WBR1075
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| Author | PageAuthor::Chetan Lokhande |
|---|---|
| Exam Type | ExamType::USMLE Step 3 |
| Main Category | MainCategory::Emergency Room |
| Sub Category | SubCategory::Poisoning |
| Prompt | [[Prompt::A 36 year old man was found unconscious in the alley. The police department brought him to emergency department where he was found to be unresponsive. On eye examinations pupils were dilated and there was a divergent squint. On cardio-vasular examination patient had tachycardia. On neuromuscular exam there is an increased muscle tone, increased reflexes and extensor plantar response. The emergency room nurses found an Amitriptyline prescription in his pocket. The patient was intubated immediately. What is the best next step ?]] |
| Answer A | AnswerA::Lorazepam |
| Answer A Explanation | AnswerAExp::Lorazepam is not given in Tricyclic antidepressant poisoning. There are no indications to prescribe lorazepam in an acute setting except when the patient has uncontrollable and refractory seizures. |
| Answer B | AnswerB::Anti-arrhythmic drugs |
| Answer B Explanation | AnswerBExp::Anti-arrhythmic drugs are not given in Tricyclic antidepressant poisoning. They may be indicated if soda bicarbonate therapy fails. |
| Answer C | AnswerC::Soda bicarbonate |
| Answer C Explanation | AnswerCExp::Soda bicarbonate is the effective treatment for resolving the metabolic acidosis and cardiovascular complications of Tricyclic antidepressant poisoning . |
| Answer D | AnswerD::Activated Charcoal |
| Answer D Explanation | AnswerDExp::Activated charcoal may be the correct answer if Tricyclic antidepressant were ingested within two hrs. Since the time of ingestion is not known it may be futile to start activated charcoal now. |
| Answer E | AnswerE::Potassium |
| Answer E Explanation | AnswerEExp::There are no indications to use Potassium in the treatment of Tricyclic antidepressant poisoning . Potassium doesn't have any cardioprotective functions. |
| Right Answer | RightAnswer::C |
| Explanation | [[Explanation::Most of the toxic effects of TCAs are caused by four major pharmacological effects. TCAs have anticholinergic effects, cause excessive blockade of norepinephrine reuptake at the postganglionic synapse, direct alpha adrenergic blockade, and importantly they block sodium membrane channels with slowing of membrane depolarization, thus having quinidine like effects on the myocardium.Initial treatment of an acute overdose includes gastric decontamination of the patient. This is achieved by administering activated charcoal which adsorbs the drug in the gastrointestinal tract either orally or via a nasogastric tube. Other decontamination methods such as stomach pumps, ipecac induced emesis, or whole bowel irrigation are not recommended in TCA poisoning.Symptomatic patients are usually monitored in an intensive care unit for a minimum of 12 hours, with close attention paid to maintenance of the airways, along with monitoring of blood pressure, arterial pH, and continuous ECG monitoring. Supportive therapy is given if necessary, including respiratory assistance, maintenance of body temperature, and administration of sodium bicarbonate as an antidote. Sodium bicarbonate is given intravenously and it has been shown to be an effective treatment for resolving the metabolic acidosis and cardiovascular complications of TCA poisoning. If sodium bicarbonate therapy fails to improve cardiac symptoms, conventional antidysrhythmic drugs such as phenytoin and magnesium can be used to reverse any cardiac abnormalities. However, no benefit has been shown from lidocaine or other class 1a and 1c antiarrhythmic drugs; it appears they worsen the sodium channel blockade, slow conduction velocity, and depress contractility and should be avoided in TCA poisoning.Hypotension is initially treated with fluids along with bicarbonate to reverse metabolic acidosis (if present), if the patient remains hypotensive despite fluids then further measures such as the administration of epinephrine, norepinephrine, or dopamine can be used to increase blood pressure.[1] Another potentially severe symptom is seizures; often seizures resolve without treatment but administration of a benzodiazepine or other anticonvulsive may be required for persistent muscular overactivity. There is no role for physostigmine in the treatment of tricyclic toxicity as it may increase cardiac toxicity and cause seizures.Tricyclic antidepressants are highly protein bound and have a large volume of distribution; therefore removal of these compounds from the blood with hemodialysis, hemoperfusion or other techniques are unlikely to be of any significant benefit.
TCAs are protein bound and become less bound in more acidic conditions, so by reversing the acidosis, protein binding increases and bioavailability thus decreases – the sodium load may also help to reverse the Na+ channel blocking effects of the TCA). |
| Approved | Approved::Yes |
| Keyword | WBRKeyword::Tricyclic antidepressant, WBRKeyword::Poisoning, WBRKeyword::Soda bicarbonate |
| Linked Question | Linked:: |
| Order in Linked Questions | LinkedOrder:: |