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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)



    See Also:
       Toxicological Abbreviations
       Potassium chloride (ICSC)
       POTASSIUM CHLORIDE (JECFA Evaluation)
       Potassium chloride (SIDS)