RAISED INTRACRANIAL PRESSURE “The sul basicaly & fluid (CSF) ~ are incon twthin the skal esl in an increase in itraranil presse (ICP o Stal - ris f Diagrammatic representation of Intracranial contents ee < fa 900-1200 mt ~ ~ frat i stuctue. Since ts contents ~ bain, blood and cerebrospinal ble, an increase in one constcuentce an expanding mast 1 "Monto-Kellie ‘CAUSES OF RAISED Ic Expanding mass Increase in brain | er ateasion 1 eeeaerat + ners corse 1 | Sreroseen Bicod velo 50) wesodaaton \ ~Nenous outow orca \vse! I an) / a - impaired absorption ‘Compensatory mechanisms fr an expanding iatesceaial mas lesion (1. Delayed — 3, 1 Betracelslar Oi | CSF volume = CSF outflow to the lambar theca 2. | Cerebral blood volume| CONCEPTS AND DIAGNOSTIC APPROACH RAISED INTRACRANIAL PRESSURE coe feet eeretceces =f ‘sult of continued CSE production. ‘Witham expanding intracranial mass lesion, sormal pressure is inilly ‘paintined by CSF expulsion wo the ‘xpandable amber thes. Further ‘expansion and subsequent bra sift may obstruct the fee fo of CSF ‘ot only tthe Lumber thea bat also to the avachocid vill eauting en cute rte in intracranial presse. onamwsne eee SOT NT ay me EGS, etree ‘ajacon to tumour navn FO) ZLB @ IES cetera means et ger Coy Set Interati wnen obstrctive hyarocephalue ‘develop, CS fore throug tothe \emiculer CF ‘ct aac xeeay ne prveser snd Megendio shout ‘With ichaomic damage, ss cll metabolism fis ieraelular No and Ca* ineease and te cells small Le. cytotoniecedema, Capillary damage follows and vasogeie oedema supervenes nCLINICAL PRESENTATION, ANATOMICAL CONCEPTS AND DIAGNO: RAISED INTRACRANIAL PRESSURE " (CEREBRAL BLOOD FLOW (CBF)/CEREBRAL BLOOD VOLUME (CBV) ‘Blood flow is dependent on blood prestre and the vaacolar resistance: Presure Flow = Resistance side the skull intracranial presrure must he taken into account (Cerebral perfusion pressure (CPP) (Ge systamie BP intscranisl pressure) ‘Cerebral vascular eseance (CVR} (Cerebral blood flow (CBE) Under normal conditions the cerebral blood flow is couple to the energy requirements of brain tissue. Various regulatory mechanisms sting om the arterioles maintain 4 cerebral blood low suficient to meet the metabolic demands FACTORS AFFECTING THE CEREBRAL VASCULATURE, Chemoregulation ~ Change in extzacelllar pH or sn accumulation of metabolle by-products diecly affects the vere calibre, ~ Any chunge in arteriolar PCO bas a diec effet on cercbsal vessels but aly & redtion of PO; to. <50 mkig has sgnificont effect, Autoregulstion = A change inthe cerebral perfusion pressure results i a compensatory change in vere calle, {Foo ‘Cerebral persion] [(CERE [lroz presse Tetrecaluar pH |Limetaboe byproducts / \ {autoregulation} {chemoregustion {autoregulation} Ichemoregulation) \__s#__ ‘extracellular pH perfusion ([eeneanat vasoowaranion Limatabote by-products | broesre ‘Any change in Blood esl diameter rss in considerate variation in cerebral Bod elas fd tt, cur, dsc aot acral pressure. ncrgy requieements dif in diferent pacts ofthe brain, To meet such needs inthe ‘white mater, ow is 20 ml/100glmin, whereas inthe grey matter flow i high as 100 ‘l/min.RAISED INTRACRANIAL PRESSURE (CEREBRAL BLOOD FLOW contd) [Autoregulation iss compensatory mechaniam which permits flccuation inthe cerebral, perfusion pressure within certain iis without significantly akering cerebral Bod flow 'A drop in cerebral perfusion pressure produces vasodilation (probably due 2 cer ‘myogenic effet on the AUTOREGULATION: CBF maintained ‘asco smeoth muscle) chereby espe change in CPP maintaining flow; arse inthe cerebral | vi perfusion pressure causes ‘Nearogeni iniuences appear to nave litle direct effec on the cerebral vessels but they may alter the range of pressure changes over which ‘utoreguation acts ‘Autorepultion fils when the Carsbrl boo tow . eventual futher eal! ~ sneromarts in volume produce Isrgor nd terger increments *RAISED INTRACRANIAL PRESSURE CP (contd) ‘When intracranial pressure is monitored with a ventricular catheter, regular waves due to pulse and respiratory eects are recorded (page 51). Asan intracranial mass expands and as ‘he compensatory reserves diminish, transient presure elevations (pressure waves) aze superimposed. These become mote frequent and spore prominent asthe mean pressure "Eventully the ris i intracranial pressure and resulta alin cerebral peefsion presse reach a cial level anda significant reduction in cerebral blood flow occur. Electrical activity i the corer fils at flow rats about 20 m100 gimin. Wf astoreglation is aleady impaired these ees develop even calle. When intacranal pressure reaches ‘the mean arte blood pressure, cerebral bleed How ceases. INTERRELATIONSHIPS Many factors affect intracranial pressure and these should not be considered in iolation Inter-rlationships are complex and fedback pathways may merely seve to compound the ‘ain damage Teor a C3F outtow vt (Severe te Brin |_| Blooerain teducon —ovegulaton) ~| somase | —| armen \ 4 Bian vase cee es 76RAISED INTRACRANIAL PRESSURE CLINICAL EFFECTS OF RAISED INTRACRANIAL PRESSURE [rated ICP wil produce sympeoms and sans bur doos nt cause neuronal damage provided cerebral Sood flow is maintained. Damage does, however, result from brain shift = tenorial or tonilar herniation CClineal features due to {TCP: 1 Headache ~ worse i the mornings, aggravated by stooping and bending 2 Vomiting — secure with a acute sei ICP 3, Puplloedema ~ occurs in a proportion of patients with TICP. It is related to CSF brtniction and doesnot necessarily ocear with bean shift alone Increased CSF pressure in the opie nerve sheath impedes venous tainage and axoplasmic flow in optic neurons Swelling of the optic Sis end retinal and dise haemorrhages result. Vision i only sk ‘when pailloedema is bot eevee and prolonged BRAIN SHIFT - TYPES TENTORIAL HERMATION tater: 2 iatert expanding mate ences SSUBFALCINE ‘MIDUNE’ SHIFT: occurs early {entra une remiton ss wth ultra pace oczupying lesion the medial edge of th temporal ‘Seldom produces ory eiml ect. iobe erate ough no sthough patel nr sar tortor ht. A Slt ocson as en meenigcrinas heriaton flows. {f ‘cerebellar ona through ‘ho foramen magnum. & ree of upward namition tects ara aut to ‘etinguih rom eects of ‘rest braneteniisrain hamisperos results erie caplocement af he ‘doen and clancaphalon trough the fentorial hots. Damage to those structures oosurs ‘nr from machanea toron oF fem schoeniasocardary to tathing ofthe perforating ‘Unchecked intra tential herniation leads co cetral tentoril and tonsil ssoclated with progressive brain stem dyfinction from midbraia te medulla, ”RAISED INTRACRANIAL PRESSURE CLINICAL EFFECTS OF BRAIN SHIFT ‘TENTORIAL HERNIATION - Latera ‘The posterior cerebral otery i= tometimas ocsludee bt the Feautlont romonymous hemianop Feraroy detected Inthe seta toge Pressure against the reteviar formation | Pressure to the edge ofthe testorum eerebe tn the opposite Cerebral peduncle {Kernohan's act may produce limb weakness on the sme se athe lesion ie se Seclsing) Son reve (Optic arves and chiasma TENTORIAL HERNIATION - Centr cata Prasis an inpared eve tery movemonis aes The rat of symptom progression ie related tthe rat of fesion expansion. (te , oD se) ‘Comprasson of the 1 nen and eovlomoter ‘uses pupil ciatavon anc ‘are toract lhe Setet dv to the associated Diencophsion snd midbrain damage from buckling and distortion and stetching of performing vessels Prossure on dors aspect Cental trtri Papi ints Sf and ) tight ‘nuse diabetes insipidusRAISED INTRACRANIAL PRESSURE CLINICAL EFFECTS OF BRAIN SHIFT (con'é) ‘TONSILLAR HERNIATION A dogroe of upward cerebalier herniation wevaly present, $2 sans pressure reals I [ogee soprossion of conscious lov Tonsilar —~ oe ‘eapratory rrequaiee- Tepiatory srrest foramen magnom produces eck stitnese end head tit [An injudicious lumbar puncture in the pretence of a subtentorial mass may ‘create a pressure gradient sufficient to induce tonsillar heralation, N.B, Harvey Cushing described cardiovascular changes ~an increase in blood pressure and 2 all in pulue rate, asociated with an expanding iotracranial ass, and probably resting from direx medulary compresion.‘The clinical vlue of these observations i often cveremphasives. They are often absent; when presen they ae invatably preceded by a deterioration in conscious level INVESTIGATIONS Patients with suspected raised intracranial pressure require an urgent CT sean. Intracranial pressure monitoring where appropriate (Seepage 51) ‘TREATMENT OF RAISED INTRACRANIAL PRESSURE When a ring iatscranial prestuse fs ened by an expanding muss, or is compounded by respiratory problems, treatment is clear-ct; Ube amass must be removed and blood gies restored fo normal levels ~ by vndltion if ecesary Tn vine pants despite te above measures, cerebral sweliag may produce « marked increase in itraranal pressure, This may follow removal of «ramour or haematoma oF may complicate a diffuse ead ijury” Arficial method of lowering inracranisl pressure ‘may prevent brain damage and cent from brain shift, but some methods lead to reduced ‘etebal blood flow, which in tse may cause beain damage (see page 80) Thracranial presure is monitored with a ventricular catheter or surface pressure recording device (ate page 30). “Treatment may be snstitted when the mean ICP is > 30 mungCLNICAL PRESENTATION. ANATOMICAL CONCEPTS AND DIAGNOSTIC APPROACN RAISED INTRACRANIAL PRESSURE ‘TREATMENT (cond) ‘Methods of reducing intracranial pressure ‘Mannitol infusion: nix. bols of 100 mil of 20% mannitl infused over 15 minstes reduces intracranial pressure by establishing an osmotic gradient between the plasma and brain tse, Thi method “us time prior to craniotomy i a ations deteriorating from a sas lesion, Mantel i als used housty for 424-49 bout period in an atempt to reduce ‘ised ICP. Repeated infusions, however, lead to equilibration aad a high iaraclialar ‘osmotic pressure, thus counteracting further treatment. In addition, eepeated doses may precipitate lethal ses in ateril blood pressure and acute tabular necrosis [te ae in ‘herefore best reserved for emergency stations (Controlled hyperventilation: Bringing the PCO, dowa wo 33kPa by hypesvensating the sedated or paralysed patent cases vasoconstriction. Although this redes intracranial prestue, the reultane reduction in cerebral blood flow may in ielf ease bein damage ‘Maintaining the blood pressure andthe ceralrl perfusion prezare (CRP) (> 70 mn) appears to be as, if not more, important than lowering intracranial pressure. Only by ‘monitoriag the amount of oxygen extracted frm the brain can one determine whether oF ‘or the brain uasus can Withstand further vasoaonstrictin eaused by hyperventilation (eee age 227), CSF withdrawal: Removal of» few miles of CSP from the venticle wil immodiarly reduce the intracranial presture. Withia minutes, however, the pressure wil rise and further CSF withdrawal wil be required. In practic, thie method i of limited elo, since (CSE outflow tothe lomber thec results ian diminished itracranial CSF volume and the Leer ventricles aze often eallapied. Continuous CSF deuinage may make mort aarantage of thi method, ‘Sedatives: I intracranial pessute fis wo respond wo standard measures then sedation may help under carefully controlled conditions. ‘Propofol a short acting anaesthetic agent, reduces intracranial pressure but causes systemic ‘vasodilatation, If this cceurs pressor agen may be required wo prevent fll a Blood pressure and a rection in cerebral perfosion. Barbicwrates (siopomone) reduce neuronal activity and depress cerebral metabolism; a fll in energy requirement theoreieally protects iehoemic areas. Associated vasoconstriction ‘an reduce cerebral blood volume aad intracranial pressure but sjstemic hypotension and ‘myocardial depression also occur. Clinical tial of Barbtwate therapy have ot demonsveted 2 improvement come tomate alo provides cerebral protection by reducing cerebral metabolism and Incruceanial presnure withour proving cardicdepression. It inhibits endogenous steroid synthesis, and therefore eequits steroid cover. ‘Steroids: There is no doubt that steroids ply an important rte in eating patients with ‘ntracranial tamours and surrounding oedema. Cell membranes are sable, but iis not certain that thei Beneficial effect in tumour management isa result of reducing ICP. Steroids appeat to be of no vale in the weatment of traumatic or tchaemic damage. Experimental evidence sigests that they may help f administered before the damage ‘ocurs Dut clearly thsi seldom of practical value @