Head injury

1. HEAD INJURY: ICU MANAGEMENT AND MEANS OF CEREBRAL PROTECTION

2. INTRODUCTION TRAUMATIC BRAIN INJURY: Is a non degenerative, non congenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical and psychosocial functions, with an associated diminished or altered state of consciousness.

3. INTRACRANIAL PHYSIOLOGY AND CEREBRAL AUTOREGULATION

4. PATHOPHYSIOLOGY OF TBI Primary Injury (Brain damage at impact) Minor Concussion Diffuse Axonal Injury Brain Stem dysfunction. Followed by series of secondary events : (i) Focal hematoma / contusion (ii)Changes in CBF & CMRO2 (iii) ICP (iv) Biochemical changes at Cellular level Secondary Brain Injury (hours to days)

5. CBF AND CMRO2 CHANGES IN TBI Phase 1: Initial ischemic phase(6-12hrs) responsible for early mortality. Phase 2: Hyperemic phase(24-72 hrs.) CBF-CMRO2 uncoupling occurs. Phase 3: Delayed ischemic phase(20days) progressive hypo perfusion due to vasospasm delayed mortality. Phase 4: Recovery phase - CBF returns to normal. Both ischemia and hyperemia are associated with poor outcome. Ischemia neuronal death directly Hyperemia ICP Brain herniation's (Uncal , Tentorial , FM) with respiratory & vasomotor paralysis.

6. CEREBRAL AUTOREGULATION Normal limits of Cerebral Auto regulation: 50-150mm Hg Lower limit following TBI. So higher CPP required to protect neurons from ischemic insults like Hypotension. Recent studies recommend CPP 60-70mmHg. Pressure AR is abolished in severe TBI. But Vascular response to CO2 preserved till late & its abolition indicates bad prognosis.

7. CHANGES IN ICP ICP documented in 50-70% cases. Causes : Mass lesion (EDH, SDH, ICH ; Contusion) Cerebral hyperemia Cerebral edema ( vasogenic & cytotoxic) Hydrocephalus Uncontrolled ICH perfusion Ischemia Brain Swelling Brain herniation

8. CELLULAR EVENTS Ischaemia Biochemical events Neuronal death Mediators of Cellular cascade are : Calcium EAA ( aspartate & glutamate) Free radical (SO dismutase, H2O2, OH) Cerebral Lacto-acidosis Ionic fluxes of K+ & Mg++ Inflammatory mediators- Cytokines

9. CELLULAR EVENTS Massive Sympathetic discharge occur after TBI Sympathetic flow Impact on CVS Hypertension , Tachycardia Myocardial ischaemia & Neurogenic Pulmonary oedema. Coagulation defects

10. CLINICAL GRADING GCS Mild : 13-15 Moderate: 9-12 Severe : 8 Mortality in severe TBI is 20-25% even in neurological centers of excellence. Intensive care needed to secondary insult

11. ICU MANAGEMENT Aim is to : 1. Optimize O2 & substrate delivery 2. Detect harmful events. ICU management include : Intensive monitoring & Intensive therapy

12. ICU MONITORING 1. Clinical Neurological Assessment & serial CT 2. CVS monitoring (HR, ECG, NIBP/IBP, CVP, PCWP) 3. Respiratory : SpO2 , EtCO2, ABG, Serial chest X-ray 4. ICP monitoring 5. Jugular venous O2 saturation & ABG 6. Trans cranial Doppler monitoring 7. Evoked potential monitoring 8. Core Temp. monitoring 9. Metabolic monitoring with PET, Br. Micro dialysis. 10. Fluid intake /output, Sr. electrolytes, Glucose, BUN etc.

13. CLINICAL MONITORING Parameters need to be monitored are : 1. Level of Consciousness by GCS 2. Cranial nerve function 3. Dolls eye movement 4. Vestibulo-ocular response

14. INTENSIVE THERAPY Aim is to achieve optimum cerebral perfusion and prevent secondary ischaemic insults: CPP = MAP ICP (Ideally 60-70 mmHg) ing MAP : volume expansion , ionotropes & vasopressor ing ICP : head-up position, hyperventilation , diuretics , CNS depressants, drainage of CSF

15. BLOOD PRESSURE AND OXYGENATION Blood pressure should be monitored and hypotension avoided.(SBP 30% during Hyperventilation recommended. SaO2 must be > 95%. SjVO2 monitoring helps to detect ischemia & allows PaCO2 adjustment.

19. HYPEROSMOLAR THERAPY : Mannitol: 0.25-1gm/kg Osm. diuresis. blood viscosity, microcirculation & CPP. Side effects : ReboundICP when BBB disrupted , Fluid overload , Dilutional hyponatraemia serum osmolality >320mos/kg Renal Failure Repeated doses may lead to tachyphylaxis

20. HYPEROSMOLAR THERAPY Loop diuretics: Frusemide s brain water content s CSF production Can be used alone : Dose- 0.5- 1mg/ kg Can be used with Mannitol : 0.15- 0.3mg/kg Synergistic action & prolongs action of mannitol.

21. HYPEROSMOLAR THERAPY Hypertonic saline: (7.5%) another options. Recent report shows 23.4% effective in ICH refractory to mannitol.

22. SEDATION Necessary to avoid further ICP. Barbiturate less commonly used (only in refractory cases). Propofol (200 gm/kg/min) commonly used due to better pharmaco kinetic profile BUT may cause hypotension CPP, Ischemia Midazolam is a better option: CMRO2, CBF & CBV keeping CAR intact

23. CEREBRAL METABOLIC SUPRESSION IV anaesthetics- Barbiturates CMRO2 by 40%, Potent cerebral vasoconstrictor CBF,CBV,ICP Free radical scavenger. Loading dose- 10mg/kg given over 30 mins 5mg/kg/hr during next 3hrs. Maintained with 1mg/kg/hr.

24. ANTI- EPILEPTIC THERAPY TBI pts develop early seizure. Incidence is 42% in penetrating injury. Prophylactic ACT is a must for better prognosis.

25. NEURO PROTECTIVE MEASURES Mild- Moderate hypothermia (33-36C) Ca channel blockers eg. Nimodipine EAA antagonists ? (NMDA rec.antg-MK801)

26. STEROIDS No role in ICP control in TBI; rather hazardous as they induce hyperglycaemia.

27. OTHER MEASURES CSF drainage by intraventricular catheter in situ s ICP & helps monitoring. Complications: Hemorrhage and Infections. General measures : of Head 15-30 + Neutral position for good venous drainage Euvolaemia to maintain MAP & CPP

28. EXTRACRANIAL ORGAN FUNCTION Optimise Haemodynamic Function : Aim Euvolaemia ; adequate MAP & organ function CVP has to be 5-10mmHg & PCWP10-14 mmHg. If CVP 140mEq/L Normal saline If Na < 140 mEq/L Isotonic saline K loss due to Diuretic replace Specific syndromes ( DI, SIADH, CSW) diagnose & treat properly. Hyperglycaemia control of Bl. glucose

30. NUTRITIONAL SUPPORT TBI patients have high nutritional need. Feeding should be started within 24 hrs. Replace 140% resting metabolic expenditure with 15% of calories supply as Protein by post-trauma day 7. Encourage enteral feeding along with prokinetic agents. TPN if enteral feeding not possible

31. DVT PROPHYLAXIS (a) Low dose heparin (5000U, Subcutaneous) (b) Pneumatic Compression boot Start ACT within 24 hrs if coagulation profile normal & CT shows hemorrhage stabilized If ACT contraindicated Venacaval filter

32. CONTROL OF INFECTION Patients with severe TBI suffer from infections - Chest, UTI, Generalized septicemia, Sinusitis etc. Control of infections with proper antibiotics after C/S testing. General nursing care and hygiene has to be maintained for prevention of bed sore

33. REFERENCES Millers 8th deition Brain Trauma Foundation guidelines 2007 Recent advances in principles of neuro-critical care

34. The End THANK YOU

Head injury

Health & Medicine

icu monitoring

tbi phase

icp icp

metabolic monitoring

severe tbi

clinical monitoring

cvs monitoring hr

evoked potential monitoring