potassium disorders , comprehensive & practical approach
TRANSCRIPT
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Potassium Disorders
DrYasser Matter
Nephrology and Kidney Transplantation SpecialistUrology and Nephrology center Mansoura
University [email protected]
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Outlines • General principals and physiology.• Hypo & Hyperkalemia : causesManifestations and diagnostic approachManagement • Some updates .
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General principals and physiology
• 1 mmol k+ = 1 meq k+ = 40 mg k+ .• Total body k+ = 50 meq x body weight kg. • 95 - 98% of the body potassium is found
inside the cells. • Normal blood potassium level : 3.5 - 5.0
milimoles/litre( concentration of K is about 150mmol/L of H2O inside the cell).
• Adequate daily intake of k+ in adults :4700mg.
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• The normal ratio between extracellular and intracellular concentrations is important for maintenance of the resting membrane potential and neuromuscular functioning.
• Intracellularly, potassium participates in several vital functions, such as cell growth, maintenance of cell volume, DNA and protein synthesis, enzymatic function and acid-base balance.
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Distribution of total body potassium in organs and body
compartments
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Factors controlling k metabolism
•Factors that shift K+into cells:–Insulin.–Aldosterone.–Epinephrine (through Beta-adrenergic stimulation).–Alkalosis.
•Factors that shift K+out of cells:–Insulin deficiency (diabetes mellitus)–Aldosterone deficiency (Addisons disease)–Beta-adrenergic blockade–Acidosis–Cell lysis
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Cellular Potassium Shifts
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Aldosterone stimulates K secretion
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Transtubular Potassium Gradient TTKG (normally 6-12 )
• TTKG is indirect indicator of aldosterone activity .• TTKG = (UrineK / SerumK) * (UrineOsm / SerumOsm).
Hypokalemia from extrarenal causes
results in renal potassium conservation and a TTKG less than 2. A higher value suggests renal potassium losses,
as through hyperaldosteronism
The expected TTKG during hyperkalemia is
greater than 10.An inappropriately low TTKG in a hyperkalemic
patient suggests hypoaldosteronism or a
renal tubule defect.
After 0.05 mg 9α-fludrocortisone>10 ----- Hypoaldosteronism is likely.No change -------Suggests a renal tubule defect
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Potassium and food
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Amphotericin B
B agonists ; B12 ; Penicillin
Carbenoxolone ; CS.
Diuretics
Exogenous insulin
Folic acid
G-csf
A nti-inflamm.non-steroidals
B blockers ; blockers of RAAS
CNI; co-trimoxazole
DIuretics: k+ sparing
EPleronone(&spironolactone);EPO
Fluconazole
G Anaesthetic:succinyl choline
Heparins ; herbs
Potassium and drugs
hyperkalaemiahypokalaemia
Hormones: epinephrine
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HYPOKALEMIA
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Hypokalemia (K level < 3.5 mmol/L)
causes
• Pseudohypokalemia• Redistribution • Intake • Loss (renal & non renal)• Hyperaldosteronism• Drugs
The most common cause is acute leukemia; the large numbers of abnormal leukocytes take up potassium when the blood is stored in a collectionvial for prolonged periods at room temperature. Rapid separation of plasma and storage at 4° C is used to avoid Pseudohypokalemia.
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Manifestations
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Hypokalemia ECG changes
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Treatment of Hypokalemia
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• Every 1mmEq/ L [K+] depletion = 10 % Reduction of total body K+store.
• [Total body K+content = 50mEq/ KG]• For a 60 kg person, total body K+store = 60 x 50=
3000 mEq. Therefore, 1 mEq/ L [K+] depletion = 3000 x 10% = 300 mEq. = Total K+ deficit.
• Oral or enteral administration is preferred if the patient can take oral medication and has normal GI tract function. Acute hyperkalemia is highly unusual when potassium is given orally.
• parenteral KCl should be administered in dextrose-free solutions.
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Indications for IV potassium• Hypokalemic periodic paralysis.• Severe hypokalemia in a patient requiring urgent
surgery.• Acute myocardial infarction and significant
ventricular ectopy.• Severe diarrhea.• Severe myopathy with muscle necrosis.
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K supplement in the market
• 1 bottle ringer 2 meq• 1 bottle kadlax 13.5 meq• 1 amp KCL 10 meq• 1 tab slow k 7.5 meq• 5 ml of potassium syrup 4 meq
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Hyperkalemia
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Hyperkalemia (K level >5.0 mmol/L)
Ranges are as follows: 5.5 – 6 mEq/L - Mild condition . 6 - 6.5 mEq/L - Moderate condition. 6.5 mEq/L and greater - Severe
condition.
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causes• Pseudohyperk
alemia• Redistribution • Intake • Renal retension• Hypoaldosteronism• Drugs
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Pseudohyperkalemia
Causes Sever Leukocytosis Sever Thrombocytosis Hemolysis :Ischemia from prolonged tourniquet timeIN patients with RA or IMN or abnormalRBC membrane potassium permeability (IVH)
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Pseudohyperkalemia• There is raised serum (clotted blood) potassium concentration with concurrently normal plasma (non-clotted blood) potassium concentration
• It is the clotting process with subsequent release of potassium from cells and platelets that causes an increase in the serum potassium concentration by an average of 0.4 mmol/L.
• Pseudo-hyperkalaemia can be excluded by performing simultaneous measurements of plasma potassium in a lithium heparin anti-coagulated specimen and in a clotted sample.
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Pseudohyperkalemia
• This will provide two values with the lower being in the heparinised specimen.
• Pseudo-hyperkalaemia is detected when the serum potassium concentration exceeds that of the plasma by more than 0.4 mmol/L.• The difference in results may be in the order of
several mmol/L. A full blood count should also be performed to exclude a haematological disorder.
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PseudohyperkalemiaTechnique of blood drawing• Mechanical trauma during venipuncture can result
in the release of potassium from red cells and a characteristic reddish tint of the serum due to the concomitant release of hemoglobin.
• Potassium moves out of muscle cells with exercise. repeated fist clenching during blood drawing can acutely raise the serum potassium concentration by more than 1 to 2 meq/L in that forearm
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Pseudohyperkalemia• venipuncture without a tourniquet, repeated
fist clenching, or trauma will demonstrate the true serum potassium concentration.
• If a tourniquet is required, the tourniquet should be released after the needle has entered the vein, followed by waiting for one to two minutes before drawing the blood sample.
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Manifestations
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Hyperkalemia ECG changes
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ECG in a patient with severe hyperkalaemia (serum K+ 9.1 mmol/L) illustrating peaked T waves (a), diminished P waves (b) and wide QRS complexes (c).
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Treatment of Hyperkalemia
AVOID POTASSIUM
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There are five key steps in the treatment of hyperkalaemia (never walk away without completing all of these steps).
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STEP 1 -Protect the heart; intravenous calcium salts
• We recommend that intravenous calcium chloride or calcium gluconate, at an equivalent dose (6.8mmol), is given to patients with hyperkalaemia in the presence of ECG evidence of hyperkalaemia. (1A)
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• ca chloride salt has been recommended in the setting of haemodynamic instability, including cardiac arrest , because the active calcium is released immediately on infusion, unlike calcium gluconate, which requires liver metabolism to release the calcium.
• IV calcium antagonises the cardiac membrane excitability thereby protecting the heart against arrhythmias .
• It is effective within 3 minutes as shown by an improvement in the ECG appearance (e.g. narrowing of the QRS complex). The dose should be repeated if there is no effect within 5-10 minutes.
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ECG on admission (a) and following 30ml 10% calcium gluconate IV (b) patient with serum K+ 9.3 mmol/L
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STEP 2 – Shift K+ into cells
• Insulin-glucose infusion
• B2 agonist
• Sodium bicarbonate
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Insulin-glucose infusion &salbutamol
• We recommend that insulin-glucose (10 units soluble insulin in 25g glucose) by intravenous infusion is used to treat severe (K+ ≥ 6.5 mmol/L) hyperkalaemia. (1B)
• We recommend nebulised salbutamol 10-20mg is used as adjuvant therapy for severe (K+ ≥ 6.5 mmol/L) hyperkalaemia. (1B)
• We recommend that salbutamol is not used as monotherapy in the treatment of severe hyperkalaemia. (1A)
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• The efficacy of insulin-glucose is increased if given in combination with salbutamol. The peak K+ lowering effect with combination therapy at 60 minutes was found to be 1.2 mmol/L with nebulised beta-agonist therapy.
• Up to 40% of patients with ESRD do not respond to salbutamol, even in the absence of beta-blocker therapy, and the mechanism for this resistance is unknown.
• A frequent mistake when administering nebulizedβ2-adrenoceptor agonists is underdosage (salbutamol 10-20mg )
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1 ml farcolin 6 mg salbutamol
So , at least 2 ml farcolin should be used
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Sodium bicarbonate
• We suggest that intravenous sodium bicarbonate infusion is not used routinely for the acute treatment of hyperkalaemia. (2C)
• Do not use(NaHCO3) therapy unless the patient is frankly acidotic (pH <7.2) or unless substantial endogenous renal function is present.
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STEP 3 – Remove K+ from body, resins (30-60 gm )
• We suggest that cation-exchange resins are not used in the emergency management of severe hyperkalaemia, but may be considered in patients with mild to moderate hyperkalaemia. (2B)
• multiple doses were required over several days with the effect on lowering the serum K+ noted over 1 to 5 days.
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• These resins exchange sodium(Kayexalate) or calcium(resonium), respectively, for potassium in the GI tract to remove K . It can be administered orally or rectally as a retention enema.
• Constipation is common; therefore, resins are usually given in combination with a cathartic, (20% sorbitol).
• If given as an enema, sorbitol should be avoided, because rectal administration of cation exchange resins with sorbitol can cause colonic perforation
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STEP 3 – Remove K+ from body, Hemodialysis
• Acute hemodialysis is the primary method of potassium removal when renal function is significantly impaired, either from AKI or advanced CKD, and severe hyperkalemia.
• Serum potassium can decrease as much as 1.2 to 1.5 mmol/h.
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STEP 4 - Blood monitoring; serum K+
• We recommend that the serum K+ is monitored closely in all patients with hyperkalaemia to assess efficacy of treatment and look for rebound hyperkalaemia. (1B)
• We suggest that serum potassium be assessed at least 1, 2, 4, 6 and 24 hours after identification and treatment of hyperkalaemia. (2C)
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STEP 4 - Blood monitoring; blood glucose
• We recommend that the blood glucose concentration is monitored at regular intervals (0, 15, 30, 60, 90, 120, 180, 240, 300, 360 minutes) for a minimum of 6 hours after administration of insulin-glucose infusion in all patients with hyperkalaemia. (1C)
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Some Updates
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Zirconium cyclosilicate(ZS-9)• ZS-9 exchanges both sodium and hydrogen
ions for potassium at intestine in CKD patients.
• Dose : 10- 15 gm Once daily.• S/E : no serious se reported but edema may
occur.• Neither trial evaluated the long-term
efficacy and safety of ZS-9, and neither studied patients with acute hyperkalemia or ESRD.
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Patiromer• FDA approved October 2015and will be available
at January 2016• Patiromer binds potassium in the colon in
exchange for calcium in CKD patients.• Dose : 8.4 g once daily (maximum dose: 25.2 g/day).• S/E : Constipation (the commonest ),
Hypomagnesemia (Patiromer binds to magnesium in the colon)
• The effect of Patiromer in patients with acute hyperkalemia or ESRD was not evaluated
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References
• Potassium and its disorders. Presentation of Prof. Essam Nour Eldin at acid base and electrolytes disturbance conference ,Cairo, October ,2014 .
• ANDREOLI AND CARPENTER ’ S CECIL ESSENTIALS OF MEDICINE , 8th edition,2010.
• COMPREHENSIVE CLINICAL NEPHROLOGY , 5th edition ,2015.
• Davidsons Principles and Practice of Medicine ,22nd edition ,2014.
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References
• Uptodate , 2016.• CLINICAL PRACTICE GUIDELINES , TREATMENT OF
ACUTE HYPERKALAEMIA IN ADULTS , UK Renal Association ,2014 .