The primary underlying brain injury associated with acute subdural hematoma is generally more severe than that seen with epidural hematoma, particularly in children. In children, subdural hematoma is often caused by local extension of hemor-rhagic intracerebral contusions into the subdural space. Onset of coma at the moment of injury is common. Localizing signs, which are less frequent than with epidural hematomas, depend variably on the location of the hematoma and any underlying cerebral contusions.
With CT imaging, acute subdural hematomas appear as convex-concave ('moon-shaped') hyperdensities adjacent to the skull (see Fig. 4). Subdural hematomas are not limited by dural suture attachments and frequently tend to cover most or all of the cerebral hemisphere ('pan-hemispheric'). Poor differentiation of the underlying gray-white matter junction may be due to cerebral edema and/or ischemia.
Figure 4. Acute subdural hematoma. Axial computed tomography in this adolescent motor-vehicle crash victim demonstrates a moderate-sized hyperdensity in the left frontal region. The abnormality is crescent shaped and is not limited in extent by adherence of the dura to cranial sutures. At operation, an acute subdural hematoma was identified and successfully evacuated.
Acute subdural hematomas result from accidental and nonaccidental trauma, as well as birth trauma. Generalized seizures and severe cerebral edema are relatively common in the presence of traumatic subdural hematomas. Critical care interventions to control the impact of these complications (outlined above) should be aggressively pursued. The hematoma and edematous injured brain may result in shift of midline structures (such as the interhemispheric fissure) away from the midline skull and dural landmarks, and efface the basilar cisterns. A large amount of midline shift with only a thin hematoma generally results from severe underlying brain injury and edema and carries a particularly grim prognosis. At any time during this clinical sequence, the patient may demonstrate the Cushing reflex—systemic arterial hypertension and bradycardia—which is also a secondary sign of severe intracranial hypertension. A large, unilateral subdural hematoma may cause an 'uncal herniation syndrome.' By contrast, severe diffuse brain injury and/or bilateral subdural hematomas may cause a 'central herniation syndrome' (see Table 4). Treatment of subdural hematoma involves steps to reduce cerebral edema, as outlined above, and craniotomy for surgical removal of the hematoma. Indications for removal are:
1. Thickness greater than 5 to 10 mm.
2. Raised intracranial pressure with a hematoma of any size that might contribute to ICP elevation.
3. Local mass effect with corresponding neurological deficit.
4. Difficult-to-control seizures (controversial).
Subdural hematomas are evacuated by open craniotomy. Extreme care is taken to avoid uncontrolled bleeding from torn venous sinuses, which may be rapidly fatal due to the small blood volume of pediatric patients. Small areas of clotted hematoma over the bleeding source may be left in place or reinforced with hemostatic agents. Because of the narrow subdural space in normal children and the risk of infection, a postoperative subdural drain is rarely used, although subdural-to-peritoneal shunting may be necessary for recurrent fluid collections.
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