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Potassium chloride
1. NAME
1.1 Substance
1.2 Group
1.3 Synonyms
1.4 Identication numbers
1.4.1 CAS number
1.4.2 Other numbers
1.5 Brand names, Trade names
1.6 Manufacturers, Importers
2. SUMMARY
2.1 Main risks and target organs
2.2 Summary of clinical effects
2.3 Diagnosis
2.4 First aid measures and management principles
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
3.3 Physical properties
3.3.1 Properties of the substance
3.3.2 Properties of the locally available formulation
3.4 Other characteristics
3.4.1 Shelf-life of the substance
3.4.2 Shelf-life of the locally available formulation
3.4.3 Storage conditions
3.4.4 Bioavailability
3.4.5 Specic properties and composition
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4. USES
4.1 Indications
4.2 Therapeutic dosage
4.2.1 Adults
4.2.2 Children
4.3 Contraindications
5. ROUTES OF ENTRY
5.1 Oral
5.2 Inhalation
5.3 Dermal
5.4 Eye
5.5 Parenteral
5.6 Other
6. KINETICS
6.1 Absor
Absorption by route of exposure
6.2 Distribution by route of exposure
6.3 Biological half-life by route of exposure
6.4 Metabolism
6.5 Elimination by route of exposure
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
7.1.1 Toxicodynamics
7.1.2 Pharmacodynamics
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
7.2.1.2 Children
7.2.2 Relevant animal data
7.2.3 Relevant in vitro data
7.3 Carcinogenicity
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7.4 Teratogenicity
7.5 Mutagenicity
7.6 Interactions
7.7 Main adverse effects
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL
INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecied) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecied) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecied) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Conrmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
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10. MANAGEMENT
10.1 General principles
10.2 Relevant laboratory analyses
10.2.1 Sample collection
10.2.2 Biomedical analysis
10.2.3 Toxicological analysis
10.2.4 Other investigations
10.3 Life supportive procedures and symptomatic/specic treatment
10.4 Decontamination
10.5 Elimination
10.6 Antidote treatment
10.6.1 Adults
10.6.2 Children
10.7 Management discussion
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
11.2 Internally extracted data on cases
11.3 Internal cases
12. Additional information
12.1 Availability of antidotes
12.2 Specic preventive measures
12.3 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES),
COMPLETE ADDRESS(ES)
PHARMACEUTICALS
1. NAME
1.1 Substance
Potassium chloride
1.2 Group
Electrolytes/agents
1.3 Synonyms
Chlorure de potassium
Cloreto de potassio
Cloruro de potasio
Kalii chloridum
Kalium chloratum
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Potassi chloridum
Sylvine
1.4 Identification numbers
1.4.1 CAS number
7447-40-7
1.4.2 Other numbers
1.5 Brand names, Trade names
Camcopot; Chloropotassuril; Chlorvescent; ClK; Diffu-K; Enseal
potassium chloride; Kaleorid; Kalitabs; Kalium-Duriles; KaonCl; Kaskay; Kayback; Kay-Cll-L; K-Contin; Klor-Con; K-Norm; KTab; Lento-Kalium; Leo K; Micro K; Nu-K; Peter-Kal; PfiKlor;
Potavescent; Rekawan; Repone K; Slow-K; Span-K
Celeka, Durules-K (Argentina)
Chlorvescent, K-San, Kay Ciel, Span-K (Australia)
Chloropotassuril, Kalium Durettes, Steropotassium, Ultra-Kchlor (Belgium)
Kaochlor, Kay Ciel, K-lyte/C1, K-10 Solution, Roychlor
(Canada)
Kaleorid, Kalinorm (Denmark)
Kaleorid, Potassion (France)
Kalinor, Kalcium-Duriles, Rekawan (Germany)
Kadalex, Lento-Kalium (Italy)
Kalium-Durettes (Netherlands)
Kaleorid, Kalilente, Kalium duretter, Kali Retard (Norway)
Peter-Kal, Lento-K (South Africa)
Miopotasio, Potasion (Spain)
Kaleorid, Kalilente, Kalipor, Kalitabs, Kalium-Duretter
(Sweden)
Kaliguild (Switzerland)
Kaochlor, Kaochlor S-F, Kaon-Cl, Kato, Kay Ciel, Klor, KlorCon, K-Lor,
Klorfen, Klorvess 10% Liquid, Klotrix, K-lyte/Cl, Pan-Kloride,
PfiKlor, Rum-K
(USA)
1.6 Manufacturers, Importers
Abbott; Adria; Astra; Baxter; Beecham; Benzo; Borlex; BristolMyers; CA Roy; Ciba; Ciba-Geigy; Collett-Marwell; Columbia
Drug; Ferrosan; Fleming; Gama-Geve; Giulini; Hssle; ICN; Leo;
Liorens; Mead-Johnson; Nordmark; Panray; Petersen; Pfizer;
Proten; Robin; San-Bolagen; Sandoz-Wander; Schering
Corp/Essex; Sheuli; Sopar; Sterop; Upsher-Smith
2. SUMMARY
2.1 Main risks and target organs
Cardiac and related effects are the most important risks of
potassium chloride overdose. Neuromuscular symptoms may
occur. Gastrointestinal ulceration may be caused by entericcoated potassium chloride tablets. Local pain and
inflammation may develop from intravenous or subcutaneous
administration.
2.2 Summary of clinical effects
Vomiting, diarrhoea, listlessness, muscular cramps,
hypotension and arrhythmias.
2.3 Diagnosis
The diagnosis is based on the clinical presentation of the
patient: vomiting, diarrhoea, muscular cramps, hypotension;
the presence of hyperkalaemia and electrocardiographic
changes.
2.4 First aid measures and management principles
Basic life support measures are essential in severely poisoned
patients:
establish IV-line, obtain blood sample for electrolytes, BUN,
glucose and arterial blood gas analysis;
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of potassium.
4.3 Contraindications
Potassium should not be given to patients with hyperkalemia.
Patients with chronic renal disease or any other condition
that impairs potassium excretion should be carefully
monitored. Potassium should not be administered to patients
receiving potassium-sparing diuretics (e.g. spironolactone) in
the absence of hypokalaemia. Tablets should not be given to
patients who may have delayed gastrointestinal passage of
solid preparations.
5. ROUTES OF ENTRY
5.1 Oral
Ingestion is the most common route of exposure.
5.2 Inhalation
Unknown.
5.3 Dermal
Unknown.
5.4 Eye
Unknown.
5.5 Parenteral
Parenteral administration is common.
5.6 Other
Unknown.
6. KINETICS
6.1 Absor
Absorption by route of exposure
Almost all orally administered potassium chloride is absorbed.
The peak level and its occurrence time after ingestion depend
on the preparation administered.
6.2 Distribution by route of exposure
Orally and intravenously administered potassium chloride
reaches an equilibrium between the extracellular fluid and
intracellular space.
6.3 Biological half-life by route of exposure
Not applicable.
6.4 Metabolism
Not applicable.
6.5 Elimination by route of exposure
At steady state continuous excretion of potassium chloride in
the urine and faeces equals the daily intake.
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
7.1.1 Toxicodynamics
The cardiac effects of hyperkalemia are principal toxic
effects of potassium. They are mediated through changes
in the intra/extracellular potassium ratio, which alters
cardiac conduction. With no underlying conduction
defects a transient increase in cardiac conduction
occurs with potassium concentrations above 7 mmol/l,
but a profound depression occurs when concentrations
rise over 8.0 mmol/l. One of the effects of
hyperkalemia is the depolarisation of cardiac muscle,
which interferes with normal contractility. Potassium
chloride exerts a direct irritant effect on the
gastrointestinal mucosa.
7.1.2 Pharmacodynamics
Potassium is an essential element in the body. It is
the main intracellular cation: 98% of total body
potassium is located within the cells. There is an
active and continuous transportation of potassium into
the cell. Potassium balance is delicate. It can be
divided into internal balance, i.e. the relation between
the intracellular space (ICS) and the extracellular
fluid (ECF), and external balance, i.e. potassium intake
versus excretion (Cox et al., 1981; Martin et al.,
1986).
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1986).
Potassium is involved in numerous enzymatic reactions,
in nerve conduction, muscle contraction and carbohydrate
metabolism.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Acute ingestion of 2 to 2.5 mmol/kg can result
in hyperkalemia
LDLo (Lowest lethal dose) is:
Oral
0.51 mmol/kg (Lewis, 1992)
IV
0.77 to 0.9 mmol/kg, depending on rate
of infusion (Bhatkhande, 1977)
7.2.1.2 Children
Two to three tablets each containing 8 mmol may
be lethal to a child weighing ten kg. The LDLo
is 12.6 mmol/kg following oral administration
(Lewis, 1992)
7.2.2 Relevant animal data
LD50 (rat, oral)
2600
(mouse, oral)
383
(rat, IV)
39
(mouse, IV)
117
mg/kg
mg/kg
mg/kg
mg/kg
(Saxena, 1989)
7.2.3 Relevant in vitro data
No data available.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
No data available.
7.6 Interactions
Digitalis glycosides (in overdose) inhibit cellular uptake of
potassium thus resulting in hyperkalemia.
7.7 Main adverse effects
Gastrointestinal disturbance.
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
Serum, plasma and urine.
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
Frozen (-20C) serum and urine.
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
Frozen (-20C) serum and urine.
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
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9.1.2
9.1.3
9.1.4
9.1.5
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ultimately result in a joining of the QRS and the Twave. Ventricular fibrillation and asystole may then
occur.
Reversible heartblock and ectopic beats can be present.
(Williams et al., 1986; Borras et al., 1988; Saxena,
1989)
The ECG of hyperkalemia can mimic a myocardial
infarction (Simon, 1988).
Hypotension is a result of the cardiac effects.
9.4.2 Respiratory
Respiration is depressed primarily by weakness of the
respiratory muscles (Saxena, 1989).
9.4.3 Neurological
9.4.3.1 CNS
Cranial nerves and cerebral function remain
unimpaired (McCaughan, 1984).
Paresthesias and decreased proprioception can
occur.
9.4.3.2 Peripheral nervous system
A number of neuromuscular effects can be seen,
usually with potassium concentrations of 7.0
mmol/l or higher. General weakness and
flaccidity precede ascending paralysis. Tremor,
paresthesias, decreased vibration perception and
proprioception can be seen, but the sensory
function is usually intact. Dysarthria and
dysphagia may occur (Borras et al., 1988).
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
A number of neuromuscular effects can be seen,
usually with potassium concentrations of 7.0
mmol/l or higher. General weakness and
flaccidity precede ascending paralysis. Tremor,
paresthesias, decreased vibration and
proprioception can be seen but the sensory
function is usually intact. Dysarthria and
dysphagia may occur (Borras et al., 1988) (see
Section 9.4.3.2).
9.4.4 Gastrointestinal
The initial signs of poisoning are generally
gastrointestinal: nausea, vomiting and diarrhoea. These
symptoms can develop into abdominal pain and eventually
paralytic ileus. Gastrointestinal perforation after
oral exposure can occur (Saxena, 1989). Bleeding and
perforation have been reported in patients receiving
solid forms of potassium chloride.
9.4.5 Hepatic
Not relevant.
9.4.6 Urinary
9.4.6.1 Renal
Not relevant.
9.4.6.2 Other
Not relevant.
9.4.7 Endocrine and reproductive systems
Hyperkalemia can potentiate the effects of
hypoaldosteronism (Cox, 1981) and can complicate adrenal
insufficiency.
9.4.8 Dermatological
Local pain and inflammation may result from subcutaneous
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ECG
Abdominal X-ray may reveal intact tablets of
potassium present in the gut.
10.3 Life supportive procedures and symptomatic/specific
treatment
The usual basic life support measures should be implemented,
followed by procedures to redistribute potassium and/or
increase elimination. (see treatment protocol for
hyperkalaemia)
Bicarbonate increases blood pH
transfer of potassium into the
renal excretion of potassium.
15 minutes and the duration is
1986).
Adults:
50 ml/dose (iv over 5 minutes, to repeat every 20
to 30 minutes) Children: 1 to 2 ml/kg/dose (iv every two to
four hours)
The intravenous administration of glucose and insulin moves
potassium into the cells. Several different alternatives
for the administration exist. The regime below will lower
the potassium concentration by 1 to 2 mmol/l within 30 to 60
minutes, and the decrease will persist for several hours (De
Frenzo et al., 1982; Stein, 1986).
Adults:
minutes)
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10.4 Decontamination
If vital signs are compromised, primary stabilization should
always take precedence over decontamination procedures.
Gastric evacuation can be achieved by emesis or gastric
lavage according to the clinical status of the patient.
Activated charcoal does not bind potassium but may be used
if other agents have been ingested.
Whole gut lavage may necessary following ingestion of slowrelease potassium formulations (Illingworth & Proudfoot,
1980).
10.5 Elimination
Enhancement of elimination may be achieved by exchange
resins, haemodialysis or peritoneal dialysis.
Haemodialysis and peritoneal dialysis are effective and are
the best approach in patients who cannot tolerate fluid
loads, or when acidosis does not respond to bicarbonate
treatment (Saxena, 1989).
Cation-exchange resins
Because exchange resins take hours or days to lower serum
potassium, they may be insufficient to lower severe
hyperkalemia rapidly, especially in an emergency. The resin
usually used is polystyrene sulfonate (Kayexalate) and the
average daily dose is 20 to 50 g, divided into four doses.
Smaller children should receive a lower dose. Each dose
should be given as a suspension in water or syrup, or 20%
sorbitol (20 to 100 ml). The resin is less effective if
given as enema. The recommended doses are: (for adults) 30
to 50 g in 100 ml of a warm emulsion (e.g. sorbitol), which
should be retained as long as possible and followed by a
cleansing enema. The dose does not increase the excretion
of potassium nor facilitate the shift of potassium into the
cell.
The dose may be repeated every four hours up to four to five
times per day. Plasma electrolytes should be monitored at
least every four hours (Saxena, 1989).
10.6 Antidote treatment
10.6.1 Adults
No antidote available.
10.6.2 Children
No antidote available.
10.7 Management discussion
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Case 1: A 29-year-old female felt weak and had experienced
a period of diarrhoea. She thought she was hypokalemic and
took a potassium-containing salt substitute. On admission
to hospital (emergency room) she requested extra iv
potassium administration. Plasma potassium concentration
was 8.4 mmol/l, serum creatinine 102 micromol/l, sodium 145
mmol/l, albumin concentration 35 g/l, Hb 13.5 mmol/l.
The ECG showed absent P-waves, broadened QRS-complex and
peaked T-waves. The patient experienced cardiac arrest and,
later, generalized seizures due to hypoxia rather than
hyperkalaemia. Resuscitation, intubation, intravenous
calcium gluconate, sodium bicarbonate and 40% glucose in
combination with insulin were administered. After three
hours the potassium level was 4.8 mmol/l. The patient was
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hours the potassium level was 4.8 mmol/l. The patient was
ventilated mechanically and extubated after ten days. She
was conscious but could not speak and she was now
quadriplegic (Schim van der Loeff, 1988).
Case 2: A 24 year-old male took slow-release potassium
tablets, 30 mefenamic acid capsules and 15 tablets of a
paracetamol/phenylpropanolamine hydrochloride compound after
drinking heavily. Two hours later he was admitted to
hospital after having vomited. He was not distressed. An
ECG showed sinus rhythm with peaking of the T-waves. Serum
potassium concentrations were 6.4 mmol/l. After gastric
lavage, 30 g calcium resonium was left in his stomach. He
was given iv calcium gluconate, dextrose and insulin, and
the serum potassium fell to 5.0 mmol/l. Three hours later
serum-potassium was 7.9 mmol. The patient had three
episodes of self limiting ventricular tachycardia 21 hours
after ingestion (Colledge & Fraser, 1988).
11.2 Internally extracted data on cases
To be completed by the Poisons Centre.
11.3 Internal cases
To be completed by the Poisons Centre.
12. Additional information
12.1 Availability of antidotes
No antidote available.
12.2 Specific preventive measures
Clear guidelines on treatment with potassium salts should be
given to patients who require prevention or treatment of
potassium deficiency, especially if they are also taking
diuretics and/or digitalis preparations. Oral doses of KCl
should be taken with meals and with a full glass of water.
Patients should be advised to check with their physician if
they have trouble swallowing the tablets, if stools are
tarry or gastrointestinal bleeding is noted (PDR, 1992).
12.3 Other
Serum potassium concentrations can be substantially higher
than plasma concentrations when the platelet count is over
500 x 109/l, or the white cell count is over 50,000/mm3
(Martin et al., 1986; Saxena, 1989).
There are several situations in which the plasma or serum
potassium concentration (or both) are falsely elevated and
do not provide a true estimate of the extracellular
potassium concentration. Prolonged tourniquet application
causes potassium release from ischaemic muscle (plasma and
serum concentrations elevated); and in vitro hemolysis with
potassium release from red blood cells (plasma and serum
concentration elevated) (Cox, 1981).
13. REFERENCES
Bhatkhande CY & Joglekar VD (1977) Fatal poisoning by potassium
in human and rabbit. Forensic Sci, 9 :33-36.
Colledge NR, Northridge B, Fraser DM (1988)
massive overdose of slow-release potassium.
Cox M (1981)
Potassium Homeostasis.
Survival after
Scot Med J, 33: 279.
Medical Toxicology.
Elsevier
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Illingworth RN & Proudfoot AT (1980) Rapid poisoning with slowrelease potassium. Br Med J, 281: 485-486.
Kallen RJ, Rieger CH, Cohen HS et al. (1976) Near fatal
hyperkalemia due to ingestion of salt substitute by an infant.
JAMA, 235: 2125-2126.
Lavinsky NG (1966)
Hyperkalemia.
Potassium.
Martindale.
29th ed.
46th Ed.
Postgrad
Acute
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Sweden
Tel: 46-8-338765
Fax: 46-8-327584
Date:
August 1992
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