hypokalemia, diagnosis and management

potassium homeostasis, hypokalemia and potassium correction, electrolyte imbalance, management of hypokalemia,potassium deficit

1. hypokalemia Sheila Perillo , MD Obstetrics and Gynecology

2. Less than 3.5 mEq /L- (3.5 mmol /L) Moderate hypokalemia - 2.5-3 mEq /L Severe hypokalemia - less than 2.5 mEq /L

3. Potassium - most abundant intracellular cation - important to normal cellular function particularly of nerve and muscle cells - regulated by specific ion-exchange pumps, primarily by cellular, membrane-bound, sodium-potassium adenosine triphosphatase ( ATPase ) pumps

4. - obtained through the diet -excreted via the kidney. - Potassium homeostasis is maintained predominantly through the regulation of renal excretion

5. Hypokalemia inadequate potassium intake increased potassium excretion- most common shift of potassium from the extracellular to the intracellular space

6. Common findings include weakness, fatigue, constipation, ileus , and respiratory muscle dysfunction. Symptoms seldom occur unless plasma K+ is less than 3.0 mmol /L.

7. ECG changes

8. The treatment of hypokalemia has 4 facets Reduction of potassium losses Replenishment of potassium stores Evaluation for potential toxicities Determination of the cause to prevent future episodes

9. Pathophysiology Daily excess intake of approximately 1 mEq /kg/day (60-100 mEq ): Ninety percent is excreted through the kidneys 10 % is excreted through the gut Potassium homeostasis is maintained predominantly through the regulation of renal excretion (collecting duct)

10. Potassium excretion is increased by the following factors: Aldosterone High sodium delivery to the collecting duct ( eg , diuretics) High urine flow ( eg , osmotic diuresis ) High serum potassium levels Delivery of negatively charged ions to the collecting duct ( eg , bicarbonate)

11. Potassium excretion is decreased by the following factors: Absolute aldosterone deficiency or resistance to aldosterone effects Low sodium delivery to the collecting duct Low urine flow Low serum potassium levels Renal failure

12. increase in osmolality  exit from cells acute cell/tissue breakdown  releases potassium into extracellular space

13. Renal factors in potassium homeostasis Kidneys adapt to acute and chronic alterations in potassium intake: When potassium intake is chronically high, potassium excretion likewise is increased . obligatory renal losses are 10-15 mEq /day The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure. In the presence of renal failure, the proportion of potassium excreted through the gut increases. The colon is the major site of gut regulation of potassium excretion.

14. Potassium distribution Potassium is predominantly an intracellular cation ; therefore, serum potassium levels can be a very poor indicator of total body stores.

15. Several factors that regulate the distribution of potassium between the intracellular and extracellular space Glycoregulatory hormones: ( 1) Insulin enhances potassium entry into cells (2) glucagon impairs potassium entry into cells Adrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium entry into cells (2) alpha-adrenergic stimuli impair potassium entry into cells pH: (1) Alkalosis enhances potassium entry into cells (2) acidosis impairs potassium entry into cells

16. Pathogenic mechanisms Hypokalemia can occur via the following pathogenetic mechanisms: Deficient intake Increased excretion A shift from the extracellular to the intracellular space Although poor intake or an intracellular shift by itself is a distinctly uncommon cause

17. Increased excretion The most common mechanisms leading to increased renal potassium losses include the following: Enhanced sodium delivery to the collecting duct, as with diuretics Mineralocorticoid excess, as with primary or secondary hyperaldosteronism Increased urine flow, as with an osmotic diuresis

18. Gastrointestinal losses: Diarrhea Vomiting nasogastric suctioning, also are common causes of hypokalemia Volume depletion leads to secondary hyperaldosteronism  enhanced cortical collecting tubule secretion of potassium in response to enhanced sodium reabsorption Metabolic alkalosis  increases collecting tubule potassium secretion

19. Extracellular/intracellular shift Shift from extracellular to intracellular space often accompanies increased excretion  potentiation of the hypokalemic effect of excessive loss Intracellular shifts of potassium often are episodic frequently are self-limited ( ie ., acute insulin therapy for hyperglycemia )

20. Complications Cardiovascular complications A trial and ventricular arrhythmias Increased susceptibility to cardiac arrhythmias is observed with hypokalemia in the following settings: Congestive heart failure Underlying ischemic heart disease/acute myocardial ischemia Aggressive therapy for hyperglycemia , such as with diabetic ketoacidosis Digitalis therapy Methadone therapy  Conn syndrome  

21. Low potassium intake hypertension and/or hypertensive end-organ damage altered vascular reactivity  vasoconstriction and impaired relaxation Treatment of hypertension with diuretic exacerbates the development of end-organ damage by fueling the metabolic abnormalities high risk for lethal hypokalemia under stress conditions such as myocardial infarction, septic shock, or diabetic ketoacidosis

22. Muscular complications Muscle weakness D epression of the deep-tendon reflexes F laccid paralysis Rhabdomyolysis (severe hypokalemia )

23. Renal complications Nephrogenic diabetes insipidus - Abnormalities of renal function often accompany acute or chronic hypokalemia M etabolic alkalosis from impaired bicarbonate excretion Cystic degeneration Interstitial scarring

24. Gastrointestinal complications Decreased gut motility, which can lead to or exacerbate an ileus Hepatic encephalopathy in the setting of cirrhosis

25. Metabolic complications Dual effect on glucose regulation by decreasing insulin release and peripheral insulin sensitivity Thiazide -associated diabetes mellitus

26. Etiology Inadequate potassium intake Increased potassium excretion ** Shift of potassium from the extracellular to the intracellular space

27. Inadequate potassium intake Eating disorders   : Anorexia, bulimia, starvation, pica, and alcoholism Dental problems: Impaired ability to chew or swallow Poverty: Inadequate quantity or quality of food ( eg , "tea-and-toast" diet of elderly individuals) Hospitalization: Potassium-poor TPN

28. Increased potassium excretion Mineralocorticoid excess (endogenous or exogenous) Hyperreninism from renal artery stenosis Osmotic diuresis : Mannitol and hyperglycemia can cause osmotic diuresis Increased gastrointestinal losses Drugs Genetic disorders

29. Gastrointestinal loss of potassium Vomiting Diarrhea Small intestine drainage

30. Drugs that can cause hypokalemia include the following: Diuretics (carbonic anhydrase inhibitors, loop diuretics, thiazide diuretics): Increased collecting duct permeability or increased gradient for potassium secretion can result in losses Methylxanthines ( theophylline , aminophylline , caffeine) Verapamil (with overdose) Quetiapine (particularly in overdose) Ampicillin , carbenicillin , high-dose penicillins Bicarbonate Antifungal agents ( amphotericin B, azoles, echinocandins )  Gentamicin Cisplatin Ephedrine (from Ephedra ; banned in the United States, but available over the Internet)  Beta-agonist intoxication 

31. Genetic disorders Congenital adrenal hyperplasia (11-beta hydroxylase or 17-alpha hydroxylase deficiency) Glucocorticoid -remediable hypertension Bartter syndrome Gitelman syndrome Liddle syndrome Gullner syndrome Glucocorticoid receptor deficiency Hypokalemic period paralysis Thyrotoxic periodic paralysis (TTPP) Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance ( SeSAME syndrome)

32. Shift of potassium from extracellular to intracellular space Alkalosis (metabolic or respiratory) Insulin administration or glucose administration (the latter stimulates insulin release) Intensive beta-adrenergic stimulation Hypokalemic periodic paralysis Thyrotoxic periodic paralysis Refeeding : This is observed in prolonged starvation, eating disorders, and alcoholism Hypothermia

33. Other factors associated with a high incidence of hypokalemia include the following: Eating disorders (incidence of 4.6-19.7% in an outpatient setting) AIDS (23.1% of hospitalized patients)  Alcoholism (incidence reportedly as high as 12.6%  [33]  in the inpatient setting), likely from a hypomagnesemia -induced decrease in tubular reabsorption of potassium Bariatric surgery 

34. Treatment Therapeutic goals Prevent life-threatening complications (arrhythmias, respiratory failure, hepatic encephalopathy) Correct the K+ deficit Minimize ongoing losses Treat the underlying cause

35. Treatment K deficit= ( desired k- actual k ) x 100% 0.27 Estimation of K+ deficit 3.0 meq /L= total body K+ deficit of 200-400 meq /70kg 2.5 meq /L = 500 meq /70kg 2.0 meq /L = 700 meq /70kg

36. Treatment Oral therapy Generally safer Degree of K+ depletion does not correlate well with the plasma K+ KCl is usually the preparation of choice Kalium durule : 1 durule = 10 meqs KCl KCl syrup: 1meq/mL

37. Treatment IV therapy For severe hypokalemia or those who are unable to take anything by mouth Maximum rate at which potassium is infused into peripheral veins is usually 10 meq / hr Central – 20 meq / hr Rate of infusion should not exceed 20 meq /hour unless paralysis or malignant ventricular arrhythmias are present

38. TO GOD BE THE GLORY!