Airway obstruction caused by massive swelling of the tongue following bilateral tonsillectomy for sleep apnea syndrome

A case of airway obstruction caused by the tongue swelling is reported. The patient is a 5-year-old boy scheduled for bilateral tonsillectomy for sleep apnea syndrome. Anesthesia was slowly induced by sevoflurane and maintained with nitrous oxide, fentanyl and sevoflurane. Bilateral tonsillectomy and adenoidectomy were performed uneventfully under general anesthesia. The operation time was 2 hours and 30 minutes. Following the surgical procedure, the endotracheal tube was removed. Shortly after the extubation, the patient complained of difficult articulation and paradoxical respiration. Trachea was intubated immediately. Oxygen saturation was within normal limits throughout all the procedures. Swelling of the tongue was aggravated and was not relieved by steroid infusion. Massive swelling of the face and neck was observed on the next day. CT scan and fiberoptic scope examination showed the swollen tongue obstructing the upper airway. Additional administration of steroid was continued. On the third postoperative day, edema was relieved and the endotracheal tube was removed. Clinical course after the extubation was uneventful. No laboratory data was obtained suggesting the allergic basis. Extubation should be performed carefully and respiratory condition should be observed cautiously following the oral surgery of even a short duration.     

Histopathological factors predictive for prognosis of lung cancer

This study was done on 110 lung cancer patients who had received surgical resection consisted of two groups; one group of 43 who survived more than 5 years without recurrence and the other group of 67 who died within one year following surgery. Prognostic significance of the histopathological features at the primary tumor site as well as the regional lymph nodes were compared between the two groups. Blood vessel invasion by the tumor and lymph node metastasis appeared to be equally significant prognostic factors. Patients having the both factors had little chance for survival. Abundant lymphoid cell infiltration around the tumor was associated with longer survival. Lymphoid cell infiltration at the site of blood vessel invasion also was associated with better grognosis. Follicular hyperplasia and paracortical hyperplasia in the regional lymph nodes were favorable prognostic indicators, whereas sinus histiocytosis was poorly significant prognostic indicator.     

Effect of decreased plasma colloid osmotic pressure on development of pulmonary edema in dogs

The effect of decreased plasma colloid osmotic pressure on the development of pulmonary edema was studied in anesthetized dogs. Lung lymph flow was used as a sensitive and reliable indicator of fluid filtration rate in the lung. When plasma colloid osmotic pressure alone was reduced by slow infusion of saline, and hydrostatic pressure in the pulmonary vascular bed was maintained at normal level by exsanguination, lung lymph flow increased almost linearly with the reduction in colloid osmotic pressure, but was not increased more than five fold of the control, despite a reduction of 80% in the plasma colloid osmotic pressure. Furthermore, there was no evidence of fluid in the tracheal aspirations and no gross evidence of pulmonary edema. In contrast, both decrease in colloid osmotic pressure and increase in pulmonary capillary hydrostatic pressure produced a marked increase in lung lymph flow. This flow varied linearly with the level of the pulmonary artery wedge-plasma colloid osmotic pressure difference and approached twelve fold of the control, when the plasma colloid osmotic pressure was reduced by 73% and the pulmonary artery wedge pressure was elevated by 20 mmHg from the baseline. Our data indicate that decreased colloid osmotic pressure is not associated with the development of pulmonary edema, when there is no increase in pulmonary vascular hydrostatic pressure.     

Evaluation of the risk of postoperative pulmonary complications

Ten of 40 patients who underwent major thoracic or abdominal operations developed postoperative pulmonary complications, consisting of six massive atelectasis, three pneumonias and one edema. They were mostly thoracotomy cases and cigarette smokers. Many of these complications would have been prevented, if reliable pulmonary function tests are available to predict preoperatively such occurrence. Flow-volume curve tracing and closing volume measurement were evaluated in this respect. Both flow at the point of functional residual capacity on flow-volume curve, and the closing capacity subtracted from functional residual capacity were found to be well correlated with the occurrence of postoperative complications and can be used to evaluate the risk of pulmonary complications developing in postoperative period.     

Chronic ethanol consumption decreases serum sulfatide levels by suppressing hepatic cerebroside sulfotransferase expression in mice

Epidemiological studies demonstrate a possible relationship between chronic ethanol drinking and thrombotic diseases, such as myocardial infarction and stroke. However, the precise mechanism for this association remains unclear. Sulfatides are endogenous glycosphingolipids composed of ceramide, galactose, and sulfate, known to have anti-thrombotic properties. Low (0.5 g/kg/day), middle (1.5 g/kg/day), and high (3.0 g/kg/day) doses of ethanol were administered for 21 days intraperitoneally to female wild-type mice, and serum/liver sulfatide levels were measured. No significant changes in cholesterol and triglycerides were seen in serum and liver by ethanol treatment. However, serum/liver sulfatide levels were significantly decreased by middle- and high-dose ethanol treatment, likely due to downregulation of hepatic cerebroside sulfotransferase (CST) levels. Marked decreases in the expression of catalase and superoxide dismutases and ensuing increases in lipid peroxides were also observed in the livers of mice with middle- and high-dose ethanol treatment, suggesting the association between the suppression of hepatic CST expression and enhancement of oxidative stress. Furthermore, serum levels of tissue factor, a typical pro-coagulant molecule, were significantly increased in the mice with middle- and high-dose ethanol treatment showing decreases in serum sulfatide levels. Collectively, these results demonstrate that chronic ethanol consumption reduces serum sulfatide levels by increasing oxidative stress and decreasing the expression of CST in the liver. These findings could provide a mechanism by which chronic ethanol drinking increases thrombotic events.     

Eicosapentaenoic acid improves hepatic steatosis independent of PPARα activation through inhibition of SREBP-1 maturation in mice

Eicosapentaenoic acid (EPA) in fish oil is known to improve hepatic steatosis. However, it remains unclear whether such action of EPA is actually caused by peroxisome proliferator-activated receptor α (PPARα) activation. To explore the contribution of PPARα to the effects of EPA itself, male wild-type and Ppara-null mice were fed a saturated fat diet for 16 weeks, and highly (>98%)-purified EPA was administered in the last 12 weeks. Furthermore, the changes caused by EPA treatment were compared to those elicited by fenofibrate (FF), a typical PPARα activator. A saturated fat diet caused macrovesicular steatosis in both genotypes. However, EPA ameliorated steatosis only in wild-type mice without PPARα activation, which was evidently different from numerous previous observations. Instead, EPA inhibited maturation of sterol-responsive element-binding protein (SREBP)-1 in the presence of PPARα through down-regulation of SREBP cleavage-activating protein and site-1 protease. Additionally, EPA suppressed fatty acid uptake and promoted hydrolysis of intrahepatic triglycerides in a PPARα-independent manner. These effects were distinct from those of fenofibrate. Although fenofibrate induced NAPDH oxidase and acyl-coenzyme A oxidase and significantly increased hepatic lipid peroxides, EPA caused PPARα-dependent induction of superoxide dismutases, probably contributing to a decrease in the lipid peroxides. These results firstly demonstrate detailed mechanisms of steatosis-ameliorating effects of EPA without PPARα activation and ensuing augmentation of hepatic oxidative stress.     

Attenuation of kidney injuries maintains serum sulfatide levels dependent on hepatic synthetic ability: a possible involvement of oxidative stress

Serum sulfatides are the major glycosphingolipids in lipoproteins. Although serum sulfatides are mainly synthesized and secreted by the liver, they are significantly decreased when the kidneys are impaired. Our recent experimental study using a murine protein-overload nephropathy model suggested a hypothetical mechanism whereby serum sulfatides were reduced due to kidney dysfunction. This was the result of decreased hepatic expression of a sulfatide synthetic enzyme, cerebroside sulfotransferase (CST), which is associated with systemic enhancement of oxidative stress. However, there is a possibility that the experimental process, protein-overload itself, directly affected the sulfatide metabolism and oxidative stress in the liver. To determine whether kidney dysfunction actually reduces the hepatic synthesis of sulfatides via oxidative stress, we examined sulfatide levels, the hepatic content of metabolic sulfatide enzymes, and the degree of oxidative stress in protein-overload mice subjected to renoprotective therapy using clofibrate, a representative hypolipidemic medicine. Protein-overload mice exhibited marked kidney injuries, enhancement of hepatic oxidative stress, decreased levels of serum and hepatic sulfatides, and decreased expression of hepatic CST. The clofibrate treatment attenuated kidney damage and hepatic oxidative stress while maintaining serum/hepatic sulfatide levels and hepatic CST content in the mice. Because clofibrate monotherapy without protein-overload treatment only minimally affected these hepatic parameters, the hepatic synthesis of sulfatides appeared to be strongly influenced by kidney dysfunction and subsequent oxidative stress. This study suggests that the crosstalk between kidney dysfunction and hepatic sulfatide metabolism is mediated by oxidative stress. These results should help to understand the phenomenon in patients with end-stage kidney disease.