2 Cerebral Edema and Intracranial Pressure Ahmed Raslan, MD, and Anish Bhardwaj, MD, FAHA, FCCM Cerebral edema isa frequent and challenging prob- lem in the clinical setting and is a major cause of ‘morbidity and mortality in patients with acute Drain injury. Its simply defined as an increase in brain water content (normal brain water content is ‘approximately 80%) and is invariably aconsequence ‘of a primary brain insult Eiologes ofthese neuro- logie injuries that cause cerebral edema are diverse ‘and commonly include: ‘= Traumatic brain injury (TBI) 1 Subarachnoid hemorrhage (SAH) 1 Ischemic stroke 1m Intracerebral hemorthage (ICH) 1 Neoplasms (primary and metastatic) 1 Inflammatory diseases (meningitis, ventriculits, cerebral abscess, encephalils) ‘= Tosic-metabolic derangements (hyponatremia, fulminant hepatic encephalopathy) ‘CEREBRAL EDEMA: CLASSIFICATION ‘Traditional classification of cerebral edema into cytotoxic, vasogenic, and interstitial (hydrocepha- li) is overly simplistic in that it does not reflect the complexity of pathophysiologic and underly. ing molecular mechanisms. However, it serves asa simple therapeutic guide 1 Gytotoxic edema results from swelling ofthe ce: lular elements (neurons, glia, and endothelial cells) because of substrate and energy (Na, K’ “Ts work was supported by Public Heakh Serve NI grant pump) fallure and affects both gray and white ‘matter. This edema subtype isthe initial accom- paniment of any brain injury irrespective of etio Togy and conventionally is thought to be resistant toany known medical treatment. 1m Vasogenic edema that predominantly affects white matter, (ypically encountered in TBI, neo: plasms, and inflammatory conditions, results {rom breakdown of the blood-brain barrier (BBB) ‘due to increased vascular permeability and con- sequent leakage of plasma components. ‘This ‘edema subtype is responsive to both steroids (notably edema associated with neoplasms) and ‘osmotherapy. = Interstitial edeme, manifested as acute or chronic hydrocephalus, is a consequence of impaired absorption of cerebrospinal fluid (CSF) shat eads to Inereases in transependymal CSF flow due to elevations in hydrostatc pressure gradient. This edema subtype is also not responsive to steroids; its response to osmotherapy remains unproven aand debatable ‘bal edema may or may not result in eleva tions in intracranial pressure (ICP; normal, 5-15 ‘mm Hg: 8-18 em H,0). Most cases of brain injury that result in elevated ICP usually begin as focal cerebral edema, Consistent withthe Monroe-Kellie doctrine (see below and Chapter 8) as it applies to ‘altered intracranial vault physiology, the conse- ‘quences of focal or global cerebral edema, with or ‘without elevations in ICP, can be lethal and include cerebral Ischemia from compromised regional or ‘lobal cerebral blood flow (CBF) and intracranial compartmental shifts due to ICP gradients. un Intracranial compartmental shits can result in compression of vital brain structures ftom cerebral “herniation” and may cause death. Prompt recog nition ofthese clinical herniation syndromes war- rants institution of targeted therapies that constitute the basis for cerebral resuscitation, Herniation syn- dromes include: 1 Subfalcine or cingulate: Usually when the cingu- late gyrus herniates under thefakccerebri to cause compression of the ipsilateral anterior cerebral artery, resulting in contralateral lower extremity paresis. = Central tentoriak Downward displacement of ‘one or both cerebral hemispheres, resulting in ‘compression of the diencephalon and midbrai through thetentorialnotchand typically causedby centrally located masses. Presents with impaired consciousness and eye movements, elevated ICP, ‘and bilateral flexor or extensor posturing. = Lateral transtentorial (uncal): Most common form of herniation syndrome observed clinically, resulting from laterally located (hemispheric) ‘masses (tumors and hematomas). There is her- nation of the mesial temporal lobe, uncus, and hippocampal gyrus through the tentorial inci- sura leading «© compression of occulomotor nerve, midbrain, and posterior cerebral artery Clinically, the patient has a depressed level of consciousness, ipsilateral pupillary dilatation ‘and contralateral hemiparesis, decerebrate pos: turing, central neurogenic hyperventilation, and elevated ICP. = Tonsilar Herniation of cerebellar tonsils through the foramen magnum, leading to medullary com- pression, most frequently due to mass lesions in the posterior fossa Clinically, there are precipi- ‘ous changes in blood pressure, heart rate small pupils ataxic breathing, disturbance of conjugate gaze, and quadriparess, 18 External: Due to penetrating injuries to the skull, for example, gunshot wound or skull fractures ‘and has accompanying loss of CSF and brain ts sue, ICP may not be elevated because of dural opening. = Upward: Ni after placement of ventricular drain for external CSF drainage in the presence of a space-oceu- ping lesion in the posterior fossa. A “spinning op” appearance of midbrain and protrusion of ‘common and usually fatrogenic ‘A. Raslan and A. Bhardwaj the cerebellum through the quadrigeminal plate cistern on CT sean is characteristic. Itis imperative to underscore the importance ofthe presence ofa cerebral herniation syndrome without accompanying increments in global ICP, particu larly when cerebral edema is focal in distribution. INTRACRANIAL PRESSURE: BASIC ANATOMY AND CEREBRAL PHYSIOLOGY mn adults, the intracranial contents are encased in a rigid, nondistensible, bony skull. The foramen mag ‘num communicates direcdy with the spinal sub- arachnoid space and represents the main ext point from the calvaral fortress Within the sal folds ofthe ‘duramater compartmentalize intracranial contents, such that a tightly packed space (dhe tentorial inci- ‘sura) serves as the thruway between the middle and posterior fossa. The intracranial compartments com- posed of three main noncompressible components 18 Hrnin, with an estimated volume of approxi- ‘mately 1300-1500 mL. = CSF, representing approximately 75 ml. (20-25 ‘mL within the ventricular system) = Cerebral blood volume (CBW), accounting for approximately 75 mL. 70% ofblood volume iscon- tained inthe cerebral venoussinuses that comprise ‘low-pressure, high-capacity venous system, In pathologic conditions, with increased intrac- ranial volume (hy # tumor, hemorshage, oF beain ‘edema),compensatorymechanismsplayamajorrole in preventing or minimizing changes in ICP. Initially, (CSP is displaced from the intracranial compartment {nto the spinal thecal sac. Once this compensatory mechanism 1s exhausted, CBV is decreased, pri ‘marily atthe expense of fs venous component, but also by changes in the diameter ofthe basal arteries. ‘Ultimately, ifthe initial insult continues to progress, orifthe aforementioned compensatory mechanisms fail to contol ICP, brain herniation ensues. ‘This complementary relationship among be parenchyma, blood, and CSE has been termed the *Monro-Kellie doctrine” proposed in 1783, The doctrine simply can be interpreted as follows: Skull 1s arid box that contains elements that are incom pressble and an increase in the volume of each of ‘the intracranial components will beat the expense of other.(Cerebral Edema and Intracranial Pressure CEREBRAL EDEMA AND ICP: DIAGNOSIS AND MONITORING Determination of definitive contribution of cerebral cexiema tothe deterioration in neurologic status in a critically il patent can be challenging, as this may result from combination of the primary insult, or evolving secondary injury with accompanying cere- bral edema aver time, 1 Serial and close bedside monitoring of neurologic status with a focus on level of consciousness and new or worsening focal neurologic deficits cri caland frequently requires admission oan inten «Serial neuroimaging tudes (computed tomogea- phy [CT] and magnetic resonance imaging [MRI Scans) canbe pariculrlyuseflinconimingin- + eal hemiton syndromes, ischemic brain injury, and exacerbation of cerebral edema (lal fiace- nent and obliteration of basal cstes) and can «give valuable insights into the type of edema (focal or global, involvement of gray or white matter). {ICP montoring an important adjunctive tool in patients whom neurologic sarus is dificult 0 ‘sera serial pardculary inthe sting ofphar- nacologi sedation and newomsular paralysis > ‘The rain Trauma Foundation guidelines recom smendCP monitoring TBpaenswith Gasgow Coma Scale (GCS) sere of and shor Cx sean o Inpatient with GCS <9 and normal CT Age >40 years > Unilateral or bilateral motor posturing > Stoic blood presse <0 mm He ‘No uidelinesexistfor ICP monitoringinother brain injury paradigms (ischemic stoke, CH, cerebral neoplasms), and decisions made for ICP monitoring in this setting are frequently based on the clinical neurologic status ofthe patient and data from neuroimaging studies MEDICAL MANAGEMENT OF BRAIN EDEMA AND ELEVATED ICP. Medical management of cerebral edema (with or \without elevations in ICP) consists ofa graded algo rithmic approach from general measures to specific therapeutic interventions (Table 2.1) 3 Table 2.1. Management of cerebral edema and elevated intracranial pressure General measures ‘Optimize head position (30-60 degrees from horizontal) Neck position (midline) Normoxia (PaO, approximately 100 mm Ha); avoidance of hypoxemia Normocarbia(P3CO, approximately 35 mm Hg}; avoidance of hypercarbia 'Normathermia Normoglycemia Maintain CPP >60 mm Hy Adequate nutrition Seizure prophylaxis n select patients Specific measures Hyperventilation PaCO, 25-30 mm Ha) Corticosteroids (dexamethasone) in select patients (e.g, brain neoplasms) Loop diuretics (turosemide) ‘Osmotherapy (mannitol versus hypertonic saline) Pharmacologic coma barbiturates, propofol) Analgesia, sedation, and paralysis Hypothermia Surgical decompression General Measures ‘These measures are focused toward Limiting cere- bral edema that may or may not be accompanied by elevations in ICP, and the overriding goal oftheir application is to optimize cerebral perfusion, oxy genation, and venous drainage; minimize cerebral metabolic demands; and avoid interventions that may perturb the ionie or osmolar gradient between, the brainand the vascular compartment. These gen- ‘eral measues include: |= Head and neck postion: It has been well docu- ‘mented that in normal uninjured patients as well 1s in patients with brain injury, head elevation decreases ICP, These observations have led most clinicians to widely incorporate elevation of the hhead to 30 degrees in patients with poor intracra- nial compliance. However, head position eleva ‘don may be a significant concern in patients with4 7 Nalin armani rl pero einen ak 09%. 2% 05% ie Head Can ronetanced ‘A. Raslan and A. Bhardwaj 7 Nera Nii gh Game fp] fe ran nea | came ] 1 Coen of ot sac oi Pere] To Toop ga ra nah eae Malai someroleniahni ypencemia {loner scam Na gob oop ert accom tes et * Nama omens en ypencemia TSRINN pute 15-155 meq {stn soe a he LInp aise rod 7 Gir damage ee FaCO,2510mm tig Teap des Minin Cs on PHmi og (agai ke + Cy decor ey SSeS ae + Pharmocsogt coma pens ropto) Figure 2.1. Algorithm forthe management of cerebral edema and elevated intracranial pressure Reproduced from Raslan A, Bhardwaj A. Neurosurg Focus 2007;22 (51-12, with permission. {scheme stroke, as it may compromise perfusion toischemic tissue a isk = Ventilation and oxygenation: As dictated by prin «ciples of cerebral physiology, hypoxia and hyper- ‘capniare potent cerebral vasodilatorsand should be avoided in patients with cerebral edema. > PaCO, should be maintained at levels that sup- portadequateregional CBF (¢CBF)to the injured brain, and a value of approximately 35 mm Hgis ‘a generally accepted targetin the absence of CP ‘elevations or clinical hemiation syndromes. > Avoidance of hypoxemia and maintenance ‘of PaO, of approximately 100 mm Hg are recommended. = Maintenance of intravascular volume and cere- bral perfusion: Buvolemia or mild hypervolemia with the use ofsotonle Muids (0.9% saline) should always be maintained through rigorous monitor- ing of dally uid balance, body weight and serum electrolytes > ‘The recommended goal of CPP >60 mm Hig should be adhered o In patients with TBI > Sharp rises and precipitous falls in systemic blood pressure should be avoided. 1 Setzure prophylaxs: Seizures are deleterious in the setting of acute brain injury. Use of prophy- laetie anticonvulsants remains controversial in various brain injury paradigms. While use ofCerebral Edema and Intracranial Pressure prophylactic anticonvulsants is recommended in patients with TBI, their utility in a subarachnoid hhemorthage (SAH), ICH, ischemic stroke, and brain neoplasms curently is tailored to the indi- ‘vidual patient and is largely dependent on clnical practices = Management of fever: Numerous experimental ‘and clinical studies have demonstrated the delete rious effects offever on outcome afterbrain injury, th theoretically result from increases in oxj- igen demand, although the specific effects of fever ‘on cerebral edema have not been elucidated. > Normothermia is strongly recommended in patients with cerebral edema irespective of underlying etiology. > Acetaminophen (325-650 mg orally or rectally every 4-6 hours) is the most common agent ‘used and recommended to avoid elevations in body temperature. > Some efficacy of other surface and endovascu: lar cooling devices has been demonstrated. 18 Glycemic control: videncefromclinicalstudiesin patents with ischemic stroke, SAH, and TBI sug: gests a strong correlation between hyperglycemia ‘and adverse clinical outcomes. Hypergiycer ccan also exacerbate brain injury and cerebral edema > Significantly improved outcome has been reported in general ICU patients (including 20% of patient with TBI and post-craniotomy) ‘with adequate but, not tight contro. {= Nutritional suppose Promptinsticution and main= tenance of nutritional support is imperative in all patients with acute brain injury. Unless contrain- dicated, the enteral route of nutrition is preferred, Special attention should be given to the osmotic content of formulations, In order to avoid free water intake that may result in a hypo-osmolar state and worsen cerebral eden Specific Measures = Controlled hyperventilation: Most efficacious ‘therapeutic intervention for cerebral edema, ps ticularly when Its associated with elevations in ICP, Decrease in PaCO, by 10 mm Hg produces proportional decreases in 1CBF (and, in turn, decreases in CBV in the intracranial vault) result- rapid and prompt ICP reduction. 8 > Vasoconstrictive effect of respiratory alkalosis ‘on cerebral arterioleslasts only for 10-20 hours, ‘beyond which vascular dilation may result in ‘exacerbation of cerebral edema and rebound ‘elevations in ICP. > Prolonged hyperventilation results in worse ‘outcomes in patients with TBL Caution should be exerted in reversing hyper ventilation judiciously aver 6-24 hours to avoid ‘cerebral hyperemia and rebound elevations in ICP secondary to effects of reequilibration, © Osmotherapy: The Fundamental and simplistic {geal of smotherapy isto create an osmotic grad- tent to cause egress of water from the brain extra cellular (and possibly intracellular) compartment {into the vasculature, thereby decreasing intra- cranial volume and improving intracranial com- pliance. The goal of osmotherapy for cerebral ‘edema associated with brain injury is to mai tain a euvolemic ora slightly hypervolemic state. ‘As a fundamental principle, a hyposmolar state should always be avoided in any patlent who has an acute brain injury. > A serum osmolality in the range of 300-820 mOsmol/L has. traditionally been recom ‘mended for patients with acute rain injury who ‘demonstrate poor intracranial compliance. > Serum osmolality values >320 mOsmol/L can ‘be sed with caution, without apparent untow ard side effects, {include its inertness, being nontoxé, i its exclusion fom an intact BBB with minimalsystemicside effets, Mannitol and hypertonic saline (HS) solutions are ‘the most studied agents for elevatons in ICP ‘= The conventional osmotic agent mannitol, when administered at a dose of 0.25-1.5 g/kg by IV bolus injection, usually lowers ICP, with maximal ‘effects observed 20-40 minutes after its adminis- tration, Repeated dosing may be instituted every 6 hours and guided by serum osmolality toa ec ‘ommended target value of approximately 320 ‘mOsmol/L; higher values result in renal tubular damage. However, this therapeutic goal Is based ‘on limited evidence, and higher values can be targeted, provided the patient is not volume depleted,16 1= Variety of formulations of HS solutions (2%, 7.5%, 10%, 23%) are utllized in clinical practice forthe reatment of cerebral edema with or with- out elevations in ICP. HS solutions of 2%, 3%, oF 7.5% is used as a sodium chloride and sodium acetate mixture (50:50) to avoid hyperchloremic acidosis as continuous IV infusions (via a cen- tral venous catheter) ata variable rte to achieve euvolemia or slight hypervolemia (1-2 mL/kg perhour). > A250-mL bolus of HS can be administered cau Hiously in select patients if more aggressive and rapid resuscitation is warranted. > Normovolemic Muld status Is maintained, as ‘guided by central venous pressure or pulmo- nary artery wedge pressure (ifavailabe). > The goal in using HS is to inerease seru sodium concentration to a range of 145-155 mEq/L (serum osmolality approximately 300-320 mOsmol/L), but higher levels can be targeted cautiously. This level of serum sodium {s maintained for 48-72 hours, until patients {demonstrate clinical improvement, or there is lack of response despite the serum sodium goal being achieved. During withdrawal of therapy, spectal cau- tion is emphasized owing to the possibility of rebound hyponatremia leading to exacerba- tion of cerebral edema, Serum sodium and potassium are monitored every 4-6 hours, both during institution and withdrawal of therapy. Other serum electrolytes are mon itored dally (particular attention to caleium and magnesium). > Chest radiographs are performed atleast once every day to look for evidence of pulmonary edema from congestive heart failure, espe- cially in elderly patients with poor cardiovas- cular reserve. IV bolus injections (30 mL) of 23.4% HS have been utilized in cases of intracranial hyperten- sion refractory to conventional ICP-lowering, therapies; repeated injections of 30-mL. boluses of 23.4% HS may be given ifneeded to lower ICP. SAFETY OF HYPEROSMOLAR THERAPY 1 Safety concerne-with manmtol-inckite hypo- tension, hemolysis, hyperkalemia, renal insufi- 1cy,and pulmonary edema. AA. Raslan and A. Bhardwaj = No tials have been conducted to investigate safety with HS solutions. However, clinical expe- rence suggests thatthe side-effect profile of HS {s superior to that of mannitol, but some notable theoretical complications are possible with HS therapy, including > GNS changes (encephalopathy, lethargy, sel zures, coma) > Myelinolysis > Congestive heart fallure, cardiac stun, cardiac arrhythmias > Pulmonary edema Electrolyte derangements (hypokalemia, hypo- ‘magnesemia, hypocalcemia) ‘Metabolic academia (hyperchloremic with use ofchloride solutions) > Potentiation of nontamponaded bleeding > Subdural hematomas resulting from shearing ‘ofbridging veins due to hyperosmolar contrac- ture of brain > Hemolysis with rapid infusions, resulting in sudden osmotic gradients in serum, phlebitis ‘with infusion via the peripheral route > Coagulopathy (elevated prothrombin and par- ‘ial thromboplastin time, platelet dysfunction) > Rebound hyponatremia leading to cerebral edema with rapid withdrawal 1 Diuretic: The use of loop diuretics (commonly {urosemide) for the treatment of cerebral edema, particularly when used alone, remains controver: sial, The combination of furosemide with man- tol produces a profound dlusests; however, the Acommon strategy to rise serum sodium rapidly {sto administer an 1V bolus of furosemide (10-20 mig) toenhance ree waterexcretion and to replace ‘twit 250-mL IV bolus of 2% oF 3% HS. Corticosteroid: The main indication forthe use of steroids is for the treatment of vasogenic edema, commonly associated with brain tumors, after brain radiation, and retraction injury from surgi- cal manipulation, While the precise mechanisms ofthe beneficial effects of steroids inthis paradigm fare not known, steroids decrease tight junction permeability and, in tur, stabilize the disrupted BBB. Therapeutic role of steroidsin TBL and stroke‘Cerebral Edema and tntracra Pressure hhas been studied extensively. In TBI, steroids failed to control elevations in ICP or show any benefit in ‘outcome and may even be harmful. In stroke, ste- roids have falled to show any substantial benefit despite some suceessin animal models. > Glucocorticaids, especially dexamethasone, are the preferred agents due to its low miner alocortcoid activity. > Inlightof deleterious side effects (peptic leers, bbyperglycemia, impairment of wound healing, psychoss, and immunosuppression), until fa ther studies are published, caution is advised inthe use of steroid for cerebral edema unless absolutely Indicated. 1 Pharmacologic Come: > Warbituratas: Known over several decades from numerous experimental studies that barbitw: rates are neuroprotective and lower elevated ICP via reduction in cerebral metabolic activ- lity that is coupled to reduction in CBF (and CBV indireely, thereby decreasing intrac elastance), Use of barbiturates in clinical prac: tice isnot without controversy as experimental studies have not readily translated into clinieal paradigms. In patents with TBI, barbiturates are effective in reducing ICP but have failed {o show improvement in clinical outcome idence is limited for utility of barbiturates in the setting of cerebral pathologies that include space-occupying lesions (tumor, ICH) and ischemic stroke. P Pentobarbital is the preferred agent over thiopental (short acting: half-life approx- imately 5 hours) or phenobarbital (long- acting; halflife approximately 72-96 hours) because of is intermediate physiologic hal ie (72-96 hour). > The recommended regimen entails a load- ing 1V bolus dose of pentobarbital (3-10 mg kg), followed by a continuous TV infusion (0.5-3.0 mg/kg per hour; serum levels 3 mg/ 4), whichis titrated to sustained reduction in ICP orachievinga "burst-suppression pat tern” on continuous EEG monitoring Barbiturate (pentobarbital) coma should bbe maintained for 48-72 hour, with gradual tapering by decreasing the hourly infusion by 50% each day. Several adverse effects of barbiturates that limit their clinical use include sustained v ‘vasodepressor effect. (hypotension and decrease in CPP), myocardial depression, immunosuppression leading to increased risk of infection, and hypothermia, > The most important limitation with bark ‘urate coma is the inability o follow sub- tle changes in clinical neurologic status, Which necessitates frequent and serial neuroimaging. > Propofol: Because of the potential side effects ‘of barbiturates and relative long half-life, ‘propofol has emerged as an appealing atern tive, especially due to its ultra-short half Effcacious in controlling ICP in TBI patients, ‘talso has antiseizure properties and decreases cerebral metabolic rate. > While propofol use continues to become ‘more popular due to these properties, hypo- tension can be the limiting factor tots use in the clinieal setting, > Other adverse effects inchude hypertiglye- ceridemia and increased CO, production due tothe lipid emulsification vehicle. Careful monitoring of serum triglycerides is ‘recommended with ts use. Cases of ‘propofol infuston syndrome” that ‘can he fatal have been reported, particularly In children, when propofol Is used over @ long period of time at high doses. 1 Analgesia, Sedation, and Neuromuscular Blockade Pain and agitation can exacerbate corebral edema and raise ICP and compromise CPP significantly. Judicious bolus IV administration of short-acting narcotics such as morphine (2-5 mg) and fentanyl (25-100 pg) ora continuous titratable IV infusion of fentanyl (25-200 yg/h) are preferred agents for anal gesia, Special care must be taken for airway protec tion and not to mask the serial bedside neurologic ‘examination. Neuromuscular blockade can be a useful ‘adjunet in control of refractory elevations in ICP. Nondepolarizingagents(pancuronium, vecuronium, rocuronium) are the preferred agents, as a depolar- izing neuromuscular blocker such as succinylcho: line ean potentially cause elevations in ICP (usually transient), due to muscle contraction. Other con: siderations include hepatic and renal insuiciency, 1s these may significantly prolong metabolism and ‘excretion of these agents Inability to follow serial8 AcRaslan and A. Bhardwaj neurologic examinations may necessitate frequent ‘and sometimes unwarranted neuroimaging studies undergo early decompressive. craniectomy. However, debate continues as to long-term functional outcomes although reeent metanal- 1 Abpoibermia: Robust data from experimental anda few clinical studies demonstrate dhthyper- thermia exacerbates brain injury However, spe- tile effects of hypothermia on brain edema pet se remain unclear at present Further, beneficial effects of therapeutic hypothermia demonstrated Inlaboratory-based studies have nottranslatedin all bain injury paradigms as dictated by benef- cial effets on neurologic outcomes. > Therapeutichypothermiahasseveralaccompa- ying adverse side effects including preumo- tia, dhrombocytopenia, severe coagulopathy, hhemodynamicinstability cardiac artis hypotension, cardia fale), and pancreatitis > Recent trials of therapeutic mild hypothermia (62°C) following out-of hospital cardiac areest, accomplished within 8 hours and maintained for 12-24 hours, improved morality and fan tional outcomes. Based on these tals mild Iypothermias quickly becominga standard of cate globally in management of patients after cardiac ares. ‘The ole of hypothermia in the setting of Tis Jess cleat and previous cna was have not demonstrated eficacy. Nevertheless, achieving ysis isencouraging. > Anearly neurosurgical consultforthisinterven- tion is strongly suggested in seloct few patients ‘with poor neurologic status with severe brain injury and space-occupying pathologies on neuroimaging studies. > Technical considerations for hemicraniectomy for malignant ischemie strokes Include: > Durotomy with duroplasty is recommended, > The procedure is performed over entire region of bony decompression, > Cruciate or circumferential durotomy is acceptable. > Dural graftingis recommended. ‘he bone flap issavedina bone bank or peri- toneal cavity and replaced within 3 months > Noncompression dressing should be applied. _Ventriculostomy is not recommended. > Brain amputation is not recommended, SUMMARY AND CONCLUSIONS (Cerebral edema is frequently encountered in clin ‘and maintaining normothermia is a desirable goal In critically ill paients with brain injury inrespective of etiology. A varloty of surface ae well as endovascular ‘cooling methods are present utilized in clin ‘cal practice. 1 uggioabddecampressig: Surgical decompression via craniectomy with or without brain amputa tion Is an old therapy that is increasingly gain. ing resurgence as a rescue therapy for malignant cerebral edema that may or may not be accompa nied by elevations in ICP. Tis surgical treatment {applicable ina variety of brain injury paradigms that have space-occupying components in the {aeranial vault including malignant ischemic strokes, TBI, ICH, and encephalitis. > Timing of surgery, age of the patient, and ent- cal practice and is a major cause of morbidity end ‘mortality in crtically ill neurology and neurosurg cal patients with acute brain injury, Consequences fof corebral edema can be catastrophic and inchide cerebral ischemia from compromised regional or slobal CBF and intracranial compartmental shifts ‘due to ICP gradients in the intracranial vault that result in. compression of vital brain structures. Management of cerebral edema entails a timely, systematic, and algorithmie approach with an over arching goal of maintaining regional and global CBF tomeet the metabolicrequirements of the brain and prevent secondary neuronal injury from cerebral Ischemia, Early surgical decompression should be ‘considered in some brain injury paradigms tcl ndings “on neuroimaging studies ae wepeRENCces Important determinants decison making. Ns ney an edema, > Recent studies pariularyformalignantcere- mae Tamer ofan edema Neca. 2 bral infarctions, strongly suggest that mortality [smarkedly attenuatedin younger patients who Bhardva) A. Cerebral edemn and intracranial yperten sion. In Bhardwa) A Mik MA, Ulatowsk JA (ed)