navaz karanjia, md medical director, neurocritical care program and neuro-icu assistant professor of...

ICU management of Severe Traumatic Brain Injury

Navaz Karanjia, MDMedical Director, Neurocritical Care Program and Neuro-ICUAssistant Professor of NeurosciencesUniversity of California-San Diego Health System

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Navaz Karanjia, MD

FINANCIAL DISCLOSURE: none

UNLABELED/UNAPPROVED USE DISCLOSURE: hypertonic saline / propofol use for ICP control

Overview

Severe TBI pathophysiology

Severe TBI management

Why do we need to understand acute management of neurologic injuries?

Classification of TBI

Closed/Blunt Motor Vehicle Accidents Sports Injuries

Penetrating Gunshot wounds Stab wounds

Blast Bomb blasts Battlefield Injuries

Classification of TBI Mild

no LOC or amnesia brief amnesia or

LOC, or impaired alertness, memory

postconcussive syndrome

GCS 13-15 Moderate

LOC > 5 min, or focal neurologic deficit

GCS 9-12 Severe

GCS < 8

Pathophysiology:Primary vs. Secondary Injury

Primary Injury Epidural Subdural Subarachnoid Contusion/ICH DAI

Secondary Injury Cerebral edema

/ elevated ICP Ischemia Excitotoxicity Inflammation

Secondary Brain Injury: pathophysiology

Secondary Brain Injury Treatment: the golden triangle

Cerebral Oxygenation

PaO2 (normooxic) Hemoglobin (>8)

Cerebral Metabolism

Sedation Seizure screening/rx Thermoregulatory

mgmt

Cerebral Perfusion Blood pressure (SBP >90) Cardiac output Volume status (euvolemic) ICP / CPP (ICP<20, CPP>60) PaCO2 (normocarbic)

Severe TBI: Clinical Practice Guidelines

“Guidelines for the management of severe traumatic brain injury, 3rd Edition (2007)”

Brain Trauma Foundationand

The American Association of Neurological Surgeons Congress of Neurological Surgeons

J Neurotrauma 24 Suppl 1: p. S1-106 (2007)Download available: www.braintrauma.org


Elevate and maintain head of bed > 300, keep neck straight Provide sedation and analgesia Resuscitate with isotonic to hypertonic fluids (NS) Maintain normoxia with PaO2 target of >60 (not hyperoxic)

mmHg Maintain Hgb at least >8 or higher if intracerebral

monitoring indicates Avoid hypotension (SBP < 90mm Hg)/maintain cerebral

perfusion CPP >60mmHg (and <70mmHg) Maintain ICP < 20mmHg Maintain normocapnia with PaCO2 35-45 mmHg Maintain normothermia with temperature goal of 36.5-37.50

Antiepileptic therapy x 7 days, continue only if seizing NO steroids Early nutritional optimization Normoglycemia




Cerebral Metabolism


mgmt


Oxygenation

BTF/AANS GUIDELINE

Oxygenation is to be monitored Hypoxia (O2 sat <90% and pO2<60) is

to be avoided (Level 3)

Oxygenation

Oxygenation Hypoxia is bad

ICP by CBF Aerobic anaerobic metabolism energy failure,

dying in 4 min

Oxygenation

Oxygenation Hyperoxia is probably bad for

TBI patients

Oxygenation

Oxygenation Hyperoxia is probably bad for TBI patients

Hyperoxia (Pa02>300) 63% mortalityHypoxia (Pa02<60) 57% mortalityNormooxia 43% mortalityOR for death w/ hyperoxia = 1.8

Oxygenation

Oxygenation Normooxia is just right

Cerebral Oxygenation: Hemoglobin

Role of hemoglobin in neurovascular injury Cerebral ischemia is caused by impaired CBF

and cerebral oxygen delivery (DO2)

DO2= CBF x arterial oxygen content

Arterial oxygen content = linearly related to Hb

In normal brain, compensatory vasodilation occurs at Hb <10, brain hypoxia at Hb <6

Oddo M et al. Hemoglobin concentration and cerebral metabolism in patients with aneurysmal subarachnoid hemorrhage. Stroke 2009 Apr; 40(4): 1275-81

Percentage of episodes of brain tissue hypoxia (PbtO2 <20 mm Hg) and cell energy dysfunction (LPR >40) according to different Hgb ranges. *P<0.05 for Hgb <9 g/dl

In aneurysmal subarachnoid hemorrhage, ICH, and stroke, microdialysis and brain tissue oxygen monitoring associate Hb <9-10 with brain tissue hypoxia and metabolic distress





Cerebral Metabolism


mgmt


Cerebral Perfusion: Blood Pressure/CPP

BTF/AANS GUIDELINE

Blood pressure should be monitored SBP < 90mmHg is to avoided (Level 2)

Resuscitate patients to SBP>90 using isotonic to hypertonic, non-glucose containing fluids; use pressors if necessary


BTF/AANS GUIDELINE

Aggressive attempts to maintain CPP > 70mmHg with fluids and pressors should be avoided because of the risk of ARDS (Level 2)

Avoid CPP < 50mmHg (Level 3)

Keep CPP >60; target CPP 60-70 if using pressors


80%12%8%

92%4%

4%

79%20%

Monroe Kellie Doctrine

Skull is a rigid container (1600 cc)Cranial contents (brain, blood, CSF) are incompressibleAdditional volume (pathologic or expansile) will lead to displacement of normal cranial contents

Normal ICP = 5-20 cm H20

CSF Blood Brain

CSF Blood Brain

Blood Tumor Brain

Normal

Cerebral edema

Tumor

Saunders NR, Habgood MD, Dziegielewska KM (1999). "Barrier mechanisms in the brain, I. Adult brain". Clin. Exp. Pharmacol. Physiol.

26 (1): 11–9.


HV, mannitol, 23%

Brain Volume

No blood = BAD FOR BRAIN

CPP = MAP - ICP

Rosner M J, Rosner S D & Johnson A H. "Cerebral perfusion: management protocol and clinical results." J.Neurosurgery

1985; 83: 949-962.


CPP = MAP - ICP

CBF = CPP/CVR

CD02 = CBF x Ca02

Cerebral Perfusion: Blood Pressure

Aerobic anaerobic metabolism energy failure, dying in 4 min


Rosner M J, Rosner S D & Johnson A H. "Cerebral perfusion: management protocol and clinical results." J.Neurosurgery 1985; 83: 949-962.

Bratton SL et al. J Neurotrauma 24 (S1): S59-S64, 2007Narotam P, Morrison J et al. Brain tissue oxygen monitoring in traumatic brain injury and major trauma: outcome analysis of a brain tissue oxygen-directed

therapy. JNS (2009) 111 (4): 672-682

TBI: -1 episode of prehospital SBP<90 = 2x mortality

-If CPP < 60 over 33% of the time, mortality ~100%

-ICP<20, CPP>60 = mortality reduction by > 50%

-HOWEVER, CPP>70 = increased mortality

Healthy human subjects: normal CPP = 50-70

-CPP<50 = ischemia/decreased EEG amplitude

TARGET CPP>60, ICP<20, SBP>90


Autoregulation

Cerebral Perfusion: ICP

BTF/AANS GUIDELINE

ICP should monitored in all severe TBI patients (GCS <8) with abnormal CT (Level 2)

ICP should be monitored in all severe TBI patients (GCS <8) with normal CT and > 2 of the following (age > 40, posturing, SBP < 90mmHg) (Level 3)

Treatment should be initiated with ICP threshold > 20mmHg (Level 2)

A combination of ICP value, clinical and CT findings should be used to determine the need for treatment (Level 3)

Cerebral Perfusion: ICPClinical Syndromes

Subfalcine Herniation

Cerebral cortex under falx

Leg weakness

mental status

Central/Upward Herniation

Brainstem down/up through tentorium

mental status

Dilated pupil, eye “down and out” (CN3)

Weakness/posturing

Basilar stroke

Tonsillar Herniation

Cerebellar tonsils in foramen magnum

Awake, pharynx weakness, quadriparesis

Arrhythmia/cardiac arrest

Respiratory arrest

Uncal Herniation

Uncus over tentorial notch

mental status

Dilated pupil, eye “down and out” (CN3)

Weakness/posturing

Cerebral Perfusion: ICP

80%12%8%

92%4%

4%

79%20%

Monroe Kellie Doctrine

Skull is a rigid container (1600 cc)Cranial contents (brain, blood, CSF) are incompressibleAdditional volume (pathologic or expansile) will lead to displacement of normal cranial contents

Normal ICP = 5-20 cm H20

CSF Blood Brain

CSF Blood Brain

Blood Tumor Brain

Normal

Cerebral edema

Tumor

Saunders NR, Habgood MD, Dziegielewska KM (1999). "Barrier mechanisms in the brain, I. Adult brain". Clin. Exp. Pharmacol. Physiol.

26 (1): 11–9.

CPP = MAP - ICP

Cerebral Perufsion: ICPBrain Code guideline

UCSD Brain CodeGuideline

Cerebral Perfusion: ICPCompartment Approach

Venous blood HOB up 60 deg Neck straight No IJ lines, do not lay flat for lines Do no use venodilating BP agents

CSF Place EVD Change popoff

Brain parenchyma Osmotherapy (mannitol, hypertonic saline) Steroids only if appropriate (tumor, HACE, some infections) Surgery (hemicrani, SOC)

Lesion Blood, tumor, pus -> surgery Air-> 100% NRB, surgery

Arterial blood Normoventilate Avoid hyperemia: CPP 50-70 Avoid Hypoxia: Pa02>60 Decrease metabolism: sedation, cooling

Arterial bloodNormoventilate target Pac02 35-45 Avoid hyperemia: CPP 50-70 Avoid hypoxia: Pa02>60 Decrease metabolism: propofol IVP, propofol/pentobarb gtt, hypothermia 32-34 C

Kramer A, Zygun D. Anemia and red cell transfusion in neurocritical care. Critical Care 2009 13:R89

35

60

150

25

20

50

Cerebral Perfusion: ICPArterial Compartment

Cerebral Perfusion: Ventilation

BTF/AANS GUIDELINE

Prophylactic hyperventilation of PaCO2 < 25mmHg is not recommended (Level 2)

HV should be avoided during the first 24 hours after injury (Level 3)

If HV is used, jugular bulb monitoring or brain tissue oxygen tension measurement is recommended to monitor oxygen delivery (Level 3)

Hyperventilation (HV) is recommended as a temporizing measure for reduction of elevated ICP (Level 3)

Cerebral Perfusion: Sedation to reduce metabolism and ICPBTF/AANS GUIDELINE

Prophylactic administration of barbiturate to induce EEG burst suppression is not recommended (Level 2)

High dose barbiturate is recommended to control elevated ICP refractory to medical and surgical management; hemodynamic stability is critical before and during treatment (Level 2)

Propofol is recommended for ICP control but not for improving mortality or 6-month outcome; High dose propofol can produce significant increased morbidity (Level 2)

Sedate patients to reduce cerebral metabolism; titrate to comfort and ICP control.


Cytotoxic Vasogenic

Stroke TumorAbscess

Cerebral Perfusion: ICPOsmotherapy


Sodium=0.97 Mannitol=0.9

Glycerol=0.5 Urea=0.6

Reflection Coefficient



Increased vascular volume-> improves

CBF up to 23%

Dehydration of erythrocytes increases deformability through small capillaries

Reduces inflammatory response by reducing PMN adhesion to

microvasculature (unclear clinical significance)

Pascual J et al. Hypertonic saline resuscitation of hemorrhagic shock diminishes neutrophil rolling and adherence to endothelium and reduces in vivo vascular

leakage. Ann Surg. 2000 Nov; 236 (5): 634-642Tseng M, Pippa G et al. Effect of hypertonic saline on cerebral blood flow in poor

grade patients with subarachnoid hemorrhage. Stroke 2003;34:1389-1396



Create a GRADIENT,

DON’T

dehydrate your patient!


MA Koenig, M Bryan, JL Lewin, III, MA Mirski, RG Geocadin and RD Stevens

Neurology 2008;70;1023-1029; originally published online Feb 13, 2008

253 cases transtentorial herniation 30cc 23.4% saline bolus reversed clinical signs of TTH in 75% Transient hypotension in 17%, no CPM on MRI at 17 days

Up to 50% reduction of ICP 65% of patients below 20mmHg ICP


Long-term outcome after medical reversal of transtentorial herniation in patients with supratentorial mass lesions Qureshi,,Geocadin,Suarez, Ulatowski, CRITICAL CARE MEDICINE 2000;28:1556-1564

11/28 (40%) survived to discharge 7/11 (59%) survivors functionally independent


BTF/AANS GUIDELINE

Mannitol is effective for control of raised ICP at doses of 0.25 g/kg to 1 g/kg. Arterial hypotension (SBP <90 mm Hg) should be avoided (Level 2)

Restrict mannitol use prior to ICP monitoring to those patients who are herniating or are neurologically deteriorating (not attributable to extracranial cause) (Level 3)


BTF/AANS GUIDELINE

The use of steroids is not recommended for improving outcome or reducing ICP. (Level 1)

High dose methylprednisolone in moderate-severe TBI patients is associated with increased mortality and is contraindicated. (Level 1)

Cerebral Perfusion: ICPSteroids

Mixed results in Blunt Trauma Many case series show ICP reduction

and mortality benefit About 30% of patients have

favorable long term outcomes

Howard et al, J Trauma. 2008 Aug;65(2):380-5

Cerebral Perfusion: ICPHemicraniectomy

155 severe, diffuse TBI patients randomized

Early bifrontotemporal decompressive hemicraniectomy v. standard care

In adults with severe diffuse traumatic brain injury and refractory intracranial hypertension, early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure and the length of stay in the ICU but was associated with more unfavorable outcomes

Cooper DJ et. al. N Engl J Med 2011; 364:1493-1502

Surgical intervention for moderate to severe penetrating and blast TBI in the theater

Early hemicraniectomy as blast brain becomes hyperemic and edematous very quickly (few hours)

Life saving May allow for overseas transportLing et al, J Neurotrauma (2009)Bell et al, Neurosurg Focus. 2010 May;28(5):E1.

Cerebral Perfusion: ICPHemicraniectomy




Cerebral Metabolism


mgmt


Cerebral metabolism: thermoregulatory management

Fever increases cerebral metabolic rate by 5-7% with each degree change in temp

Fever accelerates the secondary injury cascade, causing neuronal death, infarct volume, cerebral edema, ICP, midline shift, morbidity, mortality

in temp by 1°C increases OR of death by 2.2 in ischemic patients

Henker, Brown, Marion; Neurosurgery 42:1071, 1998 Andrews, et al., J Neurosurg 97:326, 2002


Normothermia is a class I AHA recommendation for ischemic stroke, ICH, and SAH patients

Hypothermia is a class I AHA recommendation for comatose post-cardiac arrest patients (improves good neurologic outcome in survivors from ~30% to ~50% (OR 5, NNT 6) Techniques: acetaminophen, cooling

blankets, advanced thermoregulatory devices (cooling catheter, conductive surface cooling devices)


Normothermia in TBI:

Fever is associated with significantly worse outcomes

Li, J et al. J Neurotrauma. 2012 January 1; 29(1): 96–100


Hypothermia in TBI:

No clear evidence yet to support its use for neuroprotection (it IS effective for refractory ICP management)

National Acute Brain Injury Study: Hypothermia II (neuroprotection study) terminated early for futility

GL Clifton, A Valadka, D Zygun et al. Lancet Neurol, 10 (2011), pp. 131–139Sadaka F et al. Brain Inj. 2012;26(7-8):899-908.


BTF/AANS GUIDELINE

Prophylactic hypothermia does not increase nor decrease mortality when compared to normothermic controls (Level 3)

When hypothermia is maintained for > 48 hours, there is decreased mortality risk

(Level 3) Prophylactic hypothermia is associated with

higher GOS (4 and 5) than normothermic controls (Level 3)

Maintain normothermia; hypothermia is not standard of care for neuroprotection but is useful for refractory ICP treatment

Cerebral Metabolism: Sedation and Analgesia

▪ Proper sedation cuts resting cerebral metabolic rate in half

▪ No evidence that one sedative is better than another for TBI as long as ICP / CPP /SBP are controlledCrit Care Med. 2011 Dec;39(12):2743-51.

Cerebral Metabolism: Sedation and AnalgesiaBTF/AANS GUIDELINE

Prophylactic administration of barbiturate to induce EEG burst suppression is not recommended (Level 2)

High dose barbiturate is recommended to control elevated ICP refractory to medical and surgical management; hemodynamic stability is critical before and during treatment (Level 2)

Propofol is recommended for ICP control but not for improving mortality or 6-month outcome; High dose propofol can produce significant increased morbidity (Level 2)

Sedate patients to reduce cerebral metabolism; titrate to comfort and ICP control.

Cerebral Metabolism: Sedation and Analgesia

Pentobarbital Loading Dose

▪ 10 mg/kg i.v. over 30 minutes▪ 5 mg/kg i.v. every hour X 3 doses

Maintenance Dose▪ 1 mg/kg/hr, i.v. infusion

Propofol Start: 50 mg/kg/min Maintenance: 100 mg/kg/min (titrate prn)

Helpful to use EEG/SEDLINE monitoring during sedation for ICP control, to ensure excessive doses not being used

J Clin Neurophysiol. 2011 Oct;28(5):483-8.

Eisenberg et al, J Neurosurg 69:15-23 (1988)

Are seizures common in TBI patients?

22% of all moderate to severe TBI patients; 50% NCSz only (Vespa) 20-50% of all altered hypoxic-ischemic injury patients; most NCSz

(Wijdicks, Krumholz, Wright, Geocadin) 8-10% of MICU patients without known brain injury with

unexplained AMS; 67-100% were NCSz only (Towne, Oddo) 21% of MICU patients with encephalopathy due to toxic-

metabolic cause, sepsis, or renal failure; 98% were NCSz only (Classen)

48% of patients who present with status epilepticus with persistent AMS have NCSz when monitored for 24 hrs; 14% were in NCSE (DeLorenzo)

11% of all altered ischemic stroke patients; 80% were NCSz only (Claassen)

31-36% of ICH patients with AMS; 58% NCSz only (Claassen, Vespa) 19% of all altered SAH patients; 70% were in NCSE (Claassen)

Cerebral metabolism: seizure management


Are seizures problematic?

Cerebral

Increased blood flowEnergy requirements are matched by increased lactate, increased glucose

Metabolic

HyperglycemiaLactic acidosis

Autonomic

HypertensionIncreased COIncreased CVPMassiveCatecholaminesTachycardiaArrythmiasHyperpyrexiaVomiting


Physiologic Changes--compensated


Physiologic Changes--decompensated Cerebral

Failure of autoregulationHypoxiaHypoglycemiaDecreased lactateIncreased ICPCerebral edema

Metabolic

HypoglycemiaHyponatremiaHypo/HyperkalemiaAcidosisHepatic/Renal dysfunctionDICRhabdomyolysisSerum/CSFleukocytosis

Autonomic

HypoxiaDecreased blood pressureFalling COPulmonary edemaCHFArrythmiasHyperpyrexia


Vespa et al Crit Care Med 2007

Higher Microdialysis Lactate/Pyruvate with seizures

ICP in seizure patientsn = 9 pts, k = 108 hours

0.0

5.0

10.0

15.0

20.0

25.0

30.0

35.0

ICP Baseline ICP during seizure

mm

Hg

p < 0.001


Vespa et al Crit Care Med 2007

Increase in ICP in TBI patients


MRI after seizure


2012 Neurocritical Care Society Guidelines for Treatment of Status Epilepticus: Indications for Continuous EEG Monitoring


TBI:

• Phenytoin or carbamazepine are effective in preventing early post-traumatic seizures

• They do not prevent onset of late post-traumatic seizures

Newer agents lack evidence to support their use (ex: leviteracetam

Temkin et al, NEJM 323:497 (1990)Glotzner et al, Neurochir 26:66-79 (1983)

Manaka et al, JpnJ Psych Neuro 46:311-315 (1992)Amer Acad Phys Med Rehab Arch Phys Med 79: 594 (1998)

Cerebral metabolism: seizures management

BTF/AANS GUIDELINE

Anticonvulsant therapy is indicated to decrease the incidence of early post-traumatic seizures (< 7 days) (Level 2)

Phenytoin and valproate are not recommended for preventing late post-traumatic seizures (> 7 days) (Level 2)

Give AED’s for 7 days, then stop unless pt is seizing or has had craniotomy

Brain Tissue Oxygenation (PbO2) monitoring

PbO2 measures interstitial brain tissue oxygenation (PbtO2) in mmHg and brain temperature (°C)

The goal is to prevent secondary injury by ensuring viable tissue is receiving adequate oxygen

Hypoxia strongly associated with a poorer outcome

Brain Tissue Oxygen Monitoring in Traumatic Brain Injury (BOOST 2) ongoing (closes 2014)

Neurol. Res 20 Suppl 1, S71-75 (1998).J Neurosurg. 2009 Oct;111(4):672-82J Neurosurg. 2009 Oct;111(4):644-9.

BrainTissue Oxygenation (PbO2) monitoring

BTF/AANS GUIDELINE

Jugular venous saturations (< 50%) or brain tissue oxygenation tension (< 15mmHg) are treatment thresholds. (Level 3)

Cerebral Metabolism: Nutrition

Any episode of hyperglycemia >200 mg/dl associated with 3.6x risk of hospital mortality

Cerebral Metabolism: Nutrition

BTF/AANS GUIDELINE

Patients should be fed to attain full caloric replacement by day 7 post-injury. (Level 2)

Normoglycemia is probably recommended

Antibiotics

BTF/AANS GUIDELINE

Periprocedural antibiotics for intubation should be used to reduce the incidence of pneumonia but they do not change length of stay or mortality (Level 2)

Routine ventricular catheter exchanges or prophylactic antibiotic use for ventricular catheter placement is not recommended to reduce infection (Level 3)

Tracheostomy

BTF/AANS GUIDELINE

Early tracheostomy should be used to reduce the number of mechanical ventilation days; Does not reduce mortality or rate of nosocomial pneumonia (Level 2)

DVT Prophylaxis

BTF/AANS GUIDELINE

Graduated compression stockings and intermittent pneumatic stockings should be used (Level 3)

Low molecular weight heparin or low dose unfractionated heparin should be used in combination with mechanical prophylaxis (Level 3)

DVT Prophylaxis

AACP 2008 GUIDELINE

Use both Mechanical Compression Devices and heparin agents

Apply MCD as early as possible (typically upon admission)

Begin heparin agent at 36-48 hours TBI without hemorrhage is not a

contraindication to heparin agent Active bleeding or intracranial hemorrhage

is a contraindication No evidence supporting the use of

prophylactic inferior vena cava filters if heparin agent can be usedAmerican College of Chest Physicians (ACCP, 8th edition, 2008)


Elevate and maintain head of bed > 300, keep neck straight Provide sedation and analgesia Resuscitate with isotonic to hypertonic fluids (NS) Maintain normoxia with PaO2 target of >60 (not hyperoxic)

mmHg Maintain Hgb >8 or higher if intracerebral monitoring indicates Avoid hypotension (SBP < 90mm Hg)/maintain cerebral

perfusion CPP >60mmHg (and <70mmHg) Maintain ICP < 20mmHg Maintain normocapnia with PaCO2 35-45 mmHg Maintain normothermia with temperature goal of 36.5-37.5

degrees Celsius Antiepileptic therapy x 7 days, continue only if seizing NO steroids Early nutritional optimization Normoglycemia

Thank you

Josh DuckworthHolly HinsonGeoffrey LingRomer Geocadin

navaz karanjia, md medical director, neurocritical care program and neuro-icu assistant professor of...

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