Despite no reported survival benefit by inhaled nitric oxide (NO) among patients with acute respiratory distress syndrome (ARDS) until now, NO inhalation is still deemed acceptable as a rescue therapy for ARDS patients with refractory hypoxemia to various therapeutic measures. However, it is unclear whether inhaled NO exerts either detrimental or beneficial effects on the pathogenesis of ARDS. Laboratory studies suggest that inhaled NO might reduce some types of acute lung injury (ALI). By contrast, NO and nitrite could interact with neutrophil myeloperoxidase or high oxygen in the alveoli to stimulate oxidative reactions during inflammation. Recent experimental data suggest that inhaled NO might attenuate endotoxin-induced ALI. Considering the diverse role of NO as an important endogenous regulatory molecule on both proinflammatory and antiinflammatory processes, the effects of early and continued therapy with low dose of inhaled NO on ALT should be determined.

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Therapeutic strategy for severe acute pancreatitis was reviewed based on the Japanese guidelines for acute pancreatitis. Aggressive fluid resuscitation with intensive medical care is crucial as an initial step of the management of severe acute pancreatitis. Urgent endoscopic retrograde cholangiopancreatography/endoscopic sphincterotomy (ERCP/ES) should be indicated for the patients with severe gallstone pancreatitis, in whom biliary obstruction or cholangitis is suspected. CT-guided fine needle aspiration is recommended for the diagnosis of infected pancreatic necrosis. Necrosectomy with continuous closed lavage or open drainage should be mandatory for surgical management of infected pancreatic necrosis.

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A 27-year-old housewife had a miscarriage in her 5th week of pregnancy following 4 days of fever and increasing epigastric pain. She was diagnosed with acute gastritis and hyperventilation syndrome for her repeated vomiting, continuous dyspnea and thirsty in our ER three days after the abortion. As she had got worsened rather than no improvement with a prescription, she was brought in to the ER again on the same day and extremely high blood glucose with ketoacidosis was found out. Her blood glucose was 978mg·dl^-1 and her HbA_1C was 5.5% (normal). She was diagnosed as fulminant type 1 diabetes and was treated in a standard way for diabetic ketoasidocis. She complained of chest discomfort with T wave inversion on ECG during hospitalization. Although her chest discomfort improved without any specific treatment, normalization of ECG has taken no less than 6 months. As the onset of fulminant type 1 diabetes is abrupt with ketoacidosis and it may lead to death, it is important for emergency physicians as well as obstetricians and internists to have fulminant type 1 diabetes in mind not to misdiagnose nor to delay treatment.

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