Intracranial Lesions epidural hemorrhages commonly originated from tearing of the middle meningeal artery or the diploic veins subdural hemorrhages arising from tearing of bridging veins or disruption of cortical vessels Traumatic subarachnoid hemorrhage more frequent and occurred in 39% of patients
Intracranial Lesions diffuse cerebral edema present in 39% head injury patients Cerebral edema can be unilateral or diffuse and can occur even in the absence of intracranial bleeding. Severe brain edema probably occurs more commonly in children than in adults.
Causes of Secondary Brain Injury Systemic Factors Immediate: a. Hypotension b. Hypoxemia c. Anemia Delayed: a. Coagulopathy b. Hyperthermia (increased CMRO 2 ) c. Hyponatremia
Causes of Secondary Brain Injury Intracranial IICP (decreased CBF) a. Hematomas b. Edema (vascular compromised) c. Brain swelling secondary to hyperemia Brain shift (herniation, arterial compression) Vasospasm (decreased CBF) Epileptic seizures (increased CMRO 2 )
General Care for Head Injury Intravenous fluid 1. to prevent dehydration or overload 2. Normal saline or Ringer’s lactate solution recommended use 3. Prevent hyper- or hyponatremia Hyperventilation 1. Aggressive and prolonged hyperventilation cerebral ischemia 2. PaCO 2 level 30-35 mmHg
General Care for Head Injury Mannitol bolus dose as 1g/kg in acute downhill p’t Furosemide (lasix) 0.3 – 0.5 mg/kg Steroids not recommended in acute head injury
General Care for Head Injury Barbiturates often hypotension not indicated in the acute injury resuscitative phase Antiepileptic drugs 若無發生癲癇最多預防性使用一周
癲癇預防 (Seizure Prophylaxis) Ideal anticonvulsants: easy to use, provide adequate control, and generate no major side effects Phenytoin (Dilantin ) 是最常見的術後抗癲癇藥物 No difference in efficacy, cognitive function, quality of life between phenytoin or sodium valproate (Deparkin) Less toxic serum concentration and hypersensitivity skin reactions in sodium valproate