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Elevated Potassium - Hyperkalemia

Hyperkalemia, elevated serum potassium and the current approach to the diagnosis and treatment of potassium disorders.


by Kruti Vora, MD, M.C.A. Butman and M.P. Butman, MD


“Hyperkalemia” refers to an elevated serum potassium level. In most cases, this occurs when the kidneys are unable to excrete potassium and is usually due to diseases that damage the kidneys, disorders that affect their ability to excrete potassium, diseases that raise potassium levels independent of any problem with the kidneys, or a combination of the aforementioned. The most common causes of chronic kidney damage is diabetes and hypertension. Kidney damage may also occur acutely from dehydration, hypotension, kidney stones, iodinated contrast used in imaging, and the adverse effects of a myriad of medications including antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin converting enzyme inhibitors, angiotensin II blockers, immunotherapeutic agents, chemotherapy, IVIG, and antiretroviral therapy.


Disorders that raise potassium levels in a setting of normal kidney function include abnormalities of the adrenal glands (e.g. Addison’s disease/adrenal insufficiency,acquired hyporeninemic hypoaldosteronism, congenital adrenal hyperplasia), hemolysis, tumor lysis, constipation, and metabolic acidosis.


Factitious Hyperkalemia

A serum potassium level that is falsely elevated is known as factitious hyperkalemia or pseudohyperkalemia. This may occur when red blood cells within a sample of blood are damaged (hemolysis). The hemolyzed cells release potassium and artifactually elevate the serum potassium concentration in a sample, even though total body potassium may be normal or low. Hemolysis may occur at any point during the collection, transportation, handling, storage, or processing of a blood sample. If hemolysis occurs, the lab should be able to detect and report it, and the blood sample may need to be repeated.

Pseudohyperkalemia also may occur in patients with high platelet counts (thrombocytosis), leukocytosis or cancers of the white blood cells due to the fragility of the cellular membrane. or the genetic condition familial pseudohyperkalemia (no hemolysis, but a genetically leaky cell membrane). It also is seen in individuals who have had splenectomies, which can cause a secondary thrombocytosis.

If factitious hyperkalemia is suspected it is recommended to repeat the serum potassium level and also perform a plasma potassium level (drawn into a tube that contains either heparin, EDTA or citrate). Serum potassium is usually drawn into a tube that does not contain an anticoagulant.

If factitious hyperkalemia (other than leukocytosis or fragile white blood cells) is suspected, the plasma potassium should be normal or significantly lower than the serum level. If specimen hemolysis is suspected, make sure that the patient avoids squeezing their fist during the repeat blood draw. Drawing blood through a larger caliber needle or using a needle to draw the blood specimen rather than drawing through a catheter may also reduce the risk of specimen hemolysis.


Note that heparin may actually increase the fragility of white blood cells, making it difficult to confirm “pseudohyperkalemia” in the presence of leukocytosis. Factitious hyperkalemia or pseudohyperkalemia in the absence of EKG changes or other symptoms related to hyperkalemia, may not require treatment but each case should be evaluated on a case-by-case basis.


Signs and Symptoms of Significant Hyperkalemia

Hyperkalaemia Symptoms

Signs and symptoms of hyperkalemia may include muscle fatigue, weakness, nausea, arrhythmias, and even paralysis. Hyperkalemia is difficult to diagnose without an understanding of the patient’s medical history and any presenting signs or symptoms. Hyperkalemia is defined as a blood potassium level higher than the normal range of 3.6 to 5.2(mmol/L). Other factors, as discussed previously, can result in factitious hyperkalemia, such as hemolysis of blood cells in the blood sample. Misdiagnosis may be prevented by repeating the assay, especially if it seems unlikely for the particular patient to have developed hyperkalemia based on their medical history.Besides treating hyperkalemia, it is of the utmost importance to diagnose and treat the underlying process that the elevated potassium level.


ECG changes in Hypokalemia and Hyperkalemia

hyperkalemia

hyperkalemia

Treatment of Hyperkalemia

Hyperkalemia can cause fatal cardiac arrhythmias. A rapid rise or a very elevated potassium level alters the resting membrane potential of the cardiac myocyte inactivating fast sodium channels thus blocking conduction which can result in cardiac arrest.


Treatment of hyperkalemia is aimed at reducing serum potassium levels to either prevent cardiac dysrhythmias from occurring or if cardiac manifestations are present, reducing potassium levels to restore a normal cardiac rhythm while stabilizing the cardiac membrane.


The management varies depending on how urgent the situation is. The urgency depends on the potassium level, how rapidly it rose, the presence of clinical manifestations (e.g., cardiac dysrhythmias, ECG changes, or paralysis), and the underlying cause. The latter will influence treatment and long-term management.

The level required for an elevated potassium level to result in a cardiac arrhythmia is variable. However, the higher the serum potassium and the more rapid the rise, the more likely a dysrhythmia will occur. A potassium of 6.5 or greater warrants immediate treatment as does a potassium level of 5.5 in a patient with ECG changes or neuromuscular weakness and a potassium level greater than 5.5 mEq/L in a patient who is at risk of the potassium level rising further (e.g. acute kidney injury).


Treatment in such cases requires stabilization of the myocardium while lowering the potassium level. The former entails the administration of intravenous (IV) Calcium Chloride or Calcium Gluconate. Although IV calcium chloride and calcium gluconate do not reduce potassium levels, they stabilize the membrane of the cardiac myocytes, preventing the likelihood of developing an arrhythmia.


Reducing potassium can be achieved by either (a) shifting the potassium from the extracellular space (ECF) to the intracellular space (ICF), or (b) by eliminating the potassium from the body.


Shifting potassium from the ECF to the ICF is a temporizing measure that does not remove potassium from the body, but does reduce the serum levels by transiently moving it from one compartment to another. With time, potassium will eventually leak back out of the ICF into the ECF. Until that time, other measures may be implemented to remove the potassium remaining in the ECF from the body, so that when the potassium shifts back from the ICF to the ECF, the serum level will not be elevated.


One common approach is to administer dextrose in the form of D50W IV followed by 10 units of short-acting insulin IV. The movement of glucose into the cells is accompanied by an intracellular potassium shift. Another technique is to use aerosolized Albuterol, a beta agonist which is known to transiently reduce potassium levels. A third option is to use IV sodium bicarbonate. IV sodium bicarbonate increases extracellular bicarbonate leading to a shift of hydrogen ions from the ICF to the ECF which in turn drives potassium from the ECF to the ICF. As with Dextrose and insulin, this too only transiently lowers serum potassium levels.


Removal of potassium from the body can only be achieved in three ways; either (a) excreted by the kidneys (b) by the gastrointestinal tract or (c) with renal dialysis.


The intestines account for approximately 10% of daily potassium losses and so serve as a possible location to help remove potassium from the body. Several medications are available including patiromer (Veltassa), sodium zirconium cyclosilicate (Lokelma), and sodium polystyrene sulfonate (Kayexalate).


For decades sodium polystyrene sulfonate (aka Kayexalate or Kionex) has been used with great success to remove potassium. It can be given orally or rectally but may take several hours before it has its desired effect, so until then, it may be necessary to administer D50 and insulin to temporarily lower the serum potassium level. The same is true of patiromer and sodium zirconium cyclosilicate. It should be noted that sodium polystyrene sulfonate has been associated with bowel necrosis and is contraindicated in patients who are post op or have an ileus. While bowel necrosis has not been seen thus far with patiromer and sodium zirconium cyclosilicate, neither have been studied in patients who have severe constipation, bowel obstruction or who have postoperative bowel motility disorders and their use in such cases is warned against.


Finally, both peritoneal (PD) and hemodialysis dialysis (HD) are effective methods for lowering serum potassium levels if more conservative measures are not possible or if the patient’s condition deteriorates despite conservative management.


While PD may be administered acutely, some hospitals may not have the ability to place a PD catheter or have the infrastructure to do the procedure, so hemodialysis has been the default modality. Once a hemodialysis catheter has been inserted dialysis can be provided and the potassium normalized within an hour.


Other Causes of Hyperkalemia


Metabolic acidosis also affects potassium levels by causing a shift of potassium ions from the intracellular space to the extracellular space. As in factitious hyperkalemia, treatment of the hyperkalemia may or may not be necessary. If treatment is deemed necessary it will be in the form of reducing total body potassium unless there is life threatening signs and symptoms.


In DKA, both acidosis and hyperglycemia will cause a shift of potassium to the extracellular space, but total body potassium is frequently depleted yet serum potassium may be initially elevated. Treating the “hyperkalemia” in DKA unless there are life threatening effects may be lethal.


Other diseases that should be mentioned that cause the shift of potassium out of the cells into the extracellular space and blood and cause hyperkalemia. These include rhabdomyolysis, burns, hyperosmolar states, tumor lysis syndrome and familial periodic paralysis. Treatment of the hyperkalemia depends on the level of hyperkalemia, speed of onset, the projected duration of the underlying pathology and the presence of EKG changes or severe symptoms.

In severe leukocytosis or thrombocytosis hyperkalemia may be due to the fragility of the cells but may be due to the abnormal increase in cell mass.

The management of less threatening levels of hyperkalemia is based on the suspected cause of the hyperkalemia and whether it is a transient problem or a chronic problem. For example, if due to a medication, then the dose of the medication may need to be adjusted or discontinued altogether. If from dehydration, then increased fluid is indicated. If the patient is constipated, then review of diet and medications that may cause or be contributing to the constipation should be reviewed and a softener or motility agent may be necessary. In some cases permanent dietary modification may be necessary. See below.


FibonacciMD Patient Handout for chronic Hyperkalemia

For normokalemic patients the recommended AI (adequate intake) for potassium is 3,500 mg(milligrams) to 4,700 mg per day. Patients with impaired kidney function may require a low potassium diet of less than 3,000 mg per day. Consult with your physician or healthcare clinician to see what your daily intake of potassium should be.

High potassium foods (Foods to Avoid)


Fruits:
  • Tomato puree, tomato paste & sauce (canned)

  • Banana (1 banana 422 mg)

  • Currants

  • Dried fruit (raisins, sultanas, prunes, apricots, peaches, dates, sundried tomatoes)

  • Avocados

  • Oranges

  • Plantains

  • Pomegranate (1 cup 666 mg)

  • Cantaloupe

  • Watermelon

Vegetables:

  • Amaranth leaves

  • Baked potato (skin on)

  • Beans, black (1 cup 611 mg)

  • Beans, white (navy, cannellini) (1 cup 829 mg)

  • Beets (1 cup 518 mg)

  • Brussel sprouts

  • Butternut squash (1 cup 582 mg)

  • Edamame (1 cup 676 mg)

  • Lentils

  • Mushrooms (dried and fresh)

  • Spinach (1 cup cooked 540 mg)

  • Sweet potato ((1 medium 541 mg)

  • Swiss chard (1 cup cooked, 961 mg)

Meats:

  • Salmon

  • Clams

  • Mackerel

  • Chili (canned with beans)

  • Halibut

  • Tuna

  • Snapper

  • Rainbow trout

Dairy:

  • Chocolate milk

  • Yogurt, low fat (6 oz 398 mg)

  • Skim milk

Starch:
  • Cereal or granola that is bran-based or with dried fruits, nuts, or chocolate

Snacks:
  • Manufactured potato products like chips, hash browns, potato wedges, french fries, etc.

Drinks:
  • Coffee

  • Wine

  • Canned juice such as prune, carrot, tomato, and vegetable juice (1 cup coconut water 600 mg)


Low potassium foods (Foods to Include in your Diet)


Fruit: (limit to 2 portions a day)
  • Small apple or pear (1 medium apple 150 mg)

  • Only a Handful of grapes

  • Drain any canned fruits

  • Blueberries (1/2 cup 60 mg)

  • Raspberries (1/2 cup 90 mg)

  • Mandarin oranges (1/2 cup 99 mg)

  • Strawberries (1/2 cup 125 mg)

Vegetables:
  • Peas (1/2 cup 90 mg)

  • Boiled potatoes (max 1 small portion per day)

  • Cauliflower (1/2 cup 150 mg)

  • Green beans (1/2 cup 90 mg)

  • Cucumber (1/2 cup 80 mg)

  • Eggplant (1 cup cooked 60 mg)

  • Other Low Potassium Vegetables: Carrots, Broccoli, Cabbage

Dairy:
  • Cheese

  • Rice or oat milk

  • Eggs

Meats:
  • Chicken

  • Turkey

Starch:
  • Pasta, rice, noodles, couscous, bread

Snacks:
  • Popcorn

  • Marshmallows

  • Mints

  • Sponge cake

  • Corn, rice, wheat-based snacks

  • Unsalted peanut butter

  • Nutless, non-chocolate cookies

Drinks:
  • Water

  • Tea

  • Fizzy drinks

 

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ABOUT THE AUTHORS


Kruti Vora, M.D.

Dr. Vora attended Harvard Medical School and has started her internship in the Department of Medicine at Massachusetts General Hospital in Boston, Massachusetts. Her interests are in medical oncology, advocating for health equity, mentorship, and medical education.


M.C.A. Butman and M.P. Butman, MD



References:

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