Complications in Anesthesia Practice Questions

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

Halothane. ***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.

Q: Malignant hyperthermia is most commonly precipitated by:

Succinyl choline. ***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.

Q: The most appropriate immediate management of prolonged Scoline apnea is

Continuation of artificial ventilation. ***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.

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

Thiopentone. ***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**.

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

Pain. ***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.

Q: 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?

Venous air embolism. ***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.

Q: All are clinical features of Propofol infusion syndrome except:-

Metabolic alkalosis. ***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.

Q: All are seen in malignant hyperthermia except:

Bradycardia. ***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**.

Question 1

Which of the following is the most potent trigger of malignant hyperthermia?

Accepted Answer

Halothane

Answer

Thiopentone

Answer

Isoflurane

Answer

Suxamethonium

Question 2

Malignant hyperthermia is most commonly precipitated by:

Accepted Answer

Succinyl choline

Answer

Dantrolene sodium

Answer

Gallamine

Answer

Pancuronium

Question 3

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?

Accepted Answer

Administration of dantrolene sodium and termination of the procedure

Answer

Administration of intravenous steroids and an antihistamine agent with continuation of the procedure

Answer

Administration of dantrolene sodium and continuation with the procedure

Answer

Alkalinization of the urine, administration of mannitol, and continuation with the procedure

Question 4

The most appropriate immediate management of prolonged Scoline apnea is

Accepted Answer

Continuation of artificial ventilation

Answer

Reversal with neostigmine

Answer

Estimation of plasma cholinesterase

Answer

Exchange transfusion

Question 5

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

Accepted Answer

Thiopentone

Answer

Isoflurane

Answer

Suxamethonium

Answer

Halothane

Question 6

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

Accepted Answer

Pain

Answer

Paralysis

Answer

Analgesia

Answer

Skin ulceration

Question 7

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?

Accepted Answer

Venous air embolism

Answer

Sympathetic overactivity

Answer

Vagal stimulation

Answer

Carotid body stimulation

Question 8

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?

Accepted Answer

Stop the injection, remove the IV, administer local anesthetic and hyaluronidase

Answer

Apply a warm compress

Answer

Inject hydrocortisone locally

Answer

Elevate the limb

Question 9

All are clinical features of Propofol infusion syndrome except:-

Accepted Answer

Metabolic alkalosis

Answer

Lipaemia

Answer

Bradycardia

Answer

Renal failure

Question 10

All are seen in malignant hyperthermia except:

Accepted Answer

Bradycardia

Answer

Hypertension

Answer

Metabolic acidosis

Answer

Hyperkalemia

Complications in Anesthesia — MCQs

Complications in Anesthesia — MCQs

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