Potassium chloride
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification 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 Specific properties and composition |
| 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 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 |
| 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 (unspecified) 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 (unspecified) 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 (unspecified) 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 Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 CNS |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Other |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ear, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Other |
| 9.6 Summary |
| 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/specific 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 Specific 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
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; Kaon-
Cl; Kaskay; Kayback; Kay-Cll-L; K-Contin; Klor-Con; K-Norm; K-
Tab; 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-K-
chlor (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, Klor-
Con, 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; Bristol-
Myers; CA Roy; Ciba; Ciba-Geigy; Collett-Marwell; Columbia
Drug; Ferrosan; Fleming; Gama-Geve; Giulini; Hässle; 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 enteric-
coated 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;
continuous ECG monitoring should be started;
cardiac dysrhythmias should be controlled with an appropriate
drug regimen;
emesis or gastric lavage should be performed as soon as
possible.
Consult the treatment protocol on the management of
hyperkalaemia. Reduce the plasma concentration of potassium by
infusion of sodium bicarbonate, glucose plus insulin, or
dialysis. These regimes shift potassium into cells; they do
not increase its elimination. Infusion of calcium salts may be
necessary to correct ECG changes.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Potassium is a natural element which is never found free in
nature. A large number of salts exist of which potassium
chloride is one.
3.2 Chemical structure
KC1
MW: 74.55 (K 52,4%, Cl 47,6%)
3.3 Physical properties
3.3.1 Properties of the substance
Solubility in water: 35.7 g/100 ml
Solubility in alcohol: 0.25 g/100 ml
Solubility in ether: insoluble
pH: approximately 7
Normal state at room temperature: white crystals
or crystalline powder or white granular powder
or colourless crystals, with saline taste,
odourless.
Density: 1.98
Melting point 773°C
3.3.2 Properties of the locally available formulation
3.4 Other characteristics
3.4.1 Shelf-life of the substance
Solid phase in airtight container - five years.
3.4.2 Shelf-life of the locally available formulation
3.4.3 Storage conditions
Store in airtight containers. Protect from light.
3.4.4 Bioavailability
3.4.5 Specific properties and composition
4. USES
4.1 Indications
Prevention and treatment of potassium deficiency, e.g.
when thiazide diuretics or corticosteroids are used in
case of excessive vomiting or diarrhoea, or diets poor
in potassium. It is also used in the treatment of
cumulative digitalis poisoning. There is no potential
for abuse.
4.2 Therapeutic dosage
4.2.1 Adults
In case of potassium deficiency, the dose should be
adjusted to the needs of the patient. For the
prevention of hypokalaemia the usual dose is 20 to 30
mEq of potassium per day; and 40 to 100 mEq or more per
day for the treatment of potassium depletion.
3.0 g of potassium chloride contain approximately 40
mmol of potassium (Ellenhorn and Barceloux, 1988).
4.2.2 Children
The dose usually indicated in children is 2 mmol/kg/day
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 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).
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 mg/kg
(mouse, oral) 383 mg/kg
(rat, IV) 39 mg/kg
(mouse, IV) 117 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 (-20°C) 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 (-20°C) 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
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
Type of test: Advanced quantitative.
Principle of test: Ion selective electrode. Flame
photometric technique.
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
Abdominal X-ray may reveal the presence of intact potassium
tablets in the gut.
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Symptoms of acute poisoning after ingestion of potassium
chloride are usually mild, provided renal function is
adequate. In large overdoses or in patients with renal
insufficiency, the symptoms may range from nausea,
vomiting and diarrhoea, with abdominal discomfort; to
weakness, muscle cramps, ascending paralysis, dysarthria
as well as hypotension and arrhythmias (Saxena, 1989).
Gastrointestinal ulceration, bleeding, perforation and
obstruction may follow the use of the solid dosage forms
of potassium chloride tablets.
9.1.2 Inhalation
Not relevant.
9.1.3 Skin exposure
Not relevant.
9.1.4 Eye contact
Not relevant.
9.1.5 Parenteral exposure
Symptoms of acute poisoning after parenteral
administration are similar to symptoms after oral
exposure but can appear more promptly and be more
severe.
Local pain and inflammation may result from intravenous
administration of potassium chloride (Ellenhorn and
Barceloux, 1988).
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
No data available.
9.2.2 Inhalation
No data available.
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
Hyperkalemia is quite common. In one hospital, 10% of
all hospital admissions over a two-month period had a
serum potassium concentration of 5.3 mmol/l or more
(Shermes et al., 1983). Borras et al. (1988) reported
an incidence of 5.5%.
9.3 Course, prognosis, cause of death
The clinical features of hyperkalemia depend on multiple
factors, e.g. serum potassium level; the rate at which that
level was been attained; and the underlying cardiovascular,
renal and metabolic status of the patient.
Electrolyte imbalance (e.g. due to hyponatremia,
hypomagnesaemia, or an acidotic environment) can lead to
serious hyperkalemia (Cox, 1981; Martin, 1986; Saxena et al.,
1989).
Cardiac dysrhythmias and arrest are the likely cause of death
following potassium overdose.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
In an attempt to establish criteria for mild, moderate
and severe poisonings/overdoses, the following limits
have been suggested:
Mild: K+ <6.5 mmol/l with no ECG changes
Moderate: K+ 6.5 to <8 mmol/l, with minor ECG changes
Severe: K+ >8 mmol/l with significant ECG changes
(Lavinsky, 1966; Sorkin, 1980)
The cardiac effects are potentially the most life
threatening, but they rarely occur with potassium
concentrations under 6 mmol/l. Hypotension, bradycardia
and ventricular conduction arrhythmias occur.
On the ECG, the initial change is a peaking, tall T-wave,
followed by a normal or decreased QT-interval. As
potassium concentrations increase, the PR-interval is
prolonged and eventually the P-wave disappears.
Ultimately, there is a prolongation and widening of the
QRS-complex. A continuous widening of the QRS will
ultimately result in a joining of the QRS and the T-
wave. 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
injection (Ellenhorn and Barceloux, 1988). Skin rash
has rarely been reported with potassium preparations.
9.4.9 Eye, ear, nose, throat: local effects
Not relevant.
9.4.10 Haematological
Not relevant.
9.4.11 Immunological
Not relevant.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Hyperkalemia tends to be associated with
metabolic acidosis (Cox, 1981) and to
complicate diabetic acidosis.
9.4.12.2 Fluid and electrolyte disturbances
Hyperkalemia may decrease reabsorption of
bicarbonate. Hyponatremia, hypomagnesaemia
and hypocalcemia may occur. These
circumstances also potentiate the effects of
hyperkalemia (Cox, 1981). Hyperkalemia may
complicate conditions such as acute
dehydration and extensive tissue breakdown,
e.g. severe burns.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
Not relevant.
9.4.14 Other clinical effects
Local pain and inflammation may result after iv
injection.
9.4.15 Special risks
No available data.
9.5 Other
No available data.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Continuous surveillance of vital functions including close
ECG-monitoring and basic life support measures should be
implemented.
Gastric decontamination: after ingestion of potassium
chloride, gastric evacuation should be performed. Abdominal
X-ray is recommended to reveal visible tablets proximal to
the duodenum thus demanding additional gastric evacuation
(Saxena, 1989; Savitt et al., 1986).
Cardiac pacing can be necessary if the patient remains
unstable despite other therapies and manoeuvres (Saxena,
1989).
In cases of minor poisoning (e.g. asymptomatic hyperkalemia),
all foods and medication containing potassium should be
eliminated.
10.2 Relevant laboratory analyses
10.2.1 Sample collection
Serum (plasma) urine.
10.2.2 Biomedical analysis
Blood: electrolytes, acid-base-balance, BUN,
creatinine, glucose.
10.2.3 Toxicological analysis
Potassium blood concentrations.
Intracellular potassium concentrations.
10.2.4 Other investigations
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 and, therefore, induces the
transfer of potassium into the cells. It may also increase
renal excretion of potassium. The onset of action is within
15 minutes and the duration is one to two hours (Stein,
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: 50 ml (50% glucose) + 5 to 10 U insulin (iv over 5
minutes)
Children: 0.25-0.5 ml/kg/dose iv, followed by 1 U regular
insulin iv for every 4 g glucose infused.
An alternative regime for adults is infusion of 500 ml of
10% glucose (dextrose) with 10-20 U insulin.
To enhance elimination of potassium, administration of
sodium polystyrene sulfonate could be indicated:
Adults: 15 g orally or rectally, three or four times a
day.
Children: 1 g/kg/dose orally or rectally every six hours.
Peritoneal dialysis and hemodialysis are effective and
should be considered in serious cases.
In patients with cardiac signs, intravenous administration
of calcium gluconate or calcium chloride may be considered.
Adults: 5-10 ml CaCl2 10%
Children: 0.2-0.3 ml/kg/dose CaCl2 10%
The injection can be repeated in 10 minutes. The duration
of action is approx one hour (Lavinsky, 1966).
The above described procedures only redistribute potassium,
there is no increase in excretion.
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 slow-
release 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
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) Survival after
massive overdose of slow-release potassium. Scot Med J, 33: 279.
Cox M (1981) Potassium Homeostasis. Med Clin North Am, 65: 363-384.
DeFrenzo RA et al. (1982) Clinical disorder of hyperkalemia.
Annu Rev Med, 33 :521-554.
Ellenhorn MJ & Barceloux DG (1988) Medical Toxicology. Elsevier
1988.
Goodman LS & Gilman A. The Pharmacological basis of
therapeutics. 8th ed.
Illingworth RN & Proudfoot AT (1980) Rapid poisoning with slow-
release 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. N Engl J Med 274: 1076-1077.
McCaughan D (1984) Hazards of nonprescription potassium
supplements. Lancet, 1: 513-514.
Martin ML, Hamilton R, West MF (1986) Potassium. Emerg Med Clin
North Am, 4: 131-144.
Martindale. The Extra Pharmacopoeia. 29th ed.
The Merck Index, 11th ed.
PDR (Physician's Desk Reference) (1992) 46th Ed.
Savitt DL, Hawkins HH, Roberts JR (1987) The radiopacity of
ingested Medications. Ann Emerg Med, 16: 331-339.
Saxena K (1989) Clinical features and management of poisoning due
to potassium chloride. Med Toxicol Adverse Drug Exp, 4(6): 429-
443.
Saxena K (1988) Death from potassium chloride overdose. Postgrad
Med 84: 97-102.
Scherr L (1961) Management of hyperkalemia with a carbon-exchange
resin. N Engl J Med, 264: 115-119.
Schim van der Loeff (1988) Cardiac arrest due to oral potassium
intake. Intensive Care Med, 15: 58-59.
Simon BC (1988) Pseudomyocardial infarction and hyperkalemia -
case report. J Emerg Med, 6: 511-515.
Sorkin MI (1980) Hyperkalemia: causes, management and
prevention. Consultant, 7: 25-32.
Stein JH (1986) Current concepts in acute renal failure. Acute
Care Therapeutics, 1(3): 9-15.
Ward C, Hamid S, Dow J (1987) Gastric complication of massive
slow-K overdose. Br J Surg, 74: 490.
Wetli CV and Davis JH (1978) Fatal hyperkalemia from accidental
overdose of potassium chloride. JAMA, 240: 1339.
Williams ME et al. (1986) Hyperkalemia. Adv Intern Med, 31: 265-291.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: P. Myrenfors
Swedish Poison Information Centre
Box 60500
S-104 01
Stockholm
Sweden
Tel: 46-8-338765
Fax: 46-8-327584
Date: August 1992
Peer Review: Cardiff, United Kingdom, February 1994
(Members: P. Myrenfors, A. Furtado Rahde, C. Alonzo,
V. Danel, A. Kleinert, J. De Kom, L. Hodgson)