The impact of coagulopathy on the outcome of traumatic epidural hematoma.
ABSTRACT To evaluate the impact of trauma-associated coagulation disorders on the neurological outcome in patients with traumatic epidural hematoma undergoing surgical or non-surgical treatment. A retrospective analysis was performed using prospectively collected data in a consecutive patient series from a level 1 trauma center.
Eighty-five patients with traumatic epidural hematoma were identified out of 1,633 patients admitted to our emergency room with traumatic head injuries between October 2004 and December 2008. The following prospectively assessed parameters were analyzed: Glasgow Coma Scale, coagulopathy, presence of skull fractures, additional injuries, the Injury Severity Score, hematoma volume and thickness at admission, hematoma volume progression over time and neurologic symptoms. Furthermore, patients were grouped based on whether they had undergone surgical or non-surgical treatment of the epidural hematoma. Clinical outcome was determined according to the Glasgow Outcome Score (GOS) at hospital discharge.
Patients with coagulopathy showed significantly lower GOS values compared to patients with intact blood coagulation. Initial and progressive hematoma volumes did not influence neurological outcome. Patients with multiple injuries did not show a worse outcome compared to those with isolated epidural hematoma. There was no difference in patient's outcome after surgical or non-surgical treatment.
Poor outcome after traumatic epidural hematoma was associated with coagulopathy. Progression of epidural hematoma volume was not associated with coagulopathy or with poor neurological outcome. Prospective studies are needed to confirm these results.
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ABSTRACT: The purpose of this study was to evaluate the influence of additional, extracranial injuries and subsequent neurological complications in the intensive care unit on the functional outcome after head injury with extradural haematoma. The retrospective analysis included 139 adult patients with acute extradural haematomas admitted to the intensive care unit. Fifty-seven patients (41 per cent) were multiply injured (Injury Severity Score (ISS) = 36.5), and 82 (59 per cent) had a single head injury (ISS = 24.9). Fifty-four patients (39 per cent) developed neurological complications such as intracranial pressure (ICP) increase alone (N = 16), intracranial bleeding, ischaemic brain lesions or epileptic seizures with an associated ICP increase (N = 24) or without (N = 14). Overall, 77 per cent of the patients had a functional outcome (Glasgow outcome score 4 or 5); 46 per cent had a good recovery, 31 per cent were moderately disabled, 10 per cent were severely disabled, 4 per cent were persistently vegetative, and 9 per cent died. Differences were found between (1) patients with and without complications, (2) patients with extradural haematomas and patients with additional intracranial lesions, and (3) patients with a 'severe' Glasgow Coma Score (GCS) of 3-8 and patients with a GCS of 9-15. The presence of additional intracerebral injuries, and not extracerebral injuries, as well as the management of elevated ICP determines the final outcome in patients with extradural haematomas.Injury 07/1996; 27(5):345-9. · 1.93 Impact Factor
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ABSTRACT: Although coagulopathy is known to be the major contributor to a poor outcome of traumatic brain injury (TBI), the mechanisms that trigger coagulation abnormalities have not been studied in detail. We undertook a prospective observational study at a neurosurgical ICU (NICU) in a university hospital. We examined 11 patients with severe isolated TBI, at admittance to the hospital and during the next 3 days. We collected cerebrovenous blood samples from a jugular bulb catheter, arterial blood, and cerebrospinal fluid (CSF) samples. We measured concentrations of thrombin-antithrombin complex (TAT), fibrin D-dimer (DD), prothrombin fragment 1 + 2 (F1 + 2), interleukin-6 (IL-6), and complement complex (C5b-9). All patients had some degree of consumption coagulopathy at the study start and a tendency to thrombocytopenia during the next few days. Levels of DD (3.6 +/- 2.7 mg/L), TAT (86 +/- 72 microg/L) and F1 + 2 (5.9 +/- 6.8 nmol/L) were significantly increased shortly after the trauma compared to reference values, with considerable transcranial gradients for TAT (49 microg/L) and F1 + 2 (3.2 nmol/L). Compared to controls, IL-6 levels were increased more than a hundredfold in both blood (283 +/- 192 ng/L) and CSF (424 +/- 355 ng/L) samples, with a transcranial gradient at the study start (107 ng/L). C5b-9 levels were moderately increased in blood samples, 270 +/- 114 microg/L, versus controls, 184 +/- 39 (p < 0.05). We conclude that activation of the coagulation system takes place during the passage of blood through the damaged brain, and is already evident hours after the trauma. IL-6 and activation of the complement system (C5b-9) co-vary with hemostatic parameters in TBI patients.Journal of Neurotrauma 01/2007; 24(1):174-80. · 4.30 Impact Factor
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ABSTRACT: Mortality due to epidural hematoma is virtually restricted to patients who undergo surgery for that condition while in coma. The authors have analyzed the factors influencing the outcome of 64 patients who underwent epidural hematoma evacuation while in coma. These patients represented 41% of the 156 patients operated on for epidural hematoma at their centers after the introduction of computerized tomography (CT). Eighteen patients (28.1%) died, two (3.1%) became severely disabled, and 44 (68.8%) made a functional recovery. The mortality rate for the entire series was 12%, significantly lower than the 30% rate observed when only angiographic studies were available. A significant correlation was found between the final result and the mechanism of injury, the interval between trauma and surgery, the motor score at operation, the hematoma CT density (homogeneous vs. heterogeneous), and the hematoma volume. The patient's age, the course of consciousness before operation (whether there was a lucid interval), and the clot location did not correlate with the final outcome. The mortality rate was significantly higher in patients operated on within 6 hours or between 6 and 12 hours after injury than in those undergoing surgery 12 to 48 hours after injury. Compared with the patients operated on later, the patients undergoing surgery in the early period were, on the average, older and had more rapidly developing symptoms, more pupillary changes, lower motor scores at surgery, larger hematomas, a higher incidence of mixed CT density clots, more severe associated intracranial lesions, and higher postoperative intracranial pressure (ICP). The mechanism of trauma seems to influence the course of consciousness before and after surgery. Passengers injured in traffic accidents had a lower incidence of a lucid interval and longer postoperative coma than patients with low-speed trauma, suggesting more frequent association of diffuse white matter-shearing injury. The duration of postoperative coma correlated with the morbidity rate in survivors. Forty-eight patients (75%) had one or more associated intracranial lesions, and 70% of these required treatment for elevation of ICP after hematoma evacuation. An ICP of over 35 mm Hg strongly correlated with poor outcome; administration of high-dose barbiturates was the only effective means for lowering ICP in nine of 15 patients who developed severe intracranial hypertension after surgery. This study attempts to identify patients at greater risk for presenting postoperative complications and to define a strategy for control CT scanning and ICP monitoring.Journal of Neurosurgery 02/1988; 68(1):48-57. · 3.15 Impact Factor