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Traumatic Brain Injury - Management in Africa

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Intro&uction An African 'erspective 'athophysiology of Brain Injury (ormal )omeostasis Autoregulation Intracranial )ypertension 'hysiology of Injury *lassification of )ea& Injury *lassification !y Severity *lassification !y 'athology "iffuse Injury Focal Injury Initial Management The (eurological +,amination Brain "eath Imaging in )ea& Trauma Alternate Imaging Mo&alities Managment of Brain Injury Invasive Monitoring Measures to Treat Intracranial 'ressure Basic (eurosurgical 'roce&ures in Trauma +,ternal -entricular "rainage +,ploratory./0oo&pec1er/ Surgery *raniotomy . *raniectomy 2eneral Measures 2ui&elines for the Management of )ea& Injury Management Algorithm *onclusion eferences Intro&uction The brain has monumental functions, mediating consciousness as well as neural and hormonal control of the body. Brain injury thus has a special place amongst traumatic insults due to its uniquely intimate and profound impact on the person. Patients with brain injury are often a challenge to manage, requiring difficult decisions and an

infrequently used skill-set for most physicians. This task is made even more difficult when one is practicing in an environment without resources such as T scanners which have become instrumental to the management of such patients in neurosurgical centers over the past !" years. This review is designed to assist physicians managing traumatic brain injury #TB$% while working in environments with limited resources. &e will present details on the current guidelines and management paradigms as they e'ist in the literature. Though craniotomies have been performed in (frica for centuries #)% we anticipate that the majority of our readers will have insufficient resources to provide the type of care described in the current literature. This review will therefore try to help practitioners to provide the highest level of care possible with the resources at their disposal. An African 'erspective $n (frica, the epidemiology of traumatic brain injury is very similar to that seen in the &est, though this may be because (frica*s publishing neurosurgical centres are located in urban, industriali+ed centres. (s in the &est, young males are disproportionately affected and traffic accidents are a predominant mechanism of injury #,, !%. -urthermore, like .orth (merica, TB$ is the most common cause of traumatic death in the young #,, /-0% and age is one of the strongest predictors of outcome #,, 1%. 2ifferent from the &est, however, is the fact that injured (fricans face a median distance of 0" km to a hospital and a corresponding nine hour delay in reaching such care #/%. Police, good samaritans or relatives are frequently responsible for transport to healthcare facilities #3%. Though problems in neurotrauma care are not unique to (frica #0%, efforts to improve transport, centrali+e trauma care #0%, and improve trauma management within individual hospitals will almost certainly result in improved patient outcomes in (frica #4, )"%. The development of neurosurgical 5 entres of 6'cellence* in (frican countries, partnered with similar centres in developed countries, has been proposed as a means of improving (frican neurotrauma care, as has the development of an (dvanced Brain 7ife 8upport course which would supplement the (dvanced Trauma 7ife 8upport course #0%. 'athophysiology of Brain Injury (ormal )omeostasis - Autoregulation3 erebral blood flow is normally maintained at a constant level thanks to autoregulatory processes which match flow to the metabolic needs of the brain #)), ),%. There are numerous forms of autoregulation. Pressure autoregulation holds that between systolic blood pressures of 9" and )0" mm:g #higher in those with chronic hypertension%, the diameter of cerebral arterioles is altered to maintain a constant blood supply to the brain #)!%. ;iscosity autoregulation alters vessel diameter and thus blood flow in response to changes in viscosity #)/%. The cerebral vasculature is also highly responsive to metabolites allowing for metabolic autoregulation #)9%. Perhaps best understood, however, is the relationship between Pa <,, Pa <, and cerebral blood flow. :ypo'ia is a potent vasodilator #)0% and Pa <, levels have a similar and more profound effect on cerebrovascular tone #)1%. =nderstanding autoregulation is essential in managing traumatic brain injury. (utoregulation may be lost following a head injury, thus making the brain prone to ischemia. (voidance of hypotension is thus crucial as the ability to compensate is lost. 8ome forms of autoregulation are generally preserved, however, and are essential

for treatment #)3%. >eactivity to <, e'plains the efficacy of hyperventilation in head injury management #)4% as well as mannitol*s effects which are largely due to reduction in viscosity and resulting vasoconstriction #,"%. erebral blood volume can change up to /"cc*s as a result of these processes, effecting a ,4-fold change in intracranial pressure #$ P% #))%. Intracranial )ypertension3 $ntracranial hypertension is the end result of multiple intracranial processes that can be seen in trauma #,)%. The ?ellie-@onro 2octrine describes that the volume within the skull is fi'ed, and that an e'ponential increase in pressure occurs secondary to processes such as hemorrhage or swelling which add to that volume. 8uch pressure elevation can impair blood flow to the brain. (s a compensatory response, the body produces hypertension and bradycardiaA combined with irregular breathing, these comprise ushing*s triad #,,% which is seen in its classic form only a third of the time. &hen treating head injured patients, it is important to follow the cerebral blood flow. This is not easily measured directly so clinically we use a surrogate, the cerebral perfusion pressure # PP%, which is calculated as followsB PPC$ P-@(P where @(P is the mean arterial pressure, calculated as ,D! the diastolic pressure E )D! the systolic pressure. 'hysiology of Injury3 The damage to the brain that occurs at the time of initial injury is known as primary injury. -ollowing this the brain is sensitive to additional insults which have become known as secondary injury #,!%. These are surprisingly common, seen in perhaps 4"F of patients #,/%. -ortunately, however, many of these factors can be ameliorated by physicians. The following are important, frequent causes of secondary injuryB Cerebral Edema: Brain swelling, or edema, is very common following brain injury. $t peaks several days post-insult and can cause focal deficits and elevated $ P. Though effective for brain tumor-associated edema, steroids have shown a ,"F higher mortality rate #,9% when given to the head injured, and should not be administered. Hypotension: :ypotension, defined as one or more observation of a systolic blood pressure less than 4" mm:g, is associated with a two-fold increased risk of mortality #,0%. :ypotensive or under-resuscitated patients have been shown to have higher $ P because of compensatory cerebral vasodilation #,1, ,3%. :ypotension must thus be avoided at all costs. Hypoxemia: =nfortunately the brain is more sensitive to ischemia after trauma than in the normal state, and furthermore hypo'ia results in compensatory cerebral vasodilation, increasing intracranial pressure #,3%. :ypo'ia, defined as the observation of a single Pa<, less than 0" mm:g, is thus correlated with a much worse prognosis #,0%. (ggressive treatment is mandated. Pyrexia: @etabolism increases )"-)!F per degree centigrade and fever thus increases the needs of a brain already stretching to meets its metabolic requirements. $t can also increase cerebral blood flow by as much as 41F, raising $ P #))%. )ea& Injury *lassification :ead injury is classified in many waysB by the severity, resulting pathology #focal or diffuse injury% or mechanism of injury #blunt or penetrating%. *lassification !y Severity3 The Glasgow oma 8cale #,4% 42*S, Ta!le 56 is generally used to indicate the

severity of a head injury. $n general patients with a G 8 of )/ or )9 are considered to have a mild injury, those with G 8 4-)! a moderate injury, and those with G 8 3 or less a severe head injury. The :ead $njury 8everity 8cale 4Ta!le 76 is a slight variation on this system. *lassification !y 'athology3 &hile head injury can be classified as focal or diffuse, the reality is that both generally e'ist to varying degrees. <ne must also remember as well that up to ,"F of patients who present with a diffuse injury will develop a mass lesion, most commonly in the first day following the injury #!"%. $n severe head injury, diffuse injury predominates but focal lesions carry a higher mortality rate #!)%. "iffuse Injury3 The hallmark of diffuse brain injury is alteration of mental status out of proportion to T findings. >otational accelerationDdeceleration forces are key, causing the corte' to move at a different speed than deeper brain structures, damaging a'ons. oncussion and diffuse a'onal injury #2($% e'ist at opposite ends of a gradient, but a dividing line has been establishedB traumatic coma of less than si' hours is classified as concussion, while coma of longer duration is considered 2($. Concussion: oncussion is defined as any alteration in mental status following head injury. linical hallmarks are confusion, amnesia, and loss of consciousness. T is typically normal, however, @>$ may detect lesions. Grading schemes for concussion have fallen out of favour #!,%, but the one perhaps most widely used is that of the (merican (cademy of .eurology 4Ta!le 86. -ull recovery from a concussion is not always seen #!!%. Diffuse Axonal Injury: 2($ is seen in 3"-)""F of those with fatal head injuries #!/%. The absence of a lucid interval is said to be a hallmark. &hile most lesions in this disorder are non-hemorrhagic and microscopic, punctate hemorrhages can be seen at grey-white matter interfaces, and in the upper pons, dorsolateral midbrain and corpus callosum. 8evere 2($ has a mortality rate as high as 9"F #!9%. $nterestingly, associated a'on disruption is seen predominantly in a delayed fashion and preventing this is a subject of intensive research. Focal Injury3 Scalp Laceration: 8calp lacerations can lead to significant hemorrhage if not managed appropriately. $t must be remembered that managing circulatory compromise is a higher priority than neurological disabilityH 8calp lacerations are of special significance when they are associated with a skull fracture, #making it an open fracture%, putting patients at risk for meningitis. 8ome scalp defects may require flaps for reconstruction #!0%. Skull ractures: The skull is a comple' bony structure and can be affected by a myriad of fractures. Basal skull fractures should be suspected in the face of raccoon eyes, Battle*s sign, hemotympanum, otorrhea or rhinorrhea. The numerous important vascular and neurological structures that traverse the skull base can be compromised such as the optic nerve, and the seventh and eight cranial nerves. ( basal skull fracture is a contraindication to the insertion of nasal devices #ie. nasogastic tubes% as there is a risk of intracranial placement through a bony defect. Blows with a small area of impact are generally responsible for depressed skull fractures 4Figure 5a,!6# 2epressed skull fractures should generally be elevated if #))%B

). the depth of the depressed fragments is equal to or greater than the width of the surrounding bone ,. conservative management would result in a cosmetic deficit !. the fracture is open /. associated with a deficit from compression of underlying brain <pen skull fractures deserve special consideration. &hile many would prefer operative debridement and closure of such wounds within 0 hours of injury, the recently published surgical guidelines for head trauma are more conservative in their recommendations #!1%. They state that conservative management of open skull fractures is acceptable so long as the above indications for surgical management of a depressed skull fractures are absent, and the following additional criteria are metB ). ,. !. /. 9. 0. there is no evidence of dural penetration absence of a surgical intracranial hematoma the fracture does not involve the frontal sinus there is no evidence of infection no pneumocephalus is apparent absence of gross wound contamination

They recommend that all individuals with open skull fractures should be treated prophylactically with antibiotics, but this too is controversial and different from the practice of the authors, who prefer use of antibiotics only in the face of established infection. Intracranial )ematoma $ntracranial hematomas can be life-threatening and may require surgical intervention. They are seen more frequently as the severity of injury increases, and it must be remembered that they can develop in a delayed fashion. Cerebral Contusion: erebral contusions make up /9F of primary intra-a'ial traumatic lesions and are present in nearly half of moderate and severe closed head injuries #!)%. They occur when the brain impacts against bony prominences or dural folds 4Figure 7a,!6# oup contusions lie below the region of cranial impact. ontrecoup contusions are seen at a site distant and often #but not necessarily% contralateral to the impact can be seen. ( third of these progress in si+e and they are responsible for less mass effect than would be anticipated, though associated swelling can mandate resection or decompression. Intracerebral !ematomas: $ntracerebral hematomas account for )"F of all posttraumatic intracranial hematomas #!)%. $ntracerebral hematomas may form from contusions, but are classified as the former if blood makes up greater than ,D! of the lesion or if there is a well-defined margin. 2elayed intracerebral hematomas 4Figure 8!6 are not seen on the initial scan, but appear within ,/-/3h. Epidural Hematoma: 6pidural hematomas 4Figure 9a,!6 occur in about 0F of patients with severe head injury #!)% and are more common in younger patients. They often arise from skull fractures over the pterion which disrupt the middle meningeal artery. The clinical course classically involves a loss of consciousness followed by a lucid interval, then a subsequent decline within 0 hours of injury. ( lucid interval occurs in )"-9"F of cases and is a good prognostic signA mortality is doubled when it is not seen #!3%. >adiographically these hemorrhages tend to be lens-shaped and they do not cross suture lines but can cross the fal' cerebri and tentorium cerebelli, as well

as the dural sinuses. -ortunately 1"F of patients requiring surgery for epidural hematomas have a good outcome and with rapid treatment mortality may be as low as 9F #!4%. Subdural Hematoma: (cute subdural hematomas are the most common posttraumatic focal intracranial lesion 4Figure 8a6 #!)%. They are associated with a more significant impact force than epidural hematomas and 2($ frequently co-e'ists. 8ubdural hematomas classically arise from disruption of bridging veins as they cross from the cerebral corte' to the venous sinuses. erebral atrophy puts bridging veins on a stretch, and these hemorrhages are thus seen more commonly in older patients and alcoholics. They can also arise from cortical lacerations. They tend to spread diffusely over the hemisphere in a crescent shape. =nlike epidural hematomas they can cross sutures but not dural attachments, and they are sometimes seen along the fal' and tentorium. Patients with acute subdural hematomas fare poorly compared to those with epidural hematomas, with an associated mortality rate of 9"-4"F #/"%. $n children subdural hematomas must raise suspicion of physical abuse. Subarac!noid Hemorr!a"e: The prevalence of traumatic subarachnoid hemorrhage #8(:% in severely head injured patients is probably greater than /"F #/)% and, in fact, trauma is the most frequent cause of subarachnoid hemorrhage 4Figure :6. $t may be important to rule out aneurysmal hemorrhage in these cases. :ere history is critical, and furthermore traumatic 8(: is generally seen over the cerebral conve'ity as opposed to the basal cisterns as is typically seen with aneurysms. Intra#entricular Hemorr!a"e: Post-traumatic intraventricular hemorrhage is seen in about ,9F of severe head injuries #))%, and is most frequently an e'tension of intracerebral hematoma in periventricular areas. Temporary ventriculostomy is often indicated. Penetratin" Head Injury: Penetrating head injury is frequently seen as a result of knife or gunshot wounds, with the latter being classified as 5missile* injuries 4Figure ;a,!6. Because these wounds are open, they are inherently contaminated. The role for debridement is controversial. &e are aware that many te'tbooks advocate aggressive debridement of debris and devitali+ed tissue for all patients. -urthermore, some have advocated radical or repeated surgery to remove as much foreign body as possible #with resulting destruction of much functional brain tissue% in hopes of preventing infection. This strategy, as mandated by the =nited 8tates* military during the ;ietnam &ar, has been associated with significant morbidity and mortality #/,%. The penetrating head injury guidelines currently recommend a more conservative approach #/,%. (n e'tensive review of published data on this topic led to the recommendation that those patients with 5significant* intracranial pathology should undergo debridement in addition to the other brain surgery they require. 7evel $$$ evidence indicates, however, that those without mass effect may not benefit from debridement of the missile tract, as patients that are not debrided Iare not measurably worseJ than those who are #/,%. Initial Management The airway is the highest management priority in neurotrauma, as in all trauma. Patients with a G 8 score of 3 or less #those not locali+ing% require intubation. (irway protection helps to prevent secondary injury from hypo'ia and hypercarbia. ervical spine precautions are paramount during airway interventions. Breathing, circulation and the stabili+ation of vital signs must be the ne't priority. ( hypoperfused brain does not function normally, so a Glasgow oma 8cale score has little value unless obtained post-resuscitation.

The neurological e'amination may also be obscured iatrogenically, as when patients are sedated by physicians who inappropriately feel that movement is e'acerbating their head injury. =nfortunately this often occurs at the time of first assessment when monumental decisions must be madeB whether a patient should go to surgery, or is beyond help. These agents are often necessary, especially to facilitate imagingA short acting, reversible agents #such as short-acting ben+odia+epines% should be used whenever possible. The (eurological +,amination3 The top priorities in the neurological e'amination areB determining if there is evidence for life-threatening intracranial pathology and assessing the patient*s baseline level of neurological function such that change can be detected. The two 5neurological vital signs*- the pupillary e'amination and the G 8 K are most important for this purpose and should be assessed first. The initial pupillary e'am assesses only pupil si+e and reactivity to light. ( single dilated pupil #at least L)mm larger than the other, as differentiated from anisocoria which is normal% that does not react to light suggests ipsilateral uncal herniation and mandates aggressive measures to reduce $ P as such a patient is potentially 5salvageable.* >emember, however that traumatic mydriasis is important to consider as a causeA it is often associated with hyphema. Bilateral fi'ed and dilated pupils suggest a very poor prognosis and a patient who may not benefit from intervention. The G 8 is then scored. (ll physicians should be able to score a G 8 rapidly and accurately. ( declining e'am, defined as a , or more point drop in G 8, is also an indication for initiation of therapies to treat $ P. $n a patient who is completely unresponsive, the ne't priority is assessing brainstem integrity by means of the corneal and gag refle'es. ;estibulocaloric testing also helps to assess the integrity of the brainstem, following confirmation of an intact tympanic membrane. 2oll*s eyes testing is generally not used in trauma patients as it involves manipulation of the cervical spine. The head must then be e'amined in detail. :air removal may be needed to facilitate proper e'amination. $f a T scanner is not available, wounds should inspected to determine if a skull fracture underlies them or if there is egress of 8-. :owever these wounds should be probed with e'treme caution if at all. 8igns consistent with basal skull fracture should be sought #raccoon eyes, Battle*s sign, hemotympanum, otorrhea or rhinorrhea%. To determine the presence of cerebrospinal fluid # 8-% within bloody fluid, one can look for a halo sign when a drop of fluid is placed on tissue paper. (ttention should then turn to the face for a detailed e'amination. &here possible, a full cranial nerve e'amination should be performed. $f the eyes are markedly deviated to one side it could indicate ongoing sei+ure involving the frontal eye fields contralateral to the direction of ga+e. Tongue-biting or incontinence may also suggest sei+ure. $mpaired light reaction #relative afferent papillary defect% can suggest optic nerve compromise which may need treatment. The absence of papilledema should not be reassuring in trauma patients as they rarely develop this finding. Though impractical to assess initially, the olfactory nerve is the most frequently injured cranial nerve and is very debilitating because of its role in taste. (n abducens palsy may represent a 5false-locali+ing* sign. Because of its long intra-cranial course, elevated $ P can compromise the function of this nerve. The side involved may not correspond to that of intracranial pathology so physicians should not be misled by this finding. The neck often receives little attention in a trauma. learing the cervical spine

generally involves clinical e'am in a lucid patient and often imaging. This is not important initially and it is rarely feasible because of impaired mental status. (s such, the cervical spine must be protected until this can be completed. Brain "eath3 Brain death is considered legally equivalent to cardiac death. 7ocal protocols generally define how brain death should be diagnosed. These involve demonstrating an absence of brain function on e'am in addition to ensuring that conditions that may depress consciousness such as medications, metabolic disturbances, and hypothermia are absent. (bsent blood flow to the brain on imaging and an isoelectric 66G may be adjuncts. @ore than one physician must typically participate in a declaration of brain death. Imaging in )ea& Trauma *ompute& Tomography3 T scanning is by far the most important imaging modality in head trauma patients. (ll patients with moderate or severe head injuries should be scanned as soon as possible with repeat imaging at ,/ hours, if a T scanner is available. The anadian T :ead >ule helps to determine which patients with minor head injury should be imaged #/!%. Though intended for T scanning these rules could be e'trapolated for imaging with whatever modalities are available. @agnetic resonance imaging has little utility in acute head injuries, though it may have a role later in diagnosing 2($. Alternate Imaging Mo&alities3 Generations of neurosurgeons practiced without the lu'ury of T scanning, and the following are some techniques which they utili+ed #//%. 8ome of the imaging techniques can be very time-consuming, especially in ine'perienced handsA in many situations it may be prudent to proceed with surgery before imaging as a significant delay could prove fatal. Skull x$rays: 8kull '-rays can detect skull fractures, gross pneumocephalus, and may be able to detect midline shift based on displacement of a calcified pineal gland #/9%. The presence of a skull fracture mandates close observation as it is associated with a ," fold increased risk of hematoma in an unconscious patient, and a /"" fold increase in those that are conscious #/0%. Guidelines have been devised to help determine when skull '-rays should be employed, and following them can help to reduce costs #!%. Ec!o$Encep!alo"rap!y: Though highly operator-dependent, ultrasound can be used to image the cranium. 2isplacement of the midline greater than ,mm detected in this fashion is considered pathological, and indicates the side of the lesion #//%. (bsence of shift does not rule out a hematomaB lesions may be bilateral, located subfrontal or in the posterior fossa. Generali+ed brain edema also remains a possibility. This technique has been demonstrated to be 49.!F accurate in diagnosing midline shift #/1%. Cerebral An"io"rap!y: ( mainstay in the pre- T era #/3%, this imaging technique can assist with the diagnosis of most supra-tentorial hematomas. 2isplacement of vessels from the inner table of the skull, or shift of the peri-callosal or callosomarginal arteries can assist with locali+ation 4Figure<6# These arteries can be used to diagnose hydrocephalus #as may occur with a posterior fossa hematoma% on a lateral film when elevated with a broadened curvature. The literature, as well as the authors, have found that the requisite carotid puncture is associated with a low rate of complications. %entriculo"rap!y: $nstillation of contrast via an e'ternal ventricular drain #placement of which is to be described shortly% has utility in demonstrating ventricular compression that could indicate a deeply-located hematoma or hydrocephalus

secondary to compression of the cerebral aqueduct. This procedure was considered inferior to angiography and was rarely performed in the pre- T era. Air$Encep!alo"rap!y: Though performing this procedure is discouraged by .orthfield #//%, in the absence of contrast one can inject a few cc*s of air intraventricularly. This is obviously relatively contraindicated in a patient with elevated $ P. The injected air can be imaged readily by '-ray, providing similar information to ventriculography. (n important difference, however, comes in understanding that air will rise to the top of any fluid column, making positioning key. Generally supine positioning is used for such imaging. Management of Brain Injury $n those with mild or minor head injury, decision-making centers around deciding if a patient should be admitted for observation or discharged home, based on their risk for a life-threatening intracranial lesion. 8uch lesions are seen in about ,F of these patients #))% and generally present in the first ),-,/ hours #/4%. &e recommend the anadian T :ead >ule for assistance in determining which patients should be imaged #/!% 4Ta!le 96. (ll patients with an anomaly on T or '-ray should be admitted for ,/h of observation with a T repeated prior to discharge if possible. Those meeting criteria for observation at home 4Ta!le :6 may be discharged if the attending physician feels it is prudent to do so. Patients with moderate and severe head injuries must be admitted and are generally monitored in an intensive care setting. &eneral 'easuresB (void hypotonic intravenous fluids as these agents may e'acerbate cerebral edema. Prophyla'is for gastric stress ulceration K ushing*s ulcers K should generally be prescribed #9"%. 2espite numerous studies, the optimal agent for this purpose remains controversialA proton pump inhibitors, :, antagonist, and sucralfate are all acceptable based on current literature #9)%. Patients with brain injury are at high risk for coagulopathy such as disseminated intravascular coagulation and this must be watched for. @etabolic disorders are common, especially hyponatremia and may contribute to poor mental status and sei+ures. Blood pressure is frequently and inappropriately lowered in neurotrauma patients with disastrous consequences. @any fear that hypertension will lead to edema or e'acerbation of hemorrhage, but the reality is that this is an adaptive response directed at perfusing the brain in the face of elevated $ P. 8ei+ures occur in )/F of head injury patients and can raise the metabolic rate to )9"-,9"F of normal #9,%, as well as the $ P #9!%. (nticonvulsants decrease the incidence of early but not late sei+ures from )/ to /F #9/%. urrent recommendations are to treat all patients with traumatic hemorrhage on more than one T cut with 1 days of anticonvulsant, typically dilantin #99%. Proper nutrition has been correlated with decreased mortality in head trauma patients and is thus encouraged #90%. Invasive Monitoring3 ;entriculostomy, which is capable of both monitoring $ P and draining 8-, is recommended for all trauma patients with G 8 less than 4 with abnormal T scans, or those with normal T scans and two of the followingB age older than /", systolic blood pressure less than 4" or posturing on e'am #91%. .ormal $ P values are age-dependent 4Ta!le ;6. The treatment threshold for intracranial hypertension is accepted to be ,"-,9 mm:g, even in children #93%. 2ata correlating outcome with the length of time above an $ P of ," mm:g is suggestive of the need for aggressive treatment when this level is reached #94%. ( PP target of 0" mm:g is now recogni+ed as a guideline by the (merican (ssociation of .eurological 8urgeons 8ubsection on .eurotrauma and ritical are.

Measures to Treat Intracranial 'ressure3 Positionin": 6levation of the head of the bed to !"-/9 degrees #if no contraindication% has been shown to optimi+e arterial inflow and venous drainage #0"%. ?eeping the neck midline prevents kinking of the jugular veins. entral line placement into the jugular veins should be avoided. ervical spine collars can be removed with care if patients are sedatedDparaly+ed enough that they are not moving. They should be replaced later when elevated $ P resolves and remain in place until the cervical spine can be cleared. 'annitol: @annitol is very effective and can be life-saving. $t decreases blood viscosity by reducing erythrocyte volume, decreasing hematocrit as well as increasing erythrocyte deformability #,"%. $n the face of intact viscosity autoregulation, the result is cerebral vasoconstriction, reduced cerebral blood volume and $ P #))%. $t also works as an osmotic diuretic and draws free water out of the brain, reducing its volume. The dosage of mannitol is generally ) gDkg, followed by repeat ".,9 gDkg doses given every 0 hours as needed. (dministration should be followed by infusion of saline to maintain intravascular volume. @annitol has ma'imal effect in )" minutes and continues to work for up to 0 hours. $ntermittent bolus dosing is more effective than a continuous infusion #99%. ( serum sodium value of )99 or greater, or a serum osmolality of !," or greater are contraindications to administration because of the risk of acute tubular necrosis. aution is required in those with congestive heart failure or hyperemia because of intravascular volume e'pansion. $n fact, this property of mannitol has led to it being recommended as a rescuscitation fluid in the head injured, contrary to what many would think given its diuretic effects #93%. -urosemide has a similar duration of action and enhances free water clearance. $t can be administered every si' hours at the midway point between mannitol doses. $t appears to have a synergistic effect and may slow 8- production#0), 0,%. Hyper#entilation: :yperventilation may be the most effective measure in an acutely deteriorating patient as it has a very rapid effect, significantly reduces intracranial volume and because cerebrovascular response to <, is almost universally preserved. &hen used for chronic $ P control, however, worse outcomes are seen, perhaps by lowering cerebral blood flow e'cessively #0!%. ( low-normal p <, is now the recommended target. Prolonged hyperventilation should never be used in the first ,/h following head injury as it can further compromise reduced cerebral blood flow during this period though it remains listed in the guidelines as a possible treatment for $ P elevation refractory to other treatments #99%. Sedation and Paralysis: These agents may be needed to facilitate ventilation in intubated patients as well as in the imaging of restless patients. They also decrease cerebral metabolism, and blunt $ P elevations associated with no'ious stimuli. Barbiturates have shown mi'ed results in traumatic brain injury. $n patients with elevated $ P refractory to other measures, they achieve a , fold greater chance of control. :owever, hypotension refractory to fluid and pressors develops in 9"F of patients #0/%. $ncreased risk of pneumonia and the risk of myopathy and neuropathy are major drawbacks. Hypot!ermia: :ypothermia works by reducing cerebral metabolism and blood flow proportionately. @ild hypothermia #temperature !,-!!M % started within 0 hours of injury and maintained for ,/-/3 hours may be of benefit #09-01%. ardiac arrhythmia is a concern, especially below ,3M A coagulopathy, decreased cardiac inde', reduced renal function, pancreatitis and masking infections are also concerns. Sur"ery: >ecently guidelines were published that outline which patients are best brought to surgery, based on clinical features and imaging findings #!1%.

(symptomatic patients andDor those with intracranial hematomas with thickness less than )9mm #though many recommend )"mm%, volume less that !"cc*s, and midline shift less than 9mm can generally be watched. Posterior fossa lesions and hematomas in children should be treated more aggressively. Generally we discourage non-trained individuals from attempting burrhole drainage. Burrholes provide insufficient access and thick clot is very difficult to drain through such a hole even when blood is located in the epidural space. They can be used for diagnostic purposes, and to tempori+e a patient as will be described. .orthfield, in his pre- T era te't, provided recommendations for taking action #imaging or immediate e'ploratory surgery% and we feel his recommendations are still prudent. The following were suggested indications #//%B ). $ncreasing headache, drowsiness, or vomiting in a conscious patient. ,. ( patient who arrives to your centre unconscious with a report of earlier consciousness subsequent to the injury. !. ( patient unconscious since the injury, a deepening level of unconsciousness or increasing restlessness. /. Progressive papillary change, hemiparesis, posturing, and changes in the vital signs suggestive of a ushing*s response. 8urgery is recommended as early as possible in the evolution of these findings to optimi+e outcome. 9. -ailure to improve in the first few days following injury. .orthfield recommended special caution in patients presenting with post-traumatic cerebrospinal fluid leak, as this is increases the likelihood of a hematoma, and the loss in intracranial volume can prevent clinical diagnosis of a hematoma until a stage where decline can be precipitous. Basic (eurosurgical 'roce&ures in Trauma $n the following section we will describe several surgical procedures which can play a life-saving role in head injured patients. $deally this section would complement proper surgical instruction, however we recogni+e that even in ine'perienced hands these have the potential to be life-saving. &e trust that readers will e'ercise appropriate judgement in deciding how to implement the techniques we will describe, and seek proper surgical training if they would likely be required to perform such procedures. $t may be necessary to improvise surgical instruments in a facility not equipped for such procedures #03%. External %entricular Draina"e (E%D): This surgical technique involves placement of a tube into the lateral ventricle and is also known as ventriculostomy 4Figure =a,!6# This is the gold standard technique for measuring $ P #99%, and very importantly, this can allow 8- drainage, which can be life-saving in individuals with elevated $ P. $ndications for 6;2 insertion were previously discussed. ;entriculostomy need not be performed in an operating room, and is analogous to placement of a central line. 7ocal anaesthetic alone can be adequate for placement. Typically ventriculostomies are placed on the right side, which is non-dominant even in the majority of left-handed individuals. Placement may be a challenge following brain trauma as swelling can cause ventricular effacement. .onetheless, with e'perience even apparently effaced ventricles can be cannulated. The entry point for a ventriculostomy is generally made in the mid-pupillary line #about /cm lateral to the midline%, and ,cm anterior to the coronal suture, which can generally be palpated. ( line drawn directly superior to a point )cm anterior to the

tragus can also be used to appro'imate the antero-posterior entry point. :air in the surgical area is shaved, and a generous area is then 5prepped and draped.* (n incision ,-!cm long is made, generally in the saggital plane. ( self-retaining retractor holds the skin edges apart, and the surgeon can then drill a hole through the skull. $f the hole is small #as is commonly fashioned with commercial kits% an ))-blade can be used to incise the dura. $n a larger burrhole this is accomplished by incising the dura in cruciate fashion. The leaflets of dura are then cauteri+ed with a bipolar to cause them to shrink and retract. Bipolar cautery is then used to create an opening in the pia on the surface of the brain through which the ventriculostomy tube can be passed. The tubing is then passed through the brain into the ventricle after careful consideration of the trajectory. 8ome feel that the tubing should simply be directed as perpendicular to the surface of the brain as possible. <thers aim for the medial canthus of the ipsilateral eye and a point )cm anterior to the tragus of the ipsilateral ear. The distance of insertion must be monitored meticulously as this tubing must not be advanced more than 1cm from the surface of the skull or damage to the brainstem can #and frequently does% occur. 6ntry into the ventricle is generally associated with a 5popping* sensation. The tubing is then tunnelled subcutaneously and brought out through a separate stab incision. $t is then sutured in place, knowing that dislodgement of the tubing can otherwise occur. $f ventriculostomy is unsuccessful after ! passes or if the requisite equipment is not available, placement of an alternate measuring device is recommended. .umerous monitors are available and are too numerous to describe hereA insertion techniques are generally unique to the device. Exploratory or *+oodpecker Sur"ery,3 $n the days prior to T scanning a form of e'ploratory surgery was generally performed on patients 4Figure >6. This was done predominantly for diagnostic purposes as evacuation of a hematoma through a burrhole is nearly impossible even in e'perienced hands #04%. -ortunately this technique facilitates rapid conversion to craniotomy when an e'tra-a'ial hematoma is detected. @any referred to this colloquially as Iwoodpecker surgeryJ. &hen performing this surgery, access to both sides of the head is required, so supine positioning is used. The entire head is then shaved, sterili+ed and draped. ( series of burrholes are then placed through separate, non-contiguous incisions. Burrholes are placed in descending order of probability of locating a clot. The first burrhole is performed on the side considered most likely to harbour a clot #ie. ipsilateral to a blown pupil or contralateral to hemiparesis% recogni+ing that this may not be the appropriate side in a significant proportion of patients. #( blown pupil denotes the correct side of a hematoma only 3!F of the timeH#))%% The first burrhole is placed temporally, ,.9cm above the +ygomatic arch and just anterior to the ear. $f no hematoma is found, then the surgeon should fashion an identical burrhole on the contralateral side. $f both temporal burrholes are negative, the surgeon should then proceed to place frontal burrholes located antero-superiorly, just behind the hairline and a few centimetres off of the midline. $f both of these are negative, burrholes are then fashioned over the parietal lobes. $n general, for each pair of burrholes the one on the side of highest suspicion should be placed first. The incisions should be aligned such that they can be connected into a complete craniotomy incision. The burrholes should also be placed far apart so as to facilitate a large craniotomy which is capable of e'posing the majority of the hemisphere allowing the surgeon to surgically manage the majority of pathologies that may be encountered. are must be taken, however, to stay away from the venous sinuses.

(n epidural hematoma may be readily visible just below the skullA a subdural hematoma may be suggested by a bluish hue visible through the dural, though dural opening should routinely be conducted to rule out such a clot. $f a clot is located, the procedure is then converted to a craniotomy. $n e'treme circumstances, such as herniation in the face of an e'pected delay in surgical management, one can enlarge the temporal burrhole with a rongeur and open the dura to decompress the brain and a portion of a hematoma if present, tempori+ing until more definitive surgery can be performed. Craniotomy-Craniectomy: ( large incision is generally made to facilitate a generous craniotomy for the reasons already described. 8uch an incision is generally in the shape of a Iquestion markJ 4Figure5?a,!6. $t is started anterior to the ear, above the tragus so as to avoid the facial nerve. (fter e'tending rostrally just above the pinna it is turned posteriorly, circling around the occipitoparietal area, thusly turning anteriorly to finish in the anterior frontal region behind the hairline and a couple of centimetres off of the midline. Generally the incision is made down to bone at the time of the first cutA no special attention is paid to dissection of the temporalis muscle as might be done in other procedures. :emostasis is achieved with >ainey clips or cautery and the incision is made in a staged process to prevent significant blood loss. The temporal aspect of the incision and a generous temporal burrhole are made before completing the remainder of the incision. The dura is opened to achieve some degree of decompression while the remainder of the craniotomy is completed. The flap is then retracted forwards and secured in place. @onopolar cautery is of great utility in dissecting the superior attachment of the temporalis muscle off of the superior temporal line. ( variable number of burrholes are then made. Three are generally placed in the same locations described for Iwoodpecker surgeryJ, with additional locations being in the low posterior occipitotemporal region, and another in the 5keyhole* which is a bony depression just posterolateral to the orbit. &ith this latter burrhole, care must be taken to drill at the posterior aspect of the depression so as to avoid entry into the orbit. (n appropriate instrument #which is blunt and curved such as a Penfield !% is then passed into the burrhole in the plane between the dura and the skull so as to separate the dura from the inner table to prevent laceration when the bone flap is cut. The burrholes are then connected with a series of saw cuts. ( Gigli saw is hand-held and can be used if powered drills are not available. are is taken not to drop the slippery bone flap while it is delicately dissected off of the underlying dura and removed. (n epidural hematoma should be immediately visible, if present. 6ven when it is the only hematoma presumed present, one should make a small dural incision to ensure there is not evidence of subdural hemorrhage. ( cruciate dural incision can be made with a combination of scalpel and scissors to remove a subdural hematoma. lot should be removed carefully with suction and irrigation. Gentle brain retraction is used along with appropriate lighting #preferably a headlight% to remove hematoma beyond the margins of the craniotomy, taking care not to damage bridging veins. (ny identified sources of hemorrhage should be cauteri+ed or otherwise dealt with. <nce the evacuation is completed and hemostasis is achieved, a decision must be made as to whether or not the bone flap should be replaced. 8ome prefer to leave the bone flap out #ie. perform a craniectomy% following evacuation of an acute subdural hematoma which is very likely to be followed by significant brain swelling. This is rarely required for an epidural hematoma and in all types of brain injury little is lost if this is performed in a delayed fashion so long as it can be performed e'pediently. ( flap can be preserved in a very cold free+er, or in a pocket fashioned in the patient*s

abdominal adipose tissue. &hen the bone flap is replaced, this is optimally done with small plates and screws designed for the purpose, though holes can be drilled to facilitate passage of wire or heavy suture than can also be used to hold the skull in place. 2ui&elines for the Management of )ea& Injury Perhaps the biggest recent development in head injury has been the establishment of numerous guidelines to assist clinicians. =nfortunately, the level of evidence upon which the recommendations are based is poor, however the available evidence has been meticulously gathered and analy+ed. The Brain Trauma -oundation has made these available on their website. 8eparate evidence-based guidelines are available forB

Pre-hospital @anagement #1"% (dult TB$ @anagement #99% Pediatric TB$ @anagement #93% Penetrating :ead $njury #/,% 8urgical @anagement #!1%

Treatment Algorithm (s a summation of the literature and our clinical e'perience we present the following algorithm for (frican physicians facing the difficult decisions inherent in initial patient management. 6very clinical circumstance is unique and based on patient factors, the skills and e'perience of the physician, and the resources at hand. Physician judgement should supersede at all times. Patient age and comorbidities should also factor highly in decision-making.

*onclusion Though traumatic brain injury patients can be amongst the most intellectually and emotionally challenging patients to manage, it is important to avoid nihilism and to remember that aggressive management and adherence to guidelines is leading to improved outcomes. -urther, hope is justified because research is bringing forth new treatments that may help these often devastated patients. Gregory &. N. :awryluk, @2 and @ark Bernstein @2, -> 8 2ivision of .eurosurgery

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9/. Temkin .>, 2ikmen 88, &ilensky (N, ?eihm N, habal 8, &inn :>. A ran&omiDe&, &ou!le-!lin& stu&y of phenytoin for the prevention of posttraumatic seiDures# . 6ngl N @ed. )44"A!,!#3%B/41-9",. 99. Brain Trauma -oundation ((o., 8urgeons N8o.a . 2ui&elines for the management of severe traumatic !rain injury# N .eurotrauma. ,"""A)1B/9)K0,1. 90. >app >P, Poung B, Twyman 2, Bivins B(, :aack 2, Tibbs P(, Bean N>. The favora!le effect of early parenteral fee&ing on survival in hea&injure& patients# N .eurosurg. )43!A93#0%B4"0-),. 91. .arayan >?, ?ishore P>, Becker 2P, &ard N2, 6nas GG, Greenberg >P, 2omingues 2a 8ilva (, 7ipper @:, hoi 8 , @ayhall G, 7ut+ :( !rd, Poung :-. Intracranial pressure3 to monitor or not to monitorF A review of our e,perience with severe hea& injury# N .eurosurg. )43,A90#9%B09"-4. 93. Brain Trauma -oundation ((o.. 2ui&elines for the Acute Me&ical Management of Severe Traumatic Brain Injury in Infants, *hil&ren an& A&olescents. Pediatric ritical are @edicine ,""!A/#!%B8)-819. 94. @armarou (, (nderson >7, &ard N2, et al. Impact of I*' an& hypotension on outcome in patients with severe hea& injury# N .eurosurg )44)A19B89480/. 0". -eldman Q, ?anter @N, >obertson 8, et al. +ffect of hea& elevation on intracranial pressure, cere!ral perfusion pressure, an& cere!ral !loo& flow in hea&-injure& patients# N .eurosurg )44,A10B,"1-)). 0). Buhrley 76, >eed 2N. The effect of furosemi&e on so&ium-77 upta1e into cer!rospinal flui& an& !rain# 6'p Brain >es )41,A)/B9"!-)". 0,. @arion 2&, 7etarte PB. Management of intracranial hypertension# ontemp .eurosurg )441A)4#!%B)-0. 0!. @ui+elaar NP, &ei 6P, ?ontos :(, Becker 2P. A&verse effects of prolonge& hyperventilation in patients with severe hea& injury3 A ran&omiDe& clinical trial# N .eurosurg )43!A19B3,,-3,3. 0/. 6isenberg :@, -rankowski >-, ontant -, @arshall 7-, &alker @2. )igh&ose !ar!iturate control of elevate& intracranial pressure in patients with severe hea& injury# N .eurosurg. )433A04#)%B)9-,!. 09. lifton G7, (llen 8, Barrodale P, et al. A 'hase II Stu&y of mo&erate hypothermia in severe !rain injury# N .eurotrauma )44!A)"B,0!-,1). 00. @arion 2&, <brist &2, arlier P@, et al. The use of mo&erate therapeutic hypothermia for patients with severe hea& injuries3 A preliminary report# N .eurosurg )44!A14B!9/-!0,. 01. lifton G7, @iller 6>, hoi 8 , et al. @ac1 of effect of in&uction of hypothermia after acute !rain injury# . 6ngl N @ed ,"")A!//B990-90!. 03. &iggin T. +mergency craniotomy using improvise& instruments# Trop 2oct. ,"")A!)#!%B)1/. 04. @uhammad $. Management of hea& injuries at the A!u )ospital, Haria# 6ast (fr @ed N. )44"A01#0%B//1-9). 1". -oundation BT. 2ui&elines for 'rehospital Management of Traumatic Brain Injury# ,""". *lic1 here to join the Surgery in Africa "iscussion 2roup #Back to Top%

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