PAH M&M – 6.20.13

1. PAH M&M – 6.20.13 Attending/CRNA: Parmet/Lamb Operation: Pituitary Adenoma Resection (via transpterygoid middle fossa skull base approach) Surgeons: Lee/Newman Complication: Internal carotid artery bleeding

2. Endoscopic Transpterygoid Approach

3. History • 64 yo AA female presents for resection of invasive pituitary macroadenoma • PSH: pituitary adenoma resection 2001, B/L TKR 2013 • PMH: HTN, GERD • Meds: Amlodipine, Atorvastatin, HCTZ • Allergies: NKDA • Vitals = 142/64, 84, 98% • 5’2”, 141#

4. Pre-Op Labs Na 139, K 4.0, BUN 11, Creat 0.70, Glucose 152 Hgb 10.2, Hct 30, Platelets 185 INR 1.3

5. Case Management • Smooth IV induction, 2 large bore IVs, A-line • Oral Rae ETT • TIVA with propofol/remifentanilgtts • Neuromonitoring • Supine position with bed rotated 90°

6. Incident • Acute blood loss s/p insult to left internal carotid artery ~1L within 1min • Hgb decreased from 11.1 to 8.8 on istat • Abrupt change in BP 118/60  24/11 • Pulse ox dampened

7. 21% of patients have an incomplete circle of willis

8. Interventions • Unit of blood checked/infusing • Phenylephrine administered to support BP • BP  160/90 – NTG titrated to avoid HTN • Foley cath placed by surgeon to control bleeding • Remi/Propofol gtts increased for burst suppression • Rocuronium administered (MEPs lost but SSEPs/VEPs maintained) • 1gm Magnesium to increase seizure threshold • Normocarbia maintained • Hypothermia induced for cerebral protection

9. Case Analysis Incident: “Brisk internal carotid artery bleeding” Patient Safety: A-line, IV access in place, Pt was T&C by anesthesia with 4units PRBC in room Communication: Bleeding verbalized by surgeon, confirmed by anesthesia witnessing severe hypotension, Anesthesia STAT called for additional support Health Care System: Transport to HUP via EmSTAR for IR

10. Post-Op Status • Taken to IR for angio and coils for L ICA • PEA arrest s/p 24hrs cooling • Day 3: CSF leak repair, MRI shows small punctate stroke • Day 9: extubated, transferred to neuro step down, palsy of left CN 3 (oculomotor) and CN 6 (abducens), asa initiated for concern of stump emboli

11. Current Literature Review • 1. Normocapnia • 2. Hypothermia • 3. Transfusion • 4. IHA vs. TIVA • 5. Glucose

12. Basics Review • CBF = 50ml/100gm/min (750ml/min); 15-20% of CO • CBF maintained with a MAP of 50-150 • Current literature advocates for maintaining baseline MAP or MAP >80 • CBF decreases 3% per 1mmHg change in PaCO2 (20-60mmHg) • CPP = MAP – ICP or CVP (normal 70-100mmHg) • CMRO2 and CBF are coupled • CBF and PaCO2 are directly proportional between tensions of 20-60mmHg.

13. Why Hypocapnia? • Hypocapnia widely used today……good or bad? • Monroe-Kellie Doctrine = fixed volume (80/12/8) • Used to lower ICP by decreasing CBF and CBV • accomplished by cerebral arterial vasoconstriction • Intracranial HTN causes secondary brain injury by: • Impairing cerebral perfusion • Brain herniation

14. LuxuryPerfusion Luxury Perfusion thought to be reduced by hypocapnia – now concept of luxury perfusion is largely discredited – Why? CBF and CMRO2 have been found to be decreased after brain injury Regional CBF is markedly decreased particularly in 1st 24hrs Early hypocapnia may be harmful Only 30% of CBV located in arteries (only arteries respond to change in PaCO2) Decreasing CBF by 30% only translates to decrease of 7% in CBV Arterioles most sensitive to PaCO2 change, larger arteries least sensitive (ie: ICA) “Capacity for hypocapnia to decrease CBV is limited and achieved at a disproportionate cost to arterial CBF” (Curley, 2010, p. 1349)

15. Concerns about Hypocapnia • 1. Causes cerebral hypoperfusion • 2. Worsens cerebral vasospasm (ie: SAH) • These 2 factors worsen outcome and impair CBF that may already be at risk • Injured area my be more responsive to CO2, therefore, hypocapnia may potentiate a secondary ischemic injury by diverting CBF from the injured area of the brain

16. Hypocapnia and TBI Results in increased CMRO2 and prolongs seizure activity Increases lactate/O2 demand Causes regional cerebral ischemia Produces ischemic changes visualized on MRI PaCO2 <35mmHg does not improve outcome RCT compared PaCO2 of 25 v.s 35 Prolonged hyperventilation (>20min) worsens outcome Hypocapnia increases overall level AND variability of ICP Hypocapnia lasts 4hrs at most Rebound intracranial HTN occurs when normocapnia is restored – could potentially result in brainstem herniation Hypocapnia is ineffective/counterproductive in controlling ICP over time

17. Hypocapnia and Stroke • Decreased PaCO2 = poor prognosis • Decreased PaCO2 thought to shunt blood to ischemic area of the brain, however, inverse steal phenomenon is now known not to occur

18. Hypocapnia in Healthy Patients • Impairs healthy patients post-op x48hrs • Marked effect on older patients • PaCO2 <24mmHg = delayed rxn times for up to 6 days • PaCO2 <15mmHG = decreased basic psychomotor function • INCREASED PaCO2 during anesthesia enhances neurophysiologic performance postop • Decreased PaCO2 = decreases perfusion to heart, liver, GI • Affects myocardial O2 delivery, increases O2 demand, may result in dysrhythmias, decreases coronary blood flow

19. Oxy-Hemoglobin Dissociation Curve

20. Levels of Hypocapnia • Normocapnia = 36-45mmHg • Moderate Hypocapnia = 28-35mmHg • Temporarily improved cerebral autoregulation • Shown to be detrimental even for brief periods of 20min • Shown to produce critical reductions in regional brain tissue PaO2 in 20% of patients with TBI • Severe Hypocapnia = 23mmHg • Impairs autoregulation

21. When to use hypocapnia? • Hypocapnia is still best way to reduce ICP acutely (ie: in the event of imminent brain herniation) • Also facilitates access and decrease brain bulk intraop • More severe and greater duration, the greater the potential for adverse outcome • Must weigh risks vs. benefit • Should we be advocating for the use of brain oxygenation monitors? • “frequently harmful and rarely, if ever, beneficial” (Curley, 2010, p. 1355)

22. Hypothermia for Cerebral Protection • 32-35°C • Hypothermia: decreases CMR and CBF • CBF changes 5-7% per 1°C • Maintains BBB s/p ischemia,  metabolic demands, Constricts blood vessels =  cerebral blood volume, Inhibits inflammatory pathway • Mild hypothermia is safe but found to be ineffective as a neuroprotectant in the setting of neurosurgery (no benefit regarding M&M when compared to normothermia) • 2011: National Acute Brain Injury Study: Hypothermia II Trial – terminated prematurely d/t the “ineffectiveness of the intervention” • Sentiment supported by a 2012 cochrane review “Cooling for Cerebral Protection during Brain Surgery”

23. HUP Neurocritical Care Hypothermia Protocol • Cool to 33°C using arctic sun pads • Indications: TBI, Large Hemispheric Ischemic Stroke, ICP, Hypoxic-Ischemic brain injury s/p cardiac arrest • Maintained 24-72hrs (re-eval by NSG attending Q24hrs) • Rewarmed over 12-24hrs

24. Optimum Hgb for NSG • Low Hgb associated with poor neurological outcome and increased mortality • Anemia (<9g/dl) independent predictor of severe neurological impairment in SAH pts • Anemia resulted in decreased oxygen delivery resulting in detrimental hypoxic cell signaling pathways • Measure MetHb (marker for anemic stress) • Increasing MetHb levels are associated with poor outcomes and would signal need for prompt blood transfusion • Recommended that preop and intraopHgb levels be kept at 12g/dl preop and 9g/dl intraop in neurosurgical patients • This recommendation is in contention with TRICC (transfusion requirements in critical care) trial, which is not applicable to nsg pts who are more vulnerable to adverse neurological events

25. Transfusion • PRBC transfusion associated with improved 30day survival • Improves brain tissue oxygenation in patients with TBI and SAH • As usual……any potential benefits must be weighed against risks of excessive or unnecessary blood transfusion

26. IHA vs. TIVA • Barriers: Pharmacologic animal studies indicating one is superior to the other has not been translated to humans • No present RCTs assessing neuroprotection of pharmacological agents in pts undergoing intracranial surgery • Post Hoc study of 441 IHAST patients found TIVA did not impact odds of having improved neurological outcome • Limited data suggesting improved neuro outcome after IHA • IHA Pre/post-conditioning ischemic and traumatic pts = no benefit

27. Glucose Control for NSG patients • 2001 – began use of Intensive Insulin Therapy (IIT), kept blood glucose (BG) within range of 80-110 • 3 fold increase for iatrogenic hypoglycemia and did not improve neurological outcome evaluated at 6mos • Retrospective study including 834 pts with SAH saw increased incidence of vasospasm (22 to 34%) • Hyperglycemia: • 178 pts with mean BG >140 on days 1-5 after SAH had worse neurological outcome at 1 year follow up • Two retrospective studies involving 1806 TBI pts showed worse neurological outcome with mean BG >118 and single episode BG >200 within first 10 days postop

28. Optimal Glucose: “Normoglycemia” • NICE-SUGAR Trial (multicenter, multinational, RCT) • 6104 patients • Tight BG control (81-108) vs. conventional glucose control (144-180) • Tight BG group experienced higher mortality • Range of 140-180 is associated with lower 90day mortality • Also recommended by AACE • Intraoperative Hypothermia for Aneurysm Surgery Trial (IHAST) • Glucose levels >129-152 at time of clipping a ruptured cerebral aneurysm were associated with long term cognitive changes and neuro dysfunction

29. References Beheiry, H.E. (2012). Protecting the brain during neurosurgical procedures: strategies that can work. Current Opinion in Anesthesiology, 25, 548-555. Bilotta, F., & Rosa, G. (2010). Glucose management in the neurosurgical patient: are we yet any closer? Current Opinion in Anesthesiology, 23, 539-543. Curley, G., Kavanaugh, B.P., & Laffey, J.G. (2010). Hypocapnia and the injured brain: More harm than benefit. Critical Care Medicine, 38, 1348-1359. Milani, W.R., Antibas, P.L., & Gilmar, F.P. (2012). Cooling for cerebral protection during brain surgery. The Cochrane Collaboration, 7, 1-39. Pasternak, J.J., & Lanier, W.L. (2013). Neuroanesthesiology Update. Journal of Neurosurgical Anesthesiology, 25, 98-134.