assessment of Serum potassium levels. Description of pseudohyperkalemia and reverse pseudohyperkalemia. Causes of hyperkalemia. Clinical manifestation of hypokalemia and hyperkalemia.
Why serum has higher potassium content than plasma? Best container for serum potassium? Sample of choice for potassium? Preservative used for urinary potassium? Important Facts About Potassium
Is little affected by alteration of water balance A poor guide of total body K+ content Doesn’t change unless there is 10% alteration of body K+ content Role in body Maintains Oncotic Pressure & intracellular volume Resting Membrane, Acting membrane Potential & neuromuscular function → Tissue excitability Cardiac impulse Acid base balance Helps in NA/protein synthesis Facilitates cell growth Important Facts About Potassium
Hypokalemia Rule out Pre analytical error Sample dilution (all parameters will be low) Electrolytes exclusion effect (electrolytes will be low with indirect ISE) Causes of Hypokalemia Decrease dietary potassium (chronic starvation) Redistribution of potassium in body compartments True potassium deficit
Insulin therapy Insulin → express GLUT-4 channels on cells (muscles/adipose tissue/RBCs) →GLUT-4 channel Cotransport Glucose/K+ into the cells →shift of serum potassium into cells → Hypokalemia Alkalosis ↓ H+ in plasma → to compensation H+ comes out of cells (mainly RBCs) into plasma →K+ moves inside cells to keep electrochemical gradient constant → hypokalemia ↓ H+ in plasma → DCT (kidney) conserve H+ by decreasing its excretion →to keep electrochemical gradient K+ is secretion into lumen → ↑K+ excretion →hypokalemia Redistribution of potassium in body compartments
↑ Catecholamine activity Beta 2 receptor stimulation → dose dependent activation of Na/K ATPase pump Hypothermia Increase activity of Na/K ATPase pump in induction phase Refeeding syndrome Hypokalemia (weakness), hypophosphatemia (hypotension, fits) and hypomagnesemia (hypocalcemia, GI symptoms) after initiation of feeding in malnourished patients is called refeeding syndrome Already deficiency of nutrients → Refeeding → ↑glucose in blood → release of insulin → movement of K+, Mg+2 and PO-3 into cells along with glucose Redistribution of potassium in body compartments
Periodic hypokalemic paralysis Familial hypokalemic periodic paralysis Gene mutation →mutated Kir 2.6 potassium channel in skeletal muscles →increase K+ influx → altered muscle membrane excitability →paralysis Thyrotoxic hypokalemic periodic paralysis Kir 2.2 transcription is regulated by thyroid hormone →increase thyroid hormone → increase K+ influx → altered muscle membrane excitability →paralysis Redistribution of potassium in body compartments
Loss of potassium from body →↓ Total body Potassium K+ loss through kidneys K+ loss through extra renal source 24 Hours Urinary K + < 25 mmol/day → Extrarenal loss of K + True Potassium Deficit Through Gut Through Skin Diarrhoea Excessive sweating Fistula (involving gut) Burns Ileostomy
24 Hours Urinary K+ > 25 mmol/day → Renal loss of K+ True Potassium Deficit Defective renal tubules Drugs ↑ Mineralocorticoid effect Compensatory RTA (Type I/II) Thiazide Primary hyperaldosteronism Metabolic Alkalosis ATN (Diuretic phase) Loop diuretics Secondary hyperaldosteronism NG suction Vomiting Amphotericicn B Excess of Glucocorticoids Hypomagnessemia Penicillin AME
24 hrs urinary K+ Renal >25 mmol/L Extra renal <25 mmol/L ABGs Metabolic Alkalosis Metabolic Acidosis Normal RTA Type I/II 24 hrs urinary Cl - >10 mmol/L < 10 mmol/L ↑Aldosterone ↑Glucocorticoid Vomiting NG suction Diuretics Penicillin ATN Amphotericin B
Hyperkalemia →5.1 mmol/L Severe hyperkalemia → > 7.0 mmol/L Fatal hyperkalemia → > 10 mmol/L Rule out Pre analytical error Pseudohyperkalemia Traumatic venipuncture Prolonged tourniquet K+ - EDTA contamination Hemolytic sample Vigorous shake during transport Prolonged handling time Improper storage Hyperkalemia
Reverse pseudohyperkalemia Leukemia (>100000/uL) In vitro phenomenon in which plasma potassium concentration rises higher than serum potassium concentration, usually due to extreme leukocytosis Increase iron stores Leukemic leukocytes are more fragile than normal leukocytes, leading to in vitro lysis during centrifugation of plasma specimens and elevating potassium concentrations. In serum specimens, the formation of a fibrin clot is hypothesized to entrap and stabilize tumor cells during centrifugation. Whole blood can be used as an alternative specimen in cases of reverse pseudohyperkalemia Leukocytosis has higher energy consumption leading impaired Na/K ATPase pump Increase sensitivity to heparin induced membrane damage in haematological malignancies Hyperkalemia
Hyperkalemia Pseudohyperkalemia →False ↑ in serum K+ in comparison to the normal plasma levels Pseudohyperkalemia →False ↑ in plasma K+ in comparison to the normal serum levels What is the difference between pseudohyperkalemia and reverse pseudohyperkalemia ? Aldosterone escape phenomenon and lack of edema: Potassium-wasting effect of excess aldosterone is counterbalanced by the potassium-retaining effect of hypokalemia itself
Causes of Hyperkalemia Redistribution Acidosis ( compensatory ) Drugs Beta blocker Digoxin ↓ Insulin (type 1 DM with severe insulin deficiency) Release from ICF Hemolytic anemia Tissue hypoxia Rhabdomyolysis Heavy exercise Status epilepticus Severe burn
Causes of Hyperkalemia 2. True potassium gain Normal kidneys are able to handle potassium load. When kidneys are able to excrete out extra K+ look for underlying renal disease Increase potassium intake (supplementation with compromised renal function) Massive transfusion Hemolytic transfusion reaction