Decompressive Craniectomy in Diffuse Traumatic Brain Injury

Department of Intensive Care, Alfred Hospital, Commercial Road, Melbourne, VIC 3004, Australia.
New England Journal of Medicine (Impact Factor: 55.87). 03/2011; 364(16):1493-502. DOI: 10.1056/NEJMoa1102077
Source: PubMed


It is unclear whether decompressive craniectomy improves the functional outcome in patients with severe traumatic brain injury and refractory raised intracranial pressure.
From December 2002 through April 2010, we randomly assigned 155 adults with severe diffuse traumatic brain injury and intracranial hypertension that was refractory to first-tier therapies to undergo either bifrontotemporoparietal decompressive craniectomy or standard care. The original primary outcome was an unfavorable outcome (a composite of death, vegetative state, or severe disability), as evaluated on the Extended Glasgow Outcome Scale 6 months after the injury. The final primary outcome was the score on the Extended Glasgow Outcome Scale at 6 months.
Patients in the craniectomy group, as compared with those in the standard-care group, had less time with intracranial pressures above the treatment threshold (P<0.001), fewer interventions for increased intracranial pressure (P<0.02 for all comparisons), and fewer days in the intensive care unit (ICU) (P<0.001). However, patients undergoing craniectomy had worse scores on the Extended Glasgow Outcome Scale than those receiving standard care (odds ratio for a worse score in the craniectomy group, 1.84; 95% confidence interval [CI], 1.05 to 3.24; P=0.03) and a greater risk of an unfavorable outcome (odds ratio, 2.21; 95% CI, 1.14 to 4.26; P=0.02). Rates of death at 6 months were similar in the craniectomy group (19%) and the standard-care group (18%).
In adults with severe diffuse traumatic brain injury and refractory intracranial hypertension, early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure and the length of stay in the ICU but was associated with more unfavorable outcomes. (Funded by the National Health and Medical Research Council of Australia and others; DECRA Australian Clinical Trials Registry number, ACTRN012605000009617.).

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    • "Axonal stretching has to some extent been suggested to contribute to this unfavorable outcome [1]. Also, quantitative data from recent computerized simulations seem to give evidence that the mechanical stretching of brain tissue may interfere with normal metabolism [5]. "

    03/2015; 2015(1):1-9. DOI:10.15764/ABSE.2015.01001
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    • "The authors suggest that the craniectomy contributed to a better outcome because the brain tissue could swell outwards , preventing the regional compression of blood vessels to the area surrounding the originally infarcted region. However , craniectomy is also associated with negative outcomes because of the additional stretching, and possible damage, of axons (Cooper et al. 2011). We propose a mathematical model to investigate the propagation of damage through the brain. "
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    ABSTRACT: Brain tissue swelling, or oedema, is a dangerous consequence of traumatic brain injury and stroke. In particular, a locally swollen region can cause the injury to propagate further through the brain: swelling causes mechanical compression of the vasculature in the surrounding tissue and so can cut off that tissue's oxygen supply. We use a triphasic mathematical model to investigate this propagation, and couple tissue mechanics with oxygen delivery. Starting from a fully coupled, finite elasticity, model, we show that simplifications can be made that allow us to express the volume of the propagating region of damage analytically in terms of key parameters. Our results show that performing a craniectomy, to alleviate pressure in the brain and allow the tissue to swell outwards, reduces the propagation of damage; this finding agrees with experimental observations.
    Biomechanics and Modeling in Mechanobiology 03/2015; 14(6). DOI:10.1007/s10237-015-0665-1 · 3.15 Impact Factor
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    • "Excessive edema can damage otherwise healthy brain regions by compression and is a frequent cause of delayed neurologic deterioration in trauma patients. Pharmaceuticals able to substantially influence inflammation or edema formation in TBI are not available and decompressive surgery, which is a highly invasive procedure, failed to prove efficacy in trauma patients in a recent phase III trial (Cooper et al., 2011). "
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