Complications in Anesthesia — MCQs
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A 65-year-old man undergoes a technically difficult abdominal-perineal resection for a rectal cancer during which he receives 3 units of packed red blood cells. Four hours later, in the intensive care unit (ICU), he is bleeding heavily from his perineal wound. Emergency coagulation studies reveal normal prothrombin time, partial thromboplastin time, and bleeding times. The fibrin degradation products are not elevated, but the serum fibrinogen content is depressed and the platelet count is 70,000/mL. Which of the following is the most likely cause of his bleeding?
Which of the following is the commonest nerve injury due to maintaining the same position for a prolonged period during general anesthesia?
Which drug is used in the treatment of malignant hyperthermia?
All are true about accidental intra-arterial injection of Thiopentone except:
Neuroleptic Malignant Syndrome (NMS) is caused by which of the following medications?
Post-spinal headache is most commonly due to which of the following mechanisms?
Which of the following anesthetic agents is known to be nephrotoxic?
Complications of spinal anesthesia include all EXCEPT?
A 30-year-old female who underwent surgery under spinal anesthesia developed a post-spinal headache. How long does it typically take for the headache to subside?
A 6-year-old child who has had repeated episodes of otitis media undergoes surgical placement of pressure-equalization (PE) tubes. In the recovery room, she develops a fever of 40degC (104degF), muscle rigidity, dark colored urine, and metabolic and respiratory acidosis. Which of the following therapies is most likely to be beneficial for this child's condition?
Complications in Anesthesia Indian Medical PG Practice Questions and MCQs
Question 81: A 65-year-old man undergoes a technically difficult abdominal-perineal resection for a rectal cancer during which he receives 3 units of packed red blood cells. Four hours later, in the intensive care unit (ICU), he is bleeding heavily from his perineal wound. Emergency coagulation studies reveal normal prothrombin time, partial thromboplastin time, and bleeding times. The fibrin degradation products are not elevated, but the serum fibrinogen content is depressed and the platelet count is 70,000/mL. Which of the following is the most likely cause of his bleeding?
- A. Delayed blood transfusion reaction
- B. Autoimmune fibrinolysis
- C. A bleeding blood vessel in the surgical field (Correct Answer)
- D. Factor VIII deficiency
Explanation: ### Explanation The correct answer is **C. A bleeding blood vessel in the surgical field.** #### **Why Option C is Correct** The clinical presentation describes **dilutional thrombocytopenia and consumption of clotting factors** secondary to massive hemorrhage and subsequent volume replacement. In a post-operative patient with heavy bleeding and a history of a "technically difficult" surgery, the most common cause of hemorrhage is **inadequate surgical hemostasis** (a "surgical bleeder"). The laboratory findings support this: * **Platelet count (70,000/mL):** This is the most common laboratory abnormality after massive blood transfusion (dilutional effect). * **Low Fibrinogen:** Fibrinogen is the first coagulation factor to reach critical levels during hemorrhage and dilution. * **Normal PT/PTT/BT:** These suggest that there is no primary coagulopathy or Disseminated Intravascular Coagulation (DIC) causing the bleed; rather, the bleeding is causing the depletion. #### **Why Other Options are Incorrect** * **A. Delayed blood transfusion reaction:** Usually presents days to weeks later with extravascular hemolysis (jaundice, falling hematocrit), not acute surgical site hemorrhage. * **B. Autoimmune fibrinolysis:** This is rare. If primary fibrinolysis were occurring, FDPs (Fibrin Degradation Products) would typically be significantly elevated, and PT/PTT would likely be prolonged. * **D. Factor VIII deficiency:** This is Hemophilia A. It would present with a significantly prolonged PTT, which is normal in this patient. #### **NEET-PG Clinical Pearls** * **Most common cause of bleeding after massive transfusion:** Dilutional thrombocytopenia. * **First factor to reach deficiency levels in hemorrhage:** Fibrinogen (Critical level <100 mg/dL). * **Massive Transfusion Definition:** Replacement of >1 blood volume in 24 hours or >50% blood volume in 4 hours. * **Rule of Thumb:** If a post-op patient is bleeding and coagulation profiles are relatively preserved or only mildly deranged, always rule out a **mechanical/surgical cause** first.
Question 82: Which of the following is the commonest nerve injury due to maintaining the same position for a prolonged period during general anesthesia?
- A. Common peroneal nerve injury
- B. Brachial plexus injuries
- C. Ulnar neuropathies (Correct Answer)
- D. None of the above
Explanation: **Explanation:** **Ulnar neuropathy** is the most common peripheral nerve injury associated with general anesthesia. The nerve is particularly vulnerable at the elbow as it passes through the **cubital tunnel** (postcondylar groove of the humerus). During anesthesia, the loss of muscle tone and protective pain reflexes, combined with prolonged pressure against the operating table or improper padding, leads to ischemia or compression of the nerve. It is more common in males and patients with a high or low BMI. **Analysis of Options:** * **Ulnar Nerve (Option C):** Correct. Large-scale studies (like the ASA Closed Claims Project) consistently identify ulnar neuropathy as the most frequent nerve injury, often manifesting as "claw hand" or sensory loss in the medial 1.5 fingers. * **Brachial Plexus (Option B):** This is the second most common injury. It typically occurs due to excessive abduction of the arm (>90 degrees), external rotation of the head, or the use of shoulder braces in the Trendelenburg position. * **Common Peroneal Nerve (Option A):** This is the most common nerve injury of the **lower extremity**. It occurs when the lateral aspect of the knee (fibular head) is compressed against stirrups in the lithotomy position, leading to foot drop. **Clinical Pearls for NEET-PG:** * **Most common nerve injured (Overall):** Ulnar Nerve. * **Most common lower limb nerve injured:** Common Peroneal Nerve. * **Most common cause of Brachial Plexus injury:** Excessive arm abduction (>90°). * **Prevention:** Use of foam padding at the elbow, maintaining the forearm in a neutral or supinated position, and avoiding prolonged lithotomy time. * **Radial Nerve Injury:** Usually caused by a tight NIBP cuff or pressure against the humerus (leads to wrist drop).
Question 83: Which drug is used in the treatment of malignant hyperthermia?
- A. Dantrolene (Correct Answer)
- B. Diazepam
- C. Paracetamol
- D. Phenobarbitone
Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a rare but life-threatening pharmacogenetic hypermetabolic crisis triggered by volatile anesthetics (e.g., Halothane, Isoflurane) and the depolarizing muscle relaxant Succinylcholine. **Why Dantrolene is the Correct Answer:** The underlying pathology of MH involves a mutation in the **Ryanodine Receptor (RYR1)**, leading to an uncontrolled release of calcium from the sarcoplasmic reticulum into the skeletal muscle cytoplasm. This causes sustained muscle contraction, excessive heat production, and metabolic acidosis. **Dantrolene** is a direct-acting skeletal muscle relaxant that acts as an antagonist to the RYR1 receptor. It inhibits the release of calcium, thereby reversing the hypermetabolic state. It is the only specific antidote for MH. **Analysis of Incorrect Options:** * **B. Diazepam:** A benzodiazepine used for sedation and anxiolysis; it has no effect on the intracellular calcium release mechanism in skeletal muscles. * **C. Paracetamol:** An antipyretic that acts centrally. It is ineffective in MH because the fever in MH is caused by peripheral muscular metabolic activity, not a change in the hypothalamic set-point. * **D. Phenobarbitone:** A barbiturate used primarily as an anticonvulsant; it plays no role in treating MH. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **End-Tidal CO₂ (ETCO₂)**. * **Late Sign:** Hyperthermia (can rise 1°C every 5 minutes). * **Dose of Dantrolene:** 2.5 mg/kg IV bolus, repeated every 5–10 minutes until symptoms subside (max dose 10 mg/kg). * **Safe Agents:** Propofol, Ketamine, Etomidate, and Nitrous Oxide. * **Diagnosis:** Gold standard is the **Caffeine-Halothane Contracture Test (CHCT)**.
Question 84: All are true about accidental intra-arterial injection of Thiopentone except:
- A. Immediate intense vasoconstriction and excruciating pain
- B. Cause is precipitation of thiopental crystals in the arterial vessels
- C. To relieve pain, we have to immediately remove the misplaced arterial cannula. (Correct Answer)
- D. Sympathectomy of the upper extremity produced by stellate ganglion block may relieve vasoconstriction.
Explanation: ### Explanation Accidental intra-arterial injection of Thiopentone is a medical emergency. Thiopentone is highly alkaline (pH 10.5). When injected into an artery, it reacts with blood to form **thiopental crystals**. These crystals cause mechanical obstruction, intense chemical endarteritis, and the release of norepinephrine, leading to severe vasospasm and potential gangrene. **Why Option C is the Correct Answer (The "Except" statement):** The misplaced arterial cannula should **NEVER be removed immediately**. It serves as the primary route for administering life-saving medications (vasodilators) directly to the affected site. Removing it loses precious access for emergency treatment. **Analysis of Other Options:** * **Option A:** The high alkalinity causes immediate, excruciating pain (burning sensation) and intense vasoconstriction, which can lead to the loss of distal pulses. * **Option B:** The primary pathophysiology involves the **precipitation of thiopental crystals** in the small arterioles due to the lower pH of blood compared to the drug solution. * **Option D:** A **Stellate Ganglion Block** or brachial plexus block induces sympathectomy, which helps relieve reflex vasospasm and improves distal perfusion. **Clinical Pearls for NEET-PG:** * **Management Protocol:** 1. **Leave the needle/cannula in place.** 2. Dilute the drug by injecting **Normal Saline**. 3. Administer **Vasodilators**: Intra-arterial **Papaverine** (drug of choice), Lidocaine, or Procaine. 4. **Anticoagulation:** Heparin to prevent secondary thrombosis. 5. **Sympathetic Block:** Stellate ganglion block. * **Prevention:** Use a 2.5% solution instead of 5%; always perform a test dose and check for arterial pulsations before injection.
Question 85: Neuroleptic Malignant Syndrome (NMS) is caused by which of the following medications?
- A. Metoclopramide
- B. Phenothiazines
- C. Haloperidol
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Neuroleptic Malignant Syndrome (NMS) is a life-threatening idiosyncratic reaction to **dopamine antagonists**. The underlying pathophysiology involves a profound blockade of central **D2 receptors** in the nigrostriatal pathway and hypothalamus, leading to the classic tetrad of: 1. Hyperthermia (Fever) 2. Muscle rigidity ("Lead-pipe" rigidity) 3. Autonomic instability 4. Altered mental status **Analysis of Options:** * **Haloperidol (Option C):** This is a high-potency typical antipsychotic (butyrophenone) and is the most common causative agent associated with NMS. * **Phenothiazines (Option B):** Drugs like chlorpromazine and fluphenazine are typical antipsychotics that frequently cause NMS due to their potent dopamine-blocking properties. * **Metoclopramide (Option A):** Although primarily used as a prokinetic/antiemetic, metoclopramide is a central dopamine antagonist. It is a well-documented, though often overlooked, cause of NMS. Since all three medications act as dopamine antagonists, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Marker:** Elevated **Creatine Phosphokinase (CPK)** is a hallmark finding due to muscle rigidity and rhabdomyolysis. * **Treatment of Choice:** 1. Immediate cessation of the offending agent. 2. **Dantrolene** (muscle relaxant) or **Bromocriptine** (dopamine agonist). * **NMS vs. Malignant Hyperthermia (MH):** While both present with fever and rigidity, MH is triggered by volatile anesthetics/succinylcholine and involves the ryanodine receptor, whereas NMS is triggered by neuroleptics and involves dopamine blockade. * **Differential:** NMS can also occur upon the sudden **withdrawal of Levodopa** in Parkinson’s patients.
Question 86: Post-spinal headache is most commonly due to which of the following mechanisms?
- A. Meningitis
- B. Encephalitis
- C. Cerebrospinal fluid (CSF) leak (Correct Answer)
- D. Increased intracranial pressure (ICT)
Explanation: **Explanation:** **Post-Dural Puncture Headache (PDPH)** is a common complication following spinal anesthesia or accidental dural puncture during epidural placement. **1. Why the Correct Answer is Right:** The primary mechanism is a **persistent leak of Cerebrospinal Fluid (CSF)** through the puncture hole in the dura mater. When the rate of CSF loss exceeds the rate of production, it leads to **low CSF pressure (intracranial hypotension)**. This causes two main effects: * **Loss of Cushioning:** The brain "sags" when the patient is upright, putting traction on pain-sensitive structures like the meninges and cranial nerves. * **Compensatory Vasodilation:** According to the Monro-Kellie doctrine, a decrease in CSF volume leads to compensatory cerebral vasodilation to maintain intracranial volume, which further contributes to the headache. **2. Why Incorrect Options are Wrong:** * **Meningitis & Encephalitis:** While these can cause headaches post-procedure due to infection or chemical irritation, they are inflammatory/infectious processes characterized by fever, neck rigidity, and altered sensorium, rather than the classic positional nature of PDPH. * **Increased Intracranial Pressure (ICT):** PDPH is a syndrome of *low* pressure. Increased ICT would typically cause a headache that worsens when lying flat, whereas PDPH is characteristically relieved by the supine position. **3. High-Yield Clinical Pearls for NEET-PG:** * **Classic Presentation:** A "frontal-occipital" headache that is **exclusively positional** (worsens on standing/sitting, relieved by lying flat). * **Risk Factors:** Young age, female gender (especially pregnancy), and the use of large-bore or "cutting" needles (e.g., Quincke). * **Prevention:** Use of small-gauge (25G-27G) **non-cutting/pencil-point needles** (e.g., Sprotte or Whitacre). * **Treatment:** Conservative (bed rest, hydration, caffeine). The **Gold Standard** for persistent PDPH is an **Epidural Blood Patch**.
Question 87: Which of the following anesthetic agents is known to be nephrotoxic?
- A. Halothane
- B. Methoxyflurane (Correct Answer)
- C. Ether
- D. Cyclopropane
Explanation: **Explanation:** **Methoxyflurane** is the correct answer because it is the most potent inhalational anesthetic but is notorious for its dose-dependent **nephrotoxicity**. The underlying mechanism involves the extensive hepatic metabolism of methoxyflurane (up to 50-70%), which releases high levels of **inorganic fluoride ions (F⁻)**. These ions interfere with the concentrating mechanism of the renal tubules, leading to "high-output renal failure" (polyuric renal failure). Due to this severe side effect, its use as a general anesthetic has been largely abandoned. **Analysis of Incorrect Options:** * **Halothane:** Primarily known for **hepatotoxicity** ("Halothane Hepatitis") and sensitization of the myocardium to catecholamines, leading to arrhythmias. It does not cause significant renal damage. * **Ether:** Known for its irritating effect on the airways and high flammability. While it causes sympathetic stimulation, it is not directly nephrotoxic. * **Cyclopropane:** An explosive gas that causes significant cardiac sensitization to adrenaline. Like ether, it lacks specific nephrotoxic properties. **High-Yield Clinical Pearls for NEET-PG:** * **Fluoride Threshold:** Serum fluoride levels >50 µmol/L are typically associated with renal toxicity. * **Sevoflurane:** Another modern agent that releases fluoride ions; however, it is generally safe. Its main concern is the formation of **Compound A** (a nephrotoxic vinyl ether) when reacting with soda lime, though this is rarely clinically significant in humans. * **Metabolism Rule:** Methoxyflurane (70%) > Halothane (20%) > Sevoflurane (2-5%) > Enflurane (2%) > Isoflurane (0.2%) > Desflurane (0.02%). * **Current Use:** Methoxyflurane is now only used in low doses (via the "Penthrox" inhaler) for emergency analgesia, where fluoride levels remain below the toxic threshold.
Question 88: Complications of spinal anesthesia include all EXCEPT?
- A. Hypotension
- B. Tachycardia (Correct Answer)
- C. Bradycardia
- D. Headache
Explanation: **Explanation:** Spinal anesthesia involves the injection of local anesthetics into the subarachnoid space, resulting in a sympathetic blockade. The correct answer is **Tachycardia** because spinal anesthesia typically causes the opposite effect—**Bradycardia**. **1. Why Tachycardia is the correct answer (The Exception):** Spinal anesthesia leads to a **sympathetic block**. When the block reaches high levels (T1–T4), it inhibits the **cardioaccelerator fibers**. This results in parasympathetic dominance (vagal tone), leading to **bradycardia**, not tachycardia. Tachycardia would only occur as a compensatory mechanism for hypotension if the block is low, but it is not a direct complication of the procedure itself. **2. Analysis of Incorrect Options:** * **Hypotension (A):** This is the most common complication. It occurs due to the blockade of preganglionic sympathetic fibers (T1–L2), leading to arterial and venous vasodilation (decreased systemic vascular resistance and venous return). * **Bradycardia (C):** As explained, blocking the T1–T4 segments or a sudden decrease in venous return (triggering the Bezold-Jarisch reflex) leads to a drop in heart rate. * **Headache (D):** Specifically **Post-Dural Puncture Headache (PDPH)**. It is caused by the leakage of CSF through the dural puncture site, leading to low intracranial pressure. **Clinical Pearls for NEET-PG:** * **PDPH Character:** Typically frontal or occipital, postural in nature (worsens on sitting/standing, relieved by lying flat). * **Treatment of choice for PDPH:** Epidural Blood Patch. * **High Spinal:** Can lead to respiratory paralysis if it reaches C3–C5 (Phrenic nerve). * **Urinary Retention:** The most common reason for delayed discharge after spinal anesthesia.
Question 89: A 30-year-old female who underwent surgery under spinal anesthesia developed a post-spinal headache. How long does it typically take for the headache to subside?
- A. Up to 10 minutes
- B. Up to 4 days
- C. Up to 2 weeks (Correct Answer)
- D. Up to 2 months
Explanation: **Explanation:** Post-Dural Puncture Headache (PDPH) is a common complication following spinal anesthesia, caused by the persistent leakage of cerebrospinal fluid (CSF) through the dural puncture site. This leads to low CSF pressure and loss of the "cushioning" effect, causing traction on intracranial vascular structures when the patient is upright. **Why Option C is Correct:** While most cases of PDPH are self-limiting and resolve within **5 to 7 days**, clinical studies and standard textbooks (like Miller’s Anesthesia) state that symptoms can persist for **up to 2 weeks** in a significant number of patients. If the headache lasts longer than 14 days, clinicians should investigate alternative diagnoses or consider an epidural blood patch. **Analysis of Incorrect Options:** * **Option A (10 minutes):** This is far too short. PDPH typically has a delayed onset (24–48 hours post-procedure) and requires time for the dural hole to heal. * **Option B (4 days):** While many patients show improvement by day 4, it is not the upper limit of the typical duration. * **Option D (2 months):** Chronic headaches lasting months are rare and usually indicate a complication (like a subdural hematoma) rather than simple PDPH. **High-Yield Clinical Pearls for NEET-PG:** * **Character:** Classically **frontal or occipital** and strictly **positional** (worsens on standing/sitting, relieved by lying flat). * **Risk Factors:** Young age, female gender, pregnancy, and use of large-bore or cutting-tip needles (e.g., Quincke). * **Prevention:** Use of small-gauge (25G-27G) **non-cutting (pencil-point)** needles like **Sprotte or Whitacre**. * **Management:** Conservative (bed rest, hydration, caffeine). The **Gold Standard** treatment for persistent/severe PDPH is an **Epidural Blood Patch**.
Question 90: A 6-year-old child who has had repeated episodes of otitis media undergoes surgical placement of pressure-equalization (PE) tubes. In the recovery room, she develops a fever of 40degC (104degF), muscle rigidity, dark colored urine, and metabolic and respiratory acidosis. Which of the following therapies is most likely to be beneficial for this child's condition?
- A. Acidification of the urine
- B. Administration of intravenous antibiotics after obtaining blood cultures
- C. Intravenous administration of dantrolene (Correct Answer)
- D. Administration of tetanus immunoglobulin and a booster dose of DTaP
Explanation: ### Explanation The clinical presentation described—**hyperthermia (40°C), muscle rigidity, dark-colored urine (myoglobinuria), and mixed acidosis**—following anesthesia is a classic manifestation of **Malignant Hyperthermia (MH)**. #### 1. Why the Correct Answer is Right Malignant Hyperthermia is a pharmacogenetic hypermetabolic crisis triggered by volatile anesthetics (e.g., Halothane, Sevoflurane) or depolarizing muscle relaxants (Succinylcholine). It involves a defect in the **Ryanodine Receptor (RYR1)**, leading to an uncontrolled release of calcium from the sarcoplasmic reticulum. This causes sustained muscle contraction, massive ATP consumption, and heat production. * **Dantrolene** is the definitive treatment. It acts as a muscle relaxant by binding to the RYR1 receptor and inhibiting the release of calcium, thereby reversing the hypermetabolic state. #### 2. Why Other Options are Wrong * **Option A (Acidification of urine):** In the presence of myoglobinuria (dark urine), the goal is **alkalization** of urine (using sodium bicarbonate) to prevent myoglobin precipitation in renal tubules and subsequent acute kidney injury. Acidification would worsen the condition. * **Option B (Antibiotics):** While fever can indicate sepsis, the rapid onset of rigidity and profound acidosis post-anesthesia specifically points to MH, not an acute bacterial infection. * **Option D (Tetanus prophylaxis):** Although tetanus causes muscle rigidity (risus sardonicus/opisthotonus), it does not typically present as an acute intraoperative/postoperative metabolic crisis triggered by anesthesia. #### 3. High-Yield Clinical Pearls for NEET-PG * **Earliest Sign:** Increase in **End-Tidal CO₂ (ETCO₂)** despite increased ventilation. * **Late Sign:** Hyperthermia (can be as high as 1°C every 5 minutes). * **Diagnosis:** Gold standard is the **Caffeine-Halothane Contracture Test (CHCT)** on a muscle biopsy. * **Management Mnemonic:** "Stop, Hyperventilate, Dantrolene, Cool." (Stop triggers, 100% O₂, Dantrolene 2.5 mg/kg, active cooling). * **Safe Anesthetics:** Propofol, Ketamine, Etomidate, and Nitrous Oxide.
Practice by Chapter
Adverse Drug Reactions
Practice Questions
Anaphylaxis and Allergic Reactions
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Malignant Hyperthermia
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Local Anesthetic Toxicity
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Perioperative Cardiac Complications
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Pulmonary Complications
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Awareness Under General Anesthesia
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Neurological Complications
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Postoperative Visual Loss
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Perioperative Renal Dysfunction
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Transfusion-Related Complications
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Risk Management and Prevention
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