Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 41: Ketamine is contraindicated in which of the following conditions?

A. Status asthmaticus
B. Obstetric hemorrhage
C. Glaucoma (Correct Answer)
D. Shock

Explanation: ### Explanation **Correct Option: C. Glaucoma** Ketamine is a dissociative anesthetic that causes sympathetic stimulation. It is contraindicated in **Glaucoma** because it increases **Intraocular Pressure (IOP)**. This occurs due to an increase in choroidal blood flow and potential tonic-clonic movements of the extraocular muscles. For the same reason, it is avoided in penetrating eye injuries where an increase in IOP could lead to the expulsion of intraocular contents. **Analysis of Incorrect Options:** * **A. Status Asthmaticus:** Ketamine is actually a **drug of choice** for induction in asthmatic patients. It has potent **bronchodilatory** properties mediated by catecholamine release and direct relaxant effects on bronchial smooth muscle. * **B. Obstetric Hemorrhage:** Ketamine is frequently used in obstetric emergencies (like placental abruption or hemorrhage) because it maintains blood pressure and uterine blood flow. However, it should be used in low doses (<1 mg/kg) to avoid uterine hypertonicity. * **D. Shock:** Ketamine is the **induction agent of choice in hypovolemic/hemorrhagic shock**. Its sympathomimetic effects (increased heart rate, CO, and BP) help maintain hemodynamic stability compared to agents like propofol or thiopentone. **High-Yield Clinical Pearls for NEET-PG:** 1. **Triple Increase:** Ketamine increases **IOP** (Intraocular), **ICP** (Intracranial), and **ICT** (Intrathoracic/BP). 2. **The "Exception" in Shock:** While usually preferred in shock, Ketamine can cause **myocardial depression** in "critically ill" patients who are catecholamine-depleted. 3. **Emergence Delirium:** This common side effect (hallucinations/vivid dreams) can be prevented by pre-medicating with **Benzodiazepines** (e.g., Midazolam). 4. **Secretions:** It is a potent **sialagogue** (increases salivation); hence, it is often co-administered with Glycopyrrolate.

Question 42: Postoperative shivering is treated with:

A. Diazepam
B. Antihistaminics
C. Anticholinergics
D. Pethidine (Correct Answer)

Explanation: **Explanation:** **1. Why Pethidine is the Correct Answer:** Postoperative shivering (POS) is a common complication following general or spinal anesthesia, primarily caused by the core-to-peripheral redistribution of heat and the lowering of the shivering threshold by anesthetic agents. **Pethidine (Meperidine)** is considered the **drug of choice** for treating POS. Its unique efficacy lies in its potent **agonist action at the κ (kappa) opioid receptors**, which significantly lowers the shivering threshold in the hypothalamus. While other opioids (like Morphine or Fentanyl) act primarily on μ (mu) receptors and have limited effect on shivering, Pethidine’s kappa-receptor activity makes it highly effective at low doses (10–25 mg IV). **2. Why the Other Options are Incorrect:** * **A. Diazepam:** This is a benzodiazepine used for sedation and anxiolysis. While it may reduce muscle tension, it does not act on the thermoregulatory center to stop the shivering reflex. * **B. Antihistaminics:** These are used for allergic reactions or as mild sedatives (e.g., Diphenhydramine). They have no clinical role in modulating the thermoregulatory set point. * **C. Anticholinergics:** Drugs like Atropine or Glycopyrrolate are used to reduce secretions or treat bradycardia. They do not influence the shivering mechanism. **3. High-Yield Clinical Pearls for NEET-PG:** * **Non-Pharmacological Management:** Forced-air warming (Bair Hugger) is the most effective way to prevent and treat perioperative hypothermia. * **Other Drugs for Shivering:** If Pethidine is unavailable, **Tramadol**, **Clonidine**, and **Dexmedetomidine** (α2 agonists) are effective alternatives. * **Mechanism of POS:** It increases oxygen consumption by up to 200–500%, which can be dangerous in patients with limited cardiac reserve (CAD). * **Key Association:** Pethidine is also the only opioid that possesses local anesthetic-like properties.

Question 43: Which of the following is NOT true regarding shivering after neuraxial anesthesia?

A. Shivering increases intra-ocular and intra-cranial pressures.
B. Intravenous meperidine is used in its treatment.
C. A marked increase in plasma catecholamines can cause cardiovascular complications.
D. Shivering is associated with decreased oxygen consumption. (Correct Answer)

Explanation: ### Explanation **1. Why Option D is the correct answer (The False Statement):** Shivering is an involuntary, oscillatory muscular activity aimed at generating heat through metabolic work. Contrary to the statement, shivering causes a **massive increase in oxygen consumption** (up to 200–500%) and a significant rise in carbon dioxide production. In patients with limited cardiopulmonary reserve, this increased metabolic demand can lead to hypoxemia, lactic acidosis, and myocardial ischemia. **2. Analysis of Incorrect Options (True Statements):** * **Option A:** The vigorous muscular contractions associated with shivering lead to an increase in central venous pressure, which directly translates to a rise in **intra-ocular pressure (IOP)** and **intra-cranial pressure (ICP)**. This is particularly dangerous in patients with glaucoma or head injuries. * **Option B:** **Meperidine (Pethidine)** is the gold standard and most effective drug for treating post-anesthetic shivering. It acts primarily via **kappa (κ) opioid receptors** to lower the shivering threshold. * **Option C:** Shivering triggers a sympathetic "stress response," leading to a surge in **plasma catecholamines**. This causes tachycardia and hypertension, which can precipitate arrhythmias or heart failure in susceptible individuals. **3. NEET-PG High-Yield Pearls:** * **Mechanism in Neuraxial Anesthesia:** Shivering occurs due to **core-to-peripheral redistribution of heat** (vasodilation below the block level) and a decrease in the shivering threshold by the hypothalamus. * **Drug of Choice:** Meperidine (25 mg IV). Other agents include Tramadol, Clonidine, and Dexmedetomidine. * **Non-Pharmacological Prevention:** Forced-air warming blankets and pre-warming intravenous fluids are the most effective preventive measures. * **Grading:** Shivering is often graded using the **Bedside Shivering Assessment Scale (BSAS)**.

Question 44: In the management of sepsis, what is the primary type of fluid administered?

A. Colloids
B. Crystalloids (Correct Answer)
C. Hydroxyethyl starch
D. None of the above

Explanation: ### Explanation **1. Why Crystalloids are the Correct Answer:** According to the **Surviving Sepsis Campaign (SSC) guidelines**, crystalloids are the first-line choice for fluid resuscitation in patients with sepsis and septic shock. The primary goal in sepsis is to restore intravascular volume and improve organ perfusion. Crystalloids (such as Normal Saline or Ringer’s Lactate) are preferred because they are effective, inexpensive, and have a better safety profile regarding renal function and coagulation compared to alternatives. The current recommendation is an initial bolus of **30 mL/kg** of intravenous crystalloid within the first 3 hours. **2. Why Other Options are Incorrect:** * **Colloids (Option A):** While colloids (like Albumin) stay in the intravascular space longer, they are significantly more expensive. They are generally reserved as a second-line option when patients require substantial amounts of crystalloids. * **Hydroxyethyl Starch (HES) (Option C):** HES is a synthetic colloid that is specifically **contraindicated** in sepsis. Large clinical trials (like the CHEST and 6S trials) demonstrated that HES increases the risk of **Acute Kidney Injury (AKI)**, the need for renal replacement therapy, and increased mortality in septic patients. **3. High-Yield Clinical Pearls for NEET-PG:** * **Fluid of Choice:** Balanced salt solutions (e.g., **Ringer’s Lactate** or Plasmalyte) are increasingly preferred over Normal Saline (0.9% NaCl) to avoid hyperchloremic metabolic acidosis. * **Vasoactive Support:** If MAP remains <65 mmHg despite fluid resuscitation, **Norepinephrine** is the first-choice vasopressor. * **Dynamic Parameters:** Modern sepsis management emphasizes using dynamic measures (e.g., Passive Leg Raise, Stroke Volume Variation) rather than static measures (CVP) to assess fluid responsiveness. * **Albumin:** Consider adding Albumin only when patients require very large volumes of crystalloids.

Question 45: An ICU patient on atracurium infusion develops seizures after 2 days. What is the most probable cause?

A. Accumulation of laudanosine (Correct Answer)
B. Allergy to drug
C. Prolonged infusion
D. All of the above

Explanation: **Explanation:** The correct answer is **Accumulation of laudanosine**. **1. Why Laudanosine is the cause:** Atracurium is a benzylisoquinolinium neuromuscular blocking agent that undergoes **Hofmann elimination** (a non-enzymatic chemical degradation dependent on pH and temperature). A major metabolic byproduct of this process is **laudanosine**. Unlike the parent drug, laudanosine is a tertiary amine that easily crosses the blood-brain barrier. It acts as a **CNS stimulant** and can lower the seizure threshold. In the setting of a prolonged infusion (e.g., 2 days in the ICU), laudanosine accumulates to toxic levels, potentially triggering seizures. **2. Why other options are incorrect:** * **Allergy to drug:** While atracurium is known for histamine release, this typically presents as hypotension, flushing, or bronchospasm immediately after administration, not as delayed seizures after 48 hours. * **Prolonged infusion:** While the infusion is the *context* in which the complication occurs, it is not the *cause* itself. The physiological mechanism of the seizure is the specific metabolite produced, not the duration of the infusion alone. * **All of the above:** Incorrect because the clinical presentation (seizures) is a specific toxicological effect of laudanosine, not a generalized result of allergy. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cisatracurium:** An isomer of atracurium that is more potent, produces significantly **less laudanosine**, and triggers less histamine release. It is preferred for long-term ICU infusions. * **Hofmann Elimination:** This makes atracurium/cisatracurium the drugs of choice in patients with **renal or hepatic failure**, as their clearance is independent of these organs. * **Laudanosine Clearance:** Although produced by Hofmann elimination, laudanosine itself is cleared by the liver; therefore, toxicity is more likely in patients with hepatic impairment.

Question 46: All are true statements about malignant hyperthermia except?

A. It is an autosomal dominant condition.
B. Total intravenous anesthesia (TIVA) is safe in malignant hyperthermia.
C. Malignant hyperthermia is a hypermetabolic state with elevated end-tidal CO2, tachypnea, tachycardia, masseter spasm if succinylcholine is used, and generalized muscle rigidity.
D. Oral dantrolene is the drug of choice. (Correct Answer)

Explanation: ### Explanation **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic clinical syndrome triggered by volatile anesthetic gases and the depolarizing muscle relaxant succinylcholine. **Why Option D is the correct answer (False statement):** While **Dantrolene** is indeed the definitive treatment for MH, **oral dantrolene is ineffective** in an acute crisis. The drug of choice is **Intravenous (IV) Dantrolene**. It works by binding to the ryanodine receptor (RYR1), inhibiting the release of calcium from the sarcoplasmic reticulum into the myoplasm. The initial dose is 2.5 mg/kg IV, repeated until symptoms subside. **Analysis of other options:** * **Option A:** MH is inherited as an **autosomal dominant** trait with variable penetrance. It is most commonly associated with mutations in the **RYR1 gene** (ryanodine receptor). * **Option B:** TIVA (using drugs like Propofol and Opioids) is considered **safe**. MH is only triggered by "potent" volatile agents (Halothane, Isoflurane, Sevoflurane, Desflurane) and Succinylcholine. Nitrous oxide and Etomidate are also safe. * **Option C:** MH is a hypermetabolic state. The **earliest and most sensitive sign is a rise in End-Tidal CO2 (EtCO2)**. Masseter muscle rigidity (MMR) after succinylcholine administration is a classic warning sign. Hyperthermia is often a late sign. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Caffeine Halothane Contracture Test (CHCT) performed on a muscle biopsy. * **Earliest Sign:** Unexplained rise in EtCO2 (refractory to increased ventilation). * **Management Mnemonic:** "Help, Discontinue, Dantrolene" (Call for help, stop triggers, give IV Dantrolene). * **Associated Conditions:** Central Core Disease, King-Denborough Syndrome, and Multiminicore disease. * **Safe Agents:** Propofol, Thiopentone, Ketamine, Etomidate, Nondepolarizing NMBs (eg. Vecuronium), and Local Anesthetics.

Question 47: Which of the following is true regarding post-spinal headache?

A. It does not improve when the patient is in a recumbent position.
B. It typically improves with caffeine administration. (Correct Answer)
C. It is more pressure-dependent than volume-dependent.
D. It starts immediately after the spinal procedure.

Explanation: **Explanation:** Post-Dural Puncture Headache (PDPH) is a common complication following spinal anesthesia, caused by the persistent leakage of cerebrospinal fluid (CSF) through the dural puncture site. This leads to low CSF pressure and compensatory cerebral vasodilation. **1. Why Option B is Correct:** Caffeine is a potent **cerebral vasoconstrictor**. By constricting the dilated cerebral vessels (which occur in response to low CSF pressure), caffeine helps alleviate the characteristic throbbing pain. It is often administered orally or intravenously (e.g., 500 mg Caffeine Sodium Benzoate) as a first-line conservative treatment. **2. Why Other Options are Incorrect:** * **Option A:** PDPH is classically **positional**. It worsens when the patient is upright and **improves significantly in the recumbent (supine) position** due to reduced hydrostatic pressure on the dural leak. * **Option C:** PDPH is primarily **volume-dependent**. The symptoms arise because the rate of CSF leak exceeds the rate of CSF production, leading to a loss of the "buoyancy" effect of the brain. * **Option D:** It rarely starts immediately. Symptoms typically manifest **12 to 48 hours** after the procedure. An immediate headache is more likely to be related to other causes like accidental air injection (pneumoencephalos). **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** More common in young females, pregnant patients, and when using large-bore or cutting-tip needles (e.g., Quincke). * **Prevention:** Use of small-gauge (25G–27G) **non-cutting/pencil-point needles** (e.g., **Sprotte or Whitacre**) significantly reduces incidence. * **Gold Standard Treatment:** For persistent or severe cases, the **Epidural Blood Patch** is the most effective treatment (success rate >90%). * **Character:** Typically bifrontal or occipital, radiating to the neck and shoulders.

Question 48: Nitrous oxide is contraindicated in patients with pneumothorax, pneumopericardium, or intestinal obstruction because it:

A. Depresses an already compromised myocardium.
B. Permits the use of limited FIO2 only.
C. Is less soluble than nitrogen.
D. Causes the expansion of air-filled body cavities. (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Causes the expansion of air-filled body cavities.** **Mechanism:** This phenomenon is governed by the **difference in blood solubility** between Nitrous Oxide ($N_2O$) and Nitrogen ($N_2$). $N_2O$ is approximately **34 times more soluble** in blood than $N_2$. When $N_2O$ is administered, it diffuses from the blood into closed, air-filled spaces (which contain $N_2$) much faster than the $N_2$ can diffuse out into the blood. This rapid influx of gas leads to a significant increase in the volume or pressure of the cavity. In conditions like **pneumothorax**, $N_2O$ can double the volume of the air pocket in 10 minutes, potentially converting a simple pneumothorax into a life-threatening **tension pneumothorax**. Similarly, it can worsen bowel distension in intestinal obstruction or increase intracranial pressure in pneumocephalus. **Analysis of Incorrect Options:** * **A:** While $N_2O$ has a mild direct myocardial depressant effect, this is usually offset by sympathetic stimulation and is not the primary reason for its contraindication in these specific conditions. * **B:** While using $N_2O$ limits the maximum $FiO_2$ achievable, modern anesthesia allows for safe oxygenation levels. The mechanical expansion of gas is the more acute danger. * **C:** This is factually incorrect. $N_2O$ is significantly **more** soluble than nitrogen, which is the physiological basis for the expansion. **High-Yield Clinical Pearls for NEET-PG:** * **Contraindications for $N_2O$:** Pneumothorax, air embolism, intestinal obstruction, pneumocephalus, intraocular gas bubbles (e.g., sulfur hexafluoride used in retinal surgery), and middle ear surgeries (can dislodge tympanic grafts). * **Second Gas Effect:** $N_2O$ speeds up the uptake of a companion volatile anesthetic. * **Diffusion Hypoxia (Fink Effect):** Occurs during recovery when $N_2O$ rapidly diffuses from blood back into the alveoli, diluting oxygen. Prevention: Administer 100% $O_2$ for 5–10 minutes after stopping $N_2O$.

Question 49: In which patient position is venous air embolism most commonly encountered?

A. Sitting (Correct Answer)
B. Supine
C. Prone
D. Left lateral

Explanation: **Explanation:** **Venous Air Embolism (VAE)** occurs when there is a pressure gradient that allows atmospheric air to enter the venous circulation through an open, non-collapsible vein. **Why Sitting is Correct:** The sitting position is the most common scenario for VAE, particularly during **neurosurgical procedures** (e.g., posterior fossa surgery). In this position, the surgical site is significantly **above the level of the heart**. This creates a **negative pressure gradient** between the atmospheric air at the wound site and the sub-atmospheric pressure in the dural venous sinuses. Since dural sinuses are held open by bone or dura and cannot collapse, air is easily sucked into the venous system. **Why Other Options are Incorrect:** * **Supine:** The surgical site is generally at or near the level of the heart, minimizing the gravitational pressure gradient required for air entrainment. * **Prone:** While VAE can occur in the prone position (especially in spinal surgeries), the gradient is typically less pronounced than in the sitting position. * **Left Lateral:** This position is actually used as a **treatment** for VAE (Durant’s Maneuver). Placing the patient in the left lateral decubitus with Trendelenburg helps trap the air bubble in the apex of the right ventricle, preventing it from obstructing the pulmonary artery outflow tract. **High-Yield Clinical Pearls for NEET-PG:** * **Most Sensitive Monitor:** **Precordial Doppler** (detects the classic "mill-wheel murmur"). * **Gold Standard for Detection:** Transesophageal Echocardiography (TEE). * **Earliest Sign:** Decrease in **End-Tidal CO2 (EtCO2)** due to increased dead space. * **Management:** 100% Oxygen, flood the surgical field with saline, aspirate air via a Central Venous Catheter, and place the patient in the **Left Lateral Trendelenburg position**.

Question 50: What is the treatment for bupivacaine poisoning?

A. Esmolol
B. Sotalol
C. Diazepam
D. Lipid emulsion (Correct Answer)

Explanation: **Explanation:** Bupivacaine poisoning, a form of **Local Anesthetic Systemic Toxicity (LAST)**, occurs due to accidental intravascular injection or rapid absorption. Bupivacaine is highly lipid-soluble and cardiotoxic, as it binds strongly to cardiac sodium channels (the "fast-in, slow-out" phenomenon), leading to intractable arrhythmias and cardiovascular collapse. **Why Lipid Emulsion is Correct:** **Intravenous Lipid Emulsion (ILE) 20%** is the specific antidote. It works via the **"Lipid Sink" theory**: the lipid molecules create a separate compartment in the blood that sequesters the lipophilic bupivacaine molecules, pulling them away from the cardiac and neural tissues. It also provides a direct metabolic energy source for the struggling myocardium. **Why Other Options are Incorrect:** * **Esmolol & Sotalol:** These are beta-blockers. In LAST, the heart is already depressed and prone to bradycardia or conduction blocks. Beta-blockers would further decrease contractility and worsen heart failure. * **Diazepam:** While benzodiazepines are used to control seizures associated with LAST, they do not treat the underlying cardiac toxicity or the cause of the poisoning. **High-Yield Clinical Pearls for NEET-PG:** * **Dosing:** The initial bolus of 20% Lipid Emulsion is **1.5 mL/kg** over 1 minute, followed by an infusion of **0.25 mL/kg/min**. * **Avoid Vasopressin:** In LAST-induced cardiac arrest, avoid vasopressin and use low-dose epinephrine (<1 mcg/kg) to prevent worsening arrhythmias. * **Early Signs:** Perioral numbness, metallic taste, and tinnitus often precede seizures and cardiac arrest. * **Propofol is NOT a substitute:** Although it contains lipids, the sedative effect of propofol can worsen cardiovascular instability.

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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