ICP A Stepwise Approach Stephan A. Mayer, MD Professor, Neurology & Neurosurgery Director, Neurocritical Care, Mount Sinai Health System
ICP: Basic Concepts Monroe-Kellie doctrine: skull = fixed volume 3 components of intracranial volume Normal ICP 20 cm H20 15 mm Hg CSF 150 ml Blood 150 ml Parenchyma 1200 ml
Causes of Increased ICP: Space Occupying Lesion Increased CSF Inc. Blood Volume (Vasogenic edema) Inc. Brain Volume (Cytotoxic edema) Hematoma, Tumor, Abscess Hydrocephalus Trauma, Tumor, Abcess, Hypertensive encephalopathy Infarction, Ischemia
Methods to Reduce Elevated ICP Remove Mass Lesion Surgical Evacuation Reduce CSF Volume Ventricular Drainage Reduce Cerebral Blood Volume Reduce Parenchymal Volume Hyperventiation, Barbiturates, Hypothermia Osmotic Diuretics (Mannitol, Hypertonic Saline)
Cerebral Blood Flow (ml/100 g/min) ICP (mm Hg) CPP can influence ICP when you run out of room Passive Collapse Maximum Dilatation Zone of Normal Autoregulation Maximum Constriction 50 75 50 25 25 0 0 25 50 75 GOAL 100 125 150 0 Cerebral Perfusion Pressure (mm Hg)) Stephan A. Mayer, MD
Cerebral Blood Flow (ml/100 g/min) ICP (mm Hg) CPP can influence ICP when you run out of room Passive Collapse Vasodilatory Cascade Zone Maximum Dilatation Zone of Normal Autoregulation Autoregulation Breakthrough Zone Maximum Constriction 50 75 50 25 25 0 0 25 50 75 GOAL 100 125 150 0 Cerebral Perfusion Pressure (mm Hg)) Stephan A. Mayer, MD
Post neurological outcome % Post neurological outcome % Early neurological deterioration % Early neurological deterioration % Outcome after Acute Ischemic Stroke by A Admission Blood Pressure 90 80 70 60 50 40 30 20 10 0 n = 18 n = 29 < 120 121-140 n = 39 141-160 n = 78 161-180 n = 49 181-200 Systolic BP on admission (mm Hg) n = 87 > 200 B Castillo J, et al. Stroke. 2004;35:520-526. 90 80 70 60 50 40 30 20 10 0 n = 38 < 70 n = 39 71-80 n = 48 81-90 n = 43 91-100 n = 30 101-110 Diastolic BP on admission (mm Hg) n = 102 > 110 C 90 80 70 60 50 40 30 20 10 0 n = 18 n = 29 < 120 121-140 n = 39 141-160 n = 78 161-180 n = 49 181-200 n = 87 > 200 90 80 70 60 50 40 30 20 10 0 D n = 38 < 70 n = 39 71-80 n = 48 81-90 n = 43 91-100 n = 30 101-110 n = 102 > 110 Systolic BP on admission (mm Hg) Diastolic BP on admission (mm Hg)
Lund protocol Reduce CMRO 2 with sedation Miazolam, thiopental, fentanyl Reduce BP and capillary hydrostatic pressure (CPP 50-60 mm Hg) IV Metoprolol (.2 mg/kg/hr) and clonidine (.5 mcg/kg prn) Dihydroergotamine.1-.8 mcg/kg/hr Maintain normal hematocritt, CVP, and albumin levels
MMM: Imaging Vasodilatory Cascade Physiology MAP GOAL
MMM: Imaging Perfusion Pressure Breakthrough Physiology MAP GOAL
Indications for ICP Monitoring Coma (Glasgow Coma Scale score 8) CT evidence of intracranial mass effect Extra-axial mass lesion Midline shift Effacement of basal cisterns Exception: severe TBI with motor posturing Prognosis is such that aggressive ICU care is warranted
Clinical Signs Increased ICP Depressed level of consciousness Pressor response Projectile vomiting CN 6 palsies Brainstem herniation CN 3 palsey Motor posturing Lower extremity rigidity Loss of lateral EOMs Hyperventilation
Ventricular catheter Epidural Monitor Parenchymal Micosensor Richmond Bolt
ICP/CPP Treatment Thresholds Guideline ICP treatment should be initiated at an upper threshold of 20 mm Hg. Option Cerebral Perfusion Pressure should be maintained at a minimum of 60 mm Hg.
Emergency Treatment of Increased ICP Un-monitored patient with clinical signs of herniation Elevate head of bed 30 Normal saline 100 ml/hr Intubate and hyperventilate (pco2 30 mm Hg) Mannitol 20% 1.0 to 1.5 g/kg rapid IV infusion Foley catheter CT scan and neurosurgical evaluation
Critical Pathway for Treatment of Intracranial Hypertension in the Severe Head Injury Patient (Treatment Option) Insert ICP Monitor Maintain CPP 70 mmhg YES Intracranial Hypertension?* NO Ventricular Drainage (if available) Consider Repeating CT Scan YES YES Intracranial Hypertension? Mannitol (0.25-1.0 g/kg IV) Intracranial Hypertension? NO NO May Repeat Mannitol if Serum Osmolarity < 320 mosm/l & Pt euvolemic Carefully Withdraw ICP Treatment Hyperventilation to PaCO2 30-35 mmhg YES Intracranial Hypertension? NO Other Second Tier Therapies High Dose Barbiturate therapy Hyperventilation to PaCO2 < 30 mmhg Monitoring SjO2, AVDO2, and/orcbf Recommended Second Tier Therapy
ICP PROTOCOL
Columbia Stepwise ICP Protocol 1 2 3 4 5 6 CPP OPTIMIZATION SEDATION PENTOBARBITAL HYPERVENTILATION OSMOTHERAPY HYPOTHERMIA SURGICAL DECOMPRESSION 7 2002
Revised Columbia Stepwise ICP Protocol 1 2 3 4 5 6 CPP OPTIMIZATION SEDATION HYPOTHERMIA HYPERVENTILATION OSMOTHERAPY PENTOBARBITAL SURGICAL DECOMPRESSION 7 2010
1 3-way stopcock turned off to drainage system transpac positioned at ear level LEVEL drainage bag 100cc syringe of sterile water Ventricular Drainage
2 ICU Intravenous sedation Goal is reversibility to allow repeated neurologic assessment Alternatives (in intubated pts): Fentanyl or Remifentanyl Midazolam Propofol» Ultrashort acting» Allows wake-up in 5-15 mins» Reduces ICP, CMRO2» Drawbacks: hypotension, infection
HYPOTHERMIA IS PENTOBARBITAL IS Complications of pentobarbital Hypotension Immunosuppression An extra 4 weeks in coma ICU neuromyopathy
3 CPP OPTIMIZATION: Dopamine infusion resulting in increased MAP and CPP, and decreased ICP
4 Osmotherapy Mannitol 0.25 to 1.5 g/kg IV wide open Dose up to Q1H on an as-needed basis Mechanisms:» Acute dehydrating effect (osmotic gradient across BBB)» Secondary hyperosmolality (diuretic effect)» Reflex vasoconstriction (viscosity effect) Hypertonic Saline Varying concentrations: 3%, 7.5%, 10%, and 23.4% Optimal dosing not known
30 ml 23.4% Bullets
Effect of Hypertonic Saline in CBF in SAH patients TSENG M-Y, Stroke 2003;34:1389.) 10 poor grade SAH patients 2 ml/kg of 23.5% saline ICP fell 74% CPP rose 27% CBF rose 23% Peak effect @ 20-60 minutes MAP CPP CVR ICP TCD
5 Hyperventilation HYPERVENTILATION IS THE MOST RAPID WAY TO REDUCE ICP EXCESSIVE HYPERVENTILATION CAN WORSEN CEREBRAL ISCHEMIA MECHANISM OF ACTION: HYPOCARBIA INDUCES SERUM AND CSF ALKALOSIS ALKALOSIS INDUCES CEREBRAL VASOCONSTRICTION VASOCONSTRICTION REDUCES CEREBRAL BLOOD VOLUME TIME COURSE: ICP IS REDUCED ALMOST IMMEDIATELY PEAK REDUCTION IN 5-10 MINUTES Hyperventilation Can Have Sustained Effects In Patients With Vasodilatory Vasogenic Cerebral Edema
6 Hypothermia MECHANISM OF ACTION: PROFOUNDLY REDUCES REDUCES CEREBRAL METABOLISM, AND HENCE CEREBRAL BLOOD VOLUME TARGET 32-33 C INDICATION PENTOBARBITAL-REFRACTORY ICP COMPLICATIONS: ARRYTHMIA AND CARDIOVASCULAR DEPRESSION IMMUNOSUPPRESSION COAGULOPATHY METABOLIC: SHIVERING AND REWARMING
HYPOTHERMIA FOR ICP CONTROL: TRAUMATIC BRAIN INJURY Shiozaki (J Neurosurg 1993) Randomized controlled study of hypothermia (34 C) for ICP refractory to pentobarbital (N=33). Hypothermia resulted in:»lower ICP (36.9 to 26.5 mm Hg)»Increased CPP»Reduced CBF and CMRO2»Reduced arteriojugular venous oxygen differences Survival was 50% in hypothermia patients compared to 18% in the control group (P<.05).
6 SECOND TIER Step Up HYPOTHERMIA TO TARGET 35 C THIRD TIER Advance as Needed HYPOTHERMIA TO TARGET 33 C 4 5 HYPERVENTILATION (HV) TO pco2 30-35 mm Hg BOLUS OSMOTHERAPY TO SERUM OSMS <320 MMM-GUIDED HV <30 mm Hg and/or THAM BOLUS OSMOTHERAPY TO SERUM OSMS >320 3 SEDATION to RASS -4 to -5 (Quiet, Motionless State) PARALYSIS and/or BARBITURATES 2 TARGET CPP 50-70 mm Hg MMM-GUIDED CPP OPTIMIZATION 1 CSF DRAINAGE and/or RESCUE CRANIOTOMY HEMICRANIECTOMY or SALVAGE CRANIOTOMY
3 4 5 SECOND TIER 6 HYPOTHERMIA TO TARGET 35 C HYPERVENTILATION (HV) TO pco2 30-35 mm Hg BOLUS OSMOTHERAPY TO SERUM OSMS <320 SEDATION to RASS -4 to -5 (Quiet, Motionless State) Advance first-tier ICP interventions in stepwise fashion to avoid missing essential steps 2 TARGET CPP 50-70 mm Hg 1 CSF DRAINAGE and/or RESCUE CRANIOTOMY
Advance second-tier ICP interventions as needed to fit available resources and the clinical situation THIRD TIER HYPOTHERMIA TO TARGET 33 C MMM-GUIDED HV <30 mm Hg or THAM BOLUS OSMOTHERAPY TO SERUM OSMS >320 PARALYSIS and/or BARBITURATES MMM-GUIDED CPP OPTIMIZATION HEMICRANIECTOMY or SALVAGE CRANIOTOMY
Three very bad options for a very bad situation: medically refractory ICP! THIRD TIER HYPOTHERMIA TO TARGET 33 C MMM-GUIDED HV <30 mm Hg or THAM BOLUS OSMOTHERAPY TO SERUM OSMS >320 PARALYSIS and/or BARBITURATES MMM-GUIDED CPP OPTIMIZATION HEMICRANIECTOMY or SALVAGE CRANIOTOMY
What About the Latest Trials?
BEST-TRIP TRIAL
BEST-TRIP TRIAL 324 patients 13 years of age or older with severe TBI in Bolivia or Ecuador Protocol treating ICP based on ICP monitoring Protocol for treating ICP based on standing therapy, imaging and clinical examination Six-month mortality was 39% in the pressuremonitoring group and 41% in the imaging clinical examination group (P = 0.60). Median length of stay in the ICU was similar in the two groups
BEST-TRIP TRIAL Number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyperventilation) in the ICU was higher in the imaging clinical examination group than in the pressure-monitoring group (4.8 vs. 3.4, P = 0.002). Serious adverse events was similar in the two groups.
BEST-TRIP Conclusion For patients with severe traumatic brain injury, care focused on maintaining monitored intracranial pressure at 20 mm Hg or less was not shown to be superior to care based on imaging and clinical examination.
Survival at 14 days MUCH better with ICP monitoring!
Survival at 14 days better with ICP monitoring
Aneurysmal SAH with associated suddural hematoma and bilateral motor posturing
DECRA 155 TBI patients Early bifrontal craniectomy vfersus standard care Surgical group had Lower ICPs Fewer ICP interventions Fewer ICU days WORSE outcomes despite similar mortality
DEAD FULL RECOVERY
Communicating hydrocephalus is an almost universal finding in patients after hemicraniectomy
EUROTHERM 3235 387 severe TBI patients Randomization trigger: first episode of ICP >20 mm Hg Hypothermia group Died more Less likely to survive with good outcome 26% vs 37% Cause of this worse outcome is unclear
RESCUEicp Trial
Conclusion When the going gets tough, when ICP is medically refractory, easy options are hard to find All three THIRD TIER options likely cause harm when performed early without a trial of ICU care Prophylactic barbiturate coma Straight to the OR for hemicraniectomy Cool to 32-35 C at the first sign of ICP elevation My preference for definitive salvage intervention when ICU care is failing go to the OR
RESCUEicp Trial 408 severe TBI patients Age 18-65 Randomization trigger: Medically refractory ICP >25 mm Hg for 1-12 hours Time to randomization >72 hours after injury in 45% Hemicraniectomy group Absolute 22% reduction in mortality Better ICP control: 5 vs 17 hours with ICP >25 mm Hg More complications (mostly surgical related): 16% vs 9%
RESCUEicp Trial: Craniectomy vs Barbiturates
Rescue Hemicraniectomy Creates a 22% chance of converting death to survival in a vegetative state or with severe disability
4 5 6 SECOND TIER HYPOTHERMIA TO TARGET 35 C HYPERVENTILATION (HV) TO pco2 30-35 mm Hg BOLUS OSMOTHERAPY TO SERUM OSMS <320 Advance first-tier ICP interventions in stepwise fashion to avoid missing essential steps 3 SEDATION to RASS -4 to -5 (Quiet, Motionless State) 2 TARGET CPP 50-70 mm Hg 1 CSF DRAINAGE and/or RESCUE CRANIOTOMY
SECOND TIER THIRD TIER 2 3 4 5 6 HYPOTHERMIA to 35 C Option: TARGET 33 C HYPERVENTILATION (HV) Option: MMM-Guided HV <30 BOLUS OSMOTHERAPY Option: PUSH OSMS >320 SEDATION to RASS -4 to -5 Option: ADD PARALYTICS TARGET CPP to 50-70 mm Hg Option: MMM-TARGETED CPP Ultimately, once you realize that you are losing the battle, there is really only one effective third tier therapy for ICP: pop the lid! 1 CSF DRAINAGE and/or RESCUE CRANIOTOMY HEMICRANIECTOMY or SALVAGE CRANIOTOMY
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