Hyperkalemia resident survival guide: Difference between revisions
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{{familytree | | | C01 | | | | | | | | | | | C02 |C01=EKG changes;e.g. hyperacute T waves, widened QRS,|C02=EKG not changed}} | {{familytree | | | C01 | | | | | | | | | | | C02 |C01=EKG changes;e.g. hyperacute T waves, widened QRS,|C02=EKG not changed}} | ||
{{familytree | | | |!| | | | | | | | | | | | |!| }} | {{familytree | | | |!| | | | | | | | | | | | |!| }} | ||
{{familytree | |,|-|^|-|-|-| | {{familytree | |,|-|^|-|-|,|-|-|-|.| | | | | D01 |D01=order Kayexalate}} | ||
{{familytree | E01 | | | E02 | | | | | | | | |!| | | |E01='''STEMI'''<br>Revascularization|E02='''NSTEMI'''<br>Risk stratification}} | {{familytree | E01 | | | E02 | | E03 | | | | | | |!| | | |E01='''STEMI'''<br>Revascularization|E02='''NSTEMI'''<br>Risk stratification}} | ||
{{familytree | | | | | | | | | | |,|-|-|-|-|-|+|-|-|-|-|-|.|}} | {{familytree | | | | | | | | | | |,|-|-|-|-|-|+|-|-|-|-|-|.|}} | ||
{{familytree | | | | | | | | | | F01 | | | | F02 | | | | F03 |F01='''Pneumothorax'''|F02='''Aortic dissection'''|F03=No significant findings on CXR}} | {{familytree | | | | | | | | | | F01 | | | | F02 | | | | F03 |F01='''Pneumothorax'''|F02='''Aortic dissection'''|F03=No significant findings on CXR}} |
Revision as of 20:47, 19 July 2013
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; associate editor-in-chief: Mahmoud Sakr, M.D. [2]
Definition
Hyperkalemia is best 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
Immediate life-threatening causes are conditions which result in immediate death or disability if left untreated.
- Acute Renal Failure
- Rhabdomyolysis
- Rapid tissue necrosis
- Tumor Lysis syndrome
- Metabolic acidosis, diabetic ketoacidosis
- Massive hemolysis
- large IV doses of Calcium chloride or calcium gluconate
- Adrenal insufficiency
Common Causes
- Pseudoyperkalemia
- Renal insufficiency
- Adrenal insufficiency
- Medications; ACE inhibitors, Angiotensin receptor blockers, amiloride,spironolactone, NSAIDS, ciclosporin, Tacrolimus, Trimethoprim, Pentamidine
- Renal tubular acidosis
- Iatrogenic
Management
Please find below an algorithm that summarizes the approach to hyperkalemia
Check vital signs Stabilize the patient Order an EKG Concise history and physical exam | |||||||||||||||||||||||||||||||||||||||||||||||||||
Assess EKG | |||||||||||||||||||||||||||||||||||||||||||||||||||
EKG changes;e.g. hyperacute T waves, widened QRS, | EKG not changed | ||||||||||||||||||||||||||||||||||||||||||||||||||
order Kayexalate | |||||||||||||||||||||||||||||||||||||||||||||||||||
STEMI Revascularization | NSTEMI Risk stratification | {{{ E03 }}} | |||||||||||||||||||||||||||||||||||||||||||||||||
Pneumothorax | Aortic dissection | No significant findings on CXR | |||||||||||||||||||||||||||||||||||||||||||||||||
Control BP Obtain a CT scan Emergent surgery consult | Assess the pretest probability forpulmonary embolism | ||||||||||||||||||||||||||||||||||||||||||||||||||