Mustard gas poisoning .By- Dr mohammadullah totakhil


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Mustard gas poisoning:

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Should drugs to elevate the WBC and RBC level be used for mustard gas poisoning? Why??

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Mustard gas poisoning .By- Dr mohammadullah totakhil

  1. 1. Mustard gas poisoning Question : Should drugs to elevate the WBC and RBC level be used for mustard gas poisoning? Why??
  2. 2. To be discussed: 1. Clinical Findings of Mustard Gas Intoxication. 2. Hematological effects of mustard gas . 3. Management.
  3. 3. by: Major Dr Mohammadullah (totakhil ) (Afghanistan)
  4. 4. Clinical Findings of Mustard Gas Intoxication. The picture of such a poisoning is characterized in the beginning by a latent period ,between contact and the first symptoms. The mustard gas effects several organs like skin ,eyes ,respiratory system and other Organs (Mustard gas also affects a number of other organs and tissues because of its high solubility in lipids. Therefore, several unspecific, general symptoms follow, such as nausea, vomiting, abdominal pains, headache, fatigue, apathy, diarrhea, weight loss, and tachycardia. The majority of these symptoms are apparently caused by damage to the gastrointestinal tract . Also they are partly explained by the substance's effect on the hematopoietic system. )
  5. 5.  Sulphur mustard is an alkylating agent. Alkylating agents bind covalently to various nucleophilic molecules such as DNA, RNA, proteins and components of cell membranes.  DNA: Mustard gas causes cross linking of DNA strands. Alkylation of DNA can result in the disruption of its function.  RNA: Alkylation of RNA molecules can result in altered translation and altered protein synthesis resulting in cell death.  Proteins: Binding to proteins mainly with the thiol group of cysteine produces structural changes which may alter the normal physiology of the cell i.e. altered enzyme activity.  Membranes: Mustard gas can either alkylate structural proteins located in the cell membrane or induce lipid peroxidation which may result in irreversible changes and cell death.
  6. 6. Hematological effects of mustard gas The blood count may reveal anaemia and neutropenia four days post exposure. In general, initial leukocytosis on the first 2 to 3 days after exposure is followed by leukopenia in severe intoxicated patients. Initial leukocytosis followed by leucopenia is a usual finding in mustard gas poisoning and recovers within 14 days. Marked leucopenia is a sign of sinister prognosis, leading to overwhelming infection and multiple organ failure and death. Acute: Early leukocytosis, followed by mild leucopenia. Severe leukopenia, thrombocytopenia and erythropenia indicate bone marrow depression. Chronic: Bone marrow depression leading to leukemia.
  7. 7. Management discussion.  General principles: Management of mustard gas poisoning consists of decontamination and symptomatic treatment. The importance of rapid and efficient decontamination can not be overemphasized. Biomedical analysis: Full blood count, serum electrolytes, urea, protein levels. Arterial blood gasses determination is indicated in case of pulmonary toxicity. Culture of sputum and eye exudate. Blood cultures where indicated. Skin blisters may be aspirated and the fluid obtained analysed for thiodiglycol. (Thiodiglycol is a Chemical Weapons Convention schedule 2 chemical used in the production of sulfurbased blister agents such as mustard gas. Thiodiglycol is also a product of the hydrolysis of mustard gas. It can be detected in the urine of casualties) The same estimation may be performed in blood and urine in order to differentiate blistering produced by mustard gas from that produced by other agents such as Lewisite. Contents of blisters are not toxic to attendants.
  8. 8. Life support procedures and symptomatic/specific treatment Maintain respiratory and circulatory function. Replace extracellular fluid loss, electrolytes and proteins. Blood transfusion is indicated in case of bone marrow depression. Symptomatic treatment Antidote treatment: No specific antidote is available.
  9. 9. • Bone marrow depression in severe intoxicated patients may be seen as an irreversible consequence of mustard gas poisoning. • Granulocyte, platelet and red cell transfusions as well as bone marrow transplantation have been recommended for treatment of aplastic anaemia. The value of Granulocyte Colony Stimulating Factor has not been assessed but may be of use. • Several independent scientists (Callaway & Pearce, 1958; Fasth & Sorbo, 1973; Vojvodic et al., 1985) have shown that cysteine, thiosulfate and other thiols reduce the toxicity of sulphur and nitrogen mustards (Nitrogen mustards are used in chemotherapy of malignant diseases). • The use of thiols has been proposed in the treatment of mustard gas poisoning, but has not been established.
  10. 10. • • • • • Numerous other supportive measures were used in treating casualties from the Iran-Iraq war: H2 antagonists to prevent stress ulceration. Heparin has been used to prevent deep venous thrombosis. A single large dose of methyl prednisolone (2 g) may prevent general tissue damage. Administration of Vitamins C, B12 and folate may be of use. Haemodialysis and haemoperfusion have been suggested, although there is no firm theoretical basis for such therapy.
  11. 11. Granulocyte colony stimulating factor (G-CSF) for mustard-induced bone marrow suppression.  Source Department of Internal Medicine (Hematology/Oncology Division), Naval Hospital, San Diego, CA 92134-5000. Abstract The authors describe the development of a clinical protocol to treat mustard gas-induced myelosuppression with granulocyte colony stimulating factor (GCSF), a hematopoietic growth factor.  Limited clinical evidence suggests a significant role for mustard gas-induced myelosuppression in the overall morbidity of mustard gas victims.  Initial data from primates revealed that G-CSF could ameliorate neutropenia following nitrogen mustard exposure.  Exploiting the extensive oncologic experience with G-CSF, which demonstrated its safety and absence of serious side effects the authors developed a clinical protocol for use of this drug in potential mustard gas victims in the Persian Gulf conflict.
  12. 12. Crystal structure of 3 molecules of human G-CSF  Colony stimulating factor 3 (granulocyte)  . From PDB 1rhg
  13. 13. REFERENCE: •"Clinical and Morphological Findings on Mustard Gas [Bis(2-Chloroethyl)Sulfide] Poisoning," Journal of Forensic Sciences, JFSCA, •Department of Internal Medicine (Hematology/Oncology Division), Naval Hospital, San Diego
  14. 14. Thanks