Unconscious Museum Worker:
Formulating the Differential Diagnosis

Paul Wax
Department of Emergency Medicine
Rochester School of Medicine
Rochester, NY

January 1998; 1(1): 4

See also - CASE PRESENTATION -  1998; 1(1);3, FURTHER HISTORY & DISCUSSION - 1998; 1(2):16

  This 38 year old suicidal male presented to the ED after apparently ingesting some of the contents of a liquid found in a one pint rum bottle. He may have also ingested or been exposed to some other toxin but the drug screen for many routine drugs was negative.The pertinent history is limited to his history of depression, the discovery of the one pint rum bottle among his possessions, and his employment in a museum. Important aspects of his physical examination include an initial period of lethargy and labile emotions with a slightly decreased temperature (97.3 degrees F), and respiratory rate (14 breaths/minute), and normal pulse (69 beats/minute) and BP (124/80 mm Hg). Pupils, chest, abdominal, and extremity examination were all normal. Cardiac examination revealed a bradycardic rhythm (ECG showed sinus bradycardia with rate of 50 beats/minute and normal intervals).Neurological examination was initially normal except for the lethargy.Fifteen minutes after arrival in the ED the patient rapidly became unresponsive with hypoventilation, necessitating airway control and assisted ventilation. A determination of serum electrolytes was normal except for a low HCO3 of 18 mEq/L and an anion gap of 17 mEq/L. The drug screen was negative for APAP, drugs of abuse, sedative hypnotics and opioids. The ethanol level was 22 mg/dL. In summary it appears that this patient was exposed to some sort of sedating agent, most likely from the bottle, resulting in coma, respiratory depression, and bradycardia.

Without the results of the drug screening in this case, the differential diagnosis would be rather broad. Toxicologic etiologies to consider includes an overdose of sedative hypnotic agents such as barbiturates, chloral hydrate, glutethimide, ethchlorvynol and meprobamate. Oral benzodiazepine overdose by itself does not usually cause significant respiratory depression although combining benzodiazepines with ethanol or other sedative-hypnotics could certainly lead to coma and respiratory depression. Phenothiazines, tricyclic antidepressants and muscle relaxants may also cause CNS sedation, but the concomitant bradycardia is generally not seen with most of these agents. Of course, opioids commonly cause sedation, respiratory depression and bradycardia but their presentation is usually (but not always) associated with miosis. Clonidine, guanfacine, and imidazolines may also cause respiratory depression, bradycardia, and sedation. Anticonvulsants such as carbamazepine, phenytoin, and valproic acid may also cause sedation but the first two agents may cause nystagmus and valproic acid may cause hypotension. Hypoglycemic agents (eg. insulin, sulfonylureas) may also cause coma but their presentation is usually associated with tachycardia, and the normal serum glucose does not support this possible etiology. In this case, the drug screen excludes many but not all of these agents. For instance clonidine is not usually picked up on a routine drug screen. Evidence of clonidine use or medical problems that might be treated with clonidine would be helpful to support clonidine as an etiology (particularly in the absence of the rum bottle). Imidazolines, found in many eye drop preparations, would also not be detected in most drug screens.

Liquids that may cause sedation and respiratory depression include ethanol (but not at such a low level as in this case), isopropanol, methanol and ethylene glycol. The lack of significant anion gap excludes late methanol or ethylene glycol ingestions (unless self treated with ethanol). Early ethylene glycol may cause significant sedation although methanol usually does not. Isopropanol may cause many of these symptoms. The alcohols, however, tend to mix well with water and would not cause the fluid-fluid partition seen in the bottle or radiograph.

The contents of the rum bottle is certainly suspicious for the etiology of the patient's presentation. The photograph of the 16 ounce bottle reveals the presence of a yellowish fluid at the bottom of the bottle which appears to be in 2 separate phases. A radiograph of the bottle suggests that the uppermost part of the bottle accounting for 3/4 of the bottle volume is radiolucent and most likely corresponds to air. The radiopaque bottom 3/4 of the bottle is itself divided into two phases of differing radiodensities corresponding to 2 distinct fluid phases seen on the original picture of the bottle. An immiscible fluid such as a hydrocarbon may form such an interface with air and a hydrophilic fluid.

Halogenated hydrocarbons in particular may be sufficiently radiopaque to appear on radiographs. In fact, the standard contrast media used in radiological studies are iodinated hydrocarbons. The triple layer sign is a description on upright abdominal film of an uppermost air layer, middle hydrocarbon layer and lower gastric fluid level. In this case, the in vitro radiographs of the bottle suggests the lower layer may be another fluid such as water or ethanol. Non halogenated hydrocarbons tend not to be as radiopaque as halogenated hydrocarbons but nevertheless, radiographs may be quite revealing. Patients ingesting non-halogenated hydrocarbons such as kerosene have been found to have a "double bubble" sign on abdominal film suggesting a partitioning of gastric air bubble, kerosene, and gastric contents.

We are told that the patient's employer is a museum although we are not informed what sort of job this entails. Workers at a museum may have access to all sorts of hydrocarbons and solvents. Examples include non halogenated hydrocarbons such as turpentine and halogenated hydrocarbons such as methylene chloride.

This clinical presentation is potentially consistent with a hydrocarbon ingestion along with some ethanol such as rum. Carbon tetrachloride,chloroform, methylene chloride, tetrachloroethylene, trichloroethylene, and trichloroethane are all chlorinated hydrocarbons that may cause CNS and respiratory depression. While halogenated hydrocarbons may cause tachydysrhythmias, especially with catecholamine stress, bradycardia may also occur. Turpentine is a non halogenated hydrocarbon that is particularly well absorbed enterally, and may cause significant CNS depression.

How to Solve the Problem

In order to solve the diagnosis, I would certainly check with the employer and paramedics to find out what chemicals this patient may have used or had access to. I would check for the presence of any unusual odors from the patient or bottle. Chlorinated hydrocarbons often give off a sweetish odor. I would order chest and abdominal radiographs. The presence of a chlorinated hydrocarbon, particularly an agent with a high ratio of the number of chlorine atoms to molecular weight may be quite noticeable on radiographs. The presence of a double bubble sign may suggest a less radiopaque hydrocarbon such as kerosene. A chest radiograph may also evaluate for the presence a pulmonary aspiration, a common complication of hydrocarbon ingestion. Since many of the chlorinated hydrocarbon agents are hepatotoxins, the liver function tests should be obtained and monitored. Methanol, ethylene glycol and isopropanol levels should be obtained. Pulse oximetry and possibly arterial blood gas determination should also be obtained to check for evidence of hypoxemia secondary to aspiration. Analytical detection of halogenated hydrocarbons is not routinely available from clinical laboratories but special reference laboratories may be able to perform a halogenated screen that will qualitatively detect the presence of some of these hydrocarbons.

Since methylene chloride is metabolized, in part, to carbon monoxide, a carboxyhemoglobin level should be obtained. While a normal COHb level does not exclude such exposure an elevated level would be quite suspicious given the history.

Further Management

Recommendations for further management in this case include continuous cardiac monitoring evaluating for possible dysrhythmias. Since many of the chlorinated hydrocarbons are quite toxic, careful gastric aspiration may potentially decrease absorption. Airway protection (as has already occurred in this case) should be in place when the airway can not be protected). The patient should be treated with supportive measures. Frequent blood pressure monitoring should be performed. Significant hypotension may require catecholamine support, but in the presence of chlorinated hydrocarbons, such therapy may precipitate ventricular tachydysrhythmias.

Since carbon tetrachloride as well as some of the other chlorinated hydrocarbons are potent hepatotoxins, empiric treatment with n-acetylcysteine (NAC) should be considered to prevent or limit hepatotoxicity. Given the somewhat similar metabolic activation to a hepatotoxic metabolite of chlorinated hydrocarbons such as carbon tetrachloride and acetaminophen, NAC may provide some benefit.


Daffner RH, Jimenez JP: The double gastric fluid level in kerosene poisoning. Radiology 1973;106:383-384.

Dally S, Garnier R, Bismuth C: Diagnosis of chlorinated hydrocarbon poisoning by x ray examination. Brit J Indust Med 1987:44:424-425.

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January 1998; 1(1): 4

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