Complications in Anesthesia — MCQs

A woman is posted for elective cholecystectomy. Her preoperative clinical evaluation and airway assessment were normal. In the operating room, she was attached to the monitors and an antibiotic was administered. Suddenly she became pulseless and unresponsive. What is the immediate next step in her management?

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 61: What is true about post-dural puncture headache?

A. It is common in the elderly.
B. Using a small bore needle helps prevent it. (Correct Answer)
C. Early ambulation increases its incidence.
D. All of the above.

Explanation: ### Explanation **Post-Dural Puncture Headache (PDPH)** is a common complication following spinal anesthesia or accidental dural puncture during epidural placement. It is caused by the persistent leakage of cerebrospinal fluid (CSF) through the dural hole, leading to low CSF pressure and compensatory cerebral vasodilation. #### Why Option B is Correct: The incidence of PDPH is directly proportional to the size of the dural rent. **Using a small-bore needle** (e.g., 25G, 26G, or 27G) creates a smaller hole, significantly reducing CSF leakage. Additionally, using **non-cutting (pencil-point) needles** like Whitacre or Sprotte further reduces the risk compared to cutting-tip (Quincke) needles, as they separate rather than cut the dural fibers. #### Why Other Options are Incorrect: * **Option A:** PDPH is **less common in the elderly**. It is most frequent in young adults (20–40 years), particularly pregnant women. With age, the dura becomes less elastic and more fibrous, which may help the puncture site seal faster. * **Option C:** **Early ambulation does not increase the incidence** of PDPH. While the headache is characteristically positional (worsens when upright and improves when supine), prolonged bed rest has not been proven to prevent the occurrence of the headache itself. #### High-Yield Clinical Pearls for NEET-PG: * **Classic Presentation:** A "frontal-occipital" headache that is **positional** in nature, appearing within 48–72 hours post-procedure. * **Gold Standard Treatment:** For severe, persistent cases, the **Epidural Blood Patch (EBP)** is the most effective treatment (success rate >90%). * **Conservative Management:** Includes bed rest, aggressive hydration, and pharmacological agents like **Caffeine** (causes cerebral vasoconstriction) or Theophylline. * **Needle Orientation:** If using a cutting needle (Quincke), the bevel should be kept **parallel** to the longitudinal fibers of the dura to minimize damage.

Question 62: Which agent can cause malignant hyperthermia?

A. Succinylcholine (Correct Answer)
B. Dantrolene
C. Gallamine
D. Ketamine

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a rare but life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle. It is triggered by exposure to specific anesthetic agents in genetically susceptible individuals (primarily due to mutations in the **RYR1 gene**, which encodes the Ryanodine receptor). **Why Succinylcholine is Correct:** Succinylcholine, a depolarizing neuromuscular blocker, and all **volatile inhalational anesthetics** (e.g., Halothane, Isoflurane, Sevoflurane) are the primary triggers for MH. These agents cause an uncontrolled release of calcium from the sarcoplasmic reticulum, leading to sustained muscle contraction, hypermetabolism, excessive heat production, and rhabdomyolysis. **Analysis of Incorrect Options:** * **B. Dantrolene:** This is the **treatment of choice** for MH. It acts by binding to the RYR1 receptor and inhibiting the release of calcium from the sarcoplasmic reticulum. * **C. Gallamine:** This is a non-depolarizing neuromuscular blocker. Non-depolarizing agents (like Vecuronium or Atracurium) do not trigger MH and are considered safe. * **D. Ketamine:** This is an intravenous induction agent. It is not a trigger for MH. Other safe agents include Propofol, Etomidate, and Opioids. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **End-Tidal CO₂ (ETCO₂)** despite increased ventilation. * **Clinical Features:** Masseter muscle rigidity (often the first physical sign), tachycardia, hyperthermia (late sign), and metabolic acidosis. * **Gold Standard Test:** Caffeine Halothane Contracture Test (CHCT) on a muscle biopsy. * **Management:** Stop the trigger, 100% O₂, and administer **Dantrolene (2.5 mg/kg IV)**. Use a "charcoal filter" if the same anesthesia machine must be used.

Question 63: What is the most common cause of death after anesthesia?

A. Hypothermia
B. Hypotension
C. Cardiac arrest (Correct Answer)
D. Atelectasis

Explanation: **Explanation:** **Cardiac arrest** is the leading cause of perioperative mortality. In the context of anesthesia, cardiac arrest most commonly results from **respiratory failure** (hypoxemia due to airway obstruction or inadequate ventilation) or **cardiovascular collapse** (due to drug overdose, myocardial infarction, or severe hemorrhage). While modern monitoring like pulse oximetry and capnography has significantly reduced anesthesia-related mortality, sudden cardiac events remain the terminal event in most fatal cases. **Analysis of Incorrect Options:** * **Hypothermia (A):** While common in the OR due to cold ambient temperatures and cold IV fluids, it typically leads to morbidities like shivering, coagulopathy, and delayed drug metabolism, but is rarely a direct cause of death. * **Hypotension (B):** This is a frequent side effect of induction agents and neuraxial anesthesia. While severe hypotension can lead to organ ischemia, it is considered a *precursor* or a sign rather than the ultimate cause of death itself. * **Atelectasis (D):** This is the most common **postoperative pulmonary complication**. While it can lead to shunting and hypoxemia, it is usually manageable and does not result in immediate mortality unless it leads to severe secondary pneumonia or respiratory failure. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of anesthesia-related cardiac arrest:** Airway-related events (e.g., "cannot intubate, cannot ventilate"). * **Most common cause of death in the immediate postoperative period:** Respiratory complications (Hypoventilation). * **Most common cause of overall perioperative mortality (within 30 days):** Myocardial Infarction (MI). * **Triage Priority:** Always remember the **ABC** (Airway, Breathing, Circulation) sequence; failure in any of these leads to the final common pathway: Cardiac Arrest.

Question 64: Which of the following is NOT true about the Oculocardiac reflex?

A. It is mediated by the trigeminovagal route.
B. Preoperative glycopyrrolate is not helpful for prevention. (Correct Answer)
C. It can be induced by pressure on the eyeball.
D. It is mediated by traction on the medial rectus muscle.

Explanation: The **Oculocardiac Reflex (OCR)**, also known as the Aschner-Dagnini reflex, is a common intraoperative phenomenon, particularly in ophthalmic and maxillofacial surgeries. ### **Explanation of the Correct Option** **Option B is the correct answer because it is a false statement.** While intramuscular preoperative glycopyrrolate or atropine was historically used, it is now considered **ineffective** for preventing OCR due to its short duration of action and the "escape" phenomenon. However, **intravenous (IV) glycopyrrolate or atropine** administered immediately before or during the procedure is highly effective in preventing or treating the bradycardia associated with this reflex. ### **Analysis of Incorrect Options** * **Option A:** The reflex arc is indeed **trigeminovagal**. The afferent limb is the ophthalmic division of the **Trigeminal nerve (CN V)**, and the efferent limb is the **Vagus nerve (CN X)**, leading to bradycardia or arrhythmias. * **Option C:** Pressure on the eyeball (e.g., during retrobulbar blocks or ocular trauma) is a classic trigger for the reflex. * **Option D:** Traction on the extraocular muscles, most commonly the **medial rectus**, is the most potent stimulus for inducing the OCR during strabismus surgery. ### **High-Yield Clinical Pearls for NEET-PG** * **The 5 and 10 Reflex:** Afferent is CN **5** (Trigeminal); Efferent is CN **10** (Vagus). * **Management Protocol:** 1. Stop the stimulus (Ask the surgeon to release traction). 2. Ensure adequate oxygenation and ventilation. 3. If persistent, administer **IV Atropine** (0.02 mg/kg). 4. Infiltrate the muscle with local anesthetic if the reflex recurs. * **Fatigue Phenomenon:** The reflex exhibits "tiring" or tachyphylaxis, meaning it diminishes with repeated stimulation.

Question 65: A patient was anesthetized with halothane and nitrous oxide, and tubocurarine was used for skeletal muscle relaxation. The patient became hypertensive with marked muscle rigidity and hyperthermia. Lab reports showed hyperkalemia and acidosis. This complication was caused by:

A. Block of autonomic ganglia by tubocurarine
B. Pheochromocytoma
C. Activation of brain dopamine receptors by halothane
D. Excessive release of calcium from the sarcoplasmic reticulum (Correct Answer)

Explanation: ### Explanation The clinical presentation described—**muscle rigidity, hyperthermia, hypertension, hyperkalemia, and acidosis** following the administration of halothane (a volatile anesthetic) and tubocurarine (a muscle relaxant)—is a classic case of **Malignant Hyperthermia (MH)**. **Why the correct answer is right:** Malignant Hyperthermia is a pharmacogenetic disorder typically caused by a mutation in the **Ryanodine Receptor (RYR1)**. When exposed to triggering agents (all volatile inhalational anesthetics like halothane or depolarizing relaxants like succinylcholine), there is an **excessive release of calcium from the sarcoplasmic reticulum** into the myoplasm. This massive calcium influx causes sustained muscle contraction (rigidity), leading to hypermetabolism, heat production (hyperthermia), and cellular breakdown, which results in metabolic acidosis and hyperkalemia. **Why the incorrect options are wrong:** * **Option A:** Tubocurarine is a non-depolarizing neuromuscular blocker that can cause hypotension (due to histamine release and ganglionic blockade), not hypertension or rigidity. * **Option B:** While Pheochromocytoma causes hypertension and tachycardia, it does not typically cause generalized muscle rigidity or the specific metabolic profile associated with MH. * **Option C:** Halothane does not act on brain dopamine receptors to cause these symptoms. This mechanism is more characteristic of **Neuroleptic Malignant Syndrome (NMS)**, which is triggered by dopamine antagonists (e.g., haloperidol), not anesthetic gases. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** **Dantrolene** (a muscle relaxant that acts by inhibiting calcium release from the RYR1 receptor). * **Earliest Sign:** Increase in **End-Tidal CO2 (ETCO2)** due to hypermetabolism. * **Safe Agents:** Propofol, Ketamine, Etomidate, and Nitrous Oxide. * **Screening:** The gold standard diagnostic test is the **Caffeine-Halothane Contracture Test (CHCT)** performed on a muscle biopsy.

Question 66: A patient is placed in the Trendelenburg position during surgery. What is the primary rationale for this positioning if an air embolism is suspected?

A. To trap air in the right ventricle.
B. To keep a left ventricular air bubble away from the coronary artery ostia. (Correct Answer)
C. To prevent air from passing through the foramen ovale.
D. To prevent air from entering the left ventricle.

Explanation: **Explanation:** The primary concern during a suspected **Venous Air Embolism (VAE)** or **Paradoxical Air Embolism** is the migration of air into the arterial circulation. When air enters the left ventricle (either via a patent foramen ovale or pulmonary transit), it tends to rise to the highest point due to buoyancy. **1. Why Option B is Correct:** In the **Trendelenburg (head-down) position**, the apex of the heart is positioned higher than the base. This causes any air bubbles within the left ventricle to float toward the apex, away from the **aortic valve and coronary artery ostia** located at the base. This prevents the air from entering the coronary arteries, which would otherwise cause acute myocardial ischemia or infarction. **2. Analysis of Incorrect Options:** * **Option A:** Trapping air in the right ventricle is the goal of the **Durant maneuver (Left Lateral Decubitus + Trendelenburg)** specifically for *venous* air embolism to prevent a "vapor lock" in the pulmonary artery. However, the primary rationale for Trendelenburg in a generalized context of systemic risk is protecting the coronaries. * **Option C & D:** Positioning alone cannot physically close a foramen ovale or stop air from entering the left ventricle; it only manages the distribution of air once it is already present in the chambers. **NEET-PG High-Yield Pearls:** * **Durant’s Maneuver:** Left lateral decubitus + Trendelenburg; used to displace air from the RV outflow tract to the RV apex. * **Most Sensitive Monitor for VAE:** Precordial Doppler (detects "mill-wheel murmur"). * **Gold Standard for Detection:** Transesophageal Echocardiography (TEE). * **Initial Management:** Flood the surgical field with saline, 100% FiO2, and aspirate air via a central venous catheter (multi-orifice tip preferred).

Question 67: Use of nitrous oxide is contraindicated in all of the following surgeries except?

A. Cochlear implant
B. Microlaryngeal surgery
C. Vitrioretinal surgery
D. Exentration operation (Correct Answer)

Explanation: **Explanation:** The core pharmacological principle behind this question is the **Blood-Gas Partition Coefficient** of Nitrous Oxide ($N_2O$). $N_2O$ is 34 times more soluble in blood than Nitrogen. Consequently, it diffuses into air-filled closed cavities faster than Nitrogen can diffuse out, leading to an increase in either the **volume** (in compliant cavities) or **pressure** (in non-compliant cavities) of that space. **Why Exenteration is the Correct Answer:** * **Exenteration** (orbital or pelvic) involves the removal of the entire contents of a body cavity. Unlike the other options, it does not involve a closed, air-filled space or the use of intraocular gases. Therefore, $N_2O$ does not pose a risk of pressure-induced injury and is **not contraindicated**. **Why the Other Options are Wrong:** * **Cochlear Implant/Tympanoplasty:** The middle ear is a non-compliant space. $N_2O$ diffusion increases middle ear pressure, which can displace a tympanic membrane graft or dislodge a prosthesis/implant. * **Vitreoretinal Surgery:** During these procedures, surgeons often inject gas bubbles (like $SF_6$ or $C_3F_8$) to provide internal tamponade. $N_2O$ will rapidly diffuse into these bubbles, causing a massive increase in intraocular pressure (IOP), potentially leading to retinal artery occlusion and blindness. * **Microlaryngeal Surgery:** While not strictly about "closed spaces," $N_2O$ supports combustion. In laser-assisted microlaryngeal surgery, $N_2O$ is contraindicated due to the high risk of **airway fires**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Discontinuation Rule:** $N_2O$ should be stopped at least **15–20 minutes before** graft placement in ear surgeries and **20 minutes before** gas bubble injection in eye surgeries. 2. **Post-Op Caution:** Avoid $N_2O$ for 7–10 days after $SF_6$ injection and up to 8 weeks after $C_3F_8$ injection. 3. **Other Contraindications:** Pneumothorax (doubles in size in 10 mins), intestinal obstruction, air embolism, and Vitamin B12 deficiency (inhibits methionine synthase).

Question 68: Which of the following is the first treatment for an anesthetized patient experiencing bronchospasm?

A. Administer inhalational beta-2 agonists
B. Administer intravenous epinephrine
C. Administer additional anesthetic (Correct Answer)
D. Administer neuromuscular blocking agent

Explanation: **Explanation:** **Why "Administer additional anesthetic" is correct:** In an anesthetized patient, the most common cause of bronchospasm is **light plane of anesthesia** (inadequate depth). When the anesthetic depth is insufficient, airway manipulation (like the presence of an ETT or suctioning) triggers a reflex bronchoconstriction. Volatile anesthetics (e.g., Sevoflurane, Isoflurane) are potent **bronchodilators**. Therefore, the immediate first step is to deepen the plane of anesthesia to blunt airway reflexes and utilize the direct bronchodilatory effects of the anesthetic gases. **Analysis of Incorrect Options:** * **A. Inhalational beta-2 agonists:** While Salbutamol is a mainstay for asthma, it is usually a secondary step in the OR. Delivering metered-dose inhalers through an anesthesia circuit is technically less efficient than immediately increasing the vaporizer concentration. * **B. Intravenous epinephrine:** This is reserved for severe, life-threatening bronchospasm or anaphylaxis where the patient is hemodynamically unstable. It is not the first-line intervention for simple intraoperative bronchospasm. * **D. Neuromuscular blocking agent:** Muscle relaxants paralyze skeletal muscles but have **no effect on the smooth muscles** of the bronchi. While they may help if the "bronchospasm" is actually chest wall rigidity or "bucking," they do not treat true bronchospasm. **High-Yield Clinical Pearls for NEET-PG:** * **Signs of Bronchospasm:** Increased peak airway pressure, "shark-fin" appearance on capnography (slowed CO2 upstroke), and wheezing on auscultation. * **Drug of Choice:** **Sevoflurane** is the preferred volatile agent due to its non-pungency and potent bronchodilation. * **Avoid:** **Desflurane** should be avoided in patients with reactive airways as its pungency can actually trigger bronchospasm. **Ketamine** is the induction agent of choice for asthmatics due to its sympathomimetic bronchodilatory properties.

Question 69: What is the commonest sign of aspiration pneumonitis?

A. Cyanosis
B. Tachypnea (Correct Answer)
C. Crepitations
D. Rhonchi

Explanation: **Explanation:** **Mendelson’s Syndrome (Aspiration Pneumonitis)** occurs due to the inhalation of acidic gastric contents (pH <2.5, volume >25ml). This leads to a chemical burn of the pulmonary parenchyma, resulting in immediate physiological responses. **Why Tachypnea is the Correct Answer:** **Tachypnea** is the **earliest and most common clinical sign** of aspiration pneumonitis. The presence of acidic fluid in the alveoli triggers an inflammatory response and disrupts surfactant, leading to micro-atelectasis. This decreases lung compliance and stimulates J-receptors, causing a rapid, shallow breathing pattern. While other signs develop as the condition progresses, an increase in respiratory rate is the most sensitive initial indicator. **Analysis of Incorrect Options:** * **Cyanosis:** This is a late sign indicating severe hypoxemia and significant ventilation-perfusion (V/Q) mismatch. It is not the most common or earliest sign. * **Crepitations (Rales):** These occur due to the presence of fluid and exudate in the alveoli. While common, they may take time to develop fully and are often preceded by tachypnea. * **Rhonchi:** These represent airway narrowing or secretions in larger bronchi. While they can occur due to bronchospasm (a common feature), they are less consistent than tachypnea. **High-Yield Clinical Pearls for NEET-PG:** * **Mendelson’s Criteria:** Gastric pH **< 2.5** and volume **> 0.4 ml/kg (approx. 25 ml)**. * **Commonest Site:** The **Right Lower Lobe** (specifically the superior segment) is the most frequent site of aspiration due to the more vertical anatomy of the right main bronchus. * **Management:** Immediate treatment involves oropharyngeal suctioning. **Prophylactic antibiotics and steroids are NOT recommended** for chemical pneumonitis unless secondary bacterial infection occurs.

Question 70: A woman is posted for elective cholecystectomy. Her preoperative clinical evaluation and airway assessment were normal. In the operating room, she was attached to the monitors and an antibiotic was administered. Suddenly she became pulseless and unresponsive. What is the immediate next step in her management?

A. Check for breathing
B. Call for help/additional personnel
C. Start chest compressions (Correct Answer)
D. Give two rescue breaths

Explanation: ### Explanation **Correct Answer: C. Start chest compressions** This clinical scenario describes a sudden **cardiac arrest** in the operating room, likely triggered by **anaphylaxis** (given the immediate temporal relationship with antibiotic administration). According to the **AHA (American Heart Association) ACLS Guidelines**, once a patient is found to be pulseless and unresponsive, the sequence follows the **C-A-B (Compressions-Airway-Breathing)** algorithm. In an adult cardiac arrest, the priority is to maintain coronary and cerebral perfusion through high-quality chest compressions. Delaying compressions to check for breathing or provide ventilation significantly reduces the chances of Return of Spontaneous Circulation (ROSC). **Analysis of Incorrect Options:** * **A. Check for breathing:** In the current guidelines, the pulse and breathing check are performed simultaneously (taking no more than 10 seconds). Once the patient is confirmed pulseless, checking breathing further is a delay in life-saving intervention. * **B. Call for help:** While essential, in an operating room setting, "help" is usually already present or summoned simultaneously. The *immediate* physical action required by the primary provider is to start compressions. * **D. Give two rescue breaths:** This follows the old A-B-C sequence. Current guidelines prioritize "C" (Compressions) because oxygen levels in the blood remain adequate for several minutes after arrest, but the delivery mechanism (circulation) has failed. **High-Yield Clinical Pearls for NEET-PG:** * **Anaphylaxis in OR:** The most common causes are Neuromuscular Blocking Agents (NMBAs), followed by Antibiotics and Latex. * **Chest Compression Quality:** Depth of 2–2.4 inches (5–6 cm), rate of 100–120 bpm, and allowing complete chest recoil. * **H's and T's:** Always consider reversible causes during CPR (Hypovolemia, Hypoxia, Hydrogen ion/Acidosis, Hypo/Hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thrombosis). * **Drug of Choice for Anaphylaxis:** Epinephrine (Adrenaline). In cardiac arrest, it is given IV/IO (1 mg of 1:10,000).

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free