A 73-Year-Old Man With A Mild Headache
A 73-year-old man presents to the emergency department with a 3-day history of mild headache and somnolence. His wife notes that he has periods when he seems "off," that he has been napping frequently, and that he has had a poor appetite. They deny any history of trauma, seizures, or focal neurologic deficits. Symptomatic review of the cardiopulmonary, gastrointestinal, and genitourinary systems is unremarkable. The patient drinks 5-6 ounces of hard liquor per day, but he does not smoke or use illicit drugs. He has not travelled recently, and there have been no changes in his daily routine. He takes a baby aspirin daily for unknown reasons but no other medications. He denies allergies or any other medical conditions. He has never had major surgery.
On physical examination, the patient appears well. Despite the fact that the patient is slightly vague and tangential in answering questions, his Glasgow Coma Scale score is 15. His blood pressure is 180/90 mm Hg, and his heart rate is 80 bpm and regular. The respiratory rate is 16 breaths/min. He is afebrile, with a recorded temperature of 98.1°F (36.7°C). His heart sounds are normal, and he is euvolemic. The lungs are clear on auscultation, and his abdomen is soft, nontender, and without any masses. A detailed cranial nerve examination demonstrates no abnormalities, and funduscopy is normal. The patient's neck is supple, and his cerebellar function tests are normal. He lacks any pronator drift and has a negative Romberg sign. Motor and sensory examination of all 4 limbs is normal; however, he is slightly hyperreflexic at his biceps and patellar tendons.
A workup of the patient's altered mental status is initiated. A complete blood cell count, chest x-ray, liver enzymes examination, thyroid function test, electrocardiogram, and urinalysis are all normal. Electrolytes are normal except for a sodium of 129 mEq/L (12 mmol/L). Computed tomography (CT) of the head is performed (see Figure 1). The brain is asymmetric, and a suspected lesion is noted on the right side. Signs of increased intracranial pressure (ICP), including effacement of the right-sided ventricles, obliteration of the right-sided sulci, and midline shift, are apparent. The brain parenchyma on the left is noted to be atrophic, with prominent sulci. The right-sided lesion is hypodense-to-isodense compared with the surrounding parenchyma.
What is the diagnosis?
Hint: Consider the density of the right-sided lesion seen on the CT scan.
Correct Answer & DiscussionEpidural hematoma
Acute subdural hematoma
Subacute/chronic subdural hematoma
Intracranial tumor
Subarachnoid hemorrhage
This case of subacute/chronic subdural hematoma underscores the seriousness of even subtle neurologic changes in the elderly. A CT scan was ordered due to the subjective confusion reported by the patient, in the context of advanced age and significant alcohol consumption. As with this patient, a history of trauma is lacking in 30%-50% of cases of chronic subdural hematoma.[1] In this patient, signs of midline shift were not subtle, but the density of the clot was very similar to the brain parenchyma. Had the lesion been too small to cause the shift, it could have been easily missed on CT scans without contrast.
Subdural hematomas are extra-axial blood collections between the dura mater and the brain parenchyma. Epidural hematomas are usually ipsilateral to the side of the trauma, while subdural hematomas are typically on the contralateral side. Subdural hematomas form when bridging vessels are damaged by shear forces during an acceleration-deceleration of the head, causing the initial impact coup and secondary contra-coup injury. Patients with atrophic brains are more prone to subdural hematomas as the bridging vessels are of greater length and more susceptible to shear. As a result of the slow, low-pressure venous oozing typical in these injuries, subdural hematomas can develop slowly, and presentation can be delayed by days to weeks. This is particularly true in patients with increased brain atrophy, whose craniums can more readily accommodate additional intracranial blood volume with minimal neurologic sequelae.
Subdural hematomas may present with many different clinical pictures. Rapid accumulation of extra-axial blood, nonatrophic brain parenchyma, and the presence of other traumatic brain injuries correspond to a worsened neurologic status on presentation.[2] Neurologic deficits can result from increased ICP, sequelae from a herniation syndrome, direct pressure from the clot, or other associated injuries.
Chronic subdural hematomas present more often in the elderly, with the incidence in one series estimated as being 7.35 cases out of 100,000 patients in the 70-79 year age group.[3] The most common presentation of chronic subdural hematoma in the elderly is altered mental status, but hemiparesis is also a common finding.[1] Headache and a history of trauma, especially a minor head injury, are other common features on presentation.[4] Another series reported that 24% of elderly patients with chronic subdural hematomas were taking anticoagulants or antiplatelet agents.[5]
Acute subdural hematomas are more common in younger patients, and there is often a history of significant trauma in those cases.[6] As a younger brain is rarely atrophic, even small volumes of extra-axial blood can increase the ICP and result in severe neurologic deficits. Patients with an acute subdural hematoma and severe neurologic deficits also have a worse outcome when compared with other types of hematomas. In a study of patients with fixed and dilated pupils, those patients with an acute subdural hematoma suffered a mortality of 64%, whereas those with epidural hematomas only had an 18% mortality rate.[7]
In the pediatric population, birth trauma can be a cause of subdural hematoma; however, the presence of acute or chronic subdural hematoma should also raise suspicion for child abuse.[8] Physicians should search for other signs of "shaken baby syndrome," including retinal hemorrhage, rib fracture, and long bone fracture. Infants with increased ICP might present with a bulging fontanel, enlarged head circumference, emesis, failure to thrive, and seizure.
Up to 6% of subdural hematomas will present with a seizure, usually when there is a large lesion. Transient neurologic deficits occur in 1%-12% of patients, and cranial nerve palsies and nystagmus have also been described.[9] Gerstmann syndrome (right-left disorientation, finger agnosia, agraphia, and acalculia) has also been reported in the clinical presentation of subdural hematoma.[10]
The clinician must generate a broad differential diagnosis for any elderly patient presenting with weakness or confusion because chronic subdural hematoma can mimic many other disease entities. As such, CT scanning of the brain should be considered in any elderly patient with a change in mentation. Subdural hematoma might initially be easily mistaken for other neurologic injuries, such as ischemic stroke, epidural hematoma, tumor, or subarachnoid hemorrhage.
CT scanning is the mainstay of diagnosis, and CT findings vary depending on the age of the lesion. In the acute phase (days 0-7), the lesion appears hyperdense relative to the parenchyma. The clot is fresh and jelly-like.[2] Subacutely, between days 7 and 21, the lesion is isodense or hypodense as a result of fibrinolysis occurring within the hematoma.[11] Intravenous contrast may be helpful in illuminating isodense lesions.[11] Chronic subdural hematomas (> 2 weeks) are usually hypodense and extend past suture lines.[11] Typically, acute subdural hematomas are concave in shape, as opposed to epidural hematomas, which are convex; however, in a small number of patients, particularly those with a past history of brain surgery, subdural hematomas may appear convex due to intracranial adhesions.[12]
As a subdural hematoma grows, mass effect becomes evident. CT findings may include midline shift, effacement of the sulci, obliteration of the basal cisterns, and ventricular compression.[2] Bilateral hematomas are fairly common, leading to medial compression of both ventricles and causing them to appear slit-like. This finding is called "squeezed ventricle" or the "rabbit's ears" sign.[1] Small isodense hematomas at the vertex, the base of the skull, and in the posterior fossa can be particularly difficult to visualize. In these cases, magnetic resonance imaging (MRI) can be of assistance in making the diagnosis.[11]
Clinically significant subdural hematomas are treated surgically, although cases of spontaneous resorption during observation have been reported.[13] The current consensus is that subdural hematomas greater than 1 cm or with a midline shift of more than 5 mm should be surgically drained, regardless of the Glasgow Coma Scale score.[6] Small hematomas (a few millimeters thick at maximum width) can be closely monitored if asymptomatic, but the CT scan should be repeated as soon as any signs of clinical deterioration appear.[2,14]
Surgical therapy involves drainage by twist drill/burr hole craniostomy, craniotomy, and subduroperitoneal shunt placement.[2] Craniotomy is often used for patients with reaccumulated subdural hematomas, hematomas with membranes, or solid hematomas.[15] The most common postoperative complication in chronic subdural hematomas is hematoma reaccumulation.[4] While some residual fluid is seen in up to 80% of patients, only 8%-37% of patients are symptomatic.[1] Intracerebral hemorrhage is an uncommon but deadly complication occurring after evacuation of chronic subdural hematomas. It has been hypothesized that hyperemia in the rapidly re-expanding brain might be the cause of such postoperative bleeding.[16] Seizures and tension pneumocephalus are also rare complications.[4]
Mortality after subdural hematomas is determined by numerous factors, including age, presenting neurologic condition, presence of a lucid interval, midline shift, and promptness of surgical intervention.[1] While mortality above the age of 80 years has been cited as 100%, a recent case of successful evacuation of acute subdural hematomas in a 102-year-old woman was reported.[17]
The patient in this case was successfully treated with burr-hole evacuation of the hematoma, with return to his baseline neurologic status. He suffered no postoperative complications and was discharged to home 4 days later.
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