Ultrasound-guided cannulation of a large-bore catheter into the internal jugular vein was performed to provide temporary hemodialysis vascular access for uremia in a 65-yr-old woman with acute renal failure and sepsis superimposed on chronic renal failure. Despite the absence of any clinical evidence such as bleeding or hematoma during the procedure, a chest x-ray and computed tomographic angiogram of the neck showed that the catheter had inadvertently been inserted into the subclavian artery. Without immediately removing the catheter and applying manual external compression, the arterial misplacement of the hemodialysis catheter was successfully managed by open surgical repair. The present case suggests that attention needs to be paid to preventing iatrogenic arterial cannulation during central vein catheterization with a large-bore catheter and to the management of its potentially devastating complications, since central vein catheterization is frequently performed by nephrologists as a common clinical procedure to provide temporary hemodialysis vascular access.
Acidosis/complications ; Acute Disease ; Aged ; Catheterization, Central Venous/*adverse effects ; Female ; Hemorrhage/etiology ; Humans ; Kidney Failure, Chronic/*diagnosis ; Medical Errors/*prevention & control ; Oliguria/complications ; Renal Dialysis ; Sepsis/etiology ; Subclavian Artery/injuries/*radiography/surgery ; Tomography, X-Ray Computed ; Uremia/etiology

The objective of this study was to develop an experimental animal model of fulminant hepatic failure to test the efficacy of the bioartificial liver system. The portal vein and the hepatic artery were clamped intermittently and then the hepatic artery was ligated (ligation group, n=5). Pigs whose hepatic arteries were not ligated after clamping were assigned to the non-ligation group (n=5). The biochemical changes in blood, histologic alterations of the liver and neurologic examination for pigs were checked up. All animals died within 17 hr in the ligation group. On the other hand, all animals survived more than 7 days in the non-ligation group. In the ligation group, the levels of ammonia, lactic acid and creatinine showed a progressively increasing pattern. Prothrombin time was also prolonged gradually. Cytoplasmic condensation and nuclear pyknosis of hepatocytes were detected histologically at autopsy. Neurologic findings such as decreased pain sensation, tachypnea and no light reflex of pupils were observed. The findings shown in the ligation group are similar to the clinical features of fulminant hepatic failure in human and this animal model is reproducible. Therefore, this can be a suitable animal model to evaluate the efficacy of the bioartificial liver system for treating fulminant hepatic failure.
Acidosis/etiology/prevention & control ; Ammonia/blood ; Animals ; Aspartate Aminotransferases/blood ; Bilirubin/blood ; Blood Glucose/metabolism ; Blood Urea Nitrogen ; Comparative Study ; Creatinine/blood ; *Disease Models, Animal ; Female ; Hepatic Artery/surgery ; Lactic Acid/blood ; Ligation/adverse effects ; Liver Failure, Acute/blood/*pathology ; Portal Vein/surgery ; Potassium/blood ; Prothrombin Time ; Research Support, Non-U.S. Gov't ; Sodium Bicarbonate/pharmacology ; Swine

To investigate whether hypercapnic acidosis, induced by adding CO2 to inspired gas, would be protective effect against ventilator-induced lung injury (VILI), we ventilated 55 normal white rabbits for 6 hr or until PaO2/FIO2 <200 mmHg. Control group (n=15) was ventilated with peak inspiratory pressure (PIP) of 15 cm H2O, positive end-expiratory pressure (PEEP) of 3 cm H2O, an inspiration-to-expiration ratio of 1:2, and an inspired oxygen fraction (FIO2) of 0.40. High pressure hypercapnic group (HPHC; n=20) was ventilated with PIP of 30 cm H2O, PEEP of 0 cm H2O, and FIO2 of 0.40. Carbon dioxide was introduced into the inspiratory limb of the ventilator circuit, as necessary to maintain hypercapnia (PaCO2, 65 to 75 mmHg). High pressure normocapnic group (HPNC; n=20) was ventilated with same setting of HPHC, except normocapnia (PaCO2, 35 to 45 mmHg). Bronchoalveolar lavage fluid (BALF) lactate dehydrogenase, aspartate aminotransferase, interleukin-8 were significantly higher in high pressure ventilator group than control group (p<0.05). Wet weight to dry weight (WW/DW) and histologic scores were significantly higher in high pressure ventilator group than control group (p<0.05). However, there were no significant differences in oxygenation, BALF inflammatory markers, WW/DW and histologic scores between HPHC and HPNC groups. These findings suggest that hypercapnic acidosis at least induced by CO2 insufflation would not be protective effect against VILI in this model.
Acidosis, Respiratory/*chemically induced/complications/diagnosis/physiopathology ; Administration, Inhalation ; Animals ; Carbon Dioxide/*administration and dosage ; Hypercapnia/*chemically induced/complications/diagnosis/physiopathology ; Inhalation ; Pulmonary Gas Exchange ; Rabbits ; Research Support, Non-U.S. Gov't ; Respiration, Artificial/*adverse effects ; Respiratory Distress Syndrome, Adult/diagnosis/*etiology/physiopathology/*prevention and control ; Treatment Outcome