Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 121: Which of the following is NOT true about malignant hyperthermia?

A. Succinylcholine is the most common precipitating agent.
B. Dantrolene is the treatment of choice.
C. End-tidal carbon dioxide is increased.
D. Bradycardia is a common occurrence. (Correct Answer)

Explanation: **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle, primarily triggered by volatile anesthetics and succinylcholine. ### **Explanation of Options** * **D. Bradycardia is a common occurrence (Correct Answer):** This statement is **false**. In MH, the hypermetabolic state leads to sympathetic overactivity. **Tachycardia** is actually the earliest and most consistent clinical sign. Bradycardia only occurs as a terminal event due to severe hyperkalemia or myocardial failure. * **A. Succinylcholine is the most common precipitating agent:** This is true. Succinylcholine (a depolarizing muscle relaxant) and volatile inhalational anesthetics (like Halothane, Isoflurane, and Sevoflurane) are the primary triggers that cause uncontrolled calcium release from the sarcoplasmic reticulum. * **B. Dantrolene is the treatment of choice:** This is true. Dantrolene is a postsynaptic muscle relaxant that binds to the **Ryanodine Receptor (RYR1)**, inhibiting the release of calcium. It is the gold-standard treatment. * **C. End-tidal carbon dioxide (EtCO2) is increased:** This is true. An unexplained, rapid rise in EtCO2 (despite increasing minute ventilation) is often the **first sign** of MH, reflecting the massive increase in metabolic rate and CO2 production. ### **High-Yield Clinical Pearls for NEET-PG** * **Inheritance:** Autosomal Dominant; most commonly associated with a mutation in the **RYR1 gene**. * **Early Signs:** Tachycardia, tachypnea, and **Masseter Muscle Rigidity (MMR)** following succinylcholine administration. * **Late Signs:** Hyperthermia (can rise 1°C every 5 minutes), rhabdomyolysis, and cola-colored urine (myoglobinuria). * **Safe Agents:** Nitrous oxide, Propofol, Etomidate, Thiopental, and all local anesthetics. * **Gold Standard Diagnosis:** Caffeine-Halothane Contracture Test (CHCT) on a muscle biopsy.

Question 122: What is the most common anesthetic complication occurring within the first 24 hours after surgery under general anesthesia?

A. Hypertension
B. Renal failure
C. Atelectasis (Correct Answer)
D. Cardiac arrest

Explanation: **Explanation:** **Atelectasis** is the most common postoperative pulmonary complication (PPC) following general anesthesia, typically occurring within the first 24–48 hours. **Why Atelectasis is the Correct Answer:** During general anesthesia, several factors contribute to the collapse of alveoli: 1. **Reduced Functional Residual Capacity (FRC):** Induction of anesthesia and the use of muscle relaxants cause the diaphragm to shift cephalad, reducing FRC by approximately 20%. 2. **Compression Atelectasis:** The weight of the heart and abdominal contents compresses dependent lung regions. 3. **Absorption Atelectasis:** High concentrations of inspired oxygen ($FiO_2$) wash out nitrogen (the "structural gas" of the alveoli), leading to rapid alveolar collapse. 4. **Mucociliary Dysfunction:** Anesthetic agents impair the clearance of secretions, leading to small airway obstruction. **Analysis of Incorrect Options:** * **Hypertension:** While common in the immediate recovery period due to pain, emergence excitement, or hypercarbia, it is a transient hemodynamic sign rather than a primary systemic complication. * **Renal Failure:** Postoperative acute kidney injury (AKI) is a serious but relatively rare complication, usually associated with major vascular surgery, pre-existing renal disease, or prolonged hypotension. * **Cardiac Arrest:** This is a catastrophic but rare event (incidence approx. 1 in 10,000–20,000 cases), not a "common" complication. **NEET-PG High-Yield Pearls:** * **Most common cause of postoperative fever (Day 1-2):** Atelectasis. * **Prevention:** Preoperative smoking cessation (ideally >8 weeks), incentive spirometry, and early mobilization. * **Recruitment Maneuvers:** Applying positive pressure (e.g., 40 $cmH_2O$ for 40 seconds) intraoperatively can help reopen collapsed alveoli. * **Site of Surgery:** The risk of atelectasis is highest in upper abdominal and thoracic surgeries.

Question 123: All of the following are true regarding post-spinal headache, EXCEPT?

A. Occurs within 48 hours
B. Increased by sitting upright
C. Due to cerebrospinal fluid (CSF) leak
D. Associated with photophobia (Correct Answer)

Explanation: **Explanation:** Post-Dural Puncture Headache (PDPH) is a common complication following spinal anesthesia or accidental dural puncture during epidural placement. **1. Why Option D is the Correct Answer (The Exception):** While PDPH is characterized by severe headache, it is **not typically associated with photophobia**. Photophobia is a hallmark of meningeal irritation (meningitis) or migraine. If a patient presents with photophobia, fever, and neck stiffness after spinal anesthesia, clinicians should prioritize ruling out **meningitis** rather than assuming PDPH. **2. Analysis of Incorrect Options:** * **Option A (Occurs within 48 hours):** This is true. PDPH typically manifests within 12 to 48 hours post-procedure. It rarely occurs immediately or after 5-7 days. * **Option B (Increased by sitting upright):** This is the **pathognomonic feature** of PDPH. It is a "postural headache" that worsens significantly when the patient sits or stands and is relieved by lying flat (supine). * **Option C (Due to CSF leak):** This is the underlying pathophysiology. Persistent leakage of CSF through the dural hole leads to **low intracranial pressure**. This causes traction on pain-sensitive intracranial structures (vessels and nerves) when the patient is upright. **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) and **non-cutting (pencil-point)** needles like **Sprotte or Whitacre**. * **Treatment:** Conservative management includes bed rest, hydration, and caffeine. The **Gold Standard** treatment for persistent PDPH is an **Epidural Blood Patch**.

Question 124: Which intravenous anesthetic agent does not cause histamine release?

A. Thiopentone
B. Propofol
C. Etomidate (Correct Answer)
D. Ketamine

Explanation: **Explanation:** The release of histamine from mast cells is a common side effect of several intravenous anesthetics, leading to clinical signs such as flushing, tachycardia, hypotension, and bronchospasm. **Why Etomidate is the Correct Answer:** **Etomidate** is a carboxylated imidazole derivative known for its remarkable **hemodynamic stability**. It does not trigger histamine release, making it the induction agent of choice for patients with reactive airway disease (asthma) or those with limited cardiac reserve (valvular heart disease, hypovolemia). **Analysis of Incorrect Options:** * **Thiopentone (Option A):** A barbiturate notorious for causing significant histamine release. It is strictly contraindicated in patients with porphyria and should be avoided in asthmatics due to the risk of bronchospasm. * **Propofol (Option B):** While generally safe, propofol can occasionally cause histamine release. Furthermore, its formulation (containing soybean oil and egg lecithin) can trigger allergic reactions in sensitive individuals. * **Ketamine (Option D):** Although ketamine is a bronchodilator (due to sympathomimetic effects), it can occasionally trigger minor histamine release. However, in the context of NEET-PG questions, Etomidate is the classic answer for "no histamine release." **High-Yield Clinical Pearls for NEET-PG:** * **Etomidate Side Effects:** While it lacks histamine release, it is associated with **adrenocortical suppression** (inhibits 11-beta-hydroxylase) and a high incidence of **myoclonus** and postoperative nausea/vomiting (PONV). * **Drug of Choice:** Etomidate is the drug of choice for **cardiac induction** and **trauma** patients due to minimal effect on blood pressure. * **Muscle Relaxants:** Among NMBAs, **Mivacurium** and **Atracurium** are the most common culprits for histamine release; **Vecuronium** and **Rocuronium** do not cause it.

Question 125: Which statement is false regarding malignant hyperpyrexia?

A. Dantrolene sodium is the drug of choice.
B. Isoflurane is an absolute contraindication.
C. Characterized by muscle rigidity, hyperthermia, and metabolic acidosis.
D. Low end tidal carbon dioxide is an early sign. (Correct Answer)

Explanation: **Explanation:** Malignant Hyperthermia (MH) is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle, triggered by volatile anesthetics and succinylcholine. **Why Option D is the correct answer (False statement):** The hallmark of MH is a massive increase in metabolic rate. Therefore, a **rapid rise in End-Tidal CO₂ (ETCO₂)**—often doubling or tripling—is the **earliest and most sensitive clinical sign**. Low ETCO₂ would be seen in conditions like pulmonary embolism or cardiac arrest, not MH. **Analysis of other options:** * **Option A:** **Dantrolene sodium** is the definitive treatment. It acts by binding to the ryanodine receptor (RYR1), inhibiting the release of calcium from the sarcoplasmic reticulum. * **Option B:** All **volatile inhalational anesthetics** (Halothane, Isoflurane, Sevoflurane, Desflurane) and the depolarizing muscle relaxant **Succinylcholine** are absolute contraindications in MH-susceptible patients. * **Option C:** The clinical triad of MH includes **muscle rigidity** (due to persistent calcium release), **hyperthermia** (a late but classic sign), and **mixed respiratory/metabolic acidosis** (due to excessive CO₂ and lactate production). **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant. * **Genetic Mutation:** Most commonly involving the **RYR1 gene** (Ryanodine receptor). * **Earliest Sign:** Unexplained rise in ETCO₂. * **Early Physical Sign:** Masseter muscle rigidity (MMR) following succinylcholine administration. * **Late Signs:** Hyperthermia (can rise 1°C every 5 minutes), rhabdomyolysis, and cola-colored urine (myoglobinuria). * **Safe Agents:** Nitrous oxide, Propofol, Etomidate, Ketamine, and all Local Anesthetics. * **Gold Standard Test:** Caffeine Halothane Contracture Test (CHCT).

Question 126: Which of the following is NOT a risk factor for the development of surgery-associated chronic kidney disease?

A. Older age
B. Congestive cardiac failure (CCF)
C. Emergency procedures
D. Spinal anaesthesia (Correct Answer)

Explanation: ### **Explanation** **1. Why Spinal Anaesthesia is the Correct Answer:** Spinal anaesthesia (Neuraxial blockade) is generally considered **protective** or neutral regarding renal function compared to general anaesthesia. It provides excellent sympathetic blockade, which can reduce the stress response to surgery and improve blood flow to certain vascular beds. Unlike general anaesthesia, it avoids the use of potentially nephrotoxic volatile agents or the significant hemodynamic fluctuations associated with positive pressure ventilation. Therefore, it is not a risk factor for chronic kidney disease (CKD); rather, it is often preferred in patients with mild renal impairment. **2. Why the Other Options are Wrong:** * **Older Age (Option A):** Aging is associated with a physiological decline in the Glomerular Filtration Rate (GFR) and reduced renal functional reserve, making elderly patients highly susceptible to postoperative renal insult. * **Congestive Cardiac Failure (Option B):** CCF leads to a "low output state," resulting in chronic renal hypoperfusion. These patients are prone to venous congestion and cardiorenal syndrome, significantly increasing the risk of perioperative Acute Kidney Injury (AKI) progressing to CKD. * **Emergency Procedures (Option C):** Emergency surgeries carry a higher risk due to inadequate preoperative optimization, potential hypovolemia (dehydration/sepsis), and the high-stress nature of the procedure, all of which predispose the kidneys to ischemic injury. ### **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Postoperative AKI is a leading cause of surgery-associated CKD. * **Most Important Risk Factor:** Pre-existing renal dysfunction is the strongest predictor of postoperative renal failure. * **Nephrotoxic Drugs to Avoid:** NSAIDs, Aminoglycosides, and IV Contrast should be used with caution in high-risk surgical patients. * **Protective Strategy:** Maintaining adequate **mean arterial pressure (MAP)** and ensuring **euvolemia** are the most effective ways to prevent perioperative renal complications.

Question 127: Which of the following is least useful in the treatment of local anesthetic-induced convulsions?

A. Phenytoin sodium (Correct Answer)
B. Thiopentone sodium
C. Midazolam
D. Propofol

Explanation: **Explanation:** Local Anesthetic Systemic Toxicity (LAST) manifests primarily as CNS excitation (convulsions) followed by CNS and cardiovascular depression. The management of LAST-induced seizures focuses on immediate suppression of neuronal activity and maintaining oxygenation. **Why Phenytoin is the Correct Answer (Least Useful):** Phenytoin is ineffective in the acute management of local anesthetic-induced convulsions for two primary reasons: 1. **Mechanism of Action:** Phenytoin works by blocking voltage-gated sodium channels. Local anesthetics (LAs) already cause toxicity by blocking these same channels; adding phenytoin provides no synergistic benefit and may worsen cardiac toxicity. 2. **Onset of Action:** Phenytoin has a very slow onset of action and requires a slow infusion rate to avoid arrhythmias, making it unsuitable for an acute, life-threatening emergency like LAST. **Analysis of Other Options (Useful Agents):** * **Thiopentone Sodium:** A rapid-acting barbiturate that effectively suppresses seizure activity by enhancing GABAergic inhibition. * **Midazolam:** Benzodiazepines are considered first-line agents for LA-induced seizures due to their rapid onset and excellent safety profile in suppressing CNS excitation. * **Propofol:** Though it can suppress seizures, it should be used with extreme caution (in low doses) because it can exacerbate the cardiovascular depression often seen in LAST. **Clinical Pearls for NEET-PG:** * **Drug of Choice for LAST:** **Intravenous Lipid Emulsion (20% Intralipid)** is the definitive treatment (the "Lipid Sink" theory). * **Avoid:** Vasopressin, Calcium channel blockers, and Class I anti-arrhythmics (like Lidocaine or Phenytoin). * **Airway First:** The most critical initial step is 100% oxygenation to prevent hypoxia and acidosis, which worsen LA toxicity. * **Bupivacaine** is the most cardiotoxic local anesthetic due to its slow dissociation from cardiac sodium channels ("fast in, slow out").

Question 128: Which one of the following drugs does not produce central anticholinergic syndrome?

A. Atropine sulphate
B. Glycopyrrolate (Correct Answer)
C. Antihistamines
D. Tricyclic antidepressants

Explanation: **Explanation:** The **Central Anticholinergic Syndrome (CAS)** is caused by the blockade of muscarinic receptors in the brain, leading to symptoms ranging from confusion and agitation to hallucinations and coma. The primary factor determining whether an anticholinergic drug causes CAS is its ability to cross the **blood-brain barrier (BBB)**. **Why Glycopyrrolate is the correct answer:** Glycopyrrolate is a **quaternary ammonium compound**. Due to its ionized (charged) state, it is highly polar and cannot cross the lipid-rich blood-brain barrier. Therefore, it lacks central nervous system (CNS) effects and does **not** produce central anticholinergic syndrome. It is preferred in anesthesia when only peripheral drying or reversal of bradycardia is desired without sedation. **Analysis of Incorrect Options:** * **Atropine sulphate:** This is a **tertiary amine**. Unlike quaternary compounds, tertiary amines are non-ionized and lipid-soluble, allowing them to easily cross the BBB and trigger CAS. * **Antihistamines:** Many first-generation antihistamines (e.g., diphenhydramine, promethazine) have significant anticholinergic properties and cross the BBB, frequently causing sedation or delirium. * **Tricyclic Antidepressants (TCAs):** Drugs like amitriptyline have potent muscarinic antagonist activity and cross into the CNS, making them a common cause of anticholinergic toxicity in overdose. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for CAS:** **Physostigmine** (0.01–0.03 mg/kg). It is a tertiary amine acetylcholinesterase inhibitor that crosses the BBB to increase synaptic acetylcholine. * **Neostigmine vs. Physostigmine:** Neostigmine is a quaternary ammonium (like glycopyrrolate) and does **not** cross the BBB; hence, it cannot treat CAS. * **Mnemonic for Anticholinergic Toxicity:** "Mad as a hatter (confusion), Red as a beet (flushing), Dry as a bone (decreased secretions), Hot as a hare (hyperthermia), and Blind as a bat (mydriasis)."

Question 129: What is the most common complication of surgery performed in the lithotomy position?

A. Damage to lower limb nerves (Correct Answer)
B. Damage to upper limb nerves
C. Hypotension
D. Distal gangrene

Explanation: ### **Explanation** The **lithotomy position** is frequently used for gynecological, urological, and proctological surgeries. It involves placing the patient’s legs in stirrups, which inherently risks pressure-related injuries and nerve stretching. **1. Why "Damage to lower limb nerves" is correct:** Peripheral nerve injury is the most common complication of this position. The **Common Peroneal Nerve** is the most frequently injured nerve due to compression against the lateral support (stirrup) at the neck of the fibula. Other nerves at risk include the **Saphenous nerve** (medial compression), **Femoral nerve** (excessive hip flexion/abduction), and **Sciatic nerve** (stretching due to knee extension and hip flexion). **2. Why the other options are incorrect:** * **Damage to upper limb nerves:** While brachial plexus injuries can occur in any position (especially Trendelenburg), they are not the *most common* complication specific to the lithotomy position. * **Hypotension:** Hypotension is more common when legs are *lowered* from the lithotomy position (due to venous pooling). While in the position, venous return actually increases, which can sometimes cause transient hypertension. * **Distal gangrene:** This is a rare and extreme complication associated with **Compartment Syndrome**. While lithotomy increases intracompartmental pressure, frank gangrene is far less common than nerve injury. ### **High-Yield Clinical Pearls for NEET-PG:** * **Most common nerve injured:** Common Peroneal Nerve (leads to foot drop). * **Compartment Syndrome:** Risk increases if the surgery lasts **>2–4 hours**. * **Physiological Change:** Functional Residual Capacity (FRC) decreases as abdominal contents push against the diaphragm. * **Prevention:** Ensure adequate padding at the fibular head and avoid hip flexion greater than 90 degrees.

Question 130: Which of the following anesthetic agents can cause hepatitis?

A. Cyclopropane
B. Halothane (Correct Answer)
C. Isoflurane
D. Enflurane

Explanation: **Explanation:** **Halothane** is the correct answer because it is classically associated with **Halothane Hepatitis**, a rare but severe immune-mediated adverse reaction. **Why Halothane?** Halothane undergoes significant hepatic metabolism (up to 20%) by the Cytochrome P450 system. This process produces **trifluoroacetylated (TFA) proteins**. In susceptible individuals, these act as haptens, triggering an immune response that leads to massive hepatic necrosis. There are two types: * **Type I:** Minor, transient elevation of transaminases. * **Type II:** Fulminant hepatic failure (high mortality), typically occurring 2–14 days after repeat exposure. **Analysis of Incorrect Options:** * **Cyclopropane:** An older, flammable gas primarily known for causing "Cyclopropane shock" (hypotension upon discontinuation) and sensitizing the myocardium to catecholamines, but it is not hepatotoxic. * **Isoflurane & Enflurane:** These are newer halogenated ethers. While they also produce TFA-protein adducts, they do so at a much lower rate (Isoflurane <0.2%, Enflurane ~2%) compared to Halothane. Consequently, the risk of hepatitis is extremely negligible. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Multiple exposures to halothane (most important), obesity, female gender, and middle age. * **Metabolism:** Halothane is metabolized to **trifluoroacetic acid**. * **Other Side Effects:** Halothane causes "Halothane Shakes" (shivering), sensitizes the heart to adrenaline (arrhythmias), and is a potent trigger for **Malignant Hyperthermia**. * **Preferred Agent in Liver Disease:** **Atracurium/Cisatracurium** (muscle relaxants) are preferred due to Hoffman elimination. For induction, **Sevoflurane** is safer as it does not produce TFA-protein adducts.

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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