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~!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!~ ~~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
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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
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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
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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
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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.
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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
2S "}t
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.
2. Langfitt TW. Increased Intracranial Pressure.
ClinicalNeliroslirgery 1969: 16 : 436-71.
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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