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Course # 34442 • Caring for the Poisoned Patient

CASE STUDY 1

Patient A, a girl 14 years of age, is brought to a local emergency department by her parents at 9 p.m. The parents state that 45 minutes prior to arriving they found the patient in her room. She was very upset and stated that she had just taken "a whole bottle of pills." The parents are able to account for their daughter's actions and location since she returned from school at 3 p.m., and they state that during that time she had been awake, alert, and acting normally. She had been alone for only 5 to 10 minutes. The father found an empty bottle of acetaminophen 500-mg tablets in the patient's room. The bottle contained 60 tablets when it was purchased, but neither parent can remember how many tablets were in the bottle before the exposure. They estimate that it might have been half full.

Patient A is awake, alert, and oriented to time, place, and person. Her speech is clear. Her vital signs are: temperature 98.3°F; pulse 80 beats per minute and regular; respiratory rate 16 breaths per minute; and blood pressure 112/60 mm Hg. Her skin is warm and dry, and no cyanosis is noted. Her pupils are 5 mm in diameter, and they are equal in size and normally reactive to light. Her chest is clear to auscultation, and her heart tones are normal. She has a normal gag reflex and bowel signs, and her bladder is not distended. She weighs 55 kg. Patient A has a past medical history of bipolar disorder, for which she takes lithium carbonate 300 mg, once in the morning and once in the evening; her last dose was at 9 a.m. today. The medication is given to the patient by the parents, and they are sure that she did not and could not have access to it. The patient has no other medical problems and takes no other medications. Neither parent takes any prescription medications. They state that the only other medication in the house is antacid tablets.

Patient A's ABCs are normal, and this is to be expected. Acetaminophen causes delayed onset liver and (occasionally) kidney damage, typically about 24 hours after ingestion. If a patient had taken a massive overdose of acetaminophen, other organ systems could be affected and there would be changes in the ABCs. However, these cases are rare, and even then, it takes time for toxicity to develop. A dose of acetaminophen greater than 7.5 g or 150 mg/kg is considered potentially toxic. It is estimated that Patient A may have taken 15 g or 272 mg/kg. This is a large dose and potentially toxic, but she has presented to the emergency department soon after the ingestion. As such, the dose does not put her at risk for serious derangements of the ABCs. If the ABCs were abnormal, an exposure to another drug or toxin would need to be strongly considered. There is no indication that dextrose, oxygen, naloxone, or thiamine is needed.

It appears that the patient ingested only acetaminophen, had no access to any other medications, and the history seems accurate and reliable. The patient takes lithium carbonate, and it is very unlikely that an overdose of this medication was ingested. However, the possibility should be kept in mind. The patient does not have any signs or symptoms of a toxidrome, and the physical exam is normal.

As a part of the treatment plan, gastric decontamination is considered. The patient is awake and alert, has a normal gag reflex, and has a normally functioning gastrointestinal tract. It is very unlikely that Patient A's mental status or ability to maintain her airway will deteriorate. There are no contraindications to the use of activated charcoal and it binds very well to acetaminophen, so activated charcoal would be the gastric decontamination technique to use. Syrup of ipecac should never be used, lavage is reserved for patients who have ingested a life-threatening amount of a dangerous drug and/or drug for which there is no effective antidote, and whole bowel irrigation is reserved for drugs that are not adsorbed by activated charcoal or sustained-release preparations. One dose of plain charcoal should be given. Most activated charcoal is available in 50 g doses.

NAC is a highly effective antidote for acetaminophen poisoning. It is commonly available, easy to administer, and relatively safe. It can be given any time within eight hours of an acetaminophen overdose and be equally effective; after eight hours, the effectiveness begins to decrease. Patient A may need NAC depending on the amount of drug she took. However, the time of ingestion in this case is known and within eight hours of arrival, so there is no need to give NAC immediately. NAC should be used for acetaminophen poisoning if the patient has ingested a toxic dose, there is evidence of liver damage, or the serum acetaminophen level is toxic. In this case, the dose is unknown, and it is too early to see signs, symptoms, or laboratory evidence of liver damage, so the decision of whether or not to use NAC will depend on the serum acetaminophen level. Hospital laboratories can usually perform and report the results of serum acetaminophen level test within one hour of receiving the blood sample.

It is clear a serum acetaminophen level should be obtained, but it must be done four hours or later after the ingestion. If the level is measured sooner, it cannot be reliably interpreted. Interpreting the level as toxic or nontoxic on the basis of the numerical value alone could lead to treatment errors. The level and associated risk for hepatotoxicity should be interpreted using the Rumack-Matthew nomogram. Serum hepatic transaminases, BUN, and serum creatinine should also be obtained. Although it is unlikely the patient had access to her lithium, it would be prudent to check a lithium level as well. There is no need for other laboratory tests, an ECG, or imaging studies.

In some cases, a serum aspirin level should be checked. It is not unusual for patients to use the terms acetaminophen and aspirin interchangeably. However, because of the particulars of this case study, an aspirin level would not be needed.

When an overdose of acetaminophen is taken, the two primary metabolic pathways for the drug become saturated and a third pathway is used. This metabolic pathway produces large amounts of a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI), and it is this metabolite that causes liver and kidney damage. Manipulating the pH of the urine or serum would not affect acetaminophen metabolism or the production of NAPQI, so these techniques are not used. Acetaminophen can be quickly and easily removed with hemodialysis, but hemodialysis has risks. Because there is a highly effective antidote available, hemodialysis or any other type of extracorporeal removal would not be needed.

At this point, care of Patient A focuses on monitoring vital signs, arranging a consultation with a mental health professional, maintaining patient safety, and treating with NAC if her acetaminophen level is greater than 150 mcg/mL.

CASE STUDY 2

Patient B, a man 56 years of age, is brought to the emergency department at 4:30 p.m. His wife called EMS because the patient had reportedly taken an overdose of his prescription medications. According to the EMS personnel, the ingestion was unwitnessed; Patient B had told the wife that he wanted to die and that some time that morning he had "taken all of his pills." The exact time of ingestion is not known, but a reasonable estimate is 10 a.m. The EMS personnel report that they found empty bottles of bupropion, metoprolol, and verapamil (all three sustained-release formulations), and the patient's name was on the bottles. The patient told EMS that he had been drinking vodka and when that ran out, he drank some antifreeze. The EMS personnel did not find any bottles of antifreeze. He has a past history of chronic alcohol abuse, depression, and hypertension.

Patient B is awake and alert, but drowsy. His vital signs are: temperature 97.8°F; pulse 44 beats per minute; respiratory rate 16 breaths per minute; and blood pressure 82/38 mm Hg. The cardiac monitor shows sinus bradycardia. His oxygen saturation is 93%, and his bedside serum glucose level is 148 mg/dL. His nail beds are cyanotic, there is no peripheral edema, and his skin is cool and clammy. His pupils are 5 mm and reactive, his lungs are clear, and his heart tones are normal. His abdomen is soft and nontender, and there is no bladder distention.

The most immediate need in this situation is to stabilize the ABCs. Supplemental oxygen is applied, and IV access is obtained. It is reasonable to assume that the bradycardia and hypotension are being caused by the metoprolol and verapamil. Atropine, fluids, and vasopressors are seldom effective for the cardiovascular toxicity caused by beta blockers and calcium channel blockers. Those drugs can be tried, but if they do not quickly reverse the bradycardia and hypotension, additional treatment should not be delayed. For Patient B, antidotal care is a top priority. Antidotal care may also be needed to treat ethylene glycol poisoning.

The physician administers 10% calcium chloride 10 mL IV over 5 minutes. The dose can be repeated every 10 to 20 minutes, or a continuous infusion can be used. Concurrently, an IV bolus dose of glucagon is given, 5 mg over five minutes. This can be followed (if needed) with a continuous IV infusion at 1–5 mg/hour. If these are unsuccessful, a dextrose-insulin infusion and cardiac pacing are the next steps. Give a bolus dose of regular insulin, 1 Unit/kg, followed by a continuous infusion of regular insulin at 1–10 Units/kg/hour. As the insulin is being given, the patient should receive an IV bolus of 25 g of 50% dextrose. Additional glucose should be given to maintain the serum glucose level of 100–200 mg/dL. Consider giving fomepizole. Antifreeze almost always contains ethylene glycol, but many hospital laboratories are not prepared to measure ethylene glycol levels. If a level cannot be obtained, the decision to use fomepizole will depend on how likely it is the patient ingested ethylene glycol, the patient's arterial blood gases, and if the patient has a large anion gap and/or a large osmolar gap. The risks of fomepizole are slight, and the benefit can be enormous.

Patient B's serum glucose is normal, so he does not require dextrose. Supplemental oxygen is started immediately. He does not have signs or symptoms of an opioid poisoning, so naloxone is not appropriate. Although he chronically abuses alcohol, the patient has no signs of Wernicke-Korsakoff syndrome, so thiamine should not be given.

The circumstances of the overdose are not very clear, but if Patient B did take the medications and the antifreeze, there is a substantial risk for serious morbidity and death. The time of ingestion is not known with certainty, but it appears that it happened approximately 6.5 hours prior to arrival. Given the patient's clinical condition and the empty bottles of metoprolol and verapamil, it seems reasonable to assume that he took an overdose of these medications and took an intoxicant that can cause CNS depression—in this case, ethanol and/or ethylene glycol.

Upon physical examination there is no evidence of a toxidrome, as would be expected. Because the patient has ingested a beta blocker, a calcium channel blocker, ethanol, and a toxic alcohol, the patient should be assessed for signs and symptoms of circulatory compromise, respiratory depression, intoxication, and metabolic acidosis. Circulatory compromise is evident. The patient is drowsy, and this may be due to the bupropion, the ethanol, the ethylene glycol, or a combination of the three. There is no respiratory depression, so Patient B may not have ingested sufficient quantities of the alcohols for this to develop. There are no signs of metabolic acidosis, but this could develop in the next few hours. Laboratory confirmation is needed to detect and confirm an acid-base disturbance. If acidosis is present, it could, in part, explain the CNS depression.

Gastric decontamination should not be performed for Patient B. Although the patient has ingested medications and a toxin that can be very dangerous, it has been more than one hour since the ingestion. Also, it could cause the patient's CNS depression to worsen. Any method of gastric decontamination would put the patient at risk for aspiration and/or worsening of his cardiac status and would probably not be useful.

Measurement of Patient B's serum acetaminophen level, serum ethanol level, and serum ethylene glycol level should be attempted. Blood levels of bupropion, metoprolol, and verapamil can be done, but they cannot be obtained immediately and would not be useful in caring for the patient. Obtain electrolytes to look for an anion gap, assess arterial blood gases to check for an acid-base disturbance, and request a serum osmolarity to look for an osmolar gap. A 12-lead ECG should be done, and the patient should be on continuous cardiac monitoring. Urinalysis should also be ordered. Ethylene glycol metabolism produces oxalate crystals in the urine, which could help confirm the diagnosis.

Bupropion, metoprolol, and verapamil cannot be removed by dialysis or hemoperfusion nor can their elimination be enhanced by manipulating the pH of the urine. However, hemodialysis is very effective at removing ethylene glycol and the toxic aids produced by ethylene glycol metabolism. A nephrologist should be notified of the possible need for hemodialysis.

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