Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 21: An eye surgery was performed using propofol as the intravenous anaesthetic agent and succinylcholine as the muscle relaxant. Recovery from anaesthesia was uneventful. However, the patient complains of pain in the muscles. Which of the following is the likely reason for this?

A. Propofol
B. Succinylcholine (Correct Answer)
C. Muscle infarction
D. None of the above

Explanation: ### Explanation **Correct Option: B. Succinylcholine** The patient is experiencing **postoperative myalgia (POM)**, a well-documented side effect of Succinylcholine (Suxamethonium). Succinylcholine is a depolarizing neuromuscular blocker that acts by mimicking acetylcholine at the nicotinic receptors. This results in persistent depolarization, clinically visible as **fasciculations** (uncoordinated muscle contractions). These intense contractions lead to micro-trauma of muscle fibers and the release of lactic acid and potassium, resulting in muscle pain that typically appears 24–48 hours post-surgery. It is most common in young adults undergoing minor "day-care" procedures (like eye surgery) where early mobilization occurs. **Why other options are incorrect:** * **A. Propofol:** Propofol is an intravenous anesthetic agent known for its rapid recovery profile. While it can cause pain *on injection*, it does not cause generalized postoperative muscle pain. In fact, propofol is sometimes used to reduce the incidence of succinylcholine-induced fasciculations. * **C. Muscle infarction:** This is a rare, severe condition usually associated with vascular compromise or compartment syndrome. It would present with localized, excruciating pain, swelling, and potentially skin changes, rather than generalized muscle soreness following a routine eye surgery. **NEET-PG High-Yield Pearls:** * **Prevention:** POM can be minimized by "pre-curarization"—administering a small dose of a non-depolarizing muscle relaxant (e.g., Vecuronium) before Succinylcholine. * **Risk Factors:** Highest incidence is seen in females and "ambulatory" patients. It is ironically *less* common in children and the elderly. * **Other Side Effects of Succinylcholine:** Hyperkalemia, bradycardia (especially in children), increased intraocular/intragastric pressure, and it is a potent trigger for **Malignant Hyperthermia**.

Question 22: Which anaesthetic agent should NOT be used in a patient with a previous history of halothane-induced hepatitis?

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

Explanation: **Explanation:** The correct answer is **Methoxyflurane**. **1. Why Methoxyflurane is the correct choice:** Halothane-induced hepatitis is believed to be an immune-mediated reaction triggered by the metabolism of halothane into **trifluoroacetylated (TFA) proteins**. These proteins act as haptens, leading to the formation of autoantibodies. There is a high degree of **cross-sensitivity** between volatile anesthetics that undergo significant metabolism into TFA intermediates. Methoxyflurane, along with Halothane and Enflurane, undergoes significant hepatic metabolism (up to 50-70% for Methoxyflurane) and shares similar metabolic pathways. Therefore, it is strictly contraindicated in patients with a history of halothane-induced hepatitis to avoid a potentially fatal recurrent hepatic injury. **2. Analysis of Incorrect Options:** * **Sevoflurane:** It is not metabolized into TFA intermediates. It is primarily metabolized into inorganic fluoride and hexafluoroisopropanol, making it the safest volatile agent regarding halothane-related cross-reactivity. * **Isoflurane:** While it does produce a very small amount of TFA proteins, the metabolism is extremely low (0.2%). While caution is advised, it is not as strictly contraindicated as Methoxyflurane or Enflurane. * **Ketamine:** This is an intravenous induction agent, not a halogenated ether. It does not share the metabolic pathway or the chemical structure responsible for halothane-induced hepatitis. **3. Clinical Pearls for NEET-PG:** * **Metabolism Rule:** The risk of hepatitis correlates with the degree of hepatic metabolism: Halothane (20%) > Enflurane (2%) > Isoflurane (0.2%) > Desflurane (0.02%). * **Methoxyflurane** is also notorious for **nephrotoxicity** due to the release of inorganic fluoride ions (High-output renal failure). * **Risk Factors for Halothane Hepatitis:** Female gender, obesity, middle age, and multiple exposures to halothane.

Question 23: While inserting a central venous catheter, a patient develops respiratory distress. Which of the following is the most likely cause?

A. Hemothorax
B. Hypovolemia
C. Pneumothorax (Correct Answer)
D. Pleural effusion

Explanation: **Explanation:** **Pneumothorax** is the most common and immediate respiratory complication associated with central venous catheter (CVC) insertion, particularly when using the **subclavian** or **internal jugular** approach. The apex of the lung (cupula) extends above the level of the first rib; accidental puncture of the pleura by the introducer needle allows air to enter the pleural space, leading to lung collapse and sudden respiratory distress. **Analysis of Options:** * **Pneumothorax (Correct):** Sudden onset of dyspnea, tachypnea, and decreased breath sounds on the affected side during or immediately after the procedure are classic signs. * **Hemothorax:** While possible if a major artery (like the subclavian) is punctured, it usually presents with signs of hemorrhagic shock or slower onset respiratory distress compared to the acute presentation of a pneumothorax. * **Hypovolemia:** This is a state of volume depletion. While it makes the vein harder to hit (increasing the risk of complications), it is a pre-existing condition or a result of hemorrhage, not a direct cause of sudden respiratory distress during the procedure. * **Pleural Effusion:** This is a chronic or subacute accumulation of fluid. While an "infusothorax" (infusing IV fluids into the pleural space) can occur if the catheter is misplaced, it is less common than an immediate procedural pneumothorax. **High-Yield Clinical Pearls for NEET-PG:** * **Highest Risk Site:** The **subclavian vein** approach carries a higher risk of pneumothorax (1–2%) compared to the internal jugular vein. * **Gold Standard Diagnosis:** An upright **Expiratory Chest X-ray** is the investigation of choice to visualize a small pneumothorax. * **Prevention:** The use of **Real-time Ultrasound guidance** significantly reduces the incidence of mechanical complications during CVC insertion. * **Management:** Small asymptomatic pneumothoraces (<15-20%) may be observed; large or symptomatic ones require a chest tube (intercostal drain).

Question 24: A severely ill patient was maintained on an infusional anesthetic agent. On the 2nd day, the patient started deteriorating. What is the probable culprit?

A. Etomidate (Correct Answer)
B. Propofol
C. Opioid
D. Barbiturate

Explanation: **Explanation:** The correct answer is **Etomidate**. The clinical scenario describes a severely ill patient deteriorating after a continuous infusion of an anesthetic agent. This is a classic presentation of **Etomidate-induced Adrenocortical Suppression**. **Why Etomidate is the correct answer:** Etomidate is a potent inhibitor of the enzyme **11-beta-hydroxylase**, which is essential for the conversion of 11-deoxycortisol to cortisol. Even a single induction dose can suppress cortisol production for 24–48 hours. When used as a continuous infusion (especially in critically ill or septic patients), it leads to primary adrenal insufficiency, increased morbidity, and higher mortality rates. Consequently, etomidate is strictly contraindicated for long-term sedation or maintenance infusion. **Analysis of Incorrect Options:** * **Propofol:** While "Propofol Infusion Syndrome" (PRIS) is a known complication of long-term infusion (causing metabolic acidosis, rhabdomyolysis, and cardiac failure), it typically occurs with high doses (>4mg/kg/hr) over 48 hours. Etomidate is the more "classic" culprit for rapid deterioration in the context of adrenal suppression in a "severely ill" patient. * **Opioids:** These are commonly used for long-term sedation in ICUs. While they cause respiratory depression and bradycardia, they do not typically cause the acute systemic deterioration described. * **Barbiturates (e.g., Thiopental):** These are rarely used for maintenance infusions due to their long half-life and accumulation in fat (context-sensitive half-life), but they do not cause specific endocrine failure like etomidate. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Inhibition of 11-β-hydroxylase. * **Hemodynamics:** Etomidate is the induction agent of choice for patients with **cardiovascular instability** (minimal effect on BP/HR). * **Side Effects:** High incidence of **myoclonus** (minimized by opioid premedication) and postoperative nausea/vomiting (PONV). * **Contraindication:** Avoid in patients with **Sepsis** or known Adrenal Insufficiency.

Question 25: What is true about post-spinal headache?

A. Frontal location
B. Worse when lying down
C. Low incidence with thin (25 G) needles (Correct Answer)
D. Increased by abdominal compression

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 hole. This leads to low CSF pressure and compensatory cerebral vasodilation. ### **Explanation of Options** * **Correct Option (C):** The incidence of PDPH is directly proportional to the diameter of the needle used. Using **thinner needles (e.g., 25 G, 27 G)** or non-cutting (pencil-point) needles like **Whitacre or Sprotte** significantly reduces the size of the dural rent, thereby lowering the incidence of headache. * **Option A:** PDPH is typically **occipital or frontal**, but it characteristically radiates to the neck and shoulders. * **Option B:** A hallmark of PDPH is its **orthostatic nature**. It is worsened by sitting or standing and is characteristically **relieved by lying flat**. * **Option D:** Abdominal compression (or the Girdle test) actually **decreases** the severity of the headache. It increases intra-abdominal pressure, which is transmitted to the epidural space, thereby reducing CSF leakage and increasing intracranial pressure. ### **High-Yield Clinical Pearls for NEET-PG** * **Gold Standard Treatment:** **Epidural Blood Patch** (15–20 ml of autologous blood injected into the epidural space). * **Needle Type:** Pencil-point needles (Whitacre/Sprotte) have a lower incidence of PDPH compared to cutting-tip needles (Quincke) because they separate rather than cut dural fibers. * **Risk Factors:** Young age, female gender, pregnancy, and a history of previous PDPH. * **Conservative Management:** Bed rest, aggressive hydration, oral/IV caffeine (causes cerebral vasoconstriction), and analgesics.

Question 26: A patient is not breathing after anesthesia. This is most likely due to which of the following?

A. Prolonged anesthesia
B. Neuromuscular blockade
C. Recurrent intubation leading to cord's failure
D. All of the above (Correct Answer)

Explanation: **Explanation:** Post-operative apnea or delayed recovery from anesthesia is a common clinical scenario in the PACU (Post-Anesthesia Care Unit). The correct answer is **All of the above** because each option represents a distinct physiological or mechanical cause for a patient failing to breathe spontaneously. 1. **Prolonged Anesthesia:** Excessive depth of anesthesia or the residual effect of intravenous/inhalational agents (like Opioids or Propofol) can cause central respiratory depression. Opioids, in particular, decrease the sensitivity of the respiratory center to carbon dioxide ($CO_2$), leading to hypoventilation or apnea. 2. **Neuromuscular Blockade:** This is the most common cause of post-operative respiratory failure. Residual neuromuscular block (due to non-depolarizing muscle relaxants like Vecuronium or Rocuronium) results in peripheral muscle weakness. If the diaphragm and intercostal muscles are still blocked, the patient cannot generate enough tidal volume to breathe independently. 3. **Recurrent Intubation/Cord Failure:** Repeated attempts at intubation can cause laryngeal trauma, glottic edema, or vocal cord injury/palsy. This leads to upper airway obstruction. While the patient may attempt to breathe, the mechanical failure of the "airway gate" prevents effective ventilation, appearing as a lack of clinical breathing. **High-Yield Clinical Pearls for NEET-PG:** * **Scored Assessment:** Always check the **Train-of-Four (TOF) ratio**; a ratio of **>0.9** is required for safe extubation. * **Reversal Agents:** Neostigmine (with Glycopyrrolate) or Sugammadex (specifically for Rocuronium/Vecuronium) are used to reverse neuromuscular blockade. * **Dual Block:** Remember that Succinylcholine can cause a "Phase II block" in patients with atypical pseudocholinesterase, leading to prolonged apnea. * **Hypothermia & Acidosis:** Both conditions can potentiate the effects of muscle relaxants and delay recovery.

Question 27: What is the drug of choice for treating malignant hyperthermia?

A. Dantrolene (Correct Answer)
B. Nikethamide
C. Baclofen
D. Propofol

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a 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:** Dantrolene is the specific antidote and the drug of choice for MH. It acts as a **ryanodine receptor (RyR1) antagonist** on the sarcoplasmic reticulum of skeletal muscle. By blocking these receptors, it inhibits the massive release of intracellular calcium that causes the characteristic muscle rigidity, hypercarbia, and hyperthermia seen in MH. **Analysis of Incorrect Options:** * **Nikethamide:** A respiratory stimulant once used for CNS depression; it has no role in muscle metabolism or MH. * **Baclofen:** A GABA-B receptor agonist used for chronic spasticity (acting centrally). It does not affect the peripheral calcium release mechanism involved in MH. * **Propofol:** An intravenous anesthetic agent. While it is a "safe" drug to use in MH-susceptible patients, it cannot treat the condition once it has started. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** The earliest and most sensitive indicator of MH is an **unexplained rise in End-Tidal CO2 (ETCO2)**. * **Genetic Mutation:** Most commonly associated with the **RYR1 gene** on Chromosome 19. * **Dosing:** The initial dose of Dantrolene is **2.5 mg/kg IV**, repeated every 5–10 minutes until symptoms subside. * **Gold Standard Test:** The **Caffeine-Halothane Contracture Test (CHCT)** performed on a muscle biopsy is the definitive diagnostic tool for susceptibility.

Question 28: A patient undergoing surgical procedure under general anesthesia suddenly develops tachycardia, hypertension, sweating, and tachypnea. What is the best immediate step to manage the situation?

A. Administer an IV beta-blocker
B. Abandon the surgery
C. Deepen the plane of anesthesia (Correct Answer)
D. No intervention is required

Explanation: ### Explanation The clinical presentation described—**tachycardia, hypertension, sweating, and tachypnea**—is the classic tetrad indicating an **inadequate plane of anesthesia**. These are physiological signs of sympathetic overactivity in response to surgical stress or painful stimuli. **Why Option C is Correct:** The most common cause of sudden sympathetic stimulation during surgery is "light anesthesia." When the depth of anesthesia is insufficient to suppress the patient's response to surgical stimuli, the body releases catecholamines. The **immediate and most appropriate step** is to deepen the plane of anesthesia (e.g., by increasing the concentration of volatile anesthetic or administering an IV bolus of an induction agent/opioid) to suppress this autonomic surge. **Analysis of Incorrect Options:** * **Option A (IV Beta-blocker):** While beta-blockers treat tachycardia and hypertension, they only mask the symptoms without addressing the underlying cause (pain/awareness). Using them without deepening anesthesia may leave the patient conscious but unable to manifest physiological distress. * **Option B (Abandon surgery):** This is an extreme measure reserved for life-threatening crises like Malignant Hyperthermia or refractory cardiac arrest. Light anesthesia is easily reversible. * **Option D (No intervention):** Ignoring these signs can lead to intraoperative awareness, myocardial ischemia (due to increased oxygen demand), or surgical complications due to patient movement. **NEET-PG High-Yield Pearls:** * **Triad of General Anesthesia:** Narcosis (Unconsciousness), Analgesia, and Muscle Relaxation. * **First sign of light anesthesia in a paralyzed patient:** Tachycardia and Hypertension (since tachypnea/movement is masked by neuromuscular blockers). * **Differential Diagnosis:** If symptoms persist despite deepening anesthesia, consider **Malignant Hyperthermia** (look for hypercarbia and temperature rise) or **Thyroid Storm**. * **MAC (Minimum Alveolar Concentration):** Increasing the MAC of inhalational agents is the standard way to deepen the plane.

Question 29: Which of the following is NOT a complication of massive blood transfusion?

A. Hyperkalemia
B. Alkalosis
C. Acidosis
D. Hypercalcemia (Correct Answer)

Explanation: **Explanation:** Massive blood transfusion (MBT) is defined as the replacement of one total blood volume within 24 hours or 10 units of PRBCs within 24 hours. The correct answer is **Hypercalcemia** because MBT actually causes **Hypocalcemia**. **1. Why Hypercalcemia is the Correct Answer (The Concept):** Stored blood contains **Sodium Citrate** as an anticoagulant. When large volumes are infused rapidly, the citrate binds to the patient’s ionized calcium, forming calcium citrate. This leads to a decrease in serum ionized calcium levels (**Hypocalcemia**). It is a classic complication, especially in patients with impaired liver function who cannot metabolize citrate efficiently. **2. Why the other options are complications:** * **Hyperkalemia (Option A):** During storage, the RBC membrane becomes leaky, causing potassium to move from the intracellular to the extracellular space. Therefore, stored blood has high potassium levels. * **Acidosis (Option C):** Stored blood is acidic due to the accumulation of lactic acid and the presence of Citrate-Phosphate-Dextrose (CPD) preservative. * **Alkalosis (Option B):** While initial infusion causes acidosis, the late metabolic response is **Metabolic Alkalosis**. This occurs because the liver metabolizes the infused citrate into bicarbonate. **Clinical Pearls for NEET-PG:** * **Hypothermia:** The most common complication of MBT (due to cold blood infusion). * **Dilutional Coagulopathy:** MBT leads to a deficiency of platelets and Factors V and VIII. * **TRALI:** Transfusion-Related Acute Lung Injury is the leading cause of transfusion-related mortality. * **Shift to Left:** Stored blood has low 2,3-DPG, shifting the Oxygen Dissociation Curve to the left (increased affinity, decreased release to tissues).

Question 30: Succinylcholine causes hyperkalemia in patients with which of the following conditions?

A. Burns
B. Severe infection
C. High velocity trauma
D. All of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **D. All of the above**. **Underlying Medical Concept: Up-regulation of Acetylcholine Receptors** Succinylcholine is a depolarizing neuromuscular blocker that acts on nicotinic acetylcholine receptors (nAChRs). In certain pathological states, there is an **up-regulation** of these receptors. This involves the proliferation of mature receptors and the expression of **immature (fetal) isoforms** ($\alpha7$ subtype) across the entire surface of the muscle membrane (extrajunctional receptors), rather than just at the neuromuscular junction. When succinylcholine binds to these widespread receptors, it causes prolonged depolarization and a massive efflux of potassium from the muscle cells into the extracellular fluid. This can lead to life-threatening hyperkalemia. **Analysis of Options:** * **A. Burns:** Significant thermal injury leads to massive receptor up-regulation. The risk typically begins 24–48 hours post-injury and can persist for a year or more. * **B. Severe infection:** Prolonged immobilization and systemic inflammatory responses (sepsis) trigger the proliferation of extrajunctional receptors. * **C. High velocity trauma:** Extensive muscle crush injuries and denervation lead to a similar hyperkalemic response due to muscle cell membrane instability and receptor spread. **High-Yield Clinical Pearls for NEET-PG:** * **Safe Window:** Succinylcholine is generally considered safe within the first **24 hours** of a burn or trauma; the risk of hyperkalemia peaks after 48 hours. * **Other Contraindications:** Upper/lower motor neuron lesions (Stroke, Spinal cord injury), Muscular dystrophies (Duchenne’s), and prolonged immobilization. * **Potassium Rise:** In a healthy individual, Succinylcholine raises serum $K^+$ by **0.5 mEq/L**. In the above conditions, it can rise by **>5-10 mEq/L**, leading to cardiac arrest. * **Management:** If hyperkalemia occurs, treat with Calcium gluconate (cardioprotection), insulin/dextrose, and sodium bicarbonate.

Practice by Chapter

Adverse Drug Reactions

Practice Questions

Anaphylaxis and Allergic Reactions

Practice Questions

Malignant Hyperthermia

Practice Questions

Local Anesthetic Toxicity

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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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