Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 71: A 35-year-old male developed a headache relieved by lying down two days after a surgical procedure. What is the definitive treatment for this condition?

A. NSAIDs and caffeine
B. Physiotherapy
C. Autologous blood patch (Correct Answer)
D. Caffeine

Explanation: ### Explanation The clinical presentation of a headache that is postural in nature (relieved by lying down and worsened by sitting or standing) following a surgical procedure (likely involving spinal or epidural anesthesia) is classic for **Post-Dural Puncture Headache (PDPH)**. **1. Why "Autologous Blood Patch" is correct:** While conservative management is often tried first, the **Epidural Blood Patch (EBP)** is considered the **definitive (gold standard) treatment** for PDPH. It involves injecting 15–20 ml of the patient's own venous blood into the epidural space at or near the level of the previous dural puncture. The blood clots to "plug" the dural hole, preventing further leakage of Cerebrospinal Fluid (CSF) and restoring intracranial pressure. **2. Why other options are incorrect:** * **NSAIDs and Caffeine (Options A & D):** These are components of **conservative management**. Caffeine causes cerebral vasoconstriction, which provides symptomatic relief by counteracting the compensatory vasodilation caused by low CSF pressure. However, they do not fix the underlying dural hole and are not "definitive." * **Physiotherapy (Option B):** There is no clinical role for physiotherapy in the management of PDPH. **3. High-Yield Clinical Pearls for NEET-PG:** * **Pathophysiology:** CSF leak through a dural rent $\rightarrow$ low CSF pressure $\rightarrow$ traction on pain-sensitive intracranial structures (vessels and nerves). * **Risk Factors:** Use of large-bore cutting needles (e.g., Tuohy), female gender, pregnancy, and young age. * **Needle Types:** **Quincke** (cutting) has the highest risk; **Sprotte and Whitacre** (pencil-point/non-cutting) have the lowest risk. * **Timing:** Usually appears within 48–72 hours post-procedure. * **Associated Symptom:** Occasional involvement of the 6th Cranial Nerve (Abducens), leading to diplopia.

Question 72: Which of the following is NOT a risk factor for developing bronchospasm during anesthesia?

A. Perioperative respiratory infection
B. Endotracheal intubation
C. Presence of COPD
D. Old age (Correct Answer)

Explanation: **Explanation:** Bronchospasm is a sudden constriction of the muscles in the walls of the bronchioles, often triggered by airway hyperreactivity. **Why "Old Age" is the correct answer:** While elderly patients often have comorbidities (like COPD), **age itself is not an independent risk factor** for bronchospasm. In fact, airway hyperreactivity is generally more common and severe in children and young adults (due to smaller airway caliber and higher incidence of reactive airway diseases like asthma). Therefore, being elderly does not inherently predispose a patient to acute bronchospasm during induction or maintenance of anesthesia. **Why the other options are incorrect:** * **Perioperative Respiratory Infection (A):** This is a major risk factor. Recent viral infections (within 2–4 weeks) increase airway sensitivity and mucus production, significantly raising the risk of bronchospasm. * **Endotracheal Intubation (B):** Mechanical stimulation of the larynx and trachea by an ETT is the most common trigger for bronchospasm in the perioperative period, especially during "light" planes of anesthesia. * **Presence of COPD (C):** Patients with COPD or Asthma have baseline airway inflammation and hyperresponsiveness, making them highly susceptible to bronchoconstriction when exposed to irritants like volatile anesthetics or secretions. **Clinical Pearls for NEET-PG:** * **Management:** The first step in managing intraoperative bronchospasm is to **deepen the plane of anesthesia** (using Volatile agents like Sevoflurane, which is a potent bronchodilator) and administer 100% Oxygen. * **Drug of Choice:** In acute, severe cases, inhaled or IV **Beta-2 agonists (Salbutamol)** are the mainstay. * **Avoid:** Thiopental and Morphine should be used with caution in high-risk patients as they can trigger histamine release, potentially worsening bronchospasm. Ketamine is the induction agent of choice due to its bronchodilatory properties.

Question 73: Which disease is known to be associated with malignant hyperthermia?

A. Huntington chorea
B. Fabry disease
C. Burns
D. Denborough syndrome (Correct Answer)

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a pharmacogenetic hypermetabolic crisis of skeletal muscle triggered by volatile anesthetics (e.g., Halothane, Sevoflurane) and depolarizing muscle relaxants (Succinylcholine). It is primarily caused by a mutation in the **RYR1 gene** (ryanodine receptor), leading to massive calcium release from the sarcoplasmic reticulum. **Why Denborough Syndrome is correct:** **King-Denborough Syndrome (KDS)** is a rare congenital myopathy characterized by a specific triad: dysmorphic features (short stature, ptosis, cryptorchidism), skeletal abnormalities, and a **high susceptibility to Malignant Hyperthermia**. It is the classic syndrome associated with MH in medical literature and exams. Other strongly associated conditions include Central Core Disease and Multiminicore Disease. **Analysis of Incorrect Options:** * **Huntington Chorea:** A neurodegenerative disorder involving the basal ganglia. While it involves motor symptoms, it has no known association with the RYR1 mutation or MH. * **Fabry Disease:** A lysosomal storage disorder (alpha-galactosidase A deficiency) affecting the kidneys and heart; it does not involve skeletal muscle calcium signaling. * **Burns:** While burn patients can develop **hyperkalemia** if given Succinylcholine (due to up-regulation of extrajunctional acetylcholine receptors), they do not have an increased genetic predisposition to MH itself. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **EtCO₂** (End-tidal Carbon Dioxide) despite increasing ventilation. * **Most Specific Sign:** Muscle rigidity (especially Masseter Spasm). * **Drug of Choice:** **Dantrolene** (Mechanism: Acts on RYR1 to prevent calcium release). * **Safe Agents:** Propofol, Etomidate, Thiopentone, Ketamine, and all Non-depolarizing Neuromuscular Blockers (e.g., Vecuronium). * **Gold Standard Test:** Caffeine Halothane Contracture Test (CHCT).

Question 74: What is responsible for muscle pain after day care surgery when propofol and succinylcholine (Sch) are used?

A. Succinylcholine (Sch) (Correct Answer)
B. Propofol
C. Surgery
D. Early ambulation

Explanation: ### Explanation **Correct Option: A. Succinylcholine (Sch)** Postoperative Myalgia (POM) is a well-documented side effect of Succinylcholine, a depolarizing neuromuscular blocker. It occurs in up to 50% of patients, particularly in young adults undergoing minor "day care" procedures. The pain is attributed to **fasciculations**—uncoordinated muscle fiber contractions caused by the initial depolarization of the motor endplate. These contractions lead to microscopic muscle damage, lactic acid buildup, and the release of prostaglandins and creatine kinase. The pain typically involves the neck, shoulders, and chest, appearing 24–48 hours post-surgery. **Why other options are incorrect:** * **B. Propofol:** Propofol is an intravenous anesthetic agent known for its rapid recovery profile. While it can cause pain *on injection*, it does not cause postoperative muscle pain. In fact, using propofol for induction may slightly reduce the intensity of Sch-induced fasciculations compared to thiopentone. * **C. Surgery:** While surgical trauma causes localized pain at the incision site, generalized muscle pain (myalgia) is a systemic pharmacological effect of Succinylcholine. * **D. Early ambulation:** Early ambulation is actually a **risk factor** that exacerbates Sch-induced myalgia, but it is not the *primary cause*. Patients who are mobilized quickly (typical in day care surgery) report higher pain scores than those on bed rest. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Highest incidence in females, young adults, and "ambulatory" patients. It is less common in children and the elderly. * **Prevention:** Myalgia can be minimized by "Pre-curarization"—administering a small dose of a **Non-depolarizing Neuromuscular Blocker (NDMR)** (e.g., 1/10th dose of vecuronium) 3 minutes before Succinylcholine. * **Other Sch Complications:** Hyperkalemia (avoid in burns/trauma), Malignant Hyperthermia, and prolonged apnea in patients with atypical pseudocholinesterase.

Question 75: The caffeine-halothane test is used to diagnose which of the following conditions?

A. Malignant hyperthermia (Correct Answer)
B. Neuroleptic malignant syndrome
C. Thyrotoxicosis
D. King-Denborough syndrome

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a pharmacogenetic hypermetabolic disorder of skeletal muscle triggered by volatile anesthetics (e.g., Halothane) and depolarizing muscle relaxants (Succinylcholine). The **Caffeine-Halothane Contracture Test (CHCT)** is the **gold standard (definitive) diagnostic test** for MH. It involves a muscle biopsy (usually from the vastus lateralis) where muscle strips are exposed to caffeine and halothane. In MH-susceptible individuals, the muscle fibers exhibit an exaggerated contractile response at lower concentrations compared to normal muscle due to a defect in the Ryanodine receptor (RYR1). **Analysis of Incorrect Options:** * **B. Neuroleptic Malignant Syndrome (NMS):** While clinically similar to MH (hyperthermia, rigidity), NMS is caused by dopamine antagonists (antipsychotics) and is not triggered by anesthetic gases. It does not show a positive CHCT. * **C. Thyrotoxicosis:** This is a hypermetabolic state due to excess thyroid hormone. While it can cause intraoperative tachycardia and hyperthermia, the underlying mechanism is hormonal, not a primary skeletal muscle calcium defect. * **D. King-Denborough Syndrome:** This is a rare congenital myopathy associated with MH susceptibility. While these patients are at high risk for MH, the CHCT is specifically used to diagnose the *susceptibility to Malignant Hyperthermia* itself, rather than the syndrome's dysmorphic features. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign of MH:** Increase in EtCO₂ (End-tidal Carbon Dioxide). * **Most Specific Sign:** Muscle rigidity (Masseter spasm). * **Drug of Choice:** **Dantrolene** (Mechanism: Inhibits calcium release from the sarcoplasmic reticulum by acting on RYR1). * **Genetic Mutation:** Most commonly involves the **RYR1 gene** on Chromosome 19. * **Safe Agents:** Propofol, Ketamine, Etomidate, and Nitrous Oxide.

Question 76: Abnormal plasma choline esterase produces apnea due to which of the following?

A. Halothane
B. Lignocaine
C. Suxamethonium (Correct Answer)
D. Isoflurane

Explanation: ### Explanation **Correct Option: C. Suxamethonium** Suxamethonium (Succinylcholine) is a depolarizing neuromuscular blocking agent. Its duration of action is normally very short (5–10 minutes) because it is rapidly hydrolyzed by the enzyme **Plasma Cholinesterase** (also known as Pseudocholinesterase or Butyrylcholinesterase). In patients with **Atypical Plasma Cholinesterase** (a genetic condition inherited as an autosomal recessive trait), the enzyme has a reduced affinity for the drug. Consequently, Suxamethonium is not metabolized at the normal rate, leading to a prolonged neuromuscular block and persistent respiratory muscle paralysis. This clinical phenomenon is known as **Suxamethonium Apnea**. **Why Incorrect Options are Wrong:** * **A & D (Halothane & Isoflurane):** These are volatile inhalational anesthetics. They are primarily eliminated via the lungs through exhalation and are not metabolized by plasma cholinesterase. Their main life-threatening complication is Malignant Hyperthermia. * **B (Lignocaine):** This is an amide-type local anesthetic. Amide local anesthetics are metabolized in the **liver** by microsomal enzymes (CYP450), not by plasma cholinesterase. (Note: Ester-type local anesthetics like Procaine *are* metabolized by plasma cholinesterase, but Lignocaine is an amide). **High-Yield Clinical Pearls for NEET-PG:** * **Dibucaine Number:** This is the screening test for atypical cholinesterase. Dibucaine inhibits normal enzyme by 80%, while atypical enzyme is inhibited by only 20%. A **low Dibucaine number** indicates an atypical enzyme. * **Management:** The primary treatment for Suxamethonium apnea is **mechanical ventilation and sedation** until the block wears off spontaneously. Fresh frozen plasma (FFP) can be given as it contains the enzyme, but it is rarely required. * **Mivacurium:** This is the only non-depolarizing muscle relaxant also metabolized by plasma cholinesterase; its action is also prolonged in these patients.

Question 77: Administration of succinylcholine produces dangerous hyperkalemia in which of the following conditions?

A. Paraplegia (Correct Answer)
B. Fracture of femur
C. Conditions causing elevated intracranial pressure
D. Acute renal failure

Explanation: ### Explanation **Correct Answer: A. Paraplegia** Succinylcholine is a depolarizing neuromuscular blocker that acts as an agonist at the nicotinic acetylcholine receptors (nAChR). In healthy individuals, its administration causes a transient, clinically insignificant rise in serum potassium (~0.5 mEq/L). However, in conditions like **Paraplegia** (spinal cord injury), there is a phenomenon called **Up-regulation of Receptors**. Following denervation or prolonged immobilization, extrajunctional acetylcholine receptors (specifically the immature $\alpha_7$ subtype) proliferate across the entire surface of the muscle membrane. When succinylcholine binds to these widespread receptors, it causes massive, synchronized depolarization, leading to an efflux of potassium that can result in life-threatening hyperkalemia and cardiac arrest. **Analysis of Incorrect Options:** * **B. Fracture of femur:** While major trauma can lead to hyperkalemia, a simple fracture does not typically cause the massive receptor up-regulation required for a dangerous response. However, extensive crush injuries or burns are significant risk factors. * **C. Elevated ICP:** Succinylcholine can transiently increase intracranial pressure (ICP), making it a relative contraindication in neurosurgery, but it does not cause hyperkalemia in these patients unless there is associated denervation. * **D. Acute renal failure:** While these patients have high baseline potassium, succinylcholine does not cause an *exaggerated* release of potassium in them. It is generally avoided if the baseline K+ is >5.5 mEq/L, but the mechanism of "dangerous hyperkalemia" (up-regulation) is not present here. **High-Yield Clinical Pearls for NEET-PG:** * **Safe Window:** In spinal cord injuries, succinylcholine is generally considered safe within the first 24–48 hours. The risk of hyperkalemia peaks between 1 to 6 months post-injury. * **Other High-Risk Conditions:** Severe burns (>10% BSA), Muscular Dystrophy (Duchenne’s), Guillain-Barré Syndrome, and prolonged immobilization in the ICU. * **Antidote:** Pre-curarization (small dose of non-depolarizing agent) does **not** reliably prevent this exaggerated hyperkalemic response.

Question 78: Muscle rigidity due to opioids is because of their effect on which receptor?

A. mu (Correct Answer)
B. kappa
C. sigma
D. delta

Explanation: **Explanation:** Opioid-induced muscle rigidity (often termed "stiff person syndrome" or "wooden chest syndrome") is a well-known side effect associated with high-dose, rapid intravenous administration of potent synthetic opioids like **Fentanyl, Sufentanil, and Remifentanil**. **Why Mu (μ) is correct:** The primary mechanism involves the activation of **mu-opioid receptors** located in the **striatum and the substantia nigra** (central nervous system). This activation leads to a decrease in GABAergic inhibition and an increase in dopaminergic activity, ultimately stimulating the spinal motor neurons. This results in intense rigidity of the thoracic and abdominal muscles, which can severely impede bag-mask ventilation and intubation. **Why other options are incorrect:** * **Kappa (κ):** These receptors are primarily associated with spinal analgesia, sedation, and miosis. They are also linked to dysphoria and psychotomimetic effects, but not muscle rigidity. * **Sigma (σ):** Formerly classified as opioid receptors, they are now considered non-opioid binding sites. They are associated with hallucinations and dysphoria (e.g., with Ketamine). * **Delta (δ):** These receptors play a role in spinal/supraspinal analgesia and modulating mu-receptor activity, but they do not mediate the motor-rigidity pathway. **High-Yield Clinical Pearls for NEET-PG:** 1. **Management:** The definitive treatment for opioid-induced rigidity is the administration of a **neuromuscular blocking agent** (e.g., Succinylcholine) and controlled ventilation. Naloxone can reverse it but will also abolish analgesia. 2. **Clinical Impact:** The most dangerous aspect is "Wooden Chest Syndrome," where chest wall compliance decreases so drastically that ventilation becomes impossible. 3. **Prevention:** Rigidity can be minimized by slow drug infusion and pre-treatment with a small dose of non-depolarizing muscle relaxants.

Question 79: Which of the following are postulated mechanisms by which propofol acts as an antiemetic?

A. Antidopaminergic activity
B. Depressant effect on the chemoreceptor trigger zone
C. Decreased release of glutamate and substance P in the olfactory cortex and decreased serotonin
D. All of the above (Correct Answer)

Explanation: Propofol is unique among intravenous induction agents for its potent **antiemetic properties**, making it the drug of choice for Total Intravenous Anesthesia (TIVA) to prevent Postoperative Nausea and Vomiting (PONV). Its mechanism of action as an antiemetic is **multifactorial**, involving both central and peripheral pathways. ### **Mechanism of Action:** 1. **Antidopaminergic Activity:** Propofol exerts a weak antagonistic effect on **D2 receptors**. By inhibiting dopamine signaling, it reduces the stimulation of the emetic center. 2. **Depressant Effect on the CTZ:** It directly depresses the **Chemoreceptor Trigger Zone (CTZ)** in the area postrema and the subcortical centers, raising the threshold for vomiting. 3. **Neurotransmitter Modulation:** Propofol decreases the release of excitatory neurotransmitters like **Glutamate and Substance P** in the olfactory cortex. Furthermore, it reduces **serotonin (5-HT3)** levels in the area postrema, mimicking the action of specialized antiemetics like ondansetron. ### **Why "All of the Above" is Correct:** Since propofol utilizes all three pathways—dopamine antagonism, CTZ depression, and modulation of glutamate/serotonin—to suppress the vomiting reflex, option D is the most comprehensive and accurate answer. ### **High-Yield NEET-PG Pearls:** * **Sub-hypnotic Doses:** The antiemetic effect occurs at doses much lower than those required for induction (e.g., **10–20 mg IV** or a low-dose infusion of 10 µg/kg/min). * **PONV Gold Standard:** TIVA with Propofol is considered the most effective anesthetic strategy to reduce the baseline risk of PONV. * **PRIS:** Beware of **Propofol Related Infusion Syndrome** (metabolic acidosis, rhabdomyolysis, hyperkalemia) during prolonged high-dose infusions.

Question 80: What are the CNS affections of a local anesthetic agent?

A. Convulsion
B. Perioral numbness
C. Depression
D. All of the above (Correct Answer)

Explanation: **Explanation:** Local Anesthetic (LA) systemic toxicity (LAST) primarily affects the Central Nervous System (CNS) and the Cardiovascular system. CNS symptoms typically precede cardiovascular collapse because the brain is highly sensitive to sodium channel blockade. The progression of CNS toxicity follows a predictable pattern based on increasing plasma concentrations: 1. **Initial/Early Signs (Option B):** At low toxic levels, patients experience sensory changes such as **perioral numbness**, tingling of the tongue, a metallic taste, and tinnitus. This occurs due to the high vascularity of these areas and the sensitivity of cranial nerves. 2. **Excitatory Phase (Option A):** As levels rise, LAs selectively inhibit cortical inhibitory pathways (GABAergic neurons) while leaving excitatory pathways unopposed. This leads to agitation, muscle twitching, and eventually **grand mal convulsions**. 3. **Depressive Phase (Option C):** At very high concentrations, both inhibitory and excitatory pathways are inhibited, leading to generalized **CNS depression**. This manifests as unconsciousness, respiratory depression, and eventually coma. Since all three options represent different stages of the clinical spectrum of CNS toxicity, **Option D (All of the above)** is the correct answer. **High-Yield NEET-PG Pearls:** * **Potency vs. Toxicity:** Bupivacaine is more cardiotoxic than Lidocaine. The "CC/CNS ratio" (dose required for cardiovascular collapse vs. dose for convulsions) is lower for Bupivacaine, making it more dangerous. * **First Sign:** Perioral numbness/metallic taste is often the earliest warning sign of accidental intravascular injection. * **Management:** The specific antidote for LAST is **20% Intralipid (Lipid Emulsion Therapy)**. * **Hypercapnia/Acidosis:** Increases the risk of CNS toxicity by increasing cerebral blood flow (delivering more drug to the brain) and decreasing the seizure threshold.

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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