After treating elevated intracranial pressure, the question, then, is what those minutes or hours are buying. The answer is not simply a lower ICP. They are buying time to reverse a dangerous intracranial pressure gradient before displacement of brain tissue produces irreversible vascular injury, brainstem distortion, or death. This distinction is the key to understanding cerebral herniation. Intracranial hypertension is a pressure state; herniation is a movement syndrome. The two frequently coexist, but they are not interchangeable. A patient can have a globally elevated ICP without active herniation, while a focal temporal, posterior fossa, or compartmental mass can produce lethal tissue shift even when a monitor elsewhere in the skull reports a value that is not especially impressive. The attending-level question is therefore not merely, “How high is the ICP?” It is, “Where is the pressure being generated, where is the brain being displaced, which structures are being compressed, and how much reversible time remains?”
The falx, tentorium, and foramen magnum convert the cranial vault into partially communicating compartments. Once compliance is exhausted, a pressure difference between these compartments drives tissue across one of those rigid boundaries. Subfalcine herniation shifts the cingulate gyrus beneath the falx and may compress the anterior cerebral artery. Uncal herniation displaces the medial temporal lobe across the tentorial edge, where it can compress the ipsilateral third nerve, posterior cerebral artery, and midbrain. Central transtentorial herniation produces progressively caudal displacement of the diencephalon and brainstem. Posterior fossa lesions can push the cerebellum upward through the tentorial incisura, downward through the foramen magnum, or directly against the brainstem while simultaneously obstructing the fourth ventricle. These are not merely geometric events. Tissue displacement stretches perforating arteries, obstructs venous drainage, compresses CSF pathways, and can produce secondary ischemia in tissue that was initially uninjured. Downward brainstem displacement may tear small penetrating vessels and produce Duret hemorrhages. Those hemorrhages indicate a severe mechanical insult, although their presence alone should not automatically be treated as proof that recovery is impossible.
The classic unilateral dilated pupil of uncal herniation results from parasympathetic fiber compression along the superficial third nerve, usually on the side of the mass. This is often accompanied by contralateral weakness, but the rule is not absolute. When the opposite cerebral peduncle is forced against the tentorial edge—the Kernohan notch phenomenon—the weakness may be ipsilateral to the mass and therefore falsely localizing. Compression of the posterior cerebral artery can produce an occipital infarction. With progressive central herniation, consciousness declines as the diencephalon and ascending arousal networks are distorted; pupils may progress from small and reactive to midposition and poorly reactive, motor responses may evolve from localization to flexor and then extensor posturing, and respiratory patterns become increasingly abnormal. These textbook sequences are useful anatomically but unreliable as a bedside clock. Sedatives, ocular trauma, prior eye surgery, anticholinergic exposure, hypothermia, seizures, and direct midbrain injury can all alter the examination. Conversely, a patient does not need to complete the textbook sequence before irreversible injury occurs.
The Cushing response—hypertension, bradycardia, and irregular respiration—is particularly dangerous as a diagnostic requirement because it is late, inconsistent, and may be obscured by mechanical ventilation, medications, autonomic dysfunction, or shock. A new pupillary asymmetry, abrupt decline in arousal, new extensor posturing, unexplained vomiting, or sudden loss of previously present brainstem reflexes in a patient with a plausible intracranial lesion should be treated as impending herniation until proved otherwise. Quantitative pupillometry can improve detection of change and reduce observer variability, but a normal numerical pupil index does not exclude a focal pressure gradient, and an abnormal value does not identify its cause. Likewise, optic nerve sheath diameter, transcranial Doppler, and other noninvasive surrogates may support concern but cannot safely overrule a deteriorating clinical examination.
CT findings should be interpreted in the same physiologic way. Midline shift is useful, but the number of millimeters is not a universal severity scale. A slowly growing mass may produce substantial shift with partial compensation, whereas a smaller acute posterior fossa lesion may be devastating because there is little room for displacement. Effacement of basal cisterns, ventricular trapping, obstructive hydrocephalus, compression of the third or fourth ventricle, loss of sulci, downward displacement, and evolving vascular-territory infarction often matter more than a single shift measurement. If the patient is actively deteriorating, treatment begins before transport to CT. Imaging defines the lesion and the definitive intervention; it should not become a prerequisite for reversing hypoxia, hypotension, hypercapnia, or an obvious herniation syndrome.
The initial response should function like a neurologic resuscitation. Call neurosurgery immediately, secure oxygenation and ventilation, elevate the head approximately thirty degrees, keep the neck neutral, and remove anything that obstructs jugular drainage. In a trauma patient, that does not mean casually discarding cervical precautions; it means loosening an unnecessarily constrictive collar or endotracheal-tube fixation only while maintaining appropriate alternative stabilization. Treat pain, agitation, coughing, shivering, fever, and seizures because each can increase cerebral metabolism, cerebral blood volume, or venous pressure. Intubation may be necessary, but peri-intubation hypotension, hypoxia, and prolonged apnea can convert a potentially reversible pressure crisis into global ischemic injury. Preoxygenation, adequate induction conditions, vasopressor readiness, and immediate control of ventilation are therefore part of the neurologic treatment rather than generic airway housekeeping.
Positioning is not physiologically free. Head elevation usually improves venous drainage and lowers ICP, but it can also lower arterial pressure at the level of the brain. When CPP is being calculated in a head-elevated patient, the MAP transducer should be referenced consistently—commonly near the tragus—because a transducer left at the heart can overestimate cerebral arterial pressure. If ICP is 30 mm Hg and the true MAP at the brain is 80, the CPP is only 50, regardless of how reassuring the brachial pressure appears. Severe-TBI guidance continues to use a CPP range of approximately 60–70 mm Hg, while recognizing that the optimal point depends on autoregulatory status and that aggressively forcing CPP above 70 can produce systemic harm. The same guidance recommends treating sustained ICP above 22 mm Hg, but the clinical examination and CT remain part of the decision rather than optional modifiers. A 2024 cohort could not reproduce 22 mm Hg as a universal discriminator and found considerable variation across subgroups, reinforcing that duration, trajectory, autoregulation, and tissue vulnerability matter along with the absolute value. Brain Trauma Foundation guidance remains the clinical standard, while the newer threshold data argue against treating 22 as a biologic cliff rather than a population-derived action point. The 2024 threshold study should refine, not erase, that standard.
Hypotension must be corrected promptly with appropriate isotonic volume and vasopressors when necessary. Norepinephrine is often practical because it can restore MAP without requiring excessive fluid, but the correct hemodynamic target remains disease- and patient-specific. Reflexively treating hypertension during active herniation can be catastrophic if the pressure is supporting CPP. Conversely, an expanding intracerebral hemorrhage may still require controlled blood-pressure reduction. The solution is not to choose either “blood pressure control” or “CPP support” as an absolute principle; it is to determine whether continued hematoma expansion, inadequate perfusion, or both are the immediate threat and titrate treatment accordingly.
Ventilation provides the fastest nonoperative method of reducing cerebral blood volume. Lowering PaCO₂ raises perivascular pH, constricts cerebral arterioles, reduces cerebral blood flow and blood volume, and can lower ICP within minutes. The same mechanism can worsen ischemia when blood flow is already critically reduced. Hyperventilation is therefore a bridge for active herniation, not prophylaxis against the possibility of future swelling. A reasonable emergency goal is generally a PaCO₂ around 30–35 mm Hg while definitive therapy is mobilized, confirmed with an arterial blood gas because the end-tidal gradient may be unreliable. Empirically driving PaCO₂ to 25 mm Hg or lower for prolonged periods is not recommended, and early severe TBI is particularly vulnerable because cerebral blood flow may already be depressed. If aggressive ventilation is unavoidable, brain-tissue oxygen or jugular venous oxygen monitoring can help identify an ischemic tradeoff. As CSF bicarbonate gradually compensates for respiratory alkalosis, the ICP effect wanes; abrupt return to normocapnia can then cause rapid vasodilation and rebound ICP elevation. Hyperventilation should therefore be withdrawn deliberately once the lesion is controlled. These principles remain explicit in current Brain Trauma Foundation recommendations.
Hyperosmolar therapy is administered simultaneously when herniation is suspected; one should not wait for an ICP monitor or a new sodium result. Hypertonic saline is attractive when blood-pressure and intravascular-volume support are desirable, while mannitol may be reasonable when sodium or chloride loading is problematic and renal function and circulating volume are adequate. The agent and dose matter less than whether an effective bolus is delivered promptly and produces a cerebral response. Improvement in pupillary symmetry, motor examination, ICP, CPP, or tissue shift supports continued temporization. Serial boluses without a reproducible response suggest that the gradient is too large, the blood–brain barrier physiology is unfavorable, the dominant compartment is not tissue water, or the injury has progressed beyond what osmotherapy can reverse. The Neurocritical Care Society’s guideline similarly concludes that hyperosmolar agents can reduce ICP or edema but that evidence for improved long-term neurologic outcome remains limited. NCS cerebral-edema guideline.
CSF drainage is often the most direct treatment when hydrocephalus or ventricular enlargement contributes to the pressure crisis. If a functioning EVD is already present, opening it according to the established drainage protocol may reverse deterioration faster than another osmotic bolus. Continuous drainage can reduce ICP burden, although an open EVD cannot simultaneously provide an uninterrupted ventricular-pressure tracing unless a separate monitor is present. Failure to drain should prompt an immediate mechanical assessment: Is the stopcock configured correctly? Is the system leveled properly? Is the catheter obstructed by blood or collapsed ventricle? Has the ventricle become trapped on the side opposite the catheter? Lumbar puncture or lumbar drainage is fundamentally different and can worsen a dangerous craniospinal gradient when a mass lesion, obstructive hydrocephalus, or basal cistern effacement is present. Posterior fossa disease requires particular caution because ventricular drainage may treat hydrocephalus while leaving direct brainstem compression untouched. CSF diversion must not become a reason to delay posterior fossa decompression.
The 2026 AHA/ASA acute ischemic stroke guideline makes that point more explicitly for cerebellar infarction. Ventriculostomy is recommended for obstructive hydrocephalus, but the need for concomitant or subsequent suboccipital decompression depends on infarct size, neurologic condition, brainstem compression, and response to drainage. For deterioration caused by brainstem compression—or a cerebellar infarct volume of at least 35 mL—the guideline recommends decompressive suboccipital craniectomy with dural expansion. For large supratentorial infarction, declining consciousness attributable to swelling is considered a reasonable operative trigger. In patients sixty or younger who deteriorate from unilateral MCA swelling within forty-eight hours despite medical therapy, hemicraniectomy reduces mortality and improves the functional-outcome distribution; in patients older than sixty, surgery may reduce mortality, but the probability of survival with major disability must be discussed clearly. Prior thrombolysis does not by itself preclude decompression. 2026 AHA/ASA acute ischemic stroke guideline.
That timing distinction is crucial. In malignant hemispheric infarction, waiting for a fixed pupil before offering surgery is not proof that medical therapy was fully attempted; it may mean the useful operative window was consumed by treatments incapable of creating space. Osmotherapy can transiently reduce water in relatively intact tissue, but it cannot remove the completed infarct or enlarge the cranial vault. Surgery works by changing the compliance curve itself. Removing a sufficiently large bone flap and opening the dura permits expansion outward rather than downward across the tentorium. The operation therefore lowers ICP and reduces tissue shift with remarkable reliability. Whether it improves meaningful outcome depends on what injury existed before decompression, how long the gradient persisted, the patient’s age and baseline function, the eloquence and laterality of injured tissue, and what degrees of disability the patient would consider acceptable.
The TBI evidence demonstrates this distinction especially well. DECRA tested relatively early decompression for modest but refractory ICP elevation in diffuse injury. Surgery controlled ICP and shortened intensive-care exposure but did not improve functional outcome. RESCUEicp studied later, more severe refractory intracranial hypertension and found that decompression reduced mortality, but it also increased survival across a broad range of disability states. Follow-up showed that some patients continued to improve between six and twenty-four months, yet the central tradeoff remained: decompression can prevent death without guaranteeing recovery to independence. The current Brain Trauma Foundation update therefore recommends secondary decompression for the later refractory-ICP population represented by RESCUEicp, does not recommend early secondary decompression to improve outcome in the DECRA-type population, and favors a large frontotemporoparietal opening—at least 12 by 15 cm or approximately 15 cm in diameter—over a small decompression. Importantly, “early” and “late” here refer to the distinct trial phenotypes and ICP criteria, not to a simplistic clock-based rule applicable to every patient. Brain Trauma Foundation decompressive-craniectomy update. The twenty-four-month RESCUEicp analysis reinforces the need to discuss survival and functional state separately.
Spontaneous deep ICH provides an even cleaner example of physiology outrunning clinical evidence. The 2024 SWITCH trial tested decompressive craniectomy without hematoma evacuation in approximately two hundred patients with severe basal ganglia or thalamic hemorrhage. Death or mRS 5 at six months occurred in 44% with decompression and 58% with medical therapy, but the confidence interval crossed unity and the primary result narrowly missed conventional statistical significance. The trial stopped early because of funding, severe adverse events were similar, and substantial disability remained common among survivors. The correct conclusion is not that decompression is ineffective, nor that it is now standard for deep ICH. SWITCH provides weak, hypothesis-supporting evidence that selected patients may benefit, while leaving substantial uncertainty about patient selection and the value patients assign to the resulting outcome states. SWITCH trial.
Medical metabolic suppression occupies the final rescue tier when a surgically correctable lesion has been excluded or addressed. Propofol can reduce cerebral metabolic demand and, when flow–metabolism coupling is preserved, reduce cerebral blood flow and blood volume. Its ICP benefit can be erased by hypotension, and high-dose or prolonged administration carries the risk of propofol-infusion syndrome. Neuromuscular blockade is useful when coughing, shivering, or ventilator dyssynchrony is measurably driving ICP, but it does not directly suppress cerebral metabolism and it removes the motor examination; continuous EEG becomes increasingly important. High-dose barbiturates can control ICP refractory to maximal medical and surgical treatment, but they require hemodynamic stability and should be titrated to the ICP response with EEG providing a ceiling once adequate burst suppression is achieved. Prophylactic barbiturate coma is not beneficial. Hypothermia also lowers metabolism and ICP, yet prophylactic or routine therapeutic hypothermia in TBI has not translated into improved neurologic outcome and has produced harm in some trials. Normothermia is the goal; mild hypothermia is, at most, a highly selected last-tier maneuver after its hypotensive, infectious, coagulopathic, and rewarming risks are considered. Steroids should not be used for traumatic, ischemic, or primary hemorrhagic cerebral edema. Their role belongs principally to vasogenic edema from tumors and selected inflammatory or infectious conditions; high-dose methylprednisolone in severe TBI increased mortality.
After decompression, a normal ICP does not prove that the crisis is over. Hemorrhagic progression, external cerebral herniation through an inadequate opening, venous kinking, infarct extension, hydrocephalus, seizures, and persistently impaired brain oxygenation can all continue despite a lower global pressure. At the opposite extreme, a craniectomized patient can develop paradoxical herniation when CSF drainage, dehydration, or atmospheric pressure produces abnormally low intracranial pressure and inward deformation of the scalp flap. The treatment is then the reverse of conventional ICP therapy: stop CSF drainage, restore intravascular volume, position the patient flat or head-down when tolerated, and pursue urgent definitive correction, often cranioplasty. This exception proves the larger rule—herniation is produced by a pressure gradient, not necessarily by a high absolute ICP.
The clean bedside model is therefore this: recognize tissue shift before the full terminal syndrome appears, stabilize oxygenation and perfusion, improve venous outflow, use brief controlled hyperventilation and an effective osmotic bolus to buy time, drain CSF when CSF is the pressure-generating compartment, remove a mass when a mass is the cause, and enlarge the cranial container when swelling has become mechanically incompatible with survival. Judge success by the threatened brain—pupils, arousal, motor responses, ICP burden, CPP, imaging, and, when available, cerebral oxygenation—not by whether one isolated number became normal. Every temporizing intervention should answer the question, “What definitive change am I buying time for?” The next physiologic layer is CSF dynamics, hydrocephalus, and external ventricular drainage, because once CSF becomes both a monitored variable and a therapeutic compartment, the details of leveling, drainage strategy, waveform interpretation, obstruction, and weaning directly determine whether the ICP information can be trusted.
References
Andrews, P. J. D., Sinclair, H. L., Rodriguez, A., Harris, B. A., Battison, C. G., Rhodes, J. K. J., Murray, G. D., & Eurotherm3235 Trial Collaborators. (2015). Hypothermia for intracranial hypertension after traumatic brain injury. The New England Journal of Medicine, 373(25), 2403–2412. https://doi.org/10.1056/NEJMoa1507581
Beck, J., Fung, C., Strbian, D., Bütikofer, L., Z’Graggen, W. J., Lang, M. F., Beyeler, S., Gralla, J., Ringel, F., Schaller, K., Plesnila, N., Arnold, M., Hacke, W., Jüni, P., Mendelow, A. D., Stapf, C., Al-Shahi Salman, R., Bressan, J., Lerch, S., … Fischer, U. (2024). Decompressive craniectomy plus best medical treatment versus best medical treatment alone for spontaneous severe deep supratentorial intracerebral haemorrhage: A randomised controlled clinical trial. The Lancet, 403(10442), 2395–2404. https://doi.org/10.1016/S0140-6736(24)00702-5
Cadena, R., Shoykhet, M., & Ratcliff, J. J. (2017). Emergency Neurological Life Support: Intracranial hypertension and herniation. Neurocritical Care, 27(Suppl. 1), 82–88. https://doi.org/10.1007/s12028-017-0454-z
Carney, N., Totten, A. M., O’Reilly, C., Ullman, J. S., Hawryluk, G. W. J., Bell, M. J., Bratton, S. L., Chesnut, R., Harris, O. A., Kissoon, N., Rubiano, A. M., Shutter, L., Tasker, R. C., Vavilala, M. S., Wilberger, J., Wright, D. W., & Ghajar, J. (2017). Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery, 80(1), 6–15. https://doi.org/10.1227/NEU.0000000000001432
Cook, A. M., Morgan Jones, G., Hawryluk, G. W. J., Mailloux, P., McLaughlin, D., Papangelou, A., Samuel, S., Tokumaru, S., Venkatasubramanian, C., Zacko, C., Zimmermann, L. L., Hirsch, K., & Shutter, L. (2020). Guidelines for the acute treatment of cerebral edema in neurocritical care patients. Neurocritical Care, 32(3), 647–666. https://doi.org/10.1007/s12028-020-00959-7
Cooper, D. J., Rosenfeld, J. V., Murray, L., Arabi, Y. M., Davies, A. R., D’Urso, P., Kossmann, T., Ponsford, J., Seppelt, I. M., Reilly, P., & Wolfe, R. (2011). Decompressive craniectomy in diffuse traumatic brain injury. The New England Journal of Medicine, 364(16), 1493–1502. https://doi.org/10.1056/NEJMoa1102077
CRASH Trial Collaborators. (2005). Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury—Outcomes at 6 months. The Lancet, 365(9475), 1957–1959. https://doi.org/10.1016/S0140-6736(05)66552-X
Edlow, B. L., Threlkeld, Z. D., Fehnel, K. P., & Bodien, Y. G. (2019). Recovery of functional independence after traumatic transtentorial herniation with Duret hemorrhages. Frontiers in Neurology, 10, Article 1077. https://doi.org/10.3389/fneur.2019.01077
Fried, H. I., Nathan, B. R., Rowe, A. S., Zabramski, J. M., Andaluz, N., Bhimraj, A., Guanci, M. M., Seder, D. B., & Singh, J. M. (2016). The insertion and management of external ventricular drains: An evidence-based consensus statement. Neurocritical Care, 24(1), 61–81. https://doi.org/10.1007/s12028-015-0224-8
Hawryluk, G. W. J., Rubiano, A. M., Totten, A. M., O’Reilly, C., Ullman, J. S., Bratton, S. L., Chesnut, R., Harris, O. A., Kissoon, N., Shutter, L., Tasker, R. C., Vavilala, M. S., Wilberger, J., Wright, D. W., Lumba-Brown, A., & Ghajar, J. (2020). Guidelines for the management of severe traumatic brain injury: 2020 update of the decompressive craniectomy recommendations. Neurosurgery, 87(3), 427–434. https://doi.org/10.1093/neuros/nyaa278
Hutchinson, P. J., Kolias, A. G., Timofeev, I. S., Corteen, E. A., Czosnyka, M., Timothy, J., Anderson, I., Bulters, D. O., Belli, A., Eynon, C. A., Wadley, J., Mendelow, A. D., Mitchell, P. M., Wilson, M. H., Critchley, G., Sahuquillo, J., Unterberg, A., Servadei, F., Teasdale, G. M., … Kirkpatrick, P. J. (2016). Trial of decompressive craniectomy for traumatic intracranial hypertension. The New England Journal of Medicine, 375(12), 1119–1130. https://doi.org/10.1056/NEJMoa1605215
Jüttler, E., Unterberg, A., Woitzik, J., Bösel, J., Amiri, H., Sakowitz, O. W., Gondan, M., Schiller, P., Limprecht, R., Luntz, S., Schneider, H., Pinzer, T., Hobohm, C., Meixensberger, J., & Hacke, W. (2014). Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke. The New England Journal of Medicine, 370(12), 1091–1100. https://doi.org/10.1056/NEJMoa1311367
Kolias, A. G., Adams, H., Timofeev, I. S., Corteen, E. A., Hossain, I., Czosnyka, M., Timothy, J., Anderson, I., Bulters, D. O., Belli, A., Eynon, C. A., Wadley, J., Mendelow, A. D., Mitchell, P. M., Wilson, M. H., Critchley, G., Sahuquillo, J., Unterberg, A., Posti, J. P., … Hutchinson, P. J. (2022). Evaluation of outcomes among patients with traumatic intracranial hypertension treated with decompressive craniectomy versus standard medical care at 24 months: A secondary analysis of the RESCUEicp randomized clinical trial. JAMA Neurology, 79(7), 664–671. https://doi.org/10.1001/jamaneurol.2022.1070
Liotta, E. M. (2021). Management of cerebral edema, brain compression, and intracranial pressure. Continuum, 27(5), 1172–1200. https://doi.org/10.1212/CON.0000000000000988
Prabhakaran, S., Gonzalez, N. R., Zachrison, K. S., Adeoye, O., Alexandrov, A. W., Ansari, S. A., Chapman, S., Czap, A. L., Dumitrascu, O. M., Ishida, K., Jadhav, A. P., Johnson, B., Johnston, K. C., Khatri, P., Kimberly, W. T., Lee, V. H., Leslie-Mazwi, T. M., Mac Grory, B., Madsen, T. E., … Yaghi, S. (2026). 2026 guideline for the early management of patients with acute ischemic stroke: A guideline from the American Heart Association/American Stroke Association. Stroke, 57(8), e316–e436. https://doi.org/10.1161/STR.0000000000000513
A formal correction to the 2026 guideline appears in Stroke, 57(8), e461–e467: https://doi.org/10.1161/STR.0000000000000530
Riparbelli, A. C., Capion, T., Møller, K., Mathiesen, T. I., Olsen, M. H., & Forsse, A. (2024). Critical ICP thresholds in relation to outcome: Is 22 mmHg really the answer? Acta Neurochirurgica, 166, Article 63. https://doi.org/10.1007/s00701-024-05929-y
Taheri, M., Ghazvini, M. H., & Javadnia, P. (2024). Paradoxical brain herniation following decompressive craniectomy: A case series and systematic review of literature. International Journal of Surgery Case Reports, 125, Article 110477. https://doi.org/10.1016/j.ijscr.2024.110477
Vahedi, K., Hofmeijer, J., Jüttler, E., Vicaut, E., George, B., Algra, A., Amelink, G. J., Schmiedeck, P., Schwab, S., Rothwell, P. M., Bousser, M.-G., van der Worp, H. B., & Hacke, W. (2007). Early decompressive surgery in malignant infarction of the middle cerebral artery: A pooled analysis of three randomised controlled trials. The Lancet Neurology, 6(3), 215–222. https://doi.org/10.1016/S1474-4422(07)70036-4
Viarasilpa, T. (2025). Managing intracranial pressure crisis. Current Neurology and Neuroscience Reports, 25(1), Article 12. https://doi.org/10.1007/s11910-024-01392-5
Core clinical and physiology resources
Farkas, J. (2026, February 10). Elevated intracranial pressure (ICP). Internet Book of Critical Care. https://emcrit.org/ibcc/icp/
Yartsev, A. (2025, March 4). Brain herniation. Deranged Physiology. https://derangedphysiology.com/main/required-reading/neurological-intensive-care/Chapter-1162/brain-herniation
Yartsev, A. (2025, March 4). Decompressive craniectomy for traumatic brain injury. Deranged Physiology. https://derangedphysiology.com/main/required-reading/neurological-intensive-care/Chapter-117/decompressive-craniectomy-traumatic-brain-injury
Yartsev, A. (2025, March 4). Management of raised intracranial pressure. Deranged Physiology. https://derangedphysiology.com/main/required-reading/neurological-intensive-care/Chapter-112/management-raised-intracranial-pressure
Leave a Reply