Hyperkalemia hemodialysis

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). 

It is critically important to recognize that the treatments of hyperkalemia discussed thus far are transient, temporizing measures. They are intended to provide time to institute definitive therapy aimed at removing excess potassium from the body. Agents that increase potassium excretion from the body include sodium polystyrene sulfonate, loop diuretics, and hemodialysis or hemofiltration (used only in patients with renal failure). Sodium polystyrene sulfonate (Kayexalate , various manufacturers) can be given orally, via NG tube, or as a rectal retention enema and is dosed at 15 to 60 grams in four divided doses per day. 

The definitive treatment of severe hyperkalemia in ESRD is hemodialysis. Temporary measures include calcium gluconate, insulin and glucose, nebulized albuterol, and sodium polystyrene sulfonate. 

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]... 

Heparin-induced hypoaldosteronism is well documented, both in patients treated with standard heparin, even at low doses, and in patients treated with low molecular weight heparin (477,478). The most important mechanism of aldosterone inhibition appears to be a reduction in both the number and affinity of angiotensin II receptors in the zona glomerulosa (477). A direct effect of heparin on aldosterone synthesis, with inhibition of conversion of corticosterone to 18-hydroxycorticosterone, has also been suggested. This effect is believed to be responsible for the hyperkalemia that can occur in heparin-treated patients with impaired renal function and particularly in patients on chronic hemodialysis (479), or with diabetes mellitus, or who are taking other potentially hyperkalemic drugs. 

Hottelart C, Achard JM, Moriniere P, Zoghbi F, Dieval J, Fournier A. Heparin-induced hyperkalemia in chronic hemodialysis patients comparison of low molecular weight and unfractionated heparin. Artif Organs... 

Ventricular dysrhythmias have been reported after rapid infusion of large doses of DAMB (70) in patients with hyperkalemia and renal insufficiency, but not in patients with normal serum creatinine and potassium concentrations, even if they have received the drug over a period of 1 hour. Slower infusion rates and infusion during hemodialysis have been advocated in patients with terminal kidney insufficiency, in order to avoid hyperkalemia. 

In contrast, published case reports and case series have provided more insight into the potential nephrotoxicity associated with COX-2-selective inhibitors. Taken together, these case reports suggest that COX-2 inhibitors, like non-selective NSAIDs, produce similar and consistent renal adverse effects in patients with one or more risk factors that induce prostaglandin-dependent renal function (that is patients with renal and cardiovascular disease and taking a number of culprit medications, such as diuretics and ACE inhibitors). Acute renal insufficiency, disturbances in volume status (edema, heart failure), metabolic acidosis, hyperkalemia, and hyponatremia have been commonly described. The duration of treatment with COX-2 inhibitors before the development of chnically recognized renal impairment ranged from a few days to 3-4 weeks. Withdrawal of COX-2 inhibitors and supportive therapy most often resulted in resolution of renal dysfunction, but in some patients hemodialysis was required (102,108-112). 

Hamad A, Salameh M, Zihlif M, Feinfeld DA, Carvounis CP. Life-threatening hyperkalemia after intravenous labetolol injection for hypertensive emergency in a hemodialysis patient. Am J Nephrol 2001 21(3) 241. ... 

Polystyrene sulfonic acid has been used as sodium, potassium, and calcium salts. Sodium polystyrene sulfonate has been used to treat hyperkalemia in patients with renal insufficiency and as an adjuvant during hemodialysis. It can be given orally or rectally in all age groups (1). It has also been added to feeding formulae and nutritional supplements to reduce their potassium contents and so prevent hyperkalemia however, the reduction in potassium content was more than balanced by a concomitant increase in sodium content, presumably because of exchange of the sodium with calcium and magnesium (2,3). The uses and adverse effects of sodium polystyrene sulfonate have been reviewed (4,5). 

A 67-year-old man underwent laparotomy for a ruptured abdominal aortic aneurysm (20). Postoperatively he was treated with hemodialysis because of acute renal insufficiency. Hyperkalemia was treated with sodium polystyrene sulfonate, after which he developed ulceration of the colon and required a hemicolectomy because of intractable blood loss. 

Lin JL, Huang CC. Successful initiation of hemodialysis during cardiopulmonary resuscitation due to lethal hyperkalemia. Grit Care Med 1990 18(3) 342-3. 

Low-dose spironolactone has been shown to decrease cardiovascular mortality in patients with severe heart failure. However, since spironolactone contributes to hyperkalemia, this agent should not be used in patients with Stage 4 or 5 CKD. New studies will be required before concluding that spironolactone administration is safe in the chronic hemodialysis population to reap the potential cardiovascular benefits. 

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. ... 

The treatment of hyperkalemia is to infuse slowly intravenous calcium gluconate (10 mL of 10% solution over 3 min). Soluble insulin (15 U intravenously) and 50 mL of 50% glucose solution should also be given intravenously [26], Plasma potassium should be determined hourly. Intravenous salbutamol also causes a reduction of serum potassium possibly by activating P-adrenergically stimulated membrane Na, K -ATPase [27). Longer term treatment might involve hemodialysis. 

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. 

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. 

Preoperative serum electrolyte status should be known in patients with ESRD. Hemodialysis is indicated prior to surgery, if relevant hyperkalemia (6.0 mEq/1 or more) is present, to protect the patient from life-threatening arrhythmia. Severely abnormal serum sodium or chloride needs further workup and slow correction. In emergencies, electrolyte correction is initiated without delaying life-saving surgery. 

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