Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (105 page)
Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
CSF findings are variable: clear, bloody, or xanthochromic, depending on recent or old associated injuries (e.g., contusion, laceration).
CHRONIC
Definition
Chronic subdural hematoma
develops over days or weeks following minor injury that may not have been recognized by the patient. The bleed is slow and may be recurrent.
Chronic subdural hematoma is more commonly seen in the elderly and may present with the insidious onset of cognitive impairment, headaches, light-headedness, apathy, somnolence, or seizures. Symptoms may only appear weeks after the initial injury and may be transient or fluctuating.
3
Diagnosis is based on CT imaging with membranous encapsulation visualized surrounding the hematoma. Lumbar puncture is contraindicated due to the risk of herniation.
CSF is usually xanthochromic, and the CSF protein content is 300–2,000 mg/dL.
Anemia is often present in infants.
References
1. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas.
Neurosurgery.
2006;58:S16.
2. Victor M, Ropper A. Craniocerebral trauma. In: Victor M, Ropper A, eds.
Adams and Victor’s Principles of Neurology
, 7th ed. New York: McGraw-Hill; 2001:925.
3. Kaminski HJ, Hlavin ML, Likavec MJ, et al. Transient neurologic deficit caused by chronic subdural hematoma.
Am J Med.
1992;92:698.
STROKE
Stroke or cerebrovascular accident is the loss of function of an area of the brain due to vascular compromise. Stroke or ischemia of the brain may be transient or permanent. The causes include intracerebral (see eBook Figure 4-26) or subarachnoid hemorrhage (see eBook Figure 4-27) and thrombotic or embolic ischemia (see eBook Figure 4-28). The American Heart Association data review of strokes finds that the majority of strokes are due to ischemia (87%), followed by intracerebral hemorrhage (10%) and subarachnoid hemorrhage (3%).
1
The presenting signs depend on the size and location of the infarct. Risk factors include hypertension, trauma, drugs, smoking alcoholism, atherosclerosis, and vascular malformations.
The diagnosis of stroke is made on history, physical examination, and neurologic imaging (CT or MRI) to identify hemorrhagic versus thrombotic (or embolic) stroke and rule out mass lesion. If the blood pressure is normal, berry aneurysm, hemorrhage into tumor, angioma, or coagulopathy should be considered. Rapid diagnosis is important for the treatment of the patient as thrombolysis must be initiated within the first 4.5 hours after the initial event.
2
In hemorrhagic stroke, the most common causes include ruptured berry aneurysm (45% of patients), hypertension (15% of patients), angiomatous malformations (8% of patients), and less commonly brain tumor and blood dyscrasia. Ischemic causes of stroke include thrombosis or embolism in 80% of patients.
3,4
A genetic basis for increased risk of stroke probably exists, but a definite gene has not yet been identified, nor is genetic testing commercially available. Risk is increased in patients with a family history of stroke, and following a stroke in one twin, a monozygotic second twin has a higher risk of stroke than a fraternal twin. Studies in Iceland have found three loci revealing significant association with ischemic stroke (PITX2, ZFHX3, and HDAC9).
5
In patients with sickle cell anemia, studies have shown an increased risk for stroke is associated with SNPs in the ANXA2, TGFBR3, and TEK genes.
6
A number of biochemical markers in both blood and CSF have been studied with the hope of providing prognostic or predictive value in stroke patients. A meta-analysis of all reported biochemical tests in blood and CSF concluded that the combined results were not sufficiently predictive for clinical use.
7,8
Blood testing at the time of suspected stroke should include CBC, PT and PTT, thrombin time or ecarin clotting time (for patients taking a thrombin or factor Xa inhibitor), and lipid panel. A hypercoagulable panel including lupus anticoagulant (LA), anticardiolipin antibodies (ACAs), protein C, protein S, and factor V Leiden should also be obtained. Testing to rule out SLE may be indicated. Additional tests may include a fibrinogen level, ESR, serology for Lyme disease, and HIV, and toxicology to rule out cocaine and other drugs.
References
1. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics—2013 update: a report from the American Heart Association.
Circulation.
2013;127:e6.
2. Arnold M, Nedeltchev K, Brekenfeld C, et al. Outcome of acute stroke patients without visible occlusion on early arteriography.
Stroke.
2004;35:1135.
3. MacMahon S, Peto R, Cutler J, et al. Blood pressure, stroke, and coronary heart disease. Part 1, Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias.
Lancet.
1990;335:765.
4. Kawachi I, Colditz GA, Stampfer MJ, et al. Smoking cessation and decreased risk of stroke in women.
JAMA.
1993;269:232.
5. Traylor M, Farrall M, Holliday EG, et al. Genetic risk factors for ischaemic stroke and its subtypes (the METASTROKE collaboration): a meta-analysis of genome-wide association studies.
Lancet Neurol.
2012;11:951.
6. Flanagan JM, Frohlich DM, Howard TA, et al. Genetic predictors for stroke in children with sickle cell anemia.
Blood.
2011;117:6681.
7. Zandbergen EG, de Haan RJ, Stoutenbeek CP, et al. Systematic review of early prediction of poor outcome in anoxic-ischaemic coma.
Lancet.
1998;352:1808.
8. Zandbergen EG, de Haan RJ, Hijdra A. Systematic review of prediction of poor outcome in anoxic-ischaemic coma with biochemical markers of brain damage.
Intensive Care Med.
2001;27:1661.
CEREBRAL EMBOLISM
