Complications in Anesthesia Practice Questions

Q: The following are true of Mendelson's syndrome –

Onset of symptoms generally occurs within 30 minutes. ***Onset of symptoms generally occurs within 30 minutes*** - Mendelson's syndrome refers to **chemical pneumonitis** resulting from pulmonary aspiration of sterile gastric contents. - Symptoms like **bronchospasm**, **dyspnea**, and **tachycardia** typically manifest rapidly, often within minutes to 30 minutes post-aspiration. *Steroids have been shown to improve outcome* - **Corticosteroids** are generally **not recommended** for the treatment of Mendelson's syndrome or chemical pneumonitis caused by gastric aspiration. - Their use can potentially increase the risk of **secondary bacterial pneumonia** due to immunosuppression, without significant clinical benefit in improving lung injury. *Critical volume of aspirate is 50 mls* - The critical volume of aspirate associated with Mendelson's syndrome is generally considered to be **25 mL** or **0.3 mL/kg** of gastric contents. - Aspiration of volumes greater than this threshold significantly increases the risk of developing **severe pneumonitis**. *Critical pH of gastric aspirate is 1.5* - The critical pH of gastric aspirate associated with Mendelson's syndrome is generally considered to be **less than 2.5**. - A pH below this value indicates highly acidic gastric contents, which cause **severe chemical burns** to the tracheobronchial tree and lung parenchyma.

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**.

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: 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: Which does not cause malignant hyperthermia

N2O. **N2O** - **Nitrous oxide (N2O)**, or laughing gas, is an inhaled anesthetic that does not trigger **malignant hyperthermia (MH)**. It is considered a safe anesthetic agent for MH-susceptible patients. - MH is a genetic disorder of skeletal muscle characterized by uncontrolled **calcium release** from the **sarcoplasmic reticulum**, leading to a hypermetabolic state. *Enflurane* - **Enflurane** is a **volatile inhaled anesthetic** that can trigger malignant hyperthermia. Volatile anesthetics are a primary class of agents known to induce MH in susceptible individuals. - It works by affecting the **ryanodine receptor (RyR1)** in muscle cells, leading to excessive calcium release. *Isoflurane* - **Isoflurane** is also a **volatile inhaled anesthetic** and is a known trigger for malignant hyperthermia. - Like other volatile agents, it causes a rapid increase in **intracellular calcium**, muscle rigidity, and a systemic hypermetabolic response. *Desflurane* - **Desflurane** is another **volatile inhaled anesthetic** that is a potent trigger of malignant hyperthermia. - Its rapid onset and offset properties do not prevent it from causing the rapid **calcium release** characteristic of MH.

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.

Question 1

The following are true of Mendelson's syndrome –

Accepted Answer

Onset of symptoms generally occurs within 30 minutes

Answer

Steroids have been shown to improve outcome

Answer

Critical volume of aspirate is 50 mls

Answer

Critical pH of gastric aspirate is 1.5

Question 2

All are seen in malignant hyperthermia except:

Accepted Answer

Bradycardia

Answer

Hypertension

Answer

Metabolic acidosis

Answer

Hyperkalemia

Question 3

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 4

A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:

Accepted Answer

Hypotension

Answer

Bradycardia

Answer

Dysrhythmia

Answer

Increased peripheral vascular resistance

Question 5

All are clinical signs of malignant hyperthermia except-

Accepted Answer

Hypothermia

Answer

Hypercarbia

Answer

Hypertension

Answer

Metabolic acidosis

Question 6

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 7

Treatment of malignant hyperthermia is

Accepted Answer

Dantrolene

Answer

Propranolol

Answer

Halothane

Answer

Nitrous oxide

Question 8

Which does not cause malignant hyperthermia

Accepted Answer

N2O

Answer

Enflurane

Answer

Isoflurane

Answer

Desflurane

Question 9

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 10

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

Complications in Anesthesia — MCQs

Complications in Anesthesia — MCQs

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