SEVERE TRAUMATIC BRAIN INJURY :SEVERE TRAUMATIC BRAIN INJURY Dr Vishram Buche NAGPUR. vbuche@rediffmail.com Management Guidelines….


Treatment Modalities for TBI :Treatment Modalities for TBI


Slide 4:M.O.F is less common in children than adults Children with severe head injuries have a lower rate of mass lesions requiring intervention than adults (25 % vs 46%). Even those with low GCS generally survive and achieve social rehabilitation. GCS 3-5, 55% “satisfactory”… (Lieh-Lai, 1992) GCS 3-4, 80% good recovery or moderate disability …(Bruce 1978) FACTS ABOUT TBI IN CHILDREN BLOOD supply to Brain………… Adults and Infants ……50 ml/kg/min Children……………80-100 ml/kg/min


Categorization of Brain Injury :Categorization of Brain Injury Traumatic Brain Injury isolated multi-system injuries Hypoxic-ischemic injury Toxic/metabolic injury BBB Intact Breached


How patients present ……? :How patients present ……? Obvious--motor vehicle accident, car vs pedestrian, fall from height, etc Less obvious--sports injuries (football), delayed deterioration (epidural) Hidden--shaken baby syndrome, older child maltreatment


Slide 7:Types of Injury-Primary Impact: epidural, subdural, contusion, intracerebral hemorrhage, skull # Inertial: concussion. Hypoxic\Ischemic Types of Injury-Secondary Global Decreased CBF due to increased ICP …………results in to Hypoxia and ischemia Local Impairment of CBF due to the presence of injured brain…… …… common in TBI


GCS and Classification Traumatic Brain Injury… :GCS and Classification Traumatic Brain Injury… Mild TBI….13-15 ……… 85% Moderate TBI…9-12……10% Severe TBI…< 8 ………….5% Assess the Level of !!! Consciousness


Mild TBI…..GCS…13-15 :Mild TBI…..GCS…13-15 Absolutely normal on presentation to begin with Relative normal level of consciousness Or had transient change in mental status Or had concussion Or is slightly lethargic and confused but able to communicate and follow commands easily. No anatomical Brain damage …...OBSERVE FOR 24 Hrs


Moderate TBI… GCS …9-12 :Moderate TBI… GCS …9-12 Altered level of consciousness but not comatose Quite lethargic / obtunded & little understanding speech, but can open eyes & localize pain stimuli. NEEDS careful observation to R/O HIE Usually have severe degree of Structural damage, prone to go for severe degree.


Severe TBI…GCS…<8 :Severe TBI…GCS…<8 Comatose !!! OR extremely low level of consciousness …do not open eyes, follow commands, no speech, almost fiaccid or extensor posture AGGRESSIVE MODE OF MANAGEMENT of “3HA” …. 1. Hypotension 2. Hypercarbia 3. Hypoxia & 4. Acidosis


Slide 12:Cerebral Haemodynamics


CPP :CPP Blood pressure gradient across the brain Regulates CBF… autoregulation MAP Calculated by the formula… MAP= Diastolic + 0.4 (Pulse pressure) 5th persentile Lower limit CPP = MAP-ICP Age=70 mm hg + (2 × age in years) Normal: 60 - 80 mmHg Ischemia: 50 - 60 mmHg CBF Ceases Cell Death: < 30 mmHg


Slide 14:Cerebral Perfusion Pressure C E R E B R A L B L O O D F L O W Blood Pressure PaO2 PCO2 Changes in CBF due to PCO2 ,PO2 And CPP The brain has the ability to control its blood supply to match its metabolic requirements Adapted from: Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651


Slide 15:CBF  CO2… Cerebral Blood Flow Vasodilatation … Hyperperfused BRAIN Vasoconstriction ……Ischaemic BRAIN PCO2


Slide 16:CBF  Cerebral Blood Flow Hypoxemia Normoxia Hyperoxia PaO2 Up To 300% O2 1


Slide 17:AUTOREGULATION ZONE Systemic Blood Pressure / MAP Cerebral Autoregulation… 40 140 Cerebral hyperperfusion Ischaemia Cerebral Blood Flow Adapted from: Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651


Slide 18:AUTOREGULATION ZONE AUTOREGULATION ZONE Systemic Blood Pressure / MAP Cerebral DYS-Autoregulation… 40 140 Cerebral hyperperfusion Ischaemia Cerebral Blood Flow Adapted from: Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651 DYS - AUTOREGULATION


Slide 19:HOW ICP RISES........ ???


Slide 20:Mechanism Icp Rise ???


Slide 21:↓SABP Haemorrhage ↓CO Altered vasomotor tone Fluid restriction Dehydration Pharmacologic ↑Metabolism Hypoxia Hypercarbia Pharmacologic Venous Obstuctn Added CSF Why Icp Rises........ ???


Slide 22:↑SABP Pharmacologic Euvolemia Head position Vasopressor Spontaneous ↓Metabolism ↓PCO2 ↑O2 delivery ↓Viscosity CSF drainage ↓Venous Obstuctn How it can be improved…???


Slide 23:Final expectation……..


Slide 24:Management of TBI


ICU Management … :ICU Management … Surgical management Medical management General ICU care Prevent secondary injury Manage intracranial pressure It’s a good idea to manage TBI in association with Neursurgeon & Neurophysian


Initial Evaluation … :Initial Evaluation … Airway- any evidence of trauma, airway protection, attention to c-spine Breathing- chest trauma, aspiration, adequate respiratory effort? Circulation- hypovolemia, hemorrhage, associated injury, myocardial ischemia, “spinal shock” Neurologic assessment


Overview: (principles)Management of TBI :Overview: (principles)Management of TBI Maximize oxygenation (O2 ) Optimize Ventilation (N-CO2 ) Support circulation (SABP…MAP) …Maximize CPP Decrease ICP Decrease cerebral metabolic rate Remember the culprits of ↑ICP …….!!!! 3HA H = hypoxia H = hypotension H = hypercarbia A = acidosis


Caveats in Brain Injury :Caveats in Brain Injury Neurologic examination - the most important information you have Accurate history is often unavailable or inaccurate Potential for associated injuries or illness (cardiovascular, respiratory, c-spine)


Slide 30:↑CPP therapy Patient Flat, HOB ≥ 10 Euvolemia Facilitate ↑ BP Vasopressors PCO2= 35-40 mmHg acutely “Bag” only. Avoid Position… Fluid… SABP… Ventilation… Barbiturate Coma… Traditional and current Therapy… ↓ICP therapy Supine & midline elevate HOB≥ 300 Maintenance ……⅔ Prefers Hypotension antihypertensives Hyperventilation PCO2 = 25-30 mmHg Preffered (Burst Suppression)


Why Normoventilation……? :Why Normoventilation……? Image from: ALL-NET Pediatric Critical Care Textbook www.med.ub.es/All-Net/english/neuropage/protect/vent-5htm Originally adapted from research by Skippen et al. (1997) Critical Care Medicine, 25 CBF pre- hyperventilation CBF post-hyperventilation Airway and Ventilation…… Must when GCS< 8 Eucapnic Ventilation or near lower end of PCO2 NEVER allow HYPOVENTILATION (↑ PCO2…↑CBF… ↑ICP). AVOID therapeutic prolonged hyperventilation, AND Never prophylactic…esp in 1st 24hr… ↓CBF… ↓CPP Brief aggressive Hyperventilate “ACUTE BAGGING” only when acute deterioration / impending Herniation PEEP < 10


EFFECT OF Prolonged Hyperventilation on ICP :EFFECT OF Prolonged Hyperventilation on ICP ICP CBV PCO2 Muizelaar JP, vondre Poel Hget al: Pial art vessel diameter and CO2 reactivity during prolonged hyperventilation. J Neurosurge 69:923, 1988 Shepherd S. 2004. "Head Trauma." Emedicine.com.


Research Supporting Normoventilation :Research Supporting Normoventilation Muizelaar et al. (1991) Journal of Neurosurgery, 75(5) Marion et al. (1995) New Horizons, 3(3) McLaughlin & Marion (1996) Journal of Neurosurgery, 85(5) Newell et al. (1996) Neurosurgery, 39(1) Skippen et al. (1997) Critical Care Medicine, 25(8) Yundt & Diringer (1997) Critical Care Clinics, 13(1) Forbes et al. (1998) Journal of Neurosurgery, 88(3) Research Supporting Normoventilation Recommendations …… Eucapnic ventilation Never Hypoventilate Never give prophylactic / prolonged Hyperventilation “ACUTE BAGGING”


Slide 34:THE UNCUS WAS PUSHED THROUGH THE TENT THE OCCULOMOTOR BENT PUPIL ON THAT SIDE CONS. THE OTHER ONE FOLLOWED AND HE WAS CREMATED Indication of HYPERVENTILATION…!!!!


Circulatory Support to maintain Adequate CPP ….. :Circulatory Support to maintain Adequate CPP ….. Maintain…. Euvolemia…… AVOID Fluid restriction SYSTEMIC BLOOD PRESSURE….MAP… CPP Facilitate Blood Pressure… ↑SABP…↑MAP…↑CPP…↓ICP Vasopressors rARELY USED. BLOOD TRANSFUSION may be required Remember the cause of HYPOTENSION….. Hemorrhage Altered vasomotor tone Decreased CO Fluid restriction


Diuretic Therapy :Diuretic Therapy Osmotic Diuretic Mannitol (0.25-1 gm / kg) bolus, repeat 6-8 hrs Maintain serum Osmolarity < 320 and Euvolemia Mechanism:  blood viscosity via vasoconstriction. Need intact autoregulation. (Lasts 1H) 2. Osmotic effect. Need intact BBB (6 H) Less effective if ……CPP is < 70 and Initial increase in blood volume, BP and ICP followed by decrease Have better effect along with Loop-diuretic..Furosemide ↓ ICP ↑CPP………


Hypertonic Fluid Administration… :Hypertonic Fluid Administration… Hypertonic saline is effective for control of increased ICP after TBI Effective doses: cont. infusion of 3% saline 0.1 - 1.0 ml/kg/h, Titrate the dose Goal : minimum dose maintain ICP <20 mmHg. Reduction in mean ICP in children 2 hours after bolus administration of 3% saline Little or NO continued benefit after 72 hours of treatment Fisher et al. (1992) Journal of Neurosurgical Anesthesiology, 4 Qureshi et al. (1998) Critical Care Medicine, 26(3)


Reduction of Cerebral Metabolic Rate :Reduction of Cerebral Metabolic Rate Goal: Reduce cerebral oxygen requirement BARBITURATE COMA , Pentobarbital ?? Adverse effects include hypotension, myocardial depression and bone marrow dysfunction Used only after unsuccessful attempts to control ICP and maximize CPP with other therapies i.e. Refractory ICP Improved outcome not fully supported by research Traeger et al. (1983) Critical Care Medicine, 11 Ward et al. (1985) Journal of Neurosurgery, 62(3) ANTICONVULASANTS… Prophylactic anti-seizure therapy may be considered as a treatment option to prevent early PTS in young pediatric patients and infants at high risk for seizures following head injury. Recommended with great caution


Reduction of Cerebral Metabolic Rate: By Hypothermia :Reduction of Cerebral Metabolic Rate: By Hypothermia NO PEDIATRIC STUDIES Stroids… not indicated at any point of management


Is hyperglycemia detrimental? :Is hyperglycemia detrimental? Source: Rogers (1996) Textbook of Pediatric Intensive Care pp.702-704 Is hyperglycemia detrimental……? Avoid HYPERGLYCEMIA in early hours Associated with LACTIC ACIDOSIS and more Cellular damage. Initial IV fluid without dextrose


Summary of Recommended Practices…… :Summary of Recommended Practices…… Serial neurologic assessments Identify and treat primary brain injury Rule out neurosurgical emergency Minimize secondary ischemic brain injury by promoting CPP and ↓ ICP Maintain normovolemia and adequate BP/ CPP Maintain normocapnia, have NORMOVENTILATION and adequate oxygenation Maintain normal electrolytes and euglycemia Avoid factors that increase ICP Treat intracranial hypertension


Slide 43:Free at www.pccmjournal.com


Slide 44:GCS<8 Insert ICP Monitor Maintain CPP (Age Appropriate) ICP Sedation & Analgesia HOB@300 ICP Drain CSF if Ventriculostomy is present ICP Neuromuscular Blockade ICP Mannitol PRN HTS 3% Mild Hyperventilation PaCO2 30-35 mm Hg May continue if S. Osm<360 May continue if S. Osm<320 ICP Second Tier Therapy Consider repeating CT Carefully withdraw ICP treatment NO NO NO Surgery Indicated First tier therapy….


Slide 45:Second Tier Therapy  ICP despite first tier Rx Evidence of Hyperemia ? No Evidence of Ischemia Evidence of Ischemia? No evidence of contraindication to Hypothermia? Consider moderate hypothermia Working Ventriculostomy Consider lumbar drain Active EEG? No contraindication to Barb Consider high dose Barb Salvageable patient Consider decompressive craniectomy Hyperventilation ??


Ways of ICP monitoring……. :Ways of ICP monitoring…….


Learning Point……… :Learning Point……… Always monitor ICP whenever possible, otherwise monitor SABP…MAP…CPP. Keeping CPP (MAP) at higher end and to maintain this one may have to accept higher end of ICP. Higher the CPP (MAP) better outcome. Commonest cause of morbidity and mortality is cerebral ischemia


Slide 48:THANKS Its True That Every Effort Is Not Converted Into Success, But Its Equally True That Success Does Not Come Without Efforts


Slide 49:Endocrine CEREBRAL SALT-WASTING ANP-like substance released from brain, inducing natriuresis and diuresis SIADH Elevated level of ADH inappropriate for prevailing osmotic or volume stimuli Hyponatremia, hypo-osmolality, urine osm > plasma osm, high urine Na Treatment is water restriction


Severe TBI :Severe TBI Indications for Intubation GCS< 8 Fall in GCS of 3 Unequal pupils Inadequate respiratory effort or significant lung/chest injury Loss of gag apnea


Intubation of the Patient With Brain Injury :Intubation of the Patient With Brain Injury Considerations: Increased intracranial pressure Cardiorespiratory instability Cervical spine status may be unknown Unknown, traumatized airway Aspiration risk Unknown medical history


Intubation of the patient with Brain Injury--How to... :Intubation of the patient with Brain Injury--How to... Rapid Sequence Orotracheal Intubation Axial stabilization if C-spine in question Pre-oxygenation with 100% O2 Induction: thiopental, etomidate, benzo Consider Fentanyl, Lidocaine, defasciculation Neuromuscular blockade Intubation