PubMed · 9735697
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D C Sheppard, H F Chambers. 1998. Suppurative parotitis.. https://pubmed.ncbi.nlm.nih.gov/9735697/
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OBJECTIVE: The clinical picture of mastoiditis, sigmoid sinus thrombosis and brain abscess has changed with the advent of antibiotics. A delay in the recognition of intracranial complications in children and in the institution of appropriate therapy may result in morbidity and mortality. Increased mortality of the children has been correlated with the neurological status of the patient on admission to hospital. METHOD: A retrospective study was made of two children with acute mastoiditis and sigmoid sinus thrombosis and chronic mastoiditis with cerebellar abscess treated in 1997 in the ENT Department of the Medical University of Gdansk. RESULTS: We present two cases of intracranial complications in children (13 and 11 years old) originating from acute and chronic otitis media. The first case, of a 13-year-old boy with sigmoid sinus thrombosis as a complication of acute otitis media took its course as a typical Symonds Syndrome. Mastoidectomy, thrombectomy and jugular vein ligation associated with antibiotics and edema-reducing drugs and anticoagulants proved to be successful. The second case of an 11-year-old boy with exacerbated chronic otitis media with cholesteatoma and mastoiditis, was complicated by suppurative meningitis, cerebellar abscess, perisinual abscess and sigmoid sinus thrombophlebitis. Neurosurgical approach by suboccipital craniotomy and abscess drainage was ineffective. Otological treatments of modified radical mastoidectomy, thrombectomy, jugular vein ligation, perisinual and cerebellar abscess drainage associated with wide-spectrum antibiotics and edema-reducing drugs were performed with a very good outcome. After 3 years of follow-up the patients remain without any neurological and psychiatric consequences. CONCLUSION: The authors show different courses of both presented complications and imaging techniques and surgical procedures performed in these children. The sigmoid sinus trombosis with Symonds Syndrome may be difficult to diagnose due to previous antibiotics valuable in establishing the diagnosis and the extent of disease. The successful therapy is based on understanding of pathogenesis of the intracranial complication and the cooperation of an otolaryngologist, a neurologist, a neurosurgeon and an ophthalmologist.
Patients admitted with suspicion of an acute coronary syndrome (ACS) still constitute a diagnostic, prognostic and therapeutic challenge for the treating physician. The final diagnosis ranges from a noncardiac diagnosis to a full-blown myocardial infarction (MI). Biochemical markers of myocardial damage are essential for diagnosis and, especially troponin T and troponin I, have been shown to be valuable for early risk stratification and for selection of treatment in ACS. Patients identified to be at low risk of future cardiac events might be discharged early, and unnecessary investigations and treatments avoided. On the contrary, a more intense treatment can be started in patients identified to be at high risk. Unstable angina patients with, compared to without, elevation of troponin, have a more activated coagulation system and more frequently complex lesions and visible thrombus in their coronary arteries. Accordingly, antithrombotic and antiplatelet therapies, i.e. l.m.w heparin and GP IIb/IIIa receptor antagonists, have been proved to have beneficial effects in troponin positive patients, but little or no beneficial effects in troponin negative patients. Also, the beneficial effects of an invasive compared to a noninvasive approach seem to be much more pronounced in troponin positive patients. In patients with ST-elevation MI, an elevated troponin T level at admission are associated with an increased mortality. However, the therapeutic implications of this finding remain speculative. Patients admitted with chest pain and left bundle branch block (LBBB) and who develop an MI have a poor prognosis. Current guidelines in acute myocardial infarction state that these patients should receive thrombolysis. Despite that, only a minority of these patients do receive thrombolysis, most probably because of the great diagnostic uncertainty. Rapid testing with a cardiac marker, e.g. myoglobin, would most probably increase the proportion of patients with chest pain and LBBB who receive appropriate reperfusion treatment.
Coronary thrombosis is an important determinant of prognosis in patients with acute coronary syndromes (ACS). However, the identification of patients at high-risk for progression of coronary thrombosis is difficult in part because we currently lack clinically meaningful laboratory methods for its detection. The most promising approaches involve the measurement in plasma of markers of fibrin formation and degradation. Thrombin activity, as reflected by plasma or urine concentrations of fibrinopeptide A, is increased in patients with ACS and is associated with adverse outcome. However, the use of fibrinopeptide A as a marker of fibrin formation is limited by the very short half-life of the compound, by artifact due to sample acquisition, and by extremely long turnaround times. To overcome these limitations, measurement of soluble fibrin has been proposed. We have recently explored the prognostic value of a new fibrin-specific ELISA assay for soluble fibrin in patients with ACS and found that patients with highest levels had a twofold increased risk of early and late cardiac events. Increases in plasma concentrations of cross-linked fibrin degradation products (XL-FDPs), which reflect increased fibrin turn-over, are a marker of risk for complications of myocardial infarction. However, until recently, assays for XL-FDPs lacked specificity, because they did not distinguish between fibrin and fibrinogen degradation products. Recently, fibrin-specific ELISAs have been described and a rapid whole blood assay for D-dimer has been developed. We recently validated the prognostic value of this whole blood agglutination assay in patients with ACS. The results suggest that: (1) the detection of significant activation of the coagulation and/or fibrinolytic system may be important for rapid risk stratification of patients with ACS; (2) patients with biochemical evidence of ongoing coronary thrombosis may particularly benefit from aggressive antithrombotic strategies; (3) sequential measurements of these markers may be useful to guide antithrombotic treatment during the unstable phase of coronary artery disease.