Complications in Anesthesia — MCQs

A 56-year-old man undergoes a left upper lobectomy. An epidural catheter is inserted for postoperative pain relief. Ninety minutes after the first dose of epidural morphine, the patient complains of itching and becomes increasingly somnolent. Blood gas measurement reveals the following: pH 7.24; PaCO2 58; PaO2 100; HCO3- 28. What is the most appropriate initial therapy?

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 251: During major surgery, a patient is monitored using ROTEM. The results show reduced clot firmness and increased clotting time. Which treatment should be administered to correct these abnormalities?

A. Administer cryoprecipitate to address fibrinogen deficiency (Correct Answer)
B. Give platelet concentrate to enhance clot strength
C. Administer antifibrinolytics to stabilize the clot
D. Infuse fresh frozen plasma to provide clotting factors

Explanation: ***Administer cryoprecipitate to address fibrinogen deficiency*** - **Reduced clot firmness** on ROTEM is a direct indicator of **fibrinogen deficiency** or dysfunction. - **Cryoprecipitate** is rich in **fibrinogen**, factor VIII, and von Willebrand factor, making it the most appropriate treatment to improve clot firmness in this scenario. *Give platelet concentrate to enhance clot strength* - While platelets contribute to clot strength, ROTEM differentiates between **fibrinogen** and **platelet contributions** to clot firmness. Reduced clot firmness primarily points to fibrinogen deficiency. - Platelet concentrate would be indicated if the ROTEM showed significantly low **platelet count** or dysfunction, which is not stated as the primary abnormality here. *Administer antifibrinolytics to stabilize the clot* - **Antifibrinolytics** (e.g., tranexamic acid) inhibit the breakdown of clots but do not address the *formation* or *firmness* of the initial clot. - These are used when there is excessive **fibrinolysis**, which would manifest as clot lysis on ROTEM, not primarily as reduced clot firmness or increased clotting time. *Infuse fresh frozen plasma to provide clotting factors* - **Fresh frozen plasma (FFP)** contains all clotting factors and can address prolonged clotting time if caused by **factor deficiencies**. - However, FFP has a relatively low concentration of **fibrinogen** compared to cryoprecipitate, making it less effective for severe fibrinogen deficiency causing reduced clot firmness.

Question 252: Intra-arterial thiopentone injection leads to?

A. Ischemia (Correct Answer)
B. Vasodilatation
C. Vomiting
D. Hypertension

Explanation: ***Ischemia*** - Intra-arterial injection of **thiopentone** causes severe **vasospasm** and **precipitation of barbiturate crystals** in the arterial lumen, leading to **thrombosis** and **obstruction** of blood flow. - This results in acute **ischemia** distal to the injection site, which can progress to **gangrene** and **limb loss** if not promptly managed. *Vasodilatation* - **Thiopentone** is a potent **vasoconstrictor** when injected intra-arterially due to its highly alkaline pH and direct irritation of the vascular endothelium. - Therefore, it causes **vasospasm**, not vasodilatation, which is the opposite effect and a key mechanism of the ensuing ischemia. *Vomiting* - **Vomiting** is not a characteristic or direct consequence of intra-arterial thiopentone injection; it is more commonly associated with systemic effects of some medications or with stimulation of the **chemoreceptor trigger zone**. - The adverse effects of intra-arterial thiopentone are primarily localized to the affected limb vasculature. *Hypertension* - While thiopentone can cause transient hypotension when administered intravenously as an anesthetic, **intra-arterial injection** does not typically cause systemic **hypertension**. - The primary local effect is **vasoconstriction** and **ischemia** in the injected limb, not a systemic rise in blood pressure.

Question 253: Which of the following is NOT a feature of Propofol infusion syndrome?

A. Occurs with infusion of propofol for 48 hours or longer
B. Occurs in critically ill patients
C. Features are cardiomyopathy, hepatomegaly
D. Features are nausea and vomiting (Correct Answer)

Explanation: ***Features are nausea and vomiting*** - **Nausea and vomiting** are common side effects of many medications, including propofol, but they are not specific features of **Propofol Infusion Syndrome (PRIS)**. - PRIS is a rare but severe complication characterized by metabolic and cardiac dysfunction, not gastrointestinal upset. *Occurs with infusion of propofol for 48 hours or longer* - **PRIS** typically manifests after prolonged infusions of propofol, usually **48 hours or more**, especially at high doses. - This time frame allows for the accumulation of propofol metabolites that contribute to mitochondrial dysfunction. *Occurs in critically ill patients* - **PRIS** is predominantly observed in **critically ill patients**, particularly those with severe head injury, sepsis, or burns, who are receiving prolonged high-dose propofol. - These patients often have pre-existing metabolic stress and reduced compensatory mechanisms, making them more susceptible. *Features are cardiomyopathy, hepatomegaly* - **Cardiomyopathy**, leading to **cardiac failure**, is a prominent and often fatal feature of **PRIS**. - **Hepatomegaly**, resulting from hepatic dysfunction and fat accumulation, is also commonly observed in patients with PRIS.

Question 254: Which of the following anesthetic agents is not associated with hepatotoxicity?

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

Explanation: ***Propofol*** - **Propofol** is an intravenous anesthetic agent not typically associated with significant hepatotoxicity. - It is **metabolized in the liver** and excreted renally, but does not cause acute liver injury as seen with some inhalational agents. *Halothane* - **Halothane** is a known cause of **halothane hepatitis**, a severe and sometimes fatal form of liver injury. - This reaction involves an immune-mediated response against **trifluoroacetylated liver proteins**. *Chloroform* - **Chloroform** was historically used as an anesthetic but was largely abandoned due to its significant **hepatotoxic** and nephrotoxic effects. - It causes direct toxic injury to hepatocytes, leading to **centrilobular necrosis**. *Ether* - While *diethyl ether* is largely obsolete in modern anesthesia, prolonged exposure or high concentrations can lead to some degree of **liver dysfunction**. - However, its hepatotoxic potential is generally considered less severe than halothane or chloroform.

Question 255: Which of the following statements about malignant hyperthermia is false?

A. End tidal CO2 is increased during an episode
B. Dantrolene is the treatment of choice
C. Tachycardia occurs
D. Most common cause is succinylcholine (Correct Answer)

Explanation: ***Most common cause is succinylcholine*** - While **succinylcholine** can trigger malignant hyperthermia, it is not the *most common cause* of the condition itself. **Volatile anesthetics** are more frequently implicated. - Malignant hyperthermia is a **genetic disorder** of skeletal muscle, not primarily caused by a drug. *Dantrolene is the treatment of choice* - This statement is **true** because **dantrolene** is the specific and highly effective treatment for malignant hyperthermia, working by blocking calcium release from the sarcoplasmic reticulum. - Its rapid administration is crucial for reversing the hypermetabolic crisis caused by uncontrolled calcium efflux. *End tidal CO2 is increased during an episode* - This statement is **true**. The hallmark of malignant hyperthermia is excessive muscle metabolism, leading to increased **carbon dioxide production** and a significant rise in **end-tidal CO2**. - This rapid and unexplained increase in end-tidal CO2 is often the earliest and most sensitive indicator of an MH episode. *Tachycardia occurs* - This statement is **true**. The hypermetabolic state in malignant hyperthermia leads to increased oxygen consumption, heat production, and metabolic acidosis, all of which contribute to a compensatory **tachycardia**. - **Tachycardia** is one of the early and common clinical signs, alongside tachypnea and muscle rigidity.

Question 256: What is the best immediate management for a patient experiencing anaphylaxis during surgery?

A. Give atropine
B. Increase level of anesthesia
C. Ask the surgeon to stop the surgery
D. Give adrenaline (Correct Answer)

Explanation: ***Give adrenaline*** - **Adrenaline (epinephrine)** is the first-line and most critical treatment for anaphylaxis due to its potent **vasoconstrictive** and **bronchodilatory** effects. - It rapidly reverses **hypotension**, **bronchospasm**, and other life-threatening symptoms associated with the systemic allergic reaction. *Give atropine* - **Atropine** is primarily used to treat **bradycardia** and would not address the widespread vasodilation and bronchoconstriction characteristic of anaphylaxis. - While anaphylaxis can sometimes present with bradycardia, the primary circulatory collapse is due to **vasodilation**, which atropine does not counteract. *Increase level of anesthesia* - Increasing the level of anesthesia might **depress myocardial function** and exacerbate the **hypotension** already caused by anaphylaxis, further compromising the patient. - Anesthesia is not a treatment for an anaphylactic reaction, which requires specific pharmacological interventions to stabilize the patient. *Ask the surgeon to stop the surgery* - While it may be necessary to pause or stop the surgery, this is **not the immediate medical management** for a life-threatening anaphylactic reaction. - The priority is to administer **life-saving medication** like adrenaline, after which decisions about continuing or stopping surgery can be made.

Question 257: A patient developed fulminant hepatitis after receiving inhalational anesthesia with a drug to which he had been previously exposed. Which drug is most likely responsible?

A. Halothane (Correct Answer)
B. Enflurane
C. Isoflurane
D. N2O

Explanation: ***Halothane*** - **Halothane hepatitis** is a rare but severe complication, especially upon re-exposure, due to the formation of reactive metabolites that trigger an immune response against liver cells. - The disease can range from mild liver enzyme elevation to **fulminant hepatic failure** and death. *N2O* - **Nitrous oxide** primarily causes megaloblastic anemia and neurotoxicity with prolonged exposure by interfering with vitamin B12 metabolism, not hepatotoxicity. - It works by inhibiting methionine synthase, but does not cause dose-dependent or idiosyncratic liver damage associated with fulminant hepatitis. *Enflurane* - While enflurane can rarely cause **hepatotoxicity**, it is significantly less common and less severe than with halothane. - It is more frequently associated with **nephrotoxicity** due to fluoride ion release, especially at high doses or prolonged exposure. *Isoflurane* - **Isoflurane** is one of the safest modern inhalational anesthetics with a very low incidence of hepatotoxicity due to minimal metabolism and conversion to toxic metabolites. - It is rarely implicated in liver injury, making fulminant hepatitis highly unlikely.

Question 258: Calcium homeostasis disturbance is the predominant pathophysiological mechanism in

A. Duchenne Muscular Dystrophy (DMD)
B. Limb Girdle Muscular Dystrophy
C. Malignant hyperthermia (Correct Answer)
D. Tibial Muscular Dystrophy

Explanation: ***Malignant hyperthermia*** - Malignant hyperthermia is caused by a genetic defect in the **ryanodine receptor (RYR1)** in skeletal muscle, leading to an uncontrolled release of **intracellular calcium** from the sarcoplasmic reticulum. - This excessive calcium release results in sustained muscle contraction, increased metabolism, and a rapid rise in body temperature. *Duchenne Muscular Dystrophy (DMD)* - DMD is primarily caused by a mutation in the **dystrophin gene**, which leads to the absence or severe deficiency of the **dystrophin protein**. - This deficiency results in muscle fiber fragility, cycles of degeneration and regeneration, and eventual replacement of muscle with fibrous and fatty tissue, rather than a primary calcium homeostasis disturbance. *Limb Girdle Muscular Dystrophy* - This group of disorders is characterized by progressive weakness and wasting of muscles, primarily affecting the **shoulders and hips**. - The pathophysiology involves genetic defects in various proteins that are crucial for muscle function and integrity, such as **sarcoglycans** or **calpain-3**, not primarily calcium dysregulation. *Tibial Muscular Dystrophy* - Tibial muscular dystrophy is a rare, late-onset disorder characterized by progressive weakness of the **anterior tibial muscles**. - It is typically caused by mutations in the **TTN gene**, encoding for the protein **titin**, which plays a vital role in muscle elasticity and structural integrity, rather than a primary calcium imbalance.

Question 259: What is the consequence of using the anesthetic Trilene in conjunction with sodium bicarbonate?

A. Myocardial depression
B. Hepatitis
C. ARDS
D. Renal damage (Correct Answer)

Explanation: ***Renal damage*** - The combination of **Trilene (trichloroethylene)** and **sodium bicarbonate** can lead to the formation of **dichloroacetylene**, a nephrotoxic compound. - This compound causes **acute tubular necrosis** and significant renal dysfunction, leading to irreversible kidney damage. *ARDS* - **Acute Respiratory Distress Syndrome (ARDS)** is typically associated with direct lung injury or severe systemic inflammatory responses, not directly with this specific drug interaction. - While anesthesia can affect respiratory function, this particular combination does not primarily lead to ARDS. *Myocardial depression* - Many anesthetics can cause **myocardial depression**, but the specific interaction between Trilene and sodium bicarbonate is not primarily known for this effect. - The primary concern with this combination is **nephrotoxicity**, not direct cardiac suppression. *Hepatitis* - Drug-induced **hepatitis** is a known risk with various medications, but not specifically with the combination of Trilene and sodium bicarbonate. - While some halogenated anesthetics can rarely cause liver injury, the formation of dichloroacetylene primarily targets the kidneys.

Question 260: A 56-year-old man undergoes a left upper lobectomy. An epidural catheter is inserted for postoperative pain relief. Ninety minutes after the first dose of epidural morphine, the patient complains of itching and becomes increasingly somnolent. Blood gas measurement reveals the following: pH 7.24; PaCO2 58; PaO2 100; HCO3- 28. What is the most appropriate initial therapy?

A. Intravenous naloxone (Correct Answer)
B. Endotracheal intubation (if airway is compromised)
C. Intramuscular diphenhydramine (for itching)
D. Epidural naloxone (for localized effect)

Explanation: ***Intravenous naloxone*** - The patient exhibits classic signs of **opioid overdose** including **somnolence**, **respiratory depression** (indicated by pH 7.24 and PaCO2 58), and **itching**, occurring after epidural morphine administration. - **Naloxone** is a rapidly acting **opioid antagonist** that reverses these effects, and the intravenous route provides the quickest systemic onset for emergency situations. *Endotracheal intubation (if airway is compromised)* - While intubation may be necessary if the patient's respiratory status deteriorates further and they cannot maintain their airway, it is not the *initial* therapy for opioid overdose reversal. - The primary goal is to reverse the opioid effects with an antagonist first to see if respiratory drive improves, potentially avoiding intubation. *Intramuscular diphenhydramine (for itching)* - **Diphenhydramine** only addresses the **symptom of itching** and does not reverse the life-threatening respiratory depression or somnolence caused by opioid overdose. - Treating only a side effect while ignoring the underlying cause is inappropriate in this critical situation. *Epidural naloxone (for localized effect)* - Epidural naloxone would primarily act at the spinal cord level to reverse localized opioid effects without having significant systemic impact on **respiratory depression** or **somnolence**. - For systemic opioid toxicity, **intravenous naloxone** is required for rapid brain penetration and reversal of central respiratory depression.

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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