HYPERKALEMIA NEJM PDF

Medical Intelligence from The New England Journal of Medicine — VI. Hyperkalemia. Hyperkalemia is a potentially life-threatening condition in which serum potassium exceeds mmol/l. It can be caused by reduced renal excretion, excessive. n engl j med ;3 january 15, mmol per liter.1,2 Hyperkalemia is defined as erate hyperkalemia) and more than mmol per.

Author: Sall Akinobar
Country: Montenegro
Language: English (Spanish)
Genre: Technology
Published (Last): 22 March 2013
Pages: 328
PDF File Size: 11.4 Mb
ePub File Size: 8.49 Mb
ISBN: 682-6-63304-215-5
Downloads: 67087
Price: Free* [*Free Regsitration Required]
Uploader: Fenrisho

Hyperkalemia is a potentially life-threatening condition in which serum potassium exceeds 5. It can be caused by reduced renal excretion, excessive intake or leakage of potassium from the intracellular space. In addition to acute and chronic renal failure, hypoaldosteronism, and massive tissue breakdown as in rhabdomyolysis, are typical conditions leading to hyperkalemia. Symptoms are non-specific and predominantly related to muscular or cardiac dysfunction.

Treatment has to be initiated immediately using different therapeutic strategies to increase potassium shift into the intracellular space or to increase elimination, together with reduction of intake. Knowledge of the physiological mechanisms of potassium handling is essential in understanding the causes of hyperkalemia as well as its treatment. This article reviews the pathomechanisms leading to hyperkalemic states, its symptoms, and different treatment options.

Absorption of potassium from the gastrointestinal tract is rapid and usually complete. Depending on diet, the normal daily intake can vary. Low extracellular potassium concentrations of 3. In the presence of renal failure, the proportion of potassium excreted through the gut can increase, but is subject to high inter-individual variability [ 1 ]. Handling of potassium in the nephron depends on passive and active mechanisms.

Potassium is filtered in the glomerulus and almost completely reabsorbed in the proximal tubule and the loop of Henle. Excretion mainly occurs in the cortical collecting duct [ 2 ]. It should be noted, however, that reabsorption and secretion of potassium occur simultaneously, and that many modulators are important, such as diet, adrenal steroids, and acid-base balance. The mechanisms involved are not yet completely understood.

Several co-transporters and ion channels are involved in the complex regulatory system of potassium reabsorption. The best characterized is the Na-K-2Cl cotransporter NKCC2which transports potassium out of the tubular fluid and is inhibited by loop diuretics furosemide.

Basolateral transporters include a KCl cotransporter. It modulates excretion of not only potassium but also calcium and magnesium. There is evidence that the calcium-sensing receptor CaSR influences the renal ion transport, amongst others by inhibiting the activity of ROMK [ 5 ].

Aldosterone as key regulator of renal potassium homeostasis binds to the nuclear mineralocorticoid receptor MR within the distal tubule and the principal cells in the CCD. Acid-base balance can affect the balance between cellular and extracellular potassium concentration.

Hyperkalemia may result from an increase in total body potassium secondary to imbalance of intake vs. In patients with unimpaired renal function and intact other regulatory mechanisms, large amounts of potassium are needed to achieve hyperkalemia [ 11 ]. Hyperkalemia can be classified according to serum potassium into mild 5.

Pathogenesis, diagnosis and management of hyperkalemia

Hyperkalemia is rarely associated with symptoms, occasionally patients complain of palpitations, nausea, muscle pain, or paresthesia. However, moderate and especially severe hyperkalemia can lead to disturbances of cardiac rhythm, which can be fatal [ 2829 ].

Examination and investigations should be systematic and always include assessment of cardiac function, kidneys, and urinary tract as well as hydration status and neurological evaluation. Diagnostic algorithm in hyperkalemia; adapted from Clinical Paediatric Nephrology. Used with permission from [ 40 ] RTA renal tubular acidosis.

  HECTOR ANAYA EL ARTE DE INSULTAR PDF

If elevated serum potassium is found in an asymptomatic patient with no apparent cause, factitious hyperkalemia should be considered. This results from leakage of potassium from the intracellular space during or after blood sampling.

In these cases, elevation of serum potassium concentration does not reflect the level of serum potassium in vivo and no treatment is needed. Especially in pediatrics, mechanical hemolysis can occur during difficult blood draws, and even more in samples with lymphocytosis or thrombocytosis.

Especially when capillary samples are taken, excess alcohol on the skin should be avoided, as it is the primary cause of the hemolysis in this process. Correction factors have been discussed, but blood usually has to be drawn again [ 30 ].

Therapeutic strategies should be individualized, taking into account the degree and the cause of hyperkalemia. Management should not only rely on ECG changes but be guided by the clinical scenario and serial potassium measurements [ 2931 ]. Treatment has to be more aggressive the higher and the faster the rise of the potassium level, and the greater the evidence of toxicity ECG changes.

These therapeutic measures often are sufficient in acute hyperkalemia in patients without hyperkalemmia renal impairment, where an increase in renal potassium excretion can be achieved. The following steps often have to be addressed simultaneously. Additionally, if unknown, the cause of hyperkalemia has to be determined to prevent future episodes. In summary and conclusion, the effective and rapid diagnosis and management of acute and chronic hyperkalemia in children, especially if renal function is impaired, is clinically relevant and can be life-saving.

In hyperrkalemia of moderate to severe hyperkalemia, the combination of medications with different therapeutic approaches is usually effective, and often methods of blood purification can be avoided. In children with severe hyperkalemia and major ECG abnormalities, conservative efforts should be initiated immediately to stabilize the patient, but management should include rapid facilitation of renal replacement treatment.

National Center for Biotechnology InformationU. Pediatric Nephrology Berlin, Germany. Published online Dec Anja Lehnhardt and Markus J. Author information Article notes Copyright and License information Disclaimer. This article has been cited by other articles in PMC.

Abstract Hyperkalemia is a potentially life-threatening condition in which serum potassium exceeds 5. Hyperkalemia, Potassium, Renal failure, Salbutamol. Open in a separate window.

Renal mechanisms of potassium handling Handling of potassium in the nephron depends on passive and active mechanisms. Extrarenal regulatory mechanisms of potassium metabolism Acid-base balance can affect the balance between cellular and extracellular potassium concentration.

Pathogenesis of hyperkalemia Hyperkalemia may result from an increase in total body potassium secondary to imbalance of intake vs. Excessive intake In patients with unimpaired renal function and intact other regulatory mechanisms, large amounts of potassium are needed to achieve hyperkalemia [ 11 ]. Impaired elimination of potassium Renal insufficiency acute or chronic: Non-steroidal anti-inflammatory drugs NSAIDs; ibuprofen, naproxen and ACEI nsjm converting enzyme inhibitors as well as angiotensin receptor inhibitors can cause a decrease in aldosterone and GFR and thereby lead to hyperkalemia [ 13 ].

Combined treatment with spironolactone and ACE inhibitors, especially in patients with renal impairment or heart failure, has to be monitored very carefully. Hypoaldosteronism may either be primary e. Addison or secondary e. A similar picture can be seen in patients with obstructive uropathy and renal tubular acidosis [ 1617 ]. Pseudohypoaldosteronism PHA refers to a heterogeneous group neum disorders of electrolyte metabolism characterized by hyperkalemia, metabolic acidosis, and normal GRF [ 18 ].

  ASTM C128 - 07A PDF

PHA type I caused by autosomal dominant mutations in the human mineralocorticoid receptor MR gene is limited to the kidneys.

Pathogenesis, diagnosis and management of hyperkalemia

PHA type I secondary to loss of function mutations of the ENaC not only affects the kidney but also the lungs, colon, and sweat and salivary glands. Congenital adrenal hyperplasia CAH: The particular phenotype and degree of hyperkalemia depends on the sex of the individual, the location of the block in synthesis, and the severity of the genetic deletion or mutation. Increased shift of potassium from intra to extracellular space Acidosis: Mineral acidosis is more likely to cause a shift of potassium from intracellular space into extracellular space than organic acidosis.

Acute increase in osmolality secondary to hyperglycemia or mannitol infusion causes potassium to exit from cells [ 24 ]. This can be the case in patients with rhabdomyolysis, tumorlyis, hemolysis, or after massive transfusion.

Succinylcholine, especially when given to patients with burn injuries, immobilization, or inflammation [ 26 ]. Diagnosis of hyperkalemia Hyperkalemia can be classified according to serum potassium into mild 5.

Pseudohyperkalemia If elevated serum potassium is found in an asymptomatic patient with no apparent cause, factitious hyperkalemia should be considered. Management of hyperkalemia Therapeutic strategies should be individualized, taking into account the degree and the cause of hyperkalemia. An effect can often be seen immediately but response remains unpredictable. Close electrolyte and blood glucose monitoring is needed, hypoglycemia being the main side-effect.

Salbutamol can be applied via nebulizer or given intravenously. If given iv, the lowering effect of salbutamol is quite predictable with a mean decrease of 1. It can cause tachycardia. Salbutamol has been shown to be safe and even superior to rectal cation-exchange resin in nonoliguric preterms with hyperkalemia [ 34 ].

Sodium bicarbonate, preferably given to patients who are acidotic. In hemodialysis patients with hyperkalemia it has only a moderate effect if given as prolonged infusion [ 35 ]. Even in chronic hemodialysis patients, treatment with loop diuretics may be of value if the patient has some residual renal function [ 36 ].

Ion-exchange resins containing calcium or sodium aim to keep enteral potassium from being resorbed.

More effective if given orally. Enemas should be retained at least min. Onset within h, lasting h. Renal replacement therapy RRT is the ultimate measure in severe hyperkalemia. Continuous veno-venous hemofiltration CVVH can more satisfactorily provide long-term control of potassium. Choice of method depends on local circumstances and hemodynamics of the patients, as critical ill patients will rarely tolerate HD sessions [ 38 ].

Diarrhea if preparations come premixed with sorbitol p. Ca-Gluconate does not have a potassium-lowering effect. Which drug does not cause hyperkalemia? Which of the following clinical conditions typically causes hyperkalemia answer true or false for a through e acute renal failure.

In managing a patient with severe hyperkalemia: