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Chapter: Modern Medical Toxicology: Chemical Poisons: Heavy Metals

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Potassium (Kalium) - Chemical Poisons

Potassium is a soft silvery white metal found in the earth’s crust and is an essential electrolyte.

Potassium (Kalium)

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

Potassium is the principal cation in intracellular fluid, and along with sodium and chloride, is essential for regulation of osmotic pressure and acid-base balance. A proper balance of potassium, calcium, and magnesium ions is necessary for normal excitability of muscle tissue, especially cardiac muscle. Normal serum potassium level varies from 3.8 to 5 mEq/L. In hypokalaemic states, potassium preparations are administered orally or parenterally. Several oral rehydration solutions used in diarrhoeas also contain potassium as one of the elements. Overdose can produce dangerous consequences (hyperkalaemia). Slow release potassium preparations are particularly hazardous.

Potassium salts are available in a variety of forms and are chiefly used as supplementation with diuretic therapy. Potassium supplements are available in “slow release” (enteric-coated) tablets, which can release large amounts of KCl over a relatively short segment of small bowel. These formulations have been implicated in small bowel ulcers, some of which caused fatalities. The newer slow release KCl formulations are somewhat safer, but can cause potential adverse effects if delayed intestinal transit is present.

The concentration of potassium in some common salts is given below:

Potassium (K) Salt           mEq K/gram of salt

K-Acetate                         10.3

K-Bicarbonate                 10 

K-Chloride                       13.3

 K-Citrate H20                  9.3

 K-Iodide                           6 

K-Phosphate monobasic    7.4 

K-Phosphate dibasic         11.4

Salt substitutes containing potassium can also cause serious poisoning. Potassium is also present in large amounts in certain foods (e.g. cantaloupe, citrus fruits, bananas, tomatoes, and potatoes). Water softeners can be a significant source of potas-sium, especially in patients with underlying renal insufficiency.

Potassium salts (other than phosphate, sulfate, and tartrate) are generally readily absorbed orally. Ninety percent is absorbed in the first half hour, most being absorbed in the small intestine. The rate is 25 to 50% that of sodium. Potassium distributes primarily intracellularly by complex transport mechanisms. Transcellular K “shifts” into and out of cellular water and is governed by numerous complex physiologic phenomena (extra-cellular pH, cellular adaption to K loads, endocrine function, extent of total body potassium depletion, etc.). The intracellular compartment contains most of the body’s total of potassium (approximately 150 to 160 mEq/L). It distributes preferentially to kidney, gut, liver, skin, and muscle, in that order. Potassium leaves the plasma space very rapidly (half-life approximately 16 sec) by transcapillary transfer.

Common Causes Of Hyperkalaemia (K = > 5.5 mEq/L)

■■  Acute renal failure

■■  Use of potassium-sparing diuretics (spironolactone and triamterene)

■■  Potassium over-supplementation

■■  Drug overdose: digitalis, beta 2 agonists, NSAIDs, fluo-rides, heparin, succinylcholine, and drugs causing acidosis.

Clinical Features

■■  Vomiting, diarrhoea, listlessness, weakness, numbness of extremities, pallor, muscular cramps, hypotension, arrhyth-mias, heart block, and cardiac arrest.

  ECG Changes—Peaked T waves usually develop initially,followed by small or flattened P waves, deep S waves in the precordial leads, and widened QRS complexes. In severe cases sine waves may develop. Prolongation of the PR interval is also possible

■■  The following salts can be irritating or even corrosive in nature: potassium carbonate (potash), potassium hydroxide (caustic potash), and potassium oleate.

Diagnosis

·      Monitor serial electrolytes and obtain a serum creatinine. Normal serum potassium levels range from 3.5 mEq/L to 5 mEq/L.

o     Minimal Toxicity—Potassium levels under 6.5 mEq/L.

o     Moderate Toxicity—Potassium levels between 6.5 and8 mEq/L (lassitude, fatigue, and weakness).

o     Severe Toxicity—Potassium levels over 8 mEq/L(complete neuromuscular paralysis may dominate the clinical picture; death from cardiac arrest occurs usually at 10 to 12 mEq/L).

·              Obtain an ECG and institute continuous cardiac monitoring. The ECG is fairly characteristic (i.e. peaked T waves, small P waves, QRS widening), except in patients with Addison’s disease (i.e. the ECG may show generalised reduction and slowing).

·              Potassium preparations are reported to be consistently radiopaque. An abdominal film may be useful to assess if an ingestion has occurred or if gastric decontamination has been effective.

·              Postmortem Diagnosis: Studies have shown that the serum, plasma, and vitreous humour may be the best fluids to test for potassium overdose on postmortem.

Treatment

·              Activated charcoal is not useful. Whole bowel irrigation has been employed with benefit.

·              10 ml calcium gluconate solution (10%), or calcium chlo- ride solution (10%). May be repeated after 5 to 10 minutes. Calcium chloride is the preferred salt for resuscitation since it directly delivers ionised calcium, whereas calcium gluco- calcium. However it is very irritating, and should only be given via a central venous catheter. It can also cause hypotension and bradycardia. Caution: All calcium salts

·              Sodium bicarbonate IV: It helps to shift potassium intracel- lularly. Adult Dose—50 ml (50 mEq) intravenously over 5 minutes, repeated at 20 to 30 minute intervals. Paediatric Dose—1 to 2 ml/kg/dose (1 to 2 mEq/kg/dose) intrave- nously every 2 to 4 hours, or as required by pH. The onset is 15 minutes, the duration of action 1 to 2 hours.

·              Glucose/insulin (also enhances intracellular shift of potas- sium): Adult Dose—Administer 25 grams of dextrose (250 ml of a 10% solution) intravenously over 30 minutes, and then continue the infusion at a slower rate. Ten units of regular insulin are given subcutaneously or added to the infusion. Alternatively, 50 ml of a 50% dextrose solution with 5 to 10 units of regular insulin may be administered intrave- nously over 5 minutes. This regimen generally lowers serum potassium by 1 to 2 mEq/L within 30 to 60 minutes with the decrease lasting for several hours. Paediatric Dose—0.5 to 1 gm/kg/dose followed by 1 unit of regular insulin intrave- nously for every 4 grams of glucose infused; can be repeated every 10 to 30 minutes. Caution: 50% and 25% dextrose solutions are very hyperosmolar and can cause sclerosis of peripheral veins; administration of hypertonic solutions must always be preferred via central lines, if possible.

·              Haemodialysis (in severe cases).

Forensic Issues

·              Most cases of hyperkalaemia result from iatrogenic over- dose. Some cases result from inadvertent excessive ingestion of salt substitutes containing potassium, or mistaken identity leading to ingestion of salts such as saltpetre (potassium nitrate).

·              Ingestion of match heads containing potassium dichromate can lead to death by acute renal failure, particularly in children.

·              Poisoning with potassium permanganate has been dealt with in earlier sections (consult Index).

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