Hyperkalemia Clinical Presentation
- Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
Many individuals with hyperkalemia are asymptomatic. When present, the symptoms of hyperkalemia are nonspecific and predominantly related to muscular or cardiac function. The most common complaints are weakness and fatigue. Occasionally, a patient may complain of frank muscle paralysis or shortness of breath. Patients also may complain of palpitations or chest pain. Patients may report nausea, vomiting, and paresthesias. The history is most valuable in identifying conditions that may predispose to hyperkalemia.
When hyperkalemia is discovered, investigate potential pathophysiologic mechanisms. For excessive potassium intake, query patients about the following:
Eating disorders - Very unusual diets consisting almost exclusively of high-potassium foods, such as fruits (eg, bananas, oranges, or melons), dried fruits, raisins, fruit juices, nuts, and vegetables with little to no sodium
Heart-healthy diets - Very low–sodium and high-potassium diets recommended for patients with cardiac disease, hypertension, and diabetes mellitus
Use of potassium supplements in over-the-counter herbal supplements, sports drinks, dietary supplements such as noni ( Morinda citrifolia) juice, salt substitutes, or prescribed pharmacologic agents
Many patients with hypertension have heard the advice to eat a banana a day because the potassium in it reduces blood pressure. They may not realize that in the case of renal insufficiency and hypertension, this is potentially a life-threatening practice.
With hospitalized patients, review the medication list for potassium supplements or high-dose penicillin G potassium, and review the chart to determine whether the patient has received transfusions. With patients who have undergone cardiac surgery, consider the possibility of residual effects of cardioplegic solutions.
For decreased potassium excretion, query patients regarding a history of renal insufficiency or renal failure. In addition, elicit any history of diabetes mellitus, sickle cell disease or trait, or symptoms of lower urinary tract obstruction. These conditions predispose people to type IV renal tubular acidosis, also called hyperkalemic renal tubular acidosis. Type IV renal tubular acidosis also may accompany other tubulointerstitial disorders, such as polycystic kidney disease or amyloidosis.
Patients with ureteral diversion into the ileum can develop hyperkalemia due to reabsorption of secreted potassium.
Ask about the use of medications that impair renal potassium excretion, as follows:
Potassium-sparing diuretics, which are especially popular in the treatment of cirrhosis and chronic heart failure
Nonsteroidal anti-inflammatory drugs (NSAIDs) 
Angiotensin-converting enzyme (ACE) inhibitors
The combination of spironolactone and ACE inhibitors 
Angiotensin-receptor blockers (ARBs)
Direct renin inhibitors (eg, aliskiren)
Cyclosporine or tacrolimus
Antibiotics (eg, pentamidine and trimethoprim-sulfamethoxazole) 
Epsilon-aminocaproic acid (EACA) 
Oral contraceptive agents, such as drosperinone
For a shift of potassium into the extracellular space, query patients about the following:
Recurrent episodes of flaccid paralysis
Presence of diabetes mellitus
Use of beta-blocker therapy (eg, for hypertension or angina)
Risk factors for rhabdomyolysis, such as heat stroke, chronic alcoholism, seizures, sudden excessive exertion (as in military recruits undergoing basic training), or use of medications that interfere with heat dissipation (eg, tricyclic antidepressants or anesthesia)
Risk factors for tumor lysis syndrome, such as ongoing treatment for widespread lymphoma, leukemia, or other large tumors
Risk factors for hemolysis, such as blood transfusion and sickle cell disease
Redistribution - Metabolic acidosis (diabetic ketoacidosis [DKA]) and catabolic states
In a previously well child with acute hyperkalemia, the history should focus on the following:
How the blood sample was obtained
Potassium intake or recent blood product transfusion
Risk factors for transcellular shift of potassium (acidosis) or tissue death or necrosis
Use of medication associated with hyperkalemia (by the child, other family members, pets, or household visitors)
Presence or signs of renal insufficiency
Specific questions may be focused on the following:
Urine output (last void or number of wet diapers) and fluid intake
Cola-colored urine (which may indicate acute glomerulonephritis)
Bloody stool (which may indicate hemolytic-uremic syndrome [HUS])
Drugs present in the household (or used by recent visitors), such as potassium preparations, digoxin, and diuretics
Any history of trauma (crush injuries) or thermal injury (burns)
Medical history, family history, and review of systems should be explored for any of the following:
Acute kidney injury or chronic kidney disease
Malignancy (tumor lysis syndrome)
The family history should include questions about the following:
Hyperkalemic periodic paralysis
Deaths of very young siblings
In patients with hyperkalemia, vital signs generally are normal. Nonspecific findings can include muscle weakness, fatigue, and depression. Occasionally, cardiac examination may reveal extrasystoles, pauses, or bradycardia resulting from heart block or tachypnea resulting from respiratory muscle weakness. Skeletal muscle weakness and flaccid paralysis may be present, along with depressed or absent deep tendon reflexes. Patients with ileus may have hypoactive or absent bowel sounds.
In general, the results of the physical examination alone do not alert the physician to the diagnosis, except when severe bradycardia is present or muscle tenderness accompanies muscle weakness, suggesting rhabdomyolysis. However, when hyperkalemia has been recognized, evaluation of vital signs is essential for determining hemodynamic stability and identifying the presence of cardiac arrhythmias related to the hyperkalemia.
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|Factor||Effect on Plasma K+||Mechanism|
|Aldosterone||Decrease||Increases sodium resorption, and increases K+ excretion|
|Insulin||Decrease||Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process)|
|Beta-adrenergic agents||Decrease||Increases skeletal muscle uptake of K+|
|Alpha-adrenergic agents||Increase||Impairs cellular K+ uptake|
|Acidosis (decreased pH)||Increase||Impairs cellular K+ uptake|
|Alkalosis (increased pH)||Decrease||Enhances cellular K+ uptake|
|Cell damage||Increase||Intracellular K+ release|
|Succinylcholine||Increase||Cell membrane depolarization|