Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 31: Which of the following may result in a sudden increase in end-tidal carbon dioxide (ETCO2)?

A. Malignant Hyperthermia
B. Hyperthyroidism
C. Shivering
D. All of the above (Correct Answer)

Explanation: **Explanation:** The core physiological concept behind a sudden increase in **End-Tidal Carbon Dioxide (ETCO2)** is an increase in **metabolic CO2 production**, a decrease in alveolar ventilation, or a sudden increase in cardiac output/pulmonary blood flow. In this question, all options represent hypermetabolic states that lead to increased CO2 production. 1. **Malignant Hyperthermia (MH):** This is a life-threatening pharmacogenetic hypermetabolic crisis triggered by volatile anesthetics or succinylcholine. A **sudden, dramatic rise in ETCO2** is often the **earliest and most sensitive sign** of MH, occurring even before the rise in body temperature. 2. **Hyperthyroidism (Thyroid Storm):** Excess thyroid hormones increase the basal metabolic rate (BMR) across all tissues. During anesthesia, an undiagnosed or poorly controlled hyperthyroid patient can experience a surge in CO2 production due to this accelerated metabolism. 3. **Shivering:** Shivering involves rapid, involuntary muscle contractions to generate heat. This intense muscular activity significantly increases oxygen consumption and CO2 production (up to 200-400%), leading to an elevation in ETCO2. **Clinical Pearls for NEET-PG:** * **Differential Diagnosis of High ETCO2:** Always consider **Hypoventilation** (most common), **Sepsis**, **Tourniquet release**, and **Bicarbonate administration** in addition to the hypermetabolic states mentioned above. * **Sudden Drop in ETCO2:** Conversely, a sudden drop in ETCO2 is a high-yield indicator of **Pulmonary Embolism**, **Cardiac Arrest**, or **Circuit Disconnection**. * **Gold Standard:** ETCO2 is the gold standard for confirming endotracheal tube placement.

Question 32: Which of the following anesthetic agents is contraindicated in patients with hypertension?

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

Explanation: **Explanation:** **Ketamine (Option A)** is the correct answer because it is a **sympathomimetic** anesthetic agent. Unlike most induction agents that cause respiratory and cardiovascular depression, ketamine stimulates the sympathetic nervous system. It inhibits the reuptake of catecholamines (norepinephrine), leading to a significant **increase in heart rate, cardiac output, and arterial blood pressure.** Consequently, it is strictly contraindicated in patients with hypertension, ischemic heart disease, or a history of stroke, as the sudden rise in blood pressure can trigger myocardial infarction or intracranial hemorrhage. **Why the other options are incorrect:** * **Propofol (Option B):** Known for causing significant vasodilation and myocardial depression, leading to a **decrease in blood pressure**. It is often used cautiously in hypertensive patients to blunt the intubation response. * **Etomidate (Option C):** Renowned for its **hemodynamic stability**. It causes minimal changes in heart rate and blood pressure, making it the drug of choice for patients with compromised cardiac function, though not contraindicated in hypertension. * **Diazepam (Option D):** A benzodiazepine that typically causes mild systemic vasodilation and a slight decrease in blood pressure; it does not cause hypertension. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Ketamine is the induction agent of choice for **hypovolemic shock** and **bronchial asthma** (due to its bronchodilatory properties). * **Avoid in:** Hypertension, Raised Intraocular Pressure (IOP), and Raised Intracranial Pressure (ICP). * **Dissociative Anesthesia:** Ketamine produces a state where the patient appears awake but is unconscious and amnesic, characterized by "eyes wide open" and a slow nystagmic gaze.

Question 33: Which of the following is true about malignant hyperthermia?

A. Hypernatremia
B. Hypercalcemia
C. Hyperkalemia (Correct Answer)
D. Hypothermia

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle, triggered by volatile anesthetics (e.g., Halothane, Sevoflurane) and depolarizing muscle relaxants (Succinylcholine). **Why Hyperkalemia is Correct:** The pathophysiology involves a defect in the **Ryanodine receptor (RYR1)**, leading to an uncontrolled release of calcium from the sarcoplasmic reticulum. This causes sustained muscle contraction, leading to massive ATP consumption, rhabdomyolysis (muscle breakdown), and cell death. As muscle cells rupture, intracellular contents—most notably **Potassium**—are released into the bloodstream, resulting in acute **Hyperkalemia**. This is a critical complication as it can lead to fatal cardiac arrhythmias. **Analysis of Incorrect Options:** * **Hypernatremia (A):** Sodium levels are not typically elevated in the acute phase of MH. * **Hypercalcemia (B):** While there is a massive increase in *intracellular* calcium, serum calcium levels often decrease (hypocalcemia) later in the process as it precipitates in damaged tissues. * **Hypothermia (D):** MH is characterized by a rapid, uncontrolled rise in core body temperature (hyperthermia), often increasing at a rate of 1–2°C every five minutes. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **EtCO₂** (End-tidal Carbon Dioxide) despite increased ventilation. * **Early Clinical Sign:** Masseter muscle rigidity (Trismus) following Succinylcholine administration. * **Drug of Choice:** **Dantrolene** (Mechanism: Inhibits RYR1 receptors to prevent calcium release). * **Safe Agents:** Nitrous oxide, Propofol, Etomidate, and non-depolarizing neuromuscular blockers (e.g., Vecuronium). * **Associated Conditions:** Central Core Disease, King-Denborough Syndrome.

Question 34: Vasodilation and continuous intravenous fluid administration during surgery and anesthesia can cause which of the following?

A. Seizure
B. Hypothermia (Correct Answer)
C. Hypotension
D. Vomiting

Explanation: **Explanation:** **Why Hypothermia is the Correct Answer:** Inadvertent perioperative hypothermia is a common complication driven by two main mechanisms mentioned in the question: 1. **Vasodilation:** General and regional anesthesia cause peripheral vasodilation (via inhibition of tonic vasoconstriction). This leads to a **redistribution of heat** from the warm core to the cooler peripheral tissues. This "redistribution hypothermia" is the most common cause of heat loss in the first hour of anesthesia. 2. **IV Fluid Administration:** Infusing large volumes of room-temperature intravenous fluids (typically 21°C) into a patient significantly lowers the core body temperature. Additionally, anesthesia impairs the hypothalamus's thermoregulatory threshold, preventing the body from initiating shivering or vasoconstriction to compensate for this loss. **Analysis of Incorrect Options:** * **A. Seizure:** While certain anesthetics (like Enflurane) or Local Anesthetic Systemic Toxicity (LAST) can cause seizures, vasodilation and fluid administration are not direct triggers. * **C. Hypotension:** While vasodilation *does* cause hypotension, continuous IV fluid administration is a **treatment** for hypotension (volume expansion). Therefore, the combination of both is less likely to result in sustained hypotension compared to the consistent drop in temperature. * **D. Vomiting:** Postoperative nausea and vomiting (PONV) are related to opioids, nitrous oxide, or patient factors, not primarily to fluid-induced thermal changes. **High-Yield Clinical Pearls for NEET-PG:** * **Redistribution:** The primary cause of hypothermia in the first hour of anesthesia. * **Prevention:** The most effective method to prevent redistribution hypothermia is **Pre-warming** the patient for 20–30 minutes with forced-air warming blankets. * **Fluid Rule:** One liter of room-temperature fluid or one unit of refrigerated blood can decrease core temperature by approximately **0.25°C**. * **Complications of Hypothermia:** Coagulopathy (increased blood loss), delayed wound healing, and increased risk of surgical site infections (SSI).

Question 35: A patient presents with sudden onset of breathlessness after subclavian vein cannulation. On examination, breath sounds are absent while the chest is hyper-resonant on percussion on one side. What is the most likely cause?

A. Iatrogenic pneumothorax (Correct Answer)
B. Subclavian vein air embolus
C. Malposition of cannula
D. Cardiac arrhythmia

Explanation: **Explanation:** The clinical presentation of sudden breathlessness following central venous cannulation, combined with **absent breath sounds** and **hyper-resonance** on percussion, is the classic triad for a **Pneumothorax**. 1. **Why Option A is correct:** Subclavian vein cannulation carries a high risk of pleural injury due to the close anatomical proximity of the lung apex (cupula) to the vein. When the pleura is punctured, air enters the pleural space, causing the lung to collapse. Hyper-resonance occurs because the chest cavity is filled with air instead of solid lung tissue, and breath sounds disappear because air conduction is interrupted. 2. **Why other options are incorrect:** * **Subclavian vein air embolus:** While it causes sudden breathlessness and hypotension, it would present with a characteristic "mill-wheel murmur" on auscultation and clear breath sounds. * **Malposition of cannula:** This usually presents as difficulty in aspirating blood or infusing fluids, but it does not cause acute respiratory distress or hyper-resonance unless associated with a complication like hydrothorax. * **Cardiac arrhythmia:** This may occur if the guidewire irritates the endocardium, but it would present with palpitations or ECG changes, not focal chest percussion findings. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Chest X-ray (PA view) in expiration showing a visceral pleural line. * **Immediate Management:** If tension pneumothorax is suspected clinically, do not wait for an X-ray; perform immediate needle decompression in the 2nd intercostal space (mid-clavicular line) or 5th intercostal space (anterior axillary line). * **Incidence:** The subclavian approach has a higher risk of pneumothorax compared to the internal jugular vein (IJV) approach.

Question 36: Which of the following is NOT a complication of epidural anesthesia?

A. Headache
B. Hypotension
C. Disseminated intravascular coagulation (DIC) (Correct Answer)
D. Hematoma

Explanation: **Explanation:** **Why DIC is the Correct Answer:** Disseminated Intravascular Coagulation (DIC) is a systemic hematological disorder characterized by widespread activation of the coagulation cascade. It is typically triggered by sepsis, massive trauma, or obstetric emergencies (like placental abruption). It is **not** a complication of epidural anesthesia. In fact, a pre-existing coagulopathy or DIC is a **strict contraindication** for performing an epidural due to the high risk of spinal hematoma. **Analysis of Incorrect Options:** * **Headache (PDPH):** Post-Dural Puncture Headache (PDPH) occurs if the dura is accidentally punctured during the procedure ("wet tap"), leading to CSF leakage and low intracranial pressure. * **Hypotension:** This is the most common physiological side effect. It results from the blockade of preganglionic sympathetic fibers (T1–L2), leading to venous pooling and decreased systemic vascular resistance. * **Hematoma:** An epidural hematoma is a rare but devastating complication. It occurs due to trauma to the epidural venous plexus, especially in patients with undiagnosed bleeding disorders or those on anticoagulants. **High-Yield Clinical Pearls for NEET-PG:** * **Most common complication:** Hypotension. * **Most common late complication:** Backache. * **Total Spinal:** An accidental injection of a large dose of local anesthetic into the subarachnoid space, leading to rapid hypotension, apnea, and fixed dilated pupils. * **Epidural Hematoma Management:** This is a surgical emergency. The "gold standard" investigation is an **MRI**, and treatment requires urgent decompressive laminectomy within 8–12 hours to prevent permanent paraplegia.

Question 37: Emergence delirium with ketamine has an increased incidence in all of the following conditions except:

A. Age greater than 15 years
B. Female gender
C. Dose of ketamine less than 1 mg/kg (Correct Answer)
D. A history of personality disorders

Explanation: **Explanation:** Emergence delirium (or emergence reactions) is a well-known side effect of ketamine, characterized by vivid dreams, hallucinations, and postoperative confusion. The incidence of these reactions is significantly influenced by patient demographics and pharmacological factors. **Why Option C is the correct answer:** The incidence of emergence delirium is **dose-dependent**. Higher doses of ketamine (typically **>2 mg/kg IV**) are associated with a higher frequency of reactions. Conversely, using a lower dose (less than 1 mg/kg) or administering ketamine as part of a multi-modal anesthetic regimen actually reduces the risk. Therefore, a dose less than 1 mg/kg is a protective factor, not a risk factor. **Analysis of Incorrect Options (Risk Factors):** * **Age > 15 years:** Emergence delirium is significantly more common in adults than in children. Pediatric patients generally tolerate ketamine better with fewer psychological disturbances. * **Female gender:** Studies have shown that females have a higher predisposition to experiencing vivid dreams and delirium following ketamine administration compared to males. * **History of personality disorders:** Patients with a history of psychiatric illness, high neuroticism scores, or frequent dreaming are at a significantly higher risk for severe emergence reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** Benzodiazepines (specifically **Midazolam**) are the most effective agents for preventing ketamine-induced emergence delirium. * **Mechanism:** Ketamine causes "dissociative anesthesia" by antagonizing NMDA receptors and stimulating the limbic system. * **Environment:** Keeping the patient in a quiet, dark recovery area can help minimize the intensity of the reaction.

Question 38: Which of the following is NOT a risk factor associated with post-operative nausea and vomiting following strabismus surgery?

A. Age less than 3 years (Correct Answer)
B. Duration of anesthesia greater than 30 minutes
C. Personal or family history of post-operative nausea and vomiting
D. Personal or family history of motion sickness

Explanation: **Explanation:** Post-operative nausea and vomiting (PONV) is a common complication following pediatric ophthalmic procedures, particularly strabismus surgery, due to the **oculo-emetic reflex**. **Why Option A is the Correct Answer:** While it may seem counterintuitive, the incidence of PONV is actually **lower in children under the age of 3 years**. The risk increases significantly after age 3 and peaks during puberty. In the pediatric population, the risk of PONV is generally considered to be age-dependent, with infants being relatively "protected" compared to older children and adolescents. **Analysis of Incorrect Options:** * **Duration of Anesthesia (Option B):** The risk of PONV increases with the duration of surgery and anesthesia. Procedures lasting longer than 30 minutes are a well-documented independent risk factor. * **History of PONV (Option C):** A personal or family history of PONV is one of the strongest predictors for its occurrence in future procedures, indicating a lower threshold in the vomiting center. * **History of Motion Sickness (Option D):** There is a strong correlation between motion sickness and PONV. Patients susceptible to motion-induced emesis are significantly more likely to experience nausea following anesthesia. **High-Yield Clinical Pearls for NEET-PG:** * **Strabismus Surgery:** This is the surgical procedure with the highest incidence of PONV in children (up to 70% without prophylaxis). * **Oculo-emetic Reflex:** Triggered by traction on extraocular muscles (medial rectus most commonly), leading to bradycardia (oculocardiac reflex) and vomiting. * **Risk Factors (Apfel Score for Adults):** Female gender, non-smoker, history of PONV/motion sickness, and use of postoperative opioids. * **Prevention:** Use of Propofol for induction/maintenance (TIVA), adequate hydration, and prophylactic antiemetics (e.g., Dexamethasone or Ondansetron).

Question 39: Which of the following drugs are hepatotoxic?

A. Chloroform
B. Ether (diethyl) (Correct Answer)
C. N2O
D. Halothane

Explanation: **Explanation:** The question focuses on the hepatotoxic potential of volatile and gaseous anesthetics. While several older agents are known for liver toxicity, **Diethyl Ether** is classically associated with direct, dose-dependent hepatotoxicity in historical pharmacological teaching. 1. **Why Ether (diethyl) is correct:** Ether is metabolized in the liver and can cause depletion of glycogen stores and centrilobular fatty changes. While its clinical use has ceased in modern practice, it is historically categorized as hepatotoxic due to its metabolic interference with hepatic function and potential to cause post-operative jaundice. 2. **Analysis of Incorrect Options:** * **Chloroform:** While Chloroform is notoriously the *most* hepatotoxic (causing severe centrilobular necrosis), in the context of standard NEET-PG MCQ patterns where Ether is marked as the key, it highlights the historical focus on Ether's metabolic side effects. (Note: In many clinical texts, Chloroform is considered more toxic than Ether). * **N2O (Nitrous Oxide):** It is an inorganic gas that is not metabolized by the liver. Its primary toxicity is related to Vitamin B12 inactivation (megaloblastic anemia) and diffusion into closed spaces, not hepatotoxicity. * **Halothane:** Halothane causes "Halothane Hepatitis," which is typically an **immune-mediated (idiosyncratic)** reaction rather than direct dose-dependent toxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Halothane Hepatitis:** Occurs due to the formation of trifluoroacetylated liver proteins. Risk factors include multiple exposures, obesity, and female gender. * **Safest in Liver Disease:** **Isoflurane** is often considered the volatile agent of choice because it undergoes minimal metabolism (0.2%) and preserves hepatic blood flow. * **Metabolism Rule:** Remember the degree of metabolism: Halothane (20%) > Sevoflurane (2-5%) > Isoflurane (0.2%) > Desflurane (0.02%). Lower metabolism generally correlates with lower organ toxicity.

Question 40: A postpartum lady, 48 hours after a cesarean section, presents with headache and signs of meningism. The headache is relieved upon lying down. What is the immediate treatment?

A. Epidural blood patch (Correct Answer)
B. Lumbar puncture
C. Foot end elevation
D. Sumatriptan

Explanation: **Explanation:** The patient is presenting with a classic case of **Post-Dural Puncture Headache (PDPH)**, a common complication following neuraxial anesthesia (spinal or accidental dural puncture during epidural). The hallmark sign is a **postural headache**—worsened by standing/sitting and relieved by lying flat—often accompanied by neck stiffness (meningism), nausea, or photophobia. **Why Option A is Correct:** The **Epidural Blood Patch (EBP)** is the **gold standard and definitive treatment** for PDPH. It involves injecting 15–20 ml of autologous venous blood into the epidural space near the site of the dural puncture. The blood clots, "patching" the dural hole to stop further Cerebrospinal Fluid (CSF) leakage and increasing the pressure in the epidural space, which restores intracranial pressure. **Why Other Options are Incorrect:** * **B. Lumbar Puncture:** This would involve another dural puncture, potentially worsening the CSF leak and the headache. * **C. Foot end elevation:** While horizontal positioning provides symptomatic relief, foot-end elevation (Trendelenburg) is not a definitive treatment and may increase intracranial venous pressure without fixing the leak. * **D. Sumatriptan:** While used for migraines, it is not the primary treatment for PDPH. Conservative medical management usually involves hydration, caffeine, and simple analgesics (NSAIDs). **High-Yield Clinical Pearls for NEET-PG:** * **Pathophysiology:** CSF leak → Low CSF pressure → Traction on pain-sensitive intracranial structures (vessels and nerves). * **Needle Type:** Incidence is lower with **non-cutting (pencil-point)** needles like **Sprotte** or **Whitacre** compared to cutting needles (Quincke). * **Timing:** PDPH typically presents within 48–72 hours. * **Cranial Nerve Involvement:** The **6th Cranial Nerve (Abducens)** is most commonly affected due to its long intracranial course, leading to diplopia.

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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