk of cesarean delivery for fetal distress and low Apgar scores at 5 minutes. Most of these studies, however, had high-risk patients including IUGR (level of evidence [LOE]: 2).²¹

A recent study of high-risk patients failed to detect a difference in the incidence of nonreactive nonstress tests, meconium-stained amniotic fluid cesarean delivery for fetal distress, low Apgar scores, or infants with a cord pH of <7.10 when oligohydramnios (AFI <5.0 cm) was present (LOE: 1).² The patients with oligohydramnios were all induced, while many of the other high-risk patients were expectantly managed. The study therefore provides no guidance on the safety of expectant management for patients with oligohydramnios. To eliminate the potential effect of induction versus expectant management the same authors performed a case-control study of 79 high-risk women with AFI <5 cm matched to 79 women with the same high-risk pregnancy complication who had an AFI >5 cm at the time of induction (LOE: 2).²³ They failed to detect any significant differences in neonatal outcomes between the groups.

Studies of the “borderline” AFI (between 5 cm and 8 cm) may also demonstrate an association with adverse neonatal outcomes if researchers include fetuses with IUGR or malformations. In one retrospective case review of 214 women with AFI of 5 cm to 10 cm, the only statistically significant finding was an association with IUGR.³ The authors recommended antepartum surveillance twice a week for mothers with borderline AFI, but they did not comment on induction (LOE: 2). Correspondence regarding this study argued that this recommendation was not supported by the evidence and would lead to unnecessary antenatal testing.²⁴

Studies of isolated oligohydramnios

Investigators have conducted studies (Table 1) excluding fetuses with intrauterine growth restriction or anomalies to try to determine if isolated oligohydramnios is associated with poorer outcomes.^25-30

Rainford’s study of outcomes in exclusively term, low-risk patients failed to show significant outcome differences in Apgar scores, NICU admissions, or rates of cesarean delivery for non-reassuring fetal heart rate monitoring (LOE: 2).²⁹ This study was limited due to its retrospective design. The authors comment that the relatively good outcomes in the oligohydramnios group may be due to the widespread practice of inducing such patients.

In a case-control study by Conway, 183 low-risk, term parturients with oligohydramnios were matched to 183 women of similar gestational age and parity who presented in spontaneous labor. The patients with isolated oligohydramnios were induced and showed an increased cesarean delivery rate. The increased rate of cesarean delivery was not due to nonreassuring fetal surveillance and was attributed to the induction process (LOE: 2).²⁵

An analysis of woman diagnosed with isolated oligohydramnios (AFI <5) at any gestational age in the multicenter prospective RADIUS trial demonstrated similar perinatal outcomes and fetal growth compared with pregnancies with a normal amniotic fluid (LOE: 2).³⁰

The only randomized clinical trial of labor induction vs expectant management for term isolated oligohydramnios showed similar outcomes in each group. But this study was small (n=61) and has only been published as an abstract.³¹

TABLE 1
Isolated oligohydramnios and perinatal outcomes

Effect of maternal hydration

Maternal hydration status and plasma osmolality have an affect on amniotic fluid volume (Table 2). Maternal hydration with oral water or intravenous hypotonic solutions has been shown to increase amniotic fluid volume.^8,11-13 Oral hydration with hypotonic fluid has been demonstrated to increase fetal urine production in one observational study.³² Another observational study demonstrated increased amniotic fluid volume and uteroplacental perfusion without alteration of fetal urine production suggesting the possibility that transmembranous fluid shifts from the placenta to the amniotic cavity may be involved.¹²

Two small, randomized controlled trials (RCTs) demonstrated an increase in amniotic fluid volume in women with oligohydramnios after oral hydration.^11,13 Doi demonstrated significant increases in AFI in women with oligohydramnios beyond 35 weeks when given oral hydration with free water (increase of 3.8 cm ± 1.9; P<. 001) or hypotonic intravenous solution (increase of 2.8 cm ± 1.9; P<.001) (LOE: 3).¹¹ Interestingly, this study did not demonstrate an increase in amniotic fluid volume with intravenous hydration with isotonic fluid.

Kirkpatrick demonstrated a 30% increase in amniotic fluid compared with controls in women of unspecified gestational age with oligohydramnios given 2 liters of oral water 2 to 5 hours before repeat amniotic fluid index (LOE: 3).¹³

A randomized trial in women with normal amniotic fluid demonstrated a 16% increase in amniotic fluid index 4 to 6 hours after hydration with 2 liters of oral water, compared with an 8% decrease after fluid restriction during the same period.⁸

A recent study of daily oral hydration in women with amniotic fluid volume <10% percentile showed increased amniotic fluid volume at 1 week, suggesting long-term benefit, although the study lacked an appropriate control group (LOE: 3).³³

There are no studies of clinical outcomes such as fetal heart rate decelerations during labor, or neonatal outcomes. A Cochrane systematic review concluded that maternal hydration appears to increase amniotic fluid and may be beneficial in management of oligohydramnios; however, it recommended controlled trials to assess clinical outcome benefits (LOE: 3).³⁴

TABLE 2
Effect of hydration on amniotic fluid index

Management recommendations

The AFI has low specificity and positive predictive value for oligohydramnios, and there is scant evidence that isolated term oligohydramnios causes adverse fetal outcomes. We recommend that an AFI under 5 cm should prompt additional antenatal testing rather than immediate induction in low-risk term pregnancies (SOR: B).

Though we acknowledge the lack of high-quality studies with patient-oriented outcomes to support observation and maternal hydration, we have developed a management strategy that does not require immediate induction of labor in women with uncomplicated term pregnancies.

The following recommendations apply to women having oligohydramnios as defined by amniotic fluid volume of less than 5 cm and gestational age between 37 and 41 weeks.

Initial assessment

1. Assess for premature rupture of membranes with a thorough history and a sterile speculum exam
2. Reassess dating as oligohydramnios in post-dates pregnancy (>41 weeks) is an indication for induction (SOR: C)³⁵
3. Perform a nonstress test to assess fetal wellbeing
4. Assess for IUGR with an ultrasound for estimated fetal weight and for the ratio of head circumference (HC) to abdominal circumference (AC). A comparison with prior ultrasounds can aid in assessing interval growth. An estimated fetal weight below the 10%, an elevated HC/AC ratio, or poor interval growth would suggest IUGR
5. Arrange for an ultrasound anatomic survey for fetal anomalies, if not done previously
6. Determine if preeclampsia, chronic hypertension, diabetes, or other maternal conditions associated with uteroplacental insufficiency are present.

Action steps

With any positive findings in the initial evaluation, proceed to labor induction, as the patient does not have isolated, term oligohydramnios (SOR: C). If the initial assessment is unremarkable and the AFI is less than 5, consider hydration with oral water and repeating the AFI 2 to 6 hours later (SOR: B).

Persistent oligohydramnios at term, particularly with a ripe cervix, may lead you to consider labor induction. Continued expectant management of isolated term oligohydramnios with twice weekly fetal surveillance may also be a reasonable option due to the paucity of evidence that oligohydramnios is associated with an adverse outcome in this scenario (SOR: C). Normal results with umbilical artery Doppler flow studies have been used to decrease the need for induction in high-risk pregnancies with oligohydramnios, and this technique may eventually have a role in isolated term oligohydramnios.³⁶

It is essential that patients receive counseling and give informed consent regarding the risks and benefits of observation or induction for isolated term oligohydramnios. The ease of induction based on parity and cervical ripeness should be considered.

A primiparous woman with an unfavorable cervix who strongly desires a spontaneous, vaginal birth could be told that, although there may be a small risk for her baby, no study has demonstrated any increased long-term morbidity or mortality associated with low fluid in her situation and that labor induction may double her chance of cesarean delivery.^37,38 In such a situation, an acceptable approach for mother and clinician may be rehydration followed by a repeat AFI and close follow-up with testing for fetal well-being according to the algorithm (Figure). In a practical sense, rehydration with 2 liters of oral water for oligohydramnios may be done whether or not immediate induction is chosen, as this is a safe measure that has been shown to significantly increase AFI. Alternatively, the preferred approach for a multiparous woman with a ripe cervix by Bishop score may be labor induction.

As adverse fetal outcomes have not been demonstrated in women with isolated term oligohydramnios, there is no rationale for routinely inducing labor based on an isolated finding of a so called “borderline” amniotic fluid index in the 5-to-8 range. In this situation it is appropriate to perform the initial assessment described above and may be reasonable to repeat the amniotic fluid index in 3 to 4 days to determine if true oligohydramnios has developed.

FIGURE
Assessment of the pregnant woman with oligohydramnios at term

Acknowledgments

We appreciate the assistance of George Gilson MD, Lauren Plante MD, and William Rayburn MD in manuscript review.

Corresponding author
Lawrence Leeman, MD, MPH, University of New Mexico Depts of Family and Community Medicine, Obstetrics and Gynecology, 2400 Tucker NE, 3rd floor, Albuquerque, NM 87131. E-mail: [email protected].

Family physicians providing maternity care often face a scenario in which an otherwise low-risk, term patient is incidentally noted to have a low amniotic fluid index (AFI). Common reasons for obtaining an AFI in a woman with a low-risk pregnancy include evaluation of decreased fetal movement, spontaneous variable decelerations during monitoring to evaluate for labor, or an ultrasound evaluation for fundal height measurements discordant with gestational age. How should “isolated” oligohydramnios—an AFI <5 cm—be interpreted, and should immediate induction be recommended for such patients?

Oligohydramnios occurs in about 1% to 5% of pregnancies at term.^1,2 Because adverse outcomes occur in high-risk pregnancies complicated by low amniotic fluid volume, oligohydramnios commonly prompts labor induction.^1,3,4 At one university center, oligohydramnios is now the leading indication for labor induction.⁵ Many centers may even induce labor when the AFI is between 5 cm and 8 cm, the so-called borderline AFI.³

Labor induction increases the use of cesarean delivery, particularly for the primiparous woman with an unripe cervix.⁶ Recent studies questioning the safety of labor induction in women who have had a cesarean may increase the number of elective repeat cesarean procedures when delivery is believed indicated for oligohydramnios.⁷ (See Underlying causes of oligohydramnios.)

Oligohydramnios is difficult to assess

True oligohydramnios can be difficult to confirm due to the questionable accuracy of amniotic fluid measurement by ultrasound. There is controversy, for example, about whether (and how) to include pockets of amniotic fluid containing umbilical cord.¹⁵ The AFI was introduced in 1987² to replace the 2 cm “pocket technique” of fluid assessment, and studies continue to question to what extent the AFI reflects actual amniotic fluid volume.

AFI measurements may vary with the amount of pressure applied to the abdomen and with fetal position or movement.¹⁶

Serial measurements taken by the same ultrasound operator have been shown to differ from the true volume by 1 cm, or 10.8%; serial measurements taken by multiple operators have differed by as much as 2 cm, or 15.4%.^17,18

O’Reilly-Green compared the diagnosis of oligohydramnios in 449 post-term patients with actual amniotic fluid volume measured at rupture of membranes.¹⁹ They found a positive predictive value of 50% for oligohydramnios at an AFI of 5 cm as the lower limit of normal. A study of 144 third trimester patients using the dye-dilution technique found that, to achieve 95% confidence for ruling out oligohydramnios, a cutoff AFI of 30 cm would need to be used, a value consistent with polyhydramnios.²⁰

What is the association between oligohydramnios and poor fetal outcomes?

A number of studies over the past 15 years have shown an association between oligohydramnios and poor fetal outcomes. These were predominantly retrospective studies, which failed to control for the presence of factors known to be associated with oligohydramnios such as intrauterine growth restriction (IUGR) and urogenital malformations.

No studies have directly addressed whether labor induction improves outcomes. A meta-analysis of 18 studies examining outcomes of pregnancies with AFI <5 cm found an increased risk of cesarean delivery for fetal distress and low Apgar scores at 5 minutes. Most of these studies, however, had high-risk patients including IUGR (level of evidence [LOE]: 2).²¹

A recent study of high-risk patients failed to detect a difference in the incidence of nonreactive nonstress tests, meconium-stained amniotic fluid cesarean delivery for fetal distress, low Apgar scores, or infants with a cord pH of <7.10 when oligohydramnios (AFI <5.0 cm) was present (LOE: 1).² The patients with oligohydramnios were all induced, while many of the other high-risk patients were expectantly managed. The study therefore provides no guidance on the safety of expectant management for patients with oligohydramnios. To eliminate the potential effect of induction versus expectant management the same authors performed a case-control study of 79 high-risk women with AFI <5 cm matched to 79 women with the same high-risk pregnancy complication who had an AFI >5 cm at the time of induction (LOE: 2).²³ They failed to detect any significant differences in neonatal outcomes between the groups.

Studies of the “borderline” AFI (between 5 cm and 8 cm) may also demonstrate an association with adverse neonatal outcomes if researchers include fetuses with IUGR or malformations. In one retrospective case review of 214 women with AFI of 5 cm to 10 cm, the only statistically significant finding was an association with IUGR.³ The authors recommended antepartum surveillance twice a week for mothers with borderline AFI, but they did not comment on induction (LOE: 2). Correspondence regarding this study argued that this recommendation was not supported by the evidence and would lead to unnecessary antenatal testing.²⁴

Studies of isolated oligohydramnios

Investigators have conducted studies (Table 1) excluding fetuses with intrauterine growth restriction or anomalies to try to determine if isolated oligohydramnios is associated with poorer outcomes.^25-30

Rainford’s study of outcomes in exclusively term, low-risk patients failed to show significant outcome differences in Apgar scores, NICU admissions, or rates of cesarean delivery for non-reassuring fetal heart rate monitoring (LOE: 2).²⁹ This study was limited due to its retrospective design. The authors comment that the relatively good outcomes in the oligohydramnios group may be due to the widespread practice of inducing such patients.

In a case-control study by Conway, 183 low-risk, term parturients with oligohydramnios were matched to 183 women of similar gestational age and parity who presented in spontaneous labor. The patients with isolated oligohydramnios were induced and showed an increased cesarean delivery rate. The increased rate of cesarean delivery was not due to nonreassuring fetal surveillance and was attributed to the induction process (LOE: 2).²⁵

An analysis of woman diagnosed with isolated oligohydramnios (AFI <5) at any gestational age in the multicenter prospective RADIUS trial demonstrated similar perinatal outcomes and fetal growth compared with pregnancies with a normal amniotic fluid (LOE: 2).³⁰

The only randomized clinical trial of labor induction vs expectant management for term isolated oligohydramnios showed similar outcomes in each group. But this study was small (n=61) and has only been published as an abstract.³¹

TABLE 1
Isolated oligohydramnios and perinatal outcomes

Effect of maternal hydration

Maternal hydration status and plasma osmolality have an affect on amniotic fluid volume (Table 2). Maternal hydration with oral water or intravenous hypotonic solutions has been shown to increase amniotic fluid volume.^8,11-13 Oral hydration with hypotonic fluid has been demonstrated to increase fetal urine production in one observational study.³² Another observational study demonstrated increased amniotic fluid volume and uteroplacental perfusion without alteration of fetal urine production suggesting the possibility that transmembranous fluid shifts from the placenta to the amniotic cavity may be involved.¹²

Two small, randomized controlled trials (RCTs) demonstrated an increase in amniotic fluid volume in women with oligohydramnios after oral hydration.^11,13 Doi demonstrated significant increases in AFI in women with oligohydramnios beyond 35 weeks when given oral hydration with free water (increase of 3.8 cm ± 1.9; P<. 001) or hypotonic intravenous solution (increase of 2.8 cm ± 1.9; P<.001) (LOE: 3).¹¹ Interestingly, this study did not demonstrate an increase in amniotic fluid volume with intravenous hydration with isotonic fluid.

Kirkpatrick demonstrated a 30% increase in amniotic fluid compared with controls in women of unspecified gestational age with oligohydramnios given 2 liters of oral water 2 to 5 hours before repeat amniotic fluid index (LOE: 3).¹³

A randomized trial in women with normal amniotic fluid demonstrated a 16% increase in amniotic fluid index 4 to 6 hours after hydration with 2 liters of oral water, compared with an 8% decrease after fluid restriction during the same period.⁸

A recent study of daily oral hydration in women with amniotic fluid volume <10% percentile showed increased amniotic fluid volume at 1 week, suggesting long-term benefit, although the study lacked an appropriate control group (LOE: 3).³³

There are no studies of clinical outcomes such as fetal heart rate decelerations during labor, or neonatal outcomes. A Cochrane systematic review concluded that maternal hydration appears to increase amniotic fluid and may be beneficial in management of oligohydramnios; however, it recommended controlled trials to assess clinical outcome benefits (LOE: 3).³⁴

TABLE 2
Effect of hydration on amniotic fluid index

Management recommendations

The AFI has low specificity and positive predictive value for oligohydramnios, and there is scant evidence that isolated term oligohydramnios causes adverse fetal outcomes. We recommend that an AFI under 5 cm should prompt additional antenatal testing rather than immediate induction in low-risk term pregnancies (SOR: B).

Though we acknowledge the lack of high-quality studies with patient-oriented outcomes to support observation and maternal hydration, we have developed a management strategy that does not require immediate induction of labor in women with uncomplicated term pregnancies.

The following recommendations apply to women having oligohydramnios as defined by amniotic fluid volume of less than 5 cm and gestational age between 37 and 41 weeks.

Initial assessment

1. Assess for premature rupture of membranes with a thorough history and a sterile speculum exam
2. Reassess dating as oligohydramnios in post-dates pregnancy (>41 weeks) is an indication for induction (SOR: C)³⁵
3. Perform a nonstress test to assess fetal wellbeing
4. Assess for IUGR with an ultrasound for estimated fetal weight and for the ratio of head circumference (HC) to abdominal circumference (AC). A comparison with prior ultrasounds can aid in assessing interval growth. An estimated fetal weight below the 10%, an elevated HC/AC ratio, or poor interval growth would suggest IUGR
5. Arrange for an ultrasound anatomic survey for fetal anomalies, if not done previously
6. Determine if preeclampsia, chronic hypertension, diabetes, or other maternal conditions associated with uteroplacental insufficiency are present.

Action steps

With any positive findings in the initial evaluation, proceed to labor induction, as the patient does not have isolated, term oligohydramnios (SOR: C). If the initial assessment is unremarkable and the AFI is less than 5, consider hydration with oral water and repeating the AFI 2 to 6 hours later (SOR: B).

Persistent oligohydramnios at term, particularly with a ripe cervix, may lead you to consider labor induction. Continued expectant management of isolated term oligohydramnios with twice weekly fetal surveillance may also be a reasonable option due to the paucity of evidence that oligohydramnios is associated with an adverse outcome in this scenario (SOR: C). Normal results with umbilical artery Doppler flow studies have been used to decrease the need for induction in high-risk pregnancies with oligohydramnios, and this technique may eventually have a role in isolated term oligohydramnios.³⁶

It is essential that patients receive counseling and give informed consent regarding the risks and benefits of observation or induction for isolated term oligohydramnios. The ease of induction based on parity and cervical ripeness should be considered.

A primiparous woman with an unfavorable cervix who strongly desires a spontaneous, vaginal birth could be told that, although there may be a small risk for her baby, no study has demonstrated any increased long-term morbidity or mortality associated with low fluid in her situation and that labor induction may double her chance of cesarean delivery.^37,38 In such a situation, an acceptable approach for mother and clinician may be rehydration followed by a repeat AFI and close follow-up with testing for fetal well-being according to the algorithm (Figure). In a practical sense, rehydration with 2 liters of oral water for oligohydramnios may be done whether or not immediate induction is chosen, as this is a safe measure that has been shown to significantly increase AFI. Alternatively, the preferred approach for a multiparous woman with a ripe cervix by Bishop score may be labor induction.

As adverse fetal outcomes have not been demonstrated in women with isolated term oligohydramnios, there is no rationale for routinely inducing labor based on an isolated finding of a so called “borderline” amniotic fluid index in the 5-to-8 range. In this situation it is appropriate to perform the initial assessment described above and may be reasonable to repeat the amniotic fluid index in 3 to 4 days to determine if true oligohydramnios has developed.

FIGURE
Assessment of the pregnant woman with oligohydramnios at term

Acknowledgments

We appreciate the assistance of George Gilson MD, Lauren Plante MD, and William Rayburn MD in manuscript review.

Corresponding author
Lawrence Leeman, MD, MPH, University of New Mexico Depts of Family and Community Medicine, Obstetrics and Gynecology, 2400 Tucker NE, 3rd floor, Albuquerque, NM 87131. E-mail: [email protected].

Family physicians providing maternity care often face a scenario in which an otherwise low-risk, term patient is incidentally noted to have a low amniotic fluid index (AFI). Common reasons for obtaining an AFI in a woman with a low-risk pregnancy include evaluation of decreased fetal movement, spontaneous variable decelerations during monitoring to evaluate for labor, or an ultrasound evaluation for fundal height measurements discordant with gestational age. How should “isolated” oligohydramnios—an AFI <5 cm—be interpreted, and should immediate induction be recommended for such patients?

Oligohydramnios occurs in about 1% to 5% of pregnancies at term.^1,2 Because adverse outcomes occur in high-risk pregnancies complicated by low amniotic fluid volume, oligohydramnios commonly prompts labor induction.^1,3,4 At one university center, oligohydramnios is now the leading indication for labor induction.⁵ Many centers may even induce labor when the AFI is between 5 cm and 8 cm, the so-called borderline AFI.³

Labor induction increases the use of cesarean delivery, particularly for the primiparous woman with an unripe cervix.⁶ Recent studies questioning the safety of labor induction in women who have had a cesarean may increase the number of elective repeat cesarean procedures when delivery is believed indicated for oligohydramnios.⁷ (See Underlying causes of oligohydramnios.)

Oligohydramnios is difficult to assess

True oligohydramnios can be difficult to confirm due to the questionable accuracy of amniotic fluid measurement by ultrasound. There is controversy, for example, about whether (and how) to include pockets of amniotic fluid containing umbilical cord.¹⁵ The AFI was introduced in 1987² to replace the 2 cm “pocket technique” of fluid assessment, and studies continue to question to what extent the AFI reflects actual amniotic fluid volume.

AFI measurements may vary with the amount of pressure applied to the abdomen and with fetal position or movement.¹⁶

Serial measurements taken by the same ultrasound operator have been shown to differ from the true volume by 1 cm, or 10.8%; serial measurements taken by multiple operators have differed by as much as 2 cm, or 15.4%.^17,18

O’Reilly-Green compared the diagnosis of oligohydramnios in 449 post-term patients with actual amniotic fluid volume measured at rupture of membranes.¹⁹ They found a positive predictive value of 50% for oligohydramnios at an AFI of 5 cm as the lower limit of normal. A study of 144 third trimester patients using the dye-dilution technique found that, to achieve 95% confidence for ruling out oligohydramnios, a cutoff AFI of 30 cm would need to be used, a value consistent with polyhydramnios.²⁰

What is the association between oligohydramnios and poor fetal outcomes?

A number of studies over the past 15 years have shown an association between oligohydramnios and poor fetal outcomes. These were predominantly retrospective studies, which failed to control for the presence of factors known to be associated with oligohydramnios such as intrauterine growth restriction (IUGR) and urogenital malformations.

No studies have directly addressed whether labor induction improves outcomes. A meta-analysis of 18 studies examining outcomes of pregnancies with AFI <5 cm found an increased risk of cesarean delivery for fetal distress and low Apgar scores at 5 minutes. Most of these studies, however, had high-risk patients including IUGR (level of evidence [LOE]: 2).²¹

A recent study of high-risk patients failed to detect a difference in the incidence of nonreactive nonstress tests, meconium-stained amniotic fluid cesarean delivery for fetal distress, low Apgar scores, or infants with a cord pH of <7.10 when oligohydramnios (AFI <5.0 cm) was present (LOE: 1).² The patients with oligohydramnios were all induced, while many of the other high-risk patients were expectantly managed. The study therefore provides no guidance on the safety of expectant management for patients with oligohydramnios. To eliminate the potential effect of induction versus expectant management the same authors performed a case-control study of 79 high-risk women with AFI <5 cm matched to 79 women with the same high-risk pregnancy complication who had an AFI >5 cm at the time of induction (LOE: 2).²³ They failed to detect any significant differences in neonatal outcomes between the groups.

Studies of the “borderline” AFI (between 5 cm and 8 cm) may also demonstrate an association with adverse neonatal outcomes if researchers include fetuses with IUGR or malformations. In one retrospective case review of 214 women with AFI of 5 cm to 10 cm, the only statistically significant finding was an association with IUGR.³ The authors recommended antepartum surveillance twice a week for mothers with borderline AFI, but they did not comment on induction (LOE: 2). Correspondence regarding this study argued that this recommendation was not supported by the evidence and would lead to unnecessary antenatal testing.²⁴

Studies of isolated oligohydramnios

Investigators have conducted studies (Table 1) excluding fetuses with intrauterine growth restriction or anomalies to try to determine if isolated oligohydramnios is associated with poorer outcomes.^25-30

Rainford’s study of outcomes in exclusively term, low-risk patients failed to show significant outcome differences in Apgar scores, NICU admissions, or rates of cesarean delivery for non-reassuring fetal heart rate monitoring (LOE: 2).²⁹ This study was limited due to its retrospective design. The authors comment that the relatively good outcomes in the oligohydramnios group may be due to the widespread practice of inducing such patients.

In a case-control study by Conway, 183 low-risk, term parturients with oligohydramnios were matched to 183 women of similar gestational age and parity who presented in spontaneous labor. The patients with isolated oligohydramnios were induced and showed an increased cesarean delivery rate. The increased rate of cesarean delivery was not due to nonreassuring fetal surveillance and was attributed to the induction process (LOE: 2).²⁵

An analysis of woman diagnosed with isolated oligohydramnios (AFI <5) at any gestational age in the multicenter prospective RADIUS trial demonstrated similar perinatal outcomes and fetal growth compared with pregnancies with a normal amniotic fluid (LOE: 2).³⁰

The only randomized clinical trial of labor induction vs expectant management for term isolated oligohydramnios showed similar outcomes in each group. But this study was small (n=61) and has only been published as an abstract.³¹

TABLE 1
Isolated oligohydramnios and perinatal outcomes

Effect of maternal hydration

Maternal hydration status and plasma osmolality have an affect on amniotic fluid volume (Table 2). Maternal hydration with oral water or intravenous hypotonic solutions has been shown to increase amniotic fluid volume.^8,11-13 Oral hydration with hypotonic fluid has been demonstrated to increase fetal urine production in one observational study.³² Another observational study demonstrated increased amniotic fluid volume and uteroplacental perfusion without alteration of fetal urine production suggesting the possibility that transmembranous fluid shifts from the placenta to the amniotic cavity may be involved.¹²