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POTASSIUM

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Potassium is a soft silvery white metal found in the earth's crust and is an essential electrolyte.
    B) Uses include treatment for potassium depletion, treatment of dysrhythmias that are potassium dependent, as a salt substitute, in conjunction with anticholinesterase agents in restoring muscular strength, and in the treatment of thallium poisoning.

Specific Substances

    A) POTASSIUM
    1) NIOSH/RTECS TS 6460000
    2) CAS 7440-09-7
    CARNALLITE
    1) Molecular Formula: K-Cl.Mg-Cl2.6H2O
    MICROCLINE
    1) Molecular Formula: K-Al-Si3-O8
    ADDITIONAL SUBSTANCES
    1) Kalium
    2) Orthoclase (aluminosilicates)
    3) Sylvite (potassium chloride)
    RELATED COMPOUNDS -- POTASSIUM GLUCONATE
    1) 577
    2) Potassium D-gluconate
    3) CAS 299-27-4
    RELATED COMPOUNDS -- POTASSIUM CHLORIDE
    1) 508
    2) Cloreto de potassio
    3) Kalii chloridum
    4) Kalium chloratum
    5) Potassii chloridum
    6) CAS 7447-40-7

    1.2.1) MOLECULAR FORMULA
    1) POTASSIUM CHLORIDE: KCl
    2) POTASSIUM CITRATE: K3C6H5O7-H2O

Available Forms Sources

    A) FORMS
    1) POTASSIUM SALTS are available in a variety of forms and are chiefly used as supplementation with diuretic therapy.
    2) Potassium supplements are available in "slow release" (enteric-coated) tablets which can release large amounts of KCl over a relatively short segment of small bowel. These formulations have been implicated in small bowel ulcers, some of which were fatal.
    a) The newer slow release KCl formulations are somewhat safer, but can cause potential adverse effects if delayed intestinal transit is present.
    3)
    Potassium (K) SaltmEq K/gram of salt
    K-Acetate10.3
    K-Bicarbonate10
    K-Chloride13.3
    K-Citrate H209.3
    K-Iodide6
    K-Phosphate monobasic7.4
    K-Phosphate dibasic11.4

    4) Potassium salt substitutes may cause serious poisoning. Below is the potassium content of various salt substitutes (Hoye & Clark, 2003; Hoyt, 1986; Kallen et al, 1976; Yap et al, 1976)
    SALT SUBSTITUTEmEq/teaspoon
    Adolph's Salt Substitute (unseasoned)65
    Morton's Lite Salt38
    Morton's Salt Substitute72
    No-Salt64
    Nu-Salt67

    B) SOURCES
    1) FOODS: It is also present in large amounts in certain foods (e.g., cantaloupe, citrus fruits, bananas, tomatoes, and potatoes).
    2) WATER SOFTENER: Water softeners can be a significant source of potassium, especially in patients with underlying renal insufficiency. One softener, K-Life (IMC Kalium Canada) was found to provide 7 mmol potassium per liter of water (Graves, 1998).
    3) LOW SODIUM FOODS: Hyperkalemia developed in dialysis patients when they tripled their potassium intake by switching from the old Campbell's low sodium soups (7-1/2 ounce can containing 0.5 mEq potassium/ounce) to the new Campbell's low sodium soups (10-3/4 ounce can containing 1 mEq potassium/ounce) (Bay & Hartman, 1983).
    4) COCONUT WATER: SUMMARY: Coconut water is used as a rehydration drink. It is sold in the US and other markets as a purported health drink. It has been promoted as an electrolyte-balanced sports drink for healthy exercising individuals (Rees et al, 2012).
    a) ELECTROLYTE CONTENTS: Electrolytes per liter of coconut water: sodium 46.3 mmol/L; potassium 65 mmol/L; magnesium 10.4 mmol/L; and calcium 6.1 mmol/L (Rees et al, 2012).
    b) CASE REPORT: A 26-year-old woman with type 1 diabetes and nephropathy presented with a potassium level of 7.7 mmol/L with T wave changes on an ECG. Upon questioning, the patient reported drinking 2 L of coconut water (potassium content was at least 5 g (130 mmoles)) during the preceding 24 hours; she recovered with supportive care (Rees et al, 2012).
    5) CAUSES OF HYPERKALEMIA
    a) The most common causes of hyperkalemia are acute renal failure, use of potassium-sparing diuretics (spironolactone and triamterene), and over-supplementation.
    b) Most severe hyperkalemia occurs in the face of compromised renal function.
    c) Intentional and unintentional overdoses of KCl have been reported.
    1) CREAM OF TARTAR: A 16-year-old body builder intentionally ingested a bottle of cream of tartar, which is used as a leavening agent in baking (equivalent to 420.5 mEq of potassium), and developed severe hyperkalemia (Sanftleben et al, 2000).
    C) USES
    1) The average daily intake of potassium by adults in the United States is 70 to 100 mEq (2.8 to 3.9 grams) (Sollmann, 1957).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Potassium is a metal found naturally in the earth's crust and in most foods. It is taken medically for the prevention and treatment of hypokalemia. Tablets are readily available, including sustained-release formulations. Potassium is used as a salt substitute and is often present in "low-sodium" foods. It is also used as a water softener, and in chemistry and manufacturing processes.
    B) PHARMACOLOGY: Potassium is the human body's main intracellular cation, with only 2% of the body's stores in the intravascular compartment. It is necessary for nerve conduction, and muscle (including cardiac) contraction.
    C) TOXICOLOGY: Local irritation after ingestion causes GI upset. Severe hyperkalemia after large IV or oral overdoses causes muscular dysfunction including weakness, paralysis, cardiac dysrhythmias, and rarely death.
    D) EPIDEMIOLOGY: Potassium toxicity from overdose is rare but may result from intentional ingestion. Iatrogenic overdoses can occur.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: SPECIAL SITUATIONS: Inadvertent intrathecal injection of potassium was rapidly fatal in the only case that has been reported. Potassium permanganate crystals are caustic. Potassium carbonate and hydroxide are very alkaline and have been associated with ocular injury.
    F) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, diarrhea, paresthesias, and muscle cramps are common. Rarely, GI bleed may occur.
    2) SEVERE TOXICITY: Muscular weakness progressing to paralysis may occur. Cardiac dysrhythmias often occur with concentrations greater than 8 mEq/L and death from cardiac arrest with concentrations of 9 to 12 mEq/L or higher. Characteristic ECG findings occur in the following order: peaked T waves, QRS complex blends into the T wave, PR interval prolongation, P wave is lost and ST segments depress, merging S and T waves, and finally, sine waves. The presence of the sine wave is a near terminal event, signaling that hemodynamic collapse and cardiac arrest are near. As serum hyperkalemia is corrected, the ECG changes resolve in reverse order.
    0.2.20) REPRODUCTIVE
    A) Potassium citrate is classified as FDA pregnancy category C. Potassium chloride and potassium gluconate are classified as FDA pregnancy category A.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serial serum potassium concentrations. Monitor serum electrolytes, renal function and blood glucose concentrations. Obtain serial ECGs and institute continuous cardiac monitoring.
    C) Routine monitoring of electrolytes, renal function, and glucose levels may be helpful.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Establish IV access. Initiate ECG monitoring. Cation-binding resins (ie, kayexelate) should be given orally.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Continuous ECG monitoring should be initiated and intravenous access obtained. Treat hyperkalemia associated with ECG changes aggressively; nebulized beta agonists (eg, albuterol), intravenous sodium bicarbonate 1 mEq/kg IV, intravenous calcium chloride (preferably through a central line) or calcium gluconate (avoid calcium salts in patients taking digoxin), intravenous insulin 10 units with 25 g D50. Note: All of these therapies shift potassium intracellularly, but do NOT increase the elimination of potassium from the body; expect rebound hyperkalemia to develop, the above therapies may need to be repeated. Administer a potassium binding resin orally (usually works over hours) and administer intravenous fluids. Diuretics may be used to increase urinary potassium elimination. In severe cases, in particular, patients with renal insufficiency or those also taking potassium sparing diuretics, hemodialysis may be warranted. Orotracheal intubation for airway protection should be performed if a patient is hemodynamically unstable.
    C) DECONTAMINATION
    1) PREHOSPITAL: EMESIS: Consider inducing emesis only if a recent oral overdose and the patient is not already vomiting and can protect their airway. ACTIVATED CHARCOAL: There is no role for activated charcoal as it does not bind potassium.
    2) HOSPITAL: If a recent large oral ingestion of potassium, consider orogastric lavage to remove pills or pill fragments. Potassium tablets may be seen on X-ray. Consider whole bowel irrigation, if the patient has overdosed (particularly extended-release) and the tablets are beyond the stomach. In adults, 2 L of polyethylene glycol solution should be given initially followed by 1.5 to 2 L/hr until clear rectal effluent and an absence of tablets on X-ray. For children 6 to 12 years of age: Administer 1 L/hr of polyethylene glycol solution; children 9 months to less than 6 years: 500 cc/hr should be administered. Patients must be awake and cooperative and/or must have a protected airway for decontamination.
    D) AIRWAY MANAGEMENT
    1) Perform early in patients with severe intoxication (ie, cardiovascular collapse).
    E) ANTIDOTE
    1) There is no antidote for potassium.
    F) MONITORING OF PATIENT
    1) Monitor vital signs and mental status. Monitor serial serum potassium concentrations. Monitor serum electrolytes, renal function and blood glucose concentrations. Obtain serial ECGs and institute continuous cardiac monitoring. Routine monitoring of electrolytes, renal function, and glucose levels may be helpful.
    G) ENHANCED ELIMINATION
    1) Hemodialysis may be necessary in renal failure patients with hyperkalemia or in patients with normal renal function that have severe toxicity.
    H) INTRATHECAL INJECTION
    1) Intrathecal injection of potassium caused cerebral edema and was rapidly fatal in the only case reported. The following recommendations are derived from experience with other agents. Keep the patient upright and immediately drain at least 20 mL of CSF; drainage of up to 70 mL has been tolerated in adults. Follow with CS exchange (remove serial 20 mL aliquots CSF and replace with equivalent volumes of warmed, preservative free saline). Consult a neurosurgeon for placement of a ventricular catheter and begin ventriculolumbar perfusion (infuse warmed preservative free normal saline through a ventricular catheter, drain fluid from lumbar catheter; typical volumes 80 to 150 mL/hr for 24 hours). Dexamethasone 4 mg IV every 6 hours to prevent arachnoiditis.
    I) PATIENT DISPOSITION
    1) HOME CRITERIA: Any child who ingests more than a therapeutic dose of potassium or any intentional/suicidal ingestion by an adult should be evaluated by a healthcare professional.
    2) OBSERVATION CRITERIA: Patients with deliberate ingestions and symptomatic patients should be sent to a healthcare facility for observation for at least 4 hours. A longer observation, up to 24 hours (until serum potassium has clearly peaked and is declining without active intervention) should be considered for patients that overdose on sustained-release products.
    3) ADMISSION CRITERIA: Patients with persistent GI symptoms, ECG changes, or persistent hyperkalemia should be admitted to the hospital. Patients with dysrhythmias or cardiovascular collapse or those needing dialysis should be admitted to an intensive care unit.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (severe weakness or cardiac dysrhythmias), or in whom the diagnosis is not clear.
    J) PITFALLS
    1) Failure to rapidly recognize and treat potassium toxicity and/or not observing for rebound hyperkalemia after temporizing measures to shift potassium into intracellular space have worn off. Metabolic acidosis causes an extracellular shift of potassium and can cause intracellular depletion.
    K) PHARMACOKINETICS
    1) Potassium is rapidly and well absorbed. Under normal circumstances, 90% of potassium is eliminated via the kidneys. A small amount is eliminated in feces and sweat. Pharmacokinetics are largely unknown. Distribution is largely intracellular, but it is the intravascular concentration that is primarily responsible for toxicity.
    L) DIFFERENTIAL DIAGNOSIS
    1) Hyperkalemia may also develop due to the therapeutic use or overdose of other medications such as potassium sparing diuretics, cardiac glycosides (ie, digoxin), NSAIDs, succinylcholine, ACE inhibitors and angiotensin-converting enzymes inhibitors. Medical conditions causing hyperkalemia include renal failure, adrenal insufficiency, rhabdomyolysis and hemolysis.
    0.4.6) PARENTERAL EXPOSURE
    A) INADVERTENT INTRATHECAL INJECTION: Potassium via the intrathecal route has been rapidly fatal. Keep the patient upright and begin aggressive attempts to remove as much of the drug as possible, including immediate cerebrospinal fluid (CSF) drainage, followed by CSF exchange, and ventriculolumbar perfusion. Monitor for hyperkalemia and treat as necessary.
    1) Keep the patient upright if possible. Immediately drain AT LEAST 20 mL CSF; drainage of up to 70 mL has been tolerated in adults. Follow with CSF exchange (remove serial 20 mL aliquots CSF and replace with equivalent volumes of warmed, preservative free normal saline or lactated ringers). Consult a neurosurgeon immediately for placement of a ventricular catheter and begin ventriculolumbar perfusion (infuse warmed preservative free normal saline or LR through ventricular catheter, drain fluid from lumbar catheter; typical volumes are 80 to 150 mL/hr for at least 24 hours). Fresh frozen plasma (25 mL FFP/liter NS or LR) or albumin 5% should be added to the fluid used for perfusion to increase protein binding. Administer dexamethasone 4 mg intravenously every 6 hours to prevent arachnoiditis.

Range Of Toxicity

    A) TOXICITY: ADULT: Doses as low as 2 to 2.5 mEq/kg of potassium have been reported to cause toxicity. GENERAL: NORMAL SERUM CONCENTRATIONS: 3.5 to 5 mEq/L; MINIMAL TOXICITY: Potassium concentrations under 6.5 mEq/L; MODERATE TOXICITY: Concentrations between 6.5 and 8 mEq/L produce lassitude, fatigue, and weakness. SEVERE TOXICITY: Concentrations over 8 mEq/L, complete neuromuscular paralysis may dominate the clinical picture. Death from cardiac arrest usually occurs at 9 to 12 mEq/L. It may occur at lower levels if cellular potassium is severely depleted.
    B) THERAPEUTIC: ADULT: 40 to 80 mEq/day is a typical daily dose. In patients with renal insufficiency, the dose may be lower. PEDIATRIC: 2 to 3 mEq/kg/day is the usually daily dose.

Clinical Effects

Summary Of Exposure

    A) USES: Potassium is a metal found naturally in the earth's crust and in most foods. It is taken medically for the prevention and treatment of hypokalemia. Tablets are readily available, including sustained-release formulations. Potassium is used as a salt substitute and is often present in "low-sodium" foods. It is also used as a water softener, and in chemistry and manufacturing processes.
    B) PHARMACOLOGY: Potassium is the human body's main intracellular cation, with only 2% of the body's stores in the intravascular compartment. It is necessary for nerve conduction, and muscle (including cardiac) contraction.
    C) TOXICOLOGY: Local irritation after ingestion causes GI upset. Severe hyperkalemia after large IV or oral overdoses causes muscular dysfunction including weakness, paralysis, cardiac dysrhythmias, and rarely death.
    D) EPIDEMIOLOGY: Potassium toxicity from overdose is rare but may result from intentional ingestion. Iatrogenic overdoses can occur.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: SPECIAL SITUATIONS: Inadvertent intrathecal injection of potassium was rapidly fatal in the only case that has been reported. Potassium permanganate crystals are caustic. Potassium carbonate and hydroxide are very alkaline and have been associated with ocular injury.
    F) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, diarrhea, paresthesias, and muscle cramps are common. Rarely, GI bleed may occur.
    2) SEVERE TOXICITY: Muscular weakness progressing to paralysis may occur. Cardiac dysrhythmias often occur with concentrations greater than 8 mEq/L and death from cardiac arrest with concentrations of 9 to 12 mEq/L or higher. Characteristic ECG findings occur in the following order: peaked T waves, QRS complex blends into the T wave, PR interval prolongation, P wave is lost and ST segments depress, merging S and T waves, and finally, sine waves. The presence of the sine wave is a near terminal event, signaling that hemodynamic collapse and cardiac arrest are near. As serum hyperkalemia is corrected, the ECG changes resolve in reverse order.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) POTASSIUM CHLORIDE is not injurious to eyes.
    2) POTASSIUM CARBONATE, also known as potash, may have a pH of 11.6, and may cause eye injury. When tested in rabbits (10% solution), there was pain and slight, transient optical irregularity of the epithelium that had cleared in a couple of hours (Grant & Schuman, 1993).
    3) POTASSIUM CHLORATE in a 3% to 5% solution, and powdered potassium chlorate did not cause injury in humans or animals (Grant & Schuman, 1993).
    4) POTASSIUM HYDROXIDE, also known as caustic potash, is a strong alkali and is extremely corrosive. The injury is similar to that of sodium hydroxide (Grant & Schuman, 1993).
    5) POTASSIUM OLEATE a 12% solution caused irritation in rabbit eyes (Grant & Schuman, 1993).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Potential dysrhythmias and ECG abnormalities include (sequentially): tall peaked T waves, depressed S-T segments, decreased amplitude of R waves, PR interval prolongation, decreased or flattened P waves, wide QRS, QT lengthening, a sine wave appearance, bigeminy, wide-complex tachycardia, ventricular fibrillation, and asystole (Pang et al, 2004; Mattu et al, 2000; McLean et al, 2000; Ellenhorn & Barceloux, 1988; Kallen et al, 1976).
    b) CASE REPORTS
    1) Bigeminy, absent P waves, and widened QRS were reported in an 8-month-old who was given 26 mEq/kg of potassium (Kallen et al, 1976).
    2) Peaked T waves developed in a 27-year-old woman who ingested 100 sustained-release potassium tablets (serum potassium 6.5 mmol/L) and a 30-month-old who ingested an unknown quantity of sustained-release potassium (serum potassium 9.2 mmol/L) (Geluk & Braitberg, 2000; Whitaker & Maguire, 2000).
    3) A 75-year-old woman with a history of hypertension taking enalapril 5 mg daily presented to the ED with a heart rate of 200 bpm. ECG showed broad complex tachycardia, which spontaneously reverted to atrial fibrillation. Two weeks prior to the episode, the patient started using "low-salt", a potassium chloride table salt substitute containing 1.5 g (20 mmol) potassium per teaspoon. Blood analysis revealed a potassium level which peaked at 10.2 mmol/L. The patient received 2 sessions of hemodialysis in addition to insulin and glucose infusion and intravenous calcium chloride, and recovered (Hoye & Clark, 2003).
    4) A 54-year-old woman presented to the ED with no palpable pulses or respirations. ECG revealed a wide complex rhythm at 70 beats per minute without evidence of P waves. Based on the ECG and a limited history, the differential diagnosis was limited to massive pulmonary embolism, acute hyperkalemia, and tricyclic overdose. Initial laboratory studies revealed a potassium level of 8.2 mmol/L, and past medical history revealed her recent use of excessive amounts of a salt substitute that contains potassium and was likely the cause of the hyperkalemia. She received hemodialysis and improved significantly over the first 24 hours. She was discharged 1 week later with only minimal short-term memory impairment (Pang et al, 2004).
    5) A 67-year-old hemodialysis patient was diagnosed with severe hyperkalemia after developing unconsciousness and leg paralysis. An ECG revealed peaking of the T wave, prolongation of the PR interval, loss of the P-wave amplitude and widening of the QRS complex. Laboratory results showed potassium concentration of 9.3 mmol/L (reference levels: 3.5 to 4.7 mmol/L). Following supportive care, including treatment with calcium, insulin, glucose, sodium polystyrene sulfonate, and a hemodialysis session, the patient's condition improved and the ECG normalized. It was determined that the patient was using about 40 mmol/day of added potassium from a low-sodium/potassium-enriched spread (Becel pro.activ) to improve his blood pressure (van der Steen et al, 2012).
    B) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) PEDIATRIC: A 6-week-old infant developed severe dysrhythmias leading to circulatory arrest 34 days following cardiac surgery. Advanced cardiopulmonary resuscitation was initiated. Arterial blood samples revealed a potassium concentration of 17.7 mmol/L. Prior to the arrest, the infant had received an intravenous infusion of cotrimoxazole that had erroneously been prepared using a 15% potassium chloride solution (total 30 mmol potassium chloride) instead of a 5% glucose solution. Potassium levels were lowered with conventional measures to shift potassium from the extracellular to the intracellular compartment. Spontaneous circulation was restored after 45 minutes. The infant, now age 4, recovered without developmental sequelae, other than severe iatrogenic hearing loss(Horisberger et al, 2004).
    b) CASE REPORT: Before the termination of a second trimester pregnancy, a 29-year-old pregnant woman developed cardiac arrest immediately after an attempted feticide by cardiac injection of potassium chloride. The advanced cardiopulmonary resuscitation of the mother was successful. Within 15 minutes of the arrest, maternal serum potassium level was 3.9 mmol/L. Ultrasonography revealed persistence of fetal cardiac activity. Although she delivered a neonate with cardiac activity approximately 9 hours later, the baby soon expired. Both anterior and posterior thoracic wall puncture marks were observed on the neonate's body. The authors speculated that this posterior thoracic wall "exit wound" may be the evidence that potassium chloride was injected into an extra-fetal (and even maternal) blood vessel (Coke et al, 2004).
    C) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension may occur with high serum potassium levels (Briggs & Deal, 2014; Ellenhorn & Barceloux, 1988).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) Respiratory arrest and cyanosis occurred in a child given potassium chloride with breast milk. The measured potassium level was 10.1 mEq/L. The child died (Wetli & Davis, 1978).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Paresthesias of the extremities may occur with hyperkalemia (Franko & Banitt, 1991; Bedford, 1954).
    B) CLOUDED CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) Mental confusion and listlessness is part of the clinical syndrome of hyperkalemia (Sollmann, 1957).
    C) PARALYSIS
    1) WITH POISONING/EXPOSURE
    a) Weakness and paralysis may occur with hyperkalemia, and has been reported in animals (Udezue & Harrold, 1980; Sollmann, 1957) .
    b) CASE REPORT: A 67-year-old hemodialysis patient was diagnosed with severe hyperkalemia after developing unconsciousness and leg paralysis. An ECG revealed peaking of the T wave, prolongation of the PR interval, loss of the P-wave amplitude and widening of the QRS complex. Laboratory results showed potassium concentration of 9.3 mmol/L (reference levels: 3.5 to 4.7 mmol/L). Following supportive care, including treatment with calcium, insulin, glucose, sodium polystyrene sulfonate, and a hemodialysis session, the patient's condition improved and the ECG normalized. It was determined that the patient was using about 40 mmol/day of added potassium from a low-sodium/potassium-enriched spread (Becel pro.activ) to improve his blood pressure (van der Steen et al, 2012).
    D) PARAPLEGIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Permanent paraplegia was reported in a 35-year-old woman following inadvertent epidural administration of 15 mL of 15% potassium chloride with bupivacaine (Shanker et al, 1985).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, diarrhea, and abdominal cramps may occur (Geluk & Braitberg, 2000; Whitaker & Maguire, 2000; Stanaszek & Romandiewicz, 1985; AMA Division of Drugs, 1983; Illingworth & Proudfoot, 1980; Wetli & Davis, 1978; Sollmann, 1957; Bedford, 1954) .
    B) GASTRIC HEMORRHAGE
    1) WITH THERAPEUTIC USE
    a) Small bowel ulceration has been reported with enteric coated tablets of potassium chloride, and with liquid potassium gluconate.
    b) CASE REPORT: A 50-year-old man presented 12 weeks after successful treatment of an ingestion of 160 Slow-K(R) tablets with erosive gastritis (Ward et al, 1987).
    c) CASE REPORT: Gastric ulcer was reported in a woman taking a liquid preparation of potassium gluconate (Warr & Nash, 1967; Allen et al, 1965).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) PALE COMPLEXION
    1) WITH POISONING/EXPOSURE
    a) Pallor is often reported in cases of potassium overdose (Oseas et al, 1982; Sollmann, 1957) .
    B) NECROSIS
    1) WITH POISONING/EXPOSURE
    a) A 31-year-old man experienced chemical burns to his right and left forearms (4% of the body service area) 10 hours after injecting a potassium chloride mixture in a suicide attempt. Two 10 gram vials of potassium chloride were mixed with 50 mL of tap water and injected into both arms. The patient was alert and healthy upon arrival, except for burn lesions with the formation of vesicles and purple necrotic lesions on his arms. No systemic abnormalities developed; the patient required escharotomies and skin grafts to repair the damage of the potassium to his forearms (Park et al, 2011).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) TETANY
    1) WITH POISONING/EXPOSURE
    a) Tetany has been reported in cases of acute overdose (Bedford, 1954).

Reproductive

    3.20.1) SUMMARY
    A) Potassium citrate is classified as FDA pregnancy category C. Potassium chloride and potassium gluconate are classified as FDA pregnancy category A.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) POTASSIUM CITRATE
    a) At the time of this review, no data were available to assess the teratogenic potential of this agent (Prod Info UROCIT(R)-K extended-release oral tablets, 2009; Prod Info potassium citrate extended-release oral tablets, 2009).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) POTASSIUM CITRATE
    a) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy in humans (Prod Info UROCIT(R)-K extended-release oral tablets, 2009; Prod Info potassium citrate extended-release oral tablets, 2009).
    B) PREGNANCY CATEGORY
    1) Potassium citrate is classified as FDA pregnancy category C (Prod Info UROCIT(R)-K extended-release oral tablets, 2009; Prod Info potassium citrate extended-release oral tablets, 2009), while potassium chloride and potassium gluconate are classified as FDA pregnancy category A (Briggs et al, 1998).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) POTASSIUM CITRATE
    a) At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation in humans. It is unknown whether potassium citrate is excreted in human breast milk. In normal human milk potassium content is approximately 13 mEq/L. The effects of potassium citrate on human milk content is unknown (Prod Info UROCIT(R)-K extended-release oral tablets, 2009; Prod Info potassium citrate extended-release oral tablets, 2009).
    3.20.5) FERTILITY
    A) LACK OF INFORMATION
    1) POTASSIUM CITRATE
    a) At the time of this review, no data were available to assess the potential effects on fertility from exposure to this agent (Prod Info UROCIT(R)-K extended-release oral tablets, 2009; Prod Info potassium citrate extended-release oral tablets, 2009).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor serial serum potassium concentrations. Monitor serum electrolytes, renal function and blood glucose concentrations. Obtain serial ECGs and institute continuous cardiac monitoring.
    C) Routine monitoring of electrolytes, renal function, and glucose levels may be helpful.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor serial electrolytes and obtain a serum creatinine.
    2) NORMAL SERUM CONCENTRATIONS: 3.5 to 5 mEq/L (Prod Info KLOR-CON(R) extended release tablets, 2005; Schonwald, 2004).
    3) MINIMAL TOXICITY: Potassium concentrations under 6.5 mEq/L. Evidence of cardiac toxicity is rare below 6.5 mEq/L (Schonwald, 2004).
    4) MODERATE TOXICITY: Potassium levels between 6.5 and 8 mEq/L produce lassitude, fatigue, and weakness.
    5) SEVERE TOXICITY: Concentrations over 8 mEq/L, complete neuromuscular paralysis may dominate the clinical picture. Cardiac manifestations of toxicity are also common at concentrations above 8 mEq/L (Schonwald, 2004). Death from cardiac arrest usually occurs at 9 to 12 mEq/L (Prod Info KLOR-CON(R) extended release tablets, 2005).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Obtain an ECG and institute continuous cardiac monitoring. The ECG is fairly characteristic (ie, peaked T waves, small P waves, QRS widening), except in patients with Addison's disease (ie, the ECG may show generalized reduction and slowing).
    2) POSTMORTEM
    a) ANIMALS: Studies in rabbits have shown that the serum, plasma, and vitreous humor may be the best fluids to test for potassium overdose on postmortem (Bhatkhoude & Joglekar, 1977). However, these fluids were not helpful in determining the cause of death in one human suicide case (Chaturvedi et al, 1986).

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) Potassium preparations are reported to be consistently radiopaque in models (Savitt et al, 1987; O'Brien et al, 1986; Handy, 1971). An abdominal film may be useful to assess if an ingestion has occurred or if gastric decontamination has been effective (Whitaker & Maguire, 2000; Geluk & Braitberg, 2000).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.2) DISPOSITION/PARENTERAL EXPOSURE
    6.3.2.1) ADMISSION CRITERIA/PARENTERAL
    A) Patients with persistent GI symptoms, ECG changes, or persistent hyperkalemia should be admitted to the hospital. Patients with dysrhythmias or cardiovascular collapse or those needing dialysis should be admitted to an intensive care unit.
    6.3.2.2) HOME CRITERIA/PARENTERAL
    A) Any child who ingests more than a therapeutic dose of potassium or any intentional/suicidal ingestion by an adult should be evaluated by a healthcare professional.
    6.3.2.3) CONSULT CRITERIA/PARENTERAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (severe weakness or cardiac dysrhythmias), or in whom the diagnosis is not clear.
    6.3.2.5) OBSERVATION CRITERIA/PARENTERAL
    A) Patients with deliberate ingestions and symptomatic patients should be sent to a healthcare facility for observation for at least 4 hours. A longer observation, up to 24 hours (until serum potassium has clearly peaked and is declining without active intervention) should be considered for patients that overdose on sustained-release products.

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serial serum potassium concentrations. Monitor serum electrolytes, renal function and blood glucose concentrations. Obtain serial ECGs and institute continuous cardiac monitoring.
    C) Routine monitoring of electrolytes, renal function, and glucose levels may be helpful.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS
    1) Consider inducing emesis only if a recent oral overdose and the patient is not already vomiting and can protect their airway.
    B) ACTIVATED CHARCOAL
    1) LACK OF EFFICACY: There is no role for activated charcoal as it does not bind potassium.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) If a recent large oral ingestion of potassium, consider orogastric lavage to remove pills or pill fragments. Potassium tablets may be seen on X-ray. Consider whole bowel irrigation, if the patient has overdosed (particularly extended-release) and the tablets are beyond the stomach.
    B) EMESIS
    1) Spontaneous emesis has been associated with the removal of large quantities of potassium tablets from the GI tract, even more than 4 hours after ingestion (Geluk & Braitberg, 2000).
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    D) WHOLE BOWEL IRRIGATION
    a) WHOLE BOWEL IRRIGATION/INDICATIONS: Whole bowel irrigation with a polyethylene glycol balanced electrolyte solution appears to be a safe means of gastrointestinal decontamination. It is particularly useful when sustained release or enteric coated formulations, substances not adsorbed by activated charcoal, or substances known to form concretions or bezoars are involved in the overdose.
    1) Volunteer studies have shown significant decreases in the bioavailability of ingested drugs after whole bowel irrigation (Tenenbein et al, 1987; Kirshenbaum et al, 1989; Smith et al, 1991). There are no controlled clinical trials evaluating the efficacy of whole bowel irrigation in overdose.
    b) CONTRAINDICATIONS: This procedure should not be used in patients who are currently or are at risk for rapidly becoming obtunded, comatose, or seizing until the airway is secured by endotracheal intubation. Whole bowel irrigation should not be used in patients with bowel obstruction, bowel perforation, megacolon, ileus, uncontrolled vomiting, significant gastrointestinal bleeding, hemodynamic instability or inability to protect the airway (Tenenbein et al, 1987).
    c) ADMINISTRATION: Polyethylene glycol balanced electrolyte solution (e.g. Colyte(R), Golytely(R)) is taken orally or by nasogastric tube. The patient should be seated and/or the head of the bed elevated to at least a 45 degree angle (Tenenbein et al, 1987). Optimum dose not established. ADULT: 2 liters initially followed by 1.5 to 2 liters per hour. CHILDREN 6 to 12 years: 1000 milliliters/hour. CHILDREN 9 months to 6 years: 500 milliliters/hour. Continue until rectal effluent is clear and there is no radiographic evidence of toxin in the gastrointestinal tract.
    d) ADVERSE EFFECTS: Include nausea, vomiting, abdominal cramping, and bloating. Fluid and electrolyte status should be monitored, although severe fluid and electrolyte abnormalities have not been reported, minor electrolyte abnormalities may develop. Prolonged periods of irrigation may produce a mild metabolic acidosis. Patients with compromised airway protection are at risk for aspiration.
    2) CASE REPORT: Whole bowel irrigation (with accompanying spontaneous emesis) was associated with reduction in the number of potassium tablets visible on abdominal radiograph and falling serum potassium levels in a 30-month-old child who ingested at least 32 tablets of sustained-release potassium (Whitaker & Maguire, 2000).
    3) CASE REPORTS: Hyperkalemia was reported in 2 adults with normal renal function following intentional ingestion of sustained-released potassium tablets. In both patients, the tablets were clearly visualized using standard radiography and both were successfully decontaminated with whole bowel irrigation. Because sustained release formulations may be less of a gastrointestinal irritant as compared to other potassium products, spontaneous vomiting may not occur, resulting in an increased risk for hyperkalemia (Su et al, 2001).
    E) ACTIVATED CHARCOAL
    1) In vitro, activated charcoal was NOT shown to bind potassium from potassium chloride solution (Welch et al, 1986). Charcoal may be of use if multiple agents have been ingested.
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) SUMMARY
    a) Monitor vital signs and mental status.
    b) Monitor serial serum potassium concentrations. Monitor serum electrolytes, renal function and blood glucose concentrations. Obtain serial ECGs and institute continuous cardiac monitoring.
    c) Routine monitoring of electrolytes, renal function, and glucose levels may be helpful.
    2) ECG MONITORING
    a) Progressive ECG changes occur with increasing serum potassium levels.
    1) ECG MANIFESTATIONS: ECG abnormalities include (sequentially): tall peaked T waves in the precordial leads, depressed S-T segments, decreased amplitude of R waves, PR interval prolongation, decreased or progressive flattening of the P wave, widening of the QRS complex, QT lengthening, and merging of the QRS complex with the T wave to produce a continuous sine wave appearance. Possible dysrhythmias may include: first degree AV block, AV dissociation, bigeminy, wide-complex tachycardia, ventricular fibrillation or asystole (Ellenhorn & Barceloux, 1988; Kallen et al, 1976; Martin et al, 1986; Smith et al, 1985; Williams et al, 1986; Mattu et al, 2000; McLean et al, 2000).
    b) ECG manifestations of hyperkalemia and/or a serum potassium concentration of 7.5 mEq/L or greater indicates a medical emergency and requires aggressive therapy and continuous cardiac monitoring.
    B) VENTRICULAR ARRHYTHMIA
    1) The presence of wide-complex tachycardia can be related to systemic hyperkalemia. In this setting, treatment should initially be directed at lowering serum potassium levels (Mattu et al, 2000; McLean et al, 2000).
    a) AVOID LIDOCAINE: Profound conduction disturbances (ie, asystole, sine wave pattern without a pulse) were reported in 2 adults that were given lidocaine for wide-complex tachycardia in the presence of severe hyperkalemia (McLean et al, 2000).
    1) One patient's rhythm degenerated to asystole immediately following lidocaine, and despite cardiac resuscitation efforts and treatment, the patient died within 2 hours of admission. The second patient was initially found pulseless by paramedics and treated at the scene. Her rhythm changed to sinus tachycardia followed by a sustained wide-complex tachycardia, which was treated with lidocaine. The patient's rhythm degenerated to a slow sine wave morphology without pulse. Cardiac rhythm was restored following resuscitation efforts in the ED. However, the patient died following withdrawal of care due to a persistent vegetative state. Potassium levels at the time of initial ED admission were 9.4 and 7.8 mEq/L, respectively. The authors noted that because hyperkalemia potentiates the sodium channel blocking effect of lidocaine it can result in severe cardiac depression (McLean et al, 2000).
    C) CALCIUM
    1) Intravenous calcium has no effect on circulating potassium levels, but it antagonizes cardiac toxicity in patients demonstrating cardiac signs and/or symptoms of hyperkalemia.
    2) Use 10% calcium chloride.
    3) ADULT DOSE: 5 to 10 mL (500 to 1000 mg) IV over 1 to 5 minutes; may repeat after 10 minutes (Saxena, 1989; Anon, 2000).
    4) PEDIATRIC DOSE: 0.2 mL/kg (20 to 30 mg/kg per dose up to a maximum single dose of 5 mL (500 mg) IV over 5 to 10 minutes, repeated up to 4 times or until serum calcium increases (Barkin, 1986; Anon, 2000).
    5) CALCIUM FOR INJECTION is available as 3 salts; calcium chloride, calcium gluconate, and calcium gluceptate.
    a) While the other salts may be used, calcium chloride is the preferred salt for resuscitation since it directly delivers ionized calcium, whereas the other salts must be hepatically metabolized to release ionized calcium (Chameides, 1988).
    b) Calcium chloride is very irritating, and should only be given via a central venous catheter. It may cause hypotension and bradycardia. Calcium salts are incompatible with bicarbonate (Chameides, 1988; Saxena, 1989; Anon, 2000).
    D) SODIUM BICARBONATE
    1) Administer IV sodium bicarbonate to shift potassium intracellularly. Expect 0.5 to 1 mEq/L reduction in serum potassium for each 0.1 unit rise in blood pH.
    2) A standard syringe contains 50 mL of 8.4% solution, 1 mEq/mL (total: 50 mEq/syringe).
    3) ADULT DOSE: 50 mL (50 mEq) IV over 5 minutes, repeated at 20 to 30 minute intervals (Saxena, 1989).
    4) PEDIATRIC DOSE: 1 to 2 mL/kg/dose (1 to 2 mEq/kg/dose) IV every 2 to 4 hours or as required by pH (Barkin, 1986). The onset is 15 minutes, the duration of action 1 to 2 hours (Ellenhorn & Barceloux, 1997).
    E) INSULIN (CLASS)
    1) Enhances intracellular potassium shift.
    2) ADULT DOSE: Administer 25 g of dextrose (250 mL of a 10% solution) IV over 30 minutes, and then continue the infusion at a slower rate.
    a) Ten units of regular insulin are given subQ or added to the infusion.
    3) ALTERNATIVE DOSE: 50 mL of a 50% dextrose solution with 5 to 10 units of regular insulin may be administered IV over 5 minutes.
    a) Typically, this regimen will lower serum potassium by 1 to 2 mEq/L within 30 to 60 minutes with the decrease lasting for several hours (Saxena, 1989).
    4) PEDIATRIC DOSE: 0.5 to 1 g/kg/dose followed by 1 unit of regular insulin IV for every 4 grams of glucose infused; may repeat every 10 to 30 minutes (Barkin, 1986).
    5) HYPEROSMOLARITY: It must be remembered that 50% dextrose, and even 25% dextrose, are very hyperosmolar and may be sclerosing to peripheral veins (Chameides, 1988); administration of hypertonic solutions via central lines is preferred, if possible.
    F) SODIUM POLYSTYRENE SULFONATE
    1) SUMMARY
    a) Sodium polystyrene sulfonate, a cationic exchange resin, has been used to treat severe hyperkalemia.
    2) ADULT DOSE
    a) ORAL: Average daily adult dose is 15 g to 60 g. The dose is usually administered as a 15 g resin 1 to 4 times per day as needed in a small (20 mL to 100 mL) slurry of water or syrup (to increase palatability) (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    b) RECTAL: It may be given as a retention enema, although this method is less effective than oral administration. DOSE: 30 g to 50 g resin as a retention enema every 6 hours. Dilute each dose as a warm emulsion (body temperature) in 100 mL of an aqueous vehicle (eg 20% Dextrose in Water). Gently, agitate the solution during administration. The enema should be retained as long as possible; followed by a cleansing enema (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    3) PEDIATRIC DOSE
    a) SUMMARY: The effectiveness of sodium polystyrene sulfonate has not been established in pediatric patients (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    b) ORAL: INFANTS and SMALLER CHILDREN: Use lower doses than adults; consider utilizing the exchange rate of 1 milliequivalent of excess potassium per gram of resin as the basis for the calculation. NEONATES: Sodium polystyrene sulfonate should NOT be given by the oral route to neonates (Prod Info KAYEXALATE(R) oral suspension, rectal suspension, 2003).
    c) RECTAL: INFANTS and SMALLER CHILDREN: Use lower doses than adults; consider utilizing the exchange rate of 1 milliequivalent of potassium per gram of resin as the basis for the calculation. NEONATES and CHILDREN: Rectal administration should be performed with caution, as excessive dosage or inadequate dilution could result in impaction of the resin (Prod Info KAYEXALATE(R) oral suspension, rectal suspension, 2003).
    4) MONITORING PARAMETERS
    a) Monitor serum electrolytes, particularly potassium and sodium concentrations.
    b) Monitor ECG for conduction disturbances, dysrhythmias.
    5) ADVERSE EFFECTS
    a) Nausea, vomiting, gastric irritation, anorexia and constipation can develop. Diarrhea may occur infrequently. Electrolyte abnormalities such as hypocalcemia, hypokalemia, hypomagnesemia and sodium overload are also possible (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010). Large doses in the elderly may cause fecal impaction, and rarely colonic necrosis (Lillemoe et al, 1987).
    b) The combined use of sorbitol and sodium polystyrene sulfonate have produced intestinal necrosis, which can be fatal. Concomitant use is not recommended (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    c) Intestinal obstruction from aluminum hydroxide concretions has occurred when administered in combination with sodium polystyrene sulfonate (Townsend et al, 1973).
    G) BEZOAR
    1) CASE REPORT (BEZOAR): A 44-year-old woman developed hyperkalemia (serum potassium concentration, 7.3 mmol/L) after ingesting an unknown amount of extended-release potassium tablets and alprazolam. Based on the patient's prescription usage, it was suggested that she ingested about 600 mEq (thirty 20-mEq tablets) of extended-release potassium tablets and 60 mg (sixty 1-mg tablets) of alprazolam. Initially, she was treated with albuterol, calcium gluconate, insulin, dextrose, and sodium bicarbonate; however, a radiographic study revealed a bezoar containing potassium in the gastric fundus. Since the patient did not tolerate whole bowel irrigation using a nasogastric tube, esophagogastroduodenoscopy (EGD) was used successfully to remove the bezoar and her serum potassium concentration normalized about 11 hours after presentation (Briggs & Deal, 2014).

Enhanced Elimination

    A) HEMODIALYSIS
    1) Hemodialysis is effective for removing potassium but is often too slow to be practical in treatment of acute poisoning. Patients who cannot tolerate fluids or have kidney dysfunction may benefit from dialysis (Schonwald, 2004).

Abstracts

Case Reports

    A) ADULT
    1) A 58-year-old woman survived a potassium ingestion of approximately 20 tablets (each containing 630 mg [8 mEq] of potassium chloride). Her serum potassium at 6 hours postingestion was 9.1 mEq/L (Illingworth & Proudfoot, 1980).
    2) A 24-year-old man had 3 episodes of self-terminating ventricular tachycardia 24 hours after he took 100 slow-release potassium tablets. His serum potassium concentration was 3.9 mmol/L (Colledge et al, 1988).
    3) FATALITY: A 26-year-old man died after ingesting approximately 40 Slow-K tablets (each containing 600 mg of potassium chloride) with a serum potassium of 9.3 mEq/L (Illingworth & Proudfoot, 1980).
    4) FATALITY: A 46-year-old ingested 100 Slow-K tablets (each containing 600 mg (8 mEq) of potassium chloride) and was in full cardiopulmonary arrest within an hour. The ingested dose was 16 mEq/kg. The patient was given 1 mg of epinephrine IV 4 times, calcium gluconate 10 mg IV, 5% dextrose at 500 mL/hour, and insulin 10 units/hour. Three doses of 54 mEq each of sodium bicarbonate were given. She was defibrillated 3 times with 400 joules. A single bolus of 250 mg of bretylium was given IV, then a 2 mg/min drip was started. The patient was lavaged, given activated charcoal 50 g. Serum potassium was 9.6 mEq/L 1 hour postingestion, and was 7.6 mEq/L 3 hours later. The patient was subsequently given Kayexalate(R) 50 g in 200 mL of 20% sorbitol rectally, 10 units/500 mL of regular insulin and 45 mEq of sodium bicarbonate IV. The patient required an intermittent dopamine drip to maintain her blood pressure over the next 5 days. X-rays showed that tablets remained in the abdomen. She died 14 days after ingesting the tablets (Saxena, 1988).

Range Of Toxicity

Summary

    A) TOXICITY: ADULT: Doses as low as 2 to 2.5 mEq/kg of potassium have been reported to cause toxicity. GENERAL: NORMAL SERUM CONCENTRATIONS: 3.5 to 5 mEq/L; MINIMAL TOXICITY: Potassium concentrations under 6.5 mEq/L; MODERATE TOXICITY: Concentrations between 6.5 and 8 mEq/L produce lassitude, fatigue, and weakness. SEVERE TOXICITY: Concentrations over 8 mEq/L, complete neuromuscular paralysis may dominate the clinical picture. Death from cardiac arrest usually occurs at 9 to 12 mEq/L. It may occur at lower levels if cellular potassium is severely depleted.
    B) THERAPEUTIC: ADULT: 40 to 80 mEq/day is a typical daily dose. In patients with renal insufficiency, the dose may be lower. PEDIATRIC: 2 to 3 mEq/kg/day is the usually daily dose.

Therapeutic Dose

    7.2.1) ADULT
    A) ORAL: POWDER FOR SOLUTION OR EXTENDED RELEASE TABLET
    1) AVERAGE DIETARY INTAKE: The usual dietary potassium intake in the average adult is 50 to 100 mEq/day (Prod Info potassium chloride extended-release oral tablets, 2006).
    2) PREVENTION OF HYPOKALEMIA: The usual oral dose is 20 mEq/day. However, dosage is individualized based on the clinical needs, serum electrolyte concentration, or ECG results of each patient (Prod Info KLOR-CON(R) powder for oral solution, 2009; Prod Info potassium chloride extended-release oral tablets, 2006).
    3) POTASSIUM DEPLETION: The usual adult requirement is 40 to 100 mEq/day orally. However, dosage is individualized based on the clinical needs, serum electrolyte concentration, or ECG results of each patient (Prod Info KLOR-CON(R) powder for oral solution, 2009; Prod Info potassium chloride extended-release oral tablets, 2006). MAXIMUM DOSE: Should not exceed 20 mEq/dose (Prod Info potassium chloride extended-release oral tablets, 2006).
    4) EXTENDED-RELEASE: Extended-release oral potassium tablets should be taken with meals and a glass of water or other beverage. Ingesting the tablets on an empty stomach may result in gastric irritation. Do not crush, chew, or suck extended-release tablets (Prod Info potassium chloride extended-release oral tablets, 2006).
    5) POWDER FOR SOLUTION: Each packet of potassium powder should be dissolved completely in at least 4 to 5 ounces of cold water or other beverage and ingested after meals (Prod Info KLOR-CON(R) powder for oral solution, 2009).
    6) Some references suggest that for a person starting with a 3 mEq/L level or more, 100 to 200 mEq is necessary to raise the level 1 mEq/L (Holland & Fuchs, 1983).
    7.2.2) PEDIATRIC
    A) INTRAVENOUS
    1) HYPOKALEMIA: 0.5 to 0.75 mEq/kg IV infused over 1 to 2 hours, then reassess (Khilnani, 1992; Schaber et al, 1985; DeFronzo & Bia, 1981). MAXIMUM DOSE: Should not exceed 40 mEq/dose.
    B) ORAL
    1) The safety and efficacy of potassium in the pediatric or adolescent population have not been established (Prod Info KLOR-CON(R) powder for oral solution, 2009; Prod Info potassium chloride extended-release oral tablets, 2006). However, potassium has been used in select pediatric cases. The usual dose is 3 to 8 mEq/kg/day orally (Abdel-al et al, 1999; Jospe & Forbes, 1996; Feld et al, 1988; Linshaw, 1987) divided 1 to 5 times per day depending on tolerability and dose. Start at lower dose and adjust based on serum potassium concentrations (Prod Info KLOR-CON(R) powder for oral solution, 2009).
    2) SUPPLEMENTATION WITH DIURETICS: 1 to 3 mEq/kg/day orally (Hobbins et al, 1981; Baylen et al, 1980). MAXIMUM DOSE: Should not exceed 20 mEq/day (Prod Info KLOR-CON(R) powder for oral solution, 2009).
    3) DOSE ADJUSTMENT: Adjust dosage based on monitoring of serum potassium concentrations (Prod Info potassium chloride injection, 2004).

Minimum Lethal Exposure

    A) SUMMARY
    1) NORMAL SERUM CONCENTRATIONS: 3.5 to 5 mEq/L (Prod Info KLOR-CON(R) extended release tablets, 2005; Schonwald, 2004).
    2) MINIMAL TOXICITY: Potassium concentrations under 6.5 mEq/L. Evidence of cardiac toxicity is rare below 6.5 mEq/L (Schonwald, 2004).
    3) MODERATE TOXICITY: Concentrations between 6.5 and 8 mEq/L produce lassitude, fatigue, and weakness.
    4) SEVERE TOXICITY: Concentrations over 8 mEq/L, complete neuromuscular paralysis may dominate the clinical picture. Cardiac manifestations of toxicity are also common at concentrations above 8 mEq/L (Schonwald, 2004). Death from cardiac arrest usually occurs at 9 to 12 mEq/ L (Prod Info KLOR-CON(R) extended release tablets, 2005).
    B) ROUTE OF EXPOSURE
    1) INTRAVENOUS INJECTION: Although potassium kinetics are complicated, some useful approximations may be made. For bolus intravenous injections, the human lethal dose is 0.75 to 0.9 mEq/kg (54 to 63 mEq/70 kg).
    C) CASE REPORTS
    1) ORAL
    a) ADULT
    1) A 26-year-old man died after ingesting approximately 40 Slow-K tablets (each containing 600 mg of potassium chloride; total potassium dose 320 mEq) with a serum potassium of 9.3 mEq/L. This dose is equivalent to 4 mEq/kg based on the assumption of an 80 kg body weight (Illingworth & Proudfoot, 1980).
    2) A 32-year-old woman ingested 47 potassium chloride tablets (strength unspecified) and died. The postmortem level (18 hours later) was 10.8 mEq/L (Wetli & Davis, 1978).
    3) A 46-year-old woman ingested 100 Slow-K tablets (each containing 600 mg (8 mEq) of potassium chloride) and was in full cardiopulmonary arrest within an hour. The ingested dose was 16 mEq/kg. Her initial serum potassium was 9.6 mEq/L. She died 14 days after ingestion despite aggressive care (Saxena, 1988).
    PEDIATRIC
    4) An 8-month-old child ingested 26 mEq/kg of potassium (a blood level of 10.2 mEq/L) and nearly died (Kallen et al, 1976).

    2) INJECTION
    a) ADULT
    1) POTASSIUM ASPARTATE: A man and a woman, both in their thirties, injected potassium aspartate intravenous solutions in a fatal suicide attempt. Approximately 150 mL of a 761 mEq/L concentrated solution had been administered to the woman and approximately 30 mL of a 746 mEq solution, plus 35 mL from a syringe solution containing 690 mEq/L, had been administered to the man. Potassium levels on autopsy for the woman and man were 62.8 and 49.7 mEq/L, respectively. Serum levels also indicated toxic levels of phenobarbital, promethazine, chlorpromazine, and low plasma levels of etizolam and brotizolam for both patients(Watanabe et al, 2011).

Maximum Tolerated Exposure

    A) SUMMARY
    1) 2 to 2.5 mEq/kg: Normal homeostatic mechanisms can be overwhelmed following acute ingestion of about 2 to 2.5 mEq/kg or more in patients with normal renal function (Illingworth & Proudfoot, 1980; Saxena, 1989).
    a) This is equivalent to 2 to 3 tablets containing 8 mEq for a child weighing 10 kg. Smaller oral doses of 30 to 45 mEq can lead to hyperkalemia in adult patients with renal insufficiency (Saxena, 1989).
    2) THE AMOUNT OF POTASSIUM NEEDED TO INCREASE SERUM LEVELS is dependent on factors such as absorption rate, renal function, intracellular potassium stores, and acid-base status. Kinetics are nonlinear at higher doses (Freitag & Miller, 1980). Thus calculations used to derive doses for hypokalemic patients may not be applicable to normokalemic patients who overdose.
    B) CASE REPORTS
    1) CASE REPORT (BEZOAR): A 44-year-old woman developed hyperkalemia (serum potassium concentration, 7.3 mmol/L) after ingesting an unknown amount of extended-release potassium tablets and alprazolam. Based on the patient's prescription usage, it was suggested that she ingested about 600 mEq (thirty 20-mEq tablets) of extended-release potassium tablets and 60 mg (sixty 1-mg tablets) of alprazolam. Initially, she was treated with albuterol, calcium gluconate, insulin, dextrose, and sodium bicarbonate; however, a radiographic study revealed a bezoar containing potassium in the gastric fundus. Since the patient did not tolerate whole bowel irrigation using a nasogastric tube, esophagogastroduodenoscopy (EGD) was used successfully to remove the bezoar and her serum potassium concentration normalized about 11 hours after presentation (Briggs & Deal, 2014).
    2) ADULT: A 42-year-old woman presented to the emergency department on two separate occasions after intentionally ingesting sustained-release tablets each containing 8 mEq of potassium chloride. During the first episode she presented with a potassium level of 5.5 mmol/L 90 minutes after ingesting 40 tablets and was successfully treated with supportive care, including whole bowel irrigation. At the second episode, she presented with a potassium level of 8.5 mmol/L approximately 5 hours after ingesting 100 tablets and was successfully decontaminated during 10 hours of hemodialysis. Whole bowel irrigation was not attempted during the second episode as most of the tablets had been absorbed. In each case she was discharged to psychiatric care within 2 to 3 days without sequelae (Gunja, 2011).
    3) ADULT: A 58-year-old woman survived a potassium ingestion of approximately 20 tablets (each containing 630 mg (8 mEq) of potassium chloride). Her serum potassium peaked at 6 hours postingestion at 9.1 mEq/L (Illingworth & Proudfoot, 1980).
    4) One case where 164 mEq (2 mEq/kg based on an 80 kg body weight) was ingested acutely resulted in a peak level of 9.1 mEq/L in 6 hours (Illingworth & Proudfoot, 1980).
    5) CASE REPORT: A 67-year-old hemodialysis patient was diagnosed with severe hyperkalemia (potassium concentration: 9.3 mmol/L; reference levels: 3.5 to 4.7 mmol/L) after developing unconsciousness and leg paralysis. Following supportive care, including treatment with calcium, insulin, glucose, sodium polystyrene sulfonate, and a hemodialysis session, the patient's condition improved and the ECG normalized. It was determined that the patient was using about 40 mmol/day of added potassium from a low-sodium/potassium-enriched spread (Becel pro.activ) to improve his blood pressure (van der Steen et al, 2012).
    6) CASE REPORT: Hyperkalemia developed in a 57-year-old woman who was being treated with continuous ambulatory peritoneal dialysis (CAPD; 3 daily exchanges with 2.5% dextrose solution) for end-stage renal disease secondary to renal tuberculosis and obstructive uropathy. She was compliant with her low-potassium diet regimen and used 600 mg of potassium chloride daily to maintain normal serum potassium concentrations. During a routine blood test, more than a year after starting CAPD, hyperkalemia (potassium: 6.7 mmol/L; bicarbonate of 23 mmol/L) was discovered. Following treatment with ion-exchange resin, her potassium concentration returned to normal, but increased again to 6 mmol/L. Three weeks later, it was determined that she was using a new brand of salt (LoSalt) containing potassium chloride (estimated daily intake of LoSalt: 3750 mg; 95 mmol of potassium daily). She recovered completely following the discontinuation of the potassium-containing salt (Yip et al, 2012).
    C) PEDIATRIC
    1) A 6-year-old boy developed hyperkalemia (potassium level 7.6 mmol/L on admission) after ingesting an unknown amount of sustained-release potassium chloride tablets. Approximately 50 potassium chloride tablets (Slow-K) were recovered from the vomitus. Following supportive care, including continuous venovenous hemodialysis, he recovered and was discharged on day 3. Whole bowel irrigation was not attempted as most of the tablets had been absorbed (Gunja, 2011).
    2) A 6-week-old infant was successfully resuscitated from an iatrogenic potassium intoxication resulting in a potassium level of 17.7 mmol/L. Following cardiac surgery, the infant erroneously received a 15% potassium chloride solution (total 30 mmol) intravenously instead of a 5% glucose solution. Potassium levels were lowered with conventional measures; hemodialysis was not performed. The authors theorized that conventional measures were successful because the acute nature of the exposure had not allowed the infused potassium to be distributed into the extravascular space (Horisberger et al, 2004).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ACUTE
    a) MINIMAL TOXICITY - Potassium level under 6.5 milliequivalents/liter rarely manifest cardiac toxicity (Ellenhorn & Barceloux, 1988).
    b) MODERATE TOXICITY - Potassium levels between 6.5 and 8 milliequivalents/liter may cause lassitude, fatigue, and weakness. Neurological examination will disclose weakness or incipient ascending paralysis, decreased reflex response, and paresthesias.
    c) SEVERE TOXICITY - With serum potassium levels over 8 milliequivalents/liter, complete neuromuscular paralysis may dominate the clinical picture.
    1) Death from cardiac arrest occurs usually at 10 to 12 milliequivalents/liter. It may occur at lower levels if cellular potassium is severely depleted.
    2) Cardiac arrest has been reported in patients with serum potassium levels of 8.4 milliequivalents/liter, and 9.6 milliequivalents/liter following overdose (Saxena, 1988; Schim van der Loeff et al, 1988).
    3) The major life-threatening effect is on the cardiovascular system, where bradycardia, vascular collapse, and cardiac arrest may develop rapidly. The EKG is fairly characteristic.
    4) A progression of changes serving as a warning precedes cardiac arrhythmias. Initially there is peaking of the T waves and widening of the QRS complexes as the level exceeds 6.5 milliequivalents/liter.
    5) The P wave amplitude diminishes and P-R interval is prolonged with further serum level increases. As the level of potassium exceeds 7.5 to 8 milliequivalents/liter, the P wave may disappear. Ventricular fibrillation or standstill will follow if treatment is not started.
    6) Generally, treatment should be started if serum levels exceed 6.5 milliequivalents/liter or if cardiac arrhythmias are present.

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) Potassium (metal):
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 700 mg/kg (Bovet & Bovet-Nitti, 1984)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Potassium is the chief intracellular ion. The K gradient across the cell membrane is the principle source of the -90mV resting potential.
    1) Although physiologically crucial, plasma K is only about 0.4% of total body K. Most (90%) is intracellular, and 75% of the extracellular K is in bone. Total body K is about 52 mEq/kg, of which 45 mEq/kg (3150 mEq/70kg) is exchangeable.
    B) Plasma potassium is normally closely regulated at the expense of intracellular stores. The principal route of excretion is renal (small amount in the stool).
    1) Potassium is actively reabsorbed in the proximal tubule, and K that appears in the urine is dependent on distal tubular secretion (Edelman & Leibman, 1959).
    C) An excess hydrogen ion concentration (acidosis) inhibits secretion, while alkalosis favors potassium secretion. Elevation of K above 6 mEq/L stimulates aldosterone which enhances excretion of potassium.

Physicochemical

Physical Characteristics

    A) POTASSIUM is a silvery-white metal which tarnishes in air (Budavari, 1996)
    B) POTASSIUM CHLORIDE is a white granular powder or colorless crystals, is odorless, and has a saline taste. It is freely soluble in water and insoluble in alcohol (Prod Info KLOR-CON(R) extended release tablets, 2005).
    C) POTASSIUM CITRATE is a white granular powder that is insoluble in organic solvents, almost insoluble in alcohol, and soluble in water at 154 g/100 mL (Prod Info potassium citrate extended-release oral tablets, 2009).
    D) POTASSIUM GLUCONATE is a white, odorless crystalline powder with a slightly bitter taste.

Molecular Weight

    A) POTASSIUM CHLORIDE: 74.55 (Prod Info potassium chloride in dextrose and sodium chloride injection, 2004)
    B) POTASSIUM CITRATE: 324.41 (Prod Info potassium citrate extended-release oral tablets, 2009)

References

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