Complications in Anesthesia — MCQs

A patient presents to the emergency department with a stab injury to the left side of the abdomen. She is hemodynamically stable, and a contrast-enhanced CT scan reveals a splenic laceration. Laparoscopy is planned. The patient's pO2 suddenly drops as soon as pneumoperitoneum is created. What is the most likely cause?

Q169Medium

Shortly after the administration of an inhalational anesthetic and succinylcholine for intubation prior to an elective inguinal hernia repair in a 10-year-old boy, he becomes markedly febrile, displays a tachycardia of 160, and his urine changes color to a dark red. Which of the following is the most appropriate initial management?

Q170Medium

Following accidental intra-arterial injection of thiopentone, which of the following should not be done?

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 161: A 40-year-old paraplegic patient is scheduled for cholecystectomy due to acute cholecystitis. Succinylcholine is administered prior to intubation. Immediately after induction of anesthesia, the patient develops cardiac arrest. What is the most likely cause?

A. Esophageal intubation
B. Hyperkalemia (Correct Answer)
C. Perforation of gallbladder
D. Hypovolemic shock

Explanation: **Explanation:** The correct answer is **Hyperkalemia**. **1. Why Hyperkalemia is the correct answer:** Succinylcholine (SCh) is a depolarizing neuromuscular blocker that acts as an agonist at the nicotinic acetylcholine receptors (nAChR). In a healthy individual, SCh causes a transient rise in serum potassium by approximately 0.5 mEq/L. However, in patients with **denervation injuries** (like paraplegia, hemiplegia, or burns), there is an **upregulation of extrajunctional acetylcholine receptors** across the entire muscle membrane. When SCh is administered, these receptors open simultaneously, leading to a massive efflux of potassium into the extracellular space. This acute, severe hyperkalemia can trigger life-threatening ventricular arrhythmias and cardiac arrest within minutes of induction. **2. Why the other options are incorrect:** * **A. Esophageal intubation:** While a common cause of hypoxia and subsequent arrest, it typically presents with a gradual drop in SpO2 and absence of EtCO2, rather than immediate arrest following SCh administration in a high-risk patient. * **C. Perforation of gallbladder:** This would lead to peritonitis and sepsis, which is a chronic or subacute process, not a sudden cardiac arrest immediately following induction. * **D. Hypovolemic shock:** While acute cholecystitis can cause dehydration, it rarely leads to sudden cardiac arrest at the moment of induction unless there is massive hemorrhage or profound uncorrected hypotension. **3. High-Yield Clinical Pearls for NEET-PG:** * **Safe Window:** SCh is generally considered safe within the first 24–48 hours of a spinal cord injury. The risk of hyperkalemia peaks between **1 week to 6 months** post-injury but can persist indefinitely. * **Contraindications for SCh:** Burns (>24 hours), massive trauma, prolonged immobilization, upper/lower motor neuron lesions (Stroke, MS, ALS), and muscular dystrophies. * **Drug of Choice:** In these patients, **Rocuronium** (a non-depolarizing blocker) is the preferred agent for rapid sequence induction.

Question 162: A 64-year-old hypertensive, obese female was undergoing surgery for a fracture femur under general anesthesia. Intra-operatively, her end-tidal carbon dioxide decreased to 20 mm Hg from 40 mm Hg, followed by hypotension and an oxygen saturation of 85%. What is the most probable cause?

A. Fat embolism (Correct Answer)
B. Hypovolemia
C. Bronchospasm
D. Myocardial infarction

Explanation: ### Explanation The clinical presentation of sudden **hypotension**, **hypoxemia** ($SpO_2$ 85%), and a **precipitous drop in End-Tidal $CO_2$ ($EtCO_2$)** in a patient undergoing surgery for a long bone fracture (femur) is a classic triad for **Fat Embolism Syndrome (FES)**. **Why Fat Embolism is Correct:** In orthopedic surgeries involving long bones, fat globules from the bone marrow enter the systemic circulation. These emboli obstruct the pulmonary vasculature, leading to an increase in **alveolar dead space** (areas ventilated but not perfused). This results in a sudden drop in $EtCO_2$ because $CO_2$ cannot be exchanged. The mechanical obstruction and inflammatory response cause acute pulmonary hypertension, right heart strain, and systemic hypotension. **Why Other Options are Incorrect:** * **Hypovolemia:** While it causes hypotension, it usually presents with a gradual decline in $EtCO_2$ and does not typically cause a sudden, severe drop in oxygen saturation to 85% unless associated with shock. * **Bronchospasm:** This would cause an *increase* in $EtCO_2$ (due to obstructive physiology) and a characteristic "shark-fin" appearance on the capnograph, rather than a decrease. * **Myocardial Infarction:** While it causes hypotension, the sudden drop in $EtCO_2$ and severe hypoxemia are more characteristic of a primary pulmonary embolic event in the context of a femur fracture. **Clinical Pearls for NEET-PG:** * **Gurd’s Criteria:** Used for FES diagnosis; look for the triad of respiratory distress, petechial rashes (axilla/conjunctiva), and cerebral involvement. * **EtCO2 Drop:** A sudden decrease in $EtCO_2$ is the earliest sign of any embolism (Air, Fat, or Thromboembolism) under anesthesia. * **Management:** Primarily supportive (oxygenation and hemodynamics). Early fixation of fractures reduces the incidence of FES.

Question 163: A 28-year-old man is scheduled for shoulder surgery. He has a documented history of malignant hyperthermia during a previous general anesthesia. Which of the following neuromuscular blockers is contraindicated in this patient?

A. Succinylcholine (Correct Answer)
B. Pancuronium
C. Rocuronium
D. Vecuronium

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle. The core pathology involves a mutation in the **RYR1 receptor** (Ryanodine receptor), leading to an uncontrolled release of calcium from the sarcoplasmic reticulum in response to specific "triggering agents." **Why Succinylcholine is the Correct Answer:** Succinylcholine is a **depolarizing neuromuscular blocker** and is one of the two primary triggers for MH (the other being volatile inhalational anesthetics like Halothane, Isoflurane, and Sevoflurane). In susceptible individuals, Succinylcholine causes sustained muscle contraction, leading to hyperlactatemia, hyperkalemia, hyperthermia, and rhabdomyolysis. Therefore, it is strictly contraindicated in this patient. **Why Other Options are Incorrect:** * **Options B, C, and D (Pancuronium, Rocuronium, Vecuronium):** These are **non-depolarizing neuromuscular blockers**. They do not trigger the RYR1 receptor and do not cause the release of calcium that leads to MH. They are considered safe alternatives for muscle relaxation in MH-susceptible patients. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **End-Tidal CO₂ (ETCO₂)** despite increased minute ventilation. * **Specific Sign:** Masseter muscle rigidity (Trismus). * **Late Sign:** Hyperthermia (can rise at 1°C every 5 minutes). * **Drug of Choice:** **Dantrolene** (Mechanism: Binds to RYR1 receptors and inhibits calcium release). * **Safe Anesthesia Plan:** Total Intravenous Anesthesia (TIVA) using Propofol, Opioids, and Non-depolarizing muscle relaxants. Always flush the anesthesia machine to remove residual volatile gases before use.

Question 164: A male patient became suddenly tachypneic, hypoxic, and febrile a few hours after anesthesia during an abdominal surgery. Mendelson's syndrome is suspected. What is the likely cause of this syndrome in this patient?

A. Hypersensitivity reaction to anesthetic agent
B. Gastric aspiration (Correct Answer)
C. Faulty intubation
D. Asphyxia due to tracheal stenosis

Explanation: **Explanation:** **Mendelson’s Syndrome** is a specific type of chemical pneumonitis caused by the **aspiration of acidic gastric contents** into the lungs. It typically occurs during the induction or emergence phase of anesthesia when protective airway reflexes are depressed. **Why Gastric Aspiration is Correct:** The syndrome is defined by the aspiration of gastric juice with a **pH < 2.5** and a volume of at least **25 ml (0.4 ml/kg)**. The acidic nature of the aspirate causes immediate chemical damage to the alveolar-capillary membrane, leading to pulmonary edema, bronchospasm, and severe hypoxia. Clinical features include sudden onset of tachypnea, cyanosis, tachycardia, and wheezing (resembling asthma), often occurring within 2–12 hours post-aspiration. **Why Other Options are Incorrect:** * **Option A:** Hypersensitivity (Anaphylaxis) usually presents immediately upon drug administration with hypotension, urticaria, and angioedema, rather than delayed febrile respiratory distress. * **Option C:** Faulty intubation (e.g., esophageal intubation) would cause immediate hypoxia and lack of chest rise, not a delayed febrile syndrome. * **Option D:** Tracheal stenosis is a chronic complication of long-term intubation, presenting with inspiratory stridor weeks after the procedure, not acute post-operative distress. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Pregnancy (due to increased intra-abdominal pressure and relaxed lower esophageal sphincter), obesity, and emergency surgeries (full stomach). * **Prevention:** Pre-operative fasting (NPO guidelines), use of H2 blockers (Ranitidine), proton pump inhibitors (Pantoprazole), and non-particulate antacids (Sodium Citrate). * **Management:** Immediate suctioning of the oropharynx, supplemental oxygen, and supportive ventilation. Prophylactic antibiotics and steroids are generally **not** recommended.

Question 165: Aschner's reflex is seen in which of the following?

A. Cardiac surgery
B. Neurosurgery
C. Spinal anesthesia
D. Squint surgery (Correct Answer)

Explanation: **Explanation:** **Aschner’s Reflex**, also known as the **Oculocardiac Reflex (OCR)**, is a physiological response triggered by pressure on the globe or traction on the extraocular muscles. 1. **Why Squint Surgery is Correct:** Squint surgery involves significant manipulation and traction of the extraocular muscles (most commonly the **medial rectus**). This traction triggers the reflex arc: * **Afferent limb:** Trigeminal nerve (Ciliary nerves → Ophthalmic division $V_1$ → Gasserian ganglion). * **Efferent limb:** Vagus nerve (X). The resulting vagal stimulation leads to **bradycardia**, arrhythmias, or even asystole. It is a classic intraoperative complication in pediatric ophthalmology. 2. **Why Other Options are Incorrect:** * **Cardiac Surgery:** While bradycardia occurs, it is usually due to direct nodal manipulation or drugs, not the trigeminal-vagal reflex. * **Neurosurgery:** Can involve the Cushing reflex (hypertension + bradycardia due to increased ICP), but not the Aschner reflex unless the trigeminal nerve is directly manipulated. * **Spinal Anesthesia:** Bradycardia here is typically due to blockade of cardioaccelerator fibers (T1–T4) or a decrease in venous return (Bezold-Jarisch reflex), not ocular stimulation. **High-Yield Clinical Pearls for NEET-PG:** * **Most common muscle involved:** Medial Rectus. * **Management:** 1. **Immediate step:** Ask the surgeon to **stop** the stimulus (release traction). 2. Ensure adequate oxygenation/ventilation (hypoxia/hypercarbia exacerbates the reflex). 3. If persistent: Administer **Atropine** (0.02 mg/kg) or Glycopyrrolate. * **Fatigability:** The reflex shows "fatigue," meaning the heart rate response diminishes with repeated stimulation.

Question 166: Intraoperative wheezing can be managed by:

A. Thiopentane
B. Ketamine (Correct Answer)
C. Methohexitone
D. Propofol

Explanation: ### Explanation **Correct Answer: B. Ketamine** **Why Ketamine is the Correct Choice:** Intraoperative wheezing is often a sign of bronchospasm. **Ketamine** is the induction agent of choice in patients with reactive airway disease (like asthma or COPD) because of its potent **bronchodilatory properties**. It achieves this through two mechanisms: 1. **Sympathomimetic effect:** It triggers the release of endogenous catecholamines, which stimulate $\beta_2$ receptors in the bronchial smooth muscle. 2. **Direct action:** It has a direct relaxant effect on the bronchial smooth muscle. **Analysis of Incorrect Options:** * **A. Thiopentone:** This is a barbiturate known to cause **histamine release**. It can precipitate or worsen bronchospasm and is generally avoided in asthmatic patients. * **C. Methohexitone:** Like Thiopentone, it is a barbiturate. While it has a shorter duration of action, it does not possess bronchodilatory properties and can also trigger histamine release. * **D. Propofol:** While Propofol is generally safe for asthmatics and does not cause histamine release, it is not as effective as Ketamine for *managing* active intraoperative wheezing. (Note: Propofol is often the preferred induction agent for stable asthmatics, but Ketamine is the specific "rescue" induction agent for bronchospasm). **Clinical Pearls for NEET-PG:** * **Drug of Choice for Induction in Asthma:** Ketamine (due to bronchodilation) or Propofol (due to suppression of airway reflexes). * **Avoid in Asthma:** Thiopentone, Morphine, Atracurium (all cause histamine release). * **Management of Intraoperative Bronchospasm:** Increase $FiO_2$, deepen anesthesia (with Volatile agents like Sevoflurane), administer $\beta_2$ agonists (Salbutamol), and consider Ketamine or Hydrocortisone. * **Halothane** is also a potent bronchodilator but is rarely used now due to its potential for arrhythmias when used with catecholamines.

Question 167: Which volatile anesthetic agent causes the most renal toxicity?

A. Ether
B. Isoflurane
C. Methoxyflurane (Correct Answer)
D. Sevoflurane

Explanation: **Explanation:** The correct answer is **Methoxyflurane**. The primary mechanism behind its renal toxicity is the extensive hepatic metabolism of the drug, which releases **inorganic fluoride ions ($F^-$)**. 1. **Why Methoxyflurane is correct:** Methoxyflurane undergoes the highest degree of metabolism (approx. 50–75%) among all volatile agents. This results in high serum fluoride levels (often exceeding 50 µmol/L). These fluoride ions cause **vasopressin-resistant high-output renal failure** (polyuric renal failure) by damaging the distal convoluted tubules and collecting ducts, making them unresponsive to ADH. Due to this severe nephrotoxicity, it is no longer used for general anesthesia. 2. **Why other options are incorrect:** * **Ether:** Primarily known for its irritant effect on airways and flammability; it does not produce toxic fluoride metabolites. * **Isoflurane:** It is very stable and undergoes minimal metabolism (0.2%), making it exceptionally safe for the kidneys. * **Sevoflurane:** While it does release fluoride ions and can produce **Compound A** (a nephrotoxin in rats) when reacting with soda lime, clinical studies have shown no significant evidence of renal toxicity in humans when used at recommended flow rates. **High-Yield Clinical Pearls for NEET-PG:** * **Fluoride-induced nephrotoxicity:** Characterized by polyuria, hypernatremia, and increased serum creatinine. * **Metabolism Ranking (Highest to Lowest):** Methoxyflurane (50-75%) > Halothane (20%) > Sevoflurane (2-5%) > Enflurane (2%) > Isoflurane (0.2%) > Desflurane (0.02%). * **Compound A:** Associated with **Sevoflurane**; formed by degradation in carbon dioxide absorbers (especially with low-flow anesthesia). * **Agent of choice in Renal Failure:** Isoflurane or Desflurane.

Question 168: A patient presents to the emergency department with a stab injury to the left side of the abdomen. She is hemodynamically stable, and a contrast-enhanced CT scan reveals a splenic laceration. Laparoscopy is planned. The patient's pO2 suddenly drops as soon as pneumoperitoneum is created. What is the most likely cause?

A. Inferior vena cava compression
B. Injury to the left lobe of the diaphragm
C. Injury to the colon
D. Gaseous embolism through splenic vessels (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Gaseous embolism through splenic vessels** The sudden drop in $pO_2$ immediately following the creation of pneumoperitoneum in a patient with a known visceral injury (splenic laceration) is a classic presentation of **Venous Gas Embolism (VGE)**. During laparoscopy, $CO_2$ is insufflated into the peritoneal cavity. If there is a pre-existing vascular injury or a lacerated solid organ (like the spleen), the intra-abdominal pressure (typically 12–15 mmHg) can exceed the venous pressure, forcing gas directly into the systemic circulation through the open vessels. Once in the right heart, the gas causes a "gas lock," obstructing pulmonary blood flow, leading to a sudden V/Q mismatch and a rapid fall in $pO_2$ and $EtCO_2$. **Analysis of Incorrect Options:** * **A. Inferior vena cava compression:** While pneumoperitoneum can compress the IVC, this typically results in decreased venous return and **hypotension** rather than an isolated, sudden drop in $pO_2$. * **B. Injury to the left lobe of the diaphragm:** A diaphragmatic injury could lead to a pneumothorax upon insufflation. However, in the context of a known splenic laceration, vascular entry of gas is a more direct and common cause of sudden intraoperative desaturation. * **C. Injury to the colon:** A hollow viscus injury would lead to peritonitis or pneumoperitoneum, but it does not provide a direct conduit for gas to enter the vascular system to cause sudden hypoxia. **Clinical Pearls for NEET-PG:** * **Earliest Sign of VGE:** A sudden decrease in **End-tidal $CO_2$ ($EtCO_2$)** is often the first indicator, followed by hypoxia and hypotension. * **Gold Standard for Detection:** Transesophageal Echocardiography (TEE). * **Classic Sign:** "Mill-wheel murmur" heard on precordial auscultation (late sign). * **Management:** Immediate release of pneumoperitoneum, 100% $O_2$, and placing the patient in **Durant’s position** (Left lateral decubitus and Trendelenburg) to trap gas in the apex of the right ventricle.

Question 169: Shortly after the administration of an inhalational anesthetic and succinylcholine for intubation prior to an elective inguinal hernia repair in a 10-year-old boy, he becomes markedly febrile, displays a tachycardia of 160, and his urine changes color to a dark red. Which of the following is the most appropriate initial management?

A. Complete the procedure but pretreat with dantrolene prior to future elective surgery.
B. Administer additional inhalational anesthetic agents.
C. Administer additional succinylcholine.
D. Hyperventilate with 100% O2 and initiate cooling measures. (Correct Answer)

Explanation: ### **Explanation** **Diagnosis: Malignant Hyperthermia (MH)** The clinical presentation of rapid-onset fever, tachycardia, and dark red urine (myoglobinuria) following the administration of **succinylcholine** and **inhalational anesthetics** is a classic triad for Malignant Hyperthermia. This is a pharmacogenetic hypermetabolic state caused by a mutation in the **Ryanodine receptor (RYR1)**, leading to massive calcium release from the sarcoplasmic reticulum. **1. Why Option D is Correct:** The immediate priority in MH is to stop the triggering agents and manage the hypermetabolic crisis. * **Hyperventilation with 100% O2:** This addresses the severe respiratory and metabolic acidosis and washes out the volatile anesthetic. * **Cooling Measures:** Essential to combat life-threatening hyperthermia. * **Definitive Treatment:** Though not listed as the sole step here, the administration of **Dantrolene** (a muscle relaxant that binds to RYR1) is the gold standard. **2. Why Other Options are Wrong:** * **Option A:** MH is a surgical emergency with high mortality if not treated immediately. The procedure must be aborted, and Dantrolene must be given *now*, not just as prophylaxis for future surgeries. * **Options B & C:** Inhalational agents and succinylcholine are the **primary triggers** of MH. Administering more would worsen the muscle rigidity, hyperkalemia, and hyperthermia, likely leading to cardiac arrest. **3. NEET-PG High-Yield Pearls:** * **Earliest Sign:** Increase in **End-Tidal CO2 (ETCO2)** (due to hypermetabolism). * **Most Common Trigger:** Halothane and Succinylcholine. * **Safe Agents:** Propofol, Ketamine, Etomidate, and Nitrous Oxide. * **Gold Standard Diagnostic Test:** Caffeine Halothane Contracture Test (CHCT) on a muscle biopsy. * **Dantrolene Dosage:** 2.5 mg/kg IV bolus, repeated every 5–10 minutes until symptoms subside.

Question 170: Following accidental intra-arterial injection of thiopentone, which of the following should not be done?

A. Remove the needle (Correct Answer)
B. Intra-arterial heparin
C. Intra-arterial papaverine
D. Perform a stellate ganglion block

Explanation: ### Explanation The accidental intra-arterial injection of Thiopentone (an alkaline solution with pH 10.5) is a medical emergency. When injected into an artery, thiopentone reacts with blood to form **crystals**, leading to intense vasospasm, chemical endarteritis, and subsequent thrombosis, which can result in gangrene. **Why "Remove the needle" is the correct answer:** The most critical initial step is to **leave the needle in situ**. Removing the needle loses the only direct access to the affected arterial tree. The needle should be used immediately to administer vasodilators and anticoagulants to counteract the vasospasm and prevent clot formation. **Analysis of Incorrect Options:** * **Intra-arterial Heparin:** This is a standard treatment to prevent thrombosis and further propagation of clots distal to the site of crystal formation. * **Intra-arterial Papaverine:** This is a potent vasodilator used to relieve the intense arterial spasm caused by the alkaline drug. Other alternatives include Lidocaine or Priscoline. * **Stellate Ganglion Block:** This procedure (or a brachial plexus block) is performed to produce sympathetic blockade, which results in vasodilation and improved collateral circulation to the affected limb. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Injury:** Precipitation of thiopentone crystals in the small arterioles due to the change from high pH (drug) to lower pH (blood). * **Immediate Management:** 1. **Leave the needle in place.** 2. Dilute the drug by injecting Normal Saline through the needle. 3. Administer vasodilators (Papaverine 40-80mg or 1% Lidocaine). 4. Heparinization to prevent thrombosis. 5. Sympathetic block (Stellate ganglion block). * **Clinical Sign:** The patient typically complains of a sudden, "scalding" or shooting pain down the limb during injection.

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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