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Acute renal failure (ARF) associated with liver disease is a commonly encountered clinical problem of varied etiology and high mortality. We have prospectively analyzed patients with liver disease and ARF to determine the etiology, clinical spectrum, prognosis and factors affecting the outcome. Other than hepatorenal syndrome patients, out of 221 cases, 66 developed ARF secondary to various liver disease like cirrhosis (n = 29, mortality 8, risk factors-older age p < 0.01, grade III/IV encephalopathy p < 0.05), fulminant hepatic failure (n = 25, mortality 15, risk factor-prolonged prothrombin time p < 0.01), and obstructive jaundice (n = 12, mortality 7, risk factor-sepsis p < 0.01). In these three groups the factors leading to ARF were volume depletion (24), gastrointestinal bleed (28), sepsis (34), drugs (27) [aminoglycosides (9) and NSAID (18)] along with hyperbilirubinemia. Various types of ARF with contemporaneous liver injury were malaria (n = 37, mortality 15, risk factors-higher bilirubin p < 0.001, higher creatinine p < 0.05, anuria p < 0.05 and dialysis dependency p < 0.05), sepsis (n = 36, mortality 22, risk factors-age p < 0.001, higher bilirubin p < 0.01, oliguria p < 0.05), hypovolemia with ischemic hepatic injury (n = 14, mortality 5, risk factors-higher creatinine p < 0.05 and SGPT p < 0.01), acute pancreatitis (n = 12, mortality 4, risk factors-higher bilirubin p < 0.001, higher SGPT p < 0.01, dialysis dependency p < 0.05), rifampicin toxicity (n = 10, no mortality), paroxysmal nocturnal hemoglobinuria (n = 3, no mortality), CuSO4 poisoning (n = 3 mortality 2), post abortal (n = 11, mortality 6, risk factors higher creatinine p < 0.05 and SGPT p < 0.01), ARF following delivery including HELLP syndrome (n = 12, mortality 4, risk factors-higher bilirubin p < 0.01 and SGPT p < 0.01), and of uncertain etiology (n= 14 mortality 4). 133 patients (60.2%), required hemodialysis hemodialfiltration or peritoneal dialysis. ARF associated with liver disease is having high mortality (42.5%). Avoidance of dehydration, hypotension, nephrotoxic drugs and sepsis, with promote dialytic support are necessary to reduce mortality and morbidity.
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PMID:Acute renal failure associated with liver disease in India: etiology and outcome. 1104 Dec 94

Changes in cell hydration are critically important for the signalling towards metabolic responses to hormones, substrates and reactive oxygen intermediates. In liver insulin-induced cell swelling is due to a net K(+)-uptake resulting from the concerted activation of Na(+)/K(+)/2Cl(-) cotransport, Na(+)/H(+) exchange and the Na(+)/K(+)-ATPase. Insulin-induced swelling is essential for generating the antiproteolytic response to the hormone, which depends on activation of the MAP-kinase p38. Recent investigations show, that cell swelling induced by either hypoosmolarity or insulin triggers the activation of signalling cascades. Cell swelling by insulin is Ptdins-3-kinase mediated and contributes to the activation of Erk- and p38-type MAP-kinases. Conditions dehydrating insulin target tissues such as hyperosmolarity or amino acid deprivation are frequently associated with insulin resistance. In liver, hyperosmolarity impairs the Ptdins-3-kinase-dependent K(+) uptake and cell swelling in response to insulin, leading to resistance of MAP-kinases and proteolysis to regulation by insulin. Likewise, a reduction of insulin-induced swelling by the loop diuretics furosemide and bumetanide cause insulin resistance shown by the levels of cell swelling, MAP-kinase activation and proteolysis control. Blockage of the cell volume response to insulin may be the common denominator in dehydration-induced insulin resistance found in clinical settings such as sepsis, burn injury and diabetes mellitus.
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PMID:Cell hydration and insulin signalling. 1112 22

Cholelithiasis in neonates and infants has been rarely reported. With the current widespread use of diagnostic ultrasonography, more neonates may be found with gallstones and common bile duct stones. We describe a case of asymptomatic gallstones detected incidentally at the age of four days who presented with early onset of neonatal sepsis and dehydration.
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PMID:Asymptomatic neonatal cholelithiasis. 1123 45

Fluid imbalance can arise due to hypovolemia, normovolemia with maldistribution of fluid, and hypervolemia. Trauma is among the most frequent causes of hypovolemia, with its often profuse attendant blood loss. Another common cause is dehydration, which primarily entails loss of plasma rather than whole blood. The consequences of hypovolemia include reduction in circulating blood volume, lower venous return and, in profound cases, arterial hypotension. Myocardial failure may result from increased myocardial oxygen demand in conjunction with reduced tissue perfusion. Finally, anaerobic metabolism due to reduced perfusion may produce acidosis and, together with myocardial dysfunction, precipitate multi-organ failure. The splanchnic organs are particularly susceptible to the deleterious effects of hypotension and hypovolemic shock, and these effects, depending upon their duration and severity, may be irreversible despite restoration of normovolemia by fluid administration. Patient monitoring in the intensive care unit typically relies upon central venous pressure devices, whereas the primary focus in the operating theater is blood volume deficit estimated from suction devices. However, estimates of intraoperative blood loss can be inaccurate, potentially leading to inappropriate fluid management. Normovolemia with maldistribution of fluid can be encountered in shock-specific microcirculatory disorders secondary to hypovolemia, as well as pain and stress. Consequent vasoconstriction and reduced tissue driving pressure, as well as leukocyte and platelet adhesion, and liberation of humoral and cellular mediators, may impair or abolish blood flow in certain areas. The localized perfusion deficit may contribute to multi-organ failure. Choice of resuscitation fluid may be important in this context, since some evidence suggests that at least certain colloids might be helpful in diminishing post-ischemic microvascular leukocyte adherence. Excessive volume administration may lead to fluid overload and associated impairment of pulmonary function. However, entry of fluid into the lungs may also be facilitated by increased vascular permeability in certain pathologic conditions, especially sepsis and endotoxemia, even in the absence of substantially rising hydrostatic pressure. Another condition associated with elevated vascular permeability is systemic capillary leak syndrome. The chief goal of fluid management, based upon current understanding of the pathophysiology of fluid imbalance, should be to ensure adequate oxygen delivery by optimizing blood oxygenation, perfusion pressure, and circulating volume.
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PMID:Pathophysiology of fluid imbalance. 1125 92

Because of several factors, including a change in the hormonal behavior, the postoperative period is at high risk for the diabetic patient to present a metabolic complication. On the other hand, a diabetic metabolic disorder may be secondary and reveal a severe underlying complication (sepsis...). Ketoacidosis is the consequence of an absolute or relative lack of insulin and occurs mainly in insulin dependent diabetic patients. Its incidence should be very low during the postoperative period since insulin protocols are systematically used. The main clinical and biological signs are a polypnea, signs of dehydration, an hyperglycemia associated with a high anion gap metabolic acidosis and the presence of ketoacids in the urine. Its treatment is mainly based on an active rehydration and an insulin and potassium supply. Sodium bicarbonate should not be used systematically any more, even during severe acidosis. Hyperosmolar non ketotic states affects insulin nondependent and older diabetic patients for the most part and occurs under similar conditions than ketoacidosis, revealing most of the time a severe underlying complication. Clinical and biological manifestations include a severe dehydration, alterations in consciousness and a major hyperglycemia associated to a moderate or mild metabolic acidosis. Its main treatment is an active rehydration and insulin plus potassium in a second time. Hypoglycemia is usually the consequence of a mistake in the diabetes care and in the insulin management. Every sickness or consciousness disorder occurring in a diabetic patient treated with insulin should lead to perform a blood glucose measurement. In case of severe manifestations, glucose should be administered in emergency, orally if the patient is conscious or intravenously if he is not. Lactic acidosis occurring during the postoperative period in a diabetic patient is usually non specific of diabetic disease and reflects the existence of an underlying complication (sepsis, hemorrhage, hypoxia,...), as it would in an non diabetic patient. Lactic acidosis due to a treatment with metformin is now very rare and occurs almost only in patients having a contraindication to the use of metformin.
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PMID:Acute postoperative metabolic complications of diabetes. 1137 21

The importance of an acute encephalopathy associated with nontyphoidal salmonellosis has recently been recognized, but the disease entity has been poorly established. In this study, we describe two encephalopathic patients associated with nontyphoidal salmonellosis. The patients exhibited a rapid evolution of coma after the onset of lethargy or seizure. Fever and diarrhea due to salmonellosis preceded these events. Secondary factors inducing encephalopathies, such as severe dehydration, sepsis, meningitis, electrolyte or metabolic disturbances, acute renal failure, and multiple organ failure, were excluded in the differential diagnosis at the onset of encephalopathic features. These clinical findings and rapid development of encephalopathic features from localized intestinal infection without any significant abnormalities in a variety of blood tests may suggest a toxic etiology. However, endotoxin was not found in serum from both patients. From these results, we conclude that nontyphoidal salmonellosis can cause a toxic encephalopathy syndrome, like shigellosis or verocytotoxin-producing Escherichia coli infection.
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PMID:Acute encephalopathy associated with nontyphoidal salmonellosis. 1145 56

Significantly reduced morbidity and mortality is needed before intestinal transplantation will be applicable in most patients with intestinal failure who are on long-term total parenteral nutrition (TPN). However, transplantation does play a role if TPN fails, with failure defined by Medicare as liver failure, frequent line sepsis, major central vein thrombosis, or recurrent dehydration. Of these complications, the relationship between liver failure and subsequent death in high-risk subgroups of long-term TPN patients has been shown clearly. Patients with less than 100 cm of postduodenal small bowel, an end-jejunostomy, no ileocecal valve or cecum, or persistently elevated liver function levels are at high risk for end-stage liver disease (ESLD). Early referral to experienced centers is suggested in these circumstances. High-risk patients may also take part in clinical trials of promising therapies to increase intestinal adaptation and prevent liver failure. Living donors should be considered for transplant candidates to minimize waiting time and optimize HLA matching. ESLD patients need a liver-intestine transplant. Because their waiting-list mortality is very high, their status on the liver waiting list should be elevated if possible. High incidence of early death from sepsis is reported after intestinal transplant, even at experienced centers. Aggressive measures should be taken if uncontrolled sepsis occurs, including discontinuing immunosuppression and removing the graft. Further research is needed in intestinal immunology and in development of strategies to decrease the need for aggressive immunosuppression in these transplant recipients. The ultimate role of intestinal transplantation will be determined by its capacity to show superiority, both in effectiveness and safety, to long-term TPN.
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PMID:The role of intestinal transplantation in the management of intestinal failure. 1147 3

Thrombotic disease is rare in neonates. The main risk factors at this age are perinatal asphyxia, maternal diabetes, sepsis, polycythemia, dehydration, a low cardiac output, and in primis the catheterization of central lines. Another important risk factor is inherited thrombophilia. Arterial thrombosis is even more rare than venous thrombosis and less related to most of the risk factors listed above; it occurs more frequently in the iliac, femoral, and cerebral arteries but very rarely in the aorta. Most of the described cases of aortic thrombosis are associated with the catheterization of an umbilical artery and involve the descending tract and the renal arteries; very few relate to the ascending tract and the aortic arch. The possible role of virus-induced primary vascular endothelium damage in the etiopathogenesis of neonatal arterial thrombosis has been previously hypothesized. Herpesviruses, particularly human cytomegalovirus (HCMV), can infect endothelial cells and directly damage intact vascular endothelium, altering its thromboresistant surface as a result of procoagulant activity mediated by specific viral surface phospholipids, necessary for the coagulation enzyme complex assembly that leads to thrombin generation. We describe a case of congenital aortic arch thrombosis. The clinical, laboratory, and virologic pictures; the anatomopathologic findings (fully compatible with viral infection); the detection of HCMV in various tissues (including the aorta); and the absence of other causes of aortic thrombosis make it possible to attribute the case to a severe congenital HCMV infection with multiple organ involvement, after the primary infection of the mother. The hemostatic system disorders and hemodynamic disturbances related to viral cardiac damage explain the clinical features of the case and indicate that congenital HCMV infection should be included among the causes of neonatal aortic thrombosis.
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PMID:Neonatal aortic arch thrombosis as a result of congenital cytomegalovirus infection. 1173 41

Stones or calculi in the urinary tract affect up to 12% of men and 5% of women by the age of 70 years, with more than a third of individuals having a strong family history (Unwin, 1996). Complications include obstruction in the urinary tract, pain, nausea, vomiting and sepsis. Common causes are: urine stasis, infection, presence of foreign bodies, dehydration, diet and periods of immobility. Encouraging initial diuresis could exacerbate rather than relieve symptoms. Discharge advice is a key feature of preventing recurrence once the predisposing factors have been identified. The relationship between patient and nurse is an invaluable and ideal opportunity for nurses to educate patients in appropriately changing dietary habit and in maintaining a urine output of greater than 2 litres per day.
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PMID:Urinary tract stones: cause, complications and treatment. 1183 27

Stones or calculi in the urinary tract affect up to 12% of men and 5% of women by the age of 70 years, with more than a third of individuals having a strong family history (Unwin, 1996). Complications include obstruction in the urinary tract, pain, nausea, vomiting and sepsis. Common causes are: urine stasis, infection, presence of foreign bodies, dehydration, diet and periods of immobility. Encouraging initial diuresis could exacerbate rather than relieve symptoms. Discharge advice is a key feature of preventing recurrence once the predisposing factors have been identified. The relationship between patient and nurse is an invaluable and ideal opportunity for nurses to educate patients in appropriately changing dietary habit and in maintaining a urine output of greater than 2 litres per day.
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PMID:Urinary tract stones: causes, complications and treatment. 1184 60


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