Dialysis hyperkalemia

Hyperkalemia is more common in patients with Stage 5 CKD therefore the discussion of treatment options focuses on interventions in this population. The majority of patients can be managed with a dietary potassium restriction of 50 to 80 mEq/day and alterations in dialysate potassium concentrations for patients receiving hemodialysis or peritoneal dialysis. Hyperkalemia is less common, however, in the peritoneal dialysis population due to differences in potassium transport. Constipation in patients with CKD can interfere with colonic potassium excretion therefore a good bowel regimen is important. For severe hyperkalemia hemodialysis is often required using a low-potassium dialysate bath (see Chap. 50). 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Initiation of dialysis is dependent on the patient s clinical status. Symptoms that may indicate the need for dialysis include persistent anorexia, nausea, vomiting, fatigue, and pruritus. Other criteria that indicate the need for dialysis include declining nutritional status, declining serum albumin levels, uncontrolled hypertension, and volume overload, which may manifest as chronic heart failure, and electrolyte abnormalities, particularly hyperkalemia. Blood urea nitrogen (BUN) and serum creatinine (SCr) levels may be used as a... 

Hyperkalemia Restrict dietary intake dialysis May be exacerbated by CSA or TAC or ACEIs, acidosis, or Rl fludrocortisone acetate 0.1 mg orally every day twice daily for refractory hyperkalemia... 

Treatment of hyperkalemia depends on the desired rapidity and degree of lowering (Fig. 78-4, Table 78-6). Dialysis is the most rapid way to lower serum potassium concentration. 

This should be initiated once oliguric ATN has been established - and performed on an intermittent basis. Mental status abnormalities, pericarditis, gastrointestinal and hemorrhagic disorders are indications for dialysis other indications are fluid overload and hyperkalemia. Non-oliguric patients in general do not require as many dialyses as do patients with oliguria generally because hyperkalemia is not a problem. 

Hyperkalemia occurs occasionally in patients with chronic renal failure, usually in those who do not conform fo medication regimen, dietary guidelines, and frequency of dialysis regimen. 

When giving amphotericin to dialysed patients, it may be necessary to give it during dialysis in order to avoid hyperkalemia. 

During dialysis a patient received an accidental infusion of 30 ml of a 5.25% solution of hypochlorite. This led to cardiorespiratory arrest and massive hemolysis with hyperkalemia, although the patient eventually recovered (7). 

Examination of the urine revealed macroscopic blood and granular casts. Her serum biochemistry was abnormal with hyperkalemia and an elevated urea and creatinine. She ultimately required dialysis but recovered sufficient renal function within 3 days to allow cessation of dialysis therapy. In view of the close association between the exposure to the Jeyes... 

The transfer of intracellular K" into ECF invariably occurs in acidosis as H shifts intraceHularly and shifts outward to maintain electrical neutrality. As a general rule, K concentrations are expected to rise 0.2 to 0.7 mmol/L for every 0.1 unit drop in pH. When the underlying cause of the acidosis is treated, normokalemia will rapidly be restored. Extracellular redistribution of may also occur in (1) dehydration, (2) shock with tissue hypoxia, (3) insulin deficiency (e.g., diabetic ketoacidosis), (4) massive intravascular or extracorporeal hemolysis, (5) severe burns, (6) tumor lysis syndrome, and (7) violent muscular activity, such as that occurring in status epilepticus. Finally, important iatrogenic causes of redistribution hyperkalemia include digoxin toxicity and P adrenergic blockade, especially in patients with diabetes or on dialysis. ... 

Hyperkalemia History of renal failure, diabetes, recent dialysis, dialysis fistulas, medications Calcium chloride, insulin, glucose, sodium bicarbonate, sodium polystyrene sulfonate, dialysis... 

Monitoring of volume status and serum electrolyte levels should be done at each follow-up visit in patients with Stages 4 or 5 CKD, particularly given the risk and detrimental consequences of volume overload (e.g., hypertension and pulmonary edema) and hyperkalemia (e.g., arrhythmias). Changes in volume status may warrant a change in diuretic therapy or dialysis regimens required to maintain hemodynamic stability. Patients should be educated on modifications in dietary intake and self-evaluation for signs and symptoms of edema. 

End-stage renal disease (ESRD) patients who present with severe hyperkalemia, or with cardiac manifestations of hyperkalemia, should undergo immediate hemodialysis. Dialysis is the most rapid means of lowering potassium compared to bicarbonate, epinephrine, or insulin plus glucose therapy. Other forms of dialysis can be performed (e.g., peritoneal dialysis or continuous renal replacement therapy), although they appear to be less effective means to acutely lower an elevated serum potassium. ... 

Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial 2001 15 348-356. 

Hyperkalemia is observed frequently in ARF secondary to protein catabolism and intracellular potassium release. Hyperkalemia also results from the impaired secretion and excretion of potassium by the kidney and the endogenous release secondary to tissue breakdown. If this is severe, emergent dialysis may be indicated. Patients on CRRT, however, usually will require potassium replacement to avoid hypokalemia due to dialytic potassium losses. 

Acute hyperkalemia causes a hypopolarization of the cardiac muscle cell membrane, resulting in characteristic electrocardiographic changes followed by serious and often fatal arrhythmias in most cases there are no warning symptoms. Immediate treatment is needed and consists of giving sodium bicarbonate, glucose, and insulin intravenously to shift K+ into the cells calcium intravenously to minimize the cardiotoxicity of hyperkalemia and polysterene sodium (a Na/K exchange resin) rectally or orally to remove potassium from the body if all fails, the performance of dialysis may be required (S18). 

Perturbations in mono- and divalent cation renal handling have been reported in association with pentamidine administration. Several reports of hyperkalemia in association with pentamidine therapy have been recently published [132,134,136,137,167,168]. Lachaal and Venuto [132] in a retrospective review reported a very high incidence of hyperkalemia (5.1 to 8.7 mEq/ L) in 19 of 20 patients (95%). This incidence was greater than the 5% reported earlier [123], or the 24% reported subsequently [134] in 37 patients with AIDS, and was challenged as a possible overestimation [169]. The hyperkalemia usually correlates with the presence of decreased GFR [132,134]. In our clinical study [133] the mean serum potassium concentration tended to be higher in the AIDS patients that developed pentamidine nephrotoxicity than in those that did not (5.0+0.3 vs 4.3+0.2, respectively, p <0.055). No patient, however, had a serum potassium concentration higher than 6.0 mEq/L. Hyperkalemia induced-arrhythmias occur [170], and rarely may include cardiac arrest [171]. The hyperkalemia usually reversed on discontinuation of pentamidine, and although most patients required only conservative measures, occasionally dialysis was necessary [132]. 

In 53 patients on hemodialysis who were randomized to spironolactone 50 mg or placebo thrice weekly after dialysis, potassium concentrations were measured once a month between dialysis sessions [30 ]. There were no episodes of hyperkalemia, but there was a small increase in the plasma potassium concentration (0.012 mmol/1) in the spironolactone group however, no patients developed hyperkalemia. 

Protein breakdown is accompanied by a loss of intracellular potassium, and starvation is associated with hyperkalemia. Hyperkalemia may seriously complicate uremia observed when severe renal failure occurs, and then the excess potassium should be eliminated by extracorporeal dialysis. 

Dialysis, the common name for hemodialysis, is the procedure used to treat end-stage kidney failure, transient kidney failure, and some poisoning or drug-overdose situations. Other indications for dialysis include hyperkalemia, uremia, uremic pericarditis. 

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