Alcohol and Alcoholism Advance Access originally published online on August 1, 2008
Alcohol and Alcoholism 2008 43(6):650-652; doi:10.1093/alcalc/agn063
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Ethanol Poisoning Together with Organophosphate Exposure: A Difficult Clinical Diagnosis Because of Physician Anchoring
The Emergency Department, Peking Union Medical College Hospital, Beijing, China
* Corresponding author: The Emergency Department, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Tsinghua University, Beijing 100730, China. Tel.: +86-13693-109826; Fax: +86-10652-95301; E-mail: billliyi{at}yahoo.com
Received 18 March 2008; first review notified 12 June 2008; in revised form 26 June 2008; accepted 4 July 2008; advance access publication 1 August 2008
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ABSTRACT |
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Aims: Organophosphorus pesticide poisoning occurs frequently in China and can be diagnosed easily based on the history of ingestion and the cholinergic toxic syndrome. Yet, when combined with other toxins, organophosphorus poisoning may appear different. Methods: Here, we present a case of acute ethanol poisoning together with a dermal organophosphorus exposure. Results: Based on the history and a misinterpretation of the physical examination, the patient was treated as an organophosphorus poisoning. Ultimately, serum analysis helped clarify the diagnosis. Conclusions: Toxicologist should be aware of the error known as anchoring and take appropriate precautions to limit its occurrence.
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Introduction |
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Organophosphorus pesticide (OP) poisoning is the most common form of pesticide poisoning in China (The Disease Prevention and Control Bureau of the Chinese Ministry of Health, 2007
) and is one of the leading causes of death from poisoning worldwide (Eddleston, 2000). When the history of ingestion is considered along with the clinical findings of the cholinergic toxic syndrome, OP poisoning is easily diagnosed. The core issue for an optimal patient outcome is the early use of atropine combined with good supportive therapy (Eddleston et al., 2004). Confirming the actual diagnosis rarely affects outcome. However, when OP poisoning presents together with other kinds of poisoning, laboratory confirmation of the diagnosis may be necessary in order to provide optimal patient care. |
Case Report |
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A 43-year-old man was brought to the emergency room (ER) by his family (3 a.m.), due to alcohol overdose for 1 h and unconsciousness for 30 min.
The patient had been seen drinking 500 mL of Chinese white spirit (Chinese vodka) about 1 h before. Thirty minutes later, he was found unconscious, with an empty chlorpyrifos (a typical OP used in China) bottle beside him. He was brought to our ER by an ambulance.
His past medical history was negative except for alcohol abuse. Physical examination was notable for the following: temperature 36.3°C, pulse 102 beats/min, respiration 24 breathes/min, blood pressure 132/79 mmHg, pulse oximetry 100% with 2 L/min nasal oxygen. In general, he was agitated, had a GCS of 6 (E1M3V2), had an odour of garlic and no smell of alcohol; his skin and axillae were dry and there were no signs of injection drug use or cyanosis. Pupils were 3 mm in diameter and reactive to light. Other findings were: chest: normal, no rales; cardiovascular: tachycardia, otherwise normal; abdomen: normally active bowel sounds; extremities: normal; genitourinary: bladder not palpable.
Electrocardiography showed sinus tachycardia. A serum screen including ethanol and organophosphates was sent to the laboratory.
Initial laboratory findings were: leukocytes: 7.35 x 109/L, haemoglobin: 147 g/L, platelet 296 x 109/L; liver function test: normal. The results of the renal function test were: sodium 140 mmol/L, chloride 110 mmol/L, potassium 3.4 mmol/L, calcium 1.99 mmol/L, CO2 23.5 mmol/L, glucose 8 mmol/L, blood urea nitrogen 13 mg/dL, creatinine 0.7 mg/dL and others normal.
Initially, the treating physicians were puzzled about the cause of coma. Specifically, it was unclear if the clinical findings were likely caused by ethanol or OP poisoning or both.
Because of the patient's coma, endotracheal intubation was performed and mechanical ventilation was given. Fluids were infused accompanied by atropine 2 mg/h and pralidoxime 0.5 mg/h. Immediately after the above treatments, gastric lavage was performed with warm tap water, the patient's clothes were removed and his skin was cleaned with water. The total lavage was about 5 litres. It was yellow at the beginning, and then clear. No smell of OP or ethanol was noted.
Arterial blood-gas analysis was performed after the lavage (while the patient was on mechanical ventilation with a FiO2 of 50% oxygen): pH 7.344, PaCO2 37.5 mmHg, PaO2 378 mmHg, carboxyhaemoglobin 1.0%, glucose 8.2 mmol/L, lactate 45 mg/ dL, total bilirubin 67 µmol/L, base excess –4.8 mmol/L and anion gap 14 mmol/L.
Five and a half hours after admission (8:30 a.m.) repeat vital signs were: blood pressure 124/89 mmHg, pulse rate 115 beats/min, respiratory rate 20 breaths/min, SpO2 100% (ventilation). Sedation with benzodiazepines was required to maintain intubation. Skin and axillae remained dry. Pupils were 4 mm in diameter and reactive to light. No cyanosis was found. No rales were heard on examination of the lungs. Other findings were: cardiovascular: tachycardia, otherwise normal; abdomen: normally active bowel sounds; extremities: normal; arterial blood gas: pH 7.34, PaCO2 37 mmHg, PaO2 141 mmHg, base excess –5.2 mmol/L.
Though there are no cholinergic features all the time, the clinical impression that the main reason for the patient's coma was OP poisoning was kept on. The plan was to continue the therapy with atropine, gastric lavage, active charcoal and cathartic. Eight hours after admission (11 a.m.), charcoal haemoperfusion was done for 4 h. Sixteen hours after admission (7 p.m.), the initial cholinesterase enzyme activity was reported as within the normal range and a qualitative serum toxicology screen failed to detect any pesticide (including the OP), tricycle antidepressant, acetaminophen or salicylate. However, the ethanol concentration was extremely high at 4.1 g/L. Once this information was obtained, atropine, pralidoxime and benzodiazepine therapies were all stopped.
The patient was given the final diagnosis of acute ethanol poisoning (oral exposure) and a non-toxic dermal exposure to an organophosphate. Nineteen and a half hours after admission (10:30 p.m.) he awoke, and the endotracheal tube, gastric tube and central venous line were removed. Vital signs were: BP 110/80 mmHg, pulse 109 beats/min, respiratory rate 33 breaths/min, temperature 37.8°C, SpO2 96% in room air.
The patient was discharged the next day. At that time we had been told that he had emptied the OP bottle on his skin only to scare his relatives, but never ingested the OP.
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Discussion |
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Despite the common presentations of OP poisoning and ethanol poisoning in our ER, this is the first case that we are aware of where acute ethanol poisoning was misinterpreted as organophosphate poisoning because of circumstantial evidence.
The wrong diagnosis was made based only on the pesticide smell and the empty bottle beside, while not enough data were integrated with the findings in the physical examination. The core issue for the wrong diagnosis was the failure to appreciate the confirmation for the cholinergic toxic syndrome with its classic physical findings. Unfortunately, the physician had insisted that the primary diagnosis was OP poisoning, so there was no toxic differential diagnosis for this patient. In this circumstance, treatment with atropine that was potentially harmful was initiated. Fortunately, the last and the only thing that made a difference was the laboratory.
This type of error is called ‘anchoring’. Anchoring is the tendency of an individual to retain an early hypothesis, despite obtaining subsequent information that is inconsistent with those initial conclusions. Anchoring is different from premature closure. Premature closure is closure leading to the acceptance of a diagnosis, and thus to the conclusion that no further consideration is required. Anchoring is more severe than premature closure because it is deaf and blind to the new information, which wastes the medical resources (Kassirer and Kopelman, 1989). Anchoring has no relationship with medical knowledge and background, and in fact it seems to happen more frequently in the senior doctors (Kuhn, 2002; Sutherland, 2002).
In emergency situations, it may be impossible to obtain an accurate history or any history because the patient is often too ill to accurately communicate, or too unstable to give any information or they may hide the history intentionally (Sutherland, 2002). Patients who intent to commit suicide or smuggle drugs may have an even higher tendency to behave this way. The lesson to be learned from our case is that clinicians should not entirely rely on the history in order to establish the correct diagnosis.
The best method we think of to avoid anchoring may be the process of data collection and integration process and should be performed rigorously regardless of how familiar the clinician is with the presumed disease process.
This case also teaches us that the failure to detect the odour of ethanol on the patient cannot be used to exclude the ethanol poisoning. The presence or absence of an odour of ethanol in the breath is an unreliable means of ascertaining whether a person is intoxicated or whether ethanol was recently consumed (Moskowitz et al., 1999). Likewise, when patients with a typical OP pesticide smell lack signs of the cholinergic toxic syndrome, the smell may arise from dermal exposure. Clinical toxicity from dermal exposure typically develops more slowly than that following oral exposure and less frequently results in a coma and respiratory depression. It is usually associated with gastrointestinal discomfort, skin numbness and dizziness (Wang, 2007; Yu and Yu, 2006), so it is easy to be misdiagnosed as gastroenteritis, heat exhaustion, hypoglycaemia or neurosis.
For poisoned patients we suggest that the four stages described above are essential for every clinical diagnosis. First, when the patient arrives, collect the information about history, obtain the vital signs and perform a simple physical examination. Then diagnose one or more toxic causes for the patient. Follow with a more detailed physical examination, thinking about the hypotheses again. When there are data that are contradictory or not completely congruent with the history and physical examination, more attention should be paid on the diagnosis. Try to make a diagnosis at this stage because most can be made at this time. Third, when there are inconsistencies in the clinical or historical data, attempt should be made to obtain some special laboratory tests (in our case for example the plasma cholinesterase enzyme and the toxin screen should have been done earlier) to confirm the diagnosis. Finally, verify the diagnosis or modify it based on all the data at hand.
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Conclusion |
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A case of acute ethanol poisoning that was misinterpreted as organophosphate poisoning was presented. Patients who are unconscious without any signs of the cholinergic syndrome are unlikely to be poisoned by OP pesticides. It should remind the readers that the diagnosis of poisoned patients cannot be made solely based on the history. Careful serial observations of poisoned patients once adequate resuscitation has been done are useful for the right diagnosis. Toxicologist should be aware of the error known as anchoring and take appropriate precautions to limit its occurrence.
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ACKNOWLEDGEMENTS |
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We thank Robert S. Hoffman, MD, in New York City Poison Control Center for polishing of this manuscript.
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References |
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TOPABSTRACTIntroductionCase ReportDiscussionConclusionReferences |
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Eddleston M. Patterns and problems of deliberate self-poisoning in the developing world. QJM (2000) 93:715–31.
Eddleston M, Dawson A, Karalliedde L, et al. Early management after self-poisoning with an organophosphorus or carbamate pesticide—a treatment protocol for junior doctors. Crit Care (2004) 8:R391–7.[CrossRef][Web of Science][Medline]
Kassirer JP, Kopelman RI. Cognitive errors in diagnosis: instantiation, classification, and consequences. Am J Med (1989) 86:433–41.[CrossRef][Web of Science][Medline]
Kuhn GJ. Diagnostic Errors. Acad Emerg Med (2002) 9:740–50.[CrossRef][Web of Science][Medline]
Moskowitz H, Burns M, Ferguson S. Police officers’ detection of breath odors from alcohol ingestion. Accid Anal Prev (1999) 31:175–80.[CrossRef][Web of Science][Medline]
Sutherland DC. Improving medical diagnoses by understanding how they are made. Intern Med J (2002) 32:277–80.[CrossRef][Web of Science][Medline]
The Disease Prevention and Control Bureau of the Chinese Ministry of Health. Statistic Center of Chinese Ministry of Health, National Centre of Disease Control in China. Poisoning. In: The Injury Prevention Report (2007) Beijing: People's Hygiene Publication House. 34–6. in Chinese.
Wang XK. Analysis of 7 misdiagnosed acute organophosphate cases. Community Med Mag (2007) 5:41. in Chinese.
Yu GP, Yu JM. Analysis of 22 misdiagnosed organophophate cases. Mod J Integr Tradit Chin West Med (2006) 15:1520. in Chinese.
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