Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 101: Malignant hyperthermia is common with which of the following agents?

A. Local anesthetics
B. Succinylcholine (Correct Answer)
C. Propofol
D. Barbiturates

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle. It is triggered in genetically susceptible individuals (due to mutations in the **RYR1 receptor**) upon exposure to specific anesthetic agents. **Why Succinylcholine is correct:** Succinylcholine, a depolarizing neuromuscular blocker, is a classic **potent trigger** for MH. It causes a massive release of calcium from the sarcoplasmic reticulum into the myoplasm. This leads to sustained muscle contraction, accelerated metabolism, excessive heat production (hyperthermia), and metabolic acidosis. Volatile inhalational anesthetics (e.g., Halothane, Isoflurane, Sevoflurane) are the other primary triggers. **Why other options are incorrect:** * **Local Anesthetics (A):** Modern local anesthetics (amides and esters) are considered safe and do not trigger MH. * **Propofol (C):** This is a safe intravenous induction agent and is often the drug of choice for Total Intravenous Anesthesia (TIVA) in MH-susceptible patients. * **Barbiturates (D):** Drugs like Thiopental are non-triggering agents and are safe to use. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **End-Tidal CO₂ (ETCO₂)** due to hypermetabolism (Tachycardia is the most common early clinical sign). * **Late Sign:** Hyperthermia (can rise at 1°C every 5 minutes). * **Drug of Choice:** **Dantrolene** (Mechanism: Acts on RYR1 receptors to inhibit calcium release). * **Safe Agents:** Propofol, Etomidate, Ketamine, Opioids, and all Non-depolarizing Muscle Relaxants (e.g., Vecuronium). * **Associated Conditions:** Central Core Disease, King-Denborough Syndrome.

Question 102: Which of the following anesthetic agents is NOT safe in malignant hyperthermia?

A. Nitrous oxide
B. Xenon
C. Halothane (Correct Answer)
D. Propofol

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a rare but life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle. It is primarily caused by a mutation in the **RYR1 gene** (Ryanodine receptor), leading to massive calcium release from the sarcoplasmic reticulum upon exposure to specific triggering agents. **Why Halothane is the correct answer:** Halothane is a volatile inhalational anesthetic. **All volatile halogenated inhalational anesthetics** (e.g., Halothane, Isoflurane, Sevoflurane, Desflurane) and the depolarizing muscle relaxant **Succinylcholine** are potent triggers for MH. They provoke uncontrolled muscle contractions, leading to hyperthermia, acidosis, and rhabdomyolysis. **Why the other options are wrong:** * **Nitrous oxide (A):** This is an inorganic gas and is considered safe in MH-susceptible patients. * **Xenon (B):** An inert gas used as an anesthetic; it does not trigger the RYR1 receptor and is safe. * **Propofol (D):** An intravenous anesthetic agent. All IV agents (Propofol, Etomidate, Ketamine, Thiopental) and non-depolarizing muscle relaxants (e.g., Vecuronium, Atracurium) are safe for use in MH. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **End-Tidal CO₂ (ETCO₂)** despite increased ventilation. * **Late Sign:** Hyperthermia (can be rapid and extreme). * **Drug of Choice:** **Dantrolene** (a muscle relaxant that acts directly on the Ryanodine receptor to stop calcium release). * **Confirmatory Test:** Caffeine Halothane Contracture Test (CHCT) on a muscle biopsy. * **Management Tip:** Stop the trigger, hyperventilate with 100% $O_2$, and switch to a "clean" breathing circuit.

Question 103: Which of the following is NOT a side effect of succinylcholine?

A. Myalgias
B. Raised intracranial pressure
C. Hyperkalemia
D. Raised blood pressure (Correct Answer)

Explanation: **Explanation:** Succinylcholine (Suxamethonium) is a depolarizing neuromuscular blocker that acts as an agonist at the nicotinic acetylcholine receptors. The correct answer is **Raised blood pressure** because succinylcholine typically causes **bradycardia** (especially in children or with a second dose) due to its action on cardiac muscarinic receptors. While it can occasionally cause arrhythmias, hypertension is not a classic or direct side effect. **Analysis of Incorrect Options:** * **Myalgias:** Occur due to visible muscle fasciculations during the initial depolarization phase. This is common in young, muscular adults and can be mitigated by a small "pre-curarization" dose of a non-depolarizing agent. * **Raised Intracranial Pressure (ICP):** Succinylcholine causes a transient increase in ICP, likely due to muscle fasciculations and increased cerebral blood flow. It should be used with caution in patients with head injuries. * **Hyperkalemia:** Depolarization causes the release of potassium from intracellular to extracellular space. While it raises serum $K^+$ by only 0.5 mEq/L in healthy individuals, it can cause life-threatening hyperkalemia in patients with burns, massive trauma, or denervation injuries (upregulation of extrajunctional receptors). **High-Yield Clinical Pearls for NEET-PG:** 1. **Malignant Hyperthermia:** Succinylcholine is a potent trigger. 2. **Intraocular Pressure (IOP):** It increases IOP; avoid in penetrating eye injuries. 3. **Pseudocholinesterase Deficiency:** Leads to prolonged apnea (Suxamethonium apnea) after administration. 4. **Drug of Choice:** Still used for **Rapid Sequence Induction (RSI)** due to its rapid onset (30-60s) and short duration (5-10 mins).

Question 104: Inadequate depth of anesthesia leads to all of the following physiological responses except:

A. Lacrimation
B. Bradycardia (Correct Answer)
C. Mydriasis
D. Hypertension

Explanation: **Explanation:** Inadequate depth of anesthesia (light anesthesia) triggers a **sympathetic nervous system (SNS) surge** as a physiological response to surgical stress and noxious stimuli. **1. Why Bradycardia is the Correct Answer:** In response to surgical stimulation under light anesthesia, the body releases catecholamines (epinephrine and norepinephrine). This leads to **tachycardia** (increased heart rate), not bradycardia. Bradycardia is typically associated with deep anesthesia (halothane effects), high spinal blocks, or specific reflexes (like the oculocardiac reflex), rather than inadequate depth. **2. Analysis of Incorrect Options:** * **Lacrimation (A):** Tearing is a classic clinical sign of light anesthesia. It occurs due to autonomic stimulation and is often used by anesthesiologists to gauge the need for more analgesia or anesthetic agents. * **Mydriasis (C):** Pupillary dilation occurs during light anesthesia due to sympathetic overactivity. (Note: Very deep anesthesia can also cause mydriasis due to medullary depression, but in the context of surgical stimulation, it indicates inadequacy). * **Hypertension (D):** Increased systemic vascular resistance and cardiac output due to catecholamine release lead to a rise in blood pressure. **3. Clinical Pearls for NEET-PG:** * **Signs of Light Anesthesia:** Tachycardia, hypertension, lacrimation, sweating (diaphoresis), tachypnea, and purposeful movement. * **PRST Score:** A clinical tool used to assess anesthetic depth based on **P**ressure (BP), **R**ate (HR), **S**weating, and **T**ears. * **Gold Standard:** While clinical signs are vital, **Bispectral Index (BIS) monitoring** is the most objective way to prevent intraoperative awareness; a BIS value between 40–60 indicates an adequate depth for general anesthesia.

Question 105: Which of the following is the most common initial manifestation of malignant hyperthermia?

A. Hyperkalemia
B. Increased distal esophageal temperature
C. Increased PETCO2 (Correct Answer)
D. Red discoloration of urine

Explanation: **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.

Question 106: What is the earliest sign of syncope?

A. Pallor (Correct Answer)
B. Constriction of pupil
C. Dilation of pupil
D. Bradycardia

Explanation: **Explanation:** Syncope (fainting) is a transient loss of consciousness due to global cerebral hypoperfusion. The earliest signs are mediated by the body’s initial compensatory response to a drop in blood pressure or an overactive vagal reflex. **1. Why Pallor is the Correct Answer:** Pallor is the **earliest clinical sign** of syncope. It occurs due to intense peripheral vasoconstriction and the diversion of blood away from the skin toward vital organs (the "autonomic prodrome"). This sympathetic activation happens immediately as the body attempts to maintain mean arterial pressure before the actual loss of consciousness occurs. **2. Analysis of Incorrect Options:** * **Constriction of pupil:** This is not a characteristic feature of syncope. In the early stages of a vasovagal attack, sympathetic activity may actually cause mild dilation, not constriction. * **Dilation of pupil:** While pupillary dilation (mydriasis) can occur during syncope, it is typically a **late sign** associated with significant cerebral hypoxia or the moment of loss of consciousness, rather than the earliest warning sign. * **Bradycardia:** In vasovagal syncope (the most common type), bradycardia does occur due to parasympathetic overactivity. However, it usually follows the initial phase of tachycardia or occurs simultaneously with the drop in blood pressure. Pallor almost always precedes the detectable change in heart rate. **Clinical Pearls for NEET-PG:** * **Sequence of Syncope:** Pallor → Diaphoresis (sweating) → Nausea → Visual blurring → Loss of consciousness. * **Vasovagal Syncope (Common Faint):** The most frequent cause in clinical practice, often triggered by pain, fear, or prolonged standing. * **Management:** The immediate treatment is the **Trendelenburg position** (head low, legs elevated) to increase venous return to the heart and brain.

Question 107: Hyperkalemia due to succinylcholine is seen in all EXCEPT?

A. Crush injury
B. Burn
C. Abdominal sepsis (Correct Answer)
D. Muscular dystrophy

Explanation: **Explanation:** The primary mechanism behind succinylcholine-induced hyperkalemia is the **upregulation of extrajunctional nicotinic acetylcholine receptors (nAChRs)**. Normally, receptors are localized at the neuromuscular junction. However, in specific pathological states, these receptors proliferate across the entire muscle membrane. When succinylcholine (a depolarizing muscle relaxant) binds to these widespread receptors, it causes massive, prolonged efflux of potassium from the muscle cells into the extracellular fluid. * **Why Abdominal Sepsis is the Correct Answer:** While severe systemic inflammation can cause metabolic derangements, **abdominal sepsis** is not typically associated with the massive proliferation of extrajunctional receptors required to cause a life-threatening potassium spike. Therefore, it is considered the "exception" among the provided options. * **Why the other options are incorrect:** * **Crush Injury & Burns:** These are classic triggers for receptor upregulation. Following massive tissue trauma or thermal injury, extrajunctional receptors appear within 24–48 hours. Succinylcholine administration in these patients can raise serum potassium by >5.0 mEq/L, leading to cardiac arrest. * **Muscular Dystrophy (e.g., Duchenne’s):** In these patients, the muscle membrane is unstable. Succinylcholine can cause profound rhabdomyolysis and hyperkalemic cardiac arrest. It is generally contraindicated in children with undiagnosed myopathy. **Clinical Pearls for NEET-PG:** 1. **Safe Window:** Succinylcholine is generally safe within the first **24 hours** of a burn or trauma; the risk of hyperkalemia peaks after 48 hours and can last for years. 2. **Normal Rise:** In a healthy individual, succinylcholine increases serum $K^+$ by only **0.5 mEq/L**. 3. **Other High-Yield Contraindications:** Upper/lower motor neuron lesions (paraplegia, stroke), prolonged immobilization, and denervation injuries.

Question 108: Post-anesthetic myalgia is commonest with which of the following drugs?

A. Suxamethonium (Correct Answer)
B. Pancuronium
C. Vecuronium
D. Atracurium

Explanation: **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.

Question 109: Postoperative jaundice is most commonly associated with the use of which anesthetic agent?

A. Isoflurane
B. Nitrous Oxide
C. Methoxyflurane
D. Halothane (Correct Answer)

Explanation: **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.

Question 110: 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?

A. Myocardial infarction
B. Pulmonary thromboembolism (Correct Answer)
C. Hypothermia
D. Massive blood loss

Explanation: **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.

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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