Complications in Anesthesia Practice Questions

Q: Malignant hyperthermia is caused due to which of the following mechanism?

Increased intracellular Ca. ***Increased intracellular Ca*** - **Malignant hyperthermia** is characterized by an uncontrolled release of **calcium** from the sarcoplasmic reticulum in muscle cells. - This excessive **intracellular calcium** leads to sustained muscle contraction, increased metabolism, and a rapid rise in body temperature. *Increased serum K* - While **hyperkalemia** can occur during **malignant hyperthermia** due to muscle breakdown, it is a consequence of the underlying pathology, not the primary mechanism. - The initial trigger is the excessive **calcium release**, which then leads to muscle cell damage and subsequent **potassium efflux**. *Decreased intracellular chlorine* - Changes in **intracellular chloride** levels are not considered a primary mechanism in the pathophysiology of **malignant hyperthermia**. - The disorder is fundamentally linked to abnormal **calcium regulation** within muscle cells. *Increased intracellular Na* - While altered ion gradients can occur, a primary increase in **intracellular sodium** is not the direct mechanism for the sustained muscle contraction seen in **malignant hyperthermia**. - Increased intracellular calcium is the key event driving the hypermetabolic state.

Q: 5 year old child going for sitting craniotomy, while positioning in O.T. developed end tidal CO2- Zero mmHg, PO2- 80 mm Hg implies that :

Venous air embolism. ***Venous air embolism*** - A sudden drop in **end-tidal CO2 (ETCO2)** to zero, coupled with a normal or mildly decreased PO2, in a patient undergoing a sitting craniotomy strongly suggests a venous air embolism. The sitting position and open venous sinuses in neurosurgery create a pressure gradient favoring air entrainment. - While pulmonary issues can cause some ETCO2 changes, a **sudden complete loss** (zero mmHg) is characteristic of a circulatory collapse or severe obstruction to pulmonary blood flow, as seen with significant air emboli. *Left lung collapse* - A left lung collapse (atelectasis) would primarily cause a **decrease in PO2** due to ventilation-perfusion mismatch, and a subsequent **increase in ETCO2** due to increased dead space and shunting, rather than a sudden drop to zero. - While lung collapse can lead to some ETCO2 variations, it would not typically result in a **complete absence** of exhaled CO2. *Endotracheal tube blocked with secretions* - An endotracheal tube blocked with secretions would lead to a significant **increase in peak inspiratory pressures**, **decreased tidal volumes**, and a gradual rather than sudden drop in ETCO2, often to a measurable but low level, not zero. - The patient would also likely exhibit signs of **respiratory distress** and difficulty ventilating, which is not directly indicated by the isolated ETCO2 reading. *Endotracheal tube in Oesophagus* - If the endotracheal tube were in the esophagus, there would be no CO2 entering the breathing circuit from the lungs, leading to an **ETCO2 of zero**. - However, this would also be immediately accompanied by **very low or unmeasurable PO2** because no oxygen would be entering the lungs. The given PO2 of 80 mmHg makes this less likely.

Q: A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:

Hypotension. ***Hypotension*** - **Hypotension** is a hallmark cardiovascular sign of anaphylaxis, occurring due to widespread **vasodilation** and increased vascular permeability. - This symptom is often profound and unresponsive to initial fluid resuscitation due to the ongoing systemic release of inflammatory mediators. *Bradycardia* - While bradycardia can occur in some rare cases of anaphylaxis (e.g., **vasovagal response**), **tachycardia** is the more common cardiac response due to compensatory mechanisms. - It is not a primary or consistent indicator of anaphylaxis, making it less helpful for diagnosis in this context. *Dysrhythmia* - **Dysrhythmias** can occur during anaphylaxis due to myocardial ischemia or electrolyte imbalances, but they are not a direct or consistent diagnostic feature. - Their presence often reflects severe compromise or co-existing conditions rather than being a primary anaphylactic sign. *Increased peripheral vascular resistance* - Anaphylaxis is characterized by a significant **decrease in peripheral vascular resistance** due to mast cell and basophil degranulation releasing vasodilatory mediators like histamine. - Therefore, an increase in peripheral vascular resistance would contradict the pathophysiology of anaphylaxis.

Q: All are clinical signs of malignant hyperthermia except-

Hypothermia. ***Hypothermia*** - Malignant hyperthermia is characterized by a rapid and uncontrolled increase in **body temperature (hyperthermia)**, not hypothermia. - Reduced body temperature would imply a different physiological process and is not characteristic of this condition. *Hypercarbia* - **Hypercarbia**, or an increase in blood CO2 levels, is an early and prominent sign due to increased cellular metabolism and muscle rigidity. - The rapid rise in end-tidal CO2 despite adequate ventilation is often the first indicator of malignant hyperthermia. *Hypertension* - **Hypertension** is a common clinical sign, resulting from the massive release of catecholamines and intense sympathetic stimulation during the hypermetabolic state. - The elevated blood pressure is part of the body's generalized stress response to the crisis. *Metabolic acidosis* - **Metabolic acidosis** is a key feature due to the excessive production of lactic acid from anaerobic metabolism in hyperactive muscles. - This accumulation of acid contributes significantly to the overall physiological derangement observed in malignant hyperthermia.

Q: Malignant hyperthermia is

Succinylcholine is a triggering agent. ***Succinylcholine is a triggering agent*** - **Succinylcholine**, a depolarizing neuromuscular blocker, is a potent trigger for malignant hyperthermia due to its interaction with the **ryanodine receptor**. - Other common triggering agents include **volatile anesthetic agents** such as halothane, isoflurane, and sevoflurane, all leading to uncontrolled calcium release. *Metabolic alkalosis and hypokalemia* - Malignant hyperthermia typically presents with a rapidly developing severe **metabolic acidosis**, not alkalosis, due to increased lactic acid production from muscle hypermetabolism. - Patients usually experience **hyperkalemia** due to muscle cell breakdown and potassium release, which can lead to cardiac arrhythmias. *Calcium infusion is used for treatment.* - The immediate treatment for malignant hyperthermia is **dantrolene sodium**, which acts by blocking calcium release from the sarcoplasmic reticulum in muscle cells. - **Calcium channel blockers** are generally contraindicated in malignant hyperthermia, especially when dantrolene has been administered, due to the risk of exacerbating hyperkalemia. *Autosomal recessive pharmacogenetic disease* - Malignant hyperthermia is inherited as an **autosomal dominant** pharmacogenetic disorder, primarily linked to mutations in the **RYR1 gene** (ryanodine receptor 1 gene). - This dominant inheritance pattern means that only one copy of the mutated gene is sufficient to predispose an individual to the condition.

Q: Treatment of malignant hyperthermia is

Dantrolene. ***Dantrolene*** - **Dantrolene** is a **ryanodine receptor antagonist** that blocks calcium release from the sarcoplasmic reticulum in muscle cells, directly addressing the underlying pathophysiology of malignant hyperthermia. - Administration of dantrolene is the **first-line and specific treatment** for malignant hyperthermia, rapidly reversing its life-threatening symptoms. *Propranolol* - **Propranolol** is a **beta-blocker** primarily used to treat hypertension, angina, and arrhythmias, by reducing heart rate and contractility. - It does not have any direct action on the **ryanodine receptors** or the excessive calcium release responsible for the muscle rigidity and hypermetabolism seen in malignant hyperthermia. *Halothane* - **Halothane** is an **inhalational anesthetic** that is a well-known trigger of malignant hyperthermia, particularly in genetically susceptible individuals. - Administering halothane would **exacerbate** malignant hyperthermia due to its potent ability to induce uncontrolled calcium release from the sarcoplasmic reticulum. *Nitrous oxide* - **Nitrous oxide** is an **inhalational anesthetic** that is generally considered a weak trigger for malignant hyperthermia and is often used in combination with other agents. - While typically considered safe regarding malignant hyperthermia, it does not possess any therapeutic properties to treat the condition and would not be used once malignant hyperthermia is suspected.

Q: A patient aged 28 years, was given epidural anesthesia with 15 ml of 1.5% Lignocaine with adrenaline for hernia surgery. He developed hypotension, respiratory arrest and became unconscious within 3 minutes, most probable cause will be:-

Intravascular injection of Lignocaine. ***Intravascular injection of Lignocaine*** - Rapid onset (within 3 minutes) of **hypotension**, **respiratory arrest**, and **unconsciousness** after an epidural injection strongly indicates systemic toxicity from intravascular local anesthetic injection. - The large volume (15 mL) and concentration (1.5%) of lignocaine, especially with adrenaline, when injected directly into the bloodstream, can quickly lead to **central nervous system (CNS) depression** and cardiovascular collapse. *High spinal block* - A **high spinal block** typically results from a local anesthetic spreading too high in the intrathecal space, leading to widespread sympathetic blockade and paralysis of respiratory muscles. - While it causes hypotension and respiratory depression, the rapid onset and immediate unconsciousness, without prior signs of extensive motor block ascending, make intravascular injection a more probable cause for such acute and severe symptoms. *Anaphylaxis to lignocaine* - Anaphylaxis to local anesthetics is rare and would typically present with **urticaria**, **angioedema**, **bronchospasm**, and widespread erythema, which are not described. - While anaphylaxis can cause hypotension and cardiovascular collapse, the rapid onset of CNS depression leading to unconsciousness is more characteristic of local anesthetic systemic toxicity. *Total spinal block* - A **total spinal block** occurs when a local anesthetic meant for the epidural space accidentally enters the subarachnoid space and diffuses extensively. - This results in profound **hypotension**, **bradycardia**, and **apnea** due to high sympathetic and somatic nerve blockade; however, unconsciousness typically ensues after significant hypotension and hypoperfusion, not as immediately and severely as seen with direct intravascular injection of a toxic dose.

Q: An inhalation anaesthetic agent was used in a surgery which caused high output renal failure. The agent is:

Methoxyflurane. ***Methoxyflurane*** - **Methoxyflurane** is extensively metabolized, releasing a significant amount of **free fluoride ions**. - These **fluoride ions** are toxic to the renal tubules, leading to **high-output renal failure** by impairing the kidney's ability to concentrate urine. *Enflurane* - While enflurane also undergoes some metabolism to **fluoride ions**, the amount produced is generally lower than with methoxyflurane and is less likely to cause significant **renal toxicity** in common clinical use. - Its renal effects are typically milder and usually self-limiting, not leading to the severe **high-output renal failure** seen with methoxyflurane. *Diethyl ether* - Diethyl ether is primarily eliminated via the lungs, with very little metabolism, hence it is not associated with **renal toxicity** from fluoride ions. - Its main concerns include flammability and slower induction and emergence, not **renal impairment**. *Halothane* - Halothane is associated with **halothane hepatitis** (liver toxicity) due to its metabolism producing reactive trifluoroacetyl adducts. - It is not known to cause significant **high-output renal failure** due to fluoride toxicity.

Q: A child during anesthesia with halothane and succinylcholine develops severe stiffness of masseters. What is the most probable diagnosis?

Malignant hyperthermia. ***Malignant hyperthermia*** - **Masseter muscle rigidity** following exposure to **succinylcholine** and a **halogenated inhalational anesthetic** (like halothane) is a hallmark sign of malignant hyperthermia. - This inherited disorder results in uncontrolled **calcium release** from the sarcoplasmic reticulum in skeletal muscle, leading to hypermetabolism, severe muscle contraction, and a rapid rise in body temperature. *Halothane hepatitis* - This is an idiosyncratic liver injury that can occur hours to days after exposure to halothane, not an acute intraoperative event causing muscle stiffness. - Symptoms include elevated liver enzymes, jaundice, and often fever, but without the immediate muscle rigidity seen here. *Neuroleptic malignant syndrome* - This condition is associated with the use of **antipsychotic medications** and presents with muscle rigidity, fever, altered mental status, and autonomic instability. - It does not involve exposure to succinylcholine or inhalational anesthetics and has a slower onset, typically over days. *Anaphylaxis* - Anaphylaxis is a severe, acute allergic reaction characterized by **bronchospasm**, **hypotension**, **urticaria**, and angioedema. - While it can manifest rapidly during anesthesia, it does not typically cause severe, generalized muscle stiffness as the primary symptom.

Q: 30 year old lady was on the OT and during the mastoidectomy, after having inhalational anaesthesia, suddenly developed fever, increased heart rate, raised BP, acidosis and arrythmia. What is the next best intervention?

Dantrolene. ***Dantrolene*** - The patient's presentation with **fever**, **tachycardia**, **hypertension**, **acidosis**, and **arrhythmia** during inhalational anesthesia is highly indicative of **malignant hyperthermia**. - **Dantrolene** is the specific and most effective treatment for malignant hyperthermia as it acts by interfering with muscle contraction by blocking calcium release from the sarcoplasmic reticulum. *Antipyretics* - While the patient has a fever, **antipyretics** like paracetamol or NSAIDs are not sufficient to manage the rapidly rising core body temperature in malignant hyperthermia. - The fever is a symptom of severe metabolic dysregulation, and simple antipyresis does not address the underlying pathology. *Sodium bicarbonate* - The patient has acidosis, but **sodium bicarbonate** is used to correct metabolic acidosis by buffering excess acid only after the primary cause is addressed. - While it may be used as supportive care, it does not treat the underlying mechanism of malignant hyperthermia. *Procainamide* - **Procainamide** is an antiarrhythmic drug used to treat various arrhythmias but does not address the fundamental cause of the arrhythmias in malignant hyperthermia. - The arrhythmias in malignant hyperthermia are a consequence of severe metabolic derangements and hyperkalemia, which require dantrolene and supportive care to resolve.

Question 1

Malignant hyperthermia is caused due to which of the following mechanism?

Accepted Answer

Increased intracellular Ca

Answer

Increased serum K

Answer

Decreased intracellular chlorine

Answer

Increased intracellular Na

Question 2

5 year old child going for sitting craniotomy, while positioning in O.T. developed end tidal CO2- Zero mmHg, PO2- 80 mm Hg implies that :

Accepted Answer

Venous air embolism

Answer

Left lung collapse

Answer

Endotracheal tube blocked with secretions

Answer

Endotracheal tube in Oesophagus

Question 3

A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:

Accepted Answer

Hypotension

Answer

Bradycardia

Answer

Dysrhythmia

Answer

Increased peripheral vascular resistance

Question 4

All are clinical signs of malignant hyperthermia except-

Accepted Answer

Hypothermia

Answer

Hypercarbia

Answer

Hypertension

Answer

Metabolic acidosis

Question 5

Malignant hyperthermia is

Accepted Answer

Succinylcholine is a triggering agent

Answer

Metabolic alkalosis and hypokalemia

Answer

Calcium infusion is used for treatment.

Answer

Autosomal recessive pharmacogenetic disease

Question 6

Treatment of malignant hyperthermia is

Accepted Answer

Dantrolene

Answer

Propranolol

Answer

Halothane

Answer

Nitrous oxide

Question 7

A patient aged 28 years, was given epidural anesthesia with 15 ml of 1.5% Lignocaine with adrenaline for hernia surgery. He developed hypotension, respiratory arrest and became unconscious within 3 minutes, most probable cause will be:-

Accepted Answer

Intravascular injection of Lignocaine

Answer

High spinal block

Answer

Anaphylaxis to lignocaine

Answer

Total spinal block

Question 8

An inhalation anaesthetic agent was used in a surgery which caused high output renal failure. The agent is:

Accepted Answer

Methoxyflurane

Answer

Enflurane

Answer

Diethyl ether

Answer

Halothane

Question 9

A child during anesthesia with halothane and succinylcholine develops severe stiffness of masseters. What is the most probable diagnosis?

Accepted Answer

Malignant hyperthermia

Answer

Halothane hepatitis

Answer

Neuroleptic malignant syndrome

Answer

Anaphylaxis

Question 10

30 year old lady was on the OT and during the mastoidectomy, after having inhalational anaesthesia, suddenly developed fever, increased heart rate, raised BP, acidosis and arrythmia. What is the next best intervention?

Accepted Answer

Dantrolene

Answer

Antipyretics

Answer

Sodium bicarbonate

Answer

Procainamide

Complications in Anesthesia — MCQs

Complications in Anesthesia — MCQs

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