traumatic brain injury, icu management, neuro critical care, cerebral protection measaure, BTF guidelines 2007

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.

4. INTRACRANIAL PHYSIOLOGY
AND CEREBRAL
AUTOREGULATION

6. 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)

7. 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.

8. 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.

9. 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

10. 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

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

12. 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

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

14. 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.

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

16. 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

17. BLOOD PRESSURE
AND OXYGENATION
• Blood pressure should be monitored and hypotension
avoided.(SBP<90mmHg)
• Oxygenation should be monitored and hypoxia avoided.
• PaO2 < 60mmHg or O2 saturation <90%

18. ICU MANAGEMENT
Basic ICU management of TBI are :
(A) Management of IC Hypertension
(B) Restoration of extra cranial organ function
Lundberg’s classification of ICH :
Mild ICH  up to 20mmHg
Moderate ICH  21-40mmHg
Severe ICH  > 40mmHg.

19. HYPERVENTILATION &
HYPOCAPNOEA:
Vascular reactivity to CO2 preserved till late, so
Hyperventilation effective in ing CBF, CBV, ICP.
Onset of action within 30 seconds, peak within 8 minutes.
can avert herniation
* Caution : May produce cerebral ischemia, dangerous during
1st phase when CBF is normally low.

20. HYPERVENTILATION &
HYPOCAPNOEA:
PaCO2 < 28mmHg  intense Cerebral. Vasoconstriction 
Cerebral ischemia.
Recommendation :
Controlled hyperventilation with PaCO2= 30-35 mm Hg
Tissue O2 delivery imp.: high FIO2 and haematocrit > 30%
during Hyperventilation recommended.
SaO2 must be > 95%.
SjVO2 monitoring helps to detect ischemia & allows PaCO2
adjustment.

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

22. 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.

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

24. 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

25. 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.

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

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

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

29. 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

30. EXTRACRANIAL
ORGAN FUNCTION
Optimise Haemodynamic Function : Aim
Euvolaemia ; adequate MAP & organ function
 CVP has to be 5-10mmHg & PCWP10-14 mmHg.
 If CVP <5mmHg crystalloid/colloids ;
Blood added when PCV < 30%.
 If CPP  inspite of normal CVP and PCWP, add Ionotrope /
vasopressor

31. FLUID AND
ELECTROLYTE THERAPY
Avoid excessive dehydration
Requirement- 1.5-2.0 ml/kg/hr + loss
If Na >140mEq/L  ½ 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

32. 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

33. 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

34. 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

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

36. The End
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