Articles: brain-injuries.
-
Ischemia is one of the major factors causing secondary brain damage after severe head injury. We have investigated the value of continuous partial pressure of brain tissue oxygen (PbrO2) monitoring as a parameter for cerebral oxygenation in 22 patients with severe head injury (Glasgow Coma Scale score, < or = 8). Jugular bulb oxygenation, intracranial pressure, and cerebral perfusion pressure were simultaneously recorded. ⋯ The early occurrence of ischemia after head injury can be monitored on a continuous basis. Deficiency of oxygen autoregulatory mechanisms can be demonstrated, and their occurrence is inversely related to outcome. For practical clinical use, the method seemed to be superior to jugular oximetry.
-
Critical care medicine · Jan 1996
Hypertonic saline does not improve cerebral oxygen delivery after head injury and mild hemorrhage in cats.
To investigate the effects of hypertonic saline for resuscitation after mild hemorrhagic hypotension combined with fluid-percussion traumatic brain injury. Specifically, the effects of hypertonic saline on intracranial pressure, cerebral blood flow (radioactive microsphere method), cerebral oxygen delivery (cerebral oxygen delivery = cerebral blood flow x arterial oxygen content), and electroencephalographic activity were studied. ⋯ After a combination of hemorrhage and traumatic brain injury, neither 10% hydroxyethyl starch nor 3.0% hypertonic saline restored cerebral oxygen delivery. Although neither trauma alone nor hemorrhage alone altered electroencephalographic activity, the combination produced significant decreases in electroencephalographic activity at 60 and 120 mins after resuscitation in groups 3 and 4, suggesting that cerebral oxygen delivery is inadequately restored by either resuscitation fluid. Therefore, traumatic brain injury abolished compensatory cerebral blood flow increases to hemodilution, and neither hydroxyethyl starch nor 3.0% hypertonic saline restored cerebral blood flow, cerebral oxygen delivery, or electroencephalographic activity after hemorrhagic hypotension after traumatic brain injury.
-
The purpose of this study was to evaluate the effects of mannitol (Man), dexamethasone (DM), dichloroacetic acid (DCA) and 1,3-butanediol (BD) in reduction of posttraumatic cortical edema following brain deformation injury to rats. Ten minutes prior to fluid percussion injury, each animal received one of four pretreatments or placebo: Man, 1 g/kg intravenously, DM 3.0 mg/kg intravenously, DCA 25 mg/kg intraperitoneally BD 0.5 mg/kg intraperitoneally (n = 12 per treatment group), or equivolume saline (n = 8 per corresponding trauma group). Six hours after trauma, cortical tissue was harvested. ⋯ The measured cortical SpG from traumatized animals receiving Man (mean 1.037 +/- SEM .001), DCA (1.038 +/- .001), and BD (1.039 +/- .001) were equal to SpG from untraumitized cortex (1.041 +/- .001), and were significantly greater than SpG from traumatized cortex for animals receiving DM (1.035 +/- .001) or placebo (1.033 +/- .002). Pretreatment with DCA, Man, and BD appears to protect against development of posttraumatic cortical edema when measured 6 hours after blunt head trauma in the rat. Each of these chemical treatments appears effective in preventing or reducing posttraumatic cortical edema.
-
Acta neurochirurgica · Jan 1996
Arterio-jugular differences of oxygen (AVDO2) for bedside assessment of CO2-reactivity and autoregulation in the acute phase of severe head injury.
Autoregulation and CO2-reactivity can be impaired independently of each other in many brain insults, the so-called 'dissociated vasoparalysis'. The theoretical combination of preserved CO2-reactivity and impaired or abolished autoregulation can have many clinical implications in the daily management of brain injured patients. To optimize their treatment, a bedside assessment of autoregulation and CO2-reactivity is desirable. ⋯ All patients with an impaired CO2-reactivity also had an impaired autoregulation. Monitoring relative changes in AVDO2 permits a reliable study of CO2-reactivity and autoregulation at the bedside. Introducing these variables into the day-to-day management should be considered in treatment protocols.
-
Anesteziol Reanimatol · Jan 1996
Comparative Study[The possible mechanisms of a fibrinolytic disorder in patients with severe craniocerebral trauma].
Fibrinolysis components were studied in 32 patients with slight and 38 ones with grave craniocerebral injuries on days 1, 3, 5, and 7 after the injury. No expressed disorders of blood fibrinolytic activity were revealed in patients with slight injuries. Grave craniocerebral injuries were associated with disorders of the plasmin system. Depression of the external and internal mechanisms of fibrinolysis were the most manifest starting from day 3 and caused by a number of factors characteristic of the developing disseminated intravascular blood coagulation syndrome and, possibly, by impaired regulation of the plasmin system by the central nervous system.