Four Steps to Diagnosing Drug Overdose Bedside Basics Can Help You Determine What Was Ingested in Order to Quickly Stabilize the Patient
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Four Steps to Diagnosing Drug Overdose Bedside basics can help you determine what was ingested in order to quickly stabilize the patient. By Scott Goldstein, DO he morning starts as usual, with three testing that should be undertaken to narrow down patients to see: a 46-year-old with chest the possible toxins and ensure that a life-threatening pain, a 25-year-old with back pain, and overdose is not about to go untreated. Those phases a 27-year-old schizophrenic brought in are the subject of this article. Tby friends who believe he may have overdosed but aren’t sure what drug he might have taken. FIRST: TEST BLOOD GLUCOSE One of the many challenges faced by today’s emer- If there is any change in mental status, the first test gency departments is a rising incidence of overdoses, should be a blood glucose level. This is one of the few both intentional and accidental, in the population times in current medicine when you can treat someone as a whole but especially in schizophrenic patients.1 and see a therapeutic change within seconds—possibly Fortunately, there is a way to pursue the suspicion of avoiding intubation, unnecessary imaging, and days in overdose that’s thorough enough to pick up any life- the ICU. If a patient is obtunded, and the glucose is threatening ingestions but efficient enough to save low, an ampule of dextrose should fix the problem. both practitioner and patient time in the emergency Many drugs and substances can lower blood glu- department. The predictable actions of drugs on the cose—most obviously, the antidiabetic medications, body fall into six broad classifications—anticholin- such as biguanides and sulfonylureas, which have be- ergic, cholinergic, hallucinogenic, opiate/narcotic, come ubiquitous as more and more people develop sedative/hypnotic, and sympathomimetic—called diabetes and live longer with the condition. Not only toxidromes (Table).2 Temperature, heart rate, re- can patients overdose on their spiratory rate, pulse oximetry, and blood pressure own diabetic medications, but >>FAST TRACK<< are all clues to a specific toxidrome. Most toxicities their family members may Almost all toxidromes from overdosing either an illicit or a prescribed drug also be at risk. use the vital signs in can be treated symptomatically under the general Alcohol, so often used and evaluating what the guidance of the toxidromes. The caveat is that the abused as self-medication by patient may have picture may be clouded by multiple offending agents individuals with psychiatric ingested. that bring different toxidromes into play if the pa- diagnoses, causes hypoglyce- tient has taken drugs from more than one class. mia by dysregulating pancreatic control of insulin The physician’s first task, of course, is to ana- release and decreasing glucose production by lyze the patient’s vital signs for insight into how the the liver. body is reacting to whatever pathological process is Hypoglycemia has been associated with acetamin- happening. Almost all toxidromes use the vital signs ophen overdose in a few cases, possibly secondary to in evaluating what the patient may have ingested. liver failure.3 Once that has been done, there are four phases of SECOND: GET AN ECG Dr. Goldstein is an assistant professor of emergency medicine at Penn State Hershey Medical Center in Like the blood glucose level, the ECG is easily ob- Hershey, Pennsylvania. tainable, readily available, and full of valuable infor- www.emedmag.com APRIL 2009 | EMERGENCY MEDICINE 17 DRUG OVERDOSE TABLE. Toxidromes as a Diagnostic Guide in Suspected Overdose Toxidrome Signs and symptoms Vital sign Classic agents anticholinergic delirium, flushed skin, tachycardia atropine dilated pupils, urinary hyperthermia antihistamines retention, decreased bowel hypertension scopolamine sounds, memory loss, tricyclic seizures antidepressants (mnemonic: “hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter”) cholinergic confusion, weakness, bradycardia organophosphates salivation, lacrimation, hypothermia carbamates urination, defecation, tachypnea gastrointestinal motility, emesis, diaphoresis, muscle fasciculations, miosis, seizures, “Killer Bs”: bradycardia, bronchorrhea, bronchospasm hallucinogenic disorientation, tachycardia phencyclidine hallucinations, visual tachypnea lysergic acid illusions, panic reaction, hypertension diethylamide moist skin, hyperactive cannabis bowel sounds, seizures opiate/narcotic altered mental status, bradypnea dextromethorphan unresponsiveness, bradycardia opiates: miosis, shock, hypothermia morphine decreased respiration hypotension propoxyphene sedative/hypnotic coma, stupor, confusion, apnea ethanol sedation, CNS barbiturates dsyfunction benzodiazepines anticonvulsants sympathomimetic delusions, paranoia, tachycardia cocaine diaphoresis, piloerection, hypertension amphetamines mydriasis, hyperreflexia, hyperthermia methamphetamine seizures, anxiety phenylpropanolamine ephedrine pseudoephedrine Source: Florida Poison Information Center, Jacksonville.2 mation for the treating physician about what drug One of the main things to watch for is possible or drugs may have been taken. Keep in mind the overdose with a tricyclic antidepressant (TCA). normal heart rate (60 to 100 bpm), the normal QTc These drugs have a notoriously narrow therapeu- (less than 0.45 s for men or 0.42 s for women) and tic window and a dangerous potential for severe the normal QRS (less than 0.12 s). neurologic and cardiovascular toxicity, including 18 EMERGENCY MEDICINE | APRIL 2009 www.emedmag.com DRUG OVERDOSE life-threatening arrhythmias.4 The ECG can help do not cause hypoglycemia. In contrast, bradycar- with ruling TCA toxicity in or out and formulating dia with hyperglycemia may signal an overdose of a treatment plan. the calcium blocker nifedipine. All the information The most common ECG finding in a TCA gathered needs to be used together to formulate a overdose is sinus tachycardia. If you see evidence of safe and effective plan. tachycardia and the suspicion for TCA overdose is high, look for additional ECG clues to the use of a THIRD: CHECK THE ACETAMINOPHEN LEVEL TCA, such as a strong rightward axis or terminal R The acetaminophen level is not as easy to obtain as wave in aVR. The latter finding is very sensitive for the bedside glucose or ECG, but it’s very important TCA overdose and signals an urgent need for treat- because acetaminophen can be a silent killer—there ment, because it means that the drug has already is no toxidrome with acute ingestion. It is ubiqui- affected the cardiac electrical system. Recent studies tous in today’s society and should be considered in show that if the terminal R wave is greater than 3 all intentional overdoses; liberal testing for it will mm, there is a higher risk of seizures.4,5 help save many lives at modest cost.8 When it is not The QRS is another important place to look for picked up and treated early, acetaminophen toxicity electrocardiographic clues to a TCA overdose. Nor- takes a protracted, painful, and deadly course. mal QRS is defined for general purposes as less than Even though there are no telltale signs, there 0.12 s, but if TCA overdose is a concern, the thresh- are “phases” in acetaminophen overdose. The first old drops to 0.10 s. Numerous studies have shown phase consists of gastrointestinal upset with nausea that the risks of arrhythmia and seizure increase as the and vomiting, usually in the first 24 hours. This is QRS increases, and markedly so once it exceeds 0.16 the most important phase to consider, since most s, which occurs in about 50% of patients who have a overdoses and medical clearance cases come to the wide QRS associated with TCA overdose.6,7 ED within this time frame.9 The subsequent phases Any of the above abnormalities in a patient sus- correlate with liver injury, spanning from right up- pected of TCA overdose warrants treatment with per quadrant pain to jaundice, vomiting, and frank sodium bicarbonate and admission to the ICU. liver failure. Clues to the presence of many potentially deadly Always keep the time frame in mind. Acetamino- cardiac medications can be picked up on the ECG, phen has a half-life of four hours; after a toxic in- mostly by looking at the rate. The two most common gestion the level usually peaks at four hours.3 When are beta-blockers and calcium channel blockers—it’s there is concern for acute acetaminophen toxicity, hard to go through a shift without seeing a patient the level does not need to be tested until four hours on either of these medications. Both slow the heart have passed since ingestion, but treatment can begin rate, leading to bradycardia, first-degree heart block immediately. If you suspect a chronic overdose span- and prolonged QT interval. These similarities make ning days to weeks, check it difficult to discern which type of drug is causing the the acetaminophen level >>FAST TRACK<< changes, but the combination of hypotension with and liver functions and in- Normal QRS is defined bradycardia and conduction abnormalities should stitute treatment, if neces- for general purposes as always raise suspicion for cardiotropic drug over- sary, as soon as possible. If less than 0.12 s, but if TCA dose. The patient likely needs emergent treatment you are certain the inges- overdose is a concern, with either calcium (for hyperkalemia or calcium- tion is acute, you can plot the threshold drops channel overdose) or glucagon (for beta-blocker the level against the Ru- to 0.10 s. overdose). However, if the agent is unknown, it is