cme about hypokalemia and its management (1).pptx

Electrolyte imbalance

1. Approach to a patient with Hypokalemia Dr . Jasrin Akter Phase A Resident Medicine Unit- VIII DMCH

2. Function & source of Potassium Potassium is the main intracellular cation in the body It is principally involved in membrane potential Electrical excitation of both nerve and muscle cells & A cid-base regulation.

3. Potassium Homeostasis Total body K+ is 3000-4000 meq in normal adult. Normal homeostatic mechanism maintain serum K+ level within a narrow range (3.5 – 5.0 mmol/L)

4. Hypokalaemia Hypokalaemia is a common electrolyte disturbance and is defined as when serum K+ falls below 3.5 mmol/L. It’s seen in about 20% of hospitalized patient. The prevalence in women is twice as in men .

5. Effects of hypokalemia Increases prevalence of hypertension Ventricular tachycardia Ventricular fibrillation Risk of sudden cardiac death Cardiac Impairs insulin release Induces insulin resistance, worsened glucose control in DM patient Hormonal Musculoskeletal Skeletal muscle weakness increased sensitivity to developing exercise induced rhabdomyolysis

6. Causes

7. Pseudohypokalemia Refers to the condition in which serum potassium decreases artifactually ,after phlebotomy. The most common cause is acute leukemia. The large number of abnormal leukocytes take up potassium when the blood is stored in for prolonged peroids at room temperature. Rapid separation of plasma & storage at 4˚ C is used to confirm this diagnosis.

8. Drugs causing Hypokalemia Diuretics ( Loop & thiazide) Laxatives Glucocorticoids Amphotericin Aminoglycosides Insulin Salbutamol

9. History: History of any GIT loss by vomiting, diarrhoea , nasogastric aspiration Laxative abuse Abdominal pain, vomiting and constipation– intestinal obstruction Abdominal Surgery History of excessive electrolyte free water infusion

10. History Drugs: prolonged diuretics, corticosteroid, excess insulin Polyuria, polydipsia, edema, muscle weakness – Conn’s syndrome Prolonged steroid therapy, weight gain, muscular weakness, easy bruising, excessive hair growth– Cushing’s syndrome. Smoking history with cough, hemoptysis, dyspnoea , chest pain— Ectopic ACTH Syndrome Excessive intake of liquorice or treatment with carbenexolone

11. History (cont.): Carpopedal spasm, apathy, confusion, drowsiness— metabolic alkalosis Respiratory distress, confusion, drowsiness— metabolic acidodis Features of metabolic acidosis with no evidence of GI disturbance— Renal Tubular Acidosis Recurrent episodes of limb weakness triggered by carbohydrate meal– Hypokalemic periodic paralysis

12. Examination: High blood pressure– Conn’s Syndrome, Cushing’s syndrome, glucocorticoid excess, carbenexolone / liquorice , Liddle’s Syndrome Edema– Conn’s syndrome, Corticosteroid therapy Moon face with plethora, acne, central obesity with buffalow hump, thin skin with striae and bruises– Cushing‘s syndrome

13. Examination Loss of pulses, cyanosis or pallor, decreased skin temperature, loss of sensation, paralysis, flash pulmonary edema– Renal Artery Stenosis Deep and sighing respiration, decreased blood pressure, Altered consciousness– metabolic acidosis. Distended abdomen with visible peristalsis in central abdomen— Gastric Outlet obstruction

14. Investigation: Serum electrolytes: Serum Na+‌‌‍ – high in conn’s syndrome, Renal artery stenosis low in diuretics Serum Mg – decreased in Bartter’s and Gitelman’s syndrome, diuretic therapy Urine electrolytes: Urine potassium – (>20-30mmol/day) indicates renal K loss – (<20-30mmol/day) indicates gastrointestinal K loss.

15. Urine potassium-to-creatinine ratio  —  The urine potassium-to-creatinine ratio on a spot urine correlates with 24-hour urine potassium excretion < 13 mEq /g creatinine (1.5 mEq /mmol creatinine) when hypokalemia is caused by Diarrhoea Hypokalemic periodic paralysis Insulin Beta 2 adrenergic stimulation > 13mEq/g (1.5 mEq /mmol creatinine) with active renal potassium wasting (including diuretics, when the effect on the kidney is still present

16. Acid Base Status Metabolic acidosis with a low rate of urinary potassium excretion is suggestive of L ower gastrointestinal losses due to laxative abuse or A villous adenoma Metabolic acidosis with urinary potassium wasting is most often due to D iabetic ketoacidosis or to T ype 1 (distal) or Ty pe 2 (proximal) renal tubular acidosis (RTA). Metabolic alkalosis with a low urinary potassium excretion may be due to V omiting or D iuretic use or L axative abuse

17. Metabolic alkalosis with urinary potassium wasting Normal BP D iuretic use vomiting Gitelman Bartter syndrome Urinary chloride loop diuretics Thiazide diuretics Mg deficiency Gittleman syndrome & Bartter syndrome Increased Vomiting Decreased

18. High Blood pressure Renin Aldosterone Aldosterone Renin Aldosterone Renin Renal artery stenosis Renin secreting tumor Adrenal adenoma Bilateral Adrenal hyperplasia Glucocorticoid suppressible hyperaldosteronism 11beta hydroxylase deficiency 17alpha hydroxylase deficiency Liddle Syndrome

19. Bartter Bartter's Gitelman's Liddle’s Genetic inheritance AR AR AD Defect LOF variant NKCC2 transporter in ALH LOF variant NCCT transporter in early DCT GOF variant ENaC in CD Age of onset Infancy Early adulthood Childhood Bp Normal/low Normal Raised K+ Decreased Decreased Decreased Mg+ Normal/decreased Decreased Normal Urinary calcium Increased Decreased Normal Aldosterone 2° hyperadlosteronism 2° hyperadlosteronism Normal

20. Urinary Anion Gap The cataions normally present in urine are Na+, K+, NH4, CA++ & Mg Urinary Anion Gap =[Na+]+[K+]- [Cl-] Negative when distal acidification is intact All GI disturbances Proximal RTA Positive when urinary NH4+ excretion impaired Distal RTA Type 4 RTA Renal failure

21. Investigation (cont.): Transtubular potassium gradient  — Another widely used index of urinary potassium excretion is the " transtubular potassium gradient" (TTKG) which is defined as follows:                                     [potassium]urine  ×  serum osmolality                      TTKG  =   -------------------------------------------                                     [potassium]blood  ×  urine osmolality In the absence of renal potassium wasting, the expected value of the TTKG is less than 3 to 4 in the presence of hypokalemia. Values higher than this suggest renal potassium wasting

22. Investigation (cont.): To detect Renal artery stenosis : USG of abdomen for discrepancy in size between the kidneys and renal angiography (CT Or MRI angiography) is confirmatory. Chest X-ray : Mass lesion, pleural effusion and collapse in bronchial carcinoma (Ectopic ACTH Syndrome) and pulmonary edema in renal artery stenosis. Other investigations: CBC, Blood sugar, Urine for Ketones

23. Investigation (continued): Urine chloride: low (<30mmol/L) indicates vomiting high (>40mmol/L) indicates Bartter’s syndrome, Gitelman‘s syndrome and diuretic therapy Urinary calcium: high– Bartter’s syndrome, loop diuretics low– Gitelman’s syndrome, thiazide diuretics Arterial blood gas (ABG) Analysis

24. Investigation (cont.): ECG: Flattened T wave Prominent U wave prolonged PR interval ST depression Ventricular tachycardia Ventricular fibrillation

25. Case -1 50-year-old man with a history of congestive heart failure (CHF) presents to the ED with weakness and palpitations. His medications include furosemide, digoxin, carvedilol, Losartan and atorvastatin. ECG shows paroxysmal atrial tachycardia with 2:1 block, serum K +  is 2.9 mEq / l . How would you manage his hypokalemia?

26. Answer Patient has digoxin toxicity associated with hypokalemia. IV & oral form can be started concomitantly. Digoxin should be hold.

27. Case -2 A 40-year-old man with a known diagnosis of AML was found to have a serum K +  of 1.9 mEq /l on a routine lab. Leukocytes 290 x 10 9 /l. How would you replace his K + ?

28. answer The patient was asymptomatic Pseudohypokalemia due to AML was suspected. A second sample was drawn and placed on ice, then it was immediately analyzed in the lab. K +  in the second sample was 3.7 mEq /l. No action is required.

29. Case -3 A 20-year-old woman presents with weakness and nausea; her BP is 105/55mmhg. Electrolytes: Na +  139, K +  2.7, Cl -  109, HCO 3 -  21 ( mEq /l), Urine electrolytes (in mEq /l): Na +  50, K +   24 , Cl -   83 . Urine anion gap -9.What is the diagnosis.

30. Answer I n this patient,urinary anaion gap is -9 No GI loss.So,this is a case of RTA type 2

31. Case-4 A 26-year-old man presents with a BP of 161/101mmHg. Initial electrolyte panel: Na +  144, K +  3.5, Cl -  109, HCO 3 -  29 ( mEq /l). The patient was started on chlorthalidone 25 mg po daily for HTN. One week later his electrolyte: Na +  139, K +  2.2, Cl -  101, HCO 3 -  32. How would you manage his hypokalemia?

32. Answer Work up for secondary hypertension should be considered in patients who present with hypertension at an early age. This patient developed severe hypokalemia in response to a thiazide diuretic. This is suggestive of primary aldosteronism.

33. Case-5 A 19-year-old woman was brought to the ED by her family due to nausea, proximal muscle weakness and fatigue. Her family is concerned because she has been ingesting a large amount of a clay powder she bought on the internet. She is using it for "detoxification". Labs: Na +  135, K +  2.1, Cl -  105, HCO 3 -  23 ( mEq /l), CK was elevated at 1200 U/l, urine electrolytes: Na +  85, K +  18, Cl -  60 ( mEq /l). How would you manage her hypokalemia ?

34. Answer Her hypokalemia is due to ingestion of Bentonite clay which binds K +  in the GI tract. She has low urine K +  consistent with a non-renal cause of hypokalemia. This patient required oral and intravenous replacement of K +  with instructions to avoid the use of Bentonite .

35. Case 6 A 72- year-old man was admitted to the ICU with type 2 respiratory failure COPD e osteomyelitis and was started on BiPAP non-invasive ventilation, nebulizer & inj Meropenem & inj Vancomycin & Tab Furosemide 80 mg. He has stage 3A CKD. His serum K +  dropped from 4 to 2.4 mEq /l on his 3rd hospital day. What is the etiology of his hypokalemia ?

36. answer Hypokalemia in complicated patients is multifactorial. Salbutamol in his nebulizer therapy will also shift K +  intracellularly. Vancomycin acts as stimulating K +  excretion in the collecting duct . Finally, furosemide will cause renal loss of K + .

37. Case-7 A 25-year-old woman was referred to the ED for persistent hypokalemia. She is complaining of arms and legs cramping, fatigue, urinary frequency and nocturia. BP is 105/50mmHg . Labs: Na +  135mmol/l, K +  2.7mmol/l, HCO 3 -  29( mEq /l), Mg 2+  1 mg/dl , Ca 2+  9 (mg/dl), 24 h urine shows: Na +  130, Cl - 140, K +  45 ( mEq /24 h), Ca 2+  30 mg/24 h. What is the DX??

38. answer The patient has renal loss of K + , hypomagnesemia, metabolic alkalosis, low urine Ca ++ , high urine Na +  and Cl - . All these manifestations can be seen in a patient abusing a thiazide diuretic. This patient denied using any diuretics and her urine screen for diuretics came back negative. The diagnosis is consistent with Gitelman's syndrome.

39. Case- 8 A 16-year-old boy presented to the ED with a 4-day H/O Quadriparesis. O/E BP 150/100 mm Hg . Examination revealed bilaterally reduced ankle, and triceps reflexes; plantar responses were flexor. Lab reports revealed severe hypokalemia (k- 1.7 mmol/L). On further querry he told that last year he had consumed a half bag (25 g) of licorice candy daily.

40. Answer L icorice's active ingredient, glycyrrhizic acid, causes hypokalemia through inhibition of the renal enzyme 11 β-HSD2 which is responsible for conversion of cortisol to inactive cortisone. Diagnosis depends on history and evidence of hypokalemia. Treatment is potassium supplementation and discontinuation of licorice consumption

41. Case -9 A 22y lady came with episodic both lower limb weakness for last 3months.O/E BP 100/70mmHg,muscle power in both lower limb 1/5 & both ankle & knee jerk are diminished. Lab reports reveal- S. K+ 1.6mmo/L, S. Mg 1.9 mg/dl ABG analysis- pH 7.3, HCO3- 21mmol/l. Spot urinary calcium 1.32 mg/dl, Urinary potassium 5mmol/day , Urinary Creatinine 7 mg/dl, 24 hour spot urinary creatinine 14.16mg/dl, 24 urinary Na+ 92mmol/l , K+ 20 mmol/L, Urinary Cl- 98 mmol/l, urinary Mg 0.56 mg/day. How to interpret it??

42. Answer Patient is normotensive & having metabolic acidosis. Spot urine-potassium creatinine ratio 8.11 Urinary anaion gap is 14( 24 urinary electrolyte) So, this is a case of RTA type 1 What is the next plan?

43. Management The indications of urgent therapy include Hypokalemic periodic paralysis, Severe hypokalemia in a patient requiring urgent surgery, Acute myocardial infarction and life-threatening ventricular ectopy.

44. When to admit????? Patient with symptomatic or severe hypokalemia(less than 2.5mEq/L) Cardiac manifestation Cardiac monitoring Potassium supplementation Frequent laboratory testings

45. How to treat First determining the cause and correction where possible Potassium replacement - oral slow release potassium chloride, intravenous potassium chloride The rate of administration depends on severity of hypokalaemia an d the presence of cardiac or neuromuscular complications However should not exceed 10 mmol of potassium per hour .

46. S uppose we get an  asymptomatic patient  of  70 Kg with a serum potassium level of 3.0 mmol/L and he is on nil by mouth but having an adequate diuresis, we proceed this way.  Formula: K+ deficit= ( normal value- patient value of K)× body weight in kg× 0.4 1) Deficit of potassium in mmol = (3.5 - 3.0) x 70 x 0.4 = 14 mmol 2) Daily potassium requirement = 1 x 70 = 70 mmol 3) Total requirement = 14+70 = 84 mmol 

47. Mild (>2.5mmol/L): Oral slow- release potassium chloride 50 – 150mmol/day in divided doses (treatment limited by GI intolerability) Check K + regularly Dietary K + and ? switch to/add in K + - sparing diuretic

48. Severe or symptomatic hypokalaemia (K <2.5mmol/L, arrhythmias, liver failure, or extreme weakness): IVI 0.9% saline 1L with 20 – 40mmol KCl at no more than 10 – 20mmol KCl /h through peripheral cannula In volume- restricted patients or those with profound and ongoing hypokalaemia , KCl can be given into a central vein as 20 – 40mmol/100mL 0.9% saline (NOT glucose, risk of hypokalaemia ) at not >40mmol/h with continuous cardiac monitoring

49. In hyperchloremic acidosis, normal saline should be avoided Glucose containing solution and sodium bicarbonate should be avoided. If Mg depletion is present,replacement of Mg may be required.

50. Potassium sparing diuretics appropriate for the chronic management of hypokalemia in patients who are already on a thiazide or a loop diuretic. Aldosterone receptor antagonists (spironolactone and eplerenone) help in the management of patients with advanced heart failure and in patients with resistant hypertension. Amiloride is well tolerated as well, it blocks the epithelial sodium channel ENaC in the collecting duct.

51. Management : (cont.) Close and continuous monitoring of the serum [K+] and the electrocardiogram are necessary to reduce the risk for potentially lethal acute hyperkalemia. Oral or enteral potassium administration is preferred if the patient can take oral medication and has normal GI tract function. The underlying condition should be treated whenever possible

52. Cause of death Hypokalemia promotes Q-T prolongation & torsades de pointes, which can lead to ventricular fibrillation & sudden cardiac death. Respiratory muscles weakness can lead to respiratory failure & death.

53. When to refer? Patient with unexplained hypokalemia Refractory or persisting hypokalemia Suggestive of alternative diagnosis( eg;aldosteronism or hypokalemic periodic paralysis)

54. Take home message Hypokalemia is common in the inpatient and outpatient settings. Aldosterone is the main potassium regulating hormone. Hypokalemia should be treated orally. Intravenous treatment is reserved for severe hypokalemia (K +  < 3 mEq /l) or emergencies (e.g. arrhythmias). The cause of hypokalemia is usually ascertained by obtaining a careful history, checking BP, and ordering a few laboratory tests. Distinguishing renal loss from GI loss of potassium is essential .

55. Thank You