Octogenarian With Intermittent Confusion

December 31, 2006

Intermittent, worsening confusion recently developed inan 82-year-old man. His daughter brings him to the officefor evaluation.

Intermittent, worsening confusion recently developed inan 82-year-old man. His daughter brings him to the officefor evaluation.History. The patient lives alone and is self-sufficient;he cooks, gardens, and manages his own finances. Forthe past 2 days, however, he has becomeincreasingly forgetful. For example,he misplaced his car keys, gotlost when he returned home from awalk, and did not recognize his sonin-law. His gait has also been unsteadyrecently. Yet at times he seemsto be his former self.The patient denies fever, cough,chest pain, dyspnea, palpitations,GI symptoms, headache, vision problems,weakness, paresthesias,seizures, syncope, and bladder dysfunction.His weight has been steady.About 3 days earlier, he fell when hegot up in the middle of the night, buthe sustained no external injuries.The patient has hypertension and moderately severedegenerative joint disease of the hips, knees, and shoulders.His medications include lisinopril, 10 mg/d; ibuprofen,800 mg tid; aspirin, 81 mg/d; and a multivitamin supplementonce daily.Examination.The patient is well nourished but unkemptand unshaven. Pulse rate is 66 beats per minuteand regular; respiration rate, 22 breaths per minute; bloodpressure, 148/72 mm Hg sitting and 142/70 mm Hgstanding. He is afebrile and well hydrated. No pallor,cyanosis, clubbing, adenopathy, or rashes. Thyroid is notpalpable. Varicose veins noted in lower limbs; no sensorydeficit. Crepitus is audible when knee joints move; noswelling observed.Skull and spine are normal; carotid arteries are equaland palpable. The patient is disoriented to time and spaceand is unable to recall his address or telephone number.However, he recognizes his daughter and can recite thenames of his grandchildren. Cranial nerve function is intact;funduscopy reveals arteriosclerotic changes. His leftpupil is dilated and poorly reacting. No motor or sensorydeficit is noted. Deep tendon reflexes are equal bilaterally,and plantar reflexes are flexor. Thereare no meningeal or cerebellar signs.The remainder of the systemic examinationis normal.Laboratory studies.Whiteblood cell count is 7200/μL, with anormal differential count; hemoglobinlevel, 13.8 g/dL; platelet count,192,000/μL; erythrocyte sedimentationrate, 16 mm/h. Urinalysis resultsare normal. Serum sodium level is138 mEq/L; potassium, 4 mEq/L;chloride, 100 mEq/L. Blood bicarbonatelevel is 24 mEq/L; blood ureanitrogen, 18 mg/dL; creatinine,1 mg/dL; glucose, 108 mg/dL.An ECG shows sinus rhythmwith nonspecific ST-segment and T-wave changes. Radiographsof the chest and skull are normal.What abnormality does the noncontrast head CT scanshow, and to which of the following disorders does theclinical picture point?A.Cerebral tumorB.Subdural hematomaC.Normal-pressure hydrocephalusD.Alzheimer diseaseE. Multi-infarct dementiaWHAT'S WRONG:In an elderly man with fluctuatingcognitive functions and a historyof a fall, a subacute subduralhematoma, B, is a strong possibility.The CT scan reveals a hyperdensecrescentic mass, which confirmsthe diagnosis; evidence of raised intracranialpressure is also presenton the scan (Figure).Ruling out other possibilities.A patient with a cerebral tumor typicallypresents with headache, visionproblems, and ataxia. The CT scanshows a focal or localized lesion.Normal-pressure hydrocephalus isusually associated with progressivedementia, ataxia, and urinary incontinence.The CT scan reveals a normalventricular system. Alzheimerdisease is insidious in onset and ischaracterized by progressive irreversibledementia. The CT scanmay be normal, or it may show evidenceof cerebral atrophy. Multiinfarctdementia is usually associated with hypertension and is characterized by progressive dementia;the CT scan may show evidence of multiple lacunar infarcts.Hospital course. To exclude other causes of reversible dementia, a VDRL test, thyroid functiontests, and measurement of vitamin B12 and folic acid levels were performed. All the resultswere negative or normal.A neurosurgical consultation was obtained. The patient underwent evacuation of the subduralhematoma through bur holes. After the operation, his cognitive functions recovered fully.SUBDURAL HEMATOMA:
A subdural hematoma occurs when blood collects betweenthe dura mater and the arachnoid membrane; thisusually results from tearing of the "bridging" veins thatconnect the cerebral cortex with the dural sinuses. Lessfrequently, a subdural hematoma is caused by bleedingfrom penetrating branches of superficial cerebral arteries.Subdural hematomas may be classified as acute, subacute,or chronic.Acute subdural hematoma. An acute subduralhematoma almost always indicates severe brain injuryfrom direct cranial trauma, but it may result from accelerationforces alone (eg, whiplash injury). The latter occursmore frequently in elderly persons or in those who takeanticoagulants.Symptoms of acute subdural hematoma appear within24 to 48 hours after the injury; however, most patientshave neurologic symptoms from the moment of injury.Half of patients with an acute subdural hematoma are unconsciousat the time of injury. Ipsilateral papillary dilationand contralateral hemiparesis occur in up to two thirds ofpatients. The characteristic noncontrast CT finding is a hyperdensecrescentic lesion.In a patient like ours whose condition is rapidly deteriorating,emergent evacuation with bur holes or anothertype of craniotomy is necessary. The mortality associatedwith an acute subdural hematoma is 50% to 90%, but it canbe reduced to 30% if surgical drainage is performed in thefirst 4 hours after the injury occurs.Chronic subdural hematoma.The signs andsymptoms of chronic subdural hematoma occur weeksto months after the precipitating event. These hematomasare typically caused by trivial injuries, which maybe forgotten by the patient. Patients with chronic subduralhematoma usually are older than 50 or have diseases that cause cerebral atrophy, such as alcoholism ordementia.Headache, aphasia, fluctuating drowsiness or confusion,and mild weakness are common; these symptomsmay be mistaken for manifestations of transient ischemicattacks or other neurologic conditions. Physical findingsare often subtle; they include mild weakness, hyperreflexia,and Babinski reflex contralateral to the hematoma.The characteristic CT finding is a hyperdense crescenticmass that deforms the surface of the brain. MRI can alsobe used.Treatment of large and/or symptomatic hematomasconsists of surgical evacuation through 1 or 2 bur holes.A drain is usually placed in the subdural space for 24 to 48hours. Small asymptomatic hematomas may be followedwith serial CT scans and may resolve spontaneously.Recurrence rates range from 5% to 30%. Mortality isless than 10% in treated patients, and approximately 75% ofpatients are able to resume normal functioning.Subacute subdural hematoma.Signs and symptomsof subacute subdural hematomas occur between3 and 21 days after injury and are similar to those seen inpatients with chronic subdural hematoma. Surgicaldrainage is the primary treatment.



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