Disseminated Intravascular Coagulation After Craniotomy
Department of Anesthesiology, College of Medicine and School of Health Related Sciences, Mayo Clinic, Rochester, MN 55905, USA.Journal of Neurosurgical Anesthesiology (Impact Factor: 2.99). 02/2008; 20(1):15-20. DOI: 10.1097/ANA.0b013e318155b1c4
Disseminated intravascular coagulation (DIC) is reported in neurosurgical patients; however, the incidence of DIC after craniotomy procedures is unknown. Using a surgical database, we identified 3164 patients who underwent primary craniotomy at Mayo Clinic Rochester between January 1, 2000 and December 31, 2004. Potential cases of DIC in this population were identified using 3 search triggers, patients: (1) in whom the diagnosis of DIC was noted on their hospital discharge summary, (2) who received red blood cell-free blood products, or (3) in whom a blood fibrinogen or d-dimer concentration was assessed. Using criteria based on laboratory values, we estimated the incidence of DIC developing within 72 hours of primary craniotomy to be between 13 and 44 per 10,000 patients. Despite a low incidence of DIC, the associated mortality rate was 43% to 75%. Traumatic head injury was a significant risk factor for the development of DIC [odds ratio of trauma was in the range of 16 (95% confidence interval (CI)=5.3-49) to 29 (CI=4.0-204)]. Autologous salvaged blood was administered intraoperatively to 44 patients, and 1 of these developed DIC. Although this small sample of patients receiving salvaged blood requires caution in interpreting the results, the risk of DIC seemed to be greater with salvaged blood than without [odds ratio 24 (CI=2.5-237)]. In children, 2 of 3 patients who developed DIC had congenital malformations of the brain. Findings from this study suggest that DIC is rare after craniotomy, but is often associated with mortality.
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ABSTRACT: The incidence and risk factors for traumatic brain injury (TBI)-associated coagulopathy after severe TBI (sTBI) and the effect of this complication on outcomes have not been evaluated in any large prospective studies. Prospective study of all patients admitted to the surgical intensive care unit (ICU) of an urban, Level I trauma center from June 2005 through May 2007 with sTBI (head Abbreviated Injury Scale score of >or=3). Criteria for TBI-coagulopathy included a clinical condition consistent with coagulopathy, i.e. sTBI, in conjunction with a platelet count <100,000 mm3 and/or elevated international normalized ratio and/or activated partial thromboplastin time. The following potential risk factors with p < 0.2 on bivariate analysis were included in a stepwise logistic regression analysis to identify independent risk factors for TBI coagulopathy and its association with mortality: age, mechanism of injury (blunt [B] or penetrating [P]), presence of hypotension upon admission, Injury Severity Score (ISS), Glasgow Coma Scale (GCS), head and other body area Abbreviated Injury Scale, isolated head injury, diffuse axonal injury, cerebral edema, intracranial hemorrhage (intraventricular, parenchymal, subarachnoid, or subdural), pneumocephalus, and presence of midline shift. A total of 436 patients (392 blunt, 44 penetrating) met study criteria, of whom 387 patients had isolated SHI. TBI coagulopathy occurred in 36% of all patients (B: 33%, P: 55%; p < 0.0075) and in 34% of patients with isolated head injury (B: 32%, P: 54%; p = 0.0062). Independent risk factors for TBI-coagulopathy in isolated sTBI were found to include a GCS score of <or=8, ISS >or=16, presence of cerebral edema, subarachnoid hemorrhage, and midline shift. ICU lengths of stay were significantly longer in SHI patients who developed TBI coagulopathy (12.7 vs. 8.8 days; p = 0.006). The development of TBI coagulopathy in SHI was associated with increased mortality, adjusted odds ratio (95% confidence interval): 9.61 (4.06-25.0); p < 0.0001. The incidence of TBI coagulopathy in SHI is high, especially in penetrating injuries. Independent risk factors for coagulopathy in isolated head injuries include GCS score of <or=8, ISS >or=16, hypotension upon admission, cerebral edema, subarachnoid hemorrhage, and midline shift. The development of TBI coagulopathy is associated with longer ICU length of stay and an almost 10-fold increased risk of death.
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ABSTRACT: A rare case is described of acute disseminated intravascular coagulation (DIC) following isolated mild head injury with acute subdural haematoma, coagulopathy onset preceding craniotomy. Surgical treatment of the cause followed by swift diagnosis and treatment soon after surgery enabled a good outcome. Post-operative recollection of subdural and extadural blood was treated by further surgery. DIC following isolated mild head injury without axonal damage is rare, but fatal if missed. Thrombocytopaenia in head injured patients should be investigated expediently. Post-operative interim imaging (if not standard practice) should also be considered to exclude haemorrhagic recollection requiring further surgery.
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ABSTRACT: Development of coagulopathy is a serious complication arising from isolated traumatic brain injury, and it predicts poor outcome. The underlying mechanism has not yet been established, although coagulopathy arising from brain tissue injury and the release of tissue factor may represent the pathophysiology. The authors investigated dynamic whole-blood clot formation (ROTEM) in a recently developed porcine model of induced severe intracranial hypertension. In this prospective, randomized experimental study, 17 pigs were designated for severe intracranial hypertension or sham operation. Intracranial hypertension was induced by inflation of an intracranial balloon. Whole-blood clot formation was assessed by clot initiation, and clot propagation and clot strength through thrombelastometry. The authors also assessed thrombin generation and prothrombin time, which were obtained at baseline, immediately after intervention, and 5 h after intervention. A dramatic shortening in time to clot initiation and an increase in clot propagation were observed after induction of intracranial hypertension as compared to the control group. These results were further substantiated by a pronounced increase in thrombin generation and a significantly shortened prothrombin time in the intervention group. No difference in clot strength was detected between the groups. In a porcine model, induction of increased intracranial pressure causing severe intracranial hypertension was associated with a pronounced activation of the coagulation system. Taken together, the various results indicate that tissue factor probably represents the main trigger of hypercoagulopathy found in these pigs.
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