Neurological course and correlated computerized tomography findings after severe closed head injury

Clifton, Guy L.; Grossman, Robert G.; Makela, Merry E.; Miner, Michael E.; Handel, Stanley F.; Sadhu, Vijay K.

doi:10.3171/jns.1980.52.5.0611

Cited by 157 publications

(44 citation statements)

References 24 publications

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“…The time at which death occurs after an injury is bimodal, with 70% of all deaths occurring in the first 48 hours. 6,7 A hospital-based study revealed that 28% of the patients died during the first day of hospitalization. 28 In our cohort of TBI patients, the mortality within 48 hours was 22%.…”

Section: Discussionmentioning

confidence: 99%

“…2,10,16,36,37,39,42 Few studies have analyzed the characteristics of patients who succumbed to early death after a TBI. 2,[6][7][8] The first aim of this study was to derive a prognostic model for early death (within 48 hours) to be used within the first 6 hours after a severe TBI and to externally validate this model. The second aim was to develop a clinical prediction rule based on the previous model to identify those patients who would be most likely to die early.…”

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confidence: 99%

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Validation of a prognostic score for early mortality in severe head injury cases

Gómez¹,

De-la-Cruz

Lora

et al. 2014

JNS

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Object Traumatic brain injury (TBI) represents a large health and economic burden. Because of the inability of previous randomized controlled trials (RCTs) on TBI to demonstrate the expected benefit of reducing unfavorable outcomes, the IMPACT (International Mission on Prognosis and Analysis of Clinical Trials in TBI) and CRASH (Corticosteroid Randomisation After Significant Head Injury) studies provided new methods for performing prognostic studies of TBI. This study aimed to develop and externally validate a prognostic model for early death (within 48 hours). The secondary aim was to identify patients who were more likely to succumb to an early death to limit their inclusion in RCTs and to improve the efficiency of RCTs. Methods The derivation cohort was recruited at 1 center, Hospital 12 de Octubre, Madrid (1990–2003, 925 patients). The validation cohort was recruited in 2004–2006 from 7 study centers (374 patients). The eligible patients had suffered closed severe TBIs. The study outcome was early death (within 48 hours post-TBI). The predictors were selected using logistic regression modeling with bootstrapping techniques, and a penalized reduction was used. A risk score was developed based on the regression coefficients of the variables included in the final model. Results In the validation set, the final model showed a predictive ability of 50% (Nagelkerke R2), with an area under the receiver operating characteristic curve of 89% and an acceptable calibration (goodness-of-fit test, p = 0.32). The final model included 7 variables, and it was used to develop a risk score with a range from 0 to 20 points. Age provided 0, 1, 2, or 3 points depending on the age group; motor score provided 0 points, 2 (untestable), or 3 (no response); pupillary reactivity, 0, 2 (1 pupil reacted), or 6 (no pupil reacted); shock, 0 (no) or 2 (yes); subarachnoid hemorrhage, 0 or 1 (severe deposit); cisternal status, 0 or 3 (compressed/absent); and epidural hematoma, 0 (yes) or 2 (no). Based on the risk of early death estimated with the model, 4 risk of early death groups were established: low risk, sum score 0–3 (< 1% predicted mortality); moderate risk, sum score 4–8 (predicted mortality between 1% and 10%); high risk, sum score 9–12 (probability of early death between 10% and 50%); and very high risk, sum score 13–20 (early mortality probability > 50%). This score could be used for selecting patients for clinical studies. For example, if patients with very high risk scores were excluded from our study sample, the patients included (eligibility score < 13) would represent 80% of the original sample and only 23% of the patients who died early. Conclusions The combination of Glasgow Coma Scale score, CT scanning results, and secondary insult data into a prognostic score improved the prediction of early death and the classification of TBI patients.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Validation of a prognostic score for early mortality in severe head injury cases

Gómez¹,

De-la-Cruz

Lora

et al. 2014

JNS

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“…4) Spontaneous resolution of signs of herniation due to SDH (mainly ASDH) within 24 hours is extremely rare and may be related to a rapid decrease in intracranial pressure. 2) The signs of herniation in our patient observed on admission resolved within only 6 hours. Only eight of the many case reports on the disappearance and diminution of ASDH described the resolution of signs of herniation 1,8,10,11,15) ( Table 1).…”

Section: Discussionmentioning

confidence: 99%

Rapid Spontaneous Resolution of Signs of Intracranial Herniation Due to Subdural Hematoma. Case Report.

Imai

2003

Neurol. Med. Chir.(Tokyo)

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An 83-year-old female presented with signs of intracranial herniation due to subdural hematoma (SDH) which resolved rapidly and spontaneously. This patient showed bilateral decerebrate postures due to left SDH on admission. Since she had serious neurological symptoms and critical systemic conditions caused by an asthma attack, conservative treatment including osmotherapy and mechanical ventilation was performed instead of surgical intervention. Her signs of intracranial herniation resolved only 6 hours after admission. Although the SDH did not diminish rapidly, she showed excellent neurological improvement even with conservative treatment only. Characteristic serial changes on computed tomography corresponding to the neurological improvements were seen. She was discharged with slight right hemiparesis and slight dementia that were present prior to this admission. The rapid resolution of signs of intracranial herniation was attributable to the spontaneous diminution of SDH. The diminution or disappearance of hematomas probably depended on the redistribution of cerebrospinal fluid into the hematoma in the present case.

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“…Delayed traumatic intracerebral hematoma is a serious complication with a high mortality of from 30 to 72% reported for various series [2,3, [12][13][14][15]. Delayed diagnosis and treatment is a common cause of this high mortality [3], although the severity of the initial impact and secondary insults are also contributory [15].…”

Section: Discussionmentioning

confidence: 99%

“…Focal brain injury is thought to result in decreased vascular resistance, allowing an increased head of arterial pressure and increased blood flow to be transmitted to an already traumatized capillary-vascular bed, with resultant hemorrhage into the cerebral parenchyma [2, 7,13,16]. Compression of the brain caused by a hematoma or edema can produce ischemia, necrosis, and secondary hemorrhage [12]. Mechanical distortion producing ischemia and infarction may cause delayed traumatic intracerebral hematoma [17].…”

Section: Discussionmentioning

confidence: 99%

Delayed Traumatic Intracerebral Hematoma: Case Report and Review of Literature

1991

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Delayed traumatic intracerebral hematoma is an uncommon serious complication of severe head injury that is associated with a high mortality. By definition, it arises in an area of the brain where intracerebral hematoma had been noted on a computed tomographic (CT) scan performed in the early postinjury period. The lesion was originally described a century ago by Bollinger [1]; however, Morin and Pitis [2] found only 24 cases reported in the literature before 1970. Baratham and Dennyson [3] in 1972 reported 21 cases out of 7886 cases of head injury seen during a ten-year period. It was only after the advent of CT that it was possible to confirm the de novo occurrence of hemorrhage in areas of the brain shown to be normal on an initial scan [4][5][6][7]. Currently, the reported incidence represents between 1.5 and 7% of the cases of severe head injury [8,9]. However, French and Dublin [10] could find only one case among their 1000 consecutive cases of head injury.Because delayed traumatic intracerebral hematoma frequently occurs in patients with cerebral contusion, a deteriorating neurological state in such patients may erroneously be attributed to edema around a preexisting cerebral contusion causing an increase in mass effect [6]. Thus, correct diagnosis and treatment are not infrequently delayed, with irreversible neurological damage as the outcome. The value of repeated CT scanning as part of the clinical management of severe head injury patients cannot be overemphasized.In our prospective study of 120 patients with a severe head injury (with a Glasgow Coma Scale [GCS] of 8 or below) who were seen over a one-year period, we found only one had a solitary delayed traumatic intracerebral hematoma, and this case forms the basis of our report, along with a brief review of the literature. Case ReportA 35-year-old Omani male was admitted with a GCS of 6 (i.e., no eye opening to pain, flexion withdrawal to pain, no verbal response to pain) following a road traffic accident. He had stable vital parameters (pulse, 90 bpm; blood pressure, 130/90 mm Hg; respiration, normal) and no focal neurological deficits. There were no injuries to the chest, abdomen, or limbs. Plain x-ray studies of the skull showed no fracture and CT scan done 16 hours after the accident showed no abnormality (Figure 1). With symptomatic management, his level of consciousness improved to a GCS of 11 (i.e., spontaneous eye opening, localizing to pain, voicing noise on pain). On the fourth postinjury day, a rapid-onset left hemiplegia developed and he became restless. However, his vital signs remained stable and an urgent CT scan (Figure 2) was performed that revealed a moderate-sized right posterior frontal intracerebral hematoma with surrounding edema, producing slight mass effect. He was treated conservatively, and this consisted of mannitol and dexamethasone therapy along with nursing care and physiotherapy. Over three weeks, his level of consciousness improved to a GCS of 15, and the left hemiplegia abated to a power grade of 4-5/5. Repeat CT sca...

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Neurological course and correlated computerized tomography findings after severe closed head injury

Cited by 157 publications

References 24 publications

Validation of a prognostic score for early mortality in severe head injury cases

Validation of a prognostic score for early mortality in severe head injury cases

Rapid Spontaneous Resolution of Signs of Intracranial Herniation Due to Subdural Hematoma. Case Report.

Delayed Traumatic Intracerebral Hematoma: Case Report and Review of Literature

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