Hemodialysis acute

Medicine hemodialysis, acute renal failure treatment and drug detoxification. 

The nurse monitors the patient for signs and symptoms of acute salicylate toxicity or salicylism (see Display 17-1). Initial treatment includes induction of emesis or gastric lavage to remove any unabsorbed drug from the stomach. Activated charcoal diminishes salicylate absorption if given within 2 hours of ingestion. Further therapy is supportive (reduce hyperthermia and treat severe convulsions with diazepam). Hemodialysis is effective in removing Hie salicylate but is used only in patients with severe salicylism. 

If present and clinically feasible, treat acute severe hyperphosphatemia before calcium administration (i.e., with hemodialysis in acute tumor lysis syndrome)... 

Osmotic diuretics such as mannitol act on the proximal tubule and, in particular, the descending limb of the Loop of Henle — portions of the tubule permeable to water. These drugs are freely filtered at the glomerulus, but not reabsorbed therefore, the drug remains in the tubular filtrate, increasing the osmolarity of this fluid. This increase in osmolarity keeps the water within the tubule, causing water diuresis. Because they primarily affect water and not sodium, the net effect is a reduction in total body water content more than cation content. Osmotic diuretics are poorly absorbed and must be administered intravenously. These drugs may be used to treat patients in acute renal failure and with dialysis disequilibrium syndrome. The latter disorder is caused by the excessively rapid removal of solutes from the extracellular fluid by hemodialysis. 

Parathyroid hormone (PTH) produces CNS effects in normal subjects and neuropsychiatric symptoms are frequently encountered in patients with primary hyperparathyroidism, where EEG changes resemble those described in acute renal failure. Circulating PTH is not removed by hemodialysis. In uremic patients both EEG changes and neuropsychiatric symptoms are improved by either parathyroidectomy or medical suppression of PTH. The mechanism whereby PTH causes disturbances of CNS function is not well understood, but it has been suggested that increased PTH might facilitate the entry of Ca2+ into the cell resulting in cell death. 

Dialysis, including hemodialysis and peritoneal dialysis, relieves acute toxicity during fulminant hyperammonemia. Exchange transfusions also have been performed, but this technique has not been equally useful in removing ammonia. 

If lithium toxicity is suspected, the patient should discontinue lithium and go immediately to the emergency room. Hemodialysis is generally required when serum lithium levels are above 4 mEq/L for patients on long-term treatment, or greater than 6 to 8 mEq/L after acute poisoning. 

Kidney Failure The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH]... 

Renal Effects. The patient described by Letz et al. (1984) (see Section 2.2.3.1) who lived for 64 hours after exposure to toxic levels of 1,2-dibromoethane had acute renal failure as evidenced by severe oliguria 24 hours after exposure and abnormal clinical chemistry values (blood urea nitrogen, creatinine, and serum uric acid). Severe metabolic acidosis was present despite two hemodialysis procedures. 

In hemodialysis patients or in case of acute renal failure (Ccr less than 15 mL/min or serum creatinine more than 6 mg/dL), avoid or stop infusion of lepirudin. Consider additional IV bolus doses of 0.1 mg/kg every other day only if the aPTT ratio falls below the lower therapeutic limit of 1.5. ... 

Unlabeled Uses Cardiopulmonary bypass surgery hemodialysis pulmonary hypertension associated with acute respiratory distress syndrome, systemic lupus erythematosus, or congenital heart disease refractory CHF severe community-acquired pneumonia... 

In addition to intensive supportive care, prompt chelation with oral or intravenous unithiol, intramuscular dimercaprol, or oral succimer may be of value in diminishing nephrotoxicity after acute exposure to inorganic mercury salts. Vigorous hydration may help to maintain urine output, but if acute renal failure ensues, days to weeks of hemodialysis or hemodiafiltration in conjunction with chelation may be necessary. Because the efficacy of chelation declines with time since exposure, treatment should not be delayed until the onset of oliguria or other major systemic effects. 

Salicylism and death have occurred following topical application. In an adult, 1 g of a topically applied 6% salicylic acid preparation will raise the serum salicylate level not more than 0.5 mg/dL of plasma the threshold for toxicity is 30-50 mg/dL. Higher serum levels are possible in children, who are therefore at a greater risk for salicylism. In cases of severe intoxication, hemodialysis is the treatment of choice (see Chapter 58). It is advisable to limit both the total amount of salicylic acid applied and the frequency of application. Urticarial, anaphylactic, and erythema multiforme reactions may occur in patients who are allergic to salicylates. Topical use may be associated with local irritation, acute inflammation, and even ulceration with the use of high concentrations of salicylic acid. Particular care must be exercised when using the drug on the extremities of patients with diabetes or peripheral vascular disease. 

If the patient presents with acute burning pain, the examination of choice is erythrocytic protoporphyrins. If the free protoporphyrin is significantly elevated (more than 6 pmol/1), the diagnosis of erythropoietic protoporphyria is established. Plasma porphyrins are used in patients on chronic hemodialysis who suffer from skin blisters to differentiate between PCT and pseudoporphyria the latter does not show increased plasma porphyrins. 

Hemodialysis decreases plasma concentrations 60% in a 6-hour period. Acute Treatment of Herpes Zoster 800 mg every 4 hours orally, 5 times daily for 7 to 10 days... 

A 60-year-old woman took dexamethasone 4 mg 8-hourly for dyspnea due to a precursor T lymphoblastic lymphoma-leukemia with bilateral pleural effusions and a large mass in the anterior mediastinum (130). She developed acute renal insufficiency and laboratory evidence of the metabolic effects of massive cytolysis. She received vigorous hydration, a diuretic, allopuri-nol, and hemodialysis. She recovered within 2 weeks and then underwent six courses of CHOP chemotherapy. The mediastinal mass regressed completely. She remained asymptomatic until she developed full-blown acute lymphoblastic leukemia, which was resistant to treatment. 

A patient who deliberately took potassium iodide solution 50 ml and a small dose of mefenamic acid (six capsules) as part of a suicide attempt developed acute renal insufficiency necessitating hemodialysis (72). Normal renal function returned after 10 days of hemodialysis. 

A 61-year-old woman developed a bradydysrhythmia after a cardiac arrest (57). Her lactate concentration was 18 mmol/1, pH 6.60, blood glucose 19 mmol/1, and creatinine 1136 pmol/1. She had a 5-year history of type 2 diabetes treated with glimepiride 3 mg/day and metformin 850 mg tds, and 4 months before admission had had a serum creatinine concentration of 1.1 mg/dl. In the few days before admission she had had abdominal pain, nausea, and a speech disorder. She was treated with hemodialysis, and 6 weeks later the creatinine was 0.54 mg/dl. Further information about events leading to the acute renal insufficiency was not given, but a diagnosis of metformin-associated lactic acidosis was made. 

Five patients with metformin-associated severe lactic acidosis, seen between 1 September 1998 and 31 May 2001, have been reported (58). Two had attempted suicide. All had severe metabolic acidosis with a high anion gap and raised blood lactate concentrations. Four developed profound hypotension and three had acute respiratory failure. Three had normal preceding renal function. Three required conventional hemodialysis and two continuous renal replacement therapy. 

Treatment of acute arsenic poisoning includes removal from the exposure source, supportive measures for loss of fluids, and chelation therapy (Ibrahim et al., 2006). Chelators that can be used include dimercaprol or 2,3-dimercaptosuccinic acid. In cases of renal failure, hemodialysis should be considered. 

Acute poisoning is treated with gastric aspiration and lavage combined with intensive supportive therapy, including thorough assessment of the patient plus measures to prevent respiratory failure. In cases of very severe poisoning, peritoneal dialysis or hemodialysis may be necessary. 

Kolf s early devices were used for patients who had suffered acute kidney failure as a result of trauma or poisoning and needed dialysis only a few times. Such emergency treatment was the main application of hemodialysis until the early 1960s, because patients suffering from chronic kidney disease require dialysis two to three times per week for several years, which was not practical with these early devices. However, application of hemodialysis to this class of patient was made possible by improvements in the dialyzer design in the 1960s. The development of a plastic shunt that could be permanently fitted to the patient to allow easy access to their blood supply was also important. This shunt, developed by Scribner et al. [6], allowed dialysis without the need for surgery to connect the patient s blood vessels to the dialysis machine for each treatment. 

Bismuth compounds are used as an antidiarrheal. Topical applications are used in skin disorders. Overdose may cause acute bismuth intoxication but gastric lavage, purgation, use of chelating agents, 2,3-dimercapto-l-propane sulfonic acid, and hemodialysis are steps to be taken.170-172... 

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