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Bone marrow toxicity after yellow phosphorus ingestion
  1. A J Tafur1,
  2. J A Zapatier1,
  3. L A Idrovo1,
  4. J W Oliveros2,
  5. J C Garces2
  1. 1Toxicology Service, Luis Vernaza Hospital, Guayaquil, Ecuador
  2. 2Department of Internal Medicine, Section “Santa Elena”, Luis Vernaza Hospital
  1. Correspondence to:
 Dr J A Zapatier
 Toxicology Service, Luis Vernaza Hospital, Guayaquil, PO Box 3615, Ecuador; jzapatierhotmail.com

Abstract

Suicidal ingestions of fireworks containing yellow phosphorus occur often during holidays. A case is reported of a 17 year old woman who intentionally ingested an estimated amount of 5.5 mg of yellow phosphorus, presenting with upper abdominal pain as the only complaint, a physical examination was normal. Blood tests showed a considerable decrease in the granulocyte count; the bone marrow biopsy revealed a decreased cellular mass with degenerative changes. Spontaneous remission was observed during the next 48 hours, with no further complaints.

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Suicidal ingestions of round, penny sized fireworks known as diablillos are popular especially during the period of Christmas holiday. Each diablillo usually weighs 310 mg containing 2.4% of yellow phosphorus (YP), 39.4% of silica, and 50% of potassium chlorate.1 The estimated lethal dose of YP is 1 mg/kg.2 We present a case in which the ingestion of firework containing YP induced reversible bone marrow toxicity verified on biopsy examination.

CASE REPORT

A 17 year old woman, weighing 50 kg, was admitted to the emergency room after the intentional ingestion of three quarters of a diablillo nine hours before arrival (about 5.5 mg of YP). Her vital signs were stable and the patient was conscious and well oriented. The chief complaint was upper abdominal pain and the rest of the physical examination was normal. There was no history of previous relevant illness. Gastric lavage was started with a solution containing potassium permanganate 1:1000; followed by activated charcoal and a mineral cathartic. Blood samples were obtained, and the analysis reported white blood cell (WBC) count 6.400/μl, red blood cell (RBC) count 3.9×106/μl, haemoglobin (Hb)120 g/l, and platelet count 258 000/μl. Granulocyte count was 5900/μl. Hepatic and renal functions, as well as electrolytes were all normal. Intravenous fluids, and folic acid with iron supplementation were prescribed as support treatment.

After 24 hours in hospital, blood tests were repeated showing WBC 3.500/μl, RBC 3.73×106/μl, Hb 12.2 g/dl, platelet count 226.000/μl, and granulocytes decreased to 900/μl. A bone marrow biopsy was undertaken, and the histopathological analysis reported intense interstitial oedema, haemorrhages, and some necrotic foci. The morphology of the three cellular lines was normal, but the total cellular mass was at 50%. Neoplasic or fibrotic changes were not found; suggesting the diagnosis of unspecified degenerative toxic changes in the bone marrow (fig 1).

Figure 1

Bone marrow biopsy showing interstitial oedema, haemorrhages, and necrotic foci. The morphology of the three cellular lines is preserved. The total cellular mass is at about 50%.

The patient remained stable and no complications appeared during her stay in hospital. Spontaneous resolution of the neutropenia was observed during the next 48 hours. The patient was discharged, and returned one month later for follow up presenting no further complains.

DISCUSSION

At the beginning of industrialisation, the long term exposure with air contaminated with YP particles and dermal contact were the most common ways of intoxication. Now, self induced YP intoxication remains an important health problem and is related to a significant mortality.3

YP is rapidly absorbed through the intestinal tract and a few hours after the ingestion 69% to 73% of the total ingested dose concentrates into the liver where severe complications develop.4 Also smaller concentrations reach the brain, striated muscle, and the kidneys. The short term effects of YP intoxication include gastrointestinal symptoms, liver changes, renal failure, arrhythmias, seizures, coma, and cardiovascular collapse.5

Published data recommend that decontamination is started within two to five hours after ingestion.6–9 Decontamination procedures in our centre within the first 12 hours after ingestion are based upon high incidence of YP poisoning, and death rates. The decision about what solution should be first during gastric lavage remains undetermined.3,6 We prefer to start preventing further absorption with a substance that oxidised phosphorus.

Reports of haematological disturbances after the exposure with YP are scarce.10,11 Experimentally, YP produces a significant increase in the leucocyte count and in some cases intense erythrocyte destruction, as seen with chickens and rabbits. In humans, the effects of YP intoxication present as a temporary proliferation of the red blood cells, without a simultaneous increase in the haemoglobin titre, and a decrease in the leucocyte count.12 Our patient had a considerable decrease in the granulocyte count measured 24 hours after the admittance. This fact prompted us to perform the bone marrow biopsy. Also, a mild decrease of leucocytes, erythrocytes, and platelets, with haemoglobin titres that remained normal, was recorded.

In vitro, elemental phosphorus induces a reduction in the cellular replication rate, as the phosphorus concentration increases, arresting cells in the metaphase stage of mitosis instead of destroying them.13 Histopathological examination of the biopsy samples revealed unspecified bone marrow changes with normal cells and a decreased cellular mass, showing that this phenomenon may occur also in the human bone marrow. These data suggest the possibility of a direct toxic effect of YP in the bone marrow.

The reported mortality after YP intoxication varies from 23% to 73%, and it is directly related with the ingested dose.3 The good outcome of our patient could be explained on the basis of the ingested small amount of diablillo (5.5 mg of YP). Most of the reported deaths were attributable to hepatic complications or cardiovascular collapse; but none to secondary to haematological abnormalities. It is important to emphasise that histopathology of the bone marrow in these critically ill patients was not studied.

REFERENCES

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