Effacement Of Cisterns Research Articles

Management and outcomes of malignant posterior reversible encephalopathy syndrome

IntroductionRecognition of severe forms of posterior reversible encephalopathy syndrome (PRES) has improved. Management of these patients remains challenging, particularly in patients with the combination of edema and hemorrhage. MethodsA prospective inpatient neuro-intensive care database was queried for patients with PRES. Malignant PRES was diagnosed by clinical assessments (GCS less than 8 and clinical decline despite standard medical management for elevated intracranial pressure) and radiographic criteria (edema with associated mass effect; brain hemorrhage exerting mass effect; effacement of basal cisterns, transtentorial, tonsillar, or uncal herniation). Malignant PRES was defined as: radiology studies consistent with PRES; GCS less than 8; and clinical decline despite standard elevated intracranial pressure management. ResultsFive cases were identified over a 4 year interval. The following contributing conditions were also present: chemotherapy (1), systemic lupus erythematosis (2), pregnancy (1), and methamphetamines (1). Neurocritical care interventions included: hyperosmolar therapy (5), anticonvulsants (5), management of coagulopathy (5), and ventilatory support (5). Neurosurgical interventions included: craniectomy (5), hematoma evacuation (3), and external ventricular drain (4). Brain biopsy was performed in 5 patients and was negative for vasculitis, demyelinating disease, tumor, or infection. Cyclophosphamide was administered to the two patients with SLE. With long-term follow up, all patients achieved good functional outcomes (modified Rankin score 1–2). ConclusionIn contrast to historical reports of high mortality rates (16–29%) for severe and hemorrhagic PRES variants, we had no fatalities and observed favorable functional outcomes with intracranial pressure monitoring and craniectomy for malignant PRES cases who fail medical ICP management.

Intracerebral aneurysmal bleed presenting as acute subdural haemorrhage

Acute subdural haemorrhage (aSDH) secondary to an aneurysmal bleed is a surgical emergency that requires urgent decision making. Major dilemmas are whether preoperative diagnostic studies should precede surgery and whether obliteration of the aneurysm should be performed during haematoma evacuation or as a separate delayed intervention after resuscitation. We successfully operated on a 44-year-old patient with aneurysmal aSDH, and discuss the challenges involved with such patients. Case report A 44-year-old man was brought unconscious to hospital by paramedics. Immediate family members or friends were not available to give a reliable history. On admission his Glasgow Coma Score (GCS) was 6/15 (E1 M4 V1). His right pupil was dilated and unreactive to light and he had features of Cushing’s reflex with bradycardia and hypertension. He was immediately intubated and underwent an urgent computed tomography (CT) scan (Fig. 1), which revealed a large, right frontotemporo-parietal acute subdural haematoma with effacement of basal cisterns and evidence of mass effect and midline shift. The scan also showed thick blood in the right sylvian fissure and a thrombus in the superior temporal gyrus on the right side. Because of features of uncal herniation, an emergency craniotomy was performed immediately. On draining the aSDH, the brain became lax and pulsatile. The sylvian fissure was thereafter opened proximal to distal. The arachnoid membrane across the sylvian fissure could clearly be seen in the proximal fissure, but distally, over the aneurysm, it was obliterated by the thick thrombus surrounding the fundus of a large bi-lobed aneurysm at the middle cerebral artery (MCA) bifurcation. The thrombi were carefully removed and the aneurysm neck was dissected out and clipped using a large curved Yasargil clip. Postoperatively he was ventilated for 24 hours and then gradually weaned off the ventilator. His postoperative recovery was slow but steady. On last followup six months after surgery he had made significant recovery with a modified Rankin score of 2. He was independent for activities of daily living but had not yet resumed his earlier vocation.

Patients with brain contusions: predictors of outcome and relationship between radiological and clinical evolution

Traumatic parenchymal mass lesions are common sequelae of traumatic brain injuries (TBIs). They occur in up to 8.2% of all TBI cases and 13%-35% of severe TBI cases, and they account for up to 20% of surgical intracranial lesions. Controversy exists concerning the association between radiological and clinical evolution of brain contusions. The aim of this study was to identify predictors of unfavorable outcome, analyze the evolution of brain contusions, and evaluate specific indications for surgery. In a retrospective, multicenter study, patients with brain contusions were identified in separate patient cohorts from 11 hospitals over a 4-year period (2008-2011). Data on clinical parameters and course of the contusion were collected. Radiological parameters were registered by using CT images taken at the time of hospital admission and at subsequent follow-up times. Patients who underwent surgical procedures were identified. Outcomes were evaluated 6 months after trauma by using the Glasgow Outcome Scale-Extended. Multivariate analysis revealed the following reliable predictors of unfavorable outcome: 1) increased patient age, 2) lower Glasgow Coma Scale score at first evaluation, 3) clinical deterioration in the first hours after trauma, and 4) onset or increase of midline shift on follow-up CT images. Further multivariate analysis identified the following as statistically significant predictors of clinical deterioration during the first hours after trauma: 1) onset of or increase in midline shift on follow-up CT images (p < 0.001) and 2) increased effacement of basal cisterns on follow-up CT images (p < 0.001). In TBI patients with cerebral contusion, the onset of clinical deterioration is predictably associated with the onset or increase of midline shift and worsened status of basal cisterns but not with hematoma or edema volume increase. A combination of clinical deterioration and increased midline shift/basal cistern compression is the most reasonable indicator for surgery.

Surgical management of traumatic extra dural hematoma in children: Experiences and analysis from 24 consecutively treated patients in a developing country

Background:Children with epidural hematoma (EDH) present differently than adults. The outcome of treatment is also different. We aim to report our experiences with EDH in pediatric age group in terms of mode of injury, presenting features, management, and outcomes. We also aim to identify different prognostic indicators in pediatric patients with EDH.Methods:We prospectively collected data from 24 consecutively surgically treated pediatric patients. The data collected included presenting features, radiological imaging, details of management, and outcomes. Descriptive analysis was performed and different variables were tested for any statistical significance with Glasgow Outcome Score (GOS).Results:There were 19 male and 5 female patients. The mean Glasgow Coma Scale (GCS) score at presentation was 9.3 ± 4.4. Falls were the most common cause of EDH. Outcome assessment was done at 3 month follow up. A total of 15 patients had a GOS score of 5, 4 patients had a GOS score of 4, 2 patients had a GOS score of 3, while 3 patients had a GOS score of 1. On univariate analysis, admitting GCS score, patient's age, the time from injury to admission and injury to surgery, anisocoric pupils at presentation and effacement of basal cisterns were significantly associated with the outcome of GOS score.Conclusion:Falls are the most common mode of injury leading to EDH in children. Lower GCS at presentation, younger age at trauma, increased time since trauma to surgery and admission, anisocoria and effacement of basal cisterns are statistically significant variables in surgically treated pediatric patients of EDH that confer a poorer prognosis. A timely surgical intervention can result in excellent outcomes.

Intracranial hypotension syndrome in a patient due to suboccipital craniectomy secondary to Chiari type malformation

Intracranial hypotension syndrome (IHS) is a rare disorder characterized by a decrease in cerebrospinal fluid pressure to less than 60 mm H2O. The syndrome is associated with occipital headache radiating to the frontal and temporal zones. The current clinical case describes the manifestation of IHS in a twenty-five year old female with a history of suboccipital craniectomy due to Chiari I malformation nine years earlier. The patient was admitted to the hospital complaining about postural, mainly occipital, headache during the last three months, aggravated by being in an upright position. The magnetic resonance imaging (MRI) revealed engorgement of the dural venous sinuses, significant enlargement of the pituitary gland and download displacement or sagging of the brain with effacement of the perichiasmatic cisterns and the prepontine cistern, while the spinal T2W MRI revealed a 7 mm × 2.5 mm dural defect with an extradural cerebrospinal fluid collection at the dorsal soft tissues of the cervical spine. The previous imaging did not reveal subdural effusions.

Stroke and Death Due to Spontaneous Intracranial Hypotension

Spontaneous intracranial hypotension has become a well-recognized cause of headaches and a wide variety of other manifestations have been reported. Recently, several patients with asymptomatic spontaneous intracranial hypotension were reported. I now report two patients with spontaneous intracranial hypotension who developed multiple arterial strokes associated with death in one patient, illustrating the spectrum of disease severity in spontaneous intracranial hypotension. Medical records and radiologic imaging of the two patients were reviewed. Case 1. A 45-year-old man presented with an orthostatic headache. Neurologic examination was normal. MRI showed bilateral subdural fluid collections, brain sagging, and pachymeningeal enhancement. At lumbar puncture, the opening pressure was too low to record. He underwent two epidural blood patches with transient improvement of symptoms. His headaches progressed and a CT-myelogram showed a lower cervical CSF leak. Subsequently, periodic lethargy and confusion was noted and he then rapidly deteriorated. Examination showed coma (GCS: 4 [E1, M2, V1]), a fixed and dilated right pupil, and decerebrate posturing. Bilateral craniotomies were performed for the evacuation of chronic subdural hematomas. Immediate postoperative CT showed bilateral posterior cerebral artery infarcts and a recurrent right subdural hematoma, requiring re-evacuation. Postoperative examination was consistent with brain death and support was withdrawn. Case 2. A 42-year-old man presented with a non-positional headache. Neurologic examination was normal. CT showed bilateral acute on chronic subdural hematomas and effacement of the basilar cisterns. MRI showed brain sagging, bilateral subdural hematomas, and pachymeningeal enhancement. Bilateral craniotomies were performed and subdural hematomas were evacuated. Postoperatively, the patient became progressively lethargic (GCS: 8 [E2, M4, V2]) and variable degrees of pupillary asymmetry and quadriparesis were noted. MRI now also showed multiple areas of restricted diffusion in the pons and midbrain, consistent with multiple infarcts. CT showed worsening subdural fluid collections with midline shift and increased effacement of the basilar cisterns. Repeat bilateral craniotomies were performed for evacuation of the subdural fluid collections. Neurologic examination was then noted to be fluctuating but clearly improved when lying flat (GCS: 10T [E4, M6, VT]). CT-myelography demonstrated an extensive cervico-thoracic CSF leak. An epidural blood patch was performed. The patient made a good, but incomplete, recovery with residual quadriparesis and dysphagia. Arterial cerebral infarcts are rare, but potentially life-threatening complications of spontaneous intracranial hypotension. The strokes are due to downward displacement of the brain and can be precipitated by craniotomy for evacuation of associated subdural hematomas.

Cerebral herniation associated with central venous catheter insertion: Risk assessment

PurposeCentral venous catheters (CVCs) are often necessary to treat acute brain-injured patients. Four cases of cerebral herniation immediately following central venous catheterization were the impetus for an investigation of clinical and radiologic parameters associated with this complication. Materials and MethodsThis is a case series of 4 consecutive patients who experienced clinical cerebral herniation immediately following CVC placement in Trendelenburg or supine position. Clinical and computed tomography imaging findings were reviewed. ResultsAll 4 patients developed new-onset clinical signs of cerebral herniation (unilateral or fixed dilated pupil and Glasgow Coma Scale [GCS], 3) within 30 minutes of the procedure. All had radiographic signs of Sylvian fissure and/or basal cistern effacement on the preceding computed tomographic scan secondary to unilateral or bilateral mass lesions. Preprocedure GCS was 8 or more in all cases. Herniation was medically reversed in 3 of 4 patients, and 1 patient died of progressive brainstem ischemia. ConclusionsTrendelenburg and even flat position during CVC placement can increase intracranial pressure leading to cerebral herniation in patients with significant intracranial mass effect. Careful review of neuroimaging for signs of impending herniation before inserting CVCs and choosing an alternative treatment plan in these cases may avoid this potentially underreported complication.

Factors predicting outcome in patients with severe head injury: Multivariate analysis

BackgroundOutcome prediction after severe head injury is of great clinical importance especially for countries like India for better targeting of limited healthcare resources. This study was undertaken to evaluate various factors as predictors of outcome in severe head injury. Patients and MethodsThis study is based on prospective analysis of 110 patients admitted over a period of one and half year with severe head injury. Patients with associated severe chest, abdominal or orthopedic trauma were excluded. Clinical outcome was evaluated at the time of discharge and after six months, according to Glasgow outcome score. ResultsRoad traffic accident was commonest (83.64%) mode of severe head injury. Only 5.71% of patients were following traffic rules. Increasing age of patients, hypoxia, low GCS and abnormal pupillary reflex were found to be significant predictors of adverse clinical outcome. Early operative intervention, when indicated as per CT findings, was significantly associated with favorable outcome. Greater degree of midline shift and effacement of Basal cisterns were associated with adverse outcome. ConclusionPredicting outcome is an assimilative and integrative process of various pre-injury, injury and post-injury variables. Strict enforcement of traffic rules can help us to save precious life. Hypoxia should be avoided on absolute basis. CT scan should be done on urgent basis to look for operable mass lesions.

Quantitative CT Improves Outcome Prediction in Acute Traumatic Brain Injury

The admission noncontrast head computed tomography (CT) scan has been demonstrated to be one of several key early clinical and imaging features in the challenging problem of prediction of long-term outcome after acute traumatic brain injury (TBI). In this study, we employ two novel approaches to the problem of imaging classification and outcome prediction in acute TBI. First, we employ the novel technique of quantitative CT (qCT) image analysis to provide more objective, reproducible measures of the abnormal features of the admission head CT in acute TBI. We show that the incorporation of quantitative, rather than qualitative, CT features results in a significant improvement in prediction of the 6-month Extended Glasgow Outcome Scale (GOS-E) score over a wide spectrum of injury severity. Second, we employ principal components analysis (PCA) to demonstrate the interdependence of certain predictive variables. Relatively few prior studies of outcome prediction in acute TBI have used a multivariate approach that explicitly takes into account the potential covariance among clinical and CT predictive variables. We demonstrate that several predictors, including midline shift, cistern effacement, subdural hematoma volume, and Glasgow Coma Scale (GCS) score are related to one another. Rather than being independent features, their importance may be related to their status as surrogate measures of a more fundamental underlying clinical feature, such as the severity of intracranial mass effect. We believe that objective computational tools and data-driven analytical methods hold great promise for neurotrauma research, and may ultimately have a role in image analysis for clinical care.

Automatic Recognition of Basal Cisterns on Brain CT

Effacement of the basal cisterns (BC) and midline shift (MLS) are two most important features clinicians use to evaluate the severity of brain compression by various pathologies. Because of its complex shape, measuring the compression of the BC is not an easy task and its standardization has not been proposed until recently. Based on this standard method, we develop a method for automatic recognition of the BC on brain CT slices. Hypodense pixels of the brain area on each slice are found with a threshold derived from its own histogram. Hough transform is then applied to find the semicircular band containing largest number of hypodense pixels within the lower-central brain. This area was recognized as the normal or abnormal BC if it fits certain rules derived from human experts. Our system is tested on patient images. We found good inter-rater agreement between the results generated by our system and those evaluated by a board-certified neurosurgeon (kappa = 0.957).

Editorial: Brain sag

Alaraj and colleagues1 report on 5 patients who, following the surgical repair of ruptured anterior communicating artery (ACoA) aneurysms aided by spinal drainage with or without fenestration of the lamina terminalis, demonstrated clinical “brain sag” with classic CT features: elongation of the midbrain and effacement of the basal cisterns. In all cases the angiogram obtained during the “sag episode” showed inferior displacement of the basilar artery when compared with the “pre-sag” angiogram, and in 3 cases, this displacement was so severe that the basilar artery kinked. Vertebral artery kinking was seen in some cases as well. In 4 of the 5 cases, brain sag was recognized in a timely fashion, and patients responded favorably to conventional maneuvers, most notably placement in the Trendelenburg position. In 3 of the 4 patients who improved with positional changes together with a blood patch or clamping of the spinal drain, a “post-sag” angiogram showed marked improvement in the displacement of the basilar artery. The fourth patient whose condition improved did not undergo post-sag angiography, as it was not deemed clinically necessary. The authors are careful to note that this angiographic picture was not seen in a similar population of patients lacking clinical brain sag who were being studied for vasospasm. While the authors’ series is small, it is carefully documented and provides dramatic evidence that the clinical symptoms of brain sag may not be solely due to mechanical displacement of the brainstem. Instead, regional posterior circulation cerebral ischemia may be a contributing factor. The fact that a surprisingly high percentage of their patients also exhibited early signs of vasospasm leads one to wonder whether brain sag is more common but becomes symptomatic only when there is concomitant vascular compromise. My initial impression, based on routine examination of early postsurgical CT scans, is that it is decidedly rare to see dramatic CT evidence of sag in an otherwise stable patient, although a more systematic review is needed. Such a review should clearly focus on ACoA aneurysms treated with spinal drainage. At my institution, our initial impression was that the combination of lamina terminalis fenestration and spinal drainage predisposes to brain sag,2 but maybe it is more a function of the subarachnoid dissection in this region given that ACoA aneurysm rupture often may have already rendered the ventricles in communication with the suprasellar cistern. In any case, since we recognized this phenomenon some years ago, we have kept all patients with spinal drainage and lamina terminalis fenestration flat in the immediate postoperative period, and we are quick to place a patient in the Trendelenburg position in the rare instance that it is needed. Using this approach we rarely need to resort to blood patch, and no patient has exhibited obvious irreversible deficits from the sag episode.3 That said, we have not looked to see whether patients with brain sag were more likely to develop delayed cerebral infarction from vasospasm or neurocognitive symptoms with delayed follow-up. While assuming the Trendelenburg position, many patients may have experienced increased systemic blood pressure, as vasospasm may have been in the differential diagnosis. Whether induced hypertension led to a more rapid reversal of symptoms was not examined. In conclusion, the proceeding paper is important because it documents for the first time the angiographic features of brain sag and leads us to reexamine what we think we know about its underlying pathophysiology, as well as how best to prevent it, treat it, and determine its true sequelae.

Extensive pneumocephalus after nose blowing: an unusual cause of severe headache

A 54-year-old Afro-Caribbean woman presented to the emergency department with a 1-day history of severe headache and general malaise. The pain started suddenly after blowing her nose, was frontal in location and became rapidly severe and throbbing in nature. There were no symptoms that would suggest orthostatic headache, no dizziness or vertigo, no visual or auditory disturbance and no neurological weakness. The pain was worse on movement, coughing and bending and was associated with photophobia, nausea and the development of a clear nasal discharge. Previous medical history was unremarkable; there was no history of sinus or nasal problems, no recent headaches or migraines, no visual abnormalities and no life history of head injury or nasal trauma. Examination was largely unremarkable; on arrival her Glasgow Coma Scale was 15 and she was apyrexial with no meningism or photophobia. No evidence of intracranial hypertension was found. There was slight skull tenderness on palpation over the frontal sinus, but the remainder of her neurological (including cranial nerve) examination and general examination was unremarkable. Biochemical (electrolytes, liver function, glucose, calcium) and haematological tests revealed a mild neutrophilia (12.5×109cells/litre) but were otherwise normal. Over the course of the admission, she became increasingly unwell with increasing nausea, further vomiting and fluctuant levels of consciousness. A computed tomography scan of the head showed an extensive pneumocephalus extending to the foramen magnum with marked sulcal and basal cistern effacement (Figure 1 and 2). Bone windows revealed a hole in the roof of the right sphenoid sinus. The clear discharge was found to be CSF and sent for microbiology analysis. Prophylactic cefotaxime and metronidazole antibiotics were commenced and she underwent endoscopic endonasal exploration. The bony defect in the roof of the right sphenoid and the CSF leak were identified. The dural defect was closed with a fascia lata graft and fat harvested from the thigh. Four days after the operation, she became increasingly confused and a repeat computed tomography scan showed new hydrocephalus. A lumbar puncture was performed and showed an opening pressure of 43 cm (5–20 cm). Two days later she underwent ventricular-peritoneal shunting. She eventually made a full recovery. It is still uncertain whether the hydrocephalus was secondary to a disruption of the sinus by the air pressure in the skull or whether there was hydrocephalus before the events leaking through the ethmoidal bone, suggesting the possibility of spontaneous CSF leak syndrome complicated with pneumocephalus (Schievink, 2000).

Rapid Reduction of Syrinx Associated With Traumatic Intracranial Hypotension by Direct Surgery -Case Report-

A woman in her early twenties presented with cerebellar tonsillar herniation with syrinx in the cervicothoracic spinal cord manifesting as postural headache after suffering trauma to the hip. She was treated under a diagnosis of traumatic intracranial hypotension. Cranial magnetic resonance (MR) imaging demonstrated tonsillar herniation to the upper rim of the C1 lamina, associated with effacement of the basal cisterns and flattening of the pons against the clivus, sagging of the optic chiasm, and protrusion of the pituitary gland into the suprasellar cistern. Spinal MR imaging and computed tomography (CT) myelography showed cervicothoracic syrinx and arachnoid diverticulum. Three applications of epidural blood patches produced no improvement. Surgery identified cerebrospinal fluid leakage from two small holes in the spinal dural sac, slightly proximal from the origin of the left L1 root sleeve, and arachnoid diverticulum. These two holes were sutured and a few sheets of gelatin sponge were placed around the arachnoid diverticulum and sealed with fibrin glue. The cervicothoracic syrinx was reduced significantly and tonsillar herniation disappeared within 10 days. Simple surgical repair of the dural tears may rapidly improve symptoms and imaging findings in patients with tonsillar herniation caused by traumatic intracranial hypotension.

Long-term outcomes and prognostic factors in pediatric patients with severe traumatic brain injury and elevated intracranial pressure

The management strategies and outcomes in pediatric patients with elevated intracranial pressure (ICP) following severe traumatic brain injury (TBI) are examined in this study. This study was a retrospective review of a prospectively acquired pediatric trauma database. More than 750 pediatric patients with brain injury were seen over a 10-year period. Records were retrospectively reviewed to determine interventions for correcting ICP, and surviving patients were contacted prospectively to determine functional status and quality of life. Only patients with 2 years of follow-up were included in the study. Ninety-six pediatric patients (age range 3-18 years) were identified with a Glasgow Coma Scale score<8 and elevated ICP>20 mm Hg on presentation. The mean injury severity score was 65 (range 30-100). All patients were treated using a standardized head injury protocol. The mean time course until peak ICP was 69 hours postinjury (range 2-196 hours). Intracranial pressure control was achieved in 82 patients (85%). Methods employed to achieve ICP control included maximal medical therapy (sedation, hyperosmolar therapy, and paralysis) in 34 patients (35%), ventriculostomy in 23 patients (24%), and surgery in 39 patients (41%). Fourteen patients (15%) had refractory ICP despite all interventions, and all of these patients died. Seventy-two patients (75%) were discharged from the hospital, whereas 24 (25%) died during hospitalization. Univariate and multivariate analysis revealed that the presence of vascular injury, refractory ICP, and cisternal effacement at presentation had the highest correlation with subsequent death (p<0.05). Mean follow-up was 53 months (range 11-126 months). Three patients died during the follow-up period (2 due to infections and 1 committed suicide). The mean 2-year Glasgow Outcome Scale score was 4 (median 4, range 1-5). The mean patient competency rating at follow-up was 4.13 out of 5 (median 4.5, range 1-4.8). Univariate analysis revealed that the extent of intracranial and systemic injuries had the highest correlation with long-term quality of life (p<0.05). Controlling elevated ICP is an important factor in patient survival following severe pediatric TBI. The modality used for ICP control appears to be less important. Long-term follow-up is essential to determine neurocognitive sequelae associated with TBI.

Risk Factors Associated with Delayed Traumatic Intraparenchymal Hemorrhage

Objective: Delayed hemorrhage progression is one of the most common causes of neurologic deterioration after traumatic brain injury (TBI). We herein analyzed the risk factors related to the delayed hemorrhage progression in traumatic intraparenchymal hemorrhage (IPH) or cerebral contusion. Methods: A retrospective investigation was performed on selected 105 TBI patients with IPH or cerebral contusion associated with other types of intracranial hematoma during the last 2 years. Clinical features regarding neurologic grade, time intervals from the initial injury to delayed traumatic IPH, and initial computed tomographic (CT) findings including midline shifting, cisternal effacement, and location were studied. For majority of patients, follow-up CT scans were checked at 8, 24, 72 hours after trauma, except patients with sudden neurologic deterioration. Results: Among 105 patients with traumatic IPH, 49 patients showed hemorrhage progression. Traumatic subarachnoid hemorrhage (SAH) is the most commonly accompanied hemorrhage with IPH patients. The most frequent location of hemorrhage progression was the frontal lobe, and time interval for identifying delayed IPH was within the first 8 hours in 31 patients (63%). There was statistically significant correlation between IPH progression and presence of SAH (p=0.03) and effacement of cisterns (p<0.0001). Conclusion: We should closely observe traumatic IPH or cerebral contusion patients who have initial CT findings of traumatic SAH and cisternal effacement. It is primarily because hemorrhage progression is very likely to occur in this patient group. Although we could not draw conclusion regarding time for CT surveillance, bed-side clinical monitoring is of utmost importance. (J Kor Neurotraumatol Soc 2008;4:8-13)

広範囲脳梗塞における減圧開頭術の治療成績

Extensive cerebral hemispheric infarction is a devastating condition leading to early death in nearly 80% of cases due to the rapid rise of intracranial pressure in spite of maximum medical treatment for brain edema and swelling. Recently, decompressive craniectomy has been reevaluated to prevent the brain herniation caused by extensive hemisphelic cerebral infarction. We studied the surgical results after decompressive craniectomy for extensive cerebral infarction. Between December 1997 and August 2006, 13 consecutive patients (7 males and 6 females aged from 39 to 73 with a mean age of 59 years) with massive cerebral infarction of IC (11 patients) and MCA (2 patients) territory were treated with decompressive craniectomy and dural plasty. Five patients had a left-sided stroke with severe aphasia. The cardioembolic source of stroke was seen in 5 patients. Surgery was performed at the point of neurological deterioration, anisocoria, and effacement of perimesencephalic cistern on CT findings. The mean time between stroke onset and surgery was 39.8 hr and ranged from 13 to 102 hr. GOS on discharge was MD 1, SD 8, VS 1, and D 3 (mortality rate 30. 8%). Severe pneumoniae were the causes of death. All survivors underwent cranioplasty and were transferred with the aim of rehabilitation. In this study, we showed that the decompressive craniectomy reduced mortality after extensive cerebral infarction. However, the functional outcome and level of independence are poor. It seems that the early decompressive craniectomy should be aggressively performed for extensive cerebral infarction before neurological deterioration such as worsening of consciousness disturbance or pupil abnormalities. Further investigations will be needed to clarify the surgical indications, timing, and functional outcomes.

ACUTE TRAUMATIC INTRAPARENCHYMAL HEMORRHAGE

To characterize the natural course of traumatic intraparenchymal contusions and hematomas (IPHs) and to identify risk factors for IPH progression in the acute post-injury period. A retrospective analysis was performed on a prospective observational database containing 113 head trauma patients exhibiting 229 initially nonoperated acute IPHs. The main outcome variable was radiographic evidence of IPH progression on serially obtained head computed tomographic (CT) scans. Secondary outcomes included the actual amount of IPH growth and later surgical evacuation. Univariate and multivariate analyses (using a generalized estimate equation) were applied to both demographic and initial radiographic features to identify risk factors for IPH progression and surgery. Overall, 10 IPHs (4%) shrank, 133 (58%) remained unchanged, and 86 (38%) grew between the first and second head CT scan. IPH progression was independently associated with the presence of subarachnoid hemorrhage (odds ratio [OR], 1.6; 95% confidence interval [CI], 1.12-2.3), presence of a subdural hematoma (OR, 1.94; 95% CI, 1.1-3.43), and initial size (OR, 1.11; 95% CI, 1.02-1.21, for each cm volume). Size of initial IPH proportionately correlated with the amount of subsequent growth (linear regression, P < 0.001). Worsened Glasgow Coma Score between initial and follow-up head CT scan (OR, 8.6; 95% CI, 1.5-50), IPH growth greater than 5 cm (OR, 7.3; 95% CI, 1.6-34), and effacement of basal cisterns on initial CT scan (OR, 9.0; 95% CI, 1.5-52) were strongly associated with late surgical evacuation. A large proportion of IPHs progress in the acute post-injury period. IPHs associated with subarachnoid hemorrhage, a subdural hematoma, or large initial size should be monitored carefully for progression with repeat head CT imaging. Effacement of cisterns on the initial head CT scan was strongly predictive of failure of nonoperative management, thereby leading to surgical evacuation. These findings should be important factors in the understanding and management of IPH.

The Role of Early Follow-Up Computed Tomography Imaging in the Management of Traumatic Brain Injury Patients With Intracranial Hemorrhage

The purpose of this study was to investigate whether routine follow-up computed tomography (CT) for patients with head injury, in the absence of clinical indications, alters patient management. Nonpenetrating head injury patients admitted to San Francisco General Hospital during an 18-month period were reviewed. Patients not surgically treated at presentation and with a routine follow-up head CT within 24 hours were included. Surgical and nonsurgical interventions after repeat CT were assessed. Clinical and imaging parameters were correlated with progressive hemorrhagic injury (PHI) and with delayed development of surgical lesions. PHI was identified in 49 (42%) of 116 patients. None of these patients required a nonoperative intervention in response to the PHI. Six of these patients developed a neurologic change concurrent with routine follow-up imaging and required operative intervention. Thus, no patient underwent an intervention in response to a worsening head CT in the absence of clinical findings. Of the six patients who developed a surgical lesion, two had increased intracranial pressure, one had a change in pupillary examination, three had worsening mental status, and one had change in the motor examination. Univariate risk factors for development of a delayed surgical lesion included 5 to 10 mm of midline shift (p = 0.001), basal cistern effacement (p = 0.01), and higher Marshall score (p = 0.01) on initial CT imaging. Although PHI is common with head injury, delayed interventions in the absence of clinical indicators are uncommon. Our data suggest that early follow-up CT imaging in the setting of head trauma is not routinely indicated. We suggest that assessment, based on the severity of findings on initial brain imaging and serial clinical examinations, should guide the need for follow-up imaging in the setting of head trauma.

Intensive care management of head injury patients without routine intracranial pressure monitoring

Head injury contributes significantly to mortality and morbidity in India. Evaluation of the available trauma care facilities may help improve outcome. To evaluate the factors influencing the mortality of patients with head injury who had intensive care management and evolve strategies to improve outcome. Retrospective study in a tertiary hospital where intracranial pressure monitoring (ICPM) is not routinely practiced. All patients with head injury managed in the intensive care unit in a two-year period were included. The factors evaluated were age, vital signs, Glasgow Coma scale score (GCS) at admission, pupillary light reflex (PR), oculocephalic reflex (OCR), hemodynamic stability, computerized tomography (CT) findings, diabetes mellitus, anemia, infections and abnormalities of serum sodium. We analyzed 208 patients (202 without ICPM). In-hospital mortality was 64 (31%). Only 24 (11.5%) patients were admitted within one hour of injury, while one-third arrived after six hours. The clinical factors (at admission) that influenced mortality included age, GCS, PR, OCR and diastolic blood pressure (DBP). Effacement of the basal cisterns in the initial and repeat CT scans, hyperglycemia, hemodynamic instability and serum sodium imbalances were associated with higher mortality. The independent predictors of mortality by logistic regression were initial GCS, DBP, hemodynamic instability and effacement of cisterns on repeat CT. Mortality following head injury is high. Pre-hospital emergency medical services are disorganized. The key to reducing mortality within the limitations of our current trauma system is maintenance of DBP>70 mmHg and SBP>90 mmHg from the time of first contact.

October 24 Highlight and Commentary

Fields et al. report a patient with a cerebral contusion and a subdural hematoma who developed midline shift away from the site of hemicraniectomy—“paradoxical herniation.” This potentially life-threatening but treatable condition presents with progressive neurologic deterioration and a sunken skull defect. ![][1] Figure. CT scan showing midline shift with subfalcine herniation in the direction opposite the site of craniectomy (A) and midbrain compression with effacement of the quadrigeminal cistern (B). Repeat CT scan … [1]: /embed/graphic-1.gif