CAUSES & APPROACH TO HYPOKALEMIA & ITS COMPLICATIONS

Approach and causes of hypokalemia

1. * hypokalemia * Presenter – DR SUDHANVA K Under The Guidance of Medicine Unit-4

2. POTASSIUM Majorly an Intracellular cation (+ ve ). Along with sodium, outside the cells, it creates a phenomenon knows as MEMBRANE POTENTIAL 98% of Potassium is intracellular & 2% of is extracellular. NORMAL DAILY REQUIREMENT- 50 – 80 mEq /Day

3. POTASSIUM RICH FOODS

4. * Functions of k+- Maintains smooth muscles & skeletal muscles contraction. Maintain normal cardiac rhythm. Maintain intracellular neutrality in response to H+ & Na+. Regulate intracellular Osmolality. Generate nerve impulses. Maintenance of vascular tone Reduces bone resorption.

5. REGULATION OF K+ - The urinary system is the major site of potassium homeostasis regulation. Under normal physiological conditions, about 90% of potassium is excreted through the urine while the remaining 10% or less is excreted through sweat, vomit or Stools.

6. HYPOKALEMIA- INTRODUCTION Hypokalemia is defined as plasma K+ concentration of less than 3.5mEq/L. NORMAL VALUES – 3.5 to 5.0 mEq /L ( serum K+ concentration) 150mEq/L (Intracellular concentration)

7. GRADES OF HYPOKALEMIA- MILD – 3.5 TO 3.0 MODERATE – 3.0 TO 2.5 SEVERE - <2.5 * [ The two main systems usually most significantly affected by changes in K+ homeostasis are CARDIOVASCULAR SYSTEM, followed by NEUROMUSCULAR SYSTEM]

8. THYROTOXIC PERIODIC PARALYSIS Diagnosis & associated features – Paralytic attack that is associated with hypokalemia & hyperthyroidism (low TSH with high T4 & T3) Mechanism- Thyroid hormone increases tissue responsiveness to beta-adrenergic stimulation * Increases Na-K ATPase activity on the skeletal muscle membrane * Drive K+ into cells * Hyperpolarisation of the muscle membrane – PARALYSIS Etiology- Thyrotoxicosis. Age at onset- > 20yrs Attack duration – Hours to days

9. EPIDEMIOLOGY – Highest incidence in Asians, Men > Women Precipitants- Rest after Strenuous exercise, High carbohydrate load Stress Preventive Treatment- K+ correction (in emergency) Propranolol (3mg/kg)

10. PSEUDOHYPOKALEMIA- Potassium values can also be reported as low despite normal serum levels. This is most frequently seen when blood samples with high white cell counts (>75x109/L) are stored at room temperature. The K+ is taken up by these cells and this phenomenon encountered in conditions like sepsis & leukaemia.

11. CUSHING SYNDROME Results from an excess of Corticosteroids, either by endogenous or exogenous. Which in turn increases aldosterone levels in body. Aldosterone acts on MR receptor which acts on ENac receptor which absorbs Na. Which results in increase of K+ excretion through ROMK & Maxi-K receptors

12. BARTTER SYNDROME Bartter syndrome- Excessive loss of sodium & Water through the urine. This causes a rise in the level of the hormone aldosterone, Which in turn increases secretion of K+. This is known as potassium wasting. Site of defect – Ascending loop Henle Autosomal Recessive Disorder Genes – SLC12A1, KCNJ1, BSND Mimics LOOP DIURETIC TOXICITY

13. GITELMAN’S SYNDROME Gitelman syndrome is a salt-losing tubulopathy . Autosomal Recessive disorder Characterized by renal potassium wasting, hypokalemia , metabolic alkalosis, hypocalciuria , hypomagnesemia , and hyperreninemic hyperaldosteronism . Gitelman syndrome is also referred to as familial hypokalemia-hypomagnesemia . Site of defect- Distal convoluted tubule & Cortical collecting duct. Mimics THIAZIDE TOXICITY.

14. LIDDLE SYNDROME A genetic disorder characterized by hypertension with hypokalemic metabolic alkalosis, hyporeninemia and suppressed aldosterone secretion Liddle’s syndrome mimics the symptoms of mineralocorticoid excess MOA- The reabsorption of sodium from overactive Enac in the kidney facilitates a loss of potassium in the urine.

15. MAGNESIUM DEFICIENCY- It has inhibitory effects on muscle Na+/K+-ATPase activity, Reducing influx into muscle cells and causing a secondary kaliuresis . In addition, magnesium depletion causes exaggerated K+ secretion by the distal Nephron . T his effect is attributed to a reduction in the magnesium- dependent, intracellular block of K+ efflux through the secretory K+ channel of principal cells (ROMK). I n consequence, hypo- magnesimic patients are clinically refractory to K+ replacement in the absence of Mg2+ repletion. Notably, magnesium deficiency is also a common concomitant of hypokalemia because many disorders of the distal nephron may cause both potassium and magnesium wasting .

16. SIGNS & SYMPTOMS - CARDIOVASULAR Arrhythmias atrial & Ventricular Heart failure , Stroke, HTN Neuromuscular Muscle weakness Rhabdomyolysis Paralysis & Paralytic Ileus

17. Acid- Base balance Bi-carbonate retention Causing Metabolic acidosis HYPOKALEMIC NEPHROPATHY AKI due to relatively specific voculizing Injury to proximal tubular cells. Can lead to ESRD in patients with long standing hypokalemia due to eating disorders or Laxative abuse.

18. ECG CHANGES IN HYPOKALEMIA - Broad flat or inverted “T” waves “ST” depression “QT” prolongation Presence of “U” waves *All these signs are more marked when K+ is <2.7mmol/L.

19. Assessment of the patient History Physical examination Laboratory Evaluation -24hours urine potassium measurement More than 30ml indicates renal loss ( as per ASN) Less than 15ml indicates Extrarenal loss -Urine potassium to creatinine ratio (KCR) Less than 13mEq/G of creat indicates Extrarenal loss Value above this indicates renal loss

20. TTKG – Transtubular potassium gradient. Urine K+/ Serum K+ / Urine osmo / serum osmo Normal 8-9 If less than 2 indicates Extrarenal loss If more than 4 Indicates renal loss

21. TREATMENT OF HYPOKALEMIA A. Therapeutic goals : 1. Prevention of hypokalemia · 2. To prevent life threatening complications. (arrhythmia and respiratory failure) 3. To correct the potassium. deficit 4. To minimize on-going losses · 5. To treat underlying etiology

22. PREVENTION OF K+ DEPLETION · Normal potassium intake of about 60 mEq /day i s sufficient to Prevent hypokalemia . But patients receiving digitalis , lon g term diuretics or large doses of steroids should receive potassium Supplement. Conditions where prevention of hypokalemia is of special importance are digitalis therapy, hepatic failure, previous myocardial infarction or IHD and diabetes mellitus. Postoperative patients on parenteral fluid t herapy should receive 40-50 mEq /day of potassium to preve nt hypokalemia .

23. 3.5 to 4 mEq /L : -- No potassium supplement Increased oral intake of potassium rich food Add potassium sparing diur etics or decrease dose of diuretics 3 to 3.5 mEq /L : Treatment in selected high risk patients ( Risk of arrhythmia e.g. CHF, digitalis therapy, history of acute myocradial infarction or IHD. ) < 3 mEq /L : Needs definitive treatment

24. Precautions before initiating potassium supplements - 1. In oliguria-anuria, avoid or supplement K+ caut ious 2. Patient's receiving potassium sparing diuretics, ACE inhibitors and patients with renal failure are at high risk of developing hyperkalemia, so potassiu m supplementation should be done cautiously. 3. Digitalis therapy : In patients on digitalis, potassium enters the cell at a slower rate so there is a risk of transient hyperkalemia with faster I. v infusion . So rate of infusion should be < 20 mEq / hour 4. Continuous ECG monitoring and frequent serum potassium level estimation is advisable , i f the rate of infusion is > 20mEq/hour in any patient.

25. HOW MUCH K+ TO GIVE? HOW LONG TO TREAT? The amount of K+ required to correct potassium deficit cannot be determined by any fixed formula. When the average deficit of potassium is about 200-400mEq, 50-100mEq/day of K+ slowly can be given. With severe Hypokalemia or with high rate of ongoing loss, larger dose may be required The deficit should be corrected slowly over a period of days. It may take weeks to correct severe potassium loss. Failure to increase serum K+ after sufficient dose and duration of potassium supplement raises the possibility of associated magnesium deficiency.

26. Potassium preparations Potassium chloride KCL- Commonly used to correct hypokalemia . Potassium bicarbonate & Potassium citrate tend to alkalinize the patient and would be more appropriate for hypokalemia associated with chronic diarrhoea or distal RTA Oral potassium administration is safer than I.V. Route because I.V route carries high risk of hyperkalemia

27. Oral k+ is safer mode of correction In mild to moderate hypokalemia (3 to 3.5mEq/L) average dose of KCL is 60-80mEq/day (20mEq ; 3-4times ) Potassium chloride solution, available in the market contains 20 mEq potassium per 15 ml solution ( 1 gm KCl =13 . 4 mEq of K+) KCI tablets available contain 8 mEq potassium per tablet. Oral potassium preparation may frequently cause G.I. irritation and therefore the patient is advised to take potassium chloride solution with proper dilution in a glass of water, after food. Oesophageal or small bowel erosion and stricture are uncommon side effects.

28. INDICATIONS FOR PARENTRAL CORRECTION OF POTASSIUM - Cardiac Arrhythmias Digoxin Toxicity Severe Diarrhea Severe myopathy & muscle necrosis Paralysis

29. IV POTASSIUM THERAPY – l.V . Potassium supplementation carries higher risk of hyperkalemia . So l.V . Potassium supplementation should be reserved for severe symptomatic hypokalemia (K+ < 3 mEq /L) or for patients who cannot ingest oral potassium . Always monitor l.V . Potassium therapy closely with continuous ECG monitoring and frequent serum potassium estimation . Avoid l.V . Potassium, till urine output is established .

30. Don’t give> 10-20 mEq /hour . Don’t give> 40 mEq /Litre . Don’t give> 240 mEq /day . Never give inj. KCI directly intravenously, it can cause sudden hyperkalemia and instant death from cardiac arrest. Remember that hypokalemia is safer than hyperkalemia, so avoid over enthusiastic treatment.

31. In severe hypokalemia, KCI should be mixed with isotonic saline. Should not use D-5 % as diluent because dextrose stimulated insulin release will shift potassium intracellularly and hence initially aggravates hypokalemia. Diabetic ketoacidosis and nonketotic hyperosmolar hyperglycemia are amongst the commonest indications of l.V . Potassium therapy.

32. How to give & How Long to Give ? Depending upon etiology , readymade available l.V . Fluids can be used to provide potassium supplement e.g. Isolyte -G in vomiting
or continuous nasogastric aspiration, lsolyte -M for parenteral fluid
therapy etc. Potassium concentration more than 40mEq/L can cause Phlebitis and should be infused only into large veins (femoral or subclavian) Average rise in potassium level is 0.25 mEq /L, When 20mEq is given during one hour . Usually 80-85% of administered dose enters the cells.

33. How long to give ? As soon as cardiac rhythm returns to normal or the respiratory muscle strength is restored to normal. I.V potassium drip is gradually tapered and discontinued and oral KCL should be Initiated. I.V Potassium Preparations- Inj Potassium chloride : Most widely available and used is INJ KCL 15% 10ML ampl 10ml of 15% KCL= 20mEq of potassium 1ml of 15% KCL = 2mEq of potassium

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