Asunto(s)
Anticoagulantes/efectos adversos , Factores de Coagulación Sanguínea/uso terapéutico , Hemorragia Cerebral Intraventricular/terapia , Desamino Arginina Vasopresina/uso terapéutico , Hemostáticos/uso terapéutico , Hemorragia Intracraneal Traumática/tratamiento farmacológico , Inhibidores de Agregación Plaquetaria/efectos adversos , Anciano , Anciano de 80 o más Años , Aspirina/efectos adversos , Hemorragia Cerebral Traumática/etiología , Hemorragia Cerebral Traumática/terapia , Hemorragia Cerebral Intraventricular/inducido químicamente , Clopidogrel/efectos adversos , Femenino , Fracturas Óseas/complicaciones , Hematoma/etiología , Hematoma/terapia , Hematoma Intracraneal Subdural/etiología , Hematoma Intracraneal Subdural/terapia , Humanos , Relación Normalizada Internacional , Hemorragia Intracraneal Traumática/etiología , Masculino , Persona de Mediana Edad , Huesos Pélvicos/lesiones , Pirazoles/efectos adversos , Piridonas/efectos adversos , Estudios Retrospectivos , Rivaroxabán/efectos adversos , Hemorragia Subaracnoidea Traumática/etiología , Hemorragia Subaracnoidea Traumática/terapia , Trombosis/inducido químicamente , Trombosis/epidemiología , Warfarina/efectos adversosRESUMEN
This study analyzed the predictable factors of outcome such as neuro-parameters and systemic complications to elucidate the indications for therapeutic hypothermia. In our institute, 35 patients with severe head injury (Glasgow Coma Scale 3-7) were treated with mild hypothermia therapy (33 degrees-35 degrees C). Twenty-two of these 35 patients underwent complete neuromonitoring and outcome assessments by Glasgow Outcome Scale (GOS) at three months after injury. GOS of hypothermia group was significantly better than another patient group which was treated without mild hypothermia therapy. The hypothermia group was divided into two groups: good outcome (GOOD) (good recovery or moderate disability; n = 9, 40.9%) and poor outcome (POOR) (severe disability, vegetative state, or death; n = 13, 59.1%). The mean age (mean 30.2 years, range 9-46) was significantly lower in GOOD than in POOR (mean 45.2 years, range 17-62). Patients aged over 50 years had poor outcome. CPP was significantly higher in GOOD during hypothermia. All patients with thrombocytopenia had poor outcome. Hypothermia therapy can improve outcome in patients with traumatic brain injury who are younger than 50 years old, without severe brain damage, and if improvement of cerebral perfusion is expected. Systemic complications must be prevented as far as possible by combination with other therapies.
Asunto(s)
Lesiones Encefálicas/terapia , Encéfalo/fisiopatología , Hipertermia Inducida/estadística & datos numéricos , Adolescente , Adulto , Factores de Edad , Anciano , Temperatura Corporal/fisiología , Encéfalo/patología , Edema Encefálico/patología , Edema Encefálico/fisiopatología , Edema Encefálico/terapia , Lesiones Encefálicas/patología , Lesiones Encefálicas/fisiopatología , Causalidad , Niño , Femenino , Hematoma Subdural/patología , Hematoma Subdural/fisiopatología , Hematoma Subdural/terapia , Humanos , Masculino , Persona de Mediana Edad , Valor Predictivo de las Pruebas , Pronóstico , Recuperación de la Función/fisiología , Hemorragia Subaracnoidea Traumática/patología , Hemorragia Subaracnoidea Traumática/fisiopatología , Hemorragia Subaracnoidea Traumática/terapia , Tasa de Supervivencia , Trombocitopenia/complicaciones , Trombocitopenia/fisiopatología , Resultado del TratamientoRESUMEN
Cardiac injury and pulmonary oedema occurring after acute neurological injury have been recognised for more than a century. Catecholamines, released in massive quantities due to hypothalamic stress from subarachnoid haemorrhage (SAH), result in specific myocardial lesions and hydrostatic pressure injury to the pulmonary capillaries causing neurogenic pulmonary oedema (NPO). The acute, reversible cardiac injury ranges from hypokinesis with a normal cardiac index, to low output cardiac failure. Some patients exhibit both catastrophic cardiac failure and NPO, while others exhibit signs of either one or other, or have subclinical evidence of the same. Hypoxia and hypotension are two of the most important insults which influence outcome after acute brain injury. However, despite this, little attention has hitherto been devoted to prevention and reversal of these potentially catastrophic medical complications which occur in patients with SAH. It is not clear which patients with SAH will develop important cardiac and respiratory complications. An active approach to investigation and organ support could provide a window of opportunity to intervene before significant hypoxia and hypotension develop, potentially reducing adverse consequences for the long-term neurological status of the patient. Indeed, there is an argument for all SAH patients to have echocardiography and continuous monitoring of respiratory rate, pulse oximetry, blood pressure and electrocardiogram. In the event of cardio-respiratory compromise developing i.e. cardiogenic shock and/or NPO, full investigation, attentive monitoring and appropriate intervention are required immediately to optimise cardiorespiratory function and allow subsequent definitive management of the SAH.