Treatment Of Elevated Intracranial Pressure Research Articles

Severe Traumatic Brain Injury

Traumatic brain injury remains a leading cause of death and disability worldwide. Patients with severe traumatic brain injury are best treated with a multidisciplinary, evidence-based, protocol-directed approach, which has been shown to decrease mortality and improve functional outcomes. Therapy is directed at the prevention of secondary brain injury through optimizing cerebral blood flow and the delivery of metabolic fuel (ie, oxygen and glucose). This is accomplished through the measurement and treatment of elevated intracranial pressure (ICP), the strict avoidance of hypotension and hypoxemia, and in some instances, surgical management. The treatment of elevated ICP is approached in a protocolized, tiered manner, with escalation of care occurring in the setting of refractory intracranial hypertension, culminating in either decompressive surgery or barbiturate coma. With such an approach, the rates of mortality secondary to traumatic brain injury are declining despite an increasing incidence of traumatic brain injury. This review contains 3 figures, 5 tables and 69 reference Key Words: blast traumatic brain injury, brain oxygenation, cerebral perfusion pressure, decompressive craniectomy, hyperosmolar therapy, intracranial pressure, neurocritical care, penetrating traumatic brain injury, severe traumatic brain injury

Quality And Feasibility of Sonographic Measurement of the Optic Nerve Sheath Diameter to Estimate the Risk of Raised Intracranial Pressure After Traumatic Brain Injury in Prehospital Setting

Objective: In patients with traumatic brain injury (TBI), early detection and subsequent prompt treatment of elevated intracranial pressure (ICP) is a challenge in the prehospital setting, because physical examination is limited in comatose patients and invasive device placement is not possible. The aim of this study was to evaluate the quality and feasibility of optic nerve sheath diameter (ONSD) measurements obtained during the prehospital management of patients with TBI. Methods: This study was a prospective, observational study of 23 patients with moderate and severe TBI during prehospital medical care. The primary endpoint was the quality of ONSD measurements expressed as the percentage of ONSD validated by the experts. Secondary endpoints included the feasibility of ONSD measurements as the percentage of ONSD performed and assessment by operators of ease and duration to perform. Results: Ultrasound ONSD was performed in 19 (82%) patients and 80% of ONSD measurements were validated by the experts. The ONSD measurements were possible in 15 (79%) cases. The physicians have assessed the ease of use at 8 (interquartile range [IQR] = 2.5–8) on 10 for and the median time to obtain ONSD measurement was 4 min (IQR = 3–5). ONSD measurement was performed in 12 (63%) cases during the transport and in 7 (37%) cases on scene, with 58% (n = 7) and 71% (n = 5) validated ONSD, respectively. The success rate in the helicopter was 43% compared to 80% in the ambulance. Conclusion: This study shows that it is feasible to obtain high-quality ONSD measurements in the management of patients with TBI in a prehospital setting. A randomized study evaluating the usefulness of ONSD to guide management of TBI in the prehospital phase may be of great interest.

Cerebral venous thrombosis requiring invasive treatment for elevated intracranial pressure in women with combined hormonal contraceptive intake: risk factors, anatomical distribution, and clinical presentation.

OBJECTIVE Women taking combined hormonal contraceptives (CHCs) are generally considered to be at low risk for cerebral venous thrombosis (CVT). When it does occur, however, intensive care and neurosurgical management may, in rare cases, be needed for the control of elevated intracranial pressure (ICP). The use of nonsurgical strategies such as barbiturate coma and induced hypothermia has never been reported in this context. The objective of this study is to determine predictive factors for invasive or surgical ICP treatment and the potential complications of nonsurgical strategies in this population. METHODS The authors conducted a 2-center, retrospective chart review of 168 cases of CVT in women between 2000 and 2012. Eligible patients were classified as having had a mild or a severe clinical course, the latter category including all patients who underwent invasive or surgical ICP treatment and all who had an unfavorable outcome (modified Rankin Scale score ≥ 3 or Glasgow Outcome Scale score ≤ 3). The Mann-Whitney U-test was used for continuous parameters and Fisher's exact test for categorical parameters, and odds ratios were calculated with statistical significance set at p ≤ 0.05. RESULTS Of the 168 patients, 57 (age range 16-49 years) were determined to be eligible for the study. Six patients (10.5%) required invasive or surgical ICP treatment. Three patients (5.3%) developed refractory ICP > 30 mm Hg despite early surgical decompression; 2 of them (3.5%) were treated with barbiturate coma and induced hypothermia, with documented infectious, thromboembolic, and hemorrhagic complications. Coma on admission, thrombosis of the deep venous system with consecutive hydrocephalus, intraventricular hemorrhage, and hemorrhagic venous infarction were associated with a higher frequency of surgical intervention. Coma, quadriparesis on admission, and hydrocephalus were more commonly seen among women with unfavorable outcomes. Thrombosis of the transverse sinus was less common in patients with an unfavorable outcome, with similar distribution in patients needing invasive or surgical ICP treatment. CONCLUSIONS The need for invasive or surgical ICP treatment in women taking CHCs who have CVT is partly predictable on the basis of the clinical and radiological findings on admission. The use of nonsurgical treatments for refractory ICP, such as barbiturate coma and induced hypothermia, is associated with systemic infectious and hematological complications and may worsen morbidity in this patient population. The significance of these factors should be studied in larger multicenter cohorts.

Markedly Elevated Intracranial Pressure Treated With Cranial Vault Expansion, Instead of CSF Shunting, in a Child With Hurler-Scheie Syndrome and Multiple Suture Craniosynostosis.

Despite a known association of mucopolysaccharidoses (MPS) and craniosynostosis, treatment of elevated intracranial pressure (ICP) in these patients is primarily cerebrospinal fluid (CSF) shunting. We present a unique case of Hurler-Scheie syndrome with multisuture craniosynostosis and elevated ICP, without ventriculomegaly, where elevated ICP was successfully treated with extensive cranial vault expansion and shunt placement was avoided. Patients with MPS should be evaluated for craniosynostosis, and calvarial vault expansion may be considered as a viable treatment alternative to CSF shunting for elevated ICP in select patients.

Development of a Non-invasive Cerebrovascular Status Algorithm to Estimate Cerebral Perfusion Pressure and Intracranial Pressure in a Porcine Model of Focal Brain Injury.

New tools for diagnosis, monitoring, and treatment of elevated intracranial pressure (ICP) or compromised cerebral perfusion pressure (CPP) are urgently needed to improve outcomes after brain injury. Previous success in applying advanced data analytics to build precision monitors based on large, noisy sensor datasets suggested applying the same approach to monitor cerebrovascular status. In these experiments, a new algorithm was developed to estimate ICP and CPP using the arterial pressure waveform. Sixty-five porcine subjects were subjected to a focal brain injury to simulate a mass lesion with elevated ICP. The arterial pressure waveform and the measured ICP from these subjects during injury and treatment were then utilized to develop and calibrate an ICP and CPP estimation algorithm. These estimation algorithms were then subsequently evaluated on 14 new subjects. The root mean square difference between actual ICP and estimated ICP was 2.0961 mmHg. The root mean square difference between the actual CPP and the estimated CPP was 2.6828 mmHg. A novel ICP or CPP monitor based on the arterial pressure signal produced a very close approximation to actual measured ICP and CPP and warrants further evaluation.

Pediatric Traumatic Brain Injury: an Update on Management

This article reviews the pathophysiology, evaluation, and management of pediatric TBI, as well as highlights recent updates in the literature. Traumatic brain injury (TBI) is a leading cause of death and permanent disability worldwide, and its prevalence presents a significant public health concern. Since the second edition of the Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents was released, several recent studies have broadened our understanding of pediatric TBI. While there remains a paucity of high-level evidence on which to base precise consensus guidelines for care in pediatric patients, recent studies have addressed therapeutic hypothermia, pharmacologic treatment of elevated intracranial pressure, and abusive head trauma. Understanding the pathophysiology and treatment strategies for pediatric TBI, while preventing secondary insults, remains a cornerstone for improving patient outcomes.

Targeted temperature management in neurological intensive care unit.

Targeted temperature management (TTM) shows the most promising neuroprotective therapy against hypoxic/ischemic encephalopathy (HIE). In addition, TTM is also useful for treatment of elevated intracranial pressure (ICP). HIE and elevated ICP are common catastrophic conditions in patients admitted in Neurologic intensive care unit (ICU). The most common cause of HIE is cardiac arrest. Randomized control trials demonstrate clinical benefits of TTM in patients with post-cardiac arrest. Although clinical benefit of ICP control by TTM in some specific critical condition, for an example in traumatic brain injury, is still controversial, efficacy of ICP control by TTM is confirmed by both in vivo and in vitro studies. Several methods of TTM have been reported in the literature. TTM can apply to various clinical conditions associated with hypoxic/ischemic brain injury and elevated ICP in Neurologic ICU.

Intracranial Pressure Monitoring in Infants and Young Children With Traumatic Brain Injury.

To examine the use of intracranial pressure monitors and treatment for elevated intracranial pressure in children 24 months old or younger with traumatic brain injury in North Carolina between April 2009 and March 2012 and compare this with a similar cohort recruited 2000-2001. Prospective, observational cohort study. Twelve PICUs in North Carolina. All children 24 months old or younger with traumatic brain injury, admitted to an included PICU. None. The use of intracranial pressure monitors and treatments for elevated intracranial pressure were evaluated in 238 children with traumatic brain injury. Intracranial pressure monitoring (risk ratio, 3.7; 95% CI, 1.5-9.3) and intracranial pressure therapies were more common in children with Glasgow Coma Scale less than or equal to 8 compared with Glasgow Coma Scale greater than 8. However, only 17% of children with Glasgow Coma Scale less than or equal to 8 received a monitoring device. Treatments for elevated intracranial pressure were more common in children with monitors; yet, some children without monitors received therapies traditionally used to lower intracranial pressure. Unadjusted predictors of monitoring were Glasgow Coma Scale less than or equal to 8, receipt of cardiopulmonary resuscitation, nonwhite race. Logistic regression showed no strong predictors of intracranial pressure monitor use. Compared with the 2000 cohort, children in the 2010 cohort with Glasgow Coma Scale less than or equal to 8 were less likely to receive monitoring (risk ratio, 0.5; 95% CI, 0.3-1.0), although the estimate was not precise, or intracranial pressure management therapies. Children in the 2010 cohort with a Glasgow Coma Scale less than or equal to 8 were less likely to receive an intracranial pressure monitor or hyperosmolar therapy than children in the 2000 cohort; however, about 10% of children without monitors received therapies to decrease intracranial pressure. This suggests treatment heterogeneity in children 24 months old or younger with traumatic brain injury and a need for better evidence to support treatment recommendations for this group of children.

Comparison of Equimolar Doses of Mannitol and Hypertonic Saline for the Treatment of Elevated Intracranial Pressure After Traumatic Brain Injury

Comparison of Equimolar Doses of Mannitol and Hypertonic Saline for the Treatment of Elevated Intracranial Pressure After Traumatic Brain Injury

Complications in Posterior Cranial Vault Distraction.

The use of posterior cranial vault distraction for the treatment of elevated intracranial pressure is gaining popularity and is a standard for first-stage cranial expansion in syndromic craniosynostosis at many institutions. However, although the operation is faster and less complex than other cranial vault remodeling procedures, it is not without its own unique set of complications. We surveyed the published literature for case series and case control studies on posterior vault distraction. Complication rates and types for these series were tabulated and grouped by management. When outcomes were unclear, corresponding authors were contacted for clarification and treatment plans. Eleven reports were found from a search of all the literature on posterior cranial vault distraction with a range of 1 to 22 included patients. The average age at surgery was 16.2 ± 11.8 months. Complication rates ranged from 12.5% to 100%, with the average of 30% of patients across all studies. The most common complications reported were cerebrospinal fluid leak or dural injury, followed by wound infections or device exposures, and device failure. There were no reported patient deaths or long-term morbidities. Posterior cranial vault distraction is a relatively safe and effective therapy for the treatment of elevated intracranial pressure in the setting of syndromic craniosynostosis. The majority of described complications center on the interaction of the device with the dura, device extrusion, and infection. Extreme care must be used with the placement of these distraction devices and with handling of the dura at the osteotomy sites to ensure successful outcomes and avoid complications. III.

A Randomized Clinical Trial of Hypothermia as a Preferred Second-Line Treatment for Elevated Intracranial Pressure After Traumatic Brain Injury.

A Randomized Clinical Trial of Hypothermia as a Preferred Second-Line Treatment for Elevated Intracranial Pressure After Traumatic Brain Injury.

Sleep apnea after posterior cerebral artery aneurysm rupture and elevated intracranial pressure: a Chiari-like syndrome

• Sub-arachnoid hemorrhage may determine obstructive sleep apnea, even in patients without risk factors. • In the presence of clinical deterioration, clinicians should consider this complication. • Starting CPAP therapy should be assessed when treatment of elevated intracranial pressure is not indicated.

Ventilator-Associated Pneumonia in Pediatric Traumatic Brain Injury.

Ventilator-associated pneumonia (VAP) is a common occurrence among intubated pediatric traumatic brain injury (TBI) patients. However, little is known about the epidemiology, risk factors, and microbiology of VAP in pediatric TBI. We reviewed a cohort of 119 pediatric moderate-to-severe TBI patients and identified 42 with VAP by positive protected bronchial brush specimens. Location of intubation, severity of injury, and antibiotic administration within 2 days after injury were not associated with VAP. Most treatments for elevated intracranial pressure were associated with increased risk of VAP; however, in a multi-variable analysis barbiturate coma (hazard ratio [HR], 3.2; 95% confidence interval [CI] 1.4-7.3), neuromuscular blockade (NMBA; HR, 3.4; 95% CI 1.6-7.3), and use of a cooling blanket for euthermia (HR 2.4; 95% CI 1.1-5.5) remained independently associated with VAP. Most VAP (55%) occurred prior to hospital Day 4 and only 7% developed VAP after Day 7. Methicillin-sensitive Staphylococcus aureus (34%), Haemophilus influenzae (22%), and Streptococcus pneumoniae (15%) were the most common organisms, comprising 71% of isolated pathogens (36% of infections were polymicrobial). Patients with VAP had significantly longer intensive care unit and hospital stays, as well as increased risk of chronic care needs after discharge, but not mortality. VAP is a common occurrence in pediatric TBI patients, and early empiric therapy for patients requiring barbiturate infusion, NMBA, or use of a cooling blanket could mitigate morbidity.

Barbiturate Is Not a Risk Factor For Late Ventilator Associated Pneumonia. a Post-Hoc Analysis On 441 Tbi Patients Included in 2 Rcts

Barbiturate is a therapeutic option for the treatment of elevated intracranial pressure (eICP) in Traumatic brain injury (TBI) patients. It is used in 20% of the patients in a recent European cohort [[1]]. But, barbiturate may induce an immunosuppression. Indeed, barbiturate have been shown to induce a decrease in white blood cells in old reports [[2]] and to be associated to early ventilator associated pneumonia (VAP) [[3]]).

Comparison of Equimolar Doses of Mannitol and Hypertonic Saline for the Treatment of Elevated Intracranial Pressure After Traumatic Brain Injury

The purpose of this meta-analysis was to compare the effectiveness of mannitol and hypertonic saline for reducing intracranial pressure (ICP) after traumatic brain injury (TBI).PubMed, Cochrane, Embase, and ISI Web of Knowledge databases were searched until July 3, 2014 using the terms intracranial hypertension, mannitol, and hypertonic saline. Randomized controlled trials and 2-arm prospective studies in which elevated ICP was present after TBI treated with mannitol or hypertonic saline were included. The primary outcome was the change of ICP from baseline to termination of the infusion, while the secondary outcomes were change from baseline to 30, 60, and 120 minutes after terminating the infusion and change of osmolarity from baseline to termination.A total 7 studies with 169 patients were included. The mean age of patients receiving mannitol ranged from 30.8 to 47 years, and for patients receiving hypertonic saline ranged from 35 to 47 years. A pooled difference in means = −1.69 (95% confidence interval [CI]: −2.95 to −0.44, P = 0.008) indicated that hypertonic saline reduced ICP more effectively than mannitol when compared from the baseline value to the last measurement after treatment. At 30 minutes after intervention, there was no difference in the mean ICP change between the groups, whereas at 60 minutes after intervention (pooled difference in means = −2.58, 95% CI: −4.37 to −0.80, P = .005) and 120 min after intervention (pooled difference in means = −4.04, 95% CI: −6.75 to −1.32, P = .004) hypertonic saline resulted in a significantly greater decrease in ICP. The pooled difference in means = 1.84 (95% CI: −1.64 to 5.31, P = .301) indicated no difference in serum osmolarity between patients treated with hypertonic saline or mannitol.Hypertonic saline is more effective than mannitol for reducing ICP in cases of TBI.

Carbon dioxide in the critically ill: too much or too little of a good thing?

Hypercapnia and hypocapnia commonly complicate conditions that are present in critically ill patients. Both conditions have important physiologic effects that may impact the clinical management of these patients. For instance, hypercapnia results in bronchodilation and enhanced hypoxic vasoconstriction, leading to improved ventilation/perfusion matching. Hypocapnia reduces cerebral blood volume through arterial vasoconstriction. These effects have also been exploited for therapeutic aims. In patients with traumatic brain injury (TBI), hypocapnia is often utilized to control intracranial pressure. However, this effect is not sustained, and prolonged hypocapnia increases the risk of mortality and severe disability in patients with TBI. Hypercapnia and hypercapnic acidosis are common consequences of lung-protective ventilation in ARDS. Hypercapnic acidosis reduces ischemic lung injury and preserves lung compliance, but concern has arisen over hypercapnia-induced immunosuppression and the potential for bacterial proliferation in sepsis. Experimental studies suggest that buffering hypercapnic acidosis attenuates these effects, whereas hypocapnia appears to potentiate lung injury through increased capillary permeability and decreased lung compliance. Several areas of uncertainty surround the role of hypercapnia/hypocapnia in treating TBI and ARDS. Current data support recommendations to avoid hypocapnia in treating TBI, with the exception of emergent treatment of elevated intracranial pressure, while awaiting definitive management. Permissive hypercapnia is commonly accepted as a consequence of lung-protective ventilation in ARDS, but there is insufficient evidence to support the induction of hypercapnic acidosis in clinical practice. Buffering hypercapnic acidosis should be considered only for a specific clinical indication (eg, hemodynamic instability). For clinicians choosing to buffer hypercapnic acidosis, tris-hydroxymethyl aminomethane is recommended over sodium bicarbonate, as it is more effective in correcting pH and is not associated with increased carbon dioxide production. Future studies should aim to address these areas of uncertainty to help guide clinicians in the therapeutic use and management of hypercapnia/hypocapnia in critically ill patients.

Increased Intracranial Pressure Secondary to External Ventricular Drain Obstruction in a Teenager

OPEN ACCESSMay 8, 2014Increased Intracranial Pressure Secondary to External Ventricular Drain Obstruction in a Teenager Kim Derespina, MD, Rahul Panesar, MD Kim Derespina, MD Stony Brook Long Island Children's Hospital Google Scholar More articles by this author , Rahul Panesar, MD Stony Brook Long Island Children's Hospital Google Scholar More articles by this author https://doi.org/10.15766/mep_2374-8265.9785 SectionsAbout ToolsDownload Citations ShareFacebookTwitterEmail AbstractAbstractThe occurrence of high-risk, low frequency pediatric emergencies requires an adequate volume of training to ensure favorable outcomes. However, relying on such dire situations is an inefficient and potentially hazardous method of teaching how to manage crisis events. In so far, pediatric simulation has become one of the latest tools of providing real-time, hands-on training for the pediatric resident and fellows to improve both their confidence and their performance in actual emergencies. This is a human patient simulation using a high-fidelity simulation scenario illustrating intracranial hypertension in a teenage patient. Primary educational goals include recognition and management of intracranial hypertension, including medical management strategies and manipulation of an external ventricular drain. Set up, instructor's guide, simulation scenario, and debriefing instructions are included. This scenario has been tested and run in the Pediatric Residency Program at our institution. Residents have been educated on recognition of intracranial hypertension and have learned management strategies in caring for such patients. Educational Objectives By the end of this module, learners will be able to: Recognize patients with increased intracranial pressureUnderstand the pathophysiology leading to Cushing's triad.Address underlying causes and activate tertiary measures for the treatment of elevated intracranial pressure. Sign up for the latest publications from MedEdPORTAL Add your email below FILES INCLUDEDReferencesRelatedDetails FILES INCLUDED Included in this publication: ICP Instructor's Guide.doc ICP Scenario.docx Photo1.JPG Photo2.JPG To view all publication components, extract (i.e., unzip) them from the downloaded .zip file. Download editor’s noteThis publication may contain technology or a display format that is no longer in use. Copyright & Permissions© 2014 Derespina and Panesar. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivatives license.KeywordsIntracranial HypertensionSimulationPediatrics Disclosures None to report. Funding/Support None to report. Loading ...

Lactate and the injured brain

Energy metabolism is increasingly recognized as a key factor in the pathogenesis of acute brain injury (ABI). We review the role of cerebral lactate metabolism and summarize evidence showing that lactate may act as supplemental fuel after ABI. The role of cerebral lactate has shifted from a waste product to a potentially preferential fuel and signaling molecule. According to the astrocyte-neuron lactate shuttle model, glycolytic lactate might act as glucose-sparing substrate. Lactate also is emerging as a key signal to regulate cerebral blood flow (CBF) and a neuroprotective agent after experimental ABI. Clinical investigation using cerebral microdialysis shows the existence of two main lactate patterns, ischemic - from anaerobic metabolism - and nonischemic, from activated glycolysis, whereby lactate can be used as supplemental energy fuel. Preliminary clinical data suggests hypertonic lactate solutions improve cerebral energy metabolism and are an effective treatment for elevated intracranial pressure (ICP) after ABI. Lactate can be a supplemental fuel for the injured brain and is important to regulate glucose metabolism and CBF. Exogenous lactate supplementation may be neuroprotective after experimental ABI. Recent clinical data from ABI patients suggest hypertonic lactate solutions may be a valid therapeutic option for secondary energy dysfunction and elevated ICP.

Frequency of Hematoma Expansion After Spontaneous Intracerebral Hemorrhage in Children

Hematoma expansion is the only modifiable predictor of outcome in adult intracerebral hemorrhage; however, the frequency and clinical significance of hematoma expansion after childhood intracerebral hemorrhage are unknown. To assess the frequency and extent of hematoma expansion in children with nontraumatic intracerebral hemorrhage. Prospective observational cohort study at 3 tertiary care pediatric hospitals. Children (≥ 37 weeks' gestation to 18 years) with nontraumatic intracerebral hemorrhage were enrolled in a study from 2007 to 2012 focused on predictors of outcome. For this planned substudy of hematoma expansion, neonates 28 days or younger and participants with isolated intraventricular hemorrhage were excluded. Children with 2 head computed tomography (CT) scans within 48 hours were evaluated for hematoma expansion and were compared with children with only 1 head CT scan. Consent for the primary cohort was obtained from 73 of 87 eligible participants (84%); 41 of 73 children enrolled in the primary cohort met all inclusion/exclusion criteria for this substudy, in whom 22 had 2 head CT scans obtained within 48 hours that could be evaluated for hematoma expansion. Within our substudy cohort, 21 of 41 (51%) were male, 25 of 41 (61%) were white, 16 of 41 (39%) were black, and median age was 7.7 years (interquartile range, 2.0-13.4 years). Primary outcome was prevalence of hematoma expansion. Of 73 children, 41 (56%) met inclusion criteria, and 22 (30%) had 2 head CT scans to evaluate expansion. Among these 22 children, median time from symptom onset to first CT was 2 hours (interquartile range, 1.3-6.5 hours). Median baseline hemorrhage volume was 19.5 mL, 1.6% of brain volume. Hematoma expansion occurred in 7 of 22 (32%). Median expansion was 4 mL (interquartile range, 1-11 mL). Three children had significant (>33%) expansion; 2 required urgent hematoma evacuation. Expansion was not associated with poorer outcome. Compared with children with only 1 head CT scan within 48 hours, children with 2 head CT scans had larger baseline hemorrhage volumes (P = .05) and were more likely to receive treatment for elevated intracranial pressure (P < .001). Hematoma expansion occurs in children with intracerebral hemorrhage and may require urgent treatment. Repeat CT should be considered in children with either large hemorrhage or increased intracranial pressure.

Decompressive craniectomy and head injury: brain morphometry, ICP, cerebral hemodynamics, cerebral microvascular reactivity, and neurochemistry

There has been renewed interest in decompressive craniectomy as a surgical treatment for elevated intracranial pressure (ICP), although evidence-based clinical data are still lacking and some experimental results are conflicting. Ongoing clinical trials on the use of this operation after traumatic brain injury (TBI) may clarify the clinical application of this technique, however, some pathophysiological issues, such as the timing of this operation, its effect on brain edema formation, and its role for secondary brain damage, are still controversial. This review addresses recent clinical data on the influence of decompressive craniectomy on the brain pathophysiology in TBI. Decompressive craniectomy with dural augmentation enlarges intracranial space so that the swollen cerebral hemisphere could expand out of normal cranial limits, avoiding progression of brain herniation. The gain in intracranial volume results in both the improvement of cerebral compliance and a decrease in ICP; the latter favors a rise in both cerebral blood flow and cerebral microvascular perfusion, which can be accompanied by elevation in brain tissue oxygen tension (PbtO2) as well as the return of abnormal metabolic parameters to normal values in cases of cerebral ischemia. Enhancement of edema formation, impairment of cerebrovascular pressure reactivity, and non-restoration of brain aerobic metabolism due to metabolic crisis may occur after craniectomy and require further investigations. This review suggests that decompressive craniectomy as the sole treatment is likely to be insufficient; efforts must be made to maintain adequate brain hemodynamics, preferably coupled with brain metabolism, in addition to treating brain metabolic abnormalities, during postoperative stages.