Complications in Anesthesia — MCQs

A patient is undergoing MRND for laryngeal malignancy; while dissecting the venous tributaries the surgeon elevated the internal jugular vein for ligation. Suddenly the patient's EtCO2 dropped from 38 mmHg to 12 mmHg and the patient developed hypotension along with cardiac arrhythmia. Which of the following is the most likely cause?

Q208

A patient selected for surgery induced with thiopental i.v. through one of the antecubital veins, complains of severe pain of whole hand. What should be the next line of management in this patient?

Q209

All are clinical features of Propofol infusion syndrome except:-

Q210

All are seen in malignant hyperthermia except:

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 201: Which of the following is the most potent trigger of malignant hyperthermia?

A. Thiopentone
B. Isoflurane
C. Suxamethonium
D. Halothane (Correct Answer)

Explanation: ***Halothane*** - **Halothane** is a volatile anesthetic agent and the **most potent trigger** of malignant hyperthermia, directly acting on the **ryanodine receptor (RyR1)** to cause massive calcium release from the sarcoplasmic reticulum. - It has extensive historical documentation as the **primary MH trigger** and is used as the reference standard in MH susceptibility testing. *Suxamethonium* - **Suxamethonium** (succinylcholine) is a depolarizing neuromuscular blocking agent that can trigger malignant hyperthermia but is considered a **secondary trigger** compared to volatile anesthetics. - While it can independently cause MH episodes, volatile agents like **halothane** are recognized as more potent and primary triggers in current medical literature. *Thiopentone* - **Thiopentone** (thiopental) is an intravenous barbiturate anesthetic that is **safe** in patients susceptible to malignant hyperthermia. - It does not interact with the **ryanodine receptor (RyR1)** or cause uncontrolled calcium release, making it a preferred induction agent in MH-susceptible patients. *Isoflurane* - **Isoflurane** is a volatile anesthetic agent and a **potent trigger** of malignant hyperthermia, similar to halothane in its mechanism of action. - While equally potent as halothane, **halothane** is considered the classic reference trigger due to its historical significance and extensive research documentation.

Question 202: Malignant hyperthermia is most commonly precipitated by:

A. Dantrolene sodium
B. Gallamine
C. Succinyl choline (Correct Answer)
D. Pancuronium

Explanation: ***Succinyl choline*** - **Malignant hyperthermia** is an inherited disorder characterized by a rapid and severe rise in body temperature, muscle rigidity, and other metabolic derangements, most commonly triggered by **volatile anesthetic agents** (like halothane, sevoflurane) and the depolarizing muscle relaxant **succinylcholine**. - **Succinylcholine** triggers uncontrolled calcium release from the sarcoplasmic reticulum in susceptible individuals, leading to sustained muscle contraction and excessive heat production. *Dantrolene sodium* - **Dantrolene sodium** is the specific **antidote** for malignant hyperthermia, acting to inhibit calcium release from the sarcoplasmic reticulum. - It is used to **treat** malignant hyperthermia, not to precipitate it. *Gallamine* - **Gallamine** is a historical example of a **nondepolarizing neuromuscular blocker**; these agents generally do not trigger malignant hyperthermia. - It works by competing with acetylcholine at the neuromuscular junction, not by direct calcium release. *Pancuronium* - **Pancuronium** is a **nondepolarizing neuromuscular blocker** that blocks acetylcholine receptors, but it is not known to trigger malignant hyperthermia. - Like other nondepolarizing agents, it does not directly cause the sustained muscle contraction seen in malignant hyperthermia.

Question 203: A 12-year-old boy with a femur fracture after a motor vehicle collision undergoes operative repair. After induction of anesthesia, he develops a fever of 40degC (104degF), shaking rigors, and blood-tinged urine. Which of the following is the best treatment option?

A. Administration of intravenous steroids and an antihistamine agent with continuation of the procedure
B. Administration of dantrolene sodium and continuation with the procedure
C. Alkalinization of the urine, administration of mannitol, and continuation with the procedure
D. Administration of dantrolene sodium and termination of the procedure (Correct Answer)

Explanation: ***Administration of dantrolene sodium and termination of the procedure*** - The sudden onset of **high fever, rigors, and blood-tinged urine** during anesthesia strongly suggests **malignant hyperthermia**, a life-threatening pharmacogenetic disorder. The immediate and definitive treatment involves **dantrolene sodium** to block calcium release from the sarcoplasmic reticulum, and the procedure must be **terminated** to prevent further exposure to triggering agents and manage the crisis. - Continuation of the surgery under these conditions would be extremely dangerous and could lead to **multi-organ failure** and death. *Administration of intravenous steroids and an antihistamine agent with continuation of the procedure* - This treatment would be appropriate for an **anaphylactic reaction**, which typically presents with **hypotension, bronchospasm, and rash**, not the specific constellation of fever, rigors, and blood-tinged urine seen here. - While anaphylaxis can occur, the **elevated temperature and muscle rigidity** (implied by rigors in this context) are not characteristic, and continuing the procedure would be harmful if it were malignant hyperthermia. *Administration of dantrolene sodium and continuation with the procedure* - While **dantrolene sodium** is the correct pharmacological treatment for malignant hyperthermia, **continuing the procedure** poses a significant risk as it prolongs exposure to anesthetic agents that may be triggering the reaction. - The goal is to stabilize the patient, not to proceed with surgery while under active malignant hyperthermia crisis. *Alkalinization of the urine, administration of mannitol, and continuation with the procedure* - **Alkalinization of urine and mannitol** are interventions for preventing **renal damage** due to myoglobinuria, which can occur as a complication of malignant hyperthermia. - However, these are **supportive measures** and not the primary treatment for the underlying malignant hyperthermia itself, nor should they lead to continuation of the procedure.

Question 204: The most appropriate immediate management of prolonged Scoline apnea is

A. Reversal with neostigmine
B. Estimation of plasma cholinesterase
C. Exchange transfusion
D. Continuation of artificial ventilation (Correct Answer)

Explanation: ***Continuation of artificial ventilation*** - **Scoline (succinylcholine)** apnea is often due to a deficiency in **pseudocholinesterase (plasma cholinesterase)**, leading to prolonged paralysis. - The most appropriate immediate management is to bridge the period of paralysis with **artificial ventilation** until the drug is metabolized, supporting the patient's respiratory function. *Reversal with neostigmine* - **Neostigmine** is an acetylcholinesterase inhibitor used to reverse the effects of **non-depolarizing neuromuscular blockers**, not depolarizing ones like succinylcholine. - Using neostigmine in scoline apnea would worsen the block by inhibiting the breakdown of acetylcholine at the neuromuscular junction, potentially intensifying the paralysis. *Estimation of plasma cholinesterase* - While **estimation of plasma cholinesterase** can help diagnose the cause of prolonged scoline apnea, it is a diagnostic step, not an immediate management strategy. - The results are not immediate and will not help in the acute respiratory crisis presented by prolonged apnea. *Exchange transfusion* - **Exchange transfusion** is an extreme and invasive measure that is not indicated for managing prolonged scoline apnea. - It carries significant risks and is reserved for conditions like severe hyperbilirubinemia or certain poisonings, not for pseudocholinesterase deficiency.

Question 205: Which of the following anesthetic agents does not trigger malignant hyperthermia?

A. Isoflurane
B. Suxamethonium
C. Halothane
D. Thiopentone (Correct Answer)

Explanation: ***Thiopentone*** - **Thiopentone** is an **intravenous anesthetic agent** that does not trigger **malignant hyperthermia** because it does not interact with the **ryanodine receptor (RyR1)** or lead to uncontrolled calcium release from the sarcoplasmic reticulum. - It is a **barbiturate** and its mechanism of action involves enhancing the effect of **GABA** at the GABA-A receptor, unrelated to the calcium dysregulation seen in malignant hyperthermia. *Isoflurane* - **Isoflurane** is a **volatile anesthetic agent** (inhaled) known to be a potent trigger of **malignant hyperthermia** in susceptible individuals. - It directly activates the **ryanodine receptor type 1 (RyR1)**, leading to a massive and uncontrolled release of calcium from the **sarcoplasmic reticulum** in skeletal muscle cells. *Suxamethonium* - **Suxamethonium** (succinylcholine) is a **depolarizing neuromuscular blocker** that can trigger or exacerbate **malignant hyperthermia**, especially when given with volatile anesthetics. - It causes muscle fasciculations and can lead to a sustained muscle contraction and metabolic derangements characteristic of the condition. *Halothane* - **Halothane** is a prototype **volatile anesthetic agent** and is one of the most well-known and potent triggers of **malignant hyperthermia**. - Its use has significantly decreased due to its association with malignant hyperthermia and hepatotoxicity, but it serves as a classic example of an agent that causes massive calcium release from the **sarcoplasmic reticulum**.

Question 206: If thiopentone is injected accidently into an artery the first symptom is –

A. Pain (Correct Answer)
B. Paralysis
C. Analgesia
D. Skin ulceration

Explanation: ***Pain*** - Intra-arterial injection of thiopentone causes immediate and intense **pain** due to its highly alkaline pH (around 10.5), which irritates the arterial wall and damages endothelium. - The pain is usually felt distal to the injection site, radiating down the limb, and is a crucial warning sign of this serious complication. *Paralysis* - Paralysis is not an immediate symptom of intra-arterial thiopentone injection; rather, it can be a later complication due to **ischemic nerve damage** if severe vasoconstriction and thrombosis persist. - The initial insult is primarily to the vascular endothelium, leading to spasm and tissue damage, not direct neuromuscular blockade. *Analgesia* - Analgesia is a systemic effect of intravenous thiopentone, which is a **barbiturate anesthetic**, but it is not the first symptom of its accidental intra-arterial administration. - Intra-arterial injection causes localized pain, not pain relief, as the drug's intended action is bypassed and localized irritation dominates. *Skin ulceration* - **Skin ulceration** is a severe and delayed complication of intra-arterial thiopentone, occurring hours to days after the event due to extensive tissue ischemia and necrosis. - It is not the first symptom, which is typically immediate pain, as the tissue damage takes time to manifest visually.

Question 207: A patient is undergoing MRND for laryngeal malignancy; while dissecting the venous tributaries the surgeon elevated the internal jugular vein for ligation. Suddenly the patient's EtCO2 dropped from 38 mmHg to 12 mmHg and the patient developed hypotension along with cardiac arrhythmia. Which of the following is the most likely cause?

A. Sympathetic overactivity
B. Vagal stimulation
C. Venous air embolism (Correct Answer)
D. Carotid body stimulation

Explanation: ***Venous air embolism*** - A sudden drop in **EtCO2**, **hypotension**, and cardiac arrhythmia during neck dissection, especially with manipulation of the internal jugular vein, strongly indicates venous air embolism. - This occurs when air enters an open vein, travels to the right heart, and obstructs pulmonary blood flow, leading to increased **dead space** and decreased **CO2 exhalation**. *Sympathetic overactivity* - This would typically lead to **tachycardia** and **hypertension**, not bradycardia and hypotension as suggested by the cardiac arrhythmia and drop in blood pressure. - While sympathetic stimulation can cause arrhythmias, the combination with **hypotension** and a precipitous **EtCO2 drop** points away from this as the primary cause. *Vagal stimulation* - Vagal stimulation would primarily cause **bradycardia** and **hypotension** due to parasympathetic effects on the heart, but it would not explain a sudden, profound drop in **EtCO2**. - The drop in **EtCO2** is a key indicator of impaired pulmonary perfusion or CO2 transport, which is not a direct result of vagal stimulation. *Carotid body stimulation* - Stimulation of the carotid body (chemoreceptors) primarily affects **respiration** and can cause **bradycardia** and **hypotension** through a chemoreceptor reflex. - However, it does not explain the dramatic drop in **EtCO2** observed, which is more indicative of a circulatory or pulmonary event.

Question 208: A patient selected for surgery induced with thiopental i.v. through one of the antecubital veins, complains of severe pain of whole hand. What should be the next line of management in this patient?

A. Apply a warm compress
B. Inject hydrocortisone locally
C. Stop the injection, remove the IV, administer local anesthetic and hyaluronidase (Correct Answer)
D. Elevate the limb

Explanation: ***Stop the injection, remove the IV, administer local anesthetic and hyaluronidase*** - This is the immediate and most crucial step when extravasation or intra-arterial injection of an irritant, like **thiopental**, is suspected to minimize tissue damage and relieve pain. - **Local anesthetic** helps alleviate immediate pain, while **hyaluronidase** disperses the extravasated drug, aiding in its absorption and preventing further tissue injury. *Apply a warm compress* - While warm compresses can sometimes help with localized swelling and improve circulation, they are **insufficient** as a primary intervention for severe pain and potential extravasation/intra-arterial injection of thiopental. - Thiopental is highly alkaline and can cause severe tissue necrosis if extravasated, requiring more aggressive measures than a warm compress alone. *Inject hydrocortisone locally* - **Hydrocortisone** is a steroid with anti-inflammatory properties, but it is not the immediate treatment for acute pain and potential tissue damage from **thiopental extravasation** or intra-arterial injection. - Its effects are delayed and insufficient to disperse the drug or rapidly mitigate the severe pain caused by such events. *Elevate the limb* - Elevating the limb might help reduce swelling in some scenarios, but it does **not address the immediate problem** of an irritating drug like thiopental being in the wrong tissue compartment or artery. - This action does not remove or neutralize the drug, nor does it provide rapid pain relief, which is paramount in this situation.

Question 209: All are clinical features of Propofol infusion syndrome except:-

A. Metabolic alkalosis (Correct Answer)
B. Lipaemia
C. Bradycardia
D. Renal failure

Explanation: ***Metabolic alkalosis*** - **Propofol Infusion Syndrome (PRIS)** is characterized by **metabolic acidosis**, not alkalosis. The accumulation of lactic acid is a hallmark feature. - This is a critical distinction, as **acidosis** contributes significantly to the multi-organ dysfunction seen in PRIS. *Lipaemia* - **Hyperlipidemia** and subsequent **lipaemia** are common features of PRIS due to propofol's lipid emulsion vehicle and its impact on lipid metabolism. - This can manifest as visible **clouding of serum** or elevated triglyceride levels. *Bradycardia* - **Bradycardia** is a significant and often early clinical feature of PRIS, progressing to intractable arrhythmias. - It results from propofol's direct effects on myocardial contractility and conduction, particularly when dopamine and norepinephrine are concurrently infused. *Renal failure* - **Acute renal failure** is a serious complication of PRIS, often requiring hemodialysis. - It is thought to be multifactorial, involving direct renal toxicity, rhabdomyolysis, and hypoperfusion.

Question 210: All are seen in malignant hyperthermia except:

A. Bradycardia (Correct Answer)
B. Hypertension
C. Metabolic acidosis
D. Hyperkalemia

Explanation: ***Bradycardia*** - Malignant hyperthermia is characterized by a hypermetabolic state, which typically causes **tachycardia** (increased heart rate) due to increased oxygen demand and catecholamine release, not bradycardia. - **Bradycardia** is not a hallmark sign of malignant hyperthermia; rather, it indicates an atypical or late-stage cardiac compromise. *Hypertension* - **Hypertension** is a common early sign of malignant hyperthermia due to intense **vasoconstriction** and release of catecholamines in response to the hypermetabolic state. - The elevated blood pressure reflects the body's attempt to increase oxygen delivery to tissues. *Metabolic acidosis* - The massive increase in cellular metabolism and oxygen consumption leads to an accumulation of **lactic acid**, resulting in a profound **metabolic acidosis**. - This acidotic state can significantly impair cardiac function and cellular processes. *Hyperkalemia* - Widespread **muscle rigidity** and breakdown (rhabdomyolysis) cause the release of intracellular potassium into the bloodstream, leading to **hyperkalemia**. - Severe hyperkalemia can lead to life-threatening **cardiac arrhythmias**.

Practice by Chapter

Adverse Drug Reactions

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Anaphylaxis and Allergic Reactions

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Malignant Hyperthermia

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Local Anesthetic Toxicity

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Perioperative Cardiac Complications

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Pulmonary Complications

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Awareness Under General Anesthesia

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Neurological Complications

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Postoperative Visual Loss

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Perioperative Renal Dysfunction

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Transfusion-Related Complications

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Risk Management and Prevention

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