Neuroanesthesia and Neuromonitoring Flashcards

During awake craniotomy for eloquent cortex resection, a patient develops breakthrough seizure activity following cortical stimulation mapping. After irrigating with cold saline fails to terminate the seizure, which of the following is the MOST appropriate next pharmacological step that minimises interference with continued intraoperative neurophysiological monitoring?

Answer: IV propofol 30–50 mg bolus

A small propofol bolus (30–50 mg) rapidly terminates cortical spreading seizures within seconds and has an ultra-short context-sensitive half-time, allowing the patient to return to a cooperative state within 1–2 minutes with minimal residual EEG suppression. Benzodiazepines (lorazepam) have a prolonged sedative tail that impairs further awake mapping. Phenytoin and levetiracetam act too slowly for acute intraoperative seizure termination and the loading infusion time would abort the procedure.

Intraoperative transcranial motor-evoked potential (TcMEP) monitoring is being performed during thoracoabdominal aortic aneurysm repair. After proximal aortic cross-clamping the TcMEP amplitude in bilateral lower limbs drops by 70%. Mean arterial pressure is 85 mmHg. Which intervention is most strongly supported by evidence to restore spinal cord perfusion pressure in this context?

Answer: Drain 10–15 mL of CSF via lumbar drain to reduce CSF pressure

Spinal cord perfusion pressure = MAP − CSF pressure. During thoracoabdominal aortic surgery, reducing CSF pressure via lumbar drain (targeting CSF pressure <10 mmHg) is the most evidence-based intervention specifically indicated when TcMEP deterioration occurs, as it directly augments the perfusion gradient without the risks of extreme hypertension. While raising MAP also helps, lumbar CSF drainage is the guideline-endorsed first response to neurophysiological warning signs in this specific scenario. Methylprednisolone has no proven benefit and causes harm; retrograde cerebral perfusion does not perfuse the spinal cord.

A 58-year-old patient undergoing clipping of a giant posterior communicating artery aneurysm has baseline somatosensory evoked potentials (SSEPs) recorded. Fifteen minutes after temporary clip application, the ipsilateral cortical N20 amplitude decreases by 55% with a 3 ms latency increase. The surgeon wishes to extend the temporary clip time. According to established neurophysiological warning criteria, which statement is CORRECT?

Answer: A 55% amplitude decrease alone meets the standard alert threshold requiring action

The universally accepted SSEP warning criterion is ≥50% reduction in cortical N20 amplitude AND/OR ≥10% increase in latency compared to stable baseline. A 55% amplitude decrease alone satisfies this threshold and obligates immediate notification of the surgical team. The criterion is fulfilled by EITHER parameter, not necessarily both simultaneously. Amplitude is considered more sensitive to acute ischaemia than latency. A 55% drop is clearly outside normal variability (typically ≤10–15%).

Which of the following physiological mechanisms BEST explains the phenomenon of 'luxury perfusion' seen on cerebral blood flow studies after reperfusion of an ischaemic penumbra, and what is its primary risk?

Answer: Loss of cerebrovascular autoregulation causing pressure-passive hyperaemia, risking haemorrhagic transformation

Luxury perfusion occurs when ischaemia-injured cerebrovascular smooth muscle loses autoregulatory capacity. Blood flow then becomes passively pressure-dependent, producing CBF that exceeds metabolic demand (CMRO2). The primary clinical danger is that the disrupted blood-brain barrier combined with elevated perfusion pressure promotes haemorrhagic transformation of the infarct. This is the mechanistic basis for blood pressure control targets after reperfusion therapy (thrombolysis/thrombectomy) in stroke and after carotid endarterectomy hyperperfusion syndrome.

During posterior fossa surgery in the sitting position, a sudden increase in end-tidal CO2 from 35 to 28 mmHg, a 15% drop in ETCO2, a mill-wheel murmur on precordial Doppler, and a drop in SpO2 to 90% occur simultaneously. Transesophageal echocardiography reveals air in the right ventricle. Which sequence of interventions is MOST appropriate?

Answer: Flood surgical field with saline → compress jugular veins → aspirate air via central venous catheter → left lateral Trendelenburg position

Management of significant venous air embolism (VAE) follows a stepwise approach: (1) Flood the surgical field to stop air entrainment; (2) Compress jugular veins bilaterally (raises venous pressure, reducing air entry); (3) Aspirate via a right atrial/CVP catheter (positioned at the RA–SVC junction) to remove entrained air; (4) Place in left lateral Trendelenburg to trap air in the right ventricle apex and prevent RV outflow obstruction. Supine conversion with CPR is reserved for cardiovascular collapse. PEEP alone cannot remove air. Discontinuing N2O (if used) is correct but insufficient alone. The scenario describes haemodynamically significant VAE requiring active intervention.

A neurosurgical patient with severe traumatic brain injury (GCS 6) is being managed with multimodal neuromonitoring. Intracranial pressure is 22 mmHg, MAP is 75 mmHg, and the pressure reactivity index (PRx) calculated from continuous ICP and MAP waveform correlation is +0.45. What does this PRx value indicate, and what is its immediate clinical implication?

Answer: Impaired cerebrovascular autoregulation; ICP passively follows MAP, indicating the current CPP (53 mmHg) may be suboptimal and MAP should be increased

The PRx is calculated as the moving correlation coefficient between slow-wave ICP and MAP fluctuations. A PRx close to 0 or negative indicates intact autoregulation (ICP does not passively track MAP). A PRx >+0.3 indicates impaired autoregulation, meaning ICP rises and falls passively with MAP — the brain has lost its ability to buffer perfusion changes. In this case, CPP = MAP − ICP = 75 − 22 = 53 mmHg. The elevated PRx signals the patient is operating outside their optimal CPP (CPPopt), and a higher MAP (targeting CPPopt, often 60–70 mmHg in TBI) would be beneficial. PRx is not a marker of vasospasm.