Kawasaki's disease is a disease of unknown cause. The characteristic clinical features of Kawasaki's disease are fever> or =102 degrees F for> or =5 days accompanied by a bilateral bulbar conjunctivitis/conjunctival suffusion, erythematous rash, cervical adenopathy, pharyngeal erythema, and swelling of the dorsum of the hands/feet. Kawasaki's disease primarily affects children and is rare in adults. In children, Kawasaki's disease is more likely to be associated with aseptic meningitis, coronary artery aneurysms, and thrombocytosis. In adult Kawasaki's disease, unilateral cervical adenopathy, arthritis, conjunctival suffusion/conjunctivitis, and elevated serum transaminases (serum glutamic oxaloacetic transaminase [SGOT]/serum glutamate pyruvate transaminase [SGPT]) are more likely. Kawasaki's disease in adults may be mimicked by other acute infections with fever and rash, that is, group A streptococcal scarlet fever, toxic shock syndrome (TSS), and Rocky Mountain Spotted Fever (RMSF). Because there are no specific tests for Kawasaki's disease, diagnosis is based on clinical criteria and the syndromic approach. In addition to rash and fever, scarlet fever is characterized by circumoral pallor, oropharyngeal edema, Pastia's lines, and peripheral eosinophilia, but not conjunctival suffusion, splenomegaly, swelling of the dorsum of the hands/feet, thrombocytosis, or an elevated SGOT/SGPT. In TSS, in addition to rash and fever, there is conjunctival suffusion, oropharyngeal erythema, and edema of the dorsum of the hands/feet, an elevated SGOT/SGPT, and thrombocytopenia. Patients with TSS do not have cervical adenopathy or splenomegaly. RMSF presents with fever and a maculopapular rash that becomes petechial, first appearing on the wrists/ankles after 3 to 5 days. RMSF is accompanied by a prominent headache, periorbital edema, conjunctival suffusion, splenomegaly, thrombocytopenia, an elevated SGOT/SGPT, swelling of the dorsum of the hands/feet, but not oropharyngeal erythema. We present a case of adult Kawasaki's disease with myocarditis and splenomegaly. The patient's myocarditis rapidly resolved, and he did not develop coronary artery aneurysms. In addition to splenomegaly, this case of adult Kawasaki's disease is remarkable because the patient had highly elevated serum ferritin levels of 944-1303 ng/mL; (normal<189 ng/mL). To the best of our knowledge, this is the first report of adult Kawasaki's disease with highly elevated serum ferritin levels. This is also the first report of splenomegaly in adult Kawasaki's disease. We conclude that Kawasaki's disease should be considered in the differential diagnosis in adult patients with rash/fever for> or =5 days with conjunctival suffusion, cervical adenopathy, swelling of the dorsum of the hands/feet, thrombocytosis and otherwise unexplained highly elevated ferritin levels.
Serum neopterin concentrations have a high correlation with TIMI risk scores and may represent a marker useful in stratifying patients with acute coronary syndromes. Our results also suggest that the use of uncoated coronary stents results in macrophage activation not found with other treatment modalities.
Only 6% of aortic dissections (AoD) present with acute congestive heart failure (CHF). These patients may have an atypical presentation, including hypotension and absence of pain. CHF in the presence of AoD is due to aortic regurgitation and/or coronary hypoperfusion. CASE PRESENTATION: A 31-year-old woman with no medical history presenting with cough and nausea/vomiting was found to be hypoxic and hypotensive. Electrocardiogram (EKG) demonstrated diffuse ST segment depressions. Labs were notable for leukocytosis, hyponatremia, and acute kidney injury, as well as elevated cardiac troponin and probrain natriuretic peptide. Cardiology was consulted after point of care ultrasound showed reduced systolic function. Urgent transthoracic echocardiogram (TTE) showed a large dissection flap prolapsing across the aortic valve and causing severe aortic regurgitation. The patient was also noted to have biventricular failure with moderate mitral regurgitation. Computed tomography angiography (CTA) confirmed the presence of an extensive Type A AoD. The patient underwent urgent aortic valve, root, and arch replacement with improvement in left ventricular function. Later analysis revealed a FBN1 genetic mutation associated with Marfan Syndrome. DISCUSSION: This case illustrates an unusual presentation of AoD as CHF in a young patient without pain. Like the patient in this case, individuals presenting with AoD and CHF are more likely to present without chest pain and in shock, as well as to have a valvular abnormality and a Stanford type A dissection. CHF can lead to a delay in surgical intervention, although it did not in this case. CONCLUSIONS: AoD must be considered in the differential diagnosis of unexplained CHF, even in the absence of pain, in order to minimize surgical delay and mortality.
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