Phosphorus

• Phosphorus is an essential mineral element. Phosphorus homeostasis in the body is controlled by hormonal and renal control systems.
• Toxic exposures have been reported to occur from its industrial use or from suicidal ingestion of phosphorus-containing materials.
• There are three allotropic forms of elemental phosphorus: white, red, and black phosphorus.
• The commercial product is 99.9% pure and may have a slightly yellow color.

Sources of poisoning

• Phosphorus poisoning is of rare occurrence in farm animals because of lack of exposure.
• Accidental ingestion of fertilizers, or immediately from clumps of fertilizers on cultivated land, fireworks, baits containing lumps of white phophorus for pets, rats kept on the pastures
• Grazing of animals on the battlefield where certain explosives have been used.
• finely divided phosphorus is mixed with fats and oils to promote their absorption and over consumption of such fats and oils results in phosphorus poisoning.

Toxic levels of phosphorus in animals:

• Vary greatly depending on in which state the phosphorus is ingested.
• White phosphorus in finely divided form causes toxicity in animals.
• Horses and oxen= 0.5 – 2 gms
• Pigs= 0.05 – 0.3 gms
• Dogs=0.05 – 0.1 gm
• Fowl= 0.02 gm

Mechanism of Toxicity:

• Phosphorus can be absorbed into the systemic circulation from the skin, lungs, and intestinal tract. For all practical purposes, white and yellow phosphorus are readily absorbed while red phosphorus is not. The target organs of toxicity include the gastrointestinal tract, liver, kidney, bone, and the cardiovascular and central nervous systems.

High mortality rates seen following white phosphorus burns can be due to its absorption from the burned surface, which may result in multi-organ failure (mainly liver and kidneys), hyperphosphatemia, hypocalcemia, and electrocardiogram (ECG) abnormalities.

Clinical signs:

• Per-acute toxicity:
  • Death after showing intense abdominal pain, violent convulsions, severe CNS depression, and coma.
• Acute toxicity
  • Salivation, nausea, vomition, severe diarrhoea with mild abdominal pain, fever, polydypsia, polyuria.
  • The garlic-like odor is also detected in the vomitus.
  • Most exhibit symptoms of jaundice, hematuria, oliguria followed by delirium, convulsions, coma and death.
  • Signs of gastroenteitis appear in 1-2 hours and cause of illness is 3-5 days depending on severity of toxicity.
• Chronic toxicity

Found rarely

Post mortem lesions

• If death occurs within l-3 days, no significant changes are seen, but garlic-odour of GIT contents, is noticed.
• Liver is enlarged, pale and yellowish.
• Spleen is small and atrophied.
• Congestion and hemorrhagic inflammation of GIT.
• In birds, visible fumes of phosphorus can be appreciated opening the gizzard.
• The effect of phosphorus damage is evident by the extreme fatty changes seen on many organs; a yellowish liver with marked fatty degeneration, and severe jaundice are usually present.

Diagnosis:

• History
• Clinical symptoms particularly acute gastroenteritis.
• Garlic odour of the vomitus and intestinal contents.
• Postmortem lesions.
• Estimation of phosphorus in the blood, vomitus, intestinal contents and faeces.

Treatmeant:

• No specific antidote is available
• Copper sulphate is a very effective to treat white phosphorus burns, topical application of copper sulphate to the burnt surface.
• Only tap water irrigations were found to be effective in preventing death after white phosphorus burns.
• Activated charcoal, emetics or purgatives are used for removal of the agent.
• Having good lipid solublity, oily purgatives must be prevented from used, and hence only saline purgatives should be used.
• Supportive treatment should be provided with fluid therapy.