Complications in Anesthesia Practice Questions

Q: Which of the following is NOT typically seen in malignant hyperthermia?

Hypercalcemia. **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle, most commonly triggered by volatile anesthetics (e.g., Halothane) or succinylcholine. It is caused by a mutation in the **RYR1 receptor**, leading to an uncontrolled release of calcium from the sarcoplasmic reticulum into the cytosol. **Why Hypercalcemia is the correct answer:** While MH is triggered by a massive rise in *intracellular* calcium, this does not translate to **Hypercalcemia** in the blood. In fact, serum calcium levels are often normal or even decreased (hypocalcemia) in the acute phase as calcium is sequestered within the muscle cells. **Analysis of Incorrect Options:** * **Tachycardia:** This is the **earliest and most consistent sign** of MH, resulting from a massive sympathetic surge and increased metabolic demand. * **Hyperkalemia:** As muscle cells undergo rhabdomyolysis due to sustained contraction and ATP depletion, they rupture and release potassium into the bloodstream. This can lead to fatal arrhythmias. * **Metabolic Acidosis:** The hypermetabolic state leads to excessive production of CO2 (hypercapnia) and lactic acid, resulting in a profound mixed respiratory and metabolic acidosis. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in End-Tidal CO2 (ETCO2). * **Late Sign:** Hyperthermia (can rise at 1-2°C every 5 minutes). * **Drug of Choice:** **Dantrolene** (a muscle relaxant that acts directly on the RYR1 receptor to stop calcium release). * **Safe Agents:** Nitrous oxide, Propofol, Ketamine, and Ester/Amide local anesthetics. * **Gold Standard Test:** Caffeine Halothane Contracture Test (CHCT).

Q: Intra-arterial injection of thiopental causes:

Vasospasm. **Explanation:** The accidental intra-arterial injection of **Thiopental Sodium** is a classic anesthetic emergency. Thiopental is highly alkaline (pH 10.5). When injected into an artery, it reacts with the blood to form **crystals**. These crystals, along with the release of norepinephrine from the perivascular nerve endings, trigger intense **vasospasm**. This leads to immediate, severe pain (described as a "shooting burning sensation") and distal ischemia. * **Why A is correct:** The primary pathological event is intense vasoconstriction (vasospasm) caused by the precipitation of thiopental crystals in the small arterioles and the local release of catecholamines. * **Why B is incorrect:** Thiopental causes vasoconstriction in the arterial system, not vasodilation. * **Why C is incorrect:** While prolonged ischemia can eventually lead to tissue necrosis and gangrene, the *immediate* physiological effect and the mechanism leading to that damage is vasospasm. * **Why D is incorrect:** Intra-arterial injection causes localized effects (pain, cyanosis). Systemic hypotension is a side effect of *intravenous* thiopental due to myocardial depression and peripheral venodilation, but it is not the hallmark of intra-arterial injection. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** "Hand of Gold" (initial blanching) followed by "Hand of Blue" (cyanosis). * **Management:** 1. **Leave the needle in place** to administer drugs. 2. **Dilute** the drug with saline. 3. **Relieve Vasospasm:** Inject vasodilators (e.g., **Papaverine**, Lidocaine, or Procaine). 4. **Sympathetic Block:** Stellate ganglion block or Brachial plexus block to promote vasodilation. 5. **Anticoagulation:** Heparin to prevent secondary thrombosis.

Q: Mendelson's syndrome refers to what?

Aspiration of gastric content. **Explanation:** **Mendelson’s Syndrome** is a chemical pneumonitis caused by the aspiration of acidic gastric contents, typically occurring during general anesthesia. It was first described by Curtis Mendelson in 1946 in obstetric patients. The syndrome is characterized by the rapid onset of bronchospasm, cyanosis, tachycardia, and dyspnea, often leading to pulmonary edema or respiratory failure. **Why Option A is Correct:** The pathophysiology depends on the **pH and volume** of the aspirate. For Mendelson’s syndrome to occur, the gastric aspirate must typically have: 1. A **pH 0.4 ml/kg** (approx. 25 ml in an average adult). The acid causes immediate chemical burning of the alveolar-capillary membrane, leading to an inflammatory response rather than a bacterial infection. **Why Other Options are Incorrect:** * **Option B:** Rupture of a bronchial tuberculoma leads to endobronchial tuberculosis or localized inflammation, not the acute chemical pneumonitis described by Mendelson. * **Option C:** Transient pneumonitis of allergic origin refers to **Löffler’s syndrome**, characterized by eosinophilic pulmonary infiltrates, often due to parasites. * **Option D:** Tracheal compression due to nodal enlargement is a mechanical airway obstruction (e.g., seen in lymphomas or sarcoidosis), not an aspiration event. **High-Yield Clinical Pearls for NEET-PG:** * **Prophylaxis:** Use of H2 blockers (Ranitidine), Proton Pump Inhibitors (Pantoprazole), or non-particulate antacids (Sodium Citrate) to increase gastric pH. * **Management:** Immediate suctioning, supplemental oxygen, and supportive ventilation. **Antibiotics and Steroids** are generally not indicated unless secondary infection or specific complications arise. * **Risk Factors:** Pregnancy (due to increased intra-abdominal pressure and relaxed lower esophageal sphincter), obesity, and emergency surgeries ("Full Stomach").

Q: Which of the following complications is likely to result after several units of blood have been transfused?

Metabolic alkalosis. **Explanation:** The correct answer is **Metabolic Alkalosis**. This occurs primarily due to the metabolism of **sodium citrate**, which is used as an anticoagulant in stored blood bags. 1. **Mechanism of Correct Answer:** Each unit of stored blood contains approximately 3 grams of citrate. Once transfused, the liver metabolizes citrate into **bicarbonate (HCO₃⁻)**. In massive blood transfusions (typically defined as >10 units in 24 hours), the rapid accumulation of bicarbonate exceeds the kidney's excretory capacity, leading to an increase in blood pH and metabolic alkalosis. 2. **Why Incorrect Options are Wrong:** * **Metabolic Acidosis:** While stored blood is slightly acidic due to the accumulation of lactic acid and pyruvic acid during storage, this effect is transient. Once transfused, the metabolic conversion of citrate to bicarbonate overrides the initial acidity. * **Respiratory Alkalosis/Acidosis:** These are primarily driven by changes in CO₂ levels (ventilation). Blood transfusion does not directly alter the respiratory drive or CO₂ elimination in a way that consistently produces these states. **NEET-PG High-Yield Pearls:** * **Citrate Toxicity:** Massive transfusion can lead to **Hypocalcemia** because citrate binds to ionized calcium. This can cause arrhythmias and prolonged QT intervals. * **Electrolyte Shifts:** Stored blood undergoes "storage lesion," leading to **Hyperkalemia** (as K+ leaks out of RBCs). However, post-transfusion, hypokalemia may occur as cells take up potassium. * **Hypothermia:** Transfusing cold blood rapidly can lead to cardiac arrhythmias; hence, the use of blood warmers is essential. * **2,3-DPG:** Stored blood has decreased 2,3-DPG, causing a **left shift** of the oxygen-dissociation curve (increased affinity, decreased O₂ delivery to tissues).

Q: After induction of anesthesia, what does the anesthetist monitor for when the surgeon manipulates the medial rectus muscle?

Oculocardiac reflex. **Explanation:** The correct answer is **A. Oculocardiac reflex**. **1. Why Oculocardiac Reflex (OCR) is correct:** The Oculocardiac reflex, also known as the **Aschner-Dagnini reflex**, is a physiological response triggered by pressure on the globe or traction on the extraocular muscles. The **medial rectus** is the most sensitive muscle for eliciting this reflex. * **Pathway:** The afferent limb is the **Ophthalmic division of the Trigeminal nerve (CN V1)**, and the efferent limb is the **Vagus nerve (CN X)**. * **Clinical Manifestation:** Stimulation leads to sudden bradycardia, arrhythmias, or even asystole. It is a classic intraoperative concern during strabismus surgery. **2. Why other options are incorrect:** * **B. Hypertension:** The OCR typically causes hypotension and bradycardia due to vagal stimulation, not hypertension. * **C. Oxygen delivery:** While oxygenation is always monitored (via pulse oximetry), it is not specifically affected by muscle manipulation. * **D. Response to painful stimulus:** While traction is painful, the specific physiological reflex triggered by this anatomical manipulation is the OCR. In a general anesthesia setting, the autonomic reflex (bradycardia) is the primary concern rather than a conscious pain response. **3. High-Yield NEET-PG Pearls:** * **Mnemonic for Pathway:** "Five and Dime" (Afferent: CN **5**; Efferent: CN **10**). * **Management:** The first step is to ask the surgeon to **stop the stimulus**. If it persists, administer **Atropine** (Anticholinergic). * **Fatigability:** The reflex is known to fatigue (decrease in intensity) with repeated stimulation. * **Risk Factors:** More common in pediatric patients and during light planes of anesthesia.

Q: In malignant hyperthermia, excess heat production is due to:

Increased muscle metabolism by excess of calcium ions. **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle. **1. Why Option A is Correct:** The pathophysiology involves a mutation in the **Ryanodine Receptor (RYR1)** located on the sarcoplasmic reticulum. When triggered by volatile anesthetics (e.g., Halothane) or depolarizing muscle relaxants (e.g., Succinylcholine), there is an **uncontrolled release of Calcium ions ($Ca^{2+}$)** into the sarcoplasm. This massive calcium surge causes: * Continuous muscle contraction (rigidity). * Overactivation of $Ca^{2+}$-ATPase pumps to sequester calcium back into the reticulum. * Increased ATP consumption, leading to accelerated aerobic and anaerobic metabolism, which generates **excessive heat**, $CO_2$, and lactic acid. **2. Why Other Options are Incorrect:** * **B. Thermic effect of food:** This refers to the energy expenditure for digestion and absorption (SDA), which is unrelated to anesthetic-induced hyperthermia. * **C. Increased sympathetic discharge:** While MH causes tachycardia and hypertension due to hypermetabolism, the primary source of heat is the skeletal muscle itself, not the autonomic nervous system. * **D. Mitochondrial thermogenesis:** While mitochondria are involved in cellular respiration, the "trigger" and primary driver of heat in MH is the calcium-induced mechanical and biochemical activity in the sarcoplasm, not a primary mitochondrial defect. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant. * **Earliest Sign:** Increase in **End-Tidal $CO_2$ ($ETCO_2$)**. * **Clinical Triad:** Muscle rigidity (often Masseter spasm), hyperthermia, and metabolic acidosis. * **Drug of Choice:** **Dantrolene** (acts by inhibiting the Ryanodine receptor and preventing $Ca^{2+}$ release). * **Associated Conditions:** Central Core Disease and King-Denborough Syndrome.

Q: What is the best treatment for post-dural puncture headache?

Extradural blood patch. **Explanation:** **Post-Dural Puncture Headache (PDPH)** occurs due to the leakage of cerebrospinal fluid (CSF) through a dural rent, leading to low CSF pressure and compensatory cerebral vasodilation. This results in a characteristic positional headache (worse on standing, relieved by lying flat). **Why Option C is Correct:** The **Epidural (Extradural) Blood Patch** is considered the **gold standard and most effective treatment** for PDPH. It involves injecting 15–20 ml of autologous venous blood into the epidural space near the site of the dural puncture. It works via two mechanisms: 1. **Immediate effect:** The volume of blood increases epidural pressure, compressing the thecal sac and raising CSF pressure. 2. **Long-term effect:** The blood clots over the dural hole, acting as a "plug" to prevent further CSF leakage. **Analysis of Incorrect Options:** * **A & B (Caffeine & NSAIDs):** These are considered **conservative/symptomatic management**. Caffeine causes cerebral vasoconstriction to counteract the vasodilation, and NSAIDs help with pain. However, they do not fix the underlying dural hole. * **D (IV Fluids):** While hydration is traditionally advised to encourage CSF production, clinical evidence suggests it does not significantly resolve the headache or the leak. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Young age, female gender, pregnancy, and use of large-bore/cutting needles (e.g., Quincke). * **Prevention:** Use of small-gauge (25G-27G) **pencil-point needles** (e.g., Sprotte or Whitacre) significantly reduces the incidence of PDPH. * **Timing:** PDPH typically presents within 48 hours. If conservative management fails after 24–48 hours, a blood patch is indicated.

Q: A patient with a Ryanodine receptor 1 (RYR1) mutation should avoid which of the following anesthetic agents?

Succinylcholine. **Explanation:** The question describes a patient predisposed to **Malignant Hyperthermia (MH)**, a life-threatening hypermetabolic state of skeletal muscle. The underlying pathophysiology involves a mutation in the **RYR1 gene**, which encodes the Ryanodine receptor. This receptor is a calcium release channel in the sarcoplasmic reticulum; when mutated, it causes an uncontrolled release of calcium in response to specific "triggering agents." **Why Succinylcholine is the correct answer:** Succinylcholine (a depolarizing neuromuscular blocker) and all **volatile inhalational anesthetics** (e.g., Halothane, Isoflurane, Sevoflurane) are the primary triggers for MH. In susceptible individuals, these agents cause sustained muscle contraction, leading to hyperthermia, rhabdomyolysis, and metabolic acidosis. **Why the other options are incorrect:** * **B. Nitrous oxide:** This is a non-triggering gas and is considered safe for MH-susceptible patients. * **C. Lidocaine:** Amide and ester local anesthetics do not trigger MH and are safe for regional or local anesthesia. * **D. Propofol:** This is the intravenous induction agent of choice for MH-susceptible patients as it does not affect the RYR1 receptor. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **EtCO2** (End-tidal Carbon Dioxide) despite increased ventilation. * **Late Sign:** Hyperthermia (can be as high as 1°C every 5 minutes). * **Drug of Choice:** **Dantrolene** (a muscle relaxant that acts directly on the RYR1 receptor to prevent calcium release). * **Safe Agents:** Propofol, Etomidate, Thiopentone, Ketamine, Opioids, and all Non-depolarizing muscle relaxants (e.g., Vecuronium, Atracurium). * **Associated Conditions:** Central Core Disease and King-Denborough Syndrome are also linked to RYR1 mutations and MH risk.

Q: Following accidental intra-arterial injection of thiopentone, what should not be done?

Remove the needle. ### Explanation The accidental intra-arterial injection of **Thiopentone** is a medical emergency. Thiopentone is highly alkaline (pH 10.5). When injected into an artery, it reacts with blood to form **crystals**, leading to intense vasospasm, chemical endarteritis, and subsequent thrombosis, which can result in gangrene. **Why "Remove the needle" is the correct answer:** The most critical rule in managing intra-arterial thiopentone is to **leave the needle in situ**. Removing the needle loses the only direct access to the affected vessel. The needle should be kept in place to serve as a conduit for administering emergency vasodilators and anticoagulants directly to the site of the spasm. **Analysis of other options (Management steps):** * **Intra-arterial Papaverine:** This is a potent vasodilator used to counteract the intense arterial spasm. It should be injected through the indwelling needle. * **Intra-arterial Heparin:** Used to prevent the formation of thrombi around the thiopentone crystals and damaged endothelium. * **Stellate Ganglion Block:** This provides sympathetic blockade, leading to reflex vasodilation of the upper limb vessels, thereby improving collateral circulation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of injury:** Crystal formation and norepinephrine release leading to vasospasm. * **Clinical presentation:** Immediate, intense "burning" pain distal to the site of injection and loss of distal pulses. * **Other management steps:** * Dilute the drug by injecting Normal Saline. * Lidocaine (1%) for vasodilation and pain relief. * Brachial plexus block (alternative to Stellate block). * **Gold Standard:** Leave the needle in place!

Q: Which of the following anesthetic agents is considered safe even if inadvertently injected intra-arterially?

Propofol. **Explanation:** The correct answer is **Propofol**. **1. Why Propofol is the Correct Answer:** Intra-arterial injection of anesthetic drugs is a dreaded complication that can lead to severe vasospasm, endarteritis, and tissue necrosis. **Propofol** is considered relatively safe in this context because it does not cause significant vascular damage or crystal formation. While it may cause transient pain at the injection site, it lacks the potent vasoconstrictive and pro-thrombotic properties seen with barbiturates. **2. Why the Other Options are Incorrect:** * **Thiopentone (Option A):** This is the most classic example of a dangerous intra-arterial injection. Thiopentone is highly alkaline (pH 10.5). When injected into an artery, it reacts with blood to form **insoluble crystals** that cause mechanical obstruction, intense vasospasm, and chemical endarteritis, often leading to gangrene. * **Methohexitone (Option D):** Like Thiopentone, Methohexitone is an alkaline barbiturate. It carries a high risk of vascular injury and tissue necrosis if administered intra-arterially. * **Midazolam (Option C):** While less toxic than barbiturates, intra-arterial Midazolam can still cause significant vascular irritation and has been associated with clinical complications, making it less "safe" than Propofol. **3. Clinical Pearls for NEET-PG:** * **Management of Intra-arterial Thiopentone:** Leave the needle in situ, dilute with saline, and inject **Papaverine** (vasodilator), **Lidocaine** (to prevent spasm), or **Heparin** (to prevent thrombosis). A **Stellate Ganglion Block** or Brachial Plexus block may be performed to induce sympathetic-mediated vasodilation. * **High-Yield Fact:** The primary mechanism of injury in Thiopentone injection is the formation of crystals in the small arterioles, not just the pH itself.

Question 1

Which of the following is NOT typically seen in malignant hyperthermia?

Accepted Answer

Hypercalcemia

Answer

Tachycardia

Answer

Hyperkalemia

Answer

Metabolic acidosis

Question 2

Intra-arterial injection of thiopental causes:

Accepted Answer

Vasospasm

Answer

Vasodilation

Answer

Necrosis of vessel wall

Answer

Hypotension

Question 3

Mendelson's syndrome refers to what?

Accepted Answer

Aspiration of gastric content

Answer

Rupture of bronchial tuberculoma

Answer

Transient pneumonitis of allergic origin

Answer

Tracheal compression due to nodal enlargement

Question 4

Which of the following complications is likely to result after several units of blood have been transfused?

Accepted Answer

Metabolic alkalosis

Answer

Metabolic acidosis

Answer

Respiratory alkalosis

Answer

Respiratory acidosis

Question 5

After induction of anesthesia, what does the anesthetist monitor for when the surgeon manipulates the medial rectus muscle?

Accepted Answer

Oculocardiac reflex

Answer

Hypertension

Answer

Oxygen delivery

Answer

Response to painful stimulus

Question 6

In malignant hyperthermia, excess heat production is due to:

Accepted Answer

Increased muscle metabolism by excess of calcium ions

Answer

Thermic effect of food

Answer

Increased sympathetic discharge

Answer

Mitochondrial thermogenesis

Question 7

What is the best treatment for post-dural puncture headache?

Accepted Answer

Extradural blood patch

Answer

Caffeine

Answer

NSAIDs

Answer

IV fluids

Question 8

A patient with a Ryanodine receptor 1 (RYR1) mutation should avoid which of the following anesthetic agents?

Accepted Answer

Succinylcholine

Answer

Nitrous oxide

Answer

Lidocaine

Answer

Propofol

Question 9

Following accidental intra-arterial injection of thiopentone, what should not be done?

Accepted Answer

Remove the needle

Answer

Intra-arterial heparin

Answer

Intra-arterial papaverine

Answer

Perform a stellate ganglion block

Question 10

Which of the following anesthetic agents is considered safe even if inadvertently injected intra-arterially?

Accepted Answer

Propofol

Answer

Thiopentone

Answer

Midazolam

Answer

Methohexitone

Complications in Anesthesia — MCQs

Complications in Anesthesia — MCQs

On this page

Practice by Chapter

Want unlimited practice?