Management Of Severe Head Injury

hematoma (EDH). EDH is an abnormal collection of blood between the dura and the cranium, usually from a torn middle meningeal artery, but it may be due to torn venous sinuses or bleeding from fracture lines.

Cerebral ischemia, blood flow and metabolism after TBI.

Cerebral ischemia is at the center of the secondary injuries to the brain. Ischemia could have peripheral causes (such as anemia, shock or low SaO2) or central pathogenetic mechanisms (such as low microcirculatory flow, high ICP, diffusion difficulties or problems with electron transfer at the mito-chondrial level). More than 90% of the patients who die from head trauma have evidence of hypoxic brain damage at autopsy and up to 36% of patients in the ICU at one point during their hospitaliza-tion will have global desaturation, as evidenced by sjvO2 or brain tissue oxygen monitoring [6]. During the first 24 hours after TBI, cerebral blood flow is down, especially during the first 6 hours. After the first day, for the next 3-5 days, CBF will increase and then decrease again within the next 2 weeks. Cerebral metabolism is generally down during the post-injury course of the TBI. Hyperglycolysis and increased CBF immediately after TBI could be part of the restorative mechanisms of membrane instability and could have a relationship with good outcome [7].

Cerebral swelling.

During the first 24 hours after head trauma, cerebral swelling is usually cytotoxic, due to membrane dysfunction and excess extracellular potassium. Astrocytic footplate swelling, evident following oxidative distress, is thought generally to worsen cerebral ischemia.

Table 21.2. GCS score.

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