Riesgo de hemorragia cerebral en el traumatismo craneal leve y tratamiento antitrombótico / Risk of cerebral hemorrhage in mild traumatic brain injury and antithrombotic treatment

Objetivo El tiempo de observación en el traumatismo craneoencefálico leve (TCEL) es controvertido. Nuestro objetivo se basó en evaluar el riesgo de complicaciones neurológicas en el TCEL con y sin tratamiento antitrombótico. Método Evaluamos retrospectivamente los pacientes con TCEL atendidos en urgencias durante 3 años. Consideramos TCEL aquellos con Glasgow ≥13 al ingreso. Se realizó una TC craneal en todos los casos con >1 factor de riesgo al ingreso y a las 24h en aquellos con deterioro neurológico o TC craneal inicial patológica. Se revisó retrospectivamente las complicaciones en los siguientes 3 meses. Resultados Evaluamos 907 pacientes con una edad media de 73±19 años. El 91% presentaron factores de riesgo, con un 60% en tratamiento antitrombótico. Detectamos un 11% de hemorragia cerebral inicial, 0,4% a las 24h y ningún caso a los 3 meses. El tratamiento antitrombótico no se asoció con incremento de riesgo de hemorragia cerebral (9,9 con vs. 11,9% sin tratamiento; p=0,3). El 39% de las hemorragias presentaron síntomas neurológicos (18% amnesia postraumática, 12% cefalea, 8% vómitos, 1% convulsiones), siendo en un 78,4% síntomas leves. De las 4 hemorragias detectadas a las 24h, 3 fueron asintomáticas y un caso emporó la cefalea inicial. Ningún paciente asintomático sin lesión en la TC craneal inicial presentó clínica a las 24h. Conclusiones Nuestro estudio sugiere que los pacientes con TCEL asintomáticos, sin lesión en la TC craneal inicial no precisarían periodo de observación ni TC craneal de control, independientemente del tratamiento antitrombótico o nivel de INR (AU)

Introduction The observation time in mild traumatic brain injury (mTBI) is controversial. Our aim was to assess the risk of neurological complications in mTBI with and without antithrombotic treatment. Method We retrospectively evaluated patients with mTBI seen in the emergency room for 3 years. We considered MTBI those with Glasgow ≥13 at admission. A cranial CT was performed in all cases with >1 risk factor at admission and at 24h in those with neurological impairment or initial pathological cranial CT. Complications in the following 3 months were retrospectively reviewed. Results We evaluated 907 patients with a mean age of 73±19 years. Ninety-one percent presented risk factors, with 60% on antithrombotic treatment. We detected 11% of initial brain hemorrhage, 0.4% at 24h, and no cases at 3 months. Antithrombotic treatment was not associated with an increased risk of brain hemorrhage (9.9% with vs. 11.9% without treatment, P=.3). 39% of the hemorrhages presented neurological symptoms (18% post-traumatic amnesia, 12% headache, 8% vomiting, 1% seizures), with 78.4% having mild symptoms. Of the 4 hemorrhages detected at 24h, 3 were asymptomatic and one case that worsened the initial headache. No asymptomatic patient without lesion on initial clinical cranial CT presented at 24h. Conclusions Our study suggests that patients with asymptomatic mTBI, without a lesion on the initial cranial CT, would not require the observation period or CT control regardless of antithrombotic treatment or INR level (AU)

Antiplatelet Agent Reversal Is Unnecessary in Blunt Traumatic Brain Injury Patients Not Requiring Immediate Craniotomy.

BACKGROUND: The need to reverse the coagulation impairment caused by chronic antiplatelet agents in traumatic brain injury (TBI) patients with acute traumatic intracerebral hemorrhage (TICH) remains controversial. We sought to determine whether emergent platelet transfusion reduces the incidence of hemorrhage expansion, mortality, or need for neurosurgical intervention such as intracranial pressure (ICP) monitoring, burr holes, or craniotomy. METHODS: All adult blunt TICH patients (age ≥16 years) over a 4-year period were retrospectively reviewed. Patients with penetrating TBI, blunt TBI without TICH on admission computed tomography (CT), receiving warfarin, not on antiplatelet agents, or requiring immediate operative intervention were excluded. Patients were divided into 2 groups depending on whether they received a platelet transfusion: reversal group (RV) versus no reversal group (NR). Patient outcomes were analyzed using Mann-Whitney U and Fisher's exact tests. RESULTS: 169 blunt TBI patients on chronic antiplatelet therapy were studied (102 RV group, 67 NR group). The groups were well matched with regard to age, Injury Severity Score, Abbreviated Injury Scale-head, Glasgow Coma Score, mechanism of injury, need for intubation, time to initial CT scan, and hospital length of stay. Immediate platelet transfusion did not alter the occurrence of TICH extension on follow-up CT (26% vs 21%, P = .71), TBI-specific mortality (9% vs 13%, P = .45), need for ICP monitor (2% vs 3%, P = 1.0), burr hole (1% vs 3%, P = .56), or craniotomy (1% vs 3%, P = .56). DISCUSSION: Immediate platelet transfusion is unnecessary in blunt TBI patients on chronic antiplatelet therapy who do not require immediate craniotomy.

Effect of Internal Jugular Vein Compression on Intracranial Hemorrhage in a Porcine Controlled Cortical Impact Model.

Internal jugular vein (IJV) compression has been shown to reduce axonal injury in pre-clinical traumatic brain injury (TBI) models and clinical concussion studies. However, this novel approach to prophylactically mitigating TBI through venous congestion raises concerns of increasing the propensity for hemorrhage and hemorrhagic propagation. This study aims to test the safety of IJV compression in a large animal controlled cortical impact (CCI) injury model and the resultant effects on hemorrhage. Twelve swine were randomized to placement of a bilateral IJV compression collar (CCI+collar) or control/no collar (CCI) prior to CCI injury. A histological grading of the extent of hemorrhage, both subarachnoid (SAH) and intraparenchymal (IPH), was conducted in a blinded manner by two neuropathologists. Other various measures of TBI histology were also analyzed including: ß-amyloid precursor protein (ß-APP) expression, presence of degenerating neurons, extent of cerebral edema, and inflammatory infiltrates. Euthanized 5 h after injury, the CCI+collar animals exhibited a significant reduction in total SAH (p = 0.024-0.026) and IPH scores (p = 0.03-0.05) compared with the CCI animals. There was no statistically significant difference in scoring for the other markers of TBI (ß-APP, neuronal degeneration, cerebral edema, or inflammatory infiltration). In conclusion, IJV compression was shown to reduce hemorrhage (SAH and IPH) in the porcine CCI model when applied prior to injury. These results suggest the role of IJV compression for mitigation of not only axonal, but also hemorrhagic injury following TBI.

Tranexamic acid for patients with traumatic brain injury: a randomized, double-blinded, placebo-controlled trial.

BACKGROUND: Traumatic brain injury (TBI) is commonly accompanied by intracranial bleeding which can worsen after hospital admission. Tranexamic acid (TXA) has been shown to reduce bleeding in elective surgery and there is evidence that short courses of TXA can reduce rebleeding in spontaneous intracranial haemorrhage. We aimed to determine the effectiveness and safety of TXA in preventing progressive intracranial haemorrhage in TBI. METHODS: This is a double blinded, placebo controlled randomized trial. We enrolled 238 patients older than 16 years with moderate to severe TBI (post-resuscitation Glasgow Coma Scale (GCS) 4 to 12) who had a computerized tomography (CT) brain scan within eight hours of injury and in whom there was no immediate indication for surgery. We excluded patients if they had a coagulopathy or a serum creatinine over than 2.0 milligrams%. The treatment was a single dose of 2 grams of TXA in addition to other standard treatments. The primary outcome was progressive intracranial haemorrhage (PIH) which was defined as an intracranial haemorrhage seen on the second CT scan that was not seen on the first CT scan, or an intracranial haemorrhage seen on the first scan that had expanded by 25% or more on any dimension (height, length, or width) on the second scan. RESULTS: Progressive intracranial haemorrhage was present in 21 (18%) of 120 patients allocated to TXA and in 32 (27%) of 118 patients allocated to placebo. The difference was not statistically significant [RR = 0.65 (95% CI 0.40 to 1.05)]. There were no significant difference in the risk of death from all causes in patients allocated to TXA compared with placebo [RR = 0.69 (95% CI 0.35 to 1.39)] and the risk of unfavourable outcome on the Glasgow Outcome Scale [RR = 0.76 (95% CI 0.46 to 1.27)]. There was no evidence of increased risk of thromboembolic events in those patients allocated to TXA. CONCLUSIONS: TXA may reduce PIH in patients with TBI; however, the difference was not statistically significant in this trial. Large clinical trials are needed to confirm and to assess the effect of TXA on death or disability after TBI.

Transorbital penetrating head injury by a toilet brush handle.

BACKGROUND: Transorbital penetrating brain injuries are rare lesions without defined therapy standards. CLINICAL PRESENTATION AND INTERVENTION: A male patient presented at our institution with a toilet brush handle in the right cerebral hemisphere. CT imaging identified the object entering the right orbit and having crossed the right hemisphere in the ventricular plane. After performing a medium-sized craniotomy, the object was removed step-by-step under monitoring with an intraoperative CT scan to ensure no involving major hemorrhage. CONCLUSION: Transorbital penetrating brain injuries are treated best by utilizing all up-to-date technical developments such as intraoperative CT-scanning to increase the safety in the management of such exceptional lesions with increased risk of immediate life-threatening intracranial bleeding.

Knife blade penetrating stab wound to the brain--case report--.

A 28-year-old man attempted to kill himself with a knife stab into the parietal area. Neuroimaging showed no vascular impairment except slow venous flow around the knife due to tamponading. After obtaining informed consent, the knife was removed through a craniotomy without new brain injury. Postoperative neurological findings showed no deficit. Follow-up angiography revealed no vascular impairment. No infection occurred. Brain stab wounds cause numerous complications, such as intracranial hemorrhage, injury of important vessels, and infections. Minimal blade movement during removal and precautions to prevent massive hemorrhage are essential.

Traumatismo craneoencefálico II / Head injuries II

El TEC es una enfermedad muy común enla sociedad civilizada en general y en lospaíses violentos en particular. Las causas del TEC son múltiples, pero predominan los accidentes de tránsito y las heridas por armas de fuego. La atención rápida del paciente con TEC es fundamental, ya que el tiempo que tarda un hematoma epidural, por ejemplo, en llenar puede ser una o dos horas. En relación a las lesiones neuronales, causadas por accidentes de tránsito, pueden presentarse minutos, horas o días después, tiempo quepuede ser valioso para considerar tratamientotemprano. El mejor tratamiento contra el TEC u otraenfermedad siempre será la profilaxis. La educación de la comunidad juega papel primordial para evitarlo.