CONTENTS
1)Pathophysiology of Brain Injury
2)Autoregulation and CPP
3)CMRO2 & CBF
4)CBF VS CO2 and O2
5)Monro- Kelly Doctrine
6)Effect of various ICP Values
7)Brain Ischaemia-cellular level
8)Cerebral Protection


Pathophysiology of Brain Injury
1.Primary Brain Damage
Irriversible damage
2 types;
-Focal-Direct impact of skull into brain causing contusion, laceration, or hemorrage.
-Difuse-Difused axonal injury due to internal shearing, streaching tearing forces


2. Secondary Brain Damage
Factors that causing ischaemia and further brain damage.

Potentially reversible-role of cerebral protect

-Hypoxia
-Hypotension
-Hypercarbia
-Cerebral edema-cytotoxic/vasogenic
-Herniation


Autoregulation and CPP
-CBF is maintained by autoregulation
-Between MAP 65-160mmHg, below 50 is critical
-MAP>140mmHg; autoregulatory breakthrough a/w ­ in CBF wh. disrupts BBB resulting in cerebral oedema
-Chronic HPT shifts the curve to the right
-Aim is to maintained CPP
-Abolished by; (CBF = MAP)
eg. Severe Brain Injuries-ischaemia, edema,tumor
Deep anaesthesia, hypo/hypertension
Circulatory arrest,seisure disorder
Arterial hypoxaemia,hypercarbia
-Normal CPP 70-80 mmHg
-Critical level for Cerebral Ischaemia 30-40mmHg
-Cushing Reflex- is compensatory mechanism to maintain CPP

CMRO2 & CBF
-Brain Metabolism depend on O2 delivery
-Glucose is the main substrate
-Normal CMRO2 is 3.5ml/100ml/min
-CMRO2 reflect global C. metabolism
-Increase CMRO2 will increase CBF and CO2 production (theory of autoregulation)

CMRO2= CBF x A-V O2 content diff(Fick’s)

-CMRO2 increase in…
Symp. Stimulation
Hyperthermia
Seizure
Increase in Cerebral function

-CMRO2 decrease in…
coma

CBF VS CO2 and O2

-CO2 is potent Cerebral Vasodilator
-Linear relationship; Drop of 10mmHg PaCO2 reduces CBF by 30%
-In normal circumstances, PaCO2 is the primary CBF determinant.
-Brain injury-hypercapnia leads to Reverse Steal syndrome;Diversion CBF from damaged area to healthy area
-Very little change in CBF in normal PaO2
-With the onset of hypoxaemia (PaO2 < 60mmHg), there is prompt increase in CBF in order to maintain O2 delivery constant
-Hypoxia PaO2 < 50mmHg –Cerebral Vasodialation
-Hyperoxia PaO2 > 600mmHg –Cerebral Vasoconstriction

Monro- Kelly Doctrine
The intracranial Volume is fixed apart from some minimal ‘give’ due to meninges and foremina
60% fliuds; 40% solid
All the structures are incompressible for practical purpose
Increase in the volume one of the compartment must be buffered by others( spartial compensation)
Later-Increase in volume within cranium lead to rapid increase in pressure(elastance)
Raise ICP---reduce CPP
Reduce CPP---Cerebral iscaemia---Infaction ---Brain death

Effect of various ICP Values

Neurological Sx;
ICP Benign > 40 mmHg-No Sx
Acute <> 25 for 15 min- req. tx.
> 40 for 15 min-Severe IC-HPT
Marshal et al

Coning
Temporal (Tentorial)-ipsilat 3rd N palsy,reduce GCS,Ch. Reflx , decerebrate rigidity ? ICP.
Cerebellar(medullary) –Cheyne Stokes breathing, apnea ? ICP.

Cerebral Protection
-Methods attemp to reduce the effects of Cerebral Iscaemia and damage, in order to improve neurological out comes
-Protective measures before the second insults
-Possible neuronal recovery after period of ischaemia Brain must be ‘protected’ from such insult- Hossman KA 1973

Strategies;
1.Maintained adequate O2 supply-CPP & PaO2
2.Reduce/prevent raise in ICP
3.Reduce CMRO2
4.Reducing cell damage

Indications…
1.Post successful CPR
2.Post carotid Cerebral Protection artery surgery
3.Head injury
4.Compression - Tumour,hematoma
eg : Subdural Hematoma/Intraparenchymal.
5.Inflammatory – Meningitis.
6.Metabolic encephalopathies eg : Reyes Syndrome.
7.CVA / Cerebral haemorrhage
8.Post op

The Principles Of Management
1. Position
- neutral position
- head elevate to 30°c to 45°c.

2. Observation
- vital sign, GCS and pupillary changes.

3. Maintaining O2 / Ventilation
- hyperventilate ~ keep PCO2 30 – 35mmHg
- maintain Pa2O2 100mmHg with low PEEP

4. Control Blood Pressure
- maintain MAP ~ 70 – 100mmHg
- maintain adequate cerebral perfusion pressure (CPP)
CPP = MAP - ICP

5. Diuretics
- osmotic diuretic ( Mannitol 20% )
- loop diuretic ( Frusemide )

6. Fluid Therapy
- control fluid therapy ~ avoid hypovolumia
- use Normal Saline or Hartmann

7. Prevent Isometric Exercise
- eg: give IV Fentanyl before suctioning or any procedure

8. Steroids eg. Dexamethasone
- for brain tumour
- reduce cerebral oedema

9. Treatment Of Epilepsy
eg. Diazepam or Phenytoin
- control seizures to reduce cerebral metabolic rate

10. Temperature Control
- maintain normothermia and avoid hyperpyrexia

11. Calcium Antagonist ( Nimodipime )
- for subarachnoid haemorrhage to reduce cerebral spasm

12. Surgery
- to remove mass or lession
eg. Craniotomy,evacuation of clot,CSF drainage.

13. Nutrition
- early enteral feeding ~ high nutrient and protein
( to prevent infection )

14. Electrolytes
- regular monitoring of electrolytes,urea,creatinine,blood sugar,
osmolality are important to determine fluid and electrolyte
therapy.

Maintain CPP & O2 supply

-Subject to CPP=MAP-ICP and O2 Content
-AIMs; Maintain normotension,
-Keep CVP 5-10 cm H2O
-Reduce ICP-Head up 15-30 deg. with neutral position
Consider inotropes
-No PEEP
-Hypotension & hypoxia significantly increase mortality and morbidity
-Hypotension profoundly increase mortality up to 150%
-Randall M. Chesnut. Jounal of Trauma.Vol 34, 1993
-Nimodipine in SAH
-Haemodilution, hypervol, HPT in SAH

Reduce @ preventing Rise in ICP
-Reduce cerebral edema/ICF
Ie Mannitol, frusemide
Fluid restriction 2/3 maintenance
-IPPV /hyperventilation;Aim To maintain pCO2
between 30-35mmHg to prevent
hypercapnia(Cereb.Steal Synd)
ICP reduces by 30% per 10mmHg reduction
in CO2
-Prevention hypoxia-cytotoxic cerebral edema
-Acute change in hyperventilation return to normal value after 48H, normalise CSF pH and compensatory to CSF volume

Reduce @ preventing Rise in ICP

-Surgical decompression ie craniectomy
-Normothemia/hypothermia at 35 C
-Reduce CMRO2
-CSF Drainage-via ventriculostomy catheter
-Encourage venous drainage-head at 15-30 deg & neutral position
-Steroids ie Dexa.@ M.Pred.; mean for vasogenic
edema ie tumor & abscess situation
hyperglycaemia- to start insulin

Reduce CMRO2
-Normothermia
@Hypothermia
-Barbiturate/sedation
-Anticonvulsion ie phenytoin
-Muscle relaxants-avoid pancuronium, sux
-Adequate Analgesia

Reduce cell damage
-Avoidance of hyperglycaemia
-Ca2+ channel blocker-nimodipine
-Free radical scavanger ie barbiturate,Vit C,E
-Glutamate and NMDA receptor antagonist

Thought to increase ischaemia resulting cell damage

Maintaining other organ functions

Monitoring
-Haemodynamic; CVP,MAP, CPP
-Haematological ; PCV 35-40
-Oxygenation; Above 60mmHg
-Ventilation ; CO2 30-35mmHg
-Temperature; 35 C
-BUSE, Sr. Osmolarity; SIADH/D Insipidus
-Urine SG, Osmolarity, Na+
-I/O chart
-ICP; keep less than 20mmHg
-EEG-2 parietal electrodes ;reflex global Cerebral perfusion
-Other organ function