Burns acute renal failure

Adverse effects are flatulence, diarrhoea, constipation, nausea, abdominal pain, cramps, heart burn and dysgeusia. Rarely myopathy, rhabdomyolysis with acute renal failure may also occur. 

Renal Effects. Evidence of renal damage was observed in individuals burned once with white phosphorus. Increased blood urea nitrogen (Summerlin et al. 1967), increased urinary levels of protein and urea nitrogen (Walker et al. 1947), and signs of acute renal failure (Songetal. 1985) have been observed. No longer term human studies were identified. Some of the blood/serum chemical changes are also found in thermal bum patients and cannot necessarily be ascribed to white phosphorus toxicity. However, controlled animal studies (discussed below) have shown similar effects that have been attributed to white phosphorus. 

Burne MJ, Daniels F, El Ghandour A, Mauiyyedi S, Colvin RB, O Donnell MP, Rabb FI Identification of the CD4(-i-)T cell as a major pathogenic factor in ischemic acute renal failure. J Clin.Invest 108 1283-1290, 2001... 

H NMR spectroscopy has also been used, in conjunction with standard clinical biochemical analyses, to monitor renal function in an unusual case of phenol poisoning." A 41-year-old man fell into a shallow vat containing 40% phenol in dichloromethane, at his place of work. He did not ingest any solvent and was partially immersed for only a few seconds. However, he was found collapsed and badly burned in the nearby shower unit. Subsequently, his plasma creatinine levels began to rise, and he did not pass urine. This acute renal failure was treated by haemodialysis and the i.v. administration... 

Patients at risk for SRMB include those with respiratory failure (need for mechanical ventilation for >48 hours), coagulopathy, hypotension, sepsis, hepatic failure, acute renal failure, multiple trauma, severe burns (>35% of body surface area), head injury, traumatic spinal cord injury, major surgery, or history of GI bleeding. " ""... 

Leonard MO, Hannan K, Burne MJ, Lappin DW, Doran P, Coleman P, Stenson C, Taylor CT, Daniels F, Godson C, Petasis NA, Rabb H, Brady HR 15-Epi-16-(para-fluorophenoxy)-lipoxin A4-methyl ester, a synthetic analogue of 15-epi-lipoxin A4, is protective in experimental ischemic acute renal failure. J Am Soc Nephrol 2002 13 1657-1662. 

Bedford PD (1951) Idiosyncrasy to aureomycin. Br Med J 2 1428-1429 Beirne GJ, Hansing CE, Octaviano GN, Burns RO (1967) Acute renal failure caused by hypersensitivity to polymyxin B sulfate. JAMA 202 62-64 Bennett AH (1965) Antibiotic allergies. JAMA 194 569... 

The previous studies carried out in this area have, by and large, not been concerned with the therapy of renal failure in children. The dietary requirements in adults, in whom growth is not essential, may be easy to satisfy, on the basis of such an L-essential amino acid mixture. Whether this applies to children in chronic renal failure is another matter. However, in children with acute renal failure, the process is often a rather self limited one, since with the exception of cardiac surgery, burns and severe trauma, pediatric age group patients with acute renal failure are rare. Our studies have not to date considered other lesions such as glomerulonephritis or nephrotic syndrome but there is every reason to believe that similar benefits might apply to those patients as well. 

Two workers collapsed while inside a tank that was later found to contain a 0.1-0.3% EDB solution. Removed after 20-45 minutes in the tank, one man was intermittently comatose, and the other was delirious and combative. Both experienced vomiting, diarrhea, abdominal pain, and burning of the eyes and throat. Metabolic acidosis and acute renal and hepatic failure ensured. Death occurred 12 and 64 hours later, respectively, despite supportive measures. 

C. Acute ingestion may cause gastrointestinal burns, severe vomiting and abdominal pain, and diarrhea with smoking stools. Systemic effects include headache, delirium, shock, seizures, coma, and arrhythmias (atrial fibrillation, QT prolongation, ventricular tachycardia, and fibrillation). Metabolic derangements, including hypocalcemia and hyperphosphatemia (or hypophosphatemia), may occur. Fulminant hepatic or renal failure may occur after 2-3 days. 

Trauma (and other causes of acute blood loss), C third-spacmg of fluid (e.g., burns, pancreatitis, peritonitis), vomiting, diarrhea, diuretics, renal or adrenal (i.e., sodium wasting) disease v Heart failure, hepatic cirrhosis, nephrotic syndrome, iatrogenic (intravenous fluid overload) ... 

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