Hyperkalemia resident survival guide: Difference between revisions
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{{familytree | | | | | | | | G01 | | | | | | | | | | | | | |G01=D/C any offending medications that is associated with [[hyperkalemia]]<br><br>D/C oral or parenteral potassium<br><br>Correct [[acidosis]] with bicarb if [[pH]]<7.2<br><br>Restrict dietary potassium intake<br><br>Review potassium levels every 2-4 hours until stabilized<br><br>Check levels of other [[electrolyte|electrolytes]] such as [[magnesium]] and [[phosphorus]]}} | {{familytree | | | | | | | | G01 | | | | | | | | | | | | | |G01=D/C any offending medications that is associated with [[hyperkalemia]]<br><br>D/C oral or parenteral potassium<br><br>Correct [[acidosis]] with bicarb if [[pH]]<7.2<br><br>Restrict dietary potassium intake<br><br>Review potassium levels every 2-4 hours until stabilized<br><br>Check levels of other [[electrolyte|electrolytes]] such as [[magnesium]] and [[phosphorus]]}} | ||
{{familytree/end}} | {{familytree/end}} | ||
Diagnostic criteria | |||
{{Family tree/start}} | |||
{{Family tree | | | | | | | | | | | | | | A01 | | | | | | | | | | | |A01=Potassium >5.1meq/L}} | |||
{{Family tree | | | | | | | | | | | | | | |!| | | | | | | | | | | | }} | |||
{{Family tree | | | | | | | | | | | | | | B01 | | | | | | | | | | | B01= ECG }} | |||
{{Family tree | | | | | | | | | | | | |,|-|^|-|.| | | | | | | | | | }} | |||
{{Family tree | | | | | | | | | | | | C01 | | C02 | | | | | | | | | C01=If no changes,rule out [[pseudohyperkalemia]]| C02= If changes present then start urgent treatment}} | |||
{{Family tree | | | | | | | |,|-|-|-|-|^|-|-|-|-|.| | | | | | | | |}} | |||
{{Family tree | | | | | | | D01 | | | | | | | D02 |D01=Urine sodium <25 meq/L|D02=urine sodium >25 meq/L }} | |||
{{Family tree | | | | | | | |!| | | |,|-|-|-|-|^|-|-|-|-|.| | | | | }} | |||
{{Family tree | | | | | | | E01 | | E02 | | | | | | | | E03 | | | | | | | E01=ARF<br>CKD<br>[[Heart failure]],<br>Volume depletion|E02=Decreased K+secretion(Urine K+<20meq/L|E03=Transcellular shift(measure serum osmolarity and pH) }} | |||
{{familytree | | | | | | |,|-|-|-|-|^|-|-|.| | | | | | |!| | | | | | | | }} | |||
{{Family tree | | | | | | F01 | | | | | | F02 | | | | | F03 | | | | | | F01=Low [[aldosterone]](TTG<3)|F02=Normal aldosterone(TTG>7)|F03=[[Diabetic ketoacidosis]],<br>Metabolic [[acidosis]]}} | |||
{{Family tree | | | | |,|-|^|-|.| | | | | |!| | | | | | | | | | | }} | |||
{{Family tree | | | | G01 | | G02 | | | | G03 | | | | | | | | | | G01=Low [[renin]]|G02=Normal renin|G03=Tissue breakdown,<br>[[Pseudohypoaldosternism]] type 1 and type 2,<br>Type 1 [[RTA]] }} | |||
{{Family tree | | | | |!| | | |!| | | | | | | | | | | | }} | |||
{{Family tree | | | | H01 | | H02 | | | | | | | | | H01=[[Interstital nephritis]],<br>[[Obstructive uropathies]],<br>[[Diabetic nephropathy]],<br>[[ACE inhibitors]],Angiotensin 2 receptors|H02=Primary [[hypoaldosteronism]],<br>[[Congenital adrenal hyperplasia]],<br>Aldosterone receptor antagonists,<br>RTA type 4 | |||
}} | |||
{{familytree/end}} | |||
==Do's== | ==Do's== |
Revision as of 19:37, 31 July 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]; Mahmoud Sakr, M.D. [3]
Overview
Hyperkalemia is defined as a serum potassium concentration greater than 5.5 mEq/L in adults. Levels higher than 7 mEq/L can lead to significant hemodynamic compromise.
Causes
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Acute renal failure
- Adrenal insufficiency
- Diabetic ketoacidosis
- Large IV doses of calcium chloride or calcium gluconate
- Massive hemolysis
- Metabolic acidosis
- Rapid tissue necrosis
- Rhabdomyolysis
- Tumor lysis syndrome
Common Causes
- Adrenal insufficiency
- Blood transfusion
- Diabetic ketoacidosis
- Potassium supplementation (oral or IV)
- Potassium rich diet
- Medications: ACE inhibitors, angiotensin receptor blockers, amiloride, spironolactone, NSAIDS, ciclosporin, tacrolimus, trimethoprim, pentamidine, succinylcholine
- Pseudohyperkalemia
- Renal insufficiency
- Renal tubular acidosis type 4
Management
Shown below is an algorithm summarizing the approach to hyperkalemia.[1][2][3]
Potassium > 5.5 mEq/L | |||||||||||||||||||||||||||||||||||||||||||||||||||
If repeated potassium level is normal, check potassium level in 24 hours | R/O Pseudohyperkalemia (Artifact, hemolysis, elevated WBC, elevated RBC, elevated platelets) Repeat potassium level | ||||||||||||||||||||||||||||||||||||||||||||||||||
Check vital signs ABC's Order an EKG Obtain a concise history and physical exam Order BUN, creatinine, glucose, ABG | |||||||||||||||||||||||||||||||||||||||||||||||||||
Assess EKG | |||||||||||||||||||||||||||||||||||||||||||||||||||
Presence of EKG changes Loss of P waves, peaked T waves and wide QRS | Absence of EKG changes and Hemodynamically stable patient | ||||||||||||||||||||||||||||||||||||||||||||||||||
Do the following steps simultaneously: 1. Myocardial stabilization IV Ca gluconate (1-2 amps) Contraindicated in digoxin toxicity and hypercalcemia 2. Shift potassium from blood into cells Insulin (0.2 units for every gram of glucose administered) and 20% dextrose ( 2.5-5 ml/kg/h) (D50 1 ampule/10unit insulin) Glucose level monitoring is needed Beta2 agonists (albuterol is given 10-20mg via nebulizer or 0.5 mg IV) 3. Lower total body potassium Cation exchange resin (kayexalate 30-90g given P.O. or P.R.) Loop diuretics (furosemide 1-2 mg/kg) Hemodialysis if refractory | |||||||||||||||||||||||||||||||||||||||||||||||||||
Potassium > 6 mEq/L | 5.5mEq/L<Potassium<6mEq/L | ||||||||||||||||||||||||||||||||||||||||||||||||||
Do the following steps simultaneously: 1. Monitor for cardiac arrhythmia Place the patient on a closely monitored bed for potential arrhythmias 2. Shift potassium from blood into cells Insulin (0.2 units for every gram of glucose administered) and 20%dextrose ( 2.5-5 ml/kg/h) Glucose level monitoring is needed Beta2 agonists (albuterol is given 10-20mg via nebulizer or 0.5 mg IV) 3. Lower total body potassium Cation exchange resin (kayexalate 30-90g given P.O. or P.R. Loop diuretics (furosemide 1-2 mg/kg) Hemodialysis if refractory | Lower total body potassium Cation exchange resin (kayexalate 30-90g given P.O. or P.R.) Loop diuretics (furosemide 1-2 mg/kg) | ||||||||||||||||||||||||||||||||||||||||||||||||||
D/C any offending medications that is associated with hyperkalemia D/C oral or parenteral potassium Correct acidosis with bicarb if pH<7.2 Restrict dietary potassium intake Review potassium levels every 2-4 hours until stabilized Check levels of other electrolytes such as magnesium and phosphorus | |||||||||||||||||||||||||||||||||||||||||||||||||||
Diagnostic criteria
Potassium >5.1meq/L | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
ECG | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
If no changes,rule out pseudohyperkalemia | If changes present then start urgent treatment | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Urine sodium <25 meq/L | urine sodium >25 meq/L | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
ARF CKD Heart failure, Volume depletion | Decreased K+secretion(Urine K+<20meq/L | Transcellular shift(measure serum osmolarity and pH) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Low aldosterone(TTG<3) | Normal aldosterone(TTG>7) | Diabetic ketoacidosis, Metabolic acidosis | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Low renin | Normal renin | Tissue breakdown, Pseudohypoaldosternism type 1 and type 2, Type 1 RTA | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Interstital nephritis, Obstructive uropathies, Diabetic nephropathy, ACE inhibitors,Angiotensin 2 receptors | Primary hypoaldosteronism, Congenital adrenal hyperplasia, Aldosterone receptor antagonists, RTA type 4 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Do's
1) Calcium, insulin with glucose, beta-2-adrenergic agonists, and sodium bicarbonate (in certain group of patients) can rapidly decrease the serum potassium levels. These should be the first line in patients with hyperkalemia related electrocardiographic changes, potassium levels > 6.5, and rapidly increasing less severe hyperkalemia.
2) Cation exchange resins are effective in lowering the serum potassium after multiple doses and are not effective immediately. Thus, they should always be combined with rapidly acting agents when used. They can produce severe side effects like intestinal necrosis.
References
- ↑ Lehnhardt A, Kemper MJ (2011). "Pathogenesis, diagnosis and management of hyperkalemia". Pediatr Nephrol. 26 (3): 377–84. doi:10.1007/s00467-010-1699-3. PMC 3061004. PMID 21181208.
- ↑ Ahee P. The management of hyperkalaemia in the emergency department. J Accid Emerg Med 2000;17:188-191 doi:10.1136/emj.17.3.18
- ↑ Weisberg L. Management of severe hyperkalemia. Crit Care Med 2008 Vol. 36, No. 12.
References