~!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!~ ~~JK SCIENCEIREVIEW ARTICLEI

Raised Intracranial Pressureand its Management

Anil Sharma, MS. MCh

One of the commonest pathological phenomenaencountered by the neurosurgeon is that of increasedintracranial pressure (ICP) and it has profoundinfluence on the outcome of many intracranialproblems. If raised intracranial pressure is notrecognised promptly and managed appropriately,there is alwaysaconsiderable risk in all such patientsof secondary brain damage and long term severedisability.

Physiology

The cranium can be thought of as a hollow, rigidsphere of constant volume. There are three main

components within the intracranial space: brain(1400 ml), cerebrospinal fluid (CSF) (75 ml) andblood (app. 75 ml) [15]. All these components areessentially non-compressible. The rigid cranialsphere provides the premise of the Monro-Kellie

Common causes of increased ICPHead Injury

Cerebrovascular

HydrocephalusCrania cerebral disproportionBrain Tumour

Benign Intracranial HypertensionCNS InfectionMetabolic Encephalopathy

Status epilepticus

Intracranial haematoma (EDH, SDH, intracerebral)Diffuse brain swelling, Contusion.Subarachanoid haemorrhage, Cerebral venous thrombosis,Major cerebral infarcts, Hypertensive encephalopathy.Congenital or acquired (Obstructive or communicating).

(Cysts; benign or malignant tumour)Secondary HydrocephalusMass effectOedema

Meningitis, Encephalitis, Abscess.Hypoxic-ischaemic, Reyes syndrome, Hepatic coma,Renal failure, Diabetic ketoacidosis, Hyponatraemia,Burns, Near drowning.

Adapted from references I, 2, 3, 4.

From the Unit of Neurosurgery, Department of Surgery, Govt. Medical College, Jammu (J&K).Correspondance to: Dr. Anil Sharma, Consultant Neurosurgeon. Depn. of Surgery, Govt. Medical College, Jammu (J&K).

Vo!. I No. I. January-March 1999 13

B Wave is related to various types ofperiodic breathing with a frequency of Y, to 2 perminute.

blood or CSF [12].

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doctrine which states that a change in the volume Spontaneous waves of ICP [13] are;of brain causes a reciprocal change in the volumeof one of the intracranial components i. e. either

Normal ICP is between 0- 10 mm Hg with 15 mmbeing the upper limit of normal. Resting ICPrepresents that equilibrium pressure at which CSFproduction and absorption are in balance and isassociated with an equivalent equilibrium volumeof CSF. CSF is actively secreted by choroid plexusat about 0.35 mllminute and production remainsconstant provided cerebral perfusion pressure isadequate.

CPP is commonly defined as ; CPP = MAP - ICP[MAP ; Mean arterial pressure, CPP ; Cerebralperfusion pressure].

C Wave is related to Traube-Heting-Mayer wavesof systemic blood pressure and has a frequency of6 per minute.

Both Band C waves are of low amplitude andare not harmful.

Type A wave or Plateau wave IS an acuteelevation in ICP lasting from 5 to 20 minutesfollowed by a rapid fall in pressure to former restinglevel. The amplitude is variable but may reach veryhigh levels (50 to 100 mm Hg) and is associatedwith clinical sIgns of acute brain stemdysfunction.

Mechanisms involved in raised ICP

A Mass LesionsB CSF Accumulation

C Cerebral Oedema

Haematoma, abscess, turnOUT.

Hydrocephalus (obstructive and communicating) and including contralateralventricular dilatation from supratentorial brain shift.

Increase in brain volume as a result of increased water content:

I. Vasogenic-Vessel damage (tumour, abscess, contusion).2. Cytotoxic--

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(D) Non-invasive ICP mo,!itoring :

(2) Subdural fluid filled catheters arereasonably accurate below 30 mm. Hg.

Catheter tip transducers for ICP monitoring

intraparenchymatous and intraventricular

types and these are very useful for wave

form analysis. Ventricular catheter permits

the therapeutic drainage of CSF in

case of intraventricular bleeds, ventricular

dilatation etc.

ofaretypes)(Camino-Codman(3)

Fifty percent of head injury patients who haveraised lCP on monitoring will exhibit optic discswelling in only 4% cases. "So fundoscopy may notbe of much use in acute head injuries to detect raisedICP"

(A) Clinical features: In the non-traumapatient, there mayor may not be a clear history ofheadache, vomiting and visual disturbancessuggestive of papilloedema or a VI nerve palsy. Theabsence of papilloedema does not exclude raisedlCP in patients with acute or chronic problems.

Monitoring techniq ues

(B) CT Scanning: It may show a mass lesion,hydrocephalus or diffuse odema.

(C) Invasive methods of ICP monitoring:

(i) Transcranial Doppler: This measures flowvelocity in branches of the Circle of Willis,

most commonly the middle cerebral artery

(I) Extradural sensor. (MCA).=

Indications for ICP monitoring

HEAD INJURY(a) being artificially ventilated:- Coma with compression of3rd ventricle and/or reduction in perimesencephalic cistern on CT- Coma following removal of intracranial haematoma.- Coma with decorticate/decerebrate motor response.- Coma with mid line shift/unilateral ventricular dilatation.- Early seizures not easily controlled.- Refractory hyperpyrexia.

(b) Uncertainty over surgery for small haematoma/multiple lesions.INTRACEREBRAL AND SUBARACHONOID HAEMORRHAGE- coma.

- postoperatively following intra operative complications.- hydrocephalus.

COMA WITH BRAIN SWELLING- metabolic.- hypoxiclischaemic.- infective. Adapted from references I, 3, 6

Vol. I No. I, January-March 1999 15

Many neuro surgical un its sti II manage patientswithout lCP monitoring. ICP monitoring shouldbe selective, based in part, on the initial CT scan.Such monitoring is very educational and greatlyassists general nurs'ing and medical care.

To treat raised fCP :

(a) It must first be identified, avoidable factorsprevented or treated and finally active treatmentstarted.

a diagnostic CT scan. An intravenous bolusof mannitol (0.5 gms/Kg over 15 minutes maybe required if there is evidence of coningsuch as pupillary dilatation). Acute hydrocephalusdemands immediate ventricular drainage.Surgical clots require removal and abscessestapping.

(B) Post-emergency resuscitation Management

Patients who are rapidly deteriorating or alreadyin coma, require immediate resuscitationwith intubation and ventilation followed by

(iii) Cerebral electric activity: Electroencephalo-graphy (EEG) is helpful in deciding whethercerebral metabolic depressants may be indicatedin treatment of raised (CP.

(A) Emerg~ncy resuscitation and diagnosisMANAGEMENTSTRATEGffiS

------------.~i... JK_S.C.I.E.N.C.E _(ii) Tympanic Membrane Displacement: ICP is

transmitted via the cochlear aqueduct to theperilymph of the cochlea provided aqueductis patent. Perilymphatic pressure may beassessed indirectly by recording displacementof the tympanic membrane during stapedialreflex contraction elicited by loud sound [5].

Potential Problems Exacerbating Raised ICP

(I) Calibration of Iep transducers and monilOrs particularly to check the zero reference point.(2) Neck vein obstruction:

- Inappropriate position of head and neck - avoid constricting tape around neck.

(3) Airway obstruction:- Inappropriate PEEP. secretions. bronchospasm etc.

(4) Inadequate muscle relaxant:- Breathing against ventilation.

- Muscle spasms.

(5) Hypoxia/hypercapnia(6) Further mass lesion - rescan.(7) Incomplete analgesia. incomplete sedation and anaesthesia.(8) Seizures.(9) Pyrexia.

(10) HyponalIaemia.(II) Hypovolaemia.

16 Vol. 1 No. I. January - March 1999

inappropriate secretion of antidiuretic harmone(SIADH) and it is unwise to use fluid restrictionto treat these.

(f) Seizures must be recognized in patients who areparalysed and on ventilators. Episodes ofpupillary dilatation with increases in arterialblood pressure and ICP are suggestive.

(g) Pyrexia not only increases cerebral metabolismand cerebral vasodilatation but also cerebraledema. Severe hypothermia was usedhistorically, to treat raised ICP. But now it is notused, as mild hypothermia of few c onlyreduces cerebral ischaemia because of reasonsthat are still unclear [I I].

(h) Hyperglycaemia should be avoided. There isconsiderable evidence that cerebral ischaemiaand infarction is made worse by hyperglycaemia.Use ofhigh glucose solutions is contra indicatedunless it is hypoglycaemic encephalopathy [9].

(2) Osmotic diuretics : Intravenous mannitol isinvaluable as a first aid measure in a patient with brainherniation as a rcsult of raised ICP. :

(a) The position of patient should minimize anyobstruction to cerebral venous drainage by head-up tilt while avoiding any fall in cardiac output.Direct measurement of global CBF (cerebralblood flow) and CPP (cerebral perfusionpressure) suggests that head-up tilt of up to 30is safe.

(b) Hypovolaemi" should be avoided especially insubarachanoid haemorrhage (SAH) .Dehydration, when coupled with hyponatraemia,increases risk of cerebral infarction.

(c) Knowledge of ICP may help in prognosisand counselling of relatives. In one series ofdiffuse head injuries where ICP persistentlyexceeded 20 mm Hg, almost all patients diedcompared with mortality rate of 20% in thosewhere ICP could be kept below 20 mm Hg withtreatment [7].

(I) Prevention of intracranial hypertensionGeneral medical and nursing care-avoidable factors :

___________..~~W......S-C-IE-N-C-E--------------(b) It should be treated before herniation occurs.

(c) A stable circulation must be maintained ifnecessary with colloids and inotropes(dobutamine or dopamine for its renal sparingaction).

(d) Systemic hypertension, if seen, in cranio-cerebral trauma, should not be treated directlywith agents such as sodium nitroprusside. Thisdrug impairs auto-regulation and increases riskof boundary zone infarction [8]. The cause ofhypertension like pain or retention of urineshou Id be looked for.

(e) Majority of neurosurgical patients withhyponatraemia don't have syndrome of

(a) Mannitol removes water from both normal andedematous brain. In patients with peritumoraloedema, mannitol causes withdrawai of Walelmainly from brain areas having impaired blood-brain barrier as judged by T,-MRl studies.

(b) Mannitol administration also leads to decreasein blood viscosity and.

(c) an increase in brain compliance.(d) Mannitol increases cerebral blood flow and

cerebral 0, consumption. It opens blood-brainbarrier by dehydrating endothelial cells and thuscausing separation oftight junctions and increasecapillary diameter and blood flow.

Vol. I No. L January-March 1999 17

The cerebral vasoconstrictor effect of hypocapnia,induced by hypeTlIentilatiorr, does not persist muchbeyond 24-36 hrs., probably in part becuase thebicarbonate buffering mechanisms within the brain andcerebrovascular smooth muscle themselves readjust toreturn extracellular and intracellular pH nearer to thenriginal values. This phenomenon has been confirmedin vivo in normal subjects by magnetic resonancespectroscopy.

(4) Buffer tris hydroxy methyl aminomethane(Buffer THAM)

CSF lactate accumulation and CSF acidosis occursafter head injury. Both severity of injury and theproportion of patients with poor outcome are related tohigh and increased CSF lactate levels. The deleteriouseffect ofCSF acidosis can be ameliorated by l.v. THAMas suggested by Akiota et. aI., following epidural ballooncompression of brain in dogs [16]. Evidence isaccumulating both experimentally and in humans that

THAM is at least as effective as mannitol in reducingexperimental oedema in the brain and in lowering ICPTHAM reduces the demand for mannitol and CSF

drainage.

(I) reduces CSF production.In practice, mannitol tends to be given as intermittent

bolus whenever patient's ICP rises above threshold of25-30 mm Hg. The effects ofmannitol may be potentiatedby frusemide, the best synergistic effect being obtainedby giving frusemide after 20 minutes, when mannitolbolus is finished.

It is crucial to avoicJ dehyDration and laterrthypotension with careful attention to fluid balance. Forprolonged osmotherapy, some people continue torecommend glycerol [10].

(3) Hyperventilation

Hyperventilation is one of the most effective meansof controlling increased ICP [14]. It achieves its effectby reducing cerebral blood flow and cerebral bloodvolume. CBF changes approximately 2% per mm Hg.change in PaCO,. In normal patient, hypercapniaproduces cerebral vasodilation without a rise in ICP but,when all compensatory mechanisms regarding ICPcontrol are exhausted, even the mildest respiratoryinsufficiency with hypercarbia can produce severelyincreased ICP. Many patients with increased pressureand healthy lungs and systemic circulation oftenhyperventilate spontaneously down to a PaCO of 30,mm Hg. when intubation is necessary, it should be done

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(e) helps in scavenging free oxygen radicals. caused by cerebral vasoconstriction. When PaCO is2reduced by hyperventilation, blood may be shunted fromnormal brain, where vessels are nomally responsive tochanges in PaCO,' to areas of damaged brain wherevessels are maximally dilated. This phenomenon is ofpotential benefit since areas of ischaemia would be bett~perfused.

marked elevation in ICP (upto 10 mm Hg-a findingoften seen during ICP monitoring).

PaCO, should be reduced to 25-30 mm Hg. Moreenthusiastic hyperventilation may precipitate cerebralischaemia with EEG slowing and C.S.F. lactic acidosis.Thus cerebral ischaemia produced by increased ICP maybe relieved only to be replaced by cerebral ischaemia

(5) IndomethacinIt has been known since 1973 that cerebrovasular CO,

response is blocked by indomethacin in doses that partlyinhibit brain cyclo-oxygenase activity in vivo. Cerebral

Vol. I No.1, January - March 199918

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venous pressure is very significantly reduced suggesting and SAH may involve freeD, radicals which damagethat ICP is reduced. More trials would establish a endothelium. Non-glucosteroids analogues of methylconcrete role of indomethacin in patients who are having prednisolone as well as methyl prednisolone itselfweaklyrefractory raised fCP not responsive to hyperventilation inhibit lipid-peroxidation.and barbiturate sedation.

(6) Continuous CSF drainage andsurgical decompression

External ventricular drainage (EVD) is a rapidprocedure in emergency in a patient with acutehydrocephalus. In all cases of external drainage, CSFshould be drained gradually against a postive pressureof 15-25 cm H,O. It is an optimal method of controllingICP in patients with SAl-! where cause is disturbed CSF

circulation.

Removal of bone flaps or subtemporal decom-pression are performed much less routinely.Benign intracranial hypertension (ElH) can be treatedby optic sheath fenestration and theco-peritonealshunting.

(7) Steroids

The mechanism of remarkable effect ofglucocorticoids such as dexamethasone on focal,relatively, chronic cerebral lesions remain incompletelyunderstood. In traumatic cerebral contusions, whenpatients are put on steroids and ICP monitoring, ICPwaves and compliance improve. Brain biopsy for tumouris much safer after at least three days ofdexamethasone,

(10 -20 mg loading dose, foilowed by 4 mg 6 hourly).\1uch controversy has surrounded the use of very highdose steroids in diffuse head injury but careful controlledtrials have shown no benefit. One purported mechanismofaction for steroids .involves lipid peroxidation and free

radicals. Cerebro-vascular effects ofacute hypertension

(8) Lazaroids

The 21-aminosteroids (antioxidant family known asLazaroids) are potent inhibitors of lipid peroxidationand have Vito E sparing effect. Lazaroid U-74006 F isundergoing large scale clinical trials in head injury andSAl-!.

(9) Cerebral metabolic depressants: excitotoxic amino acid antagonists

Brain energy metabol.isrn is depressed more

conveniently by hypnotic agents like barbiturates [6],etomidate, propofol, althesin and gammahydroxybutyrate rather by deep hypothermia.Unfortunately, all these agents have side effects likesystemic hypotension often compounded by dehydrationor hypovolaemia. Short-term protection duringaneurysmal surgery with barbiturate or propofol iswidely used.

Magnesium chloride (Rectal administration) whichwas old fashioned treatment for severe head injuries, isnow known to be non-competitive NMDA receptorantagonist.

(10) Anti convulsants

Epilepsy has long been known to raise rcp andincrease the risk of cerebral ischaemia as a result ofmassive increase in cerebral electrical activity andoxidative mechanism resulting in jeopardising bothmetabolic demand and CPP. Seizures must be treatedaggressively.

'9

Below is the tracing oflCP wave analysis ofa younggirl who after a fall, had right temporal lobe contusion,rcp monitoring was instituted. Her ICP was between15-25 cm of H20. After 36 hours, suddenly rcp shot upto 35. Her [CP wave form changed and clinically, shehad deterioration with right pupillary dilatation. RepealCT showed increased brain oedema. She was put onhyperventilation-osmotic diuretic regimen and sheresponded.

The management of raised ICP in childhood must takeinto account a number offactors [1].

The critical values for [CP, ASP and CPP arelower, the younger the child. Normal lCP in thenew born is probably of the order of 2-4 mm Hg.Arterial blood pressure (ASP) at birth is about 40 mmHg, 80/50 by one year and 90/60 during early school

Management in Children

Hyperaemia plays a greater role as a cause of raisedICP in children after head injury than adults. rt isphenomenon ofdysautoregulation that is more importantin children because of immature blood-brain barrier.

years.

____________...~~.JK SCIENCEparalysed patients etc. can do wonders in managing raisedpressure. ICP monitoring may not be therapeutic, byitself, in head injuries but it definitely helps inmanagement protocol.

ICPTRACINGAuthor's Note

The author, during his tenure as Neurosurgeon 111Saudia Arabia (K.S.A.), has the personal experience ofusing intraparenchymatous and intraventricular types offibre-optic catheters with pressure-sensors at theirtips. The [CP is amplified by an amplifier and directlytransmitted to display monitor. Facility for recording ofwave forms on ECG paper is also there. He has usedthese rcp measuring techniques in patients of headinjuries having Glassgow coma scale (GCS) between5-11. These catheters can be kept for 3 to 4 days insidethe cranium through non-dominant precoronal burr hole.Zero correction is very important and must be checkedevery day especially in cases where there are reasons todoubt about the unexpected lows and highs oflCP. Thus,management oflCP can be scientifically carried out, theraised pressure being titrated by changes in ventilatorsetting and by addition of osmotic diuretics. Simplemaneouvers like raising head of the patient by 20,smooth intubations while anaesthetising cases of raised[CP, use of non-narcotic and narcotic analgesia in

20

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u ....to.

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ReferencesI. Minns RA. Problems of Ie? in childhood. Clinics

developmental medicine 113/114. London: Mackeith

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__________-;t.JK SCIENCE1991 : 1-458.

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3. Miller JO. Dearden NM. Measurement. analysis and themanagement of raised intracranial pressure. In : Teasdale GM,Miller JD. cds. Current Neurosurgery, Edinburgh: ChurchillLivingstone. 1992: 119-56.

4. Miller 10. Normal and increased intracranial pressure. In .Miller JO, cd. Northfield's Surgery of the central nervoussystem 2nd ed. London: Blackwell, 1987; 7-57.

5. Reid A. Marchbanks RJ, Martin R, Pickard JO, Bateman N.Mean intracranial pressure monitoring by an audiologicaltcchnique-a pilot study. J Nellrol Neurosurg Psychiatry1989: 52; 610-2.

6. Campkin TV. Turner 1M. Neurosurgical anaesthesia andintensive care. 2nd ed. London: Butter\\'orth. 1986.

7. Miller JO. Butterworth JF. Gudeman SK et al Furtherexperience in management of severe head injuries.J Seliroslirgery 1981 , 54 : 289-99.

8 Fritch W. Pickard JO, Tamura A. Effects of hypotensioninduced with sodium nitropsusside on the cerebral circulationbefore and one week after SAH. J Neural Neurosurg

Psychiatry 1988 ; 51 : 88-93.

9. Myres RE. Anoxic brain pathology and blood glucose.Nellrology 1976; 34: 345.

10. Smedema RJ, Gaab MR. A conparison study betweenmannitol and glycerol in reducing lep. In : Avezaat, ed.Intracracial Pressure VIIl (in Press.).

II. Welsh FA, Sims RE, Harrs VA. Mild hypotherima preventsischaemie injury in gerbil hippocampus. J Cerebral BloodFlow Metab 1990; 10: 557-63.

12. Cushing H. Studies in intracranial physiology and surgery.London, Oxford University Press, 1926; pp 19-23.

13. Lundberg N. Continuous recording and control of ventricularfluid pressure in neurosurgical practice. Acta Psychiatr NeurolScand[Suppl.] 1960: 149: 1-193.

14. Lundberg N, Kjallquist A, Bien C. Reduction of increasedintracranial pressure by hyperventilation. Acta PsychiatrNellrol Scand [Suppl.] 1959 ; 139: 1-64.

15. Lassen NA. Cerebral blood flow and oxygen consumption inman. Physiol Rev 1959 ; 39 ; 183-238.

16. Akiota T, Otak, Matsumato A, et al. The effect ofTHAM onacute intracranial hypertension. An experimental and clinicalstudy. In : Beks JWF, Bosch OA, Brock M, eds. Intracranialpressure III. Berlin; Springer-Verlag, 1976; 219-33.

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