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. |