White Phosphorus Poisoning. Report of Two Cases

Alulema AL, Lascano MF, Aman DR and Cabezas MP

Published on: 2025-03-19

Abstract

Introduction: White phosphorus is a fat-soluble substance that is absorbed mainly by the gastrointestinal tract, toxic to humans, used for pyrotechnics and ammunition. Its lethal dose in humans is 50-60 mg or 1 mg per kilogram of weight; hepatoxicity is due to the generation of free radicals that damage the outer membrane of the hepatocyte. In Ecuador there are no statistics on white phosphorus intoxication. Clinically, symptoms present in four stages: the first is characterized by gastrointestinal symptoms that evolve to progressive asymptomatic liver damage, followed by clinical symptoms of liver damage such as jaundice and coagulation disorder, and finally, stage IV presents with multiorgan failure.

Case Presentation: It describes two cases of patients aged 13 and 15 years with ingestion of "diablillos" (white phosphorus) as an autolytic attempt to develop alterations in coagulation times and liver function, classified as clinical stages II and III; whose management is based on N-acetylcysteine, Vitamin K, Lactulose and especially Hemodialysis and Hemoperfusion.

Evolution: In spite of the rapid evolution to clinical stages where a high risk of morbidity and mortality has been evidenced, with the therapy performed, normalization of liver function is achieved in approximately 9 days with a satisfactory recovery, effectively reducing hospitalization time and sequelae in the affected organs.

Conclusions: It is considered that hemoperfusion therapy in cases of severe phosphorus intoxication allows an evident clinical improvement, avoiding mortality and permanent liver damage.

Keywords

Phosphorus; Intoxication; Hepatic failure; Hemoperfusion

Introduction

Phosphorus was discovered in 1669 by Brand, by 1840 phosphorus was used to make matches, however its high toxic power was discovered, being able to cause fires and poisoning [1].

There are two forms of presentation: red phosphorus, which has limited toxicity in humans, and white phosphorus, which is toxic to humans and is used in fireworks, rodenticides, and munitions. White phosphorus is fat-soluble and is absorbed primarily through the gastrointestinal tract, increasing with the co-ingestion of ethanol and fatty foods, although it can also be absorbed through the skin or respiratory tract [2].

The toxicity of white phosphorus is due to three mechanisms of action, exothermic reaction, acid production and dehydration. [2] Each device has an average concentration of 20 mg, the lethal dose in humans is 50-60 mg or 1 mg per kilogram of body weight [3].

White phosphorus has a high distribution power to tissues, hepatoxicity is due to the oxidation of phosphorus, which generates free radicals that damage the outer membrane of the hepatocyte, resulting in massive calcium influx, mitochondrial damage and consequent cell death [4]. It also inhibits phosphatidylethanolamine which inhibits lipoprotein synthesis causing fatty infiltration and cirrhosis. In the central nervous system and renal system there is an alteration of the metabolism of carbohydrates, lipids and proteins [4].

Clinically, the symptoms of white phosphorus poisoning can be divided into four stages. Stage I occurs within the first 24 hours after ingestion and is characterized by the appearance of gastrointestinal symptoms; stage II presents with asymptomatic progressive liver damage; stage III appears 72 hours after ingestion and is characterized by clinical signs of liver injury (jaundice, hepatomegaly, acholia, choluria, coagulation disorders); and finally, stage IV ends with multi-organ failure [5].

In Ecuador, there are no statistics on white phosphorus poisoning, since the sale and distribution of illegal fireworks is prohibited, with penalties of 5 to 30 days in prison. Furthermore, those who manufacture, supply, market, or transport explosives without the corresponding authorization may be punished with three to five years in prison [6].

Case Presentations

Case 1

A 13-year-old female patient was born and lives in Quito, in eighth grade, with a family history of a mother who died 12 years ago due to white phosphorus poisoning. She lives with her grandparents and aunts and uncles, but has no other significant medical history. She was brought to the emergency room by her relative due to a history of having ingested 6 diablillos (120 mg white phosphorus) approximately 72 hours ago, apparently as a suicide attempt (remembering her mother's death). She subsequently presented progressive abdominal pain accompanied by nausea that led to vomiting on one occasion. Upon admission, the patient was observed on physical examination to be conscious, oriented, in pain, with a heart rate of 92 beats per minute, a respiratory rate of 20 per minute, a Glasgow Coma Scale of 15/15, afebrile, anicteric sclera, without cardiovascular or respiratory involvement. At the gastrointestinal level, the abdomen was soft, depressible, painful to palpation in the epigastrium, with bowel sounds present, and a normal neurological status. In the admission paraclinical tests, an increase in transamines and coagulation times was evident (Table I). It was classified as a case of liver damage associated with white phosphorus poisoning since it met the criteria for coagulopathy and biochemical evidence, so treatment was started with N-acetyl cysteine with a loading dose of 150 mg/kg intravenously, then 50 mg/kg in 4 hours and subsequently 100 mg/kg for 16 hours (maintenance dose), in addition to lactulose to reduce the absorption of ammonia and omeprazole as a gastric protector. Patient in her first 15 hours of hospitalization presents persistent abdominal pain , oral intolerance, altered state of consciousness with tendency to drowsiness, tachycardic, tachypneic with requirement of supplemental oxygen by nasal cannula, respiratory alkalosis, for which she is transferred to the adult Intensive Care Service where treatment with N acetyl cysteine continues, Vitamin K is administered for prolonged coagulation times, lactulose therapy is maintained, adjuvant therapy Complex B and Ascorbic Acid is added, in addition it is decided to perform Hemodialysis (A200 filter) and Hemoperfusion (HA230 filter) continuous cycle of 8 hours.

After 12 hours of hospitalization in the Intensive Care area, control tests were performed showing a slight decrease in bilirubin, prolongation of coagulation times (Table 1) for which reason fresh frozen plasma and vitamin K were administered to reduce the risk of bleeding, she presented alterations in three cell lines, leukopenia, anemia and thrombocytopenia, bone marrow aplasia secondary to phosphorus poisoning was suspected. Clinically, the patient was hemodynamically stable, without neurological focalization with a tendency to drowsiness, without renal failure, ventilatory mechanics preserved with the requirement of supplemental oxygen. A two-phase N-acetyl cysteine protocol was completed, Vitamin E was added, with the aim of eliminating toxic molecules and pro-inflammatory cytokines, and a second cycle of continuous hemoperfusion therapy was started for 8 hours.

After 24 hours of hospitalization, the patient showed persistent elevated liver enzymes and prolonged coagulation times (Table 1), so he continued to receive fresh frozen plasma and Vitamin K, in addition to consuming platelets from platelet concentrates.

Patient on her second day of hospitalization, control tests showed liver enzymes and bilirubin decreasing, platelets increased after platelet concentrates, hemoglobin and hematocrit decreasing (Table 1). However, there was no evidence of hemodynamic instability, no signs of tissue hypoperfusion, at the neurological level with a tendency towards drowsiness, which is why hepatic encephalopathy is suspected. Supportive treatment was maintained. Evaluated by Mental Health, finding a diagnosis of Recurrent Depressive Disorder with the need for permanent follow-up.

The patient was referred to a third-level unit where the previously established treatment was continued. She remained hospitalized for nine more days with good progress. Her liver profile and cell lines (Table 1) showed normalization sixteen days after the phosphorus intake, so she was discharged.

Table 1: Laboratory tests Case one.

Laboratory Exam

Income (Day 3 After Phosphorus Intake)

Day 4 AM

Day 5 PM

Day 6

Day 7

Day 16

UNIT

Reference Values

Leukocytes

3490

3990

2740

2420

4 .760

8,200

10?/uL

4.09 – 9-75

Neutrophils

56.70%

78%

46.70%

36.90%

4 2.6%

54%

%

41.2 – 73.5

Lymphocytes

30.80%

13.10%

40%

48.80%

4 0.5%

40%

%

19 – 48-9

Hemoglobin

12

10.2

8.8

7.7

1 1.6

12

g/dL

11.3 – 15-4

Hematocrit

36.7

30.9

27.1

22.6

3 3.6

36.8

%

34.7 – 46.6

Platelets

3,98,000

106000

54000

118000

117000

422000

10?/uL

131 – 357

Tp

22.4

20

16.1

13.4

1 1.1

11.4

Sec

9.9 – 11.8

Inr

1.97

1.75

1.39

1.14

0.94

0.96

 

0.9-1.2

Ttp

45.8

66.3

25.4

48.6

34.7

28.8

Sec

2 1.7-38

Urea

63.2

10.4

8

23.6

17.7

24.7

mg/dL

16.8 – 43.7

Creatinine

0.56

0.47

0.6

0.61

0.52

0.42

mg/dL

0.5 – 0.9

Tgo/Ast

424

 

355

280

240

28

U/L

0 – 31

Tgp/Alt

252

 

365

312

277

74

U/L

0 – 34

Total Bilirubin

4.14

3.94

3.23

2.75

 

1.6

mg/dL

0.3-1.1

Bilirubin Direct

2.66

2.43

2.1

1.87

 

1.42

mg/dL

0.1-0.4

Indirect Bilirubin

1.28

1.51

1.13

0.88

 

0.18

mg/dL

0 -0.9

Case 2

A 15-year-old female patient, born and resident in Quito, is a first-year high school student with a socioeconomic background. She works as a street vendor on weekends. She has lived in a same-sex home for 10 years. She lives with her mother, aunt, and cousin. She is the third of three siblings who are migrants. She has a poor relationship with her family. Her father is an alcoholic and a drug addict. She was physically abused by a partner three days prior to admission. She suffered bullying due to an upper limb burn. She has no significant medical, obstetric, or surgical history.

Three hours before admission, the patient ingested approximately 13 diablillos pills (93 milligrams of white phosphorus) due to an apparent suicidal attempt secondary to feelings of sadness due to the migration of siblings. After this event, he presented with diffuse abdominal pain of moderate intensity. He informed his mother and went to the emergency room.

On admission, her blood pressure was 131/82, heart rate 71 beats per minute, respiratory rate 20 breaths per minute, oxygen saturation 92% on room air. Physical examination revealed a Glasgow 15/15 reading, normoreactive isochoric pupils, normal neurological examination, normal cardiopulmonary function, and a tender abdomen in the epigastrium upon deep palpation. Gastric lavage was performed with 3000 ml of saline solution, yielding food debris mixed with a shiny whitish substance. 1 gram of activated charcoal and 40 mg of omeprazole were administered. Laboratory tests were performed (Table 2). She was assessed by intensive care for further management.

During his stay in intensive care, his Glasgow 15/15 was maintained, hemodynamically stable, an administration protocol of N-acetylcysteine was started as a liver protector, in addition to gastric lavage with potassium permanganate, initially no liver alteration was evident however on his second day of hospitalization prolonged coagulation times were evident (Table 2), for which he received phytonadione; without kidney failure (Table 2) he received Hemodialysis therapy (A200 filter) and Hemoperfusion (HA230 filter) first cycle lasting 8 hours.

Despite support measures on his third day of hospitalization he progressed to clinical phase II-III with progressive liver failure, control tests with signs of cytolysis (Table 2), he received 3 days of gastric lavage with potassium permanganate to reduce his absorption of the toxic and Hemoperfusion for the second cycle for 8 hours.

Due to clinical deterioration, she was transferred to a third level care unit. Upon admission to this health center, laboratory tests were performed again with evidence of altered liver function (Table 2), so she remained under observation, with liver function controls without adding new therapy, and on her ninth day of hospitalization, control tests showed stabilization of liver function (Table 2), so her discharge was decided.

Table 2: Laboratory tests Case two.

Exam Of Laboratory

Income (Three Hours After Phosph Orus Intake)

Da Y 1

Day 2

Day 3

Day 4

Day 6

Day 9

UNIT

Reference Values

Leukocytes

10,060

6 670

3880

2,900

 

3,000

 

10?/uL

4.09 – 9-75

Neutrophils

63.6

70.2

38.7

49.1

 

45

 

%

41.2 – 73.5

Lymphocyte S

29

20.3

17.7

33.7

 

36

 

%

19 – 48-9

Hemoglobin

14.1

12.7

12.4

10.8

 

10.1

 

g/dL

11.3 – 15-4

Hematocrit

41.6

35.9

36.3

31.3

 

30.3

 

%

34.7 – 46.6

Platelets

417,000

325,00

274,0

119,000

 

9800

 

10?/uL

131 – 357

Tp

11.4

15.1

15.6

21.7

 

15.4

 

Sec

9.9 – 11.8

Ttp

38

Does Not Clot

48.2

80.9

 

28.9

 

%

75 – 120

Inr

0.35

1.3

1.34

1.91

 

1.04

   

0.9 1.1

Urea

25.2

4.9

21.8

26.7

22.2

13.2

16.4

mg/dL

16.8 – 43.7

Creatinine

0.96

0.28

0.56

0.45

0.4

0.42

0.35

mg/dL

0.8 – 1.3

Tgo

19

17

24

40

155

68.8

29

U/L

0 – 31

Tgp

13

10

13

20

74

99.2

65

U/L

0 – 34

Total Bilirubin

0.49

0.8

1.62

1.76

1.33

0.46

0.65

mg/dL

-0.4

Bilirubin Direct

0.14

0.21

0.51

0.41

0.61

0.23

0.29

mg/dL

0 – 0.9

Indirect Bilirubin

0.35

0.59

1.21

1.35

0.72

0.23

0.36

mg/dL

0.3 – 1-1

Discussion

Poisoning is more likely to occur during or before Christmas [7]. The lack of characteristic clinical symptoms in the acute phase may lead to an underestimation of the cause of the disease; similarly, late hospitalization of patients, as in the clinical cases mentioned above, will lead to a failure to provide adequate treatment, which is the key to survival [8].

Pathophysiology of White Phosphorus Poisoning

White phosphorus poisoning occurs primarily through oral administration. Although the mechanism of toxicity is not clearly understood, lipid peroxidation is thought to be the primary cause of damage. This occurs due to the release of oxygen free radicals that cause direct damage to liver cells, affecting mitochondrial respiration [7]. The processes it alters include the Krebs cycle, the urea cycle, and the formation of diffusible neurotransmitters due to changes in the production of amino acid precursors. The previous section explains many of the signs and symptoms, of which hepatotoxicity predominates. Known pathophysiological processes occurring in poisoning include inhibition of phosphatidylolamine activity, which prevents the synthesis of lipoprotein chains absorbed by the liver and leads to steatosis and cirrhosis [3].

At the pathological level, inflammation and necrosis of the liver parenchyma are detected, as well as centrilobular damage and portosystemic anastomoses. Toxic hepatitis is detected first, followed by an increase in serum ferritin, gamma-glutamyl transpeptidase, bilirubin, aspartate aminotransferase and alanine aminotransferase (AST, ALT), with consequent steatosis and hepatic necrosis. The Zimmerman index should be considered, which includes thrombocytopenia below 80,000, PT uncorrected with vitamin K and leukopenia below 4,000 [9].

Renal and cardiac toxicity is explained by a decrease in osmolality in the context of relative hypoalbuminemia, leading to hypovolemia, changes in ventilation and perfusion parameters, and a tendency toward hypercapnia. This results in acute kidney injury or cardiac arrhythmia. Cardiopulmonary arrest may even occur due to direct damage to the phosphorus element in the myocardium [6]. Neurotoxicity is thought to be due to disruption of the Na/K/ATPase pump with reduced activity, leading to an increase in GABA, resulting in impaired alertness. Manganese deposits are found in the basal ganglia of the brain.

Clinic

The main symptoms include vomiting, jaundice from the third day, abdominal pain, and changes in consciousness from irritability, lethargy to coma. Three stages can be distinguished: the first stage is characterized by nausea and vomiting, cramping abdominal pain that may seem like an acute abdomen, diarrhea, hematemesis, which can rapidly progress to shock and coma in the first 24 hours. This stage lasts from hours to two days; The second is the latent phase that lasts from the second day to 6 weeks after ingestion, manifests with jaundice, increased transaminase and bilirubin values, at this time the patient presents an apparent recovery, but in reality the toxic levels of phosphorus will damage hepatocytes, the third stage causes progressive liver failure, kidney failure and severe damage to the central nervous system [10].

Premature death occurs due to shock, ventricular fibrillation, or asystole.

Diagnosis

It may be based on the presence of fireworks in the child's environment; known or suspected exposure to fireworks; or visible fireworks particles in the mouth or vomit. Other symptoms include foul- smelling breath, difficulty breathing, vomiting, and phosphorescent stools [11].

Another useful fact to consider is that it is most likely to occur on or around Christmas.

Treatment

There is no specific therapy against this poisoning, some measures are performed to reduce toxic absorption into the digestive tract, among the main ones we have gastric lavage with potassium permanganate, whose effectiveness has not been demonstrated; also used is gastric lavage with hydrogen peroxide diluted 1:1000 every 4-6 hours for 72 hours, the same one that has as its main effect to inactivate the white phosphorus that may remain in the gastrointestinal tract. On the other hand, because phosphorus adheres to the wall of the digestive tract for a long time, it can be dissolved with mineral oil or liquid petroleum jelly, causing it to liquefy and empty quickly [11]

It should be noted that each case of pediatric white phosphorus poisoning is of great importance due to its poor prognosis and high mortality rate depending on the phase in which it is found, being up to 100% when reaching the last phase [11].

There is currently evidence of cases treated with Hemodialysis and Hemoperfusion in adults, since being an extracorporeal therapy, the elimination of circulating phosphorus could be facilitated with hemoperfusion cartridges [12]. The experience at the Enrique Garces Hospital in the two cases described above using this therapy has shown good results since after it a decrease in bilirubin and transaminase values is identified, reaching the normalization of the liver profile values. Therefore, recovery has been satisfactory, effectively reducing the hospitalization time and the sequelae in the affected organs.

Conclusion

After analyzing the therapeutics used in cases of white phosphorus poisoning, we can conclude that hemoperfusion is a very useful technique since, thanks to its use, patients experienced evident clinical improvement and mortality and permanent liver damage were prevented.

Ethical Considerations

In this case report, the patient's informed consent, signed by the legal representative, was obtained, thus facilitating the procedure.

Conflict of Interest

The authors declare no conflict of interest.

References

  1. De Vargas, MC. "History of the discoveries of the chemical elements." Industrial Engineering. 1993; 5: 63-66.
  2. Laguado NF, Fernandez Soto DR. "White phosphorus poisoning in pediatrics." 2007.
  3. Ramirez Sanchez MS, Pacheco Fuentes J, Gomez Paredes N, Fuentes S. "Pediatric white phosphorus poisoning (white phosphorus poisoning): Survival after ingestion of potentially lethal doses." Venezuelan Archives of Childcare and Pediatrics. 2008; 71: 140-144.
  4. Rojas Rodriguez L, Fonnegra Uribe P, Rojas C, Ruiz Garzon JA. "White phosphorus." 2018.
  5. Robalino V, Rojas C, Carrera F. "Suicide attempt with white phosphorus in adolescents treated in the Pediatrics and Adolescence Service of the Eugenio Espejo Hospital in Quito, Ecuador." Medical Sciences. 2005; 17.
  6. Criminal, Comprehensive Organic Code. "Comprehensive Organic Criminal Code." Quito: Corporation for Studies and Publications, Related Legislation. Professional Version. 2014.
  7. Uribe PF, Rojas C, Rojas LC, Jar G. White phosphorus. Colombian Ministry of Health. 2016; 491-496.
  8. Figueredo L, Acosta FEG, Fernando M, Castaneda O, J LF. White phosphorus poisoning. Rev Colomb Neumol. 2004; 16: 198-203.
  9. Bustamante F, Hidalgo G, Arroba Carlos Ag. White Phosphorus Poisoning. Liver Lesions. Rev. Faculty of Medical Sciences. 1986; 36: 137-143.
  10. Zuluaga Gomez M, Estrada Atehortua AF, Berrouet Mejia MC. White phosphorus poisoning during the December holidays: a case report. Med UPB. 2020; 39: 81-85.
  11. Laguado NF, Ricardo D, Soto F. White phosphorus poisoning in pediatrics. Rev los Estud Med la Univ Ind Santander Medicas UIS. 2007; 20: 61-66.
  12. Cedeno MJP, Guacho JSG, Portilla AR, Tobar SDS. Hemoperfusion in white phosphorus poisoning: Case report. J Ecuadorian Society of Nephrology, Dialysis and Transplantation. 2024; 12: 82-87.