Neuro-Anesthesia
ICP, cerebral blood flow, SAH, TBI, AVM, neuromonitoring, awake craniotomy, spinal cord protection. ← All topics
Q1. Cerebral blood flow autoregulation
Cerebral autoregulation maintains constant CBF between MAP:
A. 30–90 mmHg in normotensive patients
B. 60–150 mmHg in normotensive patients
C. 90–200 mmHg in normotensive patients
D. 40–100 mmHg in normotensive patients
E. No autoregulation occurs at any MAP
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Answer: B. Normal cerebral blood flow is approximately 50 mL/100 g/min and is autoregulated between mean arterial pressures of 60–150 mmHg in normotensive individuals. In patients with chronic hypertension, the autoregulation curve shifts rightward, making these patients vulnerable to relative cerebral hypoperfusion at blood pressures that would be considered normal in normotensive patients. Cerebral autoregulation can be impaired by multiple factors including general anesthesia, traumatic brain injury, cerebral ischemia, intracranial tumors, and hypercapnia.
Q2. CBF and PaCO₂
For every 1 mmHg change in PaCO₂, CBF changes:
A. 0.1 mL/100g/min per mmHg change in PaCO₂
B. 1–2 mL/100g/min per mmHg change in PaCO₂
C. 10 mL/100g/min per mmHg change in PaCO₂
D. 50% per mmHg change in PaCO₂
E. No predictable change per mmHg change in PaCO₂
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Answer: B. Cerebral blood flow changes approximately 1–2 mL/100g/min per mmHg change in PaCO₂. This relationship is linear over the PaCO₂ range of 20–80 mmHg. This principle is useful for transient intracranial pressure control; decreasing PaCO₂ to 30–35 mmHg provides approximately 30 minutes of ICP reduction. The effect dissipates over 6–8 hours due to bicarbonate buffering in the cerebrospinal fluid. Extreme hyperventilation should be avoided because cerebral blood flow can drop to ischemic levels below 20 mL/100g/min, potentially causing cerebral ischemia.
Q3. Cerebral perfusion pressure
CPP is calculated as:
A. MAP minus ICP or CVP, whichever is greater
B. MAP minus CVP or PCWP, whichever is greater
C. MAP plus ICP or CVP, whichever is lower
D. Aortic diastolic pressure minus left ventricular end-diastolic pressure
E. Mean pulmonary artery pressure minus pulmonary capillary wedge pressure
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Answer: A. Cerebral perfusion pressure (CPP) is calculated as MAP minus the greater of ICP or CVP. The higher downstream pressure is the relevant one opposing cerebral blood flow. Target CPP is 60–70 mmHg in traumatic brain injury. CPP above 70 mmHg increases ARDS risk, while CPP below 50 mmHg risks cerebral ischemia. Note that spinal cord perfusion pressure uses a different formula: MAP minus CSF pressure, which is relevant for spine surgery and thoracoabdominal aortic aneurysm repair where CSF drainage to 10 mmHg and MAP maintenance above 90 mmHg are employed.
Q4. Anesthetic effect on CBF/CMRO₂
Which anesthetic increases both CBF and CMRO₂?
A. Propofol decreases both cerebral blood flow and cerebral metabolic rate of oxygen consumption
B. Etomidate decreases both cerebral blood flow and cerebral metabolic rate of oxygen consumption
C. Ketamine increases both cerebral blood flow and cerebral metabolic rate of oxygen consumption
D. Sevoflurane decreases cerebral metabolic rate but increases cerebral blood flow at clinical doses
E. Dexmedetomidine decreases both cerebral blood flow and cerebral metabolic rate of oxygen consumption
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Answer: C. Ketamine increases CBF, increases CMRO₂, and increases ICP. It has traditionally been avoided in patients with elevated ICP, though recent evidence suggests it may be less concerning when PaCO₂ is controlled. Nitrous oxide similarly increases both CBF and CMRO₂. Most other intravenous anesthetics (propofol, etomidate, barbiturates, dexmedetomidine) decrease both CBF and CMRO₂. Volatile anesthetics decrease CMRO₂ but increase CBF at concentrations above 0.5 MAC, demonstrating cerebral flow-metabolism uncoupling.
Q5. ICP management
A patient with TBI develops ICP 28 mmHg. Initial measures include all EXCEPT:
A. Head of bed elevated 30 degrees to promote venous drainage
B. Head maintained in midline position to promote venous drainage
C. Hypotonic saline infusion to reduce serum osmolality and ICP
D. PaCO₂ maintained at 35–40 mmHg to avoid prolonged hyperventilation
E. Sedation and analgesia with consideration of neuromuscular blockade if needed
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Answer: C. Hypotonic fluids should be avoided in TBI patients with elevated ICP because they worsen cerebral edema by creating an osmotic gradient that drives water into brain tissue. Instead, use isotonic crystalloid (normal saline) or hypertonic saline. Initial (Tier 1) ICP management includes: head of bed elevation to 30 degrees, head maintained in midline position without neck rotation (both promote venous drainage), adequate sedation and analgesia, maintenance of normocapnia (PaCO₂ 35–40 mmHg), and normothermia. Tier 2 measures include hyperosmolar therapy with mannitol (0.25–1 g/kg) or 3% hypertonic saline, and CSF drainage if a ventriculostomy is present. Tier 3 interventions include neuromuscular blockade, brief hyperventilation (target PaCO₂ 30–35 mmHg), and barbiturate coma. Tier 4 is decompressive craniectomy for refractory intracranial hypertension.
Q6. Cushing reflex
A patient with severe ICP elevation classically develops:
A. Hypertension, bradycardia, and irregular respirations
B. Hypotension, tachycardia, and regular respirations
C. Hypotension, bradycardia, and shallow respirations
D. Normotension, tachycardia, and rapid respirations
E. Hypertension, tachycardia, and normal respirations
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Answer: A. Cushing reflex (Cushing's triad) is a late sign of impending brainstem herniation in patients with severe intracranial pressure elevation. The triad consists of hypertension (to maintain cerebral perfusion pressure), bradycardia (baroreceptor-mediated response to hypertension), and irregular respirations (Cheyne-Stokes or apneustic breathing patterns due to brainstem compression). This is a medical emergency requiring immediate treatment of elevated ICP with hyperosmolar therapy, CSF drainage, and neurosurgical decompression. The other answer choices represent hemodynamic patterns seen in shock states or other conditions but not in Cushing reflex.
Q7. Mannitol mechanism
Mannitol reduces ICP via:
A. Direct vasoconstriction of cerebral vessels reducing cerebral blood volume
B. Osmotic shift of water from brain parenchyma into intravascular space
C. Decreased cerebrospinal fluid production by the choroid plexus epithelium
D. Decreased cerebral metabolic rate of oxygen consumption reducing blood flow
E. Beta-adrenergic receptor blockade reducing cerebral blood flow and edema
Show answer
Answer: B. Mannitol reduces intracranial pressure primarily through an osmotic mechanism. It creates an osmotic gradient that shifts water out of the brain parenchyma into the intravascular space, thereby reducing cerebral edema. Typical dosing is 0.25–1 g/kg IV bolus with onset in 5–10 minutes and duration of 4–6 hours. Side effects include diuresis leading to volume depletion, hyperosmolarity, transient hyperkalemia followed by hypokalemia, and potential rebound cerebral edema with prolonged use as mannitol can cross a damaged blood-brain barrier and reverse the osmotic gradient. Hypertonic saline is an alternative that offers better hemodynamic stability and is particularly useful in hypovolemic patients. Mannitol does not work through vasoconstriction, CSF production changes, metabolic suppression, or beta-blockade.
Q8. SAH grade
Hunt and Hess grading of aneurysmal SAH:
A. Grade 1: asymptomatic or mild headache; Grade 5: deep coma, decerebrate posturing, moribund appearance
B. Grade 1: deep coma with decerebrate posturing; Grade 5: asymptomatic or mild headache only
C. Grade 1: stupor with moderate hemiparesis; Grade 5: drowsiness with mild focal neurologic deficit
D. Grade 1: moderate headache with nuchal rigidity; Grade 5: severe headache with cranial nerve palsy
E. Grade 1: drowsiness with confusion only; Grade 5: moderate headache with isolated cranial nerve palsy
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Answer: A. The Hunt and Hess grading scale for aneurysmal subarachnoid hemorrhage ranges from Grade 1 (asymptomatic or mild headache) to Grade 5 (deep coma, decerebrate posturing, moribund). The intermediate grades are: Grade 2 (moderate to severe headache with nuchal rigidity, may have cranial nerve palsy), Grade 3 (drowsiness, confusion, or mild focal neurologic deficit), and Grade 4 (stupor with moderate to severe hemiparesis, possibly early decerebrate rigidity). Higher Hunt and Hess grades correlate with worse clinical outcomes. The WFNS scale is an alternative GCS-based grading system. The Fisher scale is a separate CT-based grading system used to predict vasospasm risk rather than clinical severity.
Q9. Vasospasm in SAH
Cerebral vasospasm after SAH peaks at:
A. Day 0–1 after the initial hemorrhage
B. Days 3–14 after the initial hemorrhage
C. Day 30 after the initial hemorrhage
D. 6 weeks after the initial hemorrhage
E. Does not occur after subarachnoid hemorrhage
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Answer: B. Cerebral vasospasm after subarachnoid hemorrhage peaks during days 3–14 post-hemorrhage, with maximal risk typically around day 7. Prophylaxis consists of nimodipine 60 mg PO every 4 hours for 21 days, which has been shown to improve neurological outcomes. Detection methods include transcranial Doppler ultrasonography (flow velocity in MCA >120 cm/s or MCA:ICA flow velocity ratio >3 suggests vasospasm) and CT angiography. Treatment strategies include induced hypertension to maintain cerebral perfusion, intra-arterial vasodilators such as verapamil or milrinone, and transluminal angioplasty for large vessel spasm refractory to medical management.
Q10. AVM embolization anesthesia
Anesthetic priority during AVM embolization includes:
A. Routine general anesthesia with standard hemodynamic targets and no specific blood pressure manipulation
B. Induced hypotension at time of glue injection using esmolol, adenosine, or vasodilators to prevent distal embolization
C. Sustained hypertension throughout the procedure to maintain adequate cerebral perfusion pressure and collateral flow
D. Complete avoidance of all anticoagulation including heparin to minimize risk of intracranial hemorrhage
E. Therapeutic hypothermia to provide neuroprotection during periods of vascular occlusion and reduced cerebral blood flow
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Answer: B. Induced hypotension during glue injection is the key anesthetic priority during AVM embolization. This prevents systemic spread of cyanoacrylate embolic material to distal vessels. Methods to achieve transient hypotension include short-acting beta-blockers (esmolol), vasodilators, transient asystole with adenosine, or rapid ventricular pacing. Heparinization is typically maintained during the procedure to prevent thromboembolic complications. Post-embolization, the anesthesiologist must monitor for normal perfusion pressure breakthrough (NPPB), which occurs when sudden vasodilation develops in chronically hypoperfused brain tissue, potentially leading to edema or hemorrhage. Routine general anesthesia without specific hemodynamic manipulation is inadequate. Sustained hypertension would increase the risk of distal embolization and hemorrhage. Complete avoidance of anticoagulation is not standard practice. Hypothermia is not routinely employed for AVM embolization.
Q11. Awake craniotomy
The primary indication for awake craniotomy is:
A. Resection of posterior fossa lesions requiring cranial nerve monitoring during tumor removal
B. Resection of lesions near eloquent cortex requiring intraoperative mapping of motor and language function
C. Resection of pediatric brain tumors requiring specialized anesthetic techniques for airway management
D. Clipping of cerebral aneurysms requiring real-time assessment of neurological status during surgery
E. Placement of ventriculoperitoneal shunts requiring confirmation of adequate cerebrospinal fluid drainage
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Answer: B. Awake craniotomy is primarily indicated for resection of tumors near eloquent cortex, including Broca's area, Wernicke's area, the motor strip, and memory centers. The awake state allows real-time cortical mapping to preserve critical neurological function during tumor resection. Common techniques include the asleep-awake-asleep approach or monitored anesthesia care throughout. Anesthetic management typically involves scalp block with local anesthetic infiltration combined with dexmedetomidine and carefully titrated propofol or remifentanil infusions. The anesthesiologist must be prepared for potential complications including intraoperative seizures (have midazolam and propofol ready), hypertension, brain swelling, and venous air embolism if a dural sinus is opened. Posterior fossa lesions, aneurysm clipping, and CSF shunt procedures are typically performed under general anesthesia, while pediatric patients are rarely candidates for awake craniotomy due to cooperation requirements.
Q12. Acute spinal cord injury
For acute traumatic spinal cord injury, the most evidence-based intervention is:
A. High-dose methylprednisolone within 8 hours of injury, continued for 24-48 hours per NASCIS protocol
B. Maintain MAP >85 mmHg for 5-7 days, avoid hypoxia, and surgical decompression within 24 hours
C. Systemic hypothermia to 32-34°C for 24-48 hours initiated within 8 hours of injury
D. Mannitol 0.25-1 g/kg bolus followed by maintenance infusion to reduce spinal cord edema
E. Magnesium sulfate loading dose followed by continuous infusion for 5-7 days after injury
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Answer: B. Maintaining mean arterial pressure greater than 85 mmHg for 5-7 days after acute spinal cord injury improves neurologic outcomes by optimizing spinal cord perfusion. Avoidance of hypoxia and hypotension is critical. Surgical decompression within 24 hours improves outcomes according to the STASCIS trial. High-dose methylprednisolone (NASCIS protocol) has fallen out of favor due to methodological criticisms of the original trials and is no longer recommended by the American Association of Neurological Surgeons. Hypothermia, mannitol, and magnesium infusions lack evidence for routine use in acute traumatic spinal cord injury.
Q13. Autonomic dysreflexia
A spinal cord injury patient at T6 develops sudden BP 220/120 with headache, flushing above the lesion, and pallor below the lesion during bladder catheterization. Initial management:
A. Administer intravenous beta-blocker to control heart rate and reduce blood pressure acutely
B. Sit patient upright, remove noxious stimulus such as bladder distention, loosen tight clothing, then give nitrate or hydralazine if hypertension persists
C. Administer vasopressin infusion to counteract the peripheral vasodilation and restore vascular tone
D. Start sodium nitroprusside infusion immediately as first-line antihypertensive therapy for severe hypertension
E. Administer intravenous calcium gluconate to stabilize cardiac membranes and treat the hypertensive crisis
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Answer: B. Autonomic dysreflexia occurs in patients with spinal cord lesions at T6 or above. A noxious stimulus below the level of the lesion triggers unopposed sympathetic outflow, causing severe hypertension with reflex bradycardia mediated by intact baroreceptors above the lesion. Initial management prioritizes identifying and removing the triggering stimulus, most commonly bladder distention or fecal impaction. Sitting the patient upright and loosening constrictive clothing helps reduce blood pressure through postural changes. If hypertension persists despite these measures, short-acting antihypertensives such as nitrates, hydralazine, or nicardipine should be administered. Pure beta-blockers should be avoided as they can lead to unopposed alpha-adrenergic stimulation and worsen hypertension. For patients with chronic spinal cord injury requiring procedures, spinal anesthesia is the preferred technique to prevent autonomic dysreflexia.
Q14. CSF formation
CSF is produced primarily by:
A. Pacchionian granulations in the superior sagittal sinus
B. Choroid plexus in the lateral, third, and fourth ventricles
C. Arachnoid villi projecting into the dural venous sinuses
D. Pia mater overlying the cerebral cortex and spinal cord
E. Ependymal cells lining the walls of the ventricular system
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Answer: B. CSF is formed primarily by the choroid plexus located in the lateral, third, and fourth ventricles. Approximately 500 mL of CSF is produced daily, while the total CSF volume is only about 150 mL, meaning the entire volume turns over 3 to 4 times per day. CSF is reabsorbed via arachnoid villi (also called Pacchionian granulations) into the superior sagittal sinus and other dural venous sinuses. The Pacchionian granulations and arachnoid villi are sites of reabsorption, not production. The pia mater is the innermost meningeal layer but does not produce CSF. Communicating hydrocephalus results from decreased CSF absorption, while non-communicating hydrocephalus results from obstruction at the ventricular level.
Q15. Posterior fossa surgery — sitting position risks
The major risks of sitting position for posterior fossa craniotomy include:
A. Venous air embolism, paradoxical embolism through patent foramen ovale, hypotension, pneumocephalus, and quadriplegia from cervical flexion
B. Venous air embolism, arterial hypotension from decreased venous return, macroglossia, sciatic nerve injury, and lower extremity compartment syndrome
C. Paradoxical air embolism, hypertension from autonomic dysreflexia, tension pneumothorax, brachial plexus injury, and cerebral hyperperfusion syndrome
D. Venous air embolism, hypotension from cardiac compression, pneumomediastinum, peripheral nerve injury from positioning, and postoperative visual loss
E. Arterial air embolism without cardiac shunt, orthostatic hypotension, subcutaneous emphysema, pressure alopecia, and intraoperative awareness from anesthetic dilution
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Answer: A. The sitting position for posterior fossa craniotomy carries multiple serious risks. Venous air embolism (VAE) is the most common, occurring when open veins above the heart entrain air; monitoring with precordial Doppler or TEE increases detection sensitivity. Paradoxical air embolism can occur through a patent foramen ovale, present in approximately 25% of the population; preoperative screening with bubble study may be considered. Hypotension results from decreased venous return and pooling in the lower extremities; adequate preoperative hydration is essential. Pneumocephalus develops when air enters the cranium and can cause delayed neurologic deterioration. Quadriplegia from excessive cervical flexion is prevented by maintaining at least two fingers' width between the mandible and sternum. The other options list complications that are either not associated with the sitting position or are far less significant than the major risks.
Q16. EEG patterns under anesthesia
EEG under volatile anesthesia at 1–2 MAC shows:
A. Beta waves with increased frequency and lower amplitude throughout
B. Slower-frequency higher-amplitude waves progressing to burst suppression at higher doses
C. No change from baseline awake patterns regardless of concentration
D. Theta waves only without any other frequency components present
E. Spikes throughout all leads with epileptiform activity and sharp waves
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Answer: B. Volatile anesthetics produce dose-dependent EEG changes. At concentrations ≤1 MAC, higher frequency activity predominates. At 1–2 MAC, the EEG shows slowing with slower-frequency, higher-amplitude waves. At concentrations >2 MAC, burst suppression appears, and even higher concentrations produce electrocortical silence. This progressive pattern is characteristic of volatile agents. In contrast, ketamine increases theta activity, nitrous oxide produces fast activity, and methohexital (uniquely among barbiturates) can activate epileptic foci.
Q17. Carotid endarterectomy — neuro monitoring
The most reliable monitor for cerebral ischemia during carotid endarterectomy under general anesthesia is:
A. Pulse oximetry with continuous waveform analysis and trending of peripheral oxygen saturation
B. EEG continuous with processed analysis, SSEP, TCD, and cerebral oximetry as adjunct modalities
C. Heart rate variability with continuous trending and automated threshold alarm system integration
D. End-tidal carbon dioxide monitoring with capnography waveform analysis and numerical trending display
E. Mean arterial pressure alone with continuous invasive monitoring and automated alarm threshold settings
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Answer: B. Under general anesthesia for carotid endarterectomy, multimodal neuromonitoring is most reliable for detecting cerebral ischemia. This includes continuous EEG (raw or processed), somatosensory evoked potentials (SSEP), transcranial Doppler (TCD), and cerebral oximetry, though none is perfect in isolation. The combination provides complementary information about brain electrical activity, sensory pathway integrity, cerebral blood flow velocity, and regional oxygen saturation. Pulse oximetry, heart rate, end-tidal CO₂, and mean arterial pressure are standard anesthetic monitors but do not directly assess cerebral perfusion or function. Under regional anesthesia (awake carotid endarterectomy), direct neurologic examination remains the gold standard for detecting ischemia. The GALA trial demonstrated no difference in outcomes between general and regional anesthesia techniques for carotid endarterectomy.
Q18. Triple-H therapy
For symptomatic vasospasm after SAH, triple-H therapy traditionally involves:
A. Hyperventilation, hypothermia, and hyperoxia to reduce cerebral metabolic demand
B. Hypertension, hemodilution, and hypervolemia with modern shift toward induced hypertension
C. Hyponatremia, hypocalcemia, and hypoglycemia to alter cerebral vascular tone
D. Hyperventilation, hypocapnia, and hypothermia to decrease intracranial blood volume
E. Hypertension with intracranial pressure monitoring and targeted cerebral perfusion pressure
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Answer: B. Traditional triple-H therapy for symptomatic vasospasm after subarachnoid hemorrhage consists of hypertension, hemodilution, and hypervolemia. The modern approach has shifted to focus primarily on induced hypertension with euvolemia rather than hypervolemia, as excessive volume can lead to complications including pulmonary edema and hyponatremia. The aneurysm must be secured before initiating therapy. Hemodilution aims to reduce blood viscosity and improve microcirculatory flow, though aggressive hemodilution is now used less commonly. The other options represent interventions used in different clinical scenarios but are not components of triple-H therapy for vasospasm.
Q19. Brain death criteria
Apnea testing for brain death requires:
A. PaCO₂ rise to >60 mmHg or ≥20 mmHg above baseline without respiratory effort
B. PaCO₂ rise to >50 mmHg or ≥15 mmHg above baseline without respiratory effort
C. PaCO₂ rise to >55 mmHg or ≥25 mmHg above baseline without respiratory effort
D. PaCO₂ rise to >45 mmHg or ≥10 mmHg above baseline without respiratory effort
E. PaCO₂ rise to >65 mmHg or ≥30 mmHg above baseline without respiratory effort
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Answer: A. The apnea test is a critical component of brain death determination. The test requires pre-oxygenation with 100% oxygen, disconnection from the ventilator, and maintenance of oxygenation via a tracheal catheter delivering oxygen at 6 L/min. The patient is observed for at least 8-10 minutes for any respiratory effort. A positive apnea test (confirming brain death) requires PaCO₂ to rise to greater than 60 mmHg or at least 20 mmHg above baseline without any observed respiratory effort. The test must be aborted if the patient becomes hemodynamically unstable (systolic BP <90 mmHg) or develops significant hypoxemia (oxygen saturation <85% for >30 seconds). Prerequisites for brain death testing include a known irreversible cause of coma, core temperature ≥36°C, systolic blood pressure ≥100 mmHg, absence of CNS-depressant drugs or neuromuscular blocking agents, and correction of severe electrolyte, acid-base, and endocrine abnormalities. Ancillary tests that may be used when clinical examination cannot be completed include cerebral angiography (gold standard showing no intracranial blood flow), transcranial Doppler (TCD), electroencephalography (EEG showing electrocerebral silence), and nuclear flow studies.
Q20. Hyperglycemia and brain injury
Hyperglycemia worsens outcomes after stroke and TBI because:
A. Anaerobic metabolism of glucose in ischemic tissue produces lactic acidosis that exacerbates neuronal injury
B. Direct neurotoxic effects of glucose molecules on compromised neurons cause additional cellular damage
C. Elevated glucose levels trigger cerebral vasospasm that reduces blood flow to injured brain tissue
D. Insulin resistance alone impairs cellular glucose uptake and disrupts normal neuronal energy metabolism
E. Hyperglycemia has no measurable effect on neurologic outcomes after acute brain injury occurs
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Answer: A. Hyperglycemia (typically defined as glucose >180–200 mg/dL) worsens outcomes after stroke and traumatic brain injury through anaerobic glycolysis in ischemic tissue. When oxygen delivery is impaired, glucose is metabolized anaerobically, producing excess lactate that accumulates in the ischemic penumbra. This increased lactate leads to tissue acidosis, which exacerbates neuronal injury and cell death. Perioperative glucose should be targeted to 140–180 mg/dL. Hypoglycemia must be avoided as it also worsens brain injury. Tight glycemic control (as in the NICE-SUGAR trial) has not shown clear benefit in this population and may increase the risk of dangerous hypoglycemia.
Q21. Spinal cord stimulator indications
Spinal cord stimulator is indicated for all EXCEPT:
A. Failed back surgery syndrome (post-laminectomy syndrome)
B. Complex regional pain syndrome types I and II
C. Refractory chronic angina unresponsive to medical therapy
D. Acute postoperative pain in the immediate perioperative period
E. Lower extremity ischemic pain from peripheral vascular disease
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Answer: D. Spinal cord stimulation is indicated for chronic refractory pain conditions including failed back surgery syndrome (post-laminectomy syndrome), complex regional pain syndrome types I and II, refractory chronic angina, peripheral vascular disease with lower extremity ischemic pain, and various neuropathic pain syndromes. It is not indicated for acute pain conditions such as acute postoperative pain, which is managed with conventional analgesic approaches. Contraindications to spinal cord stimulator placement include localized infection at the insertion site, coagulopathy, sepsis, spina bifida, psychological inability to use the device appropriately, and somatoform disorder.
Q22. Status epilepticus management
Generalized status epilepticus first-line treatment is:
A. Phenytoin 20 mg/kg IV loading dose followed by maintenance infusion if seizures persist
B. IV benzodiazepine (lorazepam 4 mg or midazolam 10 mg IM) followed by phenytoin if refractory
C. Propofol bolus 1-2 mg/kg followed by continuous infusion titrated to seizure cessation
D. Magnesium sulfate 4-6 g IV loading dose followed by continuous infusion at 1-2 g/hr
E. Mannitol 0.25-1 g/kg IV bolus followed by repeat dosing based on serum osmolality
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Answer: B. First-line treatment for generalized status epilepticus is IV benzodiazepine, specifically lorazepam 4 mg IV or midazolam 10 mg IM if no IV access is available. If seizures are refractory to benzodiazepines, second-line agents include phenytoin/fosphenytoin 20 mg/kg, valproate, or levetiracetam. For refractory status epilepticus persisting beyond 30 minutes, the patient should be intubated and treated with propofol or midazolam infusion (or pentobarbital), with EEG guidance to achieve burst suppression. Concurrent workup should identify the underlying cause with CT imaging and laboratory studies. Phenytoin alone is not first-line. Propofol is reserved for refractory cases. Magnesium is specific for eclamptic seizures. Mannitol treats elevated intracranial pressure, not seizures directly.
Q23. Methohexital and ECT
Methohexital is preferred for electroconvulsive therapy because it:
A. Suppresses seizure activity and shortens overall seizure duration
B. Lengthens or has minimal effect on seizure duration
C. Provides alpha-adrenergic blockade and attenuates sympathetic surge
D. Eliminates oral secretions and prevents vagally mediated bradycardia
E. Causes tachycardia and increases heart rate during induction
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Answer: B. Methohexital is preferred for electroconvulsive therapy because it lengthens or has minimal effect on seizure duration, unlike other barbiturates and propofol which shorten seizure duration. Etomidate and ketamine also preserve or prolong seizure activity. Seizure must last at least 25 to 30 seconds for ECT to be effective. Standard pretreatment includes glycopyrrolate to prevent oral secretions and bradycardia, succinylcholine to prevent musculoskeletal injury from motor activity, and labetalol or esmolol to blunt the sympathetic surge that occurs with ECT.
Q24. Postoperative cognitive dysfunction
Risk factors for postoperative cognitive dysfunction include:
A. Advanced age, lower education, preexisting cognitive impairment, depression, sensory deficits, alcohol abuse, major surgery
B. Outpatient surgery, young age, high education level, absence of comorbidities, normal cognitive function, social support
C. Young age, high physical fitness, absence of psychiatric history, minor surgery, short anesthetic duration, no medications
D. Healthy diet, daily exercise, normal sleep patterns, absence of substance use, strong social network, minor procedures
E. Daily exercise, Mediterranean diet, cognitive stimulation, absence of depression, good hearing and vision, elective minor surgery
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Answer: A. Postoperative cognitive dysfunction and postoperative delirium are more common in elderly patients, frail individuals, and those with baseline cognitive impairment or polypharmacy. Additional risk factors include lower education level, depression, sensory deficits (vision or hearing impairment), alcohol abuse, and major surgery. Risk reduction strategies include avoiding benzodiazepines and anticholinergics, minimizing opioids through multimodal analgesia, using depth-of-anesthesia monitoring (BIS) to avoid excessively deep anesthesia, employing regional anesthesia when appropriate, and promoting early mobilization. There is mixed evidence regarding TIVA versus inhalational anesthesia for preventing cognitive dysfunction.
Q25. Perioperative stroke timing
Elective non-cardiac surgery after a recent stroke is highest risk in the first:
A. 24 hours after stroke (defer elective surgery at least 1 week)
B. 1 week after stroke (defer elective surgery at least 2 weeks)
C. 3 months after stroke (defer elective surgery at least 6 months)
D. 5 years after stroke (defer elective surgery at least 10 years)
E. Lifetime after stroke (defer elective surgery indefinitely if possible)
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Answer: C. Recent stroke within 3 months carries the highest perioperative stroke risk for elective non-cardiac surgery. The risk of recurrent perioperative stroke levels off at approximately 9 months after the initial event. Current guidelines recommend deferring elective non-cardiac surgery for at least 6 months after stroke, with 9 months being preferable when feasible. Additional key risk factors for perioperative stroke include advancing age, renal disease, and prior history of transient ischemic attack or stroke.