White phosphorus (WP) is the most reactive among phosphorus allotropes. White phosphorus is used militarily as an incendiary agent and igniter for munitions.
White phosphorus is used in grenades, mortars, and smoke bombs. Munitions-quality white phosphorus is a waxy solid.
When exposed to air, it spontaneously ignites and is oxidized rapidly to phosphorus pentoxide.
The reaction generates heat causes a yellow flame and dense white smoke. Phosphorus glows in the dark and this trait is transferred to tracer bullets when oxygen is depleted.
White phosphorus melts at 44 °C is water-insoluble and above 30 °C oxidizes in air to form phosphorus pentoxide.
The phosphorus produced is turned into phosphoric acid, utilized in agriculture for fertilizers, rodenticides, fireworks, and silicon semiconductor doping.
White phosphorus injuries mainly stem from human or mechanical accidents. Proper handling of munitions is essential to prevent injuries and burns from white phosphorus.
White phosphorous in South American fireworks leads to a 5.9% death rate in Ecuadorian hospital patients.
Trauma and burns from ingestion significantly impact morbidity and mortality rates. White phosphorus causes frequent second and third degree burns due to ignition.
Trauma involves blunt force from blasts and penetrating injuries caused by projectiles resulting from the explosion.
Anatomy
Pathophysiology
White phosphorus poses serious injury and death risks, with military use criticized due to potential soft tissue, inhalation, and ingestion exposure.
White phosphorus skin exposure causes painful burns in yellow necrotic areas with a garlic odor. White phosphorus rapidly penetrates skin due to its high lipid solubility.
Oral ingestion of white phosphorus causes liver and kidney pathologic changes in humans.
Inhaling white phosphorus smoke is considered least severe, with no casualties reported from exposure.
Etiology
The causes of white phosphorus exposure are:
Military and Warfare Exposure
Industrial and Occupational Exposure
Environmental Exposure
Accidental Exposure
Ingestion
Genetics
Prognostic Factors
Prognosis of white phosphorus exposure varies with exposure route, dose, duration, injury extent, and treatment timing.
White phosphorus burns often cause poor healing and high infection risk.
Clinical History
Collect details including the exposure history, initial symptoms and timeline, medical history to understand clinical history of patients.
Irrigate or use saline/water pads to decontaminate phosphorus exposure.
Avoid oily dressings as they allow lipid-soluble elements to penetrate tissue.
Remove contaminated clothing to prevent white phosphorus from reigniting and causing severe burns.
Copper sulfate effectively neutralizes white phosphorus and has traditionally treated burns in vitro.
Copper sulfate and phosphorus create black cupric phosphate for visualization.
Copper inhibits various erythrocyte enzymes affect the hexose monophosphate shunt activity.
Aggressive irrigation can cause phosphorus particles to travel to unaffected skin areas and react upon air exposure.
Antioxidants glutathione and propyl gallate can counteract this triglyceride increase effectively.
White phosphorus ingestion with hepatorenal failure and cardiovascular collapse is fatal.
Transfer patients to a trauma center with burn care capabilities for scar revisions associated with burns later.
Emergency procedures for white phosphorus burns includes immediate decontamination Procedure and surgical debridement
Airway & Pulmonary Interventions include Airway Management and pulmonary support.
Ocular exposure intervention includes immediate eye irrigation and ophthalmologic evaluation
phase-of-management
In the immediate care phase, the goal is to stop WP combustion, remove the patient from the source, and start decontamination.
In the emergency and acute phase, the goal is to stabilize the patient and prevent systemic complications.
Pharmacologic therapy is effective in the treatment phase as it includes the use of toxoid, analgesics, nonsteroidal anti-inflammatory agents, and topical antibiotics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
White phosphorus (WP) is the most reactive among phosphorus allotropes. White phosphorus is used militarily as an incendiary agent and igniter for munitions.
White phosphorus is used in grenades, mortars, and smoke bombs. Munitions-quality white phosphorus is a waxy solid.
When exposed to air, it spontaneously ignites and is oxidized rapidly to phosphorus pentoxide.
The reaction generates heat causes a yellow flame and dense white smoke. Phosphorus glows in the dark and this trait is transferred to tracer bullets when oxygen is depleted.
White phosphorus melts at 44 °C is water-insoluble and above 30 °C oxidizes in air to form phosphorus pentoxide.
The phosphorus produced is turned into phosphoric acid, utilized in agriculture for fertilizers, rodenticides, fireworks, and silicon semiconductor doping.
White phosphorus injuries mainly stem from human or mechanical accidents. Proper handling of munitions is essential to prevent injuries and burns from white phosphorus.
White phosphorous in South American fireworks leads to a 5.9% death rate in Ecuadorian hospital patients.
Trauma and burns from ingestion significantly impact morbidity and mortality rates. White phosphorus causes frequent second and third degree burns due to ignition.
Trauma involves blunt force from blasts and penetrating injuries caused by projectiles resulting from the explosion.
White phosphorus poses serious injury and death risks, with military use criticized due to potential soft tissue, inhalation, and ingestion exposure.
White phosphorus skin exposure causes painful burns in yellow necrotic areas with a garlic odor. White phosphorus rapidly penetrates skin due to its high lipid solubility.
Oral ingestion of white phosphorus causes liver and kidney pathologic changes in humans.
Inhaling white phosphorus smoke is considered least severe, with no casualties reported from exposure.
The causes of white phosphorus exposure are:
Military and Warfare Exposure
Industrial and Occupational Exposure
Environmental Exposure
Accidental Exposure
Ingestion
Prognosis of white phosphorus exposure varies with exposure route, dose, duration, injury extent, and treatment timing.
White phosphorus burns often cause poor healing and high infection risk.
Collect details including the exposure history, initial symptoms and timeline, medical history to understand clinical history of patients.
Irrigate or use saline/water pads to decontaminate phosphorus exposure.
Avoid oily dressings as they allow lipid-soluble elements to penetrate tissue.
Remove contaminated clothing to prevent white phosphorus from reigniting and causing severe burns.
Copper sulfate effectively neutralizes white phosphorus and has traditionally treated burns in vitro.
Copper sulfate and phosphorus create black cupric phosphate for visualization.
Copper inhibits various erythrocyte enzymes affect the hexose monophosphate shunt activity.
Aggressive irrigation can cause phosphorus particles to travel to unaffected skin areas and react upon air exposure.
Antioxidants glutathione and propyl gallate can counteract this triglyceride increase effectively.
White phosphorus ingestion with hepatorenal failure and cardiovascular collapse is fatal.
Transfer patients to a trauma center with burn care capabilities for scar revisions associated with burns later.
Emergency Medicine
Use enclosed systems for WP handling to reduce air release.
Increase use of local exhaust ventilation systems to capture WP fumes at the source.
Provide respirators with filters for those handling WP dust or fumes.
Emergency decontamination stations should be placed with showers and eye wash.
Remove WP-contaminated soil from battlegrounds and industrial sites.
Proper awareness about white phosphorus exposure should be provided and its related causes with management strategies.
Appointments with specialist and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Tetanus toxoid adsorbed:
It induces active immunity against tetanus in selected patients.
Emergency Medicine
Meperidine:
It may produce less constipation, smooth muscle spasm, and depression of cough reflex.
Emergency Medicine
Ibuprofen:
It inhibits inflammatory reactions and pain to decrease prostaglandin synthesis.
Naproxen:
It inhibits inflammatory reactions to decrease activity of cyclooxygenase.
Emergency Medicine
Silver sulfadiazine:
It is useful in preventing infections from second- or third-degree burns.
Emergency Medicine
Emergency procedures for white phosphorus burns includes immediate decontamination Procedure and surgical debridement
Airway & Pulmonary Interventions include Airway Management and pulmonary support.
Ocular exposure intervention includes immediate eye irrigation and ophthalmologic evaluation
Emergency Medicine
In the immediate care phase, the goal is to stop WP combustion, remove the patient from the source, and start decontamination.
In the emergency and acute phase, the goal is to stabilize the patient and prevent systemic complications.
Pharmacologic therapy is effective in the treatment phase as it includes the use of toxoid, analgesics, nonsteroidal anti-inflammatory agents, and topical antibiotics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
White phosphorus (WP) is the most reactive among phosphorus allotropes. White phosphorus is used militarily as an incendiary agent and igniter for munitions.
White phosphorus is used in grenades, mortars, and smoke bombs. Munitions-quality white phosphorus is a waxy solid.
When exposed to air, it spontaneously ignites and is oxidized rapidly to phosphorus pentoxide.
The reaction generates heat causes a yellow flame and dense white smoke. Phosphorus glows in the dark and this trait is transferred to tracer bullets when oxygen is depleted.
White phosphorus melts at 44 °C is water-insoluble and above 30 °C oxidizes in air to form phosphorus pentoxide.
The phosphorus produced is turned into phosphoric acid, utilized in agriculture for fertilizers, rodenticides, fireworks, and silicon semiconductor doping.
White phosphorus injuries mainly stem from human or mechanical accidents. Proper handling of munitions is essential to prevent injuries and burns from white phosphorus.
White phosphorous in South American fireworks leads to a 5.9% death rate in Ecuadorian hospital patients.
Trauma and burns from ingestion significantly impact morbidity and mortality rates. White phosphorus causes frequent second and third degree burns due to ignition.
Trauma involves blunt force from blasts and penetrating injuries caused by projectiles resulting from the explosion.
White phosphorus poses serious injury and death risks, with military use criticized due to potential soft tissue, inhalation, and ingestion exposure.
White phosphorus skin exposure causes painful burns in yellow necrotic areas with a garlic odor. White phosphorus rapidly penetrates skin due to its high lipid solubility.
Oral ingestion of white phosphorus causes liver and kidney pathologic changes in humans.
Inhaling white phosphorus smoke is considered least severe, with no casualties reported from exposure.
The causes of white phosphorus exposure are:
Military and Warfare Exposure
Industrial and Occupational Exposure
Environmental Exposure
Accidental Exposure
Ingestion
Prognosis of white phosphorus exposure varies with exposure route, dose, duration, injury extent, and treatment timing.
White phosphorus burns often cause poor healing and high infection risk.
Collect details including the exposure history, initial symptoms and timeline, medical history to understand clinical history of patients.
Irrigate or use saline/water pads to decontaminate phosphorus exposure.
Avoid oily dressings as they allow lipid-soluble elements to penetrate tissue.
Remove contaminated clothing to prevent white phosphorus from reigniting and causing severe burns.
Copper sulfate effectively neutralizes white phosphorus and has traditionally treated burns in vitro.
Copper sulfate and phosphorus create black cupric phosphate for visualization.
Copper inhibits various erythrocyte enzymes affect the hexose monophosphate shunt activity.
Aggressive irrigation can cause phosphorus particles to travel to unaffected skin areas and react upon air exposure.
Antioxidants glutathione and propyl gallate can counteract this triglyceride increase effectively.
White phosphorus ingestion with hepatorenal failure and cardiovascular collapse is fatal.
Transfer patients to a trauma center with burn care capabilities for scar revisions associated with burns later.
Emergency Medicine
Use enclosed systems for WP handling to reduce air release.
Increase use of local exhaust ventilation systems to capture WP fumes at the source.
Provide respirators with filters for those handling WP dust or fumes.
Emergency decontamination stations should be placed with showers and eye wash.
Remove WP-contaminated soil from battlegrounds and industrial sites.
Proper awareness about white phosphorus exposure should be provided and its related causes with management strategies.
Appointments with specialist and preventing recurrence of disorder is an ongoing life-long effort.
Emergency Medicine
Tetanus toxoid adsorbed:
It induces active immunity against tetanus in selected patients.
Emergency Medicine
Meperidine:
It may produce less constipation, smooth muscle spasm, and depression of cough reflex.
Emergency Medicine
Ibuprofen:
It inhibits inflammatory reactions and pain to decrease prostaglandin synthesis.
Naproxen:
It inhibits inflammatory reactions to decrease activity of cyclooxygenase.
Emergency Medicine
Silver sulfadiazine:
It is useful in preventing infections from second- or third-degree burns.
Emergency Medicine
Emergency procedures for white phosphorus burns includes immediate decontamination Procedure and surgical debridement
Airway & Pulmonary Interventions include Airway Management and pulmonary support.
Ocular exposure intervention includes immediate eye irrigation and ophthalmologic evaluation
Emergency Medicine
In the immediate care phase, the goal is to stop WP combustion, remove the patient from the source, and start decontamination.
In the emergency and acute phase, the goal is to stabilize the patient and prevent systemic complications.
Pharmacologic therapy is effective in the treatment phase as it includes the use of toxoid, analgesics, nonsteroidal anti-inflammatory agents, and topical antibiotics.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the specialist are scheduled to check the improvement of patients along with treatment response.
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