Ronny Yusyanto. Subdural Hematoma d6r3n

SUBDURAL HEMATOMA

SUBDURAL HEMATOMA Acute SDHs are less than 72 hours old and are hyperdense compared to the brain on CT scan. Subacute SDHs are 3-20 days old and are isodense or hypodense compared to the brain. Chronic SDHs are older than 20 days and are hypodense compared to the brain. An acute SDH commonly is associated with extensive primary brain injury. This diffuse parenchymal injury correlates strongly with the outcome of the patient. In one study, 82% of comatose patients with acute SDH had parenchymal contusions (Kotwica,1993)

Most chronic SDHs are believed to be derived from SDG (Subdural hygroma). The presence of brain atrophy or loss of brain tissue due to any cause, such as old age, alcoholism, or stroke, provides a potential space between the dura and the brain surface for a SDG to form. SDG may occur after head trauma and frequently is asymptomatic. The minority of chronic SDH cases are derived from acute SDH cases that have matured for lack of treatment.

Pathophysiology  Acute subdural hematoma

The usual mechanism to produce an acute SDH is high-speed impact to the skull. This causes brain tissue to accelerate relative to a fixed dural structure, which, in turn, tears blood vessels. This mechanism also leads to associated contusions, brain edema, and diffuse axonal injury.

The ruptured blood vessel often is a vein connecting the cortical surface to the dural sinuses. Bridging veins commonly are

found along the sagittal sinus and around the anterior tip of the temporal lobe. Alternatively, a cortical vessel can be damaged by direct laceration. An acute SDH due to a ruptured cortical artery may be associated with only minor head injury, and no cerebral contusions may be associated.

 Chronic subdural hematoma

Most chronic SDHs begin as SDG. An SDG begins as a separation in the dura-arachnoid interface , which then is filled by cerebrospinal fluid (CSF). Dural border cells proliferate around this CSF collection to produce a neomembrane. Then, fragile new vessels grow into the membrane. These vessels can hemorrhage and become the source of blood into the space , which results in the growth of the chronic SDH.

Chronic SDHs that form from acute SDHs have membranes between the dura and hematoma at 1 week and between the brain and hematoma at 3 weeks. As stated above, new fragile vessels grow into these membranes. The hematoma liquefies at 13 weeks of age and becomes hypodense on CT scan. If not resorbed, the vessels in the membranes surrounding the hematoma can hemorrhage repeatedly, resulting in the enlargement of the hematoma. Kawakami (1989) discovered that the coagulation and fibrinolysis systems both were excessively activated in chronic SDH. This results in defective clot formation and recurrent hemorrhage.

CLINICAL :  Acute subdural hematoma

Older patients appear to be at greater risk for developing an acute SDH after head injury. This is believed to be due to older patients having more atrophy, which allows more sheer force against bridging veins immediately after impact.

Neurological

findings : (1) altered level of consciousness (2) a dilated pupil ipsilateral to the hematoma (3) failure of the ipsilateral pupil to react to light (4) hemiparesis contralateral to the hematoma. Less commonly, the hemiparesis may be ipsilateral if caused by direct parenchymal injury or by compression of the cerebral peduncle (contralateral to the hematoma) against the edge of the tentorium cerebelli (Kernohan notch). Less common findings include papilledema and unilateral or bilateral cranial nerve VI palsy.

 Chronic subdural hematoma

Most adults with chronic SDH are older than 50 years’. One quarter to one half of patients with chronic SDH have no identifiable history of head trauma. If a patient does have a history of head trauma, it usually is mild. The average time between head trauma and chronic SDH diagnosis is 4-5 weeks. Risk factors for a chronic SDH include chronic alcoholism, epilepsy, coagulopathy, arachnoid cysts, anticoagulant therapy (including aspirin), cardiovascular disease (hypertension, arteriosclerosis), thrombocytopenia, and diabetes.

Clinical presentation often is insidious, with symptoms of decreased level of consciousness, balance problems, cognitive dysfunction and memory loss, motor deficit (such as a hemiparesis), headache, or aphasia. Acute presentation also is possible, as in the case of a patient who presents with a seizure. Neurologic examination may demonstrate hemiparesis, papilledema, hemianopsia, or third cranial nerve dysfunction, such as unreactive dilated pupil. In patients younger than 60 years, headache is a common presenting symptom.

Workup Lab Studies :  To determine whether defective coagulation was involved in the

formation of the acute SDH and to correct any coagulation abnormalities a prothrombin time (PT), activated partial thromboplastin time (aPTT), and a platelet count should be performed. A bleeding time may detect platelet dysfunction

Imaging Studies :  Computed tomography scan of the head without contrast

Acute SDH appears on CT scan as a crescent-shaped hyperdense area between the inner table of the skull and the surface of the cerebral hemisphere. Acute SDHs usually are unilateral.

The characteristic evolution of an SDH appearance on CT scan is as follows: In the first week, the SDH is hyperdense to brain tissue. In the second and third weeks, the SDH appears isodense to brain tissue. After the third week, the SDH is hypodense to brain tissue. Typical signs of mass effect may be observed, such as midline shift and ventricular compression.

Head CT

Acute subdural hematoma. Note the bright (white) image properties of the blood on this noncontrast cranial CT scan.

Head CT Subacute subdural hematoma. The crescent-shaped clot is less white than on CT scan of acute subdural hematoma. In spite of the large clot volume, this patient was awake and ambulatory.

Treatment  Medical Therapy :

Acute subdural hematoma Small acute SDHs less than 5 mm thick on axial CT images, without sufficient mass effect to cause midline shift or neurological signs, can be followed clinically. Hematoma resolution should be documented by serial imaging because an acute SDH that is treated conservatively can evolve into a chronic hematoma.

Emergent medical treatment of an acute SDH causing impending transtentorial herniation is the bolus istration of mannitol (in the patient who is adequately fluid resuscitated with an adequate blood pressure). Surgical evacuation of the lesion is the definitive treatment and should not be delayed.

Chronic subdural hematoma Without mass effect on imaging studies and no neurological symptoms or signs except mild headache, a chronic SDH can be followed with serial scans and may resolve. No medical therapy has been shown to be effective in expediting rapid resolution of acute or chronic SDHs.

INDICATIONS of surgery Emergent surgical evacuation should occur in patients with an acute SDH larger than 5mm in thickness (as measured by axial CT scan) and causing any neurological signs, such as lethargy, unresponsiveness (coma), or focal neurological deterioration. Surgery for chronic SDH is indicated if SDH is symptomatic or producing significant mass effect on imaging studies.