Unconscious Museum Worker:
Formulating the Differential Diagnosis
Department of Emergency Medicine
Rochester School of Medicine
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
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.
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
Dally S, Garnier R, Bismuth C: Diagnosis of chlorinated hydrocarbon poisoning by x ray
examination. Brit J Indust Med 1987:44:424-425.
Readers are encouraged to send their comments and diagnoses to email@example.com. Please refer to the case by number and
try to keep comment to under 100 words. Readers opinions will be anonymously tabulated and
published along with a discussion in the next issue of IJMT.
If you have a case you would like to submit, please send the clinical information and
the appropriated image (photograph, x-ray, or ECG) to: 777 E. Park Drive, P.O. Box 8820,
Harrisburg, PA 17105-8820. Images (as tif,gif, jpg files) and clinical information may be
sent by e-mail to firstname.lastname@example.org. If the image shows
an actual patient or part of a patient's body, please include a cover letter indicating
that the paitent has given you permission to take and use their photograph.
January 1998; 1(1): 4
This article is located at http://www.ijmt.net/ijmt/1_1/1_1_4.html
IJMT Home | Current Issue | Past Issues | Search | Technical Support | Send Comments to ACMTNet
Copyright 1999-2003, American College of Medical Toxicology.