Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (107 page)
Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
The diagnosis of saccular aneurysm rupture is made by identification of symptomatology and laboratory tests. The most common presenting symptom is sudden severe headache. CT scan will identify subarachnoid clot.
Laboratory Findings
Lumbar puncture reveals increased opening pressure and elevated RBC count that does not decrease between tubes 1 and 4. In early subarachnoid hemorrhage (<8 hours after onset of symptoms), the test for occult blood may be positive before xanthochromia develops. Xanthochromia is an indicator that blood has been in the CSF for at least 2 hours.
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Bloody CSF clears by the 10th day in 40% of patients and is persistently abnormal after 21 days in 15% of patients, and approximately 5% of cerebrovascular episodes due to hemorrhage are wholly within the parenchyma, resulting in normal CSF findings.
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References
1. Broderick JP, Brott T, Tomsick T, et al. The risk of subarachnoid and intracerebral hemorrhages in blacks as compared with whites.
N Engl J Med.
1992;326:733.
2. Rinkel GJ, Djibuti M, Algra A, et al. Prevalence and risk of rupture of intracranial aneurysms: a systematic review.
Stroke.
1998;29:251.
3. de Rooij, NK, Linn, FH, van der Plas JA, et al. Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender, and time trends.
J Neurol Neurosurg Psychiatry.
2007;78:1365.
4. Farnham JM, Camp NJ, Neuhausen SL, et al. Confirmation of chromosome 7q11 locus for predisposition to intracranial aneurysm.
Hum Genet.
2004;114:250.
5. UK National External Quality Assessment Scheme for Immunochemistry Working Group. National guidelines for analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage.
Ann Clin Biochem.
2003;40:481.
6. Beetham R, UK NEQAS for Immunochemistry Working group. Recommendations for CSF analysis in subarachnoid haemorrhage.
J Neurol Neurosurg Psychiatry.
2004;75:528.
CEREBRAL VEIN OR SINUS THROMBOSIS
Cerebral venous sinus thrombosis is the presence of clot within the sinus.
Cerebral vein and dural sinus thromboses are an uncommon cause of stroke. They are more likely to occur in neonates and children than adults and more likely in women than in men.
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The causes of thrombosis include prothrombotic condi-tions in 85% of cases (oral contraception, pregnancy, malignancy), infection (e.g., otitis, mastoiditis, sinusitis, meningitis), and head injury. Genetic disorders may also be implicated, including antithrombin III deficiency, protein C and protein S deficiency, factor V Leiden mutation, and prothrombin gene mutation.
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Collagen vascular and inflammatory diseases (e.g., SLE, sarcoidosis, and Wegener granulomatosis) may also be causative.
Venous thrombosis results in elevated venous pressure followed by leakage into the surrounding parenchyma and resultant impairment of CSF reabsorption leading to increased intracranial pressure. Patients may present with headache that increases over several days, motor weakness, paresis, or seizures. Thromboses of the cerebral veins and sinuses may produce focal hemorrhagic infarcts, which can be seen on neuroimaging (see eBook Figure 4-32).
The diagnosis of cerebral vein thrombosis is made predominantly by neurologic imaging (CT or MRI).
Laboratory tests are nonspecific but may give clues to the etiology. Routine hematology, coagulation (PT, PTT), and chemistry tests are recommended and give an idea of underlying cause. Evaluation of an underlying hypercoagulable state with antithrombin, Protein C and S, factor V Leiden, prothrombin mutation, lupus anticoagulant, anticardiolipin, and anti-beta2 glycoproteins may be helpful. An elevated
D
-dimer may support the diagnosis but will not exclude it if negative.
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Lumbar puncture for evaluation of CSF to rule out infection is required. Up to 50% of patients may have CSF findings. The CSF may reveal normal or mildly increased protein to ≤100 mg/dL. The CSF cell count may be normal or ≥10 WBC/μL during the first 48 hours and rarely ≥2,000 WBC/μL transiently on the 3rd day. Red cells may be increased.
Additional blood tests may be informative. An increased CRP and ESR are risk factors for development of stroke, and an increased CRP is associated with a poorer short-term prognosis. Hematologic disorders (e.g., polycythemia, sickle cell disease, thrombotic thrombocytopenia, and macroglobulinemia) may be identified (see Chapter
9
, Hematology).
Vasculitis (e.g., polyarteritis nodosa, Takayasu syndrome, dissecting aneurysm of aorta, syphilis, meningitis; see Chapter
3
, Cardiovascular Disorders) and hypotension (e.g., myocardial infarction, shock) are other potential causes of cerebral vein thrombosis.
References
1. de Veber G, Andrew M, Adams C, et al. Cerebral sinovenous thrombosis in children.
N Engl J Med.
2001;345:417.
2. Stam J. Thrombosis of the cerebral veins and sinuses.
N Engl J Med.
2005;352:1791.
3. Marjot T, Yadav S, Hasan N, et al. Genes associated with adult cerebral venous thrombosis.
Stroke.
2011;42:913.
4. Crassard I, Soria C, Tzourio C, et al. A negative D-dimer assay does not rule out cerebral venous thrombosis: a series of seventy-three patients.
Stroke.
2005;36:1716.
HYPERTENSIVE ENCEPHALOPATHY
Hypertensive encephalopathy is usually associated with a blood pressure of ≥180/120 mm Hg and is an acute, life-threatening disorder presenting with signs of cerebral edema (see eBook Figure 4-33).
Clinical symptoms are characterized by the insidious onset of headache, nausea, and vomiting. If not treated, patients progress to mental confusion, seizures, and coma. Although these symptoms differ from the abrupt onset of stroke, an MRI scan should be obtained, which may reveal edema in the parieto-occipital regions (reversible posterior leukoencephalopathy) or in the pontine region (hypertensive brain stem encephalopathy).
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