Intracranial pressure[ICP] and its significance –
Definition– intracranial pressure by convention means supratentorial CSF pressure measured in the lateral ventricles or over cerebral cortex.
Normal range- 8-12 mm of Hg.
Cranial vault is rigid structure with fixed total volume-
1.brain -80%
2.blood -12%
3.CSF – 8% [increase in any component increases ICP].
INTRACRANIAL COMPLIANCE
-Change in intracranial pressure in response to change in intracranial volume.
Cerebrospinal fluid- In brain volume 100-150 ml.
Formed @ of 0.3 to 0.4 ml /min,21 ml /hr;500 ml /day.
CSF PATHWAY–
Primarily formed in choroid plexus of cerebral ventricles.
Lateral Ventrcles
Csf-isotonic[active secretion of na]
Absorbed in arachnoid granulations over the cerebral hemisphere.
Absorption is directly proportional to ICP and inversely proportional to cerebral venous pressure.
No lymphatics in brain and spinal cord;only CSF absorption is principle means by which perivascular inerstitial proteins returned to blood.
Increase in BRAIN /CSF/BLOOD can cause increase in intracranial pressure which leads to decrease in cerebral perfusion pressure.[CPP]
Cerebral perfusion pressure= MAP-ICP;[MAP=mean arterialpressure]
Signs and symptoms of raised ICP
Headache,nausea,vomiting and mental changes,disturbances in consciousness.[mostly present in early morning hrs becoz during sleep increase in PaCO2 causes increase in CBF leade to increase in ICP.]
Fatigue,drowsiness
Papilloedema
Systolic BP increases to compensate Increase in ICP.
Local compression of tissue by mass leads to symptoms determined by area of brain involved .e.g. Frontal cortex-mental and behaviourale symptoms.
Causes of raised ICP–
1.Tumors-Direct compression,edema of tissues and obstruction to CSF are the mechanism of increase ICP.
2.intracranial hematoma
3.intracranial infection
4.Aqueductal stenosis
5.benign intracranial hypertension
6.normal pressure hydrocephalus
Increase ICP causes herniation of brain tissues.
1.Subfalcine herniation- Cingulate gyrus under the falx.-compression ofant. Cerebral artery –midline shift on CT.
2.Trastentorial herniation- Tentorium cerebella.-Brainstem compression in rostral to caudal.
Altered consciousness ,defect in gaze,afferent ocular reflexes,Haemodynamic and respiratory instability.
Uncal herniation- Ipsilateral occulomotor dysfunction ,papillary dilation ,ptosis and lateral deviation of affected eye.
3.Through Foramen magnum-cerebellar tonsils.
Cardiorespiratory instability and death.
4.Herniation of brain content thrigu traumatic defect in cranial cavity.
Monitoring of ICP–
Indications-
1. Severe traumatic brain injury.
2.Intracranial haemorrhage
3.post –craniotomy cerebral edema
4.space occupying lesion-SOL
5.Haematoma,tumour ,abcess.
6.Reyes syndrome
7.abnormal response to noxious stimuli
8.encephalopathy
9.meningitis.
Contraindications-
CNS infection.
Coagulation defect
Anticoagulant therapy
Scalp infection
Midline shift
Cerebral edema.
ICP monitoring devices-
1.ventriculostomy catheter
2.fiberoptic [interparenchymal]catheter
3.subarachnoid
4.epidural transduser
ICP- Normal range= 0-10 mm of Hg
Above 15 m of Hg –abnormal
20 mm of Hg = moderately elevated.
40 mm of Hg =severely increased.
ICP waves- characteristics-
1. pulsatile with two different frequencies
2.synchronus with arterial pulse
3.slower in time with breathing.
Wave-P1- percussion wave
P2- tidal wave
P3- dichrotic wave
Lundberg described three types of wave amplitudes and significance.
A wave- severely decreased intracranial compliance.[ICP > 50 mm of Hg]
B wave- oscillatory waves –less adverse than A,
Rhythmic oscillations every one to two min in which mean intracranial pressure increases in crescendo manner from a variable baseline to level of 20-30 mm of Hg and then falls rapidly
Cwave-little importance .
Interpretation
1.Trends are more important than isolated readings.
2.indiacate intracranial compliance
3.changes in amplitude can allow prediction of clinical deterioration.
Noninvasive monitoring-
1.USG
2.MRI.
Methods to decrease ICP
1.Posture–
A. For optimal venous drainage –Head elevation 30 degree
B.Avoid extreme flexion or extension
2. Hyperventilation-
Decrease in paCo2
Decrease cerebral blood flow
Decreases ICP.
This mesure is applicable for 6-12 hrs.
3.Draining CSF-
A.Lumbar catheter
B.V-P shunt /V-R shunt[ventriculo-rt.atrial shunt]
4.Hyperosmotic drugs–
They increases osmolarity ,draws water from tissues and decreases edema.
e.g.1. Mannitol 0.25 -0.5 gm /kg given before dura opening over 20 -30 min .max.effect for 1-2 hrs
- Loop diuretics- useful when there is raised intravascular volume and pulmonary edema.
3.corticosteroids- mechanism unknown,but causes stabilaisation of capillary membrane and decrease production of CSF.
Not useful in closed head injuries.
Mainly useful in edema becoz of vasogenic origin around tumours.
5.Barbiturates– decreases ICP