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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
Disclosure information
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
Severe TBI: Clinical Practice Guidelines
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
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)
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 Oxygenation: Hemoglobin
Cerebral Oxygenation: Hemoglobin
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)
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
Cerebral Perfusion: Blood Pressure/CPP
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
Cerebral Perfusion: Blood Pressure/CPP
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.
Cerebral Perfusion: Blood Pressure/CPP
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.
Cerebral Perfusion: Blood Pressure/CPP
CPP = MAP - ICP
CBF = CPP/CVR
CD02 = CBF x Ca02
Cerebral Perfusion: Blood Pressure
Aerobic anaerobic metabolism energy failure, dying in 4 min
Cerebral Perfusion: Blood Pressure
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
Cerebral Perfusion: Blood Pressure
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.
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
Cerebral Perfusion: ICPCompartment Approach
Brain parenchyma Osmotherapy (mannitol, hypertonic saline) Steroids only if appropriate (tumor, HACE, some infections) Surgery (hemicrani, SOC)
Cytotoxic Vasogenic
Stroke TumorAbscess
Cerebral Perfusion: ICPOsmotherapy
Brain parenchyma Osmotherapy (mannitol, hypertonic saline) Steroids only if appropriate (tumor, HACE, some infections) Surgery (hemicrani, SOC)
Sodium=0.97 Mannitol=0.9
Glycerol=0.5 Urea=0.6
Reflection Coefficient
Cerebral Perfusion: ICPOsmotherapy
Brain parenchyma Osmotherapy (mannitol, hypertonic saline) Steroids only if appropriate (tumor, HACE, some infections) Surgery (hemicrani, SOC)
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
Cerebral Perfusion: ICPOsmotherapy
Brain parenchyma Osmotherapy (mannitol, hypertonic saline) Steroids only if appropriate (tumor, HACE, some infections) Surgery (hemicrani, SOC)
Cerebral Perfusion: ICPOsmotherapy
Brain parenchyma Osmotherapy (mannitol, hypertonic saline) Steroids only if appropriate (tumor, HACE, some infections) Surgery (hemicrani, SOC)
Create a GRADIENT,
DON’T
dehydrate your patient!
Cerebral Perfusion: ICPOsmotherapy
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
Cerebral Perfusion: ICPOsmotherapy
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
Cerebral Perfusion: ICPOsmotherapy
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)
Cerebral Perfusion: ICPOsmotherapy
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
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
Cerebral Perfusion: ICPCompartment Approach
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)
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
Cerebral metabolism: thermoregulatory management
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)
Cerebral metabolism: thermoregulatory management
Normothermia in TBI:
Fever is associated with significantly worse outcomes
Li, J et al. J Neurotrauma. 2012 January 1; 29(1): 96–100
Cerebral metabolism: thermoregulatory management
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.
Cerebral metabolism: thermoregulatory management
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
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
Cerebral metabolism: seizure management
Physiologic Changes--compensated
Cerebral metabolism: seizure management
Physiologic Changes--decompensated Cerebral
Failure of autoregulationHypoxiaHypoglycemiaDecreased lactateIncreased ICPCerebral edema
Metabolic
HypoglycemiaHyponatremiaHypo/HyperkalemiaAcidosisHepatic/Renal dysfunctionDICRhabdomyolysisSerum/CSFleukocytosis
Autonomic
HypoxiaDecreased blood pressureFalling COPulmonary edemaCHFArrythmiasHyperpyrexia
Cerebral metabolism: seizure management
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
Cerebral metabolism: seizure management
Vespa et al Crit Care Med 2007
Increase in ICP in TBI patients
Cerebral metabolism: seizure management
MRI after seizure
Cerebral metabolism: seizure management
2012 Neurocritical Care Society Guidelines for Treatment of Status Epilepticus: Indications for Continuous EEG Monitoring
Cerebral metabolism: seizure management
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)
Severe TBI: Clinical Practice Guidelines
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