Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 171: Which of the following is true about hypothermia during anesthesia?

A. Hypothermia is beneficial to patients.
B. Hypothermia can be prevented by giving warm fluids. (Correct Answer)
C. The body loses heat mainly by conduction.
D. Hypothermia always occurs irrespective of the type of anesthesia.

Explanation: ### Explanation **1. Why Option B is Correct:** Intraoperative hypothermia (defined as a core temperature <36°C) is a common complication. One of the most effective ways to maintain normothermia is by **warming intravenous fluids**. Administering room-temperature fluids (approx. 21°C) to a patient can significantly drop core temperature because the body must expend energy to warm the fluid to 37°C. Using fluid warmers prevents this heat loss, especially during major surgeries involving large volume replacements. **2. Why the Other Options are Incorrect:** * **Option A:** While "induced" hypothermia is used in specific scenarios (like cardiac surgery or neuroprotection), **accidental** perioperative hypothermia is harmful. It leads to morbid cardiac events, increased surgical site infections, impaired wound healing, and coagulopathy (due to platelet dysfunction). * **Option C:** The body loses heat via four mechanisms, but the **primary mode (60%) is Radiation**, followed by Convection, Evaporation, and lastly Conduction. * **Option D:** While common, hypothermia is not inevitable. It can be prevented through active warming measures (Forced Air Warmers/Bair Huggers, warmed fluids, and increasing ambient theater temperature). **3. High-Yield Clinical Pearls for NEET-PG:** * **Phase 1 Heat Loss:** The initial rapid drop in temperature during the first hour of anesthesia is due to **internal redistribution** of heat from the core to the periphery (vasodilation). * **Post-Anesthetic Shivering:** This increases oxygen consumption by up to **400-500%**. The drug of choice to treat shivering is **Pethidine (Meperidine)**. * **General vs. Regional:** Both cause hypothermia. Regional anesthesia (Spinal/Epidural) causes it by peripheral vasodilation and by inhibiting the brain's thermoregulatory vasoconstriction below the level of the block.

Question 172: Which of the following is not a complication of succinylcholine?

A. Increased intraocular pressure
B. Increased intracranial pressure
C. Increased blood pressure (Correct Answer)
D. Decreased heart rate

Explanation: **Explanation:** Succinylcholine is a depolarizing neuromuscular blocker (DNMB) known for its rapid onset and short duration. However, its mechanism of action—prolonged depolarization of the motor endplate—leads to several systemic side effects. **Why "Increased Blood Pressure" is the correct answer:** Succinylcholine does not typically cause a rise in blood pressure. In fact, its cardiovascular effects are unpredictable but more commonly lean toward **bradycardia** (especially in children or with second doses) due to its structural similarity to acetylcholine, which allows it to stimulate muscarinic receptors in the sinus node. While sympathetic stimulation can occur, hypertension is not a classic or reliable complication of the drug. **Analysis of other options:** * **Increased Intraocular Pressure (IOP):** Succinylcholine causes a transient rise in IOP (5–10 mmHg) due to the contraction of extraocular muscles and choroidal vascular dilatation. It should be used with caution in penetrating eye injuries. * **Increased Intracranial Pressure (ICP):** Fasciculations and increased cerebral blood flow can lead to a mild, transient increase in ICP. * **Decreased Heart Rate (Bradycardia):** This is a well-known complication, particularly in pediatric patients or upon administration of a second dose in adults, due to the activation of cardiac muscarinic receptors. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperkalemia:** Succinylcholine can raise serum potassium by **0.5 mEq/L**. It is strictly contraindicated in burns (>24 hours), crush injuries, and denervation states (e.g., stroke, spinal cord injury) due to the risk of fatal hyperkalemia. * **Malignant Hyperthermia:** It is a potent trigger for MH in genetically susceptible individuals. * **Dual Block (Phase II Block):** Occurs with high doses or prolonged infusions, where the block takes on characteristics of a non-depolarizing block. * **Muscle Soreness:** Postoperative myalgia is common due to initial fasciculations.

Question 173: Hepatitis can be a complication of which anesthetic agent?

A. Halothane (Correct Answer)
B. Enflurane
C. Methoxyflurane
D. Sevoflurane

Explanation: **Explanation:** **Halothane** is the correct answer because it is classically associated with **Halothane Hepatitis**, a rare but severe immune-mediated hepatotoxicity. This occurs due to the metabolism of halothane by cytochrome P450 to a reactive intermediate (trifluoroacetyl chloride). This intermediate binds to hepatic proteins, forming neoantigens that trigger an antibody-mediated (Type II hypersensitivity) immune response against hepatocytes. **Analysis of Options:** * **Halothane (A):** About 20% of halothane undergoes hepatic metabolism. It can cause two types of injury: Type I (mild, transient rise in transaminases) and Type II (fulminant hepatic necrosis). Risk factors include multiple exposures, obesity, female gender, and middle age. * **Enflurane (B):** While it can theoretically cause hepatitis due to similar metabolism, the incidence is significantly lower (10 times less) than halothane. * **Methoxyflurane (C):** This agent is primarily associated with **nephrotoxicity** (fluoride-induced high-output renal failure) rather than hepatitis. * **Sevoflurane (D):** It is not metabolized to trifluoroacetylated compounds and is therefore not associated with immune-mediated hepatitis. Its main concern is the formation of **Compound A** (nephrotoxic in rats). **High-Yield Clinical Pearls for NEET-PG:** * **"Halothane Shakes":** Post-operative shivering is a common side effect. * **Arrhythmogenic potential:** Halothane sensitizes the myocardium to catecholamines (avoid using adrenaline). * **Metabolism Rule:** Halothane (20%) > Enflurane (2%) > Isoflurane (0.2%) > Desflurane (0.02%). Higher metabolism correlates with higher toxicity risk. * **Gold Standard:** Halothane is no longer the first choice in adults but was historically used in pediatrics due to its non-pungent odor (smooth induction).

Question 174: Malignant hyperthermia is caused by:

A. Succinylcholine and halothane (Correct Answer)
B. Propranolol
C. Lidocaine
D. Bupivacaine

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle. It is triggered in genetically susceptible individuals (often involving a mutation in the **RYR1 gene**) when they are exposed to specific anesthetic agents. 1. **Why Option A is correct:** The primary triggers for MH are **volatile inhalational anesthetics** (e.g., Halothane, Isoflurane, Sevoflurane) and the **depolarizing muscle relaxant Succinylcholine**. These agents cause an uncontrolled release of calcium from the sarcoplasmic reticulum into the myoplasm. This leads to sustained muscle contraction, excessive ATP consumption, and a massive increase in metabolic rate, resulting in hypercapnia, acidosis, and hyperthermia. 2. **Why other options are incorrect:** * **Options C & D (Lidocaine & Bupivacaine):** Local anesthetics of the amide group were historically feared but are now considered **safe** in MH-susceptible patients. * **Option B (Propranolol):** Beta-blockers do not trigger MH. In fact, non-triggering agents include all IV induction agents (Propofol, Thiopental), opioids, and non-depolarizing muscle relaxants (Vecuronium, Rocuronium). **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) following Succinylcholine administration. * **Drug of Choice:** **Dantrolene** (a Ryanodine receptor antagonist). * **Mechanism:** Defect in the **Ryanodine Receptor (RYR1)** or Dihydropyridine receptor. * **Associated Conditions:** Central Core Disease, King-Denborough Syndrome.

Question 175: Which anesthetic agent is contraindicated in acute intermittent porphyria?

A. Halothane
B. Isoflurane
C. Propofol
D. Thiopentone (Correct Answer)

Explanation: **Explanation:** **1. Why Thiopentone is the Correct Answer:** Acute Intermittent Porphyria (AIP) is a metabolic disorder characterized by a deficiency in the enzyme porphobilinogen deaminase. **Thiopentone (and all barbiturates)** are potent inducers of the hepatic enzyme **ALA synthetase**. By inducing this enzyme, barbiturates accelerate the production of porphyrins, leading to an accumulation of toxic precursors (ALA and PBG). This can trigger a life-threatening "porphyric crisis," characterized by severe abdominal pain, neuropsychiatric symptoms, and autonomic instability. **2. Why the Other Options are Incorrect:** * **Halothane and Isoflurane (Options A & B):** Most volatile inhalational agents are considered safe in porphyria. While some older literature suggested caution, modern clinical practice regards Isoflurane as a safe choice for maintenance of anesthesia in these patients. * **Propofol (Option C):** Propofol is considered the **induction agent of choice** for patients with porphyria. It does not significantly induce ALA synthetase and is not associated with triggering acute attacks. **3. High-Yield Clinical Pearls for NEET-PG:** * **Safe Induction Agents:** Propofol, Ketamine, and Etomidate (though Etomidate is controversial, it is generally considered safer than barbiturates). * **Safe Muscle Relaxants:** Succinylcholine, Vecuronium, and Atracurium. * **Safe Analgesics:** Morphine and Fentanyl. * **Contraindicated Drugs (Porphyrogenic):** Barbiturates (Thiopentone), Sulfonamides, Etomidate (in some classifications), and Phenytoin. * **Management of Crisis:** The mainstay of treatment for an acute attack is **Intravenous Hematin** (which provides negative feedback to ALA synthetase) and high-dose **Glucose** (carbohydrate loading suppresses porphyrin synthesis).

Question 176: What is a known complication of positive pressure ventilation?

A. Pneumothorax (Correct Answer)
B. Bradycardia
C. Decreased ventilation
D. Arrhythmias

Explanation: **Explanation:** **Correct Option: A. Pneumothorax** Positive Pressure Ventilation (PPV) delivers gas into the lungs by increasing airway pressure. The primary mechanism for complications is **Barotrauma**. When high peak inspiratory pressures (PIP) or excessive tidal volumes are used, the alveoli can overdistend and rupture. Air then escapes into the pleural space, leading to a **Pneumothorax**. This is particularly common in patients with underlying lung pathology like COPD, bullous emphysema, or ARDS. **Analysis of Incorrect Options:** * **B. Bradycardia:** While PPV increases intrathoracic pressure and can decrease venous return (leading to tachycardia as a compensatory mechanism), it does not directly cause bradycardia. Bradycardia in anesthesia is more commonly associated with the oculocardiac reflex, vagal stimulation, or specific drugs (e.g., Succinylcholine, Neostigmine). * **C. Decreased ventilation:** The primary goal of PPV is to *increase* or maintain minute ventilation. While "dead space" may increase due to alveolar overdistension, the process itself is a method of active ventilation. * **D. Arrhythmias:** While hypoxia or hypercarbia (resulting from poor ventilation) can cause arrhythmias, they are not a direct mechanical complication of PPV itself, unlike barotrauma. **High-Yield Clinical Pearls for NEET-PG:** * **Hemodynamic Effects:** PPV increases intrathoracic pressure → decreases venous return (preload) → decreases cardiac output → **Hypotension**. This is a classic board-exam concept. * **Tension Pneumothorax:** If a patient on a ventilator suddenly develops high airway pressures, hypotension, and absent breath sounds, suspect Tension Pneumothorax. Immediate treatment is **needle decompression** in the 2nd/5th intercostal space. * **VILI:** Ventilator-Induced Lung Injury includes barotrauma (pressure), volutrauma (volume), and atelectrauma (shear stress).

Question 177: Epidural anesthesia is associated with a decreased risk of which of the following complications?

A. Headache, Hypotension, and Meningitis
B. Headache and Arachnoiditis
C. Hypotension and Meningitis
D. Headache, Arachnoiditis, and Hypotension (Correct Answer)

Explanation: **Explanation:** The correct answer is **D: Headache, Arachnoiditis, and Hypotension.** This question compares the complication profile of **Epidural Anesthesia** versus **Spinal (Subarachnoid) Anesthesia**. 1. **Headache:** Post-Dural Puncture Headache (PDPH) is a hallmark complication of spinal anesthesia caused by CSF leakage. Since epidural anesthesia is performed in the potential space *outside* the dura, the risk of PDPH is significantly lower (unless an accidental "dural tap" occurs). 2. **Arachnoiditis:** This is an inflammation of the arachnoid mater, usually caused by the direct injection of irritants, preservatives, or contaminants into the subarachnoid space. Because epidural drugs are deposited outside the meninges, the risk of direct chemical or infectious arachnoiditis is minimized. 3. **Hypotension:** While both techniques cause sympathetic blockade, the onset of hypotension in epidural anesthesia is **gradual** (15–20 minutes) compared to the **abrupt** onset seen in spinal anesthesia. This allows for better compensatory mechanisms and easier hemodynamic management. **Analysis of Incorrect Options:** * **Options A & C:** These include **Meningitis**. While epidural anesthesia avoids direct entry into the CSF, the risk of infection (epidural abscess or meningitis) is not necessarily "decreased" compared to spinal anesthesia; in fact, indwelling epidural catheters may pose a slightly higher risk of track infections over prolonged periods. **NEET-PG High-Yield Pearls:** * **Site of Action:** Spinal anesthesia acts on the spinal cord/nerve roots; Epidural acts primarily on the nerve roots exiting the intervertebral foramina. * **Drug Volume:** Epidural requires a much larger volume of local anesthetic (15–20 mL) compared to Spinal (2–4 mL). * **Segmental Block:** Epidural allows for a "segmental block" (e.g., thoracic epidural), whereas spinal anesthesia typically results in a block of all segments below the level of injection. * **Total Spinal:** The most dreaded acute complication of an accidental dural puncture during epidural anesthesia.

Question 178: In malignant hyperthermia, a genetic mutation in the ryanodine receptor (RYR1) leads to a life-threatening reaction to certain anesthetic agents. What is the primary ionic abnormality caused by this receptor defect?

A. Increased sodium influx into the muscle cell
B. Increased potassium uptake into the sarcoplasmic reticulum
C. Increased calcium release from the sarcoplasmic reticulum (Correct Answer)
D. Increased chloride efflux from the muscle cell

Explanation: ***Increased calcium release from the sarcoplasmic reticulum*** - The **ryanodine receptor 1 (RYR1)** mutation found in malignant hyperthermia causes the receptor channel on the sarcoplasmic reticulum (SR) to become hypersensitive and spontaneously release large, uncontrolled amounts of **calcium** into the myoplasm upon exposure to triggering agents (e.g., volatile anesthetics like halothane, succinylcholine). - This massive, sustained elevation of intracellular **calcium** drives continuous muscle contraction, leading to muscle rigidity, hypermetabolism, heat production, rhabdomyolysis, and the characteristic life-threatening features of malignant hyperthermia. - Treatment with **dantrolene** works by inhibiting calcium release from the SR, confirming calcium dysregulation as the primary mechanism. *Increased sodium influx into the muscle cell* - Sodium influx is crucial for initiating the muscle action potential via **voltage-gated sodium channels**, but it is not the primary pathological trigger or defining ionic abnormality in malignant hyperthermia. - The sustained muscle contraction in MH is driven by excessive **calcium** in the myoplasm, not sodium influx which is only involved in initial depolarization. *Increased potassium uptake into the sarcoplasmic reticulum* - The sarcoplasmic reticulum's main function is the storage and release of **calcium**, not potassium regulation. - In severe MH, rhabdomyolysis causes **hyperkalemia** due to potassium *efflux* from damaged muscle cells into the bloodstream, not uptake into the SR. *Increased chloride efflux from the muscle cell* - Chloride channels maintain resting membrane potential and regulate cell volume, but their dysregulation is not the central mechanism of malignant hyperthermia. - The life-threatening symptoms of MH (hyperthermia, rigidity, hypermetabolism, acidosis) are a direct consequence of massive, uncontrolled **calcium release** from the SR, not chloride movement.

Question 179: A patient undergoing surgery develops sudden deranged vitals following a failed attempt at subclavian vein catheterization. On examination, the trachea is shifted to one side and breath sounds are absent on the opposite side. What is the most likely diagnosis?

A. Tension pneumothorax (Correct Answer)
B. Aspiration pneumonitis
C. Pulmonary embolism
D. Bronchospasm

Explanation: ***Correct: Tension pneumothorax*** - **Classic complication of subclavian vein catheterization** - inadvertent puncture of the pleura causes air accumulation in the pleural space - **Pathognomonic clinical features** present in this case: - **Tracheal deviation away from the affected side** (toward the opposite side where breath sounds are absent) - **Absent breath sounds on the affected side** due to complete lung collapse - **Hemodynamic instability** ("deranged vitals") from mediastinal shift compressing the great vessels and heart - **Medical emergency** requiring immediate needle decompression followed by chest tube insertion - The **tension** component occurs when air enters pleural space during inspiration but cannot escape during expiration (one-way valve effect), causing progressive pressure buildup *Incorrect: Aspiration pneumonitis* - Would present with bilateral crackles, hypoxia, and potential bronchospasm - Does **not cause tracheal deviation** or unilateral absent breath sounds - Typically occurs during induction or emergence from anesthesia, not during vascular access procedures *Incorrect: Pulmonary embolism* - Presents with sudden dyspnea, hypoxia, tachycardia, and possible hypotension - Does **not cause tracheal deviation** or unilateral absent breath sounds - Breath sounds remain present bilaterally (though may have localized crackles) - Not directly related to subclavian catheterization attempts *Incorrect: Bronchospasm* - Presents with **bilateral wheezing** and increased airway pressures - Does **not cause tracheal deviation** or unilateral findings - Breath sounds present bilaterally (though may be diminished with severe bronchospasm) - Would not explain the immediate temporal relationship with failed subclavian line attempt

Question 180: A patient is in ICU and there is a failed attempt of subclavian catheterization. Shortly after, BP drops and the pulse rises. What is the diagnosis?

A. Air embolism
B. Displacement of endotracheal tube (ET)
C. Pneumothorax (Correct Answer)
D. Hemothorax

Explanation: ***Pneumothorax*** - A failed attempt at **subclavian vein catheterization** carries a high risk of puncturing the **parietal pleura** (due to the proximity of the apex of the lung), leading to a pneumothorax. - The sudden drop in **blood pressure (hypotension)** and rise in **pulse (tachycardia)** indicate acute hemodynamic compromise, often resulting from a **tension pneumothorax** which impedes venous return to the heart. - This is the **most common mechanical complication** of subclavian catheterization. *Displacement of endotracheal tube (ET)* - Displacement means the tube moves from the correct **tracheal position** (e.g., into the esophagus or mainstem bronchus), leading to acute ventilation failure and hypoxia. - While displacement causes hemodynamic instability, it is a complication of **ventilator management or patient movement**, not directly related to a preceding failed attempt at a **central venous line insertion**. *Air embolism* - An air embolism occurs when air enters the venous circulation, usually when the central line tract or needle hub is open to the atmosphere (e.g., during line insertion or removal) and the patient takes a deep breath. - Although it can cause cardiovascular collapse, the presenting feature following a needle stick is classically **pneumothorax**, unless the catheter was successfully placed and air was entrained through the line. - Classic sign: **mill-wheel murmur** on auscultation. *Hemothorax* - Hemothorax results from **vascular injury** (subclavian artery or vein) during catheterization attempts, causing blood accumulation in the pleural space. - While it can occur with subclavian catheterization, it typically presents with **more gradual hemodynamic changes** and signs of blood loss (falling hematocrit), rather than the acute decompensation seen with tension pneumothorax. - Chest X-ray would show pleural fluid rather than air.

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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