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Cranio-Cerebral Trauma: What and When to Decide Laurent Cauzinille France Head trauma, with or without skull fracture,

induces immediate primar in!ur includin", if se#ere enou"h, #essel disruption and tearin" or crushin" of brain parench ma$ %f this primar in!ur is not se#ere enou"h to induce immediate death, the de#elopment of secondar in!uries durin" the followin" hours, includin" hemorrha"e, edema, increased intracranial pressure &%C'( and o#er all, ischaemia, mi"ht$ The clinician is helpless durin" the first in!ur ) howe#er, throu"h rapid medical and sur"ical inter#ention, he ma slow or re#erse the second one$ The second in!ur mechanism Tissue ischaemia is the most de#astatin" conse*uence that ma occur after a cranio-cerebral trauma$ %schaemia is due to reduction of cerebral blood flow &C+F($ The C+F decreases when the %C' increases without concomitant au"mentation of the arterial blood pressure) the C+F ma also decrease when the cranial #enous outflow is impaired because of edema, hemorrha"e, or cer#ical trauma$ %C' starts to increase once the cerebrospinal fluid &C,F( and blood redistribution bufferin" capabilities are e-hausted respecti#el b reabsorption or displacement of C,F and brain #asoconstriction$ %ntracranial perfusion re"ulation is usuall maintained b means of #ascular constriction.dilation in a normal brain$ %n an in!ured brain, this abilit ma be lost$ 'aC/0, pH, and 'a/0 influence the autore"ulation response of the cerebro-#asculature$ %ncreased 'aC/0 and h po-emia, fre*uent findin"s in traumatized patient, will cause #asodilatation and increase %C'$ %schaemia tri""ers the Cushin" refle-, ultimate "uarantee in C+F maintenance, b increasin" the s stemic arterial pressure$ %C' will finall increase too$ +rain edema is the source of the increased %C'$ The traumatic disruption of the blood brain barrier e-plains its #aso"enic e-tracellular component$ Liberation of #asoacti#e substances and the osmotic effect of interstitial b product from dead cells will also increase its de#elopment$ The c toto-ic intracellular component of brain edema results from abnormal cell metabolism caused b ischaemia$ The all-molecular chain reaction dri#es to more #aso"enic and c toto-ic edema and hi"her and hi"her intracranial pressure$ 'atient e#aluation Cranio-cerebral traumatized patients are often multi-traumatized patients$ 'atenc of airwa s must be checked as we ha#e seen that hi"h 'aC/0 and low 'a/0 increase intracranial pressure$ Look for ma!or chest trauma$ The patient is then treated for hemod namic instabilit and the abdominal ca#it is assessed for or"an trauma.rupture &spleen, bladder, kidne detachment, etc$($ Cerebral h po-ia due to h po#olemia is rare because of the pressure autore"ulation, unless se#ere internal hemorrha"e is present$ Finall , the neurolo"ical assessment status is assessed) this will be hourl $ 1lthou"h less mechanicall unstable than #ertebro-medullar trauma, the head trauma patient must be handled with care$ The head is ele#ated no more than 23) this facilitates #enous and C,F outflow from the skull$ ,tate of consciousness, breathin" pattern, menace response, nostril sensiti#it , pupillar size and refle-, ocular position and mo#ements, limb proprioception, and skeletal motor function must be e#aluated$ 1 decreased le#el of consciousness &from depressed to delirious, stupor to coma( su""ests cortical or brainstem &reticular acti#atin" s stem( in!ur $ The pro"nosis and the treatment bein" different) it is essential to rapidl differentiate a supratentorial from an infratentorial lesion$ 1s mmetr in the menace response, in the nostril stimulation response, or in limb

proprioception without other cranial ner#e deficit, is in fa#our of a contralateral hemispheric lesion$ ,tuporous brainstem in!ured patients, showin" multiple cranial ner#e %% to 4%% deficits, ha#e a more "uarded pro"nosis$ %f no chest trauma has been identified, abnormalities in respirator pattern are either of metabolic &acidosis, h po-ia( or neurolo"ical ori"in &mesencephalic, brain stem, cer#ical($ H per#entilation and periods of apnea alternation &Che ne-,trokes respiration( is secondar to diencephalic decreased 'aC/0 responsi#eness$ When the brain stem is se#erel dama"ed, the respirator pattern becomes irre"ular in rate and amplitude and is associated with brad cardia$ 5-tensor ri"idit is a form of 678 presentation$ %f all four limbs are e-tended, both hemispheres are in#ol#ed &decerebrate ri"idit () consciousness is altered but 'L9 are normal if herniation is not a consideration$ %f the forelimbs are fle-ed and the rear limbs e-tended, the cerebellum is in#ol#ed &decerebellate ri"idit () consciousness is preser#ed but menace response ma be lost$ %ncreased %C' must be suspected when the 'L9 is abnormal &or deterioratin" toward nonresponsi#e midran"e or dilated pupils( in parallel with deterioration of consciousness, e-tensor ri"idit , and abnormal respirator pattern$ Direct bilateral unresponsi#e pupils, s mmetrical or not, indicate brainstem in!ur $ Transition from m osis to m driasis su""ests a pro"ressi#e lesion often secondar to sub-tentorial occipital herniation$ 'upillar paral sis is due to dorsal pressure of the swollen brain on the oculomotor ner#es$ 'etrosal bone and internal ear in!ur induces peripheral or central #estibular si"ns that ma be impressi#e with the animal rollin" on his side continuousl $ The neurolo"ical e-am on these patients is difficult initiall $ 'roprioception deficit on one side localizes the lesion to the ipsilateral central #estibular s stem$ Dia"nostic tools ,kull radio"raphs are difficult to read$ Howe#er, fracture lines or displacement must be looked for$ Cerebellar in!ur associated with occipital bone fracture.displacement is easil #isualized b a lateral radio"raph$ This t pe of trauma induces a ma!or ata-ia but has a "ood pro"nosis with or without sur"er $ Computed Tomodensitometr &CT( shows skull fractures and haematomas$ 1fter three to sihours, an acute infarct produces a h podense area secondar to edema$ The ma-imal effect is seen after three to fi#e da s$ Howe#er, some infarcts ma be isodense and #isible onl after contrast enhancement after 0: to :; hours, e#en more after one to two weeks because of neo#ascularization$ 1fter two to three weeks, edema resol#es and the lesion becomes isodense$ 1fter four to ei"ht weeks, necrosis creates a ca#itation with a densit close to the cerebrospinal fluid &C,F($ ,ubdural haematomas ma not be as rare as ori"inall reported in the #eterinar literature$ The ima"e densit is immediatel decreased, e#en more after a few da s when the clot or"anizes$ Haematomas become isodense after a month$ 7a"netic 9esonance %ma"in" &79%( is more suitable for brain ischaemia and edema e#aluation$ 5arl chan"es are detectable: h pointense in T< wei"hted ima"es and h perintense in T0$ 'arama"netic enhancement is identical to tomodensitometr $ %n case of hemorrha"e, the ima"e intensit depends about the hemo"lobin content and form &o- , deso- , methemo"lobin, hemochrome, hemosiderin(, its location intra or e-tra er throc tic, and the wei"ht of the ima"es$ 7a"netic resonance an"io"raph is a non-in#asi#e wa of doin" an"io"raph $ +oth CT and 79% are suitable to assess indirect si"ns of increased %C' b compression or as mmetr of the #entricles and shift of the midline$

+rainstem auditor e#oked response &+159( is interestin" to confirm a petrosal bone or middle.internal ear in!ur usuall associated with #estibular si"ns$ 1bnormal results ma indicate the need for a CT$ With %C' increase, the +159 shows re#ersible decreased amplitude and increased latenc $ This test ma be of pro"nostic #alue$ +iopsies, sur"ical or ultrasound "uided, allow a final dia"nosis to be made$ Treatment The treatment is modified accordin" to the neurolo"ical status, the neurolo"ical si"ns and their chan"es o#er time$ /ne aim is to treat edema$ While #aso"enic edema is responsi#e to therap , c toto-ic edema, once initiated, is not$ The treatment is thus directed at pre#entin" the creation of ischaemia and decreasin" its de"ree and duration b workin" with dru"s on the #aso"enic edema alread present and minimizin" the c toto-ic edema to come$ 1lthou"h h po#olemic shock is not the direct cause of brain ischaemia, h po#olemia decreases brain blood flow$ H pertonic saline &=$>? 8aCl , 2> ml.@"( is the solution of choice to restore #olemia$ %t impro#es cardiac output, restores s stemic blood pressure and has a sli"ht deh dratin" effect on brain tissues$ Colloids &h dro- eth l starch and de-tran, 03 ml.@"( are then used to maintain the intra#ascular #olume$ Central #ascular pressure is monitored$ ,econd, it is essential to "uarantee h pocapnia and "ood /0 deli#er &'a /0 A ;3 mmH"($ H percapnia &'a C/0 A :3 mm H"( and h po-ia induces #asodilatation, which increases %C'$ %ntubation is necessar if the patient is unconscious$ /- "en deli#ered b nasal catheter or b o- "en ca"e must be pro#ided if the patient is not$ 1lthou"h effecti#e in decreasin" %C', a""ressi#e h per#entilation ma a""ra#ate h po-ia because of e-cessi#e #asoconstriction and ma e-acerbate focal ischaemia and edema$ Third, the use of mannitol is a common step in cranial trauma$ 7annitol is a h perosmolar molecule that deh drates the cerebral interstitium, lowerin" %C'$ 7annitol also decreases blood #iscosit , promotin" cerebral perfusion) it also has free radical sca#en"er abilit which limits the deleterious molecular cascade induced b ischaemia$ 1fter fluid resuscitation, the risk of a rebound effect on the %C' is minimized$ 7annitol ma theoreticall be detrimental in cases of acti#e bleedin" or se#ere rupture of the blood brain barrier, howe#er, this has not been pro#en$ %ma"in" is the onl wa to detect a hemorrha"e or a lar"e edema$ Howe#er, ima"in" facilities are not alwa s a#ailable$ /ne should consider that if the patient is deterioratin" with time, mannitol is the best option to re#erse the process$ The recommended dosa"e is 3$> to <".@" o#er 0323 minutes %B$ %t will ha#e a lon"er beneficial effect if "i#en at 3$0> to 3$>".@" o#er C3 minutes potentialized with 3$= m".@" of furosemide %B, <> minutes later) howe#er, this ma lead to more serious h perosmolarit and ma a""ra#ate the rebound effect$ %C' measurement necessitates an epidural, subarachnoid or intra#entricular fluid filled catheter and a pressure transducer$ The necessit of monitorin" %C' is still debatable &risk, cost, interest, etc$($ %t is probabl an indirect wa to monitor the neurolo"ical status when the patient is comatose, or sedation or anesthesia is re*uired and neurolo"ical status cannot be e#aluated differentl $ /- metr , electroencephalo"raph , and transcranial Doppler sono"raph are used in human medicine$ The meth l prednisolone protocol as a free radical sca#en"er is not used in head trauma patients$ The classic corticotherap lar"el used in neuro-oncolo" to treat #aso"enic edema is not useful a"ainst c toto-ic edema encountered in the second in!ur t pe$ ,ide effects are not ne"li"ible: the fa#or "luconeo"enesis and maintain a h per"l cemic state known to be deleterious$ The fa#or anaerobe metabolism and increase "lutamate le#els and neuronal

death$ The D% side effects are also important in patients who alread ha#e an autonomic imbalance$ %nducin" barbiturate coma &><> m".@"( is indicated when patient disorientation ma be deleterious, or when the control of the %C' au"mentation is poor$ 9espirator rate, blood "as and arterial pressure must be monitored$ Debilitated, these patients usuall do not drink their dail water needs$ 'erfusion and control of hematocrit, total protein, electrol tes and diuresis is recommended$ %n case of seizures, diazepam &3$0 m".@"(, midazolam, and phenobarbital &><> m".@"( are used in %B bolus or continuous infusion$ The need to pursue the treatment for si- months after the initiation of anti-epileptic dru"s is contro#ersial$ Head trauma patients ha#e caloric needs much abo#e normal) a naso"astric tube for assisted enteral nutrition or parenteral nutrition should be instituted as soon as possible to a#oid chronic h per"l cemia$ Classic nursin" care for recumbent animals must be pro#ided &head up 23 ma-imum, e e lubricant, re"ular decubitus chan"e, bladder catetherization, soft ph sical therap , etc$($ ,ur"er indication is indi#idual$ Linear and ele#ated fractures will be treated conser#ati#el as well as stable depressed or trans-sinus fractures$ Haematoma with a si"nificant mass effect, penetratin" wounds or unstable depressed fractures will be treated sur"icall $ ,hort actin" barbiturates are used for induction and isoflurane is the inhalant anesthetic of choice because it does not increase %C'$ 'ro"nosis The Dlas"ow scale as used in human medicine is not suited to #eterinar medicine$ The pupillar refle- and state of consciousness ma be a "ood barometer of the neurolo"ical status$ The association of depression and m osis, uni- or bilaterall , indicates an increased %C'$ Cerebral herniation induces paras mpathetic stimulation and later paral sis e-plainin" respecti#el m osis and later m driasis$ %rre"ular respirator rate and unresponsi#e bilateral m driasis indicate a poor pro"nosis$ The modified Dlas"ow scale adds "rades for the le#el of consciousness &<: coma to C: alert(, motor acti#it &<:L78 to C: 8ormal(, and brain stem refle-es &<: complete paral sis to C: normal($ 'ro"nosis is bad from 2 to C, "uarded from E<:, "ood from <><;$ 5uthanasia should be considered on patients showin" intractable seizures or se#ere respirator failure$ /thers ma reco#er unpredictabl well, at least to be suitable, autonomous pets$

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