Poison Control Deduces Cause of Patient’s Coma

Poison control is called by the emergency department (ED) with the following information: “We just received a 72-year-old male via EMS who arrived from India yesterday. He was well last night and dined with family, but this morning his son found him unresponsive in bed. He currently remains in a coma. There’s a vague history of Ayurvedic remedy use back in India.” A poison information specialist asked for additional information, but none was available, and labs were still pending. What do you think is the problem?

When the medical toxicologist and clinical toxicologist entered the ED, they found neurology wiring the patient’s head for an electroencephalogram (EEG), cardiology wheeling advanced ultrasound color echocardiography equipment toward the bedside, two infectious disease specialists ordering a CT scan, internal medicine staff who seemed bewildered at how they lost control of the patient so quickly, and the ED physician, who had handed over care because he thought it was a toxic problem.

An RN was at the head of the patient, the resident was staring at the computer monitor hoping the lab results would momentarily appear accompanied by a diagnosis, and the intern was splitting his attention between the resident and the specialists. No one was actually looking at the patient or asking questions of his two sons, who were waiting anxiously nearby.

Poison control obtained a history from the family, who was guarded in their answers–especially related to alcohol and smoking habits. They then examined the patient, after which they asked the intern if he noticed anything unusual about the skin tone or color of the sclera, and if he knew how long his patient had been decorticate.

The patient also alternated into decerebrate posturing. Other bedside findings included hepatomegaly (enlarged liver), percussed abdominal fluids, asterixis and telangiectasias–all the stigmata of liver disease. In this setting, the likely diagnosis was hepatic encephalopathy. The family ultimately admitted that their father had an alcohol problem. Lab results–elevated ammonia with liver function test abnormalities–confirmed the diagnosis.

The patient responded to treatment, regained consciousness and was discharged five days later.

The definition of “coma” hasn’t changed much since 1934, when it was described in a review paper as “a loss of consciousness, more or less profound, transient or prolonged, excepting the physiological condition of sleep.”

A more contemporary definition describes a patient who cannot react with the surrounding environment and cannot be wakened with outside physical or auditory stimulation, which differentiates it from the sleep state.

Levels of consciousness differ proportionally to the level of brain function, which can be determined by various metrics. One such guide is the Glasgow Coma Scale (GCS), which relies upon response to eye opening as well as verbal and motor responses, but GCS doesn’t identify etiology.

Categories of causative pathologies include “cerebral anemia” or interrupted cerebral circulation; mechanical injury (trauma); seizure; stroke, either hemorrhagic, thrombotic or embolic; toxicants or exogenous agents that can be inhaled, ingested or injected; metabolic derangements, such as diabetic coma; and infections–either from the toxemia of pathogens or direct injury.

When responding to coma patients, ruling out potentially lethal and treatable causes of brain insult is critical. Toxicants usually cause systemic and bilateral effects, whereas trauma and stroke tend to cause unilateral signs.

When examining a comatose patient, ask yourself: Is there a unilateral or bilateral involvement of the nervous system? Is there increased intracranial pressure? Are there signs of meningeal irritation? What other non-neurological stigmata, physical findings or clues are present? (Odor, skin color and pupillary findings, for example.) In short, the question of poisoning must be immediately ruled out.

Coma requires aggressive and continuous management, regardless of the etiology, including protection of the airway, rapid identification of offending agent or treatable cause, and control of metabolic processes. From an EMS perspective, a thorough history at the scene is critical. You’re in a unique position to describe the situation, convey the context and report critical background information.

The ED physician was correct to suspect a toxicant as the cause of his patient’s coma, although concern over Ayurvedic herbal remedy overshadowed other potential toxic agents. It’s important to recognize patients are increasingly using herbal products, and the potential exists for drug-herbal interaction or adverse effects from unregulated biologically active nutriceuticals/botanicals.

We must also be alert in identifying “toxidromes”–a cascade of characteristic clinical findings associated with a toxicant or drug class. For example, most have been taught the “red as a beet, hot as a hare, mad as a hatter, dry as a bone” toxidrome mnemonic for anticholinergic toxicity. But some intoxication can be identified readily by context and/or history. For example, recent attendance at a rave is suggestive of ecstasy use.

This patient was subject to several blunders. Did everyone rush to judgment because the patient came from India–a nation associated with exotic diseases, widely available chemical toxicants, and somewhat mysterious Ayurvedic medicines?

It seems the clinicians involved were so concerned over their specialty, the big picture was overlooked, and one of our earliest lessons–look, listen and feel–was ignored.

Ayurvedic medicines, like other categories of herbal products, can pose a health threat. Some contain heavy metals, arsenic or other toxic ingredients. Although it’s important to cast a wide net when obtaining information, it’s just as critical to separate the likely from the unlikely.

The million-dollar workup involving CT, ECG, electroencephalograms and other testing might in fact have been necessary to diagnose the coma patient, but this individual presented with classic signs and symptoms of alcohol-related hepatic encephalopathy.

Alcohol abuse is a worldwide health problem. This patient had an enlarged liver, was jaundiced and had other stigmata of liver disease–telangiectasias, ascites, asterixis and scleral icterus.

Had a good history been obtained, and his family been immediately forthcoming about alcohol abuse, much of the effort focused on identifying something relating to his trip to India–exotic toxicants, herbal remedies, endemic infections, underlying vascular derangements–might have been avoided, leading to more rapid initiation of appropriate therapies.

It’s important to remember the category of etiologies associated with acute alteration in mental status, including coma; these primarily include infections, neurological pathology, toxicants (drugs, poisons) and metabolic derangements. In the elderly, infections are most commonly implicated and appropriate PPE should be donned, but others are also highly likely and must be ruled out rapidly.

When you’re potentially dealing with toxicants, a good history and careful physical examination are essential to guide the diagnosis and optimize medical management. In the end, sometimes the biggest medical mysteries are solved with the simplest tools–the eyes and ears.JEMS

Robin McFee,DO, MPH, FACPM, FAACT, is the medical director of Threat Science and also a toxicologist and professional education coordinator of the Long Island Regional Poison Information Center, Winthrop University Hospital, Mineola, N.Y. She’s also a member of the JEMS editorial board. Contact her at poinsondoc13@hotmail.com.

Thomas R. Caraccio,PharmD, ABAT, is the managing director of the Long Island Regional Poison and Drug Information Center at Winthrop University Hospital. He is also an associate professor of emergency medicine at the State University of New York at Stony Brook and serves as a preceptor for medical, pharmacy and nursing students from St John’s University College of Pharmacy, New York College of Osteopathic Medicine, Philadelphia College of Pharmacy and Sciences, Molloy College and Adelphi University College of Nursing.


1. Young GS. The differential diagnosis of coma. Canadian Medical Association Journal. 1934;31:381—385.

For more on hepatic encephalopathy: visit jems.com/extras

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