Prophylaxis Of Acute Renal Failure Research Articles

Upper limb replantation: Surgical strategy and the prophylaxis of acute renal failure due to ischemia reperfusion injury – A report of two cases

Introduction. The arm replantation is an extremely rare and challenging procedure. The recognized risk is myoglobinuria and, consenquently, ischemia reperfusion-induced renal failure. Case report. We presented two patients aged 24 and 46 years who were admitted after traumatic arm amputation. Ischemia time was six and two hours, respectively. Postoperative intensive care treatment with assisted ventilation, sedation, and obtaining sufficient urine output prevented myoglobin-induced renal injury. In the case where ischemia time was shorter, there was only one delayed reconstruction of skin defects after fasciotomy, but in the case where ischemia lasted longer, the patient had two secondary look procedures with acceptable definitive results. Conclusion. Arm replantation is a safe procedure even in cases with longer ischemia time. Postoperative control of urine output, correction of acidosis, and preventing myoglobin-induced tubular injury are crucial for stable postoperative recovery and.

Fluid Therapy in Pediatric Victims of the 2003 Bam, Iran Earthquake

On 26 December 2003, at 05:26 hours, an earthquake of magnitude 6.6 (Richter scale) caused a disaster in the Bam region of Southeastern Iran, which had a population of approximately 102,000. In this study, the clinical and laboratory features and therapeutic interventions in pediatric (three months to 14 years) crush victims were analyzed. Determination of the type and amount of fluid therapy for prevention of acute renal failure (ARF) was the main aim of this study. The clinical and laboratory data and therapeutic interventions provided to 31 pediatric crush victims were collected. Early and vigorous fluid resuscitation was immediately performed. Resuscitation of the children from hypovolemic shock was initiated by interavenous (IV) administration of normal saline until the signs and symptoms of shock disappeared. For victims with crush injuries, an alkaline intravenous solution, up to 3 to 5 times more than maintenance doses was provided. In this study, there were two groups with decreasing severity of injury: (1) crush injury (CI), with or without ARF; and (2) non-crush injury (Non-CI). According to the above mentioned classification, there were 15 and 16 patients in group I and II, respectively. The mean time spent under the rubble was 2.2 +/-2.5 hours and 0.5 +/-0.5 hours in Groups I and II, respectively. Seventy-five percent of ARF patients (n = 8), were admitted to the hospital the day of the earthquake (Day 0) and the day after earthquake (Day 1). In non-ARF patients (n = 7), 85.7% of the victims were admitted on Day 0 and Day 1. In Group II (ARF and non-ARF), all patients were admitted within three days after the earthquake. Although ARF did not develop in any of the children without CI, it was observed in eight of 15 patients with CI. There was no significant difference between CI with ARF (n = 8) and CI without ARF (n = 7) patients, in terms of the admission date, time of admission, hospitalization duration, and time under the rubble (TUR). Admission SGOTs were significantly different between these two groups. The ratio of the amount of delivered IV fluid (DL) to expected (EX) was based on weight of children was the only fluid therapy parameter in which there was a statistically significant difference between ARF and non-ARF groups. It was 3.6 +/-0.99 in ARF and 4.8 +/-0.74 in Non-ARF group (p = 0.01). Early intravenous volume replacement may prevent both ARF and dialysis need that may develop on the basis of rhabdomyolysis. In adults, six liters or 12-14 liters of fluids for prophylaxis of ARF in crush syndrome, were suggested. In children, it seems that DL/EX ratio (delivered to expected ratio) is the best marker for evolution of IV fluid therapy in pediatric patients. In children with crush injuries, DL/EX ratio of >4.8 was sufficient for the prevention of ARF.

Continuous Low-Dose Human Atrial Natriuretic Peptide Promotes Diuresis in Oliguric Patients After Living Donor Liver Transplantation

Human atrial natriuretic peptide (ANP) is beneficial for the prophylaxis of acute renal failure (ARF) after liver transplantation (OLT). We evaluated renal function in OLT patients with or without ARF, describing cases unresponsive to loop diuretics successfully treated with continuous low-dose ANP infusion without hemodialysis. Twenty-seven consecutive adult-to-adult living donor liver transplantations (LDLTs) were performed in 26 patients. One case was excluded due to the need for continuous hemodialysis (HD) during the operation. Of the 26 cases, 6 (23%, group 2) developed ARF in the first 30 days after LDLT; the other 20 were ARF-free (group 1). The median follow-up was 24 months. No patient required either continuous or intermittent HD. Only one patient died due to multiple liver abscesses. Mean preoperative serum creatinine (sCr) value and intraoperative blood loss in group 2 were significantly higher than those in group 1. Three cases in group 2 failed to improve on high-dose loop diuretics with low-dose dopamine, exhibiting fluid overload. The remaining three cases in group 2 responded to conventional diuretic treatments. Continuous low-dose ANP was started 2, 4, or 5 days after LDLT, and urine output significantly increased after ANP administration. The serum creatinine values were 1.1, 1.2, and 1.1 at 1 month and 1.0, 0.9, and 0.6 mg/dL at 6 months after LDLT. Massive blood loss during the operation caused ARF, but did not affect renal function after LDLT. Continuous low-dose ANP improved renal function and diuresis for oliguric ARF patients, preventing the need for HD or continuous venovenous hemodialysis.

Survival of near fatal rhabdomyolysis following flame burn in a 25-year-old patient

Skin protects the interior of the body from bacterial invasion and is a vital barrier involved in fluid homeostasis. Subcutaneous muscle accounts for approximately 40% of total body mass [1]. Extensive damage such as that associated with flame burn can cause necrosis of vital tissues including the full thickness of skin, subcutaneous fat, muscle, blood vessels, nerves, and bone. Skin necrosis results in loss of the barrier that protects against infection and helps preserve internal fluids. Muscle damage with dissolution of skeletal muscle fiber, rhabdomyolysis, results in release of potentially toxic intracellular components into the systemic circulation [1]. The standard guidelines for early management of shock and prophylaxis of acute renal failure due to rhabdomyolysis have been described [2]. However, most cases of flame burn with rhabdomyolysis have a poor prognosis [3]. The renal complications of rhabdomyolysis occur as the progressive development of hypovolemia, hemoglobinuria, myoglobinuria, oliguria, and eventually, acute renal failure [1,2,4]. The etiology of adult respiratory distress syndrome (ARDS) in burn patients is multifactorial, with evidence suggesting that inhalation injury is a major cause [5]. Most patients with severe burns die due to multiple organ failure and respiratory failure [6]. Preventing the systemic and renal complications of rhabdomyolysis requires very early and vigorous treatment to sustain circulation; preferably, such therapy is started at the site of the catastrophe [1,2,4]. We present the case of a 25-year-old patient who developed fatal rhabdomyolysis

Prophylaxis of Acute Renal Failure in Patients with Rhabdomyolysis

Patients that develop rhabdomyolysis of different causes are at high risk of acute renal failure. Efforts to minimize this risk include volume repletion, treatment with mannitol, and urinary alkalinization as soon as possible after muscle injury. This is a retrospective analysis (from January 1, 1992, to December 31, 1995) of therapeutic response to prophylactic treatment in patients with rhabdomyolysis admitted to an intensive care unit (ICU). The diagnosis of rhabdomyolysis was based on creatinine kinase (CK) level (>500 Ul/L) and the criteria for prophylaxis were: time elapsed between muscle injury to ICU admission < 48 h and serum creatinine < 3 mg/dL. Fifteen patients were treated with the association of saline, mannitol, and sodium bicarbonate (S+M+B group) and 9 patients received only saline (S group). Serum creatinine at admission was similar in both groups: 1.6 ± 0.6 mg/dL in the S+M+B group and 1.5 ± 0.6 mg/dL in the S group (p > 0.05). Maximum serum CK measured was 3351 ± 1693 μ/L in the S+M+B group and 1747 ± 2345 IU/L in the S group (p < 0.05). However the measurement of CK was earlier in S+M+B patients (1.7 vs 2.7 days after rhabdomyolysis). APACHE II scores were 16.9 ± 7.4 and 13.4 ± 4.9 in the S+M+MB and S groups, respectively (p > 0.05). Despite the treatment protocol the serum levels of creatinine had similar behavior and reached normal levels in all patients in 2 or 3 days. The saline infusion during the first 60 h on the ICU was 206 mL/h in the S group and 204 mL/h in S+M+B (p > 0.05). Mannitol dose was 56 g/day, and bicarbonate 225 mEq/day during 4.7 days. Our data show that progression to established renal failure can be totally avoided with prophylactic treatment, and that once appropriate saline expansion is provided, the association of mannitol and bicarbonate seems to be unnecessary.

Prophylaxis of Acute Renal Failure in Traumatic Rhabdomyolysis

Prophylaxis of Acute Renal Failure in Traumatic Rhabdomyolysis

Early Management of Shock and Prophylaxis of Acute Renal Failure in Traumatic Rhabdomyolysis

SEISMIC catastrophes leave in their wake survivors trapped under the rubble who suffer from extensive muscle damage and its devastating sequelae of hemodynamic and metabolic disturbances and acute renal failure.1 We review here the pathogenesis of shock and acute renal failure associated with traumatic rhabdomyolysis and suggest guidelines for the early management of shock and the prophylaxis of acute renal failure due to the crush syndrome. Rhabdomyolysis, myoglobinuria, and renal failure have been known to follow massive crush injury.2 3 4 5 6 Indeed, it is now 50 years after the classic description of the crush syndrome in patients injured during the bombing of . . .