Complications in Anesthesia Practice Questions

Q: The most appropriate treatment for hypothermia during anesthesia is

Treated with warm saline. ***Treated with warm saline*** - **Warm intravenous fluids**, particularly saline, are a primary and effective method for rewarming hypothermic patients during surgery. - This helps to directly transfer heat into the patient's core circulation and raise body temperature. *Mechanism of heat loss is conduction* - While **conduction** (heat loss to colder surfaces) is one mechanism of heat loss during anesthesia, **radiation** (heat loss to the environment) and **convection** (heat loss to moving air currents or blood) are often more significant. - Evaporation (from open surgical sites) also contributes substantially to heat loss. *Occurs in all types of Anaesthesia* - Hypothermia is a common complication of **general anesthesia** due to impaired thermoregulation, but it is less common or sometimes deliberately avoided in certain regional anesthesia techniques unless the patient is already cold. - The degree and likelihood of hypothermia vary depending on the type and duration of anesthesia, ambient temperature, and patient factors. *Is beneficial to patients* - **Hypothermia** is generally **detrimental** to most surgical patients, leading to complications like increased bleeding, impaired drug metabolism, prolonged recovery, and increased risk of wound infection. - Therapeutic hypothermia is only medically induced for specific conditions (e.g., post-cardiac arrest) and is not a general benefit during anesthesia.

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: Venous air embolism during surgery is seen with

Sitting position. ***Sitting position*** - In the **sitting position** (e.g., for posterior fossa surgery), the surgical site is often above the level of the heart, creating a negative pressure gradient in the veins. - This **negative pressure** can draw air into opened veins if they are not adequately occluded, leading to a venous air embolism. *Lateral position* - While air embolism can occur in various positions if venous sinuses are open, the **lateral position** does not inherently create the same significant negative pressure gradient as the sitting position relative to the heart. - Risk is generally lower compared to positions where the surgical field is significantly elevated above the heart. *Supine position* - In the **supine position**, the surgical field is typically at or below heart level, which minimizes the likelihood of a negative pressure gradient in the veins. - This position is generally considered to have a **lower risk** for venous air embolism compared to upright positions. *Prone position* - The **prone position** can also increase central venous pressure if abdominal compression occurs, making venous air embolism less likely due to a positive venous pressure. - Although other surgical complications can arise, a venous air embolism is **not a classic risk** specifically associated with the prone position from a negative pressure standpoint.

Q: Difference between thyrotoxicosis and malignant hyperthermia is -

Elevated serum CPK level. Elevated serum CPK level - **Elevated serum creatine phosphokinase (CPK)** is a hallmark of **malignant hyperthermia** due to widespread muscle breakdown, whereas it is typically normal or only mildly elevated in thyrotoxicosis. - This difference is crucial for differentiating these conditions, as **muscle rigidity** and subsequent damage are central to the pathogenesis of malignant hyperthermia. *Tachycardia* - **Tachycardia** (rapid heart rate) is a prominent feature of both **thyrotoxicosis** [1] and **malignant hyperthermia** [2] due to different physiological mechanisms. - In thyrotoxicosis, it results from increased metabolic demand and direct cardiac stimulation [1], while in malignant hyperthermia, it’s a response to increased metabolic rate and CO2 production. *Hyperthermia* - **Hyperthermia** (elevated body temperature) is a defining feature of both **thyrotoxicosis** (especially during a thyroid storm) and **malignant hyperthermia** [2]. - Its presence alone cannot differentiate between these two conditions, as the underlying cause of the fever differs significantly. *Muscle rigidity* - **Muscle rigidity** is a classic and early sign of **malignant hyperthermia**, caused by uncontrolled calcium release in muscle cells [3]. - While muscle weakness and tremors can occur in **thyrotoxicosis** [1], generalized severe muscle rigidity is not a typical feature and is crucial for distinguishing between the two.

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: A 48 year-old woman underwent subtotal thyroidectomy. She has a vague family history of malignant hyperthermia. She develops agitation, restlessness, fever, tremor, shivering, and tachypnea. Thyrotoxic crises can be best distinguished from malignant hyperthermia by estimating -

Muscular rigidity. ***Muscular rigidity*** - **Malignant hyperthermia** is characterized by severe **muscle rigidity** due to uncontrolled calcium release from the sarcoplasmic reticulum, which is typically absent in thyrotoxic crisis. - This rigidity, especially of the **jaw and limb muscles**, is a cardinal and specific differentiating sign for malignant hyperthermia [2]. *Increased CPK levels* - While both conditions can cause elevated **creatine phosphokinase (CPK)**, the increase is usually far more pronounced and rapid in malignant hyperthermia due to widespread muscle breakdown. - However, CPK elevation can occur in severe thyrotoxicosis due to metabolic stress, making it less specific as a primary differentiating factor. *LDH* - **Lactate dehydrogenase (LDH)** can be elevated in both conditions due to cellular damage and increased metabolic activity. - This elevation is a non-specific marker of tissue injury and does not reliably distinguish between thyrotoxic crisis and malignant hyperthermia. *Temperature variation* - Both conditions present with **hyperthermia** and significantly elevated body temperatures [1]. - While the rapidity and degree of temperature rise can vary, it is not a consistently reliable distinguishing feature in isolation because both can manifest extremely high fevers.

Question 1

The most appropriate treatment for hypothermia during anesthesia is

Accepted Answer

Treated with warm saline

Answer

Mechanism of heat loss is conduction

Answer

Occurs in all types of Anaesthesia

Answer

Is beneficial to patients

Question 2

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 3

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

Accepted Answer

Thiopentone

Answer

Isoflurane

Answer

Suxamethonium

Answer

Halothane

Question 4

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

Accepted Answer

Pain

Answer

Paralysis

Answer

Analgesia

Answer

Skin ulceration

Question 5

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 6

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 7

Venous air embolism during surgery is seen with

Accepted Answer

Sitting position

Answer

Lateral position

Answer

Supine position

Answer

Prone position

Question 8

Difference between thyrotoxicosis and malignant hyperthermia is -

Accepted Answer

Elevated serum CPK level

Answer

Tachycardia

Answer

Hyperthermia

Answer

Muscle rigidity

Question 9

All are clinical features of Propofol infusion syndrome except:-

Accepted Answer

Metabolic alkalosis

Answer

Lipaemia

Answer

Bradycardia

Answer

Renal failure

Question 10

A 48 year-old woman underwent subtotal thyroidectomy. She has a vague family history of malignant hyperthermia. She develops agitation, restlessness, fever, tremor, shivering, and tachypnea. Thyrotoxic crises can be best distinguished from malignant hyperthermia by estimating -

Accepted Answer

Muscular rigidity

Answer

Increased CPK levels

Answer

LDH

Answer

Temperature variation

Complications in Anesthesia — MCQs

Complications in Anesthesia — MCQs

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