Intracranial Pressure

Intracranial PressureSusunan saraf pusat terdiri dari: Otak (otak besar dan otak kecil) Batang otak (terdiri atas mesensefalon, pons dan medula oblongata) Medula spinalis terletak di kanalis vertebralis

Peredaran darah otakOtak mendapat darah dari arteri vertebralis dan arteri karotis interna. Arteri vertebralis adalah cabang dari arteri subklavia yang masuk rongga tengkorak melalui foremen oksipitale magnum. Kedua arteri vertebralis kanan dan kiri berjalan di permukaan ventral medula oblongata dan pada batas kaudal pons kedua arteri bersatu membentuk arteri basilaris. Arteri karotis interna setelah masuk rongga tengkorak akan memberi cabang yaitu arteri serebri anterior, arteri serebri media, arteri komunikans posterior, arteri khoroidea, arteri hipofise superior dan arteri hipofise inferior.

Peredaran darah venaSistim vena sentral terdiri atas: Aliran vena serebral eksternal atau superfisial Aliran vena serebral internal atau profunda

Kedua sistim vena ini mengalirkan darah kedalam sinus venosus. Anastomose banyak terjadi antara dua kelompok ini melalui anyaman pembuluh didalam substansi otak. Dari sinus venosus melalui vena emisries darah balik ini diteruskan ke vena ekstrakranial.

The contents of the intracranial cavity1: The brain about 1400 ml.2: The blood 75-100 ml.3: The CSF 75-100 ml. Otak, volume darah dan cairan serebrospinalis di dalam kranium pada setiap saat harus relatif konstan (hipotesa Monro-Kellie).

CSF Obstruction to the flow of CSF at any point, results in dilatation of the venticular system proximal to the obstruction with profound effect on intracranial pressure.8Indications for Access & contraindications CSF analysis: Bacteriological, Immunological , Cytology,2. Measuring CSF pressure in cases of pseudotumor cerebri, and normal pressure hydrocephalus.3. The administration of antimicrobial and antineoplastic agents normally excluded by the BBB.4. Therapeutic CSF drainage. in cases of CSF fistula, pseudotumor cerebri or communicating hydrocephalus.

Methods of access Contraindications Lumbar puncture * Local inf.2. Cisternal puncture. * high ICP. Due to SOL3. Ventricular puncture. * Blood dyscrasias. Anticoaggualnt therapy. 9C.B.FBV= 75 mlI.C.VP= ICPCBF: 50ml/100gm/minCPP=CrAP- VP(ICP)CBF= CPP/ CVR CrAP-(VP) ICPCBF=-------------------- CVR

10Cerebral Autoregulation

11Brain Volume An increase in brain volume is produced either by a: S.O.L Edema: increase in brain water.1. Vasogenic edema: extra cellular, disturbance of BBB. localized around tumors, abscesses, hemorrhages and localized cerebral contusions. It may lead to herniation.2. Cytotoxic edema: intracellular, hypoxia (cardiac arrest), Intoxication, sever hypothermia. It is usually generalized.3. Osmotic edema: ECF, Abnormal ADH sec. Sever hemodialysis, or excessive ingestion of water (Hysterical).4. Hydrostatic Edema: ECF due to acute hypertension.12

13Elastance and Compliance Compliance: Is that quality of distensibility available within the intracranial contents, which enable them to adapt to an expanding IC lesion. Elastance: Is the resistance offered by the intracranial contents to the expansion of an intracranial mass. It is the inverse of compliance Compliance is decreased by increased by: 1. Hypercarbia. Hypocarbia. 2. Hypoxia. Hyperoxia (PaO2 >1000 mm Hg) 3. Sleep. Hypothermia. 4. Anesthesia. Barbiturates.14Bila terjadi kenaikan yang relatif kecil dari volume otak, keadaan initidak akan cepat menyebabkan tekanan tinggi intrakranial. Sebabvolume yang meninggi ini dapat dikompensasi dengan memindahkan cairan serebrospinalis dari ronga tengkorak ke kanalis spinalis dandisamping itu volume darah intrakranial akan menurun oleh karenaBerkurangnya peregangan durameter. Hubungan antara tekanan danvolume ini dikenal dengan complience. Jika otak, darah dan cairanserebrospinalis volumenya terus menerus meninggi, maka mekanismepenyesuaian ini akan gagal dan terjadilah tekanan tinggi intrakranial(Adams RD, Youmans JR).

Intracranial Compensation

Intracranial pressure measurement Normal I.C.P. this is 50-200 mm. water (10 mm Hg.) it is pulsatile owing mainly to I.C. arterial pulsation. It also shows fluctuations reflecting the respiratory and cardiac cycles.Measurement1. L.P: with the patient on his side, the L.P. needle is connected to a manometer. This method is not accurate, can not be used for monitoring and can be dangerous.2. Ventricular cannulation: It is more accurate, can be used for long periods, but may be complicated by infection.3. Subdural sensor { These are the safest and most reliable, and4. Extradural sensor{ and are usually used for monitoring.17Effects of increased ICP A: Effects on vital signs: These appear to be due to compression and distortion of the brain stem. These effects are noticed in patients with critically raised intracranial pressure, and in experimental animals.1. Decrease in respiratory rate.2. Bradycardia.3. Cardiac arrhythmias.4. Pupillary constriction, followed by unilateral pupillary dilatation5. Increase in pulse pressure.6. Increase in arterial blood pressure.18 B: Effect on cerebral blood flow: CAP - JVP (ICP) CBF = -------------------- CVRWhen ICP increases, cerebral blood flow remains constant by auto regulation. the efficiency of this compensation depends on the rate of expansion of the lesion, it's nature and site. And also on the compliance of the intracranial contents. CBF is increased in response to raised ICP, by cerebral vasodilatation, However this causes increase in cerebral blood volume and produces further brain swelling. When maximal vasodilatation occurs, further increase in ICP causes reduction in cerebral BF.19C: Clinical effects (symptoms and signs): Significant raised intracranial pressure can be present with out symptoms or signs.

Global symptoms of elevated ICPHeadacheProbably mediated via the pain fibers of cranial nerve (CN) V in the dura and blood vesselsDepressed global consciousnessDue to either the local effect of mass lesions or pressure on the midbrain reticular formationVomitingFocal symptomsMay be caused by local effects in patients with mass lesions or herniation syndromes Additional features of traumatic head injuryDecreased level of consciousnessPain coming in wavesVisual changesAlterations in vital signsInfants may present with less specific symptomsIrritabilityBulging fontanelLethargyFlat affectPoor feedingNontraumaticHeadacheNocturnal awakening Worsening by cough, micturition, or defecation Recurrent and localized Progressive increase in frequency or severity Growth abnormalities Nuchal rigidity Focal neurologic deficit Persistent vomiting Known risk factor for intracranial pathology(eg, neurocutaneous syndrome, macrocephaly, hormonal abnormalities) Lethargy Personality change PapilledemaIf present can confirm the diagnosisPapilledema may be absent in acute ICP elevations because it takes several days to become apparentIs not invariably present in patients with intracranial hypertension

Retinal hemorrhages may be present in patients with increased intracranial pressure, and should raise the suspicion of nonaccidental head trauma

Infants may develop MacrocephalySplit suturesBulging fontanelHydrocephalusSun setting" appearance of the eyes may appear

Dilated pupilUsually on the side of the lesionCranial nerve palsies of the third, fourth, and sixth cranial nerves can occur3rd nerve palsy most commonMay cause double vision or abnormal head posture

Level of consciousnessCan range from irritability to obtundation or coma Hemiparesis, hyperreflexia, and hypertoniaAre late signsCushing triadSystemic hypertension, bradycardia, and respiratory depressionAnother late sign, and may be a preterminal event 1.Cingulate herniation2.Central transtentorial herniation3.Uncal herniation4.Tonsilar herniation D :Internal Brain herniation: resulting in strangulation, compression of vital structures and blood vessels.

281. Cingulate herniation: compress the internal cerebral vein and the anterior cerebral artery Unilateral or bilateral weakness, loss of bladder control, and coma2. Central transtentorial herniation: * Compression of the 3rd. nerve -------------> Dilated pupils . * Compression of the post. cerebral art. ----> Hemianopia. Total blindness. * Compression or ischemia of the brain stem.-> Decerebration. Coma. * Distortion of the brain stem --------------> Hemorrhages.3. Uncal herniation. compression of the mid-brain, 3rd nerve and the post. cerebral art. 4. Tonsilar herniation: Occurs when the cerebellar tonsils, herniate through the foramen magnum, resulting in compression of medulla, Decerebration, coma, cardiovascular and respiratory abnormalities (apnea). 29Medical Treatment of raised intra cranial pressure.1. Sedation, and positioning: 2. Hypertonic solutions: * Manitol: 0.5- 1gm/ Kg body wt. over 30 min. bolus injection. * Furosemide: is effective in reducing brain edema, and reducing CSF production. 40-120 mg daily.* Glycerol: can be given orally as well as I.V. 0.5-2 gm/ Kg. every 4 hrs.3. Steroids: Dexamethasone 4mg four times a day.4. Hyperventilation: 5. Hyperbaric oxygen: (rarely used).6. Hypothermia: 7. Induced barbiturate coma: Has been used to reduce intracranial pressure in head injuries, and to increase brain tolerance to focal ischemia in aneurysm surgery , strokes and SAH.30