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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. Endoscopic Transpterygoid Approach. History.

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pah m m 6 20 13

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

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

case management
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°
  • 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
  • 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
case analysis
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

post op status
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
current literature review
Current Literature Review
  • 1. Normocapnia
  • 2. Hypothermia
  • 3. Transfusion
  • 4. IHA vs. TIVA
  • 5. Glucose
basics review
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.
why hypocapnia
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
luxury perfusion

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)

concerns about hypocapnia
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
hypocapnia and tbi
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

hypocapnia and stroke
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
hypocapnia in healthy patients
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
levels of hypocapnia
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
when to use hypocapnia
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)
hypothermia for cerebral protection
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”
hup neurocritical care hypothermia protocol
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
optimum hgb for nsg
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
  • 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
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
glucose control for nsg patients
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
optimal glucose normoglycemia
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

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.