Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 131: A 20-year-old man complains of headache after spinal anesthesia. Which of the following is the likely cause?

A. Raised intracranial pressure
B. Meningitis
C. Cerebrospinal fluid leak (Correct Answer)
D. Encephalitis

Explanation: ### Explanation The patient is presenting with **Post-Dural Puncture Headache (PDPH)**, a classic complication of spinal anesthesia. **1. Why the correct answer is right:** PDPH is caused by a **Cerebrospinal Fluid (CSF) leak** through the puncture site in the dura mater. When CSF escapes into the epidural space faster than it is produced, it leads to **low intracranial pressure**. This loss of "cushioning" causes the brain to sag in the upright position, stretching pain-sensitive intracranial structures (vessels and nerves), resulting in a characteristic **postural headache** (worsens on sitting/standing, improves when lying flat). **2. Why the incorrect options are wrong:** * **Raised Intracranial Pressure (ICP):** PDPH is a low-pressure headache. Conditions causing raised ICP (like tumors or bleeds) typically cause headaches that worsen when lying down, the opposite of PDPH. * **Meningitis:** While a potential complication of spinal anesthesia due to poor asepsis, it presents with fever, neck rigidity, and photophobia. It is not the "likely" cause of a simple post-spinal headache unless these signs are present. * **Encephalitis:** This involves inflammation of the brain parenchyma, presenting with altered mental status, seizures, or focal deficits, which are not typical of post-anesthesia headache. **3. High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Young age, female gender, pregnancy, and use of large-bore/cutting needles. * **Needle Types:** **Whitacre and Sprotte** (pencil-point/non-cutting) needles have a lower incidence of PDPH compared to **Quincke** (cutting) needles. * **Clinical Feature:** Usually occurs within 12–48 hours; bifrontal or occipital distribution. * **Management:** * *Conservative:* Bed rest, hydration, analgesics, and caffeine (causes cerebral vasoconstriction). * *Definitive:* **Epidural Blood Patch** (Gold Standard)—injecting autologous blood into the epidural space to "plug" the dural hole.

Question 132: Intra-arterial injection of thiopentone. All are true except:

A. Intra-arterial thiopentone can form crystals in arterioles and capillaries and cause intense vasoconstriction.
B. It should be treated promptly with papaverine and lidocaine.
C. Treatment of choice is stellate ganglion block. (Correct Answer)
D. Heparinization can also be done.

Explanation: **Explanation:** Intra-arterial injection of Thiopentone is a medical emergency characterized by severe pain, intense vasoconstriction, and potential gangrene. **1. Why Option C is the correct answer (The "Except"):** While a **Stellate Ganglion Block** (or Brachial Plexus Block) is a recognized treatment modality used to achieve sympathetic blockade and subsequent vasodilation, it is **not the treatment of choice**. The immediate priority and treatment of choice is to **leave the needle in situ** and inject vasodilators (like Papaverine) directly into the artery to counteract the intense vasospasm. **2. Analysis of other options:** * **Option A:** Thiopentone is highly alkaline (pH 10.5). When injected into an artery, it reacts with blood to form **crystals** that lodge in small arterioles and capillaries. This triggers endothelial damage, platelet aggregation, and intense **vasoconstriction**, leading to distal ischemia. * **Option B:** Immediate pharmacological management involves injecting **Papaverine** (40–80 mg) or **Lidocaine** (1%) through the same needle to induce direct vasodilation and stabilize the endothelium. * **Option D:** **Heparinization** is performed to prevent secondary thrombosis and microvascular occlusion resulting from the chemical endarteritis. **Clinical Pearls for NEET-PG:** * **Presentation:** "Hand of burning fire" – sudden, excruciating pain distal to the injection site. * **Immediate Action:** Do NOT remove the needle; use it for drug administration. * **Other Treatments:** Elevation of the limb, analgesia, and sometimes surgical embolectomy if large clots form. * **Prevention:** Always use a test dose and check for arterial pulsations before injecting Thiopentone.

Question 133: Anaphylaxis is caused by which of the following agents?

A. N2O
B. Althesin (Correct Answer)
C. Halothane
D. Propofol

Explanation: ### Explanation **Correct Option: B. Althesin** Althesin was an intravenous anesthetic agent consisting of a mixture of two steroids: **Alphaxalone and Alphadolone**. It was notorious for causing severe **Type I hypersensitivity reactions (anaphylaxis)**. The primary culprit was the solvent used to dissolve these steroids, **Cremophor EL** (polyoxyethylated castor oil). Due to a high incidence of life-threatening anaphylactoid reactions (approximately 1 in 1,000 to 1 in 10,000 administrations), Althesin was withdrawn from clinical use in 1984. **Analysis of Incorrect Options:** * **A. N2O (Nitrous Oxide):** An inorganic gas that does not cause anaphylaxis. Its primary concerns are diffusion hypoxia, expansion of closed gas spaces, and megaloblastic anemia (via Vitamin B12 inhibition). * **C. Halothane:** While Halothane is associated with "Halothane Hepatitis" (an immune-mediated hepatotoxicity), it does not typically cause acute anaphylactic reactions. * **D. Propofol:** Modern Propofol is formulated in a soybean oil/egg lecithin emulsion. While it can cause allergic reactions in patients with specific sensitivities, its incidence is significantly lower than that of Althesin. Interestingly, the original formulation of Propofol also used Cremophor EL but was changed due to the same anaphylactic risks seen with Althesin. **High-Yield Clinical Pearls for NEET-PG:** * **Neuromuscular Blocking Agents (NMBAs):** These are the **most common** cause of perioperative anaphylaxis (Succinylcholine and Rocuronium being the most frequent). * **Latex:** The second most common cause of intraoperative anaphylaxis. * **Cremophor EL:** Also found in the original formulation of **Propanidid** and the chemotherapy drug **Paclitaxel**, both of which are associated with hypersensitivity. * **Management:** The drug of choice for anaphylaxis is **Adrenaline (Epinephrine)**, administered IM (0.5 mg) or IV (titrated doses).

Question 134: Post dural puncture headache is typically located in which region?

A. Retro-orbital
B. Frontal
C. Occipital (Correct Answer)
D. Temporal

Explanation: **Explanation:** Post-Dural Puncture Headache (PDPH) is a common complication following spinal anesthesia or accidental dural puncture during epidural placement. **Why Occipital is Correct:** The underlying mechanism of PDPH is the leakage of Cerebrospinal Fluid (CSF) through the dural hole, leading to **low CSF pressure**. This loss of buoyancy causes the brain to sag in the upright position, stretching pain-sensitive structures like the dura mater and cranial nerves (V, IX, and X). The pain is characteristically **positional** (worsens on standing, relieved by lying flat) and is most commonly felt in the **occipital and frontal regions**, often radiating to the neck and shoulders. In the context of standard medical examinations, the **occipital** region is the classic hallmark location. **Analysis of Incorrect Options:** * **A & B (Retro-orbital and Frontal):** While PDPH can involve the frontal region, it is rarely isolated to the retro-orbital area. The occipital distribution is more specific to the traction on the tentorium cerebelli. * **D (Temporal):** Temporal pain is more characteristic of conditions like giant cell arteritis or tension headaches, rather than the gravitational traction seen in PDPH. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Treatment:** Epidural Blood Patch (EBP) – 15-20 ml of autologous blood is injected into the epidural space. * **Risk Factors:** Young age, female gender, pregnancy, and the use of large-bore/cutting needles (e.g., Quincke). * **Prevention:** Use of small-gauge, non-cutting (pencil-point) needles like **Whitacre** or **Sprotte**. * **Associated Symptom:** Diplopia due to **6th Cranial Nerve (Abducens)** palsy is the most common cranial nerve involvement.

Question 135: Following accidental intra-arterial injection of thiopental, what is the immediate management step?

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

Explanation: **Explanation:** The accidental intra-arterial injection of **Thiopental** (an alkaline solution with pH 10.5) leads to the formation of micro-crystals upon contact with blood. these crystals cause intense chemical endarteritis, vasospasm, and subsequent distal ischemia or gangrene. **Why "Remove the needle" is the correct first step:** In any scenario involving an accidental iatrogenic injury during a procedure, the immediate priority is to **stop the administration of the offending agent** to prevent further tissue damage. Removing the needle (or stopping the injection) minimizes the volume of the drug entering the arterial circulation, thereby limiting the severity of the chemical insult. **Analysis of Incorrect Options:** * **B & C (Intra-arterial Heparin/Papaverine):** While these are vital components of the *subsequent* management (Heparin to prevent thrombosis and Papaverine/Lidocaine to relieve vasospasm), they are secondary to stopping the initial insult. * **D (Stellate Ganglion Block):** This is a definitive treatment used to achieve sympathetic blockade and promote vasodilation in the affected limb, but it is never the "immediate" first step. **NEET-PG High-Yield Pearls:** * **Mechanism of Injury:** Thiopental crystals precipitate in the small arteries, leading to **norepinephrine release** and profound vasospasm. * **Clinical Presentation:** The patient typically complains of sudden, "shooting" pain radiating distally, followed by blanching and loss of distal pulses. * **Management Protocol:** 1. Stop injection/Remove needle. 2. Dilute the drug (inject Normal Saline through the same catheter if still in situ). 3. Relieve vasospasm (intra-arterial Lidocaine or Papaverine). 4. Sympathetic block (Stellate ganglion or Brachial plexus block). 5. Anticoagulation (Heparin) to prevent secondary thrombosis.

Question 136: A 25-year-old female develops masseter muscle spasm after IV succinylcholine administration. End-tidal CO2 progressively increases, heart rate increases, and temperature rises. What is the EXCEPTIONAL management for this condition?

A. Administer halothane to decrease the heart rate. (Correct Answer)
B. Hyperventilate with 100% oxygen.
C. Implement active cooling measures.
D. Treat the acidosis.

Explanation: ### Explanation The clinical presentation—**masseter muscle spasm** following succinylcholine, rising **ETCO2** (the earliest sign), tachycardia, and hyperthermia—is diagnostic of **Malignant Hyperthermia (MH)**. MH is a pharmacogenetic hypermetabolic state triggered by volatile anesthetics and depolarizing muscle relaxants. #### 1. Why Option A is the Correct (Exceptional) Choice **Halothane** is a potent trigger for Malignant Hyperthermia. In a patient already experiencing an MH crisis, administering halothane would exacerbate the calcium release from the sarcoplasmic reticulum, worsening the hypermetabolic state and potentially leading to death. While halothane can decrease heart rate via myocardial depression, its use is **absolutely contraindicated** in this scenario. #### 2. Analysis of Incorrect Options (Standard Management) * **Option B (Hyperventilate with 100% O2):** This is a primary step. High-flow oxygen helps meet increased metabolic demands, and hyperventilation helps wash out the rapidly rising CO2. * **Option C (Active Cooling):** Hyperthermia in MH can be extreme. Cooling (cold IV fluids, surface cooling, or gastric lavage) is essential to prevent heat-induced organ damage. * **Option D (Treat Acidosis):** MH causes severe mixed respiratory and metabolic (lactic) acidosis. Administration of Sodium Bicarbonate (1-2 mEq/kg) is standard to stabilize pH and treat hyperkalemia. #### 3. NEET-PG High-Yield Pearls * **Definitive Treatment:** **Dantrolene** (a Ryanodine receptor antagonist) is the drug of choice. Dose: 2.5 mg/kg IV bolus, repeated up to 10 mg/kg. * **Earliest Sign:** Increase in End-tidal CO2 (ETCO2). * **Late Sign:** Hyperthermia (can rise 1°C every 5 minutes). * **Genetic Defect:** Mutation in the **RYR1 gene** (Ryanodine receptor) on Chromosome 19. * **Safe Agents:** Propofol, Ketamine, Etomidate, and non-depolarizing NMBs (e.g., Vecuronium).

Question 137: Suxamethonium causes all EXCEPT:

A. Muscle pain
B. Malignant hyperthermia
C. Hyperkalemia
D. Hypokalemia (Correct Answer)

Explanation: **Explanation:** **Suxamethonium (Succinylcholine)** is the only depolarizing neuromuscular blocker used clinically. It acts as an agonist at the nicotinic acetylcholine receptors, causing prolonged depolarization of the motor endplate. **Why Hypokalemia is the Correct Answer:** Suxamethonium does **not** cause hypokalemia; instead, it characteristically causes **Hyperkalemia**. During the phase of generalized muscle fasciculations, potassium is released from the intracellular compartment into the extracellular fluid. In a healthy individual, serum potassium typically rises by **0.5 mEq/L**. However, in patients with up-regulated receptors (e.g., burns, trauma, or denervation injuries), this rise can be life-threatening, leading to cardiac arrest. **Analysis of Incorrect Options:** * **A. Muscle pain:** Postoperative myalgia is a common side effect caused by the initial uncoordinated muscle fasciculations. It is most frequently seen in young adults undergoing ambulatory surgery. * **B. Malignant hyperthermia:** Suxamethonium is a potent **triggering agent** for Malignant Hyperthermia (MH) in genetically susceptible individuals (RYR1 receptor mutation). * **C. Hyperkalemia:** As explained above, the efflux of potassium during depolarization is a hallmark side effect of the drug. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** For Rapid Sequence Induction (RSI) due to its rapid onset (30–60s) and short duration (5–10 mins). * **Metabolism:** Hydrolyzed by **Pseudocholinesterase** (Plasma cholinesterase). Prolonged apnea occurs in patients with atypical pseudocholinesterase (diagnosed by Dibucaine number). * **Dual Block (Phase II Block):** Occurs with repeated doses or infusion, where the block takes on characteristics of a non-depolarizing block. * **Other Side Effects:** Bradycardia (especially in children or with a second dose), increased intraocular, intragastric, and intracranial pressure.

Question 138: Hyperkalemia is seen with succinylcholine in all of the following conditions except?

A. Tetanus
B. Burns
C. Myasthenia gravis (Correct Answer)
D. Muscular dystrophy

Explanation: **Explanation:** The correct answer is **Myasthenia Gravis (C)**. The underlying mechanism for succinylcholine-induced hyperkalemia is the **upregulation of extrajunctional acetylcholine receptors (nAChR)**. In conditions involving denervation, extensive tissue damage, or prolonged immobilization, these immature receptors spread across the entire muscle membrane. When succinylcholine (a depolarizing muscle relaxant) binds to these receptors, it causes prolonged depolarization and a massive efflux of potassium from the muscle cells into the extracellular fluid. * **Why Myasthenia Gravis is the exception:** In Myasthenia Gravis, there is an autoimmune-mediated **destruction and downregulation** of acetylcholine receptors. Since there are fewer receptors available to depolarize, succinylcholine does not cause a massive potassium release. In fact, patients with Myasthenia Gravis are often **resistant** to succinylcholine and require higher doses, but are hypersensitive to non-depolarizing agents. **Why the other options are incorrect:** * **Burns (B):** Extensive thermal injury leads to massive upregulation of extrajunctional receptors. The risk of hyperkalemia typically starts 24–48 hours post-burn and can persist for a year or more. * **Tetanus (A):** The intense muscle activity and potential denervation-like state in severe tetanus lead to receptor proliferation, making succinylcholine dangerous. * **Muscular Dystrophy (D):** In Duchenne Muscular Dystrophy, the unstable sarcolemma is prone to massive potassium release and rhabdomyolysis upon depolarization, which can lead to cardiac arrest. **High-Yield Clinical Pearls for NEET-PG:** * **Safe Window:** Succinylcholine is generally safe within the first 24 hours of a burn or spinal cord injury. * **Potassium Rise:** In healthy individuals, succinylcholine raises serum $K^+$ by **0.5 mEq/L**. In "at-risk" patients, this can rise by >5–10 mEq/L. * **Other Contraindications:** Upper/Lower motor neuron lesions (Stroke, Paraplegia), Crush injuries, and Severe intra-abdominal sepsis.

Question 139: Which of the following neuromuscular blocking agents is most commonly associated with bradycardia during anesthesia?

A. Pancuronium
B. Vecuronium
C. Atracurium (Correct Answer)
D. All of the above

Explanation: **Explanation:** The correct answer is **Atracurium**. While neuromuscular blocking agents (NMBAs) are primarily used for muscle relaxation, they often exert secondary effects on the autonomic nervous system. **1. Why Atracurium is correct:** Atracurium is unique among the listed options because it triggers a dose-dependent **histamine release** from mast cells. Histamine causes systemic vasodilation, which typically leads to hypotension. In response to rapid histamine release and the subsequent drop in blood pressure, a **reflex bradycardia** or profound cardiovascular instability can occur. Additionally, some metabolites of atracurium may have mild vagolytic effects, but the histamine-mediated response is the classic association for bradycardia/hypotension in clinical scenarios. **2. Why the other options are incorrect:** * **Pancuronium:** This is a long-acting steroid NMB known for its **vagolytic effect**. It inhibits muscarinic receptors in the SA node, leading to **tachycardia** and hypertension, making it the opposite of the correct answer. * **Vecuronium:** This is considered **cardiovascularly stable**. It does not cause significant histamine release or vagal blockade, making it unlikely to cause bradycardia. **3. Clinical Pearls for NEET-PG:** * **Hofmann Elimination:** Atracurium and Cisatracurium are metabolized via Hofmann elimination (spontaneous non-enzymatic degradation), making them the drugs of choice in **renal or hepatic failure**. * **Laudanosine Toxicity:** A metabolite of atracurium (laudanosine) can cross the blood-brain barrier and may cause **seizures** at high concentrations. * **Cisatracurium:** Unlike atracurium, it does **not** cause histamine release, offering greater cardiovascular stability. * **Suxamethonium (Succinylcholine):** Though not listed, it is the NMBA most famously associated with profound bradycardia, especially in children or upon a second dose, due to its action on cardiac muscarinic receptors.

Question 140: Dantrolene is used in the treatment of which of the following conditions?

A. Malignant hyperthermia
B. Neuroleptic malignant syndrome
C. Thyrotoxicosis-induced hyperthermia
D. All of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. All of the above**. Dantrolene sodium is a muscle relaxant that acts by binding to the **Ryanodine Receptor (RyR1)** on the sarcoplasmic reticulum of skeletal muscle. This inhibits the release of calcium ions into the cytosol, thereby preventing the sustained muscle contraction and hypermetabolic state that leads to life-threatening hyperthermia. * **Malignant Hyperthermia (MH):** Dantrolene is the **drug of choice** and the only specific treatment for MH. It halts the uncontrolled calcium release triggered by volatile anesthetics or succinylcholine. * **Neuroleptic Malignant Syndrome (NMS):** While dopamine agonists (Bromocriptine) are primary, Dantrolene is used as an adjunct to reduce muscle rigidity and core temperature in severe cases. * **Thyrotoxicosis/Thyroid Storm:** In extreme cases where hyperthermia is refractory to standard cooling and anti-thyroid measures, Dantrolene can be used to reduce the peripheral heat production from skeletal muscle. **Clinical Pearls for NEET-PG:** 1. **Mechanism:** Direct-acting skeletal muscle relaxant (does not affect cardiac or smooth muscle significantly at therapeutic doses). 2. **Dose for MH:** 2.5 mg/kg IV bolus, repeated every 5–10 minutes until symptoms subside (max dose usually 10 mg/kg). 3. **Side Effects:** Significant muscle weakness and potential hepatotoxicity (with chronic oral use). 4. **Preparation:** Each vial of Dantrolene contains **20 mg** of the drug and must be reconstituted with **60 mL of sterile water**. It contains **mannitol** to improve solubility and promote diuresis.

Practice by Chapter

Adverse Drug Reactions

Practice Questions

Anaphylaxis and Allergic Reactions

Practice Questions

Malignant Hyperthermia

Practice Questions

Local Anesthetic Toxicity

Practice Questions

Perioperative Cardiac Complications

Practice Questions

Pulmonary Complications

Practice Questions

Awareness Under General Anesthesia

Practice Questions

Neurological Complications

Practice Questions

Postoperative Visual Loss

Practice Questions

Perioperative Renal Dysfunction

Practice Questions

Transfusion-Related Complications

Practice Questions

Risk Management and Prevention

Practice Questions

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