Abstract:Severe cerebrospinal fluid hypovolemia after craniotomy may produce a dramatic herniation syndrome that is completely reversed by the Trendelenburg position. Brain sag should be included in the differential diagnosis for acute postoperative clinical deterioration in this patient population.
“…5,6,42,72,73 With a large skull defect, a lumbar puncture exacerbates the negative pressure gradient between the atmosphere and the cranium. 93 Based on this, we have adopted a high threshold for performing lumbar puncture in patients with a decompressive craniectomy.…”
Section: Postoperative Complications Within 30 Daysmentioning
Decompressive craniectomy is widely used to treat intracranial hypertension following traumatic brain injury (TBI). Two randomized trials are currently underway to further evaluate the effectiveness of decompressive craniectomy for TBI. Complications of this procedure have major ramifications on the risk-benefit balance in decision-making during evaluation of potential surgical candidates. To further evaluate the complications of decompressive craniectomy, a review of the literature was performed following a detailed search of PubMed between 1980 and 2009. The author restricted her study to literature pertaining to decompressive craniectomy for patients with TBI. An understanding of the pathophysiological events that accompany removal of a large piece of skull bone provides a foundation for understanding many of the complications associated with decompressive craniectomy. The author determined that decompressive craniectomy is not a simple, straightforward operation without adverse effects. Rather, numerous complications may arise, and they do so in a sequential fashion at specific time points following surgical decompression. Expansion of contusions, new subdural and epidural hematomas contralateral to the decompressed hemisphere, and external cerebral herniation typify the early perioperative complications of decompressive craniectomy for TBI. Within the 1st week following decompression, CSF circulation derangements manifest commonly as subdural hygromas. Paradoxical herniation following lumbar puncture in the setting of a large skull defect is a rare, potentially fatal complication that can be prevented and treated if recognized early. During the later phases of recovery, patients may develop a new cognitive, neurological, or psychological deficit termed syndrome of the trephined. In the longer term, a persistent vegetative state is the most devastating of outcomes of decompressive craniectomy. The risk of complications following decompressive craniectomy is weighed against the life-threatening circumstances under which this surgery is performed. Ongoing trials will define whether this balance supports surgical decompression as a first-line treatment for TBI.
“…5,6,42,72,73 With a large skull defect, a lumbar puncture exacerbates the negative pressure gradient between the atmosphere and the cranium. 93 Based on this, we have adopted a high threshold for performing lumbar puncture in patients with a decompressive craniectomy.…”
Section: Postoperative Complications Within 30 Daysmentioning
Decompressive craniectomy is widely used to treat intracranial hypertension following traumatic brain injury (TBI). Two randomized trials are currently underway to further evaluate the effectiveness of decompressive craniectomy for TBI. Complications of this procedure have major ramifications on the risk-benefit balance in decision-making during evaluation of potential surgical candidates. To further evaluate the complications of decompressive craniectomy, a review of the literature was performed following a detailed search of PubMed between 1980 and 2009. The author restricted her study to literature pertaining to decompressive craniectomy for patients with TBI. An understanding of the pathophysiological events that accompany removal of a large piece of skull bone provides a foundation for understanding many of the complications associated with decompressive craniectomy. The author determined that decompressive craniectomy is not a simple, straightforward operation without adverse effects. Rather, numerous complications may arise, and they do so in a sequential fashion at specific time points following surgical decompression. Expansion of contusions, new subdural and epidural hematomas contralateral to the decompressed hemisphere, and external cerebral herniation typify the early perioperative complications of decompressive craniectomy for TBI. Within the 1st week following decompression, CSF circulation derangements manifest commonly as subdural hygromas. Paradoxical herniation following lumbar puncture in the setting of a large skull defect is a rare, potentially fatal complication that can be prevented and treated if recognized early. During the later phases of recovery, patients may develop a new cognitive, neurological, or psychological deficit termed syndrome of the trephined. In the longer term, a persistent vegetative state is the most devastating of outcomes of decompressive craniectomy. The risk of complications following decompressive craniectomy is weighed against the life-threatening circumstances under which this surgery is performed. Ongoing trials will define whether this balance supports surgical decompression as a first-line treatment for TBI.
“…Since Yamamura et al 15) reported in 1977, the syndrome of the sinking skin flap with neurological deterioration has been reported in the literature 2,5,7,8,11,12) . Many investigators have sought to explain the pathophysiology of this phenomenon.…”
Section: Discussionmentioning
confidence: 99%
“…Several authors 4,5) suggested that severe CSF hypovolemia after craniotomy may produce a dramatic herniation syndrome that is completely reversed by the Trendelenberg position. Also, it was reported that intrathecal saline infusion reverses impending transtentorial herniation in patient with decline of mental status due to intracranial hypotnesion 1) .…”
“…3 The Trendelenburg position reversed the symptoms in all patients. Thalamus/basal ganglia hypodensities on CT scan have neither been described in these patients nor in various case reports, [12][13][14][15][16][17] whereas global cerebral edema on admission CT scan and a longer operative time were identified as risk factors for the development of symptomatic CSF hypovolemia.…”
mentioning
confidence: 83%
“…1 MR imaging signs include thickening and enhancement of the dura after contrast administration, subdural fluid collections, sagging of the brain, engorgement of venous structures with dilation of the intracranial dural sinuses and spinal epidural plexuses, and enlargement of the pituitary gland. [1][2][3][4][5][6] CSF loss is suggested as a possible pathogenetic mechanism, though the exact location of CSF loss often remains undetected. 7,8 According to the Monro-Kellie doctrine, in a closed compartment (as within the skull) the volume loss of 1 compartment-CSF in this disease entity-is compensated by an increase of the volume in the other ones.…”
BACKGROUND AND PURPOSE: CSF loss with consecutive intracranial hypotension has been discussed as a possible pathogenetic mechanism in poor clinical outcome after uneventful neurosurgery and appears to be correlated to specific imaging findings. The purpose of this study was to describe the clinical and imaging findings of symptomatic intracranial hypotension likely induced by wound suction drainage.
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