Malpractice Counsel

Acute Coronary Syndromes

A 53-year-old obese man presented to the ED complaining of pain in his chest, bilateral jaw, and back. He stated that his symptoms had started the previous evening and had increased in severity the morning of presentation. He denied any change in breathing, or any nausea or vomiting. The patient’s medical history was significant for hypertension and chronic back pain. Regarding his social history, the patient noted that he smoked one pack of cigarettes per day; he denied alcohol use.

On physical examination, the patient’s weight was 350 lb, and he was profusely diaphoretic. Vital signs were remarkable for an elevated blood pressure (BP) of 214/106 mm Hg; respiratory rate (RR), heart rate (HR), temperature (T), and oxygen saturation were normal. The head, eyes, ears, nose, and throat examination was normal, and there was no jugular venous distention. The lung and heart examinations were also normal, and the abdominal examination was unremarkable. The patient had 2+ pitting edema in his lower extremities, which he said had been present for the past few weeks. The back examination was unremarkable, and the neurological examination was completely normal, including deep tendon reflexes.

The emergency physician (EP) ordered a 12-lead electrocardiogram (ECG), chest X-ray, and blood work, including evaluation of cardiac enzymes. The initial ECG was nondiagnostic, and the chest X-ray was read as normal. The initial serum troponin level was mildly elevated (sometimes referred to as the “gray zone of uncertainty”).

Because of the presence of chest and back pain and history of hypertension, the EP ordered a computed tomography (CT) scan of the chest with intravenous (IV) contrast to rule out aortic dissection. He also administered 0.2 mg of clonidine orally for the elevated BP. Approximately 20 minutes later, the patient was given 2 mg morphine IV for the back pain and another 0.2 mg of clonidine orally. The elevated BP responded to the clonidine, and the patient stated he was feeling better.

The CT scan of the chest was interpreted by radiology services as normal. The patient was then administered 325 mg of aspirin by mouth. Since the EP’s hospital did not have facilities for cardiac catheterization, the EP consulted with a physician at another facility regarding a possible transfer. The consulted physician did not accept the patient for transfer, but instead recommended keeping the patient at the EP’s institution for observation and continuing treatment for the elevated BP and pain. The EP agreed, and diagnosed the patient with a hypertensive emergency and a flare-up of his chronic back pain.

In the ED, the patient’s BP decreased to near normal levels, and he was feeling much improved. Approximately 5.5 hours after his arrival to the ED, he was admitted to a monitored bed under the care of a hospitalist.

A few hours later, the patient began to complain of burning in the epigastric area; analgesics and nitroglycerin were administered and a repeat ECG was ordered. A second troponin level, drawn approximately 6 hours after the original, was found to be significantly elevated. The repeat ECG demonstrated sinus tachycardia with ST-segment depression.

The hospitalist was concerned about an acute coronary syndrome (ACS) and attempted to make contact with the other facility to transfer the patient for an emergent cardiac catheterization. The consulted physician agreed to accept the patient and recommended starting an IV heparin drip and giving clopidogrel bisulfate (Plavix). While arranging for the transfer, the patient suffered a cardiac arrest; resuscitation attempts were unsuccessful. 

The family of the patient sued the hospital, the EP, and the hospitalist, alleging the EP failed to recognize that the initial ECG and elevated troponin level were suggestive of an ACS. They also complained that the morphine, oxygen, nitroglycerin, and aspirin were not started in a timely manner. In addition, the family claimed the decedent should have been immediately transferred to another facility because the defendant’s hospital could not perform cardiac catheterization. They further alleged that the hospitalist failed to perform an independent evaluation of the patient and also failed to obtain a repeat 12-lead ECG sooner. Lastly, the plaintiffs claimed that the hospital’s nursing staff was negligent in failing to provide nursing care for 3 hours prior to the patient being found unresponsive.

The defendant EP asserted that the initial ECG was nondiagnostic and that the initial troponin level, while elevated, was nonspecific. He argued the ED evaluation and care provided was appropriate. Following trial, a defense verdict was returned.

Discussion

Fortunately, the jury ruled correctly in this case. Acute coronary sydromes can be some of the most challenging medical conditions to evaluate and manage in the ED. The EP’s initial cardiac workup and evaluation for a possible acute thoracic aortic dissection were appropriate—an acute thoracic aortic dissection is a true cardiovascular emergency. After interpreting the initial ECG as nondiagnostic (specifically, to rule out evidence of ST-segment elevation, myocardial infarction [MI], or STEMI), obtaining the contrast CT scan of the chest emergently was critically important. This patient had multiple risk factors for aortic dissection: he was a male between the ages of 50 and 55 years old (the mean age for proximal thoracic aortic dissection); he had a history of hypertension; and he was experiencing chest and back pain.¹

 

Once an acute aortic dissection was excluded, focusing on a cardiac etiology, as the EP did, was appropriate. The only criticism is that this patient probably should have been managed with an IV antihypertensive agent to allow for a more controlled BP reduction; this, however, does not seem to have played any role in the patient’s ultimate outcome.

Acute coronary syndromes are a dynamic process and progress over time. The EP was clearly concerned about an ACS very early in the case, as evidenced by his attempt to transfer the patient to a facility with specialized cardiac capabilities. After not being able to do so, the most appropriate next step was his admission of the patient to a monitored bed with serial cardiac enzymes and ECGs. It is well known that initial evaluation of both ECG and cardiac enzymes can be normal early on in an ACS. Patients with a normal or nonspecific ECG have a 1% to 5% incidence of MI and a 4% to 23% incidence of unstable angina.²

This patient ultimately experienced a non-ST-segment elevation myocardial infarction (NSTEMI). However, this diagnosis did not become evident until several hours after the patient’s admission to the hospital. It is unfortunate the physician consulted by the EP at the onset did not agree to accept this patient. This patient’s best chance for survival was at a facility capable of percutaneous coronary intervention.

Serotonin Syndrome

A 20-year-old man was brought to the ED by his friends for concerns of an overdose. Just prior to arrival, the patient reportedly drank the entire contents of a bottle of cough medicine containing dextromethorphan. His friends reported the patient had been depressed lately, but was otherwise in good health. The patient was not known to abuse alcohol or use illicit drugs. The EP was unable to obtain any history from the patient, who was extremely agitated and yelling frequently. A review of the hospital records revealed the patient had been admitted a few months prior for a suicide attempt. On physical examination, the patient’s vital signs were: pulse, 126 beats/minute; BP, 144/92 mm Hg, RR 22 breaths/minute; and T, 100.6˚F. Oxygen saturation was 99% on room air. The patient was diaphoretic, agitated, and only able to provide one-word answers between screaming episodes. His pupils were mildly dilated but reactive. The cardiac examination revealed a tachycardic rate with a normal rhythm, and no murmurs, rubs, or gallops. The lungs were clear to auscultation bilaterally. The abdomen was soft and nontender, without guarding or rebound. The patient would not cooperate for a neurological examination, but was found to be moving all four extremities with good strength. He was noted to have myoclonus. The EP immediately called the Poison Control Center for advice about treatment. In the meantime, laboratory studies were drawn, including an alcohol level, acetaminophen level, salicylate level, and a urine drug screen. A 12-lead ECG demonstrated a sinus tachycardia with a normal axis. The patient was given IV lorazepam to treat the agitation. The patient’s alcohol, acetaminophen, and salicylate levels were all negative. The EP attempted to transfer the patient to another facility with a higher level of care, but unfortunately, the patient went into cardiac arrest and died in the ED. An autopsy showed that the patient died from serotonin syndrome as a result of acute dextromethorphan and selegiline toxicity. It was later discovered that the patient had been prescribed selegiline as an antidepressant following his recent hospitalization for the suicide attempt. Unfortunately, this information was not available in the records from his previous presentation or from the patient or his friends during the history taking. The patient’s family sued the EP for failing to diagnose serotonin syndrome. They argued the patient did not die from a suicide, but rather from serotonin syndrome. The EP contended the patient had deliberately combined the two drugs to commit suicide. Both parties argued application of the state’s “dead man’s statute” (also known as a “dead man’s act” or “dead man’s rule”). Following trial, a defense verdict was returned. Discussion Serotonin syndrome (or serotonin toxicity) is a drug-induced syndrome characterized by a cluster of dose-related adverse effects due to increased serotonin concentrations in the central nervous system.1 Severe toxicity, as seen in this case, usually occurs only when two or more serotonergic drugs (even when each is at therapeutic dose) are combined. One of the drugs is usually a monoamine oxidase inhibitor (MAOI).1 While selegiline is used primarily as an adjunct treatment for Parkinson disease, it is also used to treat depression, attention deficit and hyperactivity disorder, and Alzheimer disease. Its primary mechanism of action is as an irreversible inhibitor of MAO. Dextromethorphan is used primarily as an antitussive (cough suppressant). It is also used recreationally for its reported effects as a hallucinogen. Its mechanism of action occurs through several effects, one of which is as a nonselective serotonin reuptake inhibitor (NSRI). Although the label on all NSRIs clearly states  this medication should not be taken with MAOIs (ie, selegiline), few lay people know the mechanism of action of their medications. The patient in this case took a combination of medications that are known to cause severe serotonin toxicity. It is unclear whether or not he was aware of the dangers associated with combining these two medications. The classic triad of clinical features of serotonin syndrome are neuromuscular excitation (eg, clonus, hyperreflexia, myoclonus, rigidity); autonomic nervous system excitation (eg, hyperthermia, tachycardia); and altered mental status (eg, agitation, confusion).1 The onset of symptoms typically occurs within a few hours of ingestion. Serotonin syndrome can be confused with neuroleptic malignant syndrome (NMS), but there are three key differentiating features: (1) In NMS, symptom onset is slow, usually over days, not hours; (2) extrapyramidal features and rigidity are much more prominent in NMS; and (3) clonus is usually pronounced and easily elicited (especially with ankle dorsiflexion) in serotonin syndrome, but minimal to absent in NMS.1 The initial treatment of serotonin syndrome involves symptomatic care and discontinuation of all serotonergic drugs.2 Benzodiazepines can be used for muscle relaxation and treatment of agitation. All patients with serotonin syndrome require hospital admission, and those with severe toxicity should be admitted to an intensive care unit. Cyproheptadine is the most effective antiserotonergic agent, but it is only available in oral formulation. Chlorpromazine IV has also been used to treat serotonin syndrome, but resulting hypotension is a drawback.1 Approximately 25% of patients with severe serotonin toxicity require intubation and mechanical ventilation. Most patients show dramatic improvement within 24 hours of symptom onset.2 Regarding the dead man statute, according to Cornell University Law School, this statute states that in a civil action, a party with an interest in the litigation may not testify against a dead party about communications with the dead party. This is a state statute and therefore the exact wording varies from state to state. The Federal Rules of Evidence does not contain a dead man’s statute.

Acute Coronary Syndromes

A 53-year-old obese man presented to the ED complaining of pain in his chest, bilateral jaw, and back. He stated that his symptoms had started the previous evening and had increased in severity the morning of presentation. He denied any change in breathing, or any nausea or vomiting. The patient’s medical history was significant for hypertension and chronic back pain. Regarding his social history, the patient noted that he smoked one pack of cigarettes per day; he denied alcohol use.

On physical examination, the patient’s weight was 350 lb, and he was profusely diaphoretic. Vital signs were remarkable for an elevated blood pressure (BP) of 214/106 mm Hg; respiratory rate (RR), heart rate (HR), temperature (T), and oxygen saturation were normal. The head, eyes, ears, nose, and throat examination was normal, and there was no jugular venous distention. The lung and heart examinations were also normal, and the abdominal examination was unremarkable. The patient had 2+ pitting edema in his lower extremities, which he said had been present for the past few weeks. The back examination was unremarkable, and the neurological examination was completely normal, including deep tendon reflexes.

The emergency physician (EP) ordered a 12-lead electrocardiogram (ECG), chest X-ray, and blood work, including evaluation of cardiac enzymes. The initial ECG was nondiagnostic, and the chest X-ray was read as normal. The initial serum troponin level was mildly elevated (sometimes referred to as the “gray zone of uncertainty”).

Because of the presence of chest and back pain and history of hypertension, the EP ordered a computed tomography (CT) scan of the chest with intravenous (IV) contrast to rule out aortic dissection. He also administered 0.2 mg of clonidine orally for the elevated BP. Approximately 20 minutes later, the patient was given 2 mg morphine IV for the back pain and another 0.2 mg of clonidine orally. The elevated BP responded to the clonidine, and the patient stated he was feeling better.

The CT scan of the chest was interpreted by radiology services as normal. The patient was then administered 325 mg of aspirin by mouth. Since the EP’s hospital did not have facilities for cardiac catheterization, the EP consulted with a physician at another facility regarding a possible transfer. The consulted physician did not accept the patient for transfer, but instead recommended keeping the patient at the EP’s institution for observation and continuing treatment for the elevated BP and pain. The EP agreed, and diagnosed the patient with a hypertensive emergency and a flare-up of his chronic back pain.

In the ED, the patient’s BP decreased to near normal levels, and he was feeling much improved. Approximately 5.5 hours after his arrival to the ED, he was admitted to a monitored bed under the care of a hospitalist.

A few hours later, the patient began to complain of burning in the epigastric area; analgesics and nitroglycerin were administered and a repeat ECG was ordered. A second troponin level, drawn approximately 6 hours after the original, was found to be significantly elevated. The repeat ECG demonstrated sinus tachycardia with ST-segment depression.

The hospitalist was concerned about an acute coronary syndrome (ACS) and attempted to make contact with the other facility to transfer the patient for an emergent cardiac catheterization. The consulted physician agreed to accept the patient and recommended starting an IV heparin drip and giving clopidogrel bisulfate (Plavix). While arranging for the transfer, the patient suffered a cardiac arrest; resuscitation attempts were unsuccessful. 

The family of the patient sued the hospital, the EP, and the hospitalist, alleging the EP failed to recognize that the initial ECG and elevated troponin level were suggestive of an ACS. They also complained that the morphine, oxygen, nitroglycerin, and aspirin were not started in a timely manner. In addition, the family claimed the decedent should have been immediately transferred to another facility because the defendant’s hospital could not perform cardiac catheterization. They further alleged that the hospitalist failed to perform an independent evaluation of the patient and also failed to obtain a repeat 12-lead ECG sooner. Lastly, the plaintiffs claimed that the hospital’s nursing staff was negligent in failing to provide nursing care for 3 hours prior to the patient being found unresponsive.

The defendant EP asserted that the initial ECG was nondiagnostic and that the initial troponin level, while elevated, was nonspecific. He argued the ED evaluation and care provided was appropriate. Following trial, a defense verdict was returned.

Discussion

Fortunately, the jury ruled correctly in this case. Acute coronary sydromes can be some of the most challenging medical conditions to evaluate and manage in the ED. The EP’s initial cardiac workup and evaluation for a possible acute thoracic aortic dissection were appropriate—an acute thoracic aortic dissection is a true cardiovascular emergency. After interpreting the initial ECG as nondiagnostic (specifically, to rule out evidence of ST-segment elevation, myocardial infarction [MI], or STEMI), obtaining the contrast CT scan of the chest emergently was critically important. This patient had multiple risk factors for aortic dissection: he was a male between the ages of 50 and 55 years old (the mean age for proximal thoracic aortic dissection); he had a history of hypertension; and he was experiencing chest and back pain.¹

 

Once an acute aortic dissection was excluded, focusing on a cardiac etiology, as the EP did, was appropriate. The only criticism is that this patient probably should have been managed with an IV antihypertensive agent to allow for a more controlled BP reduction; this, however, does not seem to have played any role in the patient’s ultimate outcome.

Acute coronary syndromes are a dynamic process and progress over time. The EP was clearly concerned about an ACS very early in the case, as evidenced by his attempt to transfer the patient to a facility with specialized cardiac capabilities. After not being able to do so, the most appropriate next step was his admission of the patient to a monitored bed with serial cardiac enzymes and ECGs. It is well known that initial evaluation of both ECG and cardiac enzymes can be normal early on in an ACS. Patients with a normal or nonspecific ECG have a 1% to 5% incidence of MI and a 4% to 23% incidence of unstable angina.²

This patient ultimately experienced a non-ST-segment elevation myocardial infarction (NSTEMI). However, this diagnosis did not become evident until several hours after the patient’s admission to the hospital. It is unfortunate the physician consulted by the EP at the onset did not agree to accept this patient. This patient’s best chance for survival was at a facility capable of percutaneous coronary intervention.

Serotonin Syndrome

A 20-year-old man was brought to the ED by his friends for concerns of an overdose. Just prior to arrival, the patient reportedly drank the entire contents of a bottle of cough medicine containing dextromethorphan. His friends reported the patient had been depressed lately, but was otherwise in good health. The patient was not known to abuse alcohol or use illicit drugs. The EP was unable to obtain any history from the patient, who was extremely agitated and yelling frequently. A review of the hospital records revealed the patient had been admitted a few months prior for a suicide attempt. On physical examination, the patient’s vital signs were: pulse, 126 beats/minute; BP, 144/92 mm Hg, RR 22 breaths/minute; and T, 100.6˚F. Oxygen saturation was 99% on room air. The patient was diaphoretic, agitated, and only able to provide one-word answers between screaming episodes. His pupils were mildly dilated but reactive. The cardiac examination revealed a tachycardic rate with a normal rhythm, and no murmurs, rubs, or gallops. The lungs were clear to auscultation bilaterally. The abdomen was soft and nontender, without guarding or rebound. The patient would not cooperate for a neurological examination, but was found to be moving all four extremities with good strength. He was noted to have myoclonus. The EP immediately called the Poison Control Center for advice about treatment. In the meantime, laboratory studies were drawn, including an alcohol level, acetaminophen level, salicylate level, and a urine drug screen. A 12-lead ECG demonstrated a sinus tachycardia with a normal axis. The patient was given IV lorazepam to treat the agitation. The patient’s alcohol, acetaminophen, and salicylate levels were all negative. The EP attempted to transfer the patient to another facility with a higher level of care, but unfortunately, the patient went into cardiac arrest and died in the ED. An autopsy showed that the patient died from serotonin syndrome as a result of acute dextromethorphan and selegiline toxicity. It was later discovered that the patient had been prescribed selegiline as an antidepressant following his recent hospitalization for the suicide attempt. Unfortunately, this information was not available in the records from his previous presentation or from the patient or his friends during the history taking. The patient’s family sued the EP for failing to diagnose serotonin syndrome. They argued the patient did not die from a suicide, but rather from serotonin syndrome. The EP contended the patient had deliberately combined the two drugs to commit suicide. Both parties argued application of the state’s “dead man’s statute” (also known as a “dead man’s act” or “dead man’s rule”). Following trial, a defense verdict was returned. Discussion Serotonin syndrome (or serotonin toxicity) is a drug-induced syndrome characterized by a cluster of dose-related adverse effects due to increased serotonin concentrations in the central nervous system.1 Severe toxicity, as seen in this case, usually occurs only when two or more serotonergic drugs (even when each is at therapeutic dose) are combined. One of the drugs is usually a monoamine oxidase inhibitor (MAOI).1 While selegiline is used primarily as an adjunct treatment for Parkinson disease, it is also used to treat depression, attention deficit and hyperactivity disorder, and Alzheimer disease. Its primary mechanism of action is as an irreversible inhibitor of MAO. Dextromethorphan is used primarily as an antitussive (cough suppressant). It is also used recreationally for its reported effects as a hallucinogen. Its mechanism of action occurs through several effects, one of which is as a nonselective serotonin reuptake inhibitor (NSRI). Although the label on all NSRIs clearly states  this medication should not be taken with MAOIs (ie, selegiline), few lay people know the mechanism of action of their medications. The patient in this case took a combination of medications that are known to cause severe serotonin toxicity. It is unclear whether or not he was aware of the dangers associated with combining these two medications. The classic triad of clinical features of serotonin syndrome are neuromuscular excitation (eg, clonus, hyperreflexia, myoclonus, rigidity); autonomic nervous system excitation (eg, hyperthermia, tachycardia); and altered mental status (eg, agitation, confusion).1 The onset of symptoms typically occurs within a few hours of ingestion. Serotonin syndrome can be confused with neuroleptic malignant syndrome (NMS), but there are three key differentiating features: (1) In NMS, symptom onset is slow, usually over days, not hours; (2) extrapyramidal features and rigidity are much more prominent in NMS; and (3) clonus is usually pronounced and easily elicited (especially with ankle dorsiflexion) in serotonin syndrome, but minimal to absent in NMS.1 The initial treatment of serotonin syndrome involves symptomatic care and discontinuation of all serotonergic drugs.2 Benzodiazepines can be used for muscle relaxation and treatment of agitation. All patients with serotonin syndrome require hospital admission, and those with severe toxicity should be admitted to an intensive care unit. Cyproheptadine is the most effective antiserotonergic agent, but it is only available in oral formulation. Chlorpromazine IV has also been used to treat serotonin syndrome, but resulting hypotension is a drawback.1 Approximately 25% of patients with severe serotonin toxicity require intubation and mechanical ventilation. Most patients show dramatic improvement within 24 hours of symptom onset.2 Regarding the dead man statute, according to Cornell University Law School, this statute states that in a civil action, a party with an interest in the litigation may not testify against a dead party about communications with the dead party. This is a state statute and therefore the exact wording varies from state to state. The Federal Rules of Evidence does not contain a dead man’s statute.

Acute Coronary Syndromes

A 53-year-old obese man presented to the ED complaining of pain in his chest, bilateral jaw, and back. He stated that his symptoms had started the previous evening and had increased in severity the morning of presentation. He denied any change in breathing, or any nausea or vomiting. The patient’s medical history was significant for hypertension and chronic back pain. Regarding his social history, the patient noted that he smoked one pack of cigarettes per day; he denied alcohol use.

On physical examination, the patient’s weight was 350 lb, and he was profusely diaphoretic. Vital signs were remarkable for an elevated blood pressure (BP) of 214/106 mm Hg; respiratory rate (RR), heart rate (HR), temperature (T), and oxygen saturation were normal. The head, eyes, ears, nose, and throat examination was normal, and there was no jugular venous distention. The lung and heart examinations were also normal, and the abdominal examination was unremarkable. The patient had 2+ pitting edema in his lower extremities, which he said had been present for the past few weeks. The back examination was unremarkable, and the neurological examination was completely normal, including deep tendon reflexes.

The emergency physician (EP) ordered a 12-lead electrocardiogram (ECG), chest X-ray, and blood work, including evaluation of cardiac enzymes. The initial ECG was nondiagnostic, and the chest X-ray was read as normal. The initial serum troponin level was mildly elevated (sometimes referred to as the “gray zone of uncertainty”).

Because of the presence of chest and back pain and history of hypertension, the EP ordered a computed tomography (CT) scan of the chest with intravenous (IV) contrast to rule out aortic dissection. He also administered 0.2 mg of clonidine orally for the elevated BP. Approximately 20 minutes later, the patient was given 2 mg morphine IV for the back pain and another 0.2 mg of clonidine orally. The elevated BP responded to the clonidine, and the patient stated he was feeling better.

The CT scan of the chest was interpreted by radiology services as normal. The patient was then administered 325 mg of aspirin by mouth. Since the EP’s hospital did not have facilities for cardiac catheterization, the EP consulted with a physician at another facility regarding a possible transfer. The consulted physician did not accept the patient for transfer, but instead recommended keeping the patient at the EP’s institution for observation and continuing treatment for the elevated BP and pain. The EP agreed, and diagnosed the patient with a hypertensive emergency and a flare-up of his chronic back pain.

In the ED, the patient’s BP decreased to near normal levels, and he was feeling much improved. Approximately 5.5 hours after his arrival to the ED, he was admitted to a monitored bed under the care of a hospitalist.

A few hours later, the patient began to complain of burning in the epigastric area; analgesics and nitroglycerin were administered and a repeat ECG was ordered. A second troponin level, drawn approximately 6 hours after the original, was found to be significantly elevated. The repeat ECG demonstrated sinus tachycardia with ST-segment depression.

The hospitalist was concerned about an acute coronary syndrome (ACS) and attempted to make contact with the other facility to transfer the patient for an emergent cardiac catheterization. The consulted physician agreed to accept the patient and recommended starting an IV heparin drip and giving clopidogrel bisulfate (Plavix). While arranging for the transfer, the patient suffered a cardiac arrest; resuscitation attempts were unsuccessful. 

The family of the patient sued the hospital, the EP, and the hospitalist, alleging the EP failed to recognize that the initial ECG and elevated troponin level were suggestive of an ACS. They also complained that the morphine, oxygen, nitroglycerin, and aspirin were not started in a timely manner. In addition, the family claimed the decedent should have been immediately transferred to another facility because the defendant’s hospital could not perform cardiac catheterization. They further alleged that the hospitalist failed to perform an independent evaluation of the patient and also failed to obtain a repeat 12-lead ECG sooner. Lastly, the plaintiffs claimed that the hospital’s nursing staff was negligent in failing to provide nursing care for 3 hours prior to the patient being found unresponsive.

The defendant EP asserted that the initial ECG was nondiagnostic and that the initial troponin level, while elevated, was nonspecific. He argued the ED evaluation and care provided was appropriate. Following trial, a defense verdict was returned.

Discussion

Fortunately, the jury ruled correctly in this case. Acute coronary sydromes can be some of the most challenging medical conditions to evaluate and manage in the ED. The EP’s initial cardiac workup and evaluation for a possible acute thoracic aortic dissection were appropriate—an acute thoracic aortic dissection is a true cardiovascular emergency. After interpreting the initial ECG as nondiagnostic (specifically, to rule out evidence of ST-segment elevation, myocardial infarction [MI], or STEMI), obtaining the contrast CT scan of the chest emergently was critically important. This patient had multiple risk factors for aortic dissection: he was a male between the ages of 50 and 55 years old (the mean age for proximal thoracic aortic dissection); he had a history of hypertension; and he was experiencing chest and back pain.¹

 

Once an acute aortic dissection was excluded, focusing on a cardiac etiology, as the EP did, was appropriate. The only criticism is that this patient probably should have been managed with an IV antihypertensive agent to allow for a more controlled BP reduction; this, however, does not seem to have played any role in the patient’s ultimate outcome.

Acute coronary syndromes are a dynamic process and progress over time. The EP was clearly concerned about an ACS very early in the case, as evidenced by his attempt to transfer the patient to a facility with specialized cardiac capabilities. After not being able to do so, the most appropriate next step was his admission of the patient to a monitored bed with serial cardiac enzymes and ECGs. It is well known that initial evaluation of both ECG and cardiac enzymes can be normal early on in an ACS. Patients with a normal or nonspecific ECG have a 1% to 5% incidence of MI and a 4% to 23% incidence of unstable angina.²

This patient ultimately experienced a non-ST-segment elevation myocardial infarction (NSTEMI). However, this diagnosis did not become evident until several hours after the patient’s admission to the hospital. It is unfortunate the physician consulted by the EP at the onset did not agree to accept this patient. This patient’s best chance for survival was at a facility capable of percutaneous coronary intervention.

Serotonin Syndrome

A 20-year-old man was brought to the ED by his friends for concerns of an overdose. Just prior to arrival, the patient reportedly drank the entire contents of a bottle of cough medicine containing dextromethorphan. His friends reported the patient had been depressed lately, but was otherwise in good health. The patient was not known to abuse alcohol or use illicit drugs. The EP was unable to obtain any history from the patient, who was extremely agitated and yelling frequently. A review of the hospital records revealed the patient had been admitted a few months prior for a suicide attempt. On physical examination, the patient’s vital signs were: pulse, 126 beats/minute; BP, 144/92 mm Hg, RR 22 breaths/minute; and T, 100.6˚F. Oxygen saturation was 99% on room air. The patient was diaphoretic, agitated, and only able to provide one-word answers between screaming episodes. His pupils were mildly dilated but reactive. The cardiac examination revealed a tachycardic rate with a normal rhythm, and no murmurs, rubs, or gallops. The lungs were clear to auscultation bilaterally. The abdomen was soft and nontender, without guarding or rebound. The patient would not cooperate for a neurological examination, but was found to be moving all four extremities with good strength. He was noted to have myoclonus. The EP immediately called the Poison Control Center for advice about treatment. In the meantime, laboratory studies were drawn, including an alcohol level, acetaminophen level, salicylate level, and a urine drug screen. A 12-lead ECG demonstrated a sinus tachycardia with a normal axis. The patient was given IV lorazepam to treat the agitation. The patient’s alcohol, acetaminophen, and salicylate levels were all negative. The EP attempted to transfer the patient to another facility with a higher level of care, but unfortunately, the patient went into cardiac arrest and died in the ED. An autopsy showed that the patient died from serotonin syndrome as a result of acute dextromethorphan and selegiline toxicity. It was later discovered that the patient had been prescribed selegiline as an antidepressant following his recent hospitalization for the suicide attempt. Unfortunately, this information was not available in the records from his previous presentation or from the patient or his friends during the history taking. The patient’s family sued the EP for failing to diagnose serotonin syndrome. They argued the patient did not die from a suicide, but rather from serotonin syndrome. The EP contended the patient had deliberately combined the two drugs to commit suicide. Both parties argued application of the state’s “dead man’s statute” (also known as a “dead man’s act” or “dead man’s rule”). Following trial, a defense verdict was returned. Discussion Serotonin syndrome (or serotonin toxicity) is a drug-induced syndrome characterized by a cluster of dose-related adverse effects due to increased serotonin concentrations in the central nervous system.1 Severe toxicity, as seen in this case, usually occurs only when two or more serotonergic drugs (even when each is at therapeutic dose) are combined. One of the drugs is usually a monoamine oxidase inhibitor (MAOI).1 While selegiline is used primarily as an adjunct treatment for Parkinson disease, it is also used to treat depression, attention deficit and hyperactivity disorder, and Alzheimer disease. Its primary mechanism of action is as an irreversible inhibitor of MAO. Dextromethorphan is used primarily as an antitussive (cough suppressant). It is also used recreationally for its reported effects as a hallucinogen. Its mechanism of action occurs through several effects, one of which is as a nonselective serotonin reuptake inhibitor (NSRI). Although the label on all NSRIs clearly states  this medication should not be taken with MAOIs (ie, selegiline), few lay people know the mechanism of action of their medications. The patient in this case took a combination of medications that are known to cause severe serotonin toxicity. It is unclear whether or not he was aware of the dangers associated with combining these two medications. The classic triad of clinical features of serotonin syndrome are neuromuscular excitation (eg, clonus, hyperreflexia, myoclonus, rigidity); autonomic nervous system excitation (eg, hyperthermia, tachycardia); and altered mental status (eg, agitation, confusion).1 The onset of symptoms typically occurs within a few hours of ingestion. Serotonin syndrome can be confused with neuroleptic malignant syndrome (NMS), but there are three key differentiating features: (1) In NMS, symptom onset is slow, usually over days, not hours; (2) extrapyramidal features and rigidity are much more prominent in NMS; and (3) clonus is usually pronounced and easily elicited (especially with ankle dorsiflexion) in serotonin syndrome, but minimal to absent in NMS.1 The initial treatment of serotonin syndrome involves symptomatic care and discontinuation of all serotonergic drugs.2 Benzodiazepines can be used for muscle relaxation and treatment of agitation. All patients with serotonin syndrome require hospital admission, and those with severe toxicity should be admitted to an intensive care unit. Cyproheptadine is the most effective antiserotonergic agent, but it is only available in oral formulation. Chlorpromazine IV has also been used to treat serotonin syndrome, but resulting hypotension is a drawback.1 Approximately 25% of patients with severe serotonin toxicity require intubation and mechanical ventilation. Most patients show dramatic improvement within 24 hours of symptom onset.2 Regarding the dead man statute, according to Cornell University Law School, this statute states that in a civil action, a party with an interest in the litigation may not testify against a dead party about communications with the dead party. This is a state statute and therefore the exact wording varies from state to state. The Federal Rules of Evidence does not contain a dead man’s statute.