Current Psychiatry

CASE: ‘Like a sledgehammer’

Mr. J, age 54, is admitted to the cardiac critical care unit after repeated tachycardia episodes over 3 years. He also has depressive symptoms including social isolation, passive suicidal thoughts, lack of interest in sex, weight loss, difficulty sleeping, sadness, and decreased appetite, energy, and ability to concentrate. The psychiatry consult team subsequently evaluates him.

Shortly after retiring as a police officer, Mr. J started having 10-second episodes of loss of consciousness and suffered 30 episodes within 1 year. After diagnosing chronic idiopathic ventricular tachycardia, a cardiologist ablated an aberrant left ventricular pathway and inserted a single-lead implantable cardioverter-defibrillator (ICD). He also prescribed the antiarrhythmic amiodarone, but Mr. J could not tolerate the medication’s side effects.

Mr. J’s tachycardia persisted, and repeated episodes triggered an estimated 13 electrical shocks from the ICD over 5 months. At this point, the cardiologist performed a second ablation, removed the single-lead ICD, and implanted a two-lead ICD, which he hoped would more accurately discern between lethal and nonlethal fast heart rhythms.

In addition, the cardiologist prescribed the antiarrhythmic sotalol—which did not suppress the arrhythmia—before switching to flecainide, 100 mg bid, which did. However, Mr. J still suffered fatigue, exercise intolerance, near-syncope, and chest heaviness.

One week after receiving the first ICD, Mr. J recalls, he felt his first shock while out for a walk. He said the shock lasted 5 to 10 seconds and “felt like somebody took a sledgehammer to my chest.” Another time, he suffered 6 successive shocks that threw him to the ground. Motorists pulled over to assist him, which made him feel ashamed.

Before long, Mr. J became increasingly afraid of repeat discharges. As soon as he began a task, he would feel a “thumping” in the back of his neck and start panicking, fearful that a heart rate increase would trigger another shock.

The stress forced Mr. J to abandon his favorite retirement hobbies—remodeling houses and yard work—and to spend his days lying around watching television. Fearing another discharge in public, he has stopped seeing friends and going to church. He has also stopped driving and depends on his female partner of 14 years for daily visits, grocery shopping, and rides to medical appointments. She feels frustrated by his debility.

The authors’ observations

By delivering electrical shocks when ventricles beat too quickly, an ICD shocks the heart back into a normal rhythm. Based on our observation, Mr. J probably had both anxiety-induced tachycardia and recurrent atrial fibrillation.

Although ICDs have prolonged survival for patients with potentially fatal ventricular arrhythmias,^1,2 painful discharges can occur without warning. Patients liken the discharge to an electric shock or to being kicked or punched in the chest.³

Depending on the patient’s activity level, cardiologists routinely program ICDs to discharge at approximately 10 beats per minute above expected heart rates during typical activities. Because ICD leads cannot differentiate between ventricular and supraventricular rhythm disturbances, a rapid supraventricular rhythm might precipitate a discharge intended to treat a more serious ventricular rhythm disturbance.

Frequent ICD discharges could indicate:

• the patient needs a more effective antiarrhythmic
  
• the device needs to be set at a higher rate to avoid discharge during periods of anxiety/exertion
  
• or the device is defective.
  

ICD-induced psychopathology

Depression or tachycardia could have caused Mr. J’s fatigue. Either way, he showed numerous other depressive symptoms.

Fear of implant discharge or malfunction often induces psychiatric disorders, particularly in patients who have experienced discharge. As many as 87% of ICD patients suffer anxiety, depression, or other psychiatric symptoms after implantation,⁵ and 13% to 38% meet DSM-IV-TR criteria for an anxiety spectrum disorder.⁶

Multiple psychological theories explain iatrogenic anxiety disorders resulting from ICD firing. Behaviorally, ICD discharge represents an initially unconditioned stimulus that the patient associates with the activity he was engaging in when shocked. The shock discourages the patient from that activity—however benign—for fear it triggered the discharge and could cause future shocks.

ICD recipients often fear the device will malfunction or discharge while they are in public, driving, or operating machinery—leading some to become homebound and cease activities of daily living. The discharge’s unpredictability shatters a patient’s perception of control over his or her life and might induce a learned helplessness⁷ that can strain relationships, as it did with Mr. J and his partner. The patient also could develop anticipatory anxiety, mistaking benign body symptoms or increasing shock frequency for signs of a potentially fatal heart problem.⁸

Detecting ICD maladjustment

Patients with ICD maladjustment typically show anticipatory anxiety and negative cognitive attributions, and many engage in fruitless maneuvers to prevent device firing.⁵ Nervousness, dizziness, weakness, and fear are common responses to shock by ICD.¹¹

Most patients with new-onset, post-ICD anxiety disorders have no pre-implant psychiatric history.¹² Only one trial assessing state and trait anxiety before and after ICD placement reported increased trait anxiety in some patients before implantation.¹³

HISTORY: Nights in the cornfield

During psychiatric evaluation, Mr. J reveals that his parents physically and emotionally abused him as a child. He says his father frequently beat him with farm tools, and sometimes the beatings were so severe that his parents kept him home from school to prevent teachers from noticing his bruises. He never received medical treatment for his injuries.

For Mr. J, the inescapable threat of painful, unannounced ICD discharges has brought back the anticipatory terror and helplessness of his childhood. Just as he feared his father’s sudden rages, the specter of repeat ICD shocks now haunts him. He says he’d rather have the ICD removed and risk death from tachycardia than live another minute in fear.

The authors’ observations

Mr. J meets DSM-IV-TR criteria for PTSD. He associates ICD discharge with childhood abuse and experiences new-onset flashbacks, hyperarousal, and avoidance behavior.

To our knowledge, ICD shock-induced flashbacks to pre-implant trauma have not been reported, although some data associate ICDs with posttraumatic stress related to heart disease and treatment.^14-16 In one case series,¹⁴ patients showed:

• cluster B re-experiencing symptoms (cognitive preoccupation with trauma or psychophysiologic reactivity to reminders of the ICD and heart disease)
  
• cluster C avoidance symptoms (avoiding activities they thought might activate the ICD)
  
• cluster D hyperarousal symptoms (insomnia, decreased concentration, hypervigilance, and irritability).
  

The authors’ observations

Treating comorbid anxiety or depression in ICD recipients is critical. A number of psychiatric interventions might alleviate behavioral and psychological effects of body-device interactions.

CBT. In a retrospective study¹⁷ of 36 ICD recipients, those who received 9 months of CBT reported decreased depression, anxiety, distress, and sexual problems compared with those who did not. Interestingly, more CBT-group patients (11 of 18) suffered ICD shocks than did controls (6 of 18).

Peer support groups. Out of 58 ICD recipients who answered a post-implant questionnaire, 23 (39%) attended a peer support group.¹⁸ Of these, 22 (96%) found the group helpful and were happier, less hostile, and more sociable after participating. Peer group participants also were more likely to return to work than nonparticipants.

Box

In a double-blind, placebo-controlled crossover study, implantable atrial defibrillator recipients reported decreased pain and anxiety while taking the short-acting benzodiazepine triazolam, 0.375 mg, before patient-activated shock.¹⁹

We recommend trying a combination regimen that acts acutely and subacutely. A long-acting benzodiazepine such as clonazepam can calm acute, overwhelming anxiety, and a selective serotonin reuptake inhibitor (SSRI) such as fluoxetine or paroxetine can help manage chronic depressive and generalized anxiety symptoms.

SSRIs are relatively benign but more research on their cardiac safety is needed.^20,21 Tricyclic antidepressants, which prolong cardiac conduction, should be avoided.

In addition to psychotropics, concomitant psychotherapy can reduce chronic symptoms.

The authors’ observations

Preparing patients for ICD problems. Anxiety after an ICD shock and the dread of repeat shocks are normal; the goal is to prevent that anxiety from destroying quality of life.

As with Mr. J, many ICD recipients are emotionally unprepared for device-related complications. Most cardiologists do not screen patients for pre-existing anxiety before ICD placement, nor do many adequately address ICD-induced anxiety once the device has been placed.

Psychological screening before implantation can help detect and manage preexisting anxiety disorders. Small-scale evaluations have used anxiety scales to continuously measure anxiety before and after ICD placement.^13,23

Increased patient education on how ICDs work can help patients decide whether to proceed with implantation and tolerate discharges should they occur. Psychological screening and brief, routine communication between providers and patients about psychosocial issues can help patients adjust and identify those who need extended psychological services.⁴

• develop a plan for how a shock would be handled
  
• perform relaxation exercises immediately after the shock
  
• resume activities they were involved with when the shock occurred to prevent avoidance.²⁴
  

TREATMENT: Third attempt

The cardiology team discontinues flecainide and performs a third radioablation, which eradicates ectopic ventricular activity.

Acting on the psychiatry consult team’s advice, Mr. J is transferred to the inpatient mood disorders unit to aggressively treat his PTSD. He undergoes 4 days of intensive CBT designed to explore the connection between his response to the discharges and his father’s abuse. We prescribe clonazepam, 0.5 mg bid, to reduce Mr. J’s agitation and anxiety, and recommend outpatient counseling to help manage his stress—particularly his anxious response to stimuli that remind him of the ICD discharge.

Mr. J is discharged after 12 days in the cardiac and psychiatric units. He has no suicidal thoughts, his sadness has decreased, and his energy, concentration, sleep, and outlook on his future have improved. He also is resolving relationship issues with his partner.

As Mr. J’s anxiety declines and he is increasingly reassured that his arrhythmias are under control, he decides to keep the ICD. His function gradually improves with continued cardiac rehabilitation, although he does not continue psychotherapy.

Related resources

• Stutts LA, Cross NJ, Conti JB, Sears SF. Examination of research trends on patient factors in patients with implantable cardioverter defibrillators. Clin Cardiol 2007;30:64-8.
  
• Sears SF, Shea JB, Conti JB. How to respond to an implantable cardioverter-defibrillator shock. Circulation 2005;111;380-2. http://circ.ahajournals.org/cgi/reprint/111/23/e380.
  
• Pauli P, Wiedemann G, Dengler W, et al. Anxiety in patients with an automatic implantable cardioverter defibrillator: what differentiates them from panic patients? Psychosom Med 1999;61:69-76. www.psychosomaticmedicine.org/cgi/reprint/61/1/69.
  

• Amiodarone • Cordarone
  
• Clonazepam • Klonopin
  
• Flecainide • Tambocor
  
• Fluoxetine • Prozac
  
• Paroxetine • Paxil
  
• Sotalol • Betapace
  
• Triazolam • Halcion, others
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: ‘Like a sledgehammer’

Mr. J, age 54, is admitted to the cardiac critical care unit after repeated tachycardia episodes over 3 years. He also has depressive symptoms including social isolation, passive suicidal thoughts, lack of interest in sex, weight loss, difficulty sleeping, sadness, and decreased appetite, energy, and ability to concentrate. The psychiatry consult team subsequently evaluates him.

Shortly after retiring as a police officer, Mr. J started having 10-second episodes of loss of consciousness and suffered 30 episodes within 1 year. After diagnosing chronic idiopathic ventricular tachycardia, a cardiologist ablated an aberrant left ventricular pathway and inserted a single-lead implantable cardioverter-defibrillator (ICD). He also prescribed the antiarrhythmic amiodarone, but Mr. J could not tolerate the medication’s side effects.

Mr. J’s tachycardia persisted, and repeated episodes triggered an estimated 13 electrical shocks from the ICD over 5 months. At this point, the cardiologist performed a second ablation, removed the single-lead ICD, and implanted a two-lead ICD, which he hoped would more accurately discern between lethal and nonlethal fast heart rhythms.

In addition, the cardiologist prescribed the antiarrhythmic sotalol—which did not suppress the arrhythmia—before switching to flecainide, 100 mg bid, which did. However, Mr. J still suffered fatigue, exercise intolerance, near-syncope, and chest heaviness.

One week after receiving the first ICD, Mr. J recalls, he felt his first shock while out for a walk. He said the shock lasted 5 to 10 seconds and “felt like somebody took a sledgehammer to my chest.” Another time, he suffered 6 successive shocks that threw him to the ground. Motorists pulled over to assist him, which made him feel ashamed.

Before long, Mr. J became increasingly afraid of repeat discharges. As soon as he began a task, he would feel a “thumping” in the back of his neck and start panicking, fearful that a heart rate increase would trigger another shock.

The stress forced Mr. J to abandon his favorite retirement hobbies—remodeling houses and yard work—and to spend his days lying around watching television. Fearing another discharge in public, he has stopped seeing friends and going to church. He has also stopped driving and depends on his female partner of 14 years for daily visits, grocery shopping, and rides to medical appointments. She feels frustrated by his debility.

The authors’ observations

By delivering electrical shocks when ventricles beat too quickly, an ICD shocks the heart back into a normal rhythm. Based on our observation, Mr. J probably had both anxiety-induced tachycardia and recurrent atrial fibrillation.

Although ICDs have prolonged survival for patients with potentially fatal ventricular arrhythmias,^1,2 painful discharges can occur without warning. Patients liken the discharge to an electric shock or to being kicked or punched in the chest.³

Depending on the patient’s activity level, cardiologists routinely program ICDs to discharge at approximately 10 beats per minute above expected heart rates during typical activities. Because ICD leads cannot differentiate between ventricular and supraventricular rhythm disturbances, a rapid supraventricular rhythm might precipitate a discharge intended to treat a more serious ventricular rhythm disturbance.

Frequent ICD discharges could indicate:

• the patient needs a more effective antiarrhythmic
  
• the device needs to be set at a higher rate to avoid discharge during periods of anxiety/exertion
  
• or the device is defective.
  

ICD-induced psychopathology

Depression or tachycardia could have caused Mr. J’s fatigue. Either way, he showed numerous other depressive symptoms.

Fear of implant discharge or malfunction often induces psychiatric disorders, particularly in patients who have experienced discharge. As many as 87% of ICD patients suffer anxiety, depression, or other psychiatric symptoms after implantation,⁵ and 13% to 38% meet DSM-IV-TR criteria for an anxiety spectrum disorder.⁶

Multiple psychological theories explain iatrogenic anxiety disorders resulting from ICD firing. Behaviorally, ICD discharge represents an initially unconditioned stimulus that the patient associates with the activity he was engaging in when shocked. The shock discourages the patient from that activity—however benign—for fear it triggered the discharge and could cause future shocks.

ICD recipients often fear the device will malfunction or discharge while they are in public, driving, or operating machinery—leading some to become homebound and cease activities of daily living. The discharge’s unpredictability shatters a patient’s perception of control over his or her life and might induce a learned helplessness⁷ that can strain relationships, as it did with Mr. J and his partner. The patient also could develop anticipatory anxiety, mistaking benign body symptoms or increasing shock frequency for signs of a potentially fatal heart problem.⁸

Detecting ICD maladjustment

Patients with ICD maladjustment typically show anticipatory anxiety and negative cognitive attributions, and many engage in fruitless maneuvers to prevent device firing.⁵ Nervousness, dizziness, weakness, and fear are common responses to shock by ICD.¹¹

Most patients with new-onset, post-ICD anxiety disorders have no pre-implant psychiatric history.¹² Only one trial assessing state and trait anxiety before and after ICD placement reported increased trait anxiety in some patients before implantation.¹³

HISTORY: Nights in the cornfield

During psychiatric evaluation, Mr. J reveals that his parents physically and emotionally abused him as a child. He says his father frequently beat him with farm tools, and sometimes the beatings were so severe that his parents kept him home from school to prevent teachers from noticing his bruises. He never received medical treatment for his injuries.

For Mr. J, the inescapable threat of painful, unannounced ICD discharges has brought back the anticipatory terror and helplessness of his childhood. Just as he feared his father’s sudden rages, the specter of repeat ICD shocks now haunts him. He says he’d rather have the ICD removed and risk death from tachycardia than live another minute in fear.

The authors’ observations

Mr. J meets DSM-IV-TR criteria for PTSD. He associates ICD discharge with childhood abuse and experiences new-onset flashbacks, hyperarousal, and avoidance behavior.

To our knowledge, ICD shock-induced flashbacks to pre-implant trauma have not been reported, although some data associate ICDs with posttraumatic stress related to heart disease and treatment.^14-16 In one case series,¹⁴ patients showed:

• cluster B re-experiencing symptoms (cognitive preoccupation with trauma or psychophysiologic reactivity to reminders of the ICD and heart disease)
  
• cluster C avoidance symptoms (avoiding activities they thought might activate the ICD)
  
• cluster D hyperarousal symptoms (insomnia, decreased concentration, hypervigilance, and irritability).
  

The authors’ observations

Treating comorbid anxiety or depression in ICD recipients is critical. A number of psychiatric interventions might alleviate behavioral and psychological effects of body-device interactions.

CBT. In a retrospective study¹⁷ of 36 ICD recipients, those who received 9 months of CBT reported decreased depression, anxiety, distress, and sexual problems compared with those who did not. Interestingly, more CBT-group patients (11 of 18) suffered ICD shocks than did controls (6 of 18).

Peer support groups. Out of 58 ICD recipients who answered a post-implant questionnaire, 23 (39%) attended a peer support group.¹⁸ Of these, 22 (96%) found the group helpful and were happier, less hostile, and more sociable after participating. Peer group participants also were more likely to return to work than nonparticipants.

Box

In a double-blind, placebo-controlled crossover study, implantable atrial defibrillator recipients reported decreased pain and anxiety while taking the short-acting benzodiazepine triazolam, 0.375 mg, before patient-activated shock.¹⁹

We recommend trying a combination regimen that acts acutely and subacutely. A long-acting benzodiazepine such as clonazepam can calm acute, overwhelming anxiety, and a selective serotonin reuptake inhibitor (SSRI) such as fluoxetine or paroxetine can help manage chronic depressive and generalized anxiety symptoms.

SSRIs are relatively benign but more research on their cardiac safety is needed.^20,21 Tricyclic antidepressants, which prolong cardiac conduction, should be avoided.

In addition to psychotropics, concomitant psychotherapy can reduce chronic symptoms.

The authors’ observations

Preparing patients for ICD problems. Anxiety after an ICD shock and the dread of repeat shocks are normal; the goal is to prevent that anxiety from destroying quality of life.

As with Mr. J, many ICD recipients are emotionally unprepared for device-related complications. Most cardiologists do not screen patients for pre-existing anxiety before ICD placement, nor do many adequately address ICD-induced anxiety once the device has been placed.

Psychological screening before implantation can help detect and manage preexisting anxiety disorders. Small-scale evaluations have used anxiety scales to continuously measure anxiety before and after ICD placement.^13,23

Increased patient education on how ICDs work can help patients decide whether to proceed with implantation and tolerate discharges should they occur. Psychological screening and brief, routine communication between providers and patients about psychosocial issues can help patients adjust and identify those who need extended psychological services.⁴

• develop a plan for how a shock would be handled
  
• perform relaxation exercises immediately after the shock
  
• resume activities they were involved with when the shock occurred to prevent avoidance.²⁴
  

TREATMENT: Third attempt

The cardiology team discontinues flecainide and performs a third radioablation, which eradicates ectopic ventricular activity.

Acting on the psychiatry consult team’s advice, Mr. J is transferred to the inpatient mood disorders unit to aggressively treat his PTSD. He undergoes 4 days of intensive CBT designed to explore the connection between his response to the discharges and his father’s abuse. We prescribe clonazepam, 0.5 mg bid, to reduce Mr. J’s agitation and anxiety, and recommend outpatient counseling to help manage his stress—particularly his anxious response to stimuli that remind him of the ICD discharge.

Mr. J is discharged after 12 days in the cardiac and psychiatric units. He has no suicidal thoughts, his sadness has decreased, and his energy, concentration, sleep, and outlook on his future have improved. He also is resolving relationship issues with his partner.

As Mr. J’s anxiety declines and he is increasingly reassured that his arrhythmias are under control, he decides to keep the ICD. His function gradually improves with continued cardiac rehabilitation, although he does not continue psychotherapy.

Related resources

• Stutts LA, Cross NJ, Conti JB, Sears SF. Examination of research trends on patient factors in patients with implantable cardioverter defibrillators. Clin Cardiol 2007;30:64-8.
  
• Sears SF, Shea JB, Conti JB. How to respond to an implantable cardioverter-defibrillator shock. Circulation 2005;111;380-2. http://circ.ahajournals.org/cgi/reprint/111/23/e380.
  
• Pauli P, Wiedemann G, Dengler W, et al. Anxiety in patients with an automatic implantable cardioverter defibrillator: what differentiates them from panic patients? Psychosom Med 1999;61:69-76. www.psychosomaticmedicine.org/cgi/reprint/61/1/69.
  

• Amiodarone • Cordarone
  
• Clonazepam • Klonopin
  
• Flecainide • Tambocor
  
• Fluoxetine • Prozac
  
• Paroxetine • Paxil
  
• Sotalol • Betapace
  
• Triazolam • Halcion, others
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: ‘Like a sledgehammer’

Mr. J, age 54, is admitted to the cardiac critical care unit after repeated tachycardia episodes over 3 years. He also has depressive symptoms including social isolation, passive suicidal thoughts, lack of interest in sex, weight loss, difficulty sleeping, sadness, and decreased appetite, energy, and ability to concentrate. The psychiatry consult team subsequently evaluates him.

Shortly after retiring as a police officer, Mr. J started having 10-second episodes of loss of consciousness and suffered 30 episodes within 1 year. After diagnosing chronic idiopathic ventricular tachycardia, a cardiologist ablated an aberrant left ventricular pathway and inserted a single-lead implantable cardioverter-defibrillator (ICD). He also prescribed the antiarrhythmic amiodarone, but Mr. J could not tolerate the medication’s side effects.

Mr. J’s tachycardia persisted, and repeated episodes triggered an estimated 13 electrical shocks from the ICD over 5 months. At this point, the cardiologist performed a second ablation, removed the single-lead ICD, and implanted a two-lead ICD, which he hoped would more accurately discern between lethal and nonlethal fast heart rhythms.

In addition, the cardiologist prescribed the antiarrhythmic sotalol—which did not suppress the arrhythmia—before switching to flecainide, 100 mg bid, which did. However, Mr. J still suffered fatigue, exercise intolerance, near-syncope, and chest heaviness.

One week after receiving the first ICD, Mr. J recalls, he felt his first shock while out for a walk. He said the shock lasted 5 to 10 seconds and “felt like somebody took a sledgehammer to my chest.” Another time, he suffered 6 successive shocks that threw him to the ground. Motorists pulled over to assist him, which made him feel ashamed.

Before long, Mr. J became increasingly afraid of repeat discharges. As soon as he began a task, he would feel a “thumping” in the back of his neck and start panicking, fearful that a heart rate increase would trigger another shock.

The stress forced Mr. J to abandon his favorite retirement hobbies—remodeling houses and yard work—and to spend his days lying around watching television. Fearing another discharge in public, he has stopped seeing friends and going to church. He has also stopped driving and depends on his female partner of 14 years for daily visits, grocery shopping, and rides to medical appointments. She feels frustrated by his debility.

The authors’ observations

By delivering electrical shocks when ventricles beat too quickly, an ICD shocks the heart back into a normal rhythm. Based on our observation, Mr. J probably had both anxiety-induced tachycardia and recurrent atrial fibrillation.

Although ICDs have prolonged survival for patients with potentially fatal ventricular arrhythmias,^1,2 painful discharges can occur without warning. Patients liken the discharge to an electric shock or to being kicked or punched in the chest.³

Depending on the patient’s activity level, cardiologists routinely program ICDs to discharge at approximately 10 beats per minute above expected heart rates during typical activities. Because ICD leads cannot differentiate between ventricular and supraventricular rhythm disturbances, a rapid supraventricular rhythm might precipitate a discharge intended to treat a more serious ventricular rhythm disturbance.

Frequent ICD discharges could indicate:

• the patient needs a more effective antiarrhythmic
  
• the device needs to be set at a higher rate to avoid discharge during periods of anxiety/exertion
  
• or the device is defective.
  

ICD-induced psychopathology

Depression or tachycardia could have caused Mr. J’s fatigue. Either way, he showed numerous other depressive symptoms.

Fear of implant discharge or malfunction often induces psychiatric disorders, particularly in patients who have experienced discharge. As many as 87% of ICD patients suffer anxiety, depression, or other psychiatric symptoms after implantation,⁵ and 13% to 38% meet DSM-IV-TR criteria for an anxiety spectrum disorder.⁶

Multiple psychological theories explain iatrogenic anxiety disorders resulting from ICD firing. Behaviorally, ICD discharge represents an initially unconditioned stimulus that the patient associates with the activity he was engaging in when shocked. The shock discourages the patient from that activity—however benign—for fear it triggered the discharge and could cause future shocks.

ICD recipients often fear the device will malfunction or discharge while they are in public, driving, or operating machinery—leading some to become homebound and cease activities of daily living. The discharge’s unpredictability shatters a patient’s perception of control over his or her life and might induce a learned helplessness⁷ that can strain relationships, as it did with Mr. J and his partner. The patient also could develop anticipatory anxiety, mistaking benign body symptoms or increasing shock frequency for signs of a potentially fatal heart problem.⁸

Detecting ICD maladjustment

Patients with ICD maladjustment typically show anticipatory anxiety and negative cognitive attributions, and many engage in fruitless maneuvers to prevent device firing.⁵ Nervousness, dizziness, weakness, and fear are common responses to shock by ICD.¹¹

Most patients with new-onset, post-ICD anxiety disorders have no pre-implant psychiatric history.¹² Only one trial assessing state and trait anxiety before and after ICD placement reported increased trait anxiety in some patients before implantation.¹³

HISTORY: Nights in the cornfield

During psychiatric evaluation, Mr. J reveals that his parents physically and emotionally abused him as a child. He says his father frequently beat him with farm tools, and sometimes the beatings were so severe that his parents kept him home from school to prevent teachers from noticing his bruises. He never received medical treatment for his injuries.

For Mr. J, the inescapable threat of painful, unannounced ICD discharges has brought back the anticipatory terror and helplessness of his childhood. Just as he feared his father’s sudden rages, the specter of repeat ICD shocks now haunts him. He says he’d rather have the ICD removed and risk death from tachycardia than live another minute in fear.

The authors’ observations

Mr. J meets DSM-IV-TR criteria for PTSD. He associates ICD discharge with childhood abuse and experiences new-onset flashbacks, hyperarousal, and avoidance behavior.

To our knowledge, ICD shock-induced flashbacks to pre-implant trauma have not been reported, although some data associate ICDs with posttraumatic stress related to heart disease and treatment.^14-16 In one case series,¹⁴ patients showed:

• cluster B re-experiencing symptoms (cognitive preoccupation with trauma or psychophysiologic reactivity to reminders of the ICD and heart disease)
  
• cluster C avoidance symptoms (avoiding activities they thought might activate the ICD)
  
• cluster D hyperarousal symptoms (insomnia, decreased concentration, hypervigilance, and irritability).
  

The authors’ observations

Treating comorbid anxiety or depression in ICD recipients is critical. A number of psychiatric interventions might alleviate behavioral and psychological effects of body-device interactions.

CBT. In a retrospective study¹⁷ of 36 ICD recipients, those who received 9 months of CBT reported decreased depression, anxiety, distress, and sexual problems compared with those who did not. Interestingly, more CBT-group patients (11 of 18) suffered ICD shocks than did controls (6 of 18).

Peer support groups. Out of 58 ICD recipients who answered a post-implant questionnaire, 23 (39%) attended a peer support group.¹⁸ Of these, 22 (96%) found the group helpful and were happier, less hostile, and more sociable after participating. Peer group participants also were more likely to return to work than nonparticipants.

Box

In a double-blind, placebo-controlled crossover study, implantable atrial defibrillator recipients reported decreased pain and anxiety while taking the short-acting benzodiazepine triazolam, 0.375 mg, before patient-activated shock.¹⁹

We recommend trying a combination regimen that acts acutely and subacutely. A long-acting benzodiazepine such as clonazepam can calm acute, overwhelming anxiety, and a selective serotonin reuptake inhibitor (SSRI) such as fluoxetine or paroxetine can help manage chronic depressive and generalized anxiety symptoms.

SSRIs are relatively benign but more research on their cardiac safety is needed.^20,21 Tricyclic antidepressants, which prolong cardiac conduction, should be avoided.

In addition to psychotropics, concomitant psychotherapy can reduce chronic symptoms.

The authors’ observations

Preparing patients for ICD problems. Anxiety after an ICD shock and the dread of repeat shocks are normal; the goal is to prevent that anxiety from destroying quality of life.

As with Mr. J, many ICD recipients are emotionally unprepared for device-related complications. Most cardiologists do not screen patients for pre-existing anxiety before ICD placement, nor do many adequately address ICD-induced anxiety once the device has been placed.

Psychological screening before implantation can help detect and manage preexisting anxiety disorders. Small-scale evaluations have used anxiety scales to continuously measure anxiety before and after ICD placement.^13,23

Increased patient education on how ICDs work can help patients decide whether to proceed with implantation and tolerate discharges should they occur. Psychological screening and brief, routine communication between providers and patients about psychosocial issues can help patients adjust and identify those who need extended psychological services.⁴

• develop a plan for how a shock would be handled
  
• perform relaxation exercises immediately after the shock
  
• resume activities they were involved with when the shock occurred to prevent avoidance.²⁴
  

TREATMENT: Third attempt

The cardiology team discontinues flecainide and performs a third radioablation, which eradicates ectopic ventricular activity.

Acting on the psychiatry consult team’s advice, Mr. J is transferred to the inpatient mood disorders unit to aggressively treat his PTSD. He undergoes 4 days of intensive CBT designed to explore the connection between his response to the discharges and his father’s abuse. We prescribe clonazepam, 0.5 mg bid, to reduce Mr. J’s agitation and anxiety, and recommend outpatient counseling to help manage his stress—particularly his anxious response to stimuli that remind him of the ICD discharge.

Mr. J is discharged after 12 days in the cardiac and psychiatric units. He has no suicidal thoughts, his sadness has decreased, and his energy, concentration, sleep, and outlook on his future have improved. He also is resolving relationship issues with his partner.

As Mr. J’s anxiety declines and he is increasingly reassured that his arrhythmias are under control, he decides to keep the ICD. His function gradually improves with continued cardiac rehabilitation, although he does not continue psychotherapy.

Related resources

• Stutts LA, Cross NJ, Conti JB, Sears SF. Examination of research trends on patient factors in patients with implantable cardioverter defibrillators. Clin Cardiol 2007;30:64-8.
  
• Sears SF, Shea JB, Conti JB. How to respond to an implantable cardioverter-defibrillator shock. Circulation 2005;111;380-2. http://circ.ahajournals.org/cgi/reprint/111/23/e380.
  
• Pauli P, Wiedemann G, Dengler W, et al. Anxiety in patients with an automatic implantable cardioverter defibrillator: what differentiates them from panic patients? Psychosom Med 1999;61:69-76. www.psychosomaticmedicine.org/cgi/reprint/61/1/69.
  

• Amiodarone • Cordarone
  
• Clonazepam • Klonopin
  
• Flecainide • Tambocor
  
• Fluoxetine • Prozac
  
• Paroxetine • Paxil
  
• Sotalol • Betapace
  
• Triazolam • Halcion, others
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Bioethics of clinical practice change during disasters, as our staff learned when providing emergency care to Hurricane Katrina evacuees. During crises such as severe weather, terrorist acts, and epidemics, physicians can be torn between advocating for individual patients’ needs or the public good.¹

As the storm’s 2-year anniversary approaches (Box),^2,3 we share our experiences to help you prepare for disasters in your community and to contribute to the limited data on ethics in disaster psychiatry. This article describes 3 cases to show how mental health clinicians balanced issues such as conflict, consequences, patient rights, physician virtues, and justice when making treatment decisions in the Houston Astrodome clinic.

CASE 1: Benzodiazepines for anxiety?

Mr. R, age 23, presented to the Astrodome mental health clinic requesting “Xanax for my nerves.” He said he had been taking 6 mg/d “for years and years, and it’s the only thing that helps.” Mr. R claimed he had been without his medicines at least 48 hours.

The assessing psychiatrist found no evidence of benzodiazepine withdrawal or other psychiatric emergency. The dilemma: How to provide appropriate acute treatment of a chronic problem, without continuity of care and follow-up.

As a hurricane survivor, Mr. R experienced a traumatic event that could have exacerbated an underlying anxiety disorder. But patients’ use of and physicians’ prescription of benzodiazepines can have adverse short- and long-term consequences. Mr. R’s case highlights the conflict between establishing patient-physician trust vs enabling a patient’s suspected misuse of prescription medication.

Box

Recommended postdisaster treatment now integrates 4 elements:

• providing for basic needs (food, shelter, clothing, and safety)
  
• psychological first aid
  
• needs assessment
  
• psychoeducation about normal responses to disasters.⁸
  

To make its decisions, the Astrodome clinic team considered the potential problems of prescribing benzodiazepines to patients such as Mr. R:

• Large numbers of traumatized victims might visit the clinic to request benzodiazepines, addictive drugs that for many would be inappropriate and potentially harmful.
  
• Resources such as medications, information, and time were limited. The team could not contact each patient’s health care provider or pharmacy to verify prescription records.
  
• Using benzodiazepines to manage anxiety in the acute aftermath of a traumatic event is not supported by the literature.¹⁰
  

In general, patients were not given benzodiazepines for acute anxiety or acute stress disorder. Evacuees who presented to the clinic were educated about normal responses to trauma, received supportive care, and were referred to on-site social service agencies for help finding housing and lost family members.

CASE 2: Urgent care for chronic illness?

Ms. J, age 46, presented to the mental health clinic for evaluation and treatment of chronic depression and anxiety. When asked how she was coping with the storm, she replied, “I wasn’t in the storm. I live in Houston, and I’ve been waiting 6 months to see doctors at the public hospital. I decided to come here and see everyone I needed to see.”

Because of news coverage, Houston residents were well-informed about the hurricane and the Astrodome clinics. Ms. J was resourceful in seeking needed treatment.

The Astrodome clinics were intended to provide acute care to evacuees who lacked alternate resources. Ms. J had chronic mental health problems, but her symptoms could have been exacerbated by graphic media reports of the storm’s devastation.

A challenge in treating chronic health problems in an acute setting is the inability to provide follow-up and continuity of care. An “emergency” clinic is meant to serve as a bridge to later care providers.

Four principles guide ethical decision-making: respect for autonomy, beneficence, nonmaleficence, and justice (Table 1). Would it be an injustice to allocate scarce resources—number of personnel, physician time, space, and medication—to a patient with chronic rather than acute needs?

One could argue that a patient-physician relationship and duty to treat began when Ms. J presented herself as a patient in need and began a dialogue with a physician. The treating physician felt Ms. J’s interest would be served best by continuing the evaluation and acutely managing her symptoms while trying to help her obtain treatment in a more stable setting.

The staff correctly anticipated that this case was unique; no other patients who were not evacuees are known to have requested treatment at the Astrodome clinic.

Table 1

Ethical principles that guide disaster psychiatry

CASE 3: Compassion vs confidentiality

Mrs. C, age 67, came to the mental health clinic in tears because she had been separated from her son when she boarded a bus to evacuate from New Orleans. Her son has schizophrenia, and she asked if we had seen him at our clinic. In fact, he had visited our clinic shortly before she arrived.

As healthcare professionals, we value compassion but also are bound by tenets of the physician-patient relationship—in this case, maintaining confidentiality. Physicians are ethically and legally obligated to refrain from disclosing information obtained from a patient without the patient’s permission.¹¹

“Health care providers can share patient information as necessary to provide treatment. Health care providers can share patient information as necessary to identify, locate, and notify family members, guardians, or anyone else responsible for the individual’s care of the individual’s location, general condition, or death.”¹²

Based on these arguments, the treatment team believed that working with Mrs. C and, if necessary, informing her of her son’s location outweighed the conflicting need to maintain his right to confidentiality.

Therapeutic resources

Catastrophes evoke powerful emotions that can blur responders’ therapeutic boundaries and interfere with how we care for individuals in need (Table 2).¹³ Some Web-based resources to help you prepare for disasters are available from:

• American Psychiatric Association. www.psych.org/disasterpsych.
  
• Centers for Disease Control and Prevention. www.bt.cdc.gov/mentalhealth.
  
• Duke University. http://psychiatry.mc.duke.edu/clinical/disastermentalhealth.html.
  

Emotional dynamics that motivate disaster response

Bioethics of clinical practice change during disasters, as our staff learned when providing emergency care to Hurricane Katrina evacuees. During crises such as severe weather, terrorist acts, and epidemics, physicians can be torn between advocating for individual patients’ needs or the public good.¹

As the storm’s 2-year anniversary approaches (Box),^2,3 we share our experiences to help you prepare for disasters in your community and to contribute to the limited data on ethics in disaster psychiatry. This article describes 3 cases to show how mental health clinicians balanced issues such as conflict, consequences, patient rights, physician virtues, and justice when making treatment decisions in the Houston Astrodome clinic.

CASE 1: Benzodiazepines for anxiety?

Mr. R, age 23, presented to the Astrodome mental health clinic requesting “Xanax for my nerves.” He said he had been taking 6 mg/d “for years and years, and it’s the only thing that helps.” Mr. R claimed he had been without his medicines at least 48 hours.

The assessing psychiatrist found no evidence of benzodiazepine withdrawal or other psychiatric emergency. The dilemma: How to provide appropriate acute treatment of a chronic problem, without continuity of care and follow-up.

As a hurricane survivor, Mr. R experienced a traumatic event that could have exacerbated an underlying anxiety disorder. But patients’ use of and physicians’ prescription of benzodiazepines can have adverse short- and long-term consequences. Mr. R’s case highlights the conflict between establishing patient-physician trust vs enabling a patient’s suspected misuse of prescription medication.

Box

Recommended postdisaster treatment now integrates 4 elements:

• providing for basic needs (food, shelter, clothing, and safety)
  
• psychological first aid
  
• needs assessment
  
• psychoeducation about normal responses to disasters.⁸
  

To make its decisions, the Astrodome clinic team considered the potential problems of prescribing benzodiazepines to patients such as Mr. R:

• Large numbers of traumatized victims might visit the clinic to request benzodiazepines, addictive drugs that for many would be inappropriate and potentially harmful.
  
• Resources such as medications, information, and time were limited. The team could not contact each patient’s health care provider or pharmacy to verify prescription records.
  
• Using benzodiazepines to manage anxiety in the acute aftermath of a traumatic event is not supported by the literature.¹⁰
  

In general, patients were not given benzodiazepines for acute anxiety or acute stress disorder. Evacuees who presented to the clinic were educated about normal responses to trauma, received supportive care, and were referred to on-site social service agencies for help finding housing and lost family members.

CASE 2: Urgent care for chronic illness?

Ms. J, age 46, presented to the mental health clinic for evaluation and treatment of chronic depression and anxiety. When asked how she was coping with the storm, she replied, “I wasn’t in the storm. I live in Houston, and I’ve been waiting 6 months to see doctors at the public hospital. I decided to come here and see everyone I needed to see.”

Because of news coverage, Houston residents were well-informed about the hurricane and the Astrodome clinics. Ms. J was resourceful in seeking needed treatment.

The Astrodome clinics were intended to provide acute care to evacuees who lacked alternate resources. Ms. J had chronic mental health problems, but her symptoms could have been exacerbated by graphic media reports of the storm’s devastation.

A challenge in treating chronic health problems in an acute setting is the inability to provide follow-up and continuity of care. An “emergency” clinic is meant to serve as a bridge to later care providers.

Four principles guide ethical decision-making: respect for autonomy, beneficence, nonmaleficence, and justice (Table 1). Would it be an injustice to allocate scarce resources—number of personnel, physician time, space, and medication—to a patient with chronic rather than acute needs?

One could argue that a patient-physician relationship and duty to treat began when Ms. J presented herself as a patient in need and began a dialogue with a physician. The treating physician felt Ms. J’s interest would be served best by continuing the evaluation and acutely managing her symptoms while trying to help her obtain treatment in a more stable setting.

The staff correctly anticipated that this case was unique; no other patients who were not evacuees are known to have requested treatment at the Astrodome clinic.

Table 1

Ethical principles that guide disaster psychiatry

CASE 3: Compassion vs confidentiality

Mrs. C, age 67, came to the mental health clinic in tears because she had been separated from her son when she boarded a bus to evacuate from New Orleans. Her son has schizophrenia, and she asked if we had seen him at our clinic. In fact, he had visited our clinic shortly before she arrived.

As healthcare professionals, we value compassion but also are bound by tenets of the physician-patient relationship—in this case, maintaining confidentiality. Physicians are ethically and legally obligated to refrain from disclosing information obtained from a patient without the patient’s permission.¹¹

“Health care providers can share patient information as necessary to provide treatment. Health care providers can share patient information as necessary to identify, locate, and notify family members, guardians, or anyone else responsible for the individual’s care of the individual’s location, general condition, or death.”¹²

Based on these arguments, the treatment team believed that working with Mrs. C and, if necessary, informing her of her son’s location outweighed the conflicting need to maintain his right to confidentiality.

Therapeutic resources

Catastrophes evoke powerful emotions that can blur responders’ therapeutic boundaries and interfere with how we care for individuals in need (Table 2).¹³ Some Web-based resources to help you prepare for disasters are available from:

• American Psychiatric Association. www.psych.org/disasterpsych.
  
• Centers for Disease Control and Prevention. www.bt.cdc.gov/mentalhealth.
  
• Duke University. http://psychiatry.mc.duke.edu/clinical/disastermentalhealth.html.
  

Emotional dynamics that motivate disaster response

Bioethics of clinical practice change during disasters, as our staff learned when providing emergency care to Hurricane Katrina evacuees. During crises such as severe weather, terrorist acts, and epidemics, physicians can be torn between advocating for individual patients’ needs or the public good.¹

As the storm’s 2-year anniversary approaches (Box),^2,3 we share our experiences to help you prepare for disasters in your community and to contribute to the limited data on ethics in disaster psychiatry. This article describes 3 cases to show how mental health clinicians balanced issues such as conflict, consequences, patient rights, physician virtues, and justice when making treatment decisions in the Houston Astrodome clinic.

CASE 1: Benzodiazepines for anxiety?

Mr. R, age 23, presented to the Astrodome mental health clinic requesting “Xanax for my nerves.” He said he had been taking 6 mg/d “for years and years, and it’s the only thing that helps.” Mr. R claimed he had been without his medicines at least 48 hours.

The assessing psychiatrist found no evidence of benzodiazepine withdrawal or other psychiatric emergency. The dilemma: How to provide appropriate acute treatment of a chronic problem, without continuity of care and follow-up.

As a hurricane survivor, Mr. R experienced a traumatic event that could have exacerbated an underlying anxiety disorder. But patients’ use of and physicians’ prescription of benzodiazepines can have adverse short- and long-term consequences. Mr. R’s case highlights the conflict between establishing patient-physician trust vs enabling a patient’s suspected misuse of prescription medication.

Box

Recommended postdisaster treatment now integrates 4 elements:

• providing for basic needs (food, shelter, clothing, and safety)
  
• psychological first aid
  
• needs assessment
  
• psychoeducation about normal responses to disasters.⁸
  

To make its decisions, the Astrodome clinic team considered the potential problems of prescribing benzodiazepines to patients such as Mr. R:

• Large numbers of traumatized victims might visit the clinic to request benzodiazepines, addictive drugs that for many would be inappropriate and potentially harmful.
  
• Resources such as medications, information, and time were limited. The team could not contact each patient’s health care provider or pharmacy to verify prescription records.
  
• Using benzodiazepines to manage anxiety in the acute aftermath of a traumatic event is not supported by the literature.¹⁰
  

In general, patients were not given benzodiazepines for acute anxiety or acute stress disorder. Evacuees who presented to the clinic were educated about normal responses to trauma, received supportive care, and were referred to on-site social service agencies for help finding housing and lost family members.

CASE 2: Urgent care for chronic illness?

Ms. J, age 46, presented to the mental health clinic for evaluation and treatment of chronic depression and anxiety. When asked how she was coping with the storm, she replied, “I wasn’t in the storm. I live in Houston, and I’ve been waiting 6 months to see doctors at the public hospital. I decided to come here and see everyone I needed to see.”

Because of news coverage, Houston residents were well-informed about the hurricane and the Astrodome clinics. Ms. J was resourceful in seeking needed treatment.

The Astrodome clinics were intended to provide acute care to evacuees who lacked alternate resources. Ms. J had chronic mental health problems, but her symptoms could have been exacerbated by graphic media reports of the storm’s devastation.

A challenge in treating chronic health problems in an acute setting is the inability to provide follow-up and continuity of care. An “emergency” clinic is meant to serve as a bridge to later care providers.

Four principles guide ethical decision-making: respect for autonomy, beneficence, nonmaleficence, and justice (Table 1). Would it be an injustice to allocate scarce resources—number of personnel, physician time, space, and medication—to a patient with chronic rather than acute needs?

One could argue that a patient-physician relationship and duty to treat began when Ms. J presented herself as a patient in need and began a dialogue with a physician. The treating physician felt Ms. J’s interest would be served best by continuing the evaluation and acutely managing her symptoms while trying to help her obtain treatment in a more stable setting.

The staff correctly anticipated that this case was unique; no other patients who were not evacuees are known to have requested treatment at the Astrodome clinic.

Table 1

Ethical principles that guide disaster psychiatry

CASE 3: Compassion vs confidentiality

Mrs. C, age 67, came to the mental health clinic in tears because she had been separated from her son when she boarded a bus to evacuate from New Orleans. Her son has schizophrenia, and she asked if we had seen him at our clinic. In fact, he had visited our clinic shortly before she arrived.

As healthcare professionals, we value compassion but also are bound by tenets of the physician-patient relationship—in this case, maintaining confidentiality. Physicians are ethically and legally obligated to refrain from disclosing information obtained from a patient without the patient’s permission.¹¹

“Health care providers can share patient information as necessary to provide treatment. Health care providers can share patient information as necessary to identify, locate, and notify family members, guardians, or anyone else responsible for the individual’s care of the individual’s location, general condition, or death.”¹²

Based on these arguments, the treatment team believed that working with Mrs. C and, if necessary, informing her of her son’s location outweighed the conflicting need to maintain his right to confidentiality.

Therapeutic resources

Catastrophes evoke powerful emotions that can blur responders’ therapeutic boundaries and interfere with how we care for individuals in need (Table 2).¹³ Some Web-based resources to help you prepare for disasters are available from:

• American Psychiatric Association. www.psych.org/disasterpsych.
  
• Centers for Disease Control and Prevention. www.bt.cdc.gov/mentalhealth.
  
• Duke University. http://psychiatry.mc.duke.edu/clinical/disastermentalhealth.html.
  

Emotional dynamics that motivate disaster response

Supportive psychotherapy began as a second-class treatment whose only operating principle was “being friendly” with the patient (Box).¹ Critics called it “simple-minded”² and sniffed, “if it is supportive, it is not therapy…if it is therapy, it is not supportive.”³

Since its lowly beginning, however, supportive psychotherapy has been proven highly effective, and clinicians have developed operating principles that distinguish it from expressive psychotherapy (Table 1).⁴

To help you make good use of supportive psychotherapy, this article describes its evolution and:

• evidence that demonstrates its effectiveness
  
• 5 key components for clinical practice
  
• how to use it when treating challenging patients.
  

Table 1

Differences between expressive and supportive psychotherapy

A proven treatment

Effective long-term therapy. Much research on supportive psychotherapy comes from studies in which supportive psychotherapy was included as a “treatment as usual” comparison. In an extensive longitudinal study, for example, the Meninger Psychotherapy Research Project examined 42 patients receiving psychoanalysis, psychodynamic psychotherapy, or supportive psychotherapy over 25 years.⁵

Despite the institutional expertise in psychoanalysis and expressive psychotherapy, patients in supportive psychotherapy did just as well as those receiving the other treatments. Researchers found that each therapy carried more supportive elements than was intended, and supportive elements accounted for many of the observed changes. They concluded that:

• thinking of change in terms of “structural” vs “behavioral” was not useful
  
• change did not occur in proportion to resolving unconscious conflict.
  

Therapists in the behavior therapy group used a manualized, highly structured treatment protocol that included in vivo desensitization and homework. Therapists who used supportive psychotherapy simply encouraged patients to ventilate their feelings and discuss problems. Supportive therapists were instructed to be nondirective and avoid confrontation unless the patient proposed it.

Improving personality disorders. Several studies examined a form of supportive psychotherapy that used a manualized, structured protocol for treating higher functioning patients who traditionally have been treated with expressive psychotherapy. The protocol used a conversation-based, dyadic style to improve self-esteem and adaptive skills through data-based praise, advice, education, appropriate reassurance, anticipatory guidance, clarification, and confrontation. Under these reproducible conditions, supportive psychotherapy showed good efficacy compared with dynamic therapies for patients with depressive, anxiety, and personality disorders.

A review of studies from 1986 to 1992 found that supportive psychotherapy was effective for a variety of psychiatric and medical conditions, including schizophrenia, bipolar disorder, depression, posttraumatic stress disorder, anxiety disorders, personality disorders, substance abuse, and stress associated with breast cancer and back pain.⁹

CASE STUDY: A negative experience

Mrs. S, a 32-year-old grant writer, is referred to a psychiatrist by an emergency department physician after she cut herself following an argument with her husband. She has chronic dysthymia, thoughts of harming herself, low self-esteem, and indecision about her marriage.

Mrs. S was not receiving mental health treatment because her first experience with a psychiatrist had a poor outcome: “He hardly ever said anything; in fact, sometimes I wondered if he was sleeping. I needed advice desperately, and I was hoping to get some help and direction for my life. Instead he answered every question with a question, and I ended up getting more confused. I felt guilty, like I wasn’t being a good patient because I couldn’t think for myself. I felt like he thought I was stupid. He gave me some antidepressants, but after a few months of feeling even worse I stopped going and vowed to never see a therapist again.”

5 key components

Although all psychotherapies have some elements of support, effective supportive psychotherapy has 5 key components (Table 2).

• asking directive questions
  
• allowing inflection in your voice
  
• making gestures
  
• discussing opinions.
  

Table 2

5 components of supportive psychotherapy

CASE CONTINUED: Learning to cope

Mrs. S’ new psychiatrist starts her on an antidepressant and once-weekly supportive psychotherapy. For the initial sessions, the psychiatrist helps Mrs. S explore options for her highly conflicted marriage and strategies for coping with panic symptoms.

Mrs. S develops a strong feeling of attachment to the psychiatrist, sometimes projecting anger onto him by declaring that he does not care enough. Instead of interpreting this transference, the psychiatrist uses it as an opportunity to explore coping options Mrs. S can try when she feels unloved or rejected.

Nurture positive transference. A positive relationship is essential for the therapeutic alliance. In most instances, a patient naturally develops good feelings toward the therapist over time as a result of repeated empathic interchange. In supportive psychotherapy, you may acknowledge these good feelings but do not interpret them for unconscious underpinnings.

Address transference only if it is negative. If the patient develops hostility or anger toward you, use techniques to improve the relationship, such as:

• acknowledging the validity of the patient’s angry feelings
  
• gaining an understanding of your role in the conflict and apologizing if sincere
  
• offering solutions to improve the conflict
  
• providing reassurance that working through the conflict will strengthen the therapeutic relationship.
  

Reduce anxiety. In supportive psychotherapy, the primary goal is to lessen the patient’s suffering. Although the patient often must talk about stressful or painful topics, you can help him or her do so in a tolerable manner. Focus on making it easier for the patient to talk.

Reducing anxiety means not only helping the patient talk about painful matters but also allowing him or her to avoid topics that are too uncomfortable to endure. You can always “earmark” areas of concern for later discussion. This modulation of anxiety is consistent with the object relations approach proposed by Kohut,¹⁰ in which emotional pain is addressed in “small, psychologically manageable portions.”

Enhance self-esteem. Virtually all patients in supportive psychotherapy suffer from low self-esteem, so it is beneficial to help them feel better about themselves. Take an active role by using positive comments and acknowledgements (“plussing”) as well as compliments when appropriate.

Most patients with low self-esteem have defects in the ability to nurture or forgive themselves (“self-soothe”). Work with patients to enhance this ability by:

• plussing where appropriate
  
• correcting negative self-distortions or self-reproach
  
• educating patients on how to both placate and reward themselves.
  

Strengthen coping mechanisms. In supportive psychotherapy the therapist acts as a coach, giving the patient suggestions on how to cope with difficult matters. As part of treatment, you might assign the patient homework and instruct him to practice specific coping strategies.

CASE CONTINUED: Feeling stronger

Eventually Mrs. S is able to talk in a limited fashion about childhood sexual abuse. With her psychiatrist’s encouragement, she begins to write about her feelings in a journal and exercising to help her “feel strong.” The psychiatrist often acknowledges her struggle and compliments her attempts at coping in healthy ways. After a year of supportive psychotherapy Mrs. S is better able to modulate her feelings and make decisions without feeling overwhelmed.

An option for challenging patients

Psychotic disorders. Although it may seem intuitive that psychotic conditions are a contraindication for psychotherapy, patients with schizophrenia and other psychotic disorders often benefit immensely from supportive psychotherapy. A supportive therapist’s guiding influence can help psychotic patients cope with fractured social and family life, struggles with independence, loneliness, frequent disturbances of reality, stigmatization from society, and difficulty with decision-making.

During a patient’s acute psychotic episodes, you can draw on the therapeutic relationship you have established, strongly advising the patient to accept treatment when he or she is paranoid and rejecting help. In such situations, you might say, “Joe, you know me. You know that in the past I have helped you get through some tough times. You are going to have to trust me that you need this medicine now, even if you don’t want to take it.”

Borderline personality disorder. Supportive psychotherapy’s emphasis on reducing anxiety and nurturing a therapeutic relationship makes it a good treatment for patients with borderline personality disorder. The focus on adaptive skills, self-esteem, and higher order defenses—such as repression, sublimation, rationalization, intellectualization, inhibition, displacement, and humor—is particularly suitable for self-injurious and suicidal patients.¹¹

In addition, dialectical behavior therapy is congruent with supportive psychotherapy.¹² I have found it useful to let patients know I am experienced and strong enough to undergo therapy with them and can live with the chaos of their lives. This often comforts patients with borderline personality disorder, as their internal state conveys a sense of destruction not only for them but anyone close to them. From a psychoanalytic perspective, conveying a sense of safety is a core healing component of supportive therapy.¹³

Substance abuse. A lack of treatment response and therapist burn-out are recurrent problems when treating patients with substance abuse.¹⁴ I have found it useful to “stretch” my treatment timeline—for example, by measuring change in years instead of months—so that I don’t continually feel unsuccessful. This allows me to focus not on the patient’s immediate sobriety but instead on the supportive relationship, especially on helping the patient address his or her sense of guilt and failure, which frequently underpins substance abuse.

Helping your patient to reframe his or her substance abuse as “bad choices” instead of the actions of a “bad person” is essential. Accompanying the patient to an Alcoholics Anonymous meeting—“I’ll go with you to the first one, after that it is up to you”—can be a powerful intervention with lasting benefits.

Related resources

• Werman DS. The practice of supportive psychotherapy. New York: Brunner/Mazel; 1984.
  
• Winston A, Rosenthal RN, Pinsker H. Introduction to supportive psychotherapy. Arlington, VA: American Psychiatric Publishing, Inc; 2004.
  
• Pinsker H. A primer of supportive psychotherapy. Hillsdale, NJ. The Analytic Press; 1997.
  

• Imipramine • Tofranil
  

Dr. Battaglia is a consultant to Eli Lilly and Company.

Supportive psychotherapy began as a second-class treatment whose only operating principle was “being friendly” with the patient (Box).¹ Critics called it “simple-minded”² and sniffed, “if it is supportive, it is not therapy…if it is therapy, it is not supportive.”³

Since its lowly beginning, however, supportive psychotherapy has been proven highly effective, and clinicians have developed operating principles that distinguish it from expressive psychotherapy (Table 1).⁴

To help you make good use of supportive psychotherapy, this article describes its evolution and:

• evidence that demonstrates its effectiveness
  
• 5 key components for clinical practice
  
• how to use it when treating challenging patients.
  

Table 1

Differences between expressive and supportive psychotherapy

A proven treatment

Effective long-term therapy. Much research on supportive psychotherapy comes from studies in which supportive psychotherapy was included as a “treatment as usual” comparison. In an extensive longitudinal study, for example, the Meninger Psychotherapy Research Project examined 42 patients receiving psychoanalysis, psychodynamic psychotherapy, or supportive psychotherapy over 25 years.⁵

Despite the institutional expertise in psychoanalysis and expressive psychotherapy, patients in supportive psychotherapy did just as well as those receiving the other treatments. Researchers found that each therapy carried more supportive elements than was intended, and supportive elements accounted for many of the observed changes. They concluded that:

• thinking of change in terms of “structural” vs “behavioral” was not useful
  
• change did not occur in proportion to resolving unconscious conflict.
  

Therapists in the behavior therapy group used a manualized, highly structured treatment protocol that included in vivo desensitization and homework. Therapists who used supportive psychotherapy simply encouraged patients to ventilate their feelings and discuss problems. Supportive therapists were instructed to be nondirective and avoid confrontation unless the patient proposed it.

Improving personality disorders. Several studies examined a form of supportive psychotherapy that used a manualized, structured protocol for treating higher functioning patients who traditionally have been treated with expressive psychotherapy. The protocol used a conversation-based, dyadic style to improve self-esteem and adaptive skills through data-based praise, advice, education, appropriate reassurance, anticipatory guidance, clarification, and confrontation. Under these reproducible conditions, supportive psychotherapy showed good efficacy compared with dynamic therapies for patients with depressive, anxiety, and personality disorders.

A review of studies from 1986 to 1992 found that supportive psychotherapy was effective for a variety of psychiatric and medical conditions, including schizophrenia, bipolar disorder, depression, posttraumatic stress disorder, anxiety disorders, personality disorders, substance abuse, and stress associated with breast cancer and back pain.⁹

CASE STUDY: A negative experience

Mrs. S, a 32-year-old grant writer, is referred to a psychiatrist by an emergency department physician after she cut herself following an argument with her husband. She has chronic dysthymia, thoughts of harming herself, low self-esteem, and indecision about her marriage.

Mrs. S was not receiving mental health treatment because her first experience with a psychiatrist had a poor outcome: “He hardly ever said anything; in fact, sometimes I wondered if he was sleeping. I needed advice desperately, and I was hoping to get some help and direction for my life. Instead he answered every question with a question, and I ended up getting more confused. I felt guilty, like I wasn’t being a good patient because I couldn’t think for myself. I felt like he thought I was stupid. He gave me some antidepressants, but after a few months of feeling even worse I stopped going and vowed to never see a therapist again.”

5 key components

Although all psychotherapies have some elements of support, effective supportive psychotherapy has 5 key components (Table 2).

• asking directive questions
  
• allowing inflection in your voice
  
• making gestures
  
• discussing opinions.
  

Table 2

5 components of supportive psychotherapy

CASE CONTINUED: Learning to cope

Mrs. S’ new psychiatrist starts her on an antidepressant and once-weekly supportive psychotherapy. For the initial sessions, the psychiatrist helps Mrs. S explore options for her highly conflicted marriage and strategies for coping with panic symptoms.

Mrs. S develops a strong feeling of attachment to the psychiatrist, sometimes projecting anger onto him by declaring that he does not care enough. Instead of interpreting this transference, the psychiatrist uses it as an opportunity to explore coping options Mrs. S can try when she feels unloved or rejected.

Nurture positive transference. A positive relationship is essential for the therapeutic alliance. In most instances, a patient naturally develops good feelings toward the therapist over time as a result of repeated empathic interchange. In supportive psychotherapy, you may acknowledge these good feelings but do not interpret them for unconscious underpinnings.

Address transference only if it is negative. If the patient develops hostility or anger toward you, use techniques to improve the relationship, such as:

• acknowledging the validity of the patient’s angry feelings
  
• gaining an understanding of your role in the conflict and apologizing if sincere
  
• offering solutions to improve the conflict
  
• providing reassurance that working through the conflict will strengthen the therapeutic relationship.
  

Reduce anxiety. In supportive psychotherapy, the primary goal is to lessen the patient’s suffering. Although the patient often must talk about stressful or painful topics, you can help him or her do so in a tolerable manner. Focus on making it easier for the patient to talk.

Reducing anxiety means not only helping the patient talk about painful matters but also allowing him or her to avoid topics that are too uncomfortable to endure. You can always “earmark” areas of concern for later discussion. This modulation of anxiety is consistent with the object relations approach proposed by Kohut,¹⁰ in which emotional pain is addressed in “small, psychologically manageable portions.”

Enhance self-esteem. Virtually all patients in supportive psychotherapy suffer from low self-esteem, so it is beneficial to help them feel better about themselves. Take an active role by using positive comments and acknowledgements (“plussing”) as well as compliments when appropriate.

Most patients with low self-esteem have defects in the ability to nurture or forgive themselves (“self-soothe”). Work with patients to enhance this ability by:

• plussing where appropriate
  
• correcting negative self-distortions or self-reproach
  
• educating patients on how to both placate and reward themselves.
  

Strengthen coping mechanisms. In supportive psychotherapy the therapist acts as a coach, giving the patient suggestions on how to cope with difficult matters. As part of treatment, you might assign the patient homework and instruct him to practice specific coping strategies.

CASE CONTINUED: Feeling stronger

Eventually Mrs. S is able to talk in a limited fashion about childhood sexual abuse. With her psychiatrist’s encouragement, she begins to write about her feelings in a journal and exercising to help her “feel strong.” The psychiatrist often acknowledges her struggle and compliments her attempts at coping in healthy ways. After a year of supportive psychotherapy Mrs. S is better able to modulate her feelings and make decisions without feeling overwhelmed.

An option for challenging patients

Psychotic disorders. Although it may seem intuitive that psychotic conditions are a contraindication for psychotherapy, patients with schizophrenia and other psychotic disorders often benefit immensely from supportive psychotherapy. A supportive therapist’s guiding influence can help psychotic patients cope with fractured social and family life, struggles with independence, loneliness, frequent disturbances of reality, stigmatization from society, and difficulty with decision-making.

During a patient’s acute psychotic episodes, you can draw on the therapeutic relationship you have established, strongly advising the patient to accept treatment when he or she is paranoid and rejecting help. In such situations, you might say, “Joe, you know me. You know that in the past I have helped you get through some tough times. You are going to have to trust me that you need this medicine now, even if you don’t want to take it.”

Borderline personality disorder. Supportive psychotherapy’s emphasis on reducing anxiety and nurturing a therapeutic relationship makes it a good treatment for patients with borderline personality disorder. The focus on adaptive skills, self-esteem, and higher order defenses—such as repression, sublimation, rationalization, intellectualization, inhibition, displacement, and humor—is particularly suitable for self-injurious and suicidal patients.¹¹

In addition, dialectical behavior therapy is congruent with supportive psychotherapy.¹² I have found it useful to let patients know I am experienced and strong enough to undergo therapy with them and can live with the chaos of their lives. This often comforts patients with borderline personality disorder, as their internal state conveys a sense of destruction not only for them but anyone close to them. From a psychoanalytic perspective, conveying a sense of safety is a core healing component of supportive therapy.¹³

Substance abuse. A lack of treatment response and therapist burn-out are recurrent problems when treating patients with substance abuse.¹⁴ I have found it useful to “stretch” my treatment timeline—for example, by measuring change in years instead of months—so that I don’t continually feel unsuccessful. This allows me to focus not on the patient’s immediate sobriety but instead on the supportive relationship, especially on helping the patient address his or her sense of guilt and failure, which frequently underpins substance abuse.

Helping your patient to reframe his or her substance abuse as “bad choices” instead of the actions of a “bad person” is essential. Accompanying the patient to an Alcoholics Anonymous meeting—“I’ll go with you to the first one, after that it is up to you”—can be a powerful intervention with lasting benefits.

Related resources

• Werman DS. The practice of supportive psychotherapy. New York: Brunner/Mazel; 1984.
  
• Winston A, Rosenthal RN, Pinsker H. Introduction to supportive psychotherapy. Arlington, VA: American Psychiatric Publishing, Inc; 2004.
  
• Pinsker H. A primer of supportive psychotherapy. Hillsdale, NJ. The Analytic Press; 1997.
  

• Imipramine • Tofranil
  

Dr. Battaglia is a consultant to Eli Lilly and Company.

Supportive psychotherapy began as a second-class treatment whose only operating principle was “being friendly” with the patient (Box).¹ Critics called it “simple-minded”² and sniffed, “if it is supportive, it is not therapy…if it is therapy, it is not supportive.”³

Since its lowly beginning, however, supportive psychotherapy has been proven highly effective, and clinicians have developed operating principles that distinguish it from expressive psychotherapy (Table 1).⁴

To help you make good use of supportive psychotherapy, this article describes its evolution and:

• evidence that demonstrates its effectiveness
  
• 5 key components for clinical practice
  
• how to use it when treating challenging patients.
  

Table 1

Differences between expressive and supportive psychotherapy

A proven treatment

Effective long-term therapy. Much research on supportive psychotherapy comes from studies in which supportive psychotherapy was included as a “treatment as usual” comparison. In an extensive longitudinal study, for example, the Meninger Psychotherapy Research Project examined 42 patients receiving psychoanalysis, psychodynamic psychotherapy, or supportive psychotherapy over 25 years.⁵

Despite the institutional expertise in psychoanalysis and expressive psychotherapy, patients in supportive psychotherapy did just as well as those receiving the other treatments. Researchers found that each therapy carried more supportive elements than was intended, and supportive elements accounted for many of the observed changes. They concluded that:

• thinking of change in terms of “structural” vs “behavioral” was not useful
  
• change did not occur in proportion to resolving unconscious conflict.
  

Therapists in the behavior therapy group used a manualized, highly structured treatment protocol that included in vivo desensitization and homework. Therapists who used supportive psychotherapy simply encouraged patients to ventilate their feelings and discuss problems. Supportive therapists were instructed to be nondirective and avoid confrontation unless the patient proposed it.

Improving personality disorders. Several studies examined a form of supportive psychotherapy that used a manualized, structured protocol for treating higher functioning patients who traditionally have been treated with expressive psychotherapy. The protocol used a conversation-based, dyadic style to improve self-esteem and adaptive skills through data-based praise, advice, education, appropriate reassurance, anticipatory guidance, clarification, and confrontation. Under these reproducible conditions, supportive psychotherapy showed good efficacy compared with dynamic therapies for patients with depressive, anxiety, and personality disorders.

A review of studies from 1986 to 1992 found that supportive psychotherapy was effective for a variety of psychiatric and medical conditions, including schizophrenia, bipolar disorder, depression, posttraumatic stress disorder, anxiety disorders, personality disorders, substance abuse, and stress associated with breast cancer and back pain.⁹

CASE STUDY: A negative experience

Mrs. S, a 32-year-old grant writer, is referred to a psychiatrist by an emergency department physician after she cut herself following an argument with her husband. She has chronic dysthymia, thoughts of harming herself, low self-esteem, and indecision about her marriage.

Mrs. S was not receiving mental health treatment because her first experience with a psychiatrist had a poor outcome: “He hardly ever said anything; in fact, sometimes I wondered if he was sleeping. I needed advice desperately, and I was hoping to get some help and direction for my life. Instead he answered every question with a question, and I ended up getting more confused. I felt guilty, like I wasn’t being a good patient because I couldn’t think for myself. I felt like he thought I was stupid. He gave me some antidepressants, but after a few months of feeling even worse I stopped going and vowed to never see a therapist again.”

5 key components

Although all psychotherapies have some elements of support, effective supportive psychotherapy has 5 key components (Table 2).

• asking directive questions
  
• allowing inflection in your voice
  
• making gestures
  
• discussing opinions.
  

Table 2

5 components of supportive psychotherapy

CASE CONTINUED: Learning to cope

Mrs. S’ new psychiatrist starts her on an antidepressant and once-weekly supportive psychotherapy. For the initial sessions, the psychiatrist helps Mrs. S explore options for her highly conflicted marriage and strategies for coping with panic symptoms.

Mrs. S develops a strong feeling of attachment to the psychiatrist, sometimes projecting anger onto him by declaring that he does not care enough. Instead of interpreting this transference, the psychiatrist uses it as an opportunity to explore coping options Mrs. S can try when she feels unloved or rejected.

Nurture positive transference. A positive relationship is essential for the therapeutic alliance. In most instances, a patient naturally develops good feelings toward the therapist over time as a result of repeated empathic interchange. In supportive psychotherapy, you may acknowledge these good feelings but do not interpret them for unconscious underpinnings.

Address transference only if it is negative. If the patient develops hostility or anger toward you, use techniques to improve the relationship, such as:

• acknowledging the validity of the patient’s angry feelings
  
• gaining an understanding of your role in the conflict and apologizing if sincere
  
• offering solutions to improve the conflict
  
• providing reassurance that working through the conflict will strengthen the therapeutic relationship.
  

Reduce anxiety. In supportive psychotherapy, the primary goal is to lessen the patient’s suffering. Although the patient often must talk about stressful or painful topics, you can help him or her do so in a tolerable manner. Focus on making it easier for the patient to talk.

Reducing anxiety means not only helping the patient talk about painful matters but also allowing him or her to avoid topics that are too uncomfortable to endure. You can always “earmark” areas of concern for later discussion. This modulation of anxiety is consistent with the object relations approach proposed by Kohut,¹⁰ in which emotional pain is addressed in “small, psychologically manageable portions.”

Enhance self-esteem. Virtually all patients in supportive psychotherapy suffer from low self-esteem, so it is beneficial to help them feel better about themselves. Take an active role by using positive comments and acknowledgements (“plussing”) as well as compliments when appropriate.

Most patients with low self-esteem have defects in the ability to nurture or forgive themselves (“self-soothe”). Work with patients to enhance this ability by:

• plussing where appropriate
  
• correcting negative self-distortions or self-reproach
  
• educating patients on how to both placate and reward themselves.
  

Strengthen coping mechanisms. In supportive psychotherapy the therapist acts as a coach, giving the patient suggestions on how to cope with difficult matters. As part of treatment, you might assign the patient homework and instruct him to practice specific coping strategies.

CASE CONTINUED: Feeling stronger

Eventually Mrs. S is able to talk in a limited fashion about childhood sexual abuse. With her psychiatrist’s encouragement, she begins to write about her feelings in a journal and exercising to help her “feel strong.” The psychiatrist often acknowledges her struggle and compliments her attempts at coping in healthy ways. After a year of supportive psychotherapy Mrs. S is better able to modulate her feelings and make decisions without feeling overwhelmed.

An option for challenging patients

Psychotic disorders. Although it may seem intuitive that psychotic conditions are a contraindication for psychotherapy, patients with schizophrenia and other psychotic disorders often benefit immensely from supportive psychotherapy. A supportive therapist’s guiding influence can help psychotic patients cope with fractured social and family life, struggles with independence, loneliness, frequent disturbances of reality, stigmatization from society, and difficulty with decision-making.

During a patient’s acute psychotic episodes, you can draw on the therapeutic relationship you have established, strongly advising the patient to accept treatment when he or she is paranoid and rejecting help. In such situations, you might say, “Joe, you know me. You know that in the past I have helped you get through some tough times. You are going to have to trust me that you need this medicine now, even if you don’t want to take it.”

Borderline personality disorder. Supportive psychotherapy’s emphasis on reducing anxiety and nurturing a therapeutic relationship makes it a good treatment for patients with borderline personality disorder. The focus on adaptive skills, self-esteem, and higher order defenses—such as repression, sublimation, rationalization, intellectualization, inhibition, displacement, and humor—is particularly suitable for self-injurious and suicidal patients.¹¹

In addition, dialectical behavior therapy is congruent with supportive psychotherapy.¹² I have found it useful to let patients know I am experienced and strong enough to undergo therapy with them and can live with the chaos of their lives. This often comforts patients with borderline personality disorder, as their internal state conveys a sense of destruction not only for them but anyone close to them. From a psychoanalytic perspective, conveying a sense of safety is a core healing component of supportive therapy.¹³

Substance abuse. A lack of treatment response and therapist burn-out are recurrent problems when treating patients with substance abuse.¹⁴ I have found it useful to “stretch” my treatment timeline—for example, by measuring change in years instead of months—so that I don’t continually feel unsuccessful. This allows me to focus not on the patient’s immediate sobriety but instead on the supportive relationship, especially on helping the patient address his or her sense of guilt and failure, which frequently underpins substance abuse.

Helping your patient to reframe his or her substance abuse as “bad choices” instead of the actions of a “bad person” is essential. Accompanying the patient to an Alcoholics Anonymous meeting—“I’ll go with you to the first one, after that it is up to you”—can be a powerful intervention with lasting benefits.

Related resources

• Werman DS. The practice of supportive psychotherapy. New York: Brunner/Mazel; 1984.
  
• Winston A, Rosenthal RN, Pinsker H. Introduction to supportive psychotherapy. Arlington, VA: American Psychiatric Publishing, Inc; 2004.
  
• Pinsker H. A primer of supportive psychotherapy. Hillsdale, NJ. The Analytic Press; 1997.
  

• Imipramine • Tofranil
  

Dr. Battaglia is a consultant to Eli Lilly and Company.

Patients voluntarily admitted to locked psychiatric intensive care units sometimes ask to leave against medical advice. They may minimize the severity of their acute illness or deny psychiatric symptoms to obtain a discharge.

Patient characteristics and provider procedures contribute to patients’ decisions to request a discharge against medical advice (DAMA) (Table).¹

Table

Risk factors for discharge against medical advice

Not for everyone. Acutely psychotic, delusional, delirious, or demented patients or those with suicidal and homicidal ideation are not candidates for DAMA. For others, approach the patient calmly, explain with empathy what DAMA entails, and support the reasons for admission. Emphasize that following the treatment plan will alleviate psychiatric symptoms sooner and may shorten their stay.

Know the involuntary commitment procedures for your jurisdiction, and be prepared to discuss them with the patient. Assess the patient’s decision-making capacity, including awareness of the severity of his or her psychiatric illness and potential consequences of leaving against medical advice.

Arrange follow-up care for DAMA patients:

• Provide the patient with a brief summary of diagnosis, medications, and follow-up plans.
  
• Arrange the next available office or telephone appointment.
  
• Obtain contact information of those responsible for the patient’s safety.
  
• Provide the patient with emergency room and other phone numbers for crisis intervention.
  

DAMA does not absolve the physician of responsibility for poor outcomes. Carefully document the DAMA process because these patients are at increased risk of harm.² Make sure the patient signs, dates, and notes the time on the DAMA request.

Patients voluntarily admitted to locked psychiatric intensive care units sometimes ask to leave against medical advice. They may minimize the severity of their acute illness or deny psychiatric symptoms to obtain a discharge.

Patient characteristics and provider procedures contribute to patients’ decisions to request a discharge against medical advice (DAMA) (Table).¹

Table

Risk factors for discharge against medical advice

Not for everyone. Acutely psychotic, delusional, delirious, or demented patients or those with suicidal and homicidal ideation are not candidates for DAMA. For others, approach the patient calmly, explain with empathy what DAMA entails, and support the reasons for admission. Emphasize that following the treatment plan will alleviate psychiatric symptoms sooner and may shorten their stay.

Know the involuntary commitment procedures for your jurisdiction, and be prepared to discuss them with the patient. Assess the patient’s decision-making capacity, including awareness of the severity of his or her psychiatric illness and potential consequences of leaving against medical advice.

Arrange follow-up care for DAMA patients:

• Provide the patient with a brief summary of diagnosis, medications, and follow-up plans.
  
• Arrange the next available office or telephone appointment.
  
• Obtain contact information of those responsible for the patient’s safety.
  
• Provide the patient with emergency room and other phone numbers for crisis intervention.
  

DAMA does not absolve the physician of responsibility for poor outcomes. Carefully document the DAMA process because these patients are at increased risk of harm.² Make sure the patient signs, dates, and notes the time on the DAMA request.

Patients voluntarily admitted to locked psychiatric intensive care units sometimes ask to leave against medical advice. They may minimize the severity of their acute illness or deny psychiatric symptoms to obtain a discharge.

Patient characteristics and provider procedures contribute to patients’ decisions to request a discharge against medical advice (DAMA) (Table).¹

Table

Risk factors for discharge against medical advice

Not for everyone. Acutely psychotic, delusional, delirious, or demented patients or those with suicidal and homicidal ideation are not candidates for DAMA. For others, approach the patient calmly, explain with empathy what DAMA entails, and support the reasons for admission. Emphasize that following the treatment plan will alleviate psychiatric symptoms sooner and may shorten their stay.

Know the involuntary commitment procedures for your jurisdiction, and be prepared to discuss them with the patient. Assess the patient’s decision-making capacity, including awareness of the severity of his or her psychiatric illness and potential consequences of leaving against medical advice.

Arrange follow-up care for DAMA patients:

• Provide the patient with a brief summary of diagnosis, medications, and follow-up plans.
  
• Arrange the next available office or telephone appointment.
  
• Obtain contact information of those responsible for the patient’s safety.
  
• Provide the patient with emergency room and other phone numbers for crisis intervention.
  

DAMA does not absolve the physician of responsibility for poor outcomes. Carefully document the DAMA process because these patients are at increased risk of harm.² Make sure the patient signs, dates, and notes the time on the DAMA request.

Advances in neuroimaging, cell biology, and post mortem analysis are starting to explain what happens in the brain of a person who develops schizophrenia. Schizophrenia appears to be a developmental disorder of disrupted neural connection within and between regions of the brain. These disruptions seem to result from genetic predispositions interacting with negative environmental events.

A matter of gray and white

Individuals with schizophrenia have deficits in gray matter and white matter, as illustrated by studies linking auditory hallucinations with brain regions associated with normal hearing (Box).

Gray matter. Magnetic resonance imaging (MRI) indicates that gray matter volume peaks in early adolescence and declines with age. The normal adolescent brain shrinks as inefficient neural connections are pruned away, a process that refines and matures gray matter. In individuals with schizophrenia, this reduction is more aggressive—perhaps because of excessive pruning—and occurs in the time frame when schizophrenia symptoms typically emerge.

Rapoport et al¹ documented this process through sequential MRI scans in children with early-onset schizophrenia (mean age 14.5). Compared with age-matched healthy controls, youths with schizophrenia show greater and more rapid gray matter loss during late adolescence (Figure 1).²

Increased density. Reduced neuronal branching and spine formation also likely causes subtle reductions in gray matter volume (Figure 2). The resulting lack of dendritic connectivity may produce cognitive impairments and negative symptoms seen in schizophrenia.

Postmortem studies of gray matter cells show increased neuron density in patients with schizophrenia when compared with controls.³ Patients with schizophrenia have the same number of neurons as controls, but the neurons are more tightly packed because of reduced cell size, branching, and synapse formation.⁴

Research over the past decade has revealed schizophrenia to be a neurodegenerative disorder characterized by substantial brain tissue loss during first and subsequent psychotic episodes.⁵ Neuroimaging studies show that clinical and functional deterioration accompanies progressive loss of cortical gray matter volume and enlargement of cerebral ventricles. Thus, preventing relapses has come to be regarded as critical to long-term schizophrenia management.

Box

Do auditory hallucinations follow sound pathways in the brain?

Auditory hallucinations appear to emanate from the temporal lobe, the same brain region that processes external sound. Thus, it may be that patients experiencing hallucinations are misidentifying inner speech as coming from an outside source.

Using functional MRI to differentiate brain activity signals associated with hallucinating and nonhallucinating states, Dierks et al²¹ documented increased activity in auditory cortical gray matter during hallucinations in schizophrenia patients.

Auditory signals make synaptic connections in the thalamus (left) before reaching the auditory cortex. White matter fiber tracts called the arcuate fasciculus (right) connect the auditory cortex in the temporal lobe with Broca’s area in the frontal cortex.

Source: Adapted from reference 2

Using MR diffusion tensor imaging, Hubl et al²² identified white matter changes in the arcuate fasciculus of schizophrenia patients prone to hallucinations, compared with healthy controls and patients who had schizophrenia but not hallucinations.

These findings support the understanding that auditory hallucinations originate from altered connectivity of the same regions that process normal hearing and speech. The schizophrenia patient may perceive external voices from aberrant internal signals.

Figure 1 Rates of gray matter volume loss during adolescence

Youths with early-onset schizophrenia show greater gray matter volume loss during adolescence, compared with normal controls.

Source: Adapted from reference 2

Figure 2 Structural differences between neurons
in patients with schizophrenia and controls

Schizophrenic neurons show reduced soma size, spine formation, and dendritic branching

Source: Adapted from reference 2White matter. Recent research suggests that white matter deficits also may be involved in schizophrenia’s pathophysiology. Studies using diffusion tensor imaging (DTI)—which measures the sum of vectors of water diffusion along axons—have documented white matter impairments in patients with schizophrenia.⁶

White matter tracks—myelinated axons that transport electrical signals among neurons—connect regions within the cortex and between the cortex and deeper brain structures. Disruption of white matter tracks may degrade signals and confuse neuronal communication.

Myelination. Genetic studies in patients with schizophrenia also have suggested that decreased neuron myelination may play a role in white matter deficits. Hakak et al⁸ examined more than 6,000 genes using microarray analysis and found only 17 genes were significantly down-regulated in patients with schizophrenia. Of those 17 genes, 6 were related to myelin and 11 showed no pattern.

Oligodendrocytes are glial cells that insulate axons with myelin and allow faster transmission of electrical impulses in the brain. In a postmortem study, Hof et al⁷ found 7 patients schizophrenia had 28% fewer oligodendrocytes per section of the superior frontal gyrus and 27% less white matter compared with 7 age-matched controls (Figure 3).

Figure 3 Reduced neuron myelination possible in schizophrenia

In a postmortem analysis, stained white matter sections taken from schizophrenia patients had fewer oligodendrocytes, cells that insulate axons with myelin and facilitate electrical transmission.

Source: Adapted from reference 2

Genes and the environment

Schizophrenia’s heritability is among the most repeated research findings in psychiatry.⁹ Other mechanisms besides genetics must be involved, however, as studies consistently show that monozygotic twins have a concordance rate of approximately 50% for the development of schizophrenia.

Environmental factors. Adverse environmental events may act in conjuction with genetic predisposition to trigger schizophrenia development. Ischemia or an impoverished diet, for example, have the potential to change DNA methylation.

Environmental factors associated with increased risk for schizophrenia include:

• maternal starvation during pregnancy¹⁰
• prenatal exposure to influenza¹¹
• obstetrical complications with hypoxia¹²
• being born and raised in an urban environment¹³
• using marijuana during adolescence.¹⁴

Gene expression. Important genes may be silenced in individuals with increased DNA methylation and a susceptible genetic profile. Alterations in gene expression are the fundamental mechanism of behavioral change. Research shows that environmental events can alter gene expression without changing the genetic code, such as by adding methyl groups to DNA.^15,16 The silencing of important developmental genes in this way can have devastating effects on development.

One explanation for the development of schizophrenia is that environmental events in susceptible individuals silence the production of proteins essential for maintaining neuronal connections through methylation of DNA. Postmortem analysis of brains of patients with schizophrenia show reduced mRNA of reelin,¹⁷ a protein produced in gamma-aminobutyric acid neurons involved in neuronal migration, axon branching, and synapse formation during brain development. Lowered production of proteins such as reelin may reduce connections between neurons and cause schizophrenia symptoms. Two research groups also have reported increased methylation of reelin DNA in postmortem studies of the brains of patients with schizophrenia.^18,19 Increased methylation of DNA would silence production of this important protein.

Preventing neural disconnects? If schizophrenia is a developmental disorder resulting from failures in brain connectivity, then the ultimate treatment may be prevention. Recent research suggests that intervening with second-generation antipsychotics during the prodromal stage can prevent or delay the emergence of the disorder.²⁰ Further research is needed to establish whether early intervention can prevent schizophrenia’s neuronal disruption.

Advances in neuroimaging, cell biology, and post mortem analysis are starting to explain what happens in the brain of a person who develops schizophrenia. Schizophrenia appears to be a developmental disorder of disrupted neural connection within and between regions of the brain. These disruptions seem to result from genetic predispositions interacting with negative environmental events.

A matter of gray and white

Individuals with schizophrenia have deficits in gray matter and white matter, as illustrated by studies linking auditory hallucinations with brain regions associated with normal hearing (Box).

Gray matter. Magnetic resonance imaging (MRI) indicates that gray matter volume peaks in early adolescence and declines with age. The normal adolescent brain shrinks as inefficient neural connections are pruned away, a process that refines and matures gray matter. In individuals with schizophrenia, this reduction is more aggressive—perhaps because of excessive pruning—and occurs in the time frame when schizophrenia symptoms typically emerge.

Rapoport et al¹ documented this process through sequential MRI scans in children with early-onset schizophrenia (mean age 14.5). Compared with age-matched healthy controls, youths with schizophrenia show greater and more rapid gray matter loss during late adolescence (Figure 1).²

Increased density. Reduced neuronal branching and spine formation also likely causes subtle reductions in gray matter volume (Figure 2). The resulting lack of dendritic connectivity may produce cognitive impairments and negative symptoms seen in schizophrenia.

Postmortem studies of gray matter cells show increased neuron density in patients with schizophrenia when compared with controls.³ Patients with schizophrenia have the same number of neurons as controls, but the neurons are more tightly packed because of reduced cell size, branching, and synapse formation.⁴

Research over the past decade has revealed schizophrenia to be a neurodegenerative disorder characterized by substantial brain tissue loss during first and subsequent psychotic episodes.⁵ Neuroimaging studies show that clinical and functional deterioration accompanies progressive loss of cortical gray matter volume and enlargement of cerebral ventricles. Thus, preventing relapses has come to be regarded as critical to long-term schizophrenia management.

Box

Do auditory hallucinations follow sound pathways in the brain?

Auditory hallucinations appear to emanate from the temporal lobe, the same brain region that processes external sound. Thus, it may be that patients experiencing hallucinations are misidentifying inner speech as coming from an outside source.

Using functional MRI to differentiate brain activity signals associated with hallucinating and nonhallucinating states, Dierks et al²¹ documented increased activity in auditory cortical gray matter during hallucinations in schizophrenia patients.

Auditory signals make synaptic connections in the thalamus (left) before reaching the auditory cortex. White matter fiber tracts called the arcuate fasciculus (right) connect the auditory cortex in the temporal lobe with Broca’s area in the frontal cortex.

Source: Adapted from reference 2

Using MR diffusion tensor imaging, Hubl et al²² identified white matter changes in the arcuate fasciculus of schizophrenia patients prone to hallucinations, compared with healthy controls and patients who had schizophrenia but not hallucinations.

These findings support the understanding that auditory hallucinations originate from altered connectivity of the same regions that process normal hearing and speech. The schizophrenia patient may perceive external voices from aberrant internal signals.

Figure 1 Rates of gray matter volume loss during adolescence

Youths with early-onset schizophrenia show greater gray matter volume loss during adolescence, compared with normal controls.

Source: Adapted from reference 2

Figure 2 Structural differences between neurons
in patients with schizophrenia and controls

Schizophrenic neurons show reduced soma size, spine formation, and dendritic branching

Source: Adapted from reference 2White matter. Recent research suggests that white matter deficits also may be involved in schizophrenia’s pathophysiology. Studies using diffusion tensor imaging (DTI)—which measures the sum of vectors of water diffusion along axons—have documented white matter impairments in patients with schizophrenia.⁶

White matter tracks—myelinated axons that transport electrical signals among neurons—connect regions within the cortex and between the cortex and deeper brain structures. Disruption of white matter tracks may degrade signals and confuse neuronal communication.

Myelination. Genetic studies in patients with schizophrenia also have suggested that decreased neuron myelination may play a role in white matter deficits. Hakak et al⁸ examined more than 6,000 genes using microarray analysis and found only 17 genes were significantly down-regulated in patients with schizophrenia. Of those 17 genes, 6 were related to myelin and 11 showed no pattern.

Oligodendrocytes are glial cells that insulate axons with myelin and allow faster transmission of electrical impulses in the brain. In a postmortem study, Hof et al⁷ found 7 patients schizophrenia had 28% fewer oligodendrocytes per section of the superior frontal gyrus and 27% less white matter compared with 7 age-matched controls (Figure 3).

Figure 3 Reduced neuron myelination possible in schizophrenia

In a postmortem analysis, stained white matter sections taken from schizophrenia patients had fewer oligodendrocytes, cells that insulate axons with myelin and facilitate electrical transmission.

Source: Adapted from reference 2

Genes and the environment

Schizophrenia’s heritability is among the most repeated research findings in psychiatry.⁹ Other mechanisms besides genetics must be involved, however, as studies consistently show that monozygotic twins have a concordance rate of approximately 50% for the development of schizophrenia.

Environmental factors. Adverse environmental events may act in conjuction with genetic predisposition to trigger schizophrenia development. Ischemia or an impoverished diet, for example, have the potential to change DNA methylation.

Environmental factors associated with increased risk for schizophrenia include:

• maternal starvation during pregnancy¹⁰
• prenatal exposure to influenza¹¹
• obstetrical complications with hypoxia¹²
• being born and raised in an urban environment¹³
• using marijuana during adolescence.¹⁴

Gene expression. Important genes may be silenced in individuals with increased DNA methylation and a susceptible genetic profile. Alterations in gene expression are the fundamental mechanism of behavioral change. Research shows that environmental events can alter gene expression without changing the genetic code, such as by adding methyl groups to DNA.^15,16 The silencing of important developmental genes in this way can have devastating effects on development.

One explanation for the development of schizophrenia is that environmental events in susceptible individuals silence the production of proteins essential for maintaining neuronal connections through methylation of DNA. Postmortem analysis of brains of patients with schizophrenia show reduced mRNA of reelin,¹⁷ a protein produced in gamma-aminobutyric acid neurons involved in neuronal migration, axon branching, and synapse formation during brain development. Lowered production of proteins such as reelin may reduce connections between neurons and cause schizophrenia symptoms. Two research groups also have reported increased methylation of reelin DNA in postmortem studies of the brains of patients with schizophrenia.^18,19 Increased methylation of DNA would silence production of this important protein.

Preventing neural disconnects? If schizophrenia is a developmental disorder resulting from failures in brain connectivity, then the ultimate treatment may be prevention. Recent research suggests that intervening with second-generation antipsychotics during the prodromal stage can prevent or delay the emergence of the disorder.²⁰ Further research is needed to establish whether early intervention can prevent schizophrenia’s neuronal disruption.

Advances in neuroimaging, cell biology, and post mortem analysis are starting to explain what happens in the brain of a person who develops schizophrenia. Schizophrenia appears to be a developmental disorder of disrupted neural connection within and between regions of the brain. These disruptions seem to result from genetic predispositions interacting with negative environmental events.

A matter of gray and white

Individuals with schizophrenia have deficits in gray matter and white matter, as illustrated by studies linking auditory hallucinations with brain regions associated with normal hearing (Box).

Gray matter. Magnetic resonance imaging (MRI) indicates that gray matter volume peaks in early adolescence and declines with age. The normal adolescent brain shrinks as inefficient neural connections are pruned away, a process that refines and matures gray matter. In individuals with schizophrenia, this reduction is more aggressive—perhaps because of excessive pruning—and occurs in the time frame when schizophrenia symptoms typically emerge.

Rapoport et al¹ documented this process through sequential MRI scans in children with early-onset schizophrenia (mean age 14.5). Compared with age-matched healthy controls, youths with schizophrenia show greater and more rapid gray matter loss during late adolescence (Figure 1).²

Increased density. Reduced neuronal branching and spine formation also likely causes subtle reductions in gray matter volume (Figure 2). The resulting lack of dendritic connectivity may produce cognitive impairments and negative symptoms seen in schizophrenia.

Postmortem studies of gray matter cells show increased neuron density in patients with schizophrenia when compared with controls.³ Patients with schizophrenia have the same number of neurons as controls, but the neurons are more tightly packed because of reduced cell size, branching, and synapse formation.⁴

Research over the past decade has revealed schizophrenia to be a neurodegenerative disorder characterized by substantial brain tissue loss during first and subsequent psychotic episodes.⁵ Neuroimaging studies show that clinical and functional deterioration accompanies progressive loss of cortical gray matter volume and enlargement of cerebral ventricles. Thus, preventing relapses has come to be regarded as critical to long-term schizophrenia management.

Box

Do auditory hallucinations follow sound pathways in the brain?

Auditory hallucinations appear to emanate from the temporal lobe, the same brain region that processes external sound. Thus, it may be that patients experiencing hallucinations are misidentifying inner speech as coming from an outside source.

Using functional MRI to differentiate brain activity signals associated with hallucinating and nonhallucinating states, Dierks et al²¹ documented increased activity in auditory cortical gray matter during hallucinations in schizophrenia patients.

Auditory signals make synaptic connections in the thalamus (left) before reaching the auditory cortex. White matter fiber tracts called the arcuate fasciculus (right) connect the auditory cortex in the temporal lobe with Broca’s area in the frontal cortex.

Source: Adapted from reference 2

Using MR diffusion tensor imaging, Hubl et al²² identified white matter changes in the arcuate fasciculus of schizophrenia patients prone to hallucinations, compared with healthy controls and patients who had schizophrenia but not hallucinations.

These findings support the understanding that auditory hallucinations originate from altered connectivity of the same regions that process normal hearing and speech. The schizophrenia patient may perceive external voices from aberrant internal signals.

Figure 1 Rates of gray matter volume loss during adolescence

Youths with early-onset schizophrenia show greater gray matter volume loss during adolescence, compared with normal controls.

Source: Adapted from reference 2

Figure 2 Structural differences between neurons
in patients with schizophrenia and controls

Schizophrenic neurons show reduced soma size, spine formation, and dendritic branching

Source: Adapted from reference 2White matter. Recent research suggests that white matter deficits also may be involved in schizophrenia’s pathophysiology. Studies using diffusion tensor imaging (DTI)—which measures the sum of vectors of water diffusion along axons—have documented white matter impairments in patients with schizophrenia.⁶

White matter tracks—myelinated axons that transport electrical signals among neurons—connect regions within the cortex and between the cortex and deeper brain structures. Disruption of white matter tracks may degrade signals and confuse neuronal communication.

Myelination. Genetic studies in patients with schizophrenia also have suggested that decreased neuron myelination may play a role in white matter deficits. Hakak et al⁸ examined more than 6,000 genes using microarray analysis and found only 17 genes were significantly down-regulated in patients with schizophrenia. Of those 17 genes, 6 were related to myelin and 11 showed no pattern.

Oligodendrocytes are glial cells that insulate axons with myelin and allow faster transmission of electrical impulses in the brain. In a postmortem study, Hof et al⁷ found 7 patients schizophrenia had 28% fewer oligodendrocytes per section of the superior frontal gyrus and 27% less white matter compared with 7 age-matched controls (Figure 3).

Figure 3 Reduced neuron myelination possible in schizophrenia

In a postmortem analysis, stained white matter sections taken from schizophrenia patients had fewer oligodendrocytes, cells that insulate axons with myelin and facilitate electrical transmission.

Source: Adapted from reference 2

Genes and the environment

Schizophrenia’s heritability is among the most repeated research findings in psychiatry.⁹ Other mechanisms besides genetics must be involved, however, as studies consistently show that monozygotic twins have a concordance rate of approximately 50% for the development of schizophrenia.

Environmental factors. Adverse environmental events may act in conjuction with genetic predisposition to trigger schizophrenia development. Ischemia or an impoverished diet, for example, have the potential to change DNA methylation.

Environmental factors associated with increased risk for schizophrenia include:

• maternal starvation during pregnancy¹⁰
• prenatal exposure to influenza¹¹
• obstetrical complications with hypoxia¹²
• being born and raised in an urban environment¹³
• using marijuana during adolescence.¹⁴

Gene expression. Important genes may be silenced in individuals with increased DNA methylation and a susceptible genetic profile. Alterations in gene expression are the fundamental mechanism of behavioral change. Research shows that environmental events can alter gene expression without changing the genetic code, such as by adding methyl groups to DNA.^15,16 The silencing of important developmental genes in this way can have devastating effects on development.

One explanation for the development of schizophrenia is that environmental events in susceptible individuals silence the production of proteins essential for maintaining neuronal connections through methylation of DNA. Postmortem analysis of brains of patients with schizophrenia show reduced mRNA of reelin,¹⁷ a protein produced in gamma-aminobutyric acid neurons involved in neuronal migration, axon branching, and synapse formation during brain development. Lowered production of proteins such as reelin may reduce connections between neurons and cause schizophrenia symptoms. Two research groups also have reported increased methylation of reelin DNA in postmortem studies of the brains of patients with schizophrenia.^18,19 Increased methylation of DNA would silence production of this important protein.

Preventing neural disconnects? If schizophrenia is a developmental disorder resulting from failures in brain connectivity, then the ultimate treatment may be prevention. Recent research suggests that intervening with second-generation antipsychotics during the prodromal stage can prevent or delay the emergence of the disorder.²⁰ Further research is needed to establish whether early intervention can prevent schizophrenia’s neuronal disruption.

Mrs. W, age 53, is referred by her primary provider for consultation on depressive symptoms, including worsening depressed mood, anhedonia, anxiety, and suicidal thoughts for 2 months. She reports at least 2 similar episodes in the past 15 years. Mrs. W has a remote history of IV drug use and history of alcohol abuse, but she attends Alcoholics Anonymous and has 10 years of sobriety. She has no history of hospitalizations for medical illness and denies any medical problems.

Mrs. W is taking amitriptyline, 50 mg, for insomnia. She has no history of manic or psychotic symptoms, and the mental status examination is consistent with major depression. Her past depressive episodes were treated successfully with a medication that she does not recall.

The psychiatrist diagnoses recurrent and severe major depression and prescribes cognitive-behavioral therapy and sertraline, 25 mg/d, titrated to 50 mg/d over the next 2 weeks. Amitriptyline is discontinued.

When the psychiatrist receives Mrs. W’s medical records, electrolytes, complete blood count, thyroid stimulating hormone level, and fasting glucose are within normal limits, but alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are greatly elevated at 250 U/L and 150 U/L, respectively. Progress notes contain no references to liver disease.

Interpreting psychiatric patients’ liver function tests (LFTs) can be challenging, especially in those with polypharmacy, co-occurring substance abuse, or risk factors for viral hepatitis. You can improve collaboration with primary care providers by understanding:

• what an LFT measures
• how to interpret abnormal results
• which conditions to suspect, based on the results.

A standard LFT usually measures several enzymes and proteins, typically ALT, AST, alkaline phosphatase (ALP), total bilirubin (TBIL), albumin (ALB), and total protein (TP). Measures of gamma-glutamyl transpeptidase (GGT) and prothrombin time (PT) are often requested with an LFT. Table 1 provides normal ranges and ranges that indicate liver damage for several of these parameters.^1,2

“Liver function test” is a misnomer because LFTs do not directly measure liver function. Rather, they reflect hepatocyte injury or cholestasis (blockage or damage in the biliary system). ALB and PT measure liver synthetic function, but are nonspecific. ALB levels can be altered by nutritional status, protein-losing enteropathies, or nephropathies, whereas PT may be modified by warfarin, vitamin K deficiency, or consumptive coagulopathy.

Table 1

Test results: what’s normal, what suggests liver damage

CASE CONTINUED: Spotting a pattern of injury

Mrs. W’s elevated ALT and AST levels are of unknown duration. Her AST:ALT ratio is approximately 2:1, suggesting hepatocellular injury.

Interpreting abnormal LFT results

To properly interpret LFTs, consider the patient’s symptoms, physical exam findings, medical history, medical illnesses, potential substance use, risk factors for HIV and viral hepatitis, and medication list. Collaborate with the patient’s primary care provider or facilitate primary care (Figure 1).

ALT and AST are highly concentrated in the liver, but ALT is a more specific indicator of liver injury. For both, levels may vary according to age, sex, and ethnicity but in general, levels <30 U/L are considered normal.^1,2

ALP originates predominately from the liver and from bone. Persistently elevated ALP levels in the liver may indicate chronic cholestasis or infiltrative liver disease.

GGT is best used to evaluate the meaning of elevations in other serum enzymes.³ Elevated GGT can help confirm hepatic origin of elevated ALP or support a suspicion of alcohol use in patients with an AST: ALT ratio >2:1.

If an asymptomatic patient has elevated LFT results, first repeat the test. If repeat results are normal, perform the test again in 3-6 months. Keep in mind, however, that normal LFT results do not always indicate the absence of disease. For example, up to 16% of patients with hepatitis C and 13% of patients with nonalcoholic steatohepatitis (NASH) have normal LFT results despite histologic abnormalities.⁴

If repeat results are abnormal, obtain the patient’s consent to inform the primary care provider. Then take a thorough history and perform a focused physical exam. In the history, focus on use of prescription and nonprescription medications, including over-the-counter and herbal therapies, alcohol, and drugs of abuse, such as MDMA (“ecstasy”), phencyclidine (“angel dust”), and glues or solvents. Also assess for risk factors for infectious hepatitis, such as IV drug use, work-related blood exposure, and tattoos. Ask about a family history of liver disease. Focus your physical exam on visible stigmata of chronic liver disease, such as jaundice, temporal wasting, ascites, and palmar erythema.

Next, analyze the severity and pattern of the LFT abnormality. Liver injury is defined as:

• ALT >3 times the upper limit of normal
• ALP >2 times the upper limit of normal
• or total bilirubin >2 times the upper limit of normal if associated with any elevation of ALT or ALP.⁵

If ALT elevations predominate, consider hepatocellular injury. If ALP elevations predominate, suspect cholestatic injury. Elevations of both ALT and ALP suggest a mixed pattern of hepatocellular and cholestatic injury.

Figure 1 Interpreting liver function test results

ALB: albumin; ALP: alkaline phosphatase; ALT: alanine aminotransferase; AST: aspartate aminotransferase; GGT: gamma-glutamyl transpeptidase; HBV: hepatitis B virus; HCV: hepatitis C virus; HIV: human immunodeficiency virus; LFT: liver function test; PCP: primary care provider; TBIL: total bilirubin; TP: total protein

CASE CONTINUED: Pinpointing a diagnosis

Mrs. W undergoes repeat LFTs with GGT testing, screening tests for hepatitis B and C, and a comprehensive physical exam. The psychiatrist screens for alcohol use, asks the patient about her use of herbal therapies and substance abuse relapse, and evaluates cognitive mental status for symptoms of encephalopathy. Results reveal that Mrs. W’s ALT and AST are elevated because of chronic active hepatitis C.

Causes of hepatocellular injury

Further evaluation of your patient’s test results can help narrow down potential causes of liver damage. If your patient’s ALT is disproportionately elevated, estimate the:

• severity of aminotransferase elevation
• ratio of AST:ALT
• rate of change over multiple LFTs.

If AST or ALT is >10 times normal, consider toxin-induced or ischemic injury.⁶ An AST:ALT ratio of 2:1 or 3:1, especially when associated with elevated GGT, strongly suggests alcohol-induced injury. With acute mild transaminase elevations—ALT>AST, 2 to 3 times normal—suspect medication-related injury.

A variety of factors and conditions can result in hepatocellular damage:

Common causes

Medications. Many drugs, including common psychotropics, can cause elevated liver enzymes (Table 2).⁵ As little as 4 grams per day of acetaminophen can cause mild transaminitis.⁴ Antidepressants, second-generation antipsychotics (SGAs), and anticonvulsants can cause increases in AST and ALT.⁷ If liver enzymes rise after a patient starts a new medication, drug-related liver toxicity is likely. Remember to consider a patient’s use of drugs of abuse and herbal therapies.

Discontinuing the suspect agent usually produces steady (although sometimes slow) improvement in LFTs. Use serial LFT testing and focused history and physical examinations to confirm improvement.