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Query: UMLS:C0012739 (disseminated intravascular coagulation)
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We report a case who was born with extremely low birth weight infant and had experienced abdominal operation for necrotizing enterocolitis, eventually developed ileus due to fatty acid calcium stones after giving human milk fortifier. He had developed necrotizing enterocolitis on day 30 of his age, such that we performed enterectomy and ileostomy. He could not tolerate enteral feeding fully, because intestinal fistula infection was repeated. Although we administered hindmilk, he grew up slowly and he suffered cholestasis as well. We performed end-to-end anastomosis to prevent fistula infections on day 87. After this operation, breast milk feeding volume was increased easily. However, we started to add HMF of half-strength on day 124, because his body weight gain remained very poor. And we confirmed to intensify the ratio of HMF full-strength on day 128. After that his abdomen had distended on day 131. As there is no effect of conservative therapy to occlusive ileus, we did emergency laparotomy on day 139. Intestinal calculi were impacted at anastomic portion. Although all stones were removed, he died on 144 days due to disseminated intravascular coagulation and renal failure. Calculi analysis revealed that all of them were fatty acid calcium stones. There is no report about like our case. We speculate that the construction of fatty acid calcium result from either high concentration of calcium/phosphorus or rapid increase in the fortification. We could have prevented this case happened by slower increment of fortification.
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PMID:Development of fatty acid calcium stone ileus after initiation of human milk fortifier. 2340 91

An adult male chinchilla (Chinchilla lanigera) presented with severe lethargy and tachypnea; the physical examination was otherwise unremarkable. Due to the animal's clinical condition, it was submitted for necropsy but died immediately prior to euthanasia. Clinicopathologic findings included leukocytosis with a left-shift neutrophilia and lymphopenia, azotemia, hyperphosphatemia, hyperglycemia, hyperlipemia, electrolyte imbalance, cholestasis, and hepatocellular damage. Neutrophilic enteritis with gramnegative bacterial colonization, hepatic lipidosis, interstitial pneumonia, suppurative tubulonephritis, erosive gastritis, cerebral edema, and lymphoid depletion were present microscopically. Attaching and effacing, eae-positive, Escherichia coli characterized by the presence of the intimin virulence factor was isolated from both the kidney and spleen. The cause of death was attributed to acute E. coli septicemia and subsequent disseminated intravascular coagulation.
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PMID:Enteric infection and subsequent septicemia due to attaching and effacing Escherichia coli in a Chinchilla. 2432 26

Acute pancreatitis is an inflammatory disease of the pancreas. The most common cause of acute pancreatitis is gallstone impacting the distal common bile-pancreatic duct (38%) and alcoholism (36%). There have been a few reports in the literature of acute pancreatitis associated with an obstructed urinary system. This case describes a 38-year-old male with acute pancreatitis occurring in the setting of hydronephrosis. A magnetic resonance cholangiopancreaticography (MRCP) showed right-sided severe hydronephrosis pushing the duodenum and head of pancreas anteriorly, thus obliterating distal segment of the common bile duct. There were also multiple right renal stones causing ureteral obstruction and hydronephrosis. Right nephrostomy was performed to release bile duct obstruction. However, sepsis and disseminated intravascular coagulation developed as a complication of acute pancreatitis, and the patient passed away. Although gallstone and alcoholism are the most common causes of acute pancreatitis, other causes should always be considered. Physicians should be aware of right hydronephrosis as one of the possible causes of acute pancreatitis in their workup of patients.
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PMID:Hydronephrosis as an unusual cause of acute pancreatitis. 2597 85

Liver diseases may be accompanied by profound changes in the hemostatic system including thrombocytopenia, decreased plasma levels of pro- and anticoagulants, and alterations in plasma levels of fibrinolysis. The net effect of the hemostatic changes in chronic and acute liver diseases is a hemostatic system that is in relative balance due to the simultaneous decline in pro- and antihemostatic drivers. A unique category of liver diseases are those induced by pregnancy. In acute fatty liver of pregnancy, profound hemostatic changes occur, which may be caused by a combination of liver failure and disseminated intravascular coagulation. Hemostatic changes in preeclampsia and HELLP syndrome are dominated by thrombocytopenia, although alterations in plasmatic coagulation may also occur. Post-partum bleeds, bleeding from cesarean section wounds, and hepatobiliary bleeds may occur in both patient groups. Patients with intrahepatic cholestasis of pregnancy do not show clinically relevant hemostatic alterations, despite biochemical evidence of liver injury.
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PMID:Hemostatic issues in pregnancy-induced liver disease. 2826 41


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