Complications in Anesthesia Practice Questions

Q: Which of the following is the most common initial manifestation of malignant hyperthermia?

Increased PETCO2. **Explanation:** **Malignant Hyperthermia (MH)** is a pharmacogenetic hypermetabolic state triggered by volatile anesthetics (e.g., Halothane, Sevoflurane) or succinylcholine. It involves an uncontrolled release of calcium from the sarcoplasmic reticulum via defective **ryanodine receptors (RYR1)**. 1. **Why Increased PETCO2 is Correct:** The hallmark of MH is a massive increase in metabolic rate. The earliest and most sensitive sign of this hypermetabolism is a **rapid, unexplained rise in End-Tidal Carbon Dioxide (PETCO2)**, which often persists despite increasing minute ventilation. This occurs long before the body temperature rises. 2. **Why Other Options are Incorrect:** * **Hyperkalemia (A):** While hyperkalemia occurs due to rhabdomyolysis and cell membrane instability, it is a secondary consequence and usually follows the initial metabolic surge. * **Increased distal esophageal temperature (B):** Despite the name, **hyperthermia is a late sign** of MH. While the distal esophagus is the preferred site for core temperature monitoring, it is not the earliest indicator. * **Red discoloration of urine (D):** This is due to **myoglobinuria** resulting from muscle necrosis (rhabdomyolysis). This is a late complication and indicates significant muscle damage. **Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increased PETCO2 (Hypercarbia). * **Earliest Physical Sign:** Masseter Muscle Rigidity (MMR) / Trismus (especially after Succinylcholine). * **Drug of Choice:** **Dantrolene** (Mechanism: Binds to RYR1 receptors to inhibit calcium release). * **Safe Agents:** Nitrous oxide, Propofol, Etomidate, Ketamine, and all Local Anesthetics. * **Gold Standard Test:** Caffeine Halothane Contracture Test (CHCT) on a muscle biopsy.

Q: Post-anesthetic myalgia is commonest with which of the following drugs?

Suxamethonium. **Explanation:** **Suxamethonium (Succinylcholine)** is the correct answer because it is a **depolarizing neuromuscular blocker**. Its mechanism of action involves binding to nicotinic acetylcholine receptors, causing prolonged depolarization of the motor endplate. This results in disorganized muscle fiber contractions known as **fasciculations** before the onset of flaccid paralysis. These intense fasciculations lead to micro-trauma of muscle fibers and the release of lactic acid, resulting in **post-anesthetic myalgia**. This pain typically occurs 24–48 hours postoperatively, most commonly in the neck, shoulders, and abdominal muscles. It is more frequent in young adults undergoing minor ambulatory surgery. **Why the other options are incorrect:** * **Pancuronium, Vecuronium, and Atracurium:** These are all **non-depolarizing neuromuscular blockers**. They act as competitive antagonists at the acetylcholine receptor and do not cause initial depolarization or fasciculations. Consequently, they are not associated with post-anesthetic myalgia. In fact, a small "pre-curarizing" dose of these drugs is often used to *prevent* suxamethonium-induced myalgia. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** Myalgia can be reduced by pre-treatment with a small dose of a non-depolarizing agent (e.g., Vecuronium) or NSAIDs. * **Specific Risk Group:** Post-suxamethonium myalgia is notably more common in **females** and **ambulatory (day-care) patients** who mobilize early. * **Associated Findings:** Suxamethonium can also cause a transient rise in serum potassium (0.5 mEq/L) and creatine kinase due to muscle activity. * **Contraindication:** Avoid in patients with major burns, crush injuries, or neuromuscular disorders (e.g., Duchenne muscular dystrophy) due to the risk of life-threatening hyperkalemia.

Q: Postoperative jaundice is most commonly associated with the use of which anesthetic agent?

Halothane. **Explanation:** **Halothane** is the most common anesthetic agent associated with postoperative jaundice, a condition historically referred to as **"Halothane Hepatitis."** 1. **Mechanism of Correct Answer:** Halothane undergoes significant hepatic metabolism (up to 20%) by the Cytochrome P450 system. This produces reactive intermediates (trifluoroacetylated proteins) that act as haptens. In susceptible individuals, the immune system produces **anti-trifluoroacetylated protein antibodies**, leading to massive hepatic necrosis. This typically manifests as fever, jaundice, and elevated transaminases 3–14 days post-exposure. Risk factors include multiple exposures, obesity, female gender, and middle age. 2. **Analysis of Incorrect Options:** * **Isoflurane:** Undergoes minimal metabolism (0.2%). While it can theoretically cause liver injury due to its trifluoroacetyl group, the risk is negligible compared to Halothane. * **Nitrous Oxide:** It is not metabolized by the liver and is excreted unchanged via the lungs. Its primary toxicities are megaloblastic anemia and subacute combined degeneration of the cord (due to Vitamin B12 inhibition). * **Methoxyflurane:** This agent is primarily known for **nephrotoxicity** (fluoride-induced high-output renal failure) rather than hepatotoxicity. 3. **NEET-PG High-Yield Pearls:** * **Metabolism Rule:** Halothane (20%) > Sevoflurane (2-5%) > Isoflurane (0.2%) > Desflurane (0.02%). Lower metabolism correlates with lower hepatotoxicity. * **Agent of Choice in Liver Disease:** **Isoflurane** is often preferred because it maintains hepatic blood flow better than other volatile agents. * **Modern Practice:** Due to the risk of hepatitis and cardiac arrhythmias (sensitization to catecholamines), Halothane has been largely replaced by Sevoflurane and Isoflurane in adult practice.

Q: An 85-year-old lady with a history of fracture neck of femur, undergoing general anesthesia with halothane for internal fixation, suddenly develops severe hypotension and bradycardia. The capnogram shows a sudden fall in end-tidal carbon dioxide. What is the most probable diagnosis?

Pulmonary thromboembolism. **Explanation:** The clinical presentation of sudden hypotension, bradycardia, and a **precipitous drop in End-Tidal Carbon Dioxide (EtCO2)** in an elderly patient with a hip fracture is a classic triad for **Pulmonary Thromboembolism (PTE)**. **Why Pulmonary Thromboembolism is correct:** In PTE, a clot obstructs pulmonary blood flow, creating **alveolar dead space** (areas that are ventilated but not perfused). Since blood cannot reach the alveoli to exchange CO2, the concentration of CO2 in exhaled air drops sharply. The sudden increase in right ventricular afterload leads to acute right heart failure, manifesting as severe hypotension and bradycardia (often a pre-terminal sign in massive PE). Elderly patients with long-bone fractures are at the highest risk due to Virchow’s triad (stasis and orthopedic injury). **Why other options are incorrect:** * **Myocardial Infarction:** While it causes hypotension and bradycardia, it does not typically cause a *sudden* drop in EtCO2 unless it leads to full cardiac arrest. * **Hypothermia:** This causes a gradual, progressive decline in EtCO2 due to decreased metabolic rate, not a sudden drop. * **Massive Blood Loss:** This leads to hemorrhagic shock and tachycardia (compensatory), with a gradual decline in EtCO2 as perfusion decreases, rather than an abrupt "step-down" on the capnogram. **High-Yield Clinical Pearls for NEET-PG:** 1. **Capnography** is the most sensitive monitor for the early detection of pulmonary embolism intraoperatively. 2. **Differential for sudden drop in EtCO2:** Pulmonary embolism (thrombus, air, or fat), cardiac arrest, or circuit disconnection. 3. **Fat Embolism Syndrome:** Specifically associated with long-bone fractures; look for the triad of respiratory distress, petechial rashes, and cerebral involvement. 4. **Halothane** sensitizes the myocardium to catecholamines but is not the primary cause of the EtCO2 drop here.

Q: Which of the following drugs is NOT implicated in triggering malignant hyperthermia?

Propofol. **Explanation:** **Malignant Hyperthermia (MH)** is a rare but life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle. It is primarily caused by an abnormal release of calcium from the sarcoplasmic reticulum via mutated **Ryanodine receptors (RYR1)**. **Why Propofol is the correct answer:** Propofol is a phenol derivative used for induction and maintenance of anesthesia. It is considered a **"safe" drug** in patients susceptible to MH. It does not trigger the massive intracellular calcium release associated with the condition. In fact, Total Intravenous Anesthesia (TIVA) using Propofol is the technique of choice for MH-susceptible individuals. **Analysis of incorrect options:** * **Succinylcholine (Option B):** This depolarizing neuromuscular blocker is a potent **triggering agent**. It causes prolonged muscle depolarization, which, in susceptible individuals, leads to the catastrophic metabolic cascade of MH. * **Halothane (Option D):** All **volatile inhalational anesthetics** (Halothane, Sevoflurane, Desflurane, Isoflurane) are classic triggers for MH. Halothane is historically the most frequently implicated volatile agent. * **Lignocaine (Option A):** While older literature once suggested caution with amide locals, modern evidence confirms that **all local anesthetics (including Lignocaine)** are safe and do not trigger MH. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **EtCO₂** (End-tidal Carbon Dioxide) despite increased ventilation. * **Specific Sign:** Masseter muscle rigidity (Trismus) following Succinylcholine administration. * **Late Sign:** Hyperthermia (can be as high as 1°C every 5 minutes). * **Drug of Choice:** **Dantrolene Sodium** (Mechanism: Binds to RYR1 receptors to inhibit calcium release). * **Safe Drugs:** Propofol, Etomidate, Thiopentone, Ketamine, Nitrous Oxide, and all Non-depolarizing muscle relaxants (e.g., Vecuronium).

Q: Which statement is false regarding intra-arterial injection of thiopental?

Stop the injection and remove the cannula.. **Explanation:** The management of accidental intra-arterial injection of Thiopental is a high-yield topic in anesthesia. Thiopental is highly alkaline (pH 10.5). When injected into an artery, it reacts with the relatively acidic blood, leading to the formation of **thiopental crystals**. These crystals cause mechanical obstruction, intense vasospasm, and endarteritis, which can lead to gangrene. **Why Option D is the correct (False) statement:** When an accidental intra-arterial injection is suspected, the most critical step is to **leave the cannula in situ**. The cannula serves as a direct portal for administering emergency drugs (like vasodilators or local anesthetics) to the affected area. Removing it loses this vital access. Therefore, the statement "remove the cannula" is clinically incorrect. **Analysis of other options:** * **Option A:** A **Stellate Ganglion Block** is a recognized treatment. It provides a chemical sympathectomy, which relieves vasospasm and promotes collateral circulation to the limb. * **Option B:** **Papaverine** (40–80 mg) is a potent direct-acting vasodilator used to counteract the intense arterial spasm caused by the drug. * **Option C:** This is the **pathophysiological basis** of the injury. The precipitation of thiopental crystals in the small arterioles leads to thrombosis and distal ischemia. **Clinical Pearls for NEET-PG:** * **Immediate Management:** Stop the injection, leave the needle/cannula in place, and inject **1% Lidocaine (5-10 ml)** or **Heparin** to dilute the drug and prevent thrombosis. * **Clinical Sign:** The patient typically complains of a sudden, severe "shooting" or "burning" pain radiating down the limb. * **Other Treatments:** Brachial plexus block (for vasodilation) and systemic anticoagulation.

Q: Biphasic respiratory depression is usually seen after which type of anesthesia?

Neuroleptanesthesia. **Explanation:** **Neuroleptanesthesia** is a technique traditionally involving the combination of a potent opioid (typically **Fentanyl**), a neuroleptic (typically **Droperidol**), and Nitrous Oxide. The phenomenon of **biphasic respiratory depression** (also known as "re-narcotization") is a classic complication associated with this technique. The underlying mechanism involves the redistribution and enterohepatic circulation of Fentanyl. Initially, the patient recovers from respiratory depression as the drug redistributes from the brain to muscle and fat. However, a secondary peak in plasma concentration occurs later due to: 1. **Release of sequestered fentanyl** from muscle and fat stores back into the systemic circulation. 2. **Enterohepatic circulation:** Fentanyl is secreted into the gastric juice, sequestered in the acidic environment of the stomach, and later reabsorbed in the alkaline small intestine. This causes a delayed "second peak" of respiratory depression, often when the patient is in the recovery room. **Analysis of Incorrect Options:** * **Regional Anesthesia:** While it can cause respiratory depression (e.g., high spinal block), it does not exhibit a biphasic pattern once the block wears off. * **Halothane & Isoflurane:** These volatile anesthetics cause dose-dependent respiratory depression. Once the agent is washed out of the system, the depression resolves linearly without a secondary recurrence. **High-Yield Clinical Pearls for NEET-PG:** * **Neuroleptanalgesia:** Fentanyl + Droperidol. * **Neuroleptanesthesia:** Fentanyl + Droperidol + $N_2O$. * **Droperidol Warning:** It is associated with **QT interval prolongation** and potential Torsades de Pointes. * **Management:** Biphasic depression requires vigilant postoperative monitoring and may necessitate a repeat dose of **Naloxone** (opioid antagonist).

Question 1

A patient developed fever and severe back pain following surgery performed under spinal anesthesia. On examination, a fluctuant swelling was noted at the site of spinal anesthesia. A non-contrast CT scan of the region showed a hypodense soft tissue mass, leading to a diagnosis of epidural abscess. What is the treatment of choice for an epidural abscess?

Accepted Answer

Immediate surgical evacuation

Answer

Conservative management

Answer

Antibiotics

Answer

Aggressive debridement

Question 2

Which of the following is the most common initial manifestation of malignant hyperthermia?

Accepted Answer

Increased PETCO2

Answer

Hyperkalemia

Answer

Increased distal esophageal temperature

Answer

Red discoloration of urine

Question 3

Post-anesthetic myalgia is commonest with which of the following drugs?

Accepted Answer

Suxamethonium

Answer

Pancuronium

Answer

Vecuronium

Answer

Atracurium

Question 4

Postoperative jaundice is most commonly associated with the use of which anesthetic agent?

Accepted Answer

Halothane

Answer

Isoflurane

Answer

Nitrous Oxide

Answer

Methoxyflurane

Question 5

An 85-year-old lady with a history of fracture neck of femur, undergoing general anesthesia with halothane for internal fixation, suddenly develops severe hypotension and bradycardia. The capnogram shows a sudden fall in end-tidal carbon dioxide. What is the most probable diagnosis?

Accepted Answer

Pulmonary thromboembolism

Answer

Myocardial infarction

Answer

Hypothermia

Answer

Massive blood loss

Question 6

A 26-year-old female who underwent cesarean section complains of severe occipital headache since day 2 after surgery. The headache is associated with neck pain and stiffness. What is the most accurate statement regarding this clinical presentation?

Accepted Answer

Seepage of cerebrospinal fluid (CSF) resulted in the present condition.

Answer

Epidural blood patch is the next step in management.

Answer

This is a major complication requiring immediate intervention.

Answer

Early ambulation resulted in the present condition.

Question 7

Which of the following drugs is NOT implicated in triggering malignant hyperthermia?

Accepted Answer

Propofol

Answer

Lignocaine

Answer

Succinylcholine

Answer

Halothane

Question 8

Which statement is false regarding intra-arterial injection of thiopental?

Accepted Answer

Stop the injection and remove the cannula.

Answer

Stellate ganglion block can cause sympathectomy and vasodilation.

Answer

Papaverine is used for dilatation of an artery that is in spasm.

Answer

Crystallization of thiopental in arterial blood is the main cause of complications.

Question 9

Biphasic respiratory depression is usually seen after which type of anesthesia?

Accepted Answer

Neuroleptanesthesia

Answer

Regional anesthesia

Answer

Halothane anesthesia

Answer

Isoflurane anesthesia

Question 10

A patient presents with systemic symptoms of pallor and unconsciousness following local anesthesia. What is the patient experiencing?

Accepted Answer

Syncope

Answer

CNS depression

Answer

Tonic reaction to local anesthesia

Answer

Allergic response

Complications in Anesthesia — MCQs

Complications in Anesthesia — MCQs

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