Correlation of Urine Ammonium with Urine Osmolal Gap in High Anion Gap Matabolic Acidosis: Comparison to Urine Anion Gap / 대한내과학회지

OBJECTIVES: Urine anion gap(UAG) and urine osmolal gap(UOG) were proposed as indirect measures of urine ammonium(NF4+). While the former is known to have its usefulness limited to hyperchloremic metabolic acidosis, the latter is reported to have its correlation with urine NE4+ in ketoacidosis. This study was undertaken to evaluate the correlation of urine NH with IJOG in high anion gap metabolic acidosis(AGMA) and to compare it with UAG. METHODS: We measured urine NH' by enzymatic determination, UOG(=0.5 X [urine osmolality-{2 X (Na++K+)+urea+glucose)]), and UAG(=Na++K+-Cl-) in 18 patients(serum AG=24.4+/-1.6mmol/L ) with AGMA. RESULTS: When they were grouped into those with acute disorders(n=11) and those with chronic disorder(n=7), urine Nk4+ concentration was higher (p40mmol/d) had the UOG>40mmol/L. CONCLUSION: In contrast to the UAG, the UOG has a significant correlation with urine NH4+ in AGMA.

Acute Massive Pulmonary Thromboembolism Occupying both Whole Pulmonary Arteries

Massive pulmonary embolism is a major cause of morbidity and death in hospital. Most episodes of acute pulmonary embolism occurred from multiple emboli. When pulmonary embolism is suspected, the definitive diagnosis is pulmonary arteriography, but high degree of certainty can also be achieved with ventilation-perfusion scanning. The therapeutic modalities available for patients with acute pulmonary embolism are prophylatic and definitive therapy. Prophylatic therapy including anticoagulant with heparin is used to prevent further emboli episodes that might be fatal. Definitive therapy for pulmonary embolism including thrombolytic agents and pulmonary embolectomy attempts to dissolve and remove the resolution of the pathophysiologic sequelae of pulmonary embolism. We experienced a case of acute massive pulmonary embolism which occupied the pulmonary arteries bilaterally. Patient with orthopedic surgery one month before developedd dyspnea and chest tightness. Eventhough continuing enough amount of anticoagulant therapy, rapid hemodynamic deterioration and severe hypoxia occurred progressively. Urgent pulmonary embolectomy was succeeded and he has been followed up at out patient department.