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201103 hydrogen sulfide poisoning
Two Filipino workers suffered sudden loss of consciousness while cleaning a pig farm. One worker was found to have no signs of life and could not be resuscitated. The other was conscious but confused upon arrival at the emergency room. Both workers exhibited signs of hypoxemia, hypercapnia, acute renal failure, and lactic acidosis. Their symptoms and exposure history were consistent with hydrogen sulfide poisoning from sewer gas. Nitrite salts such as amyl nitrite and sodium nitrite were administered as antidotes to oxidize hemoglobin and protect cytochrome oxidase from the toxic effects of hydrogen sulfide gas.
201103 hydrogen sulfide poisoning
- 1. ACUTE RENAL FAILURE,LACTIC ACIDOSIS, AND SUDDEN COLLAPSE FOLLOWING HYDROGEN SULFIDE SEWER GAS POISONING 潘恆之, 林杰樑, 顏宗海 硫化氫沼氣中毒導致急性腎衰竭, 乳酸中毒及突發性心肺停止 林口長庚紀念醫院 腎臟系 臨床毒物科
- 2. Patient's Profiles Case 1 Age:28 Gender: male Ethnic: Filipino Marital status: married Occupation: worker Case 2 Age: 34 Gender: male Ethnic: Filipino Marital status: married Occupation: worker
- 3. Present Illness Twootherwise healthy, Filipino workers from a poultry meat-processing factory suffered sudden loss of consciousness while cleaning pig slotted floors.
- 4. Case 1 (28y/o male) -- Physical examination Vital signs: T: 35.8 ℃ P: 0 bpm R: 0 cpm BP: 0/0 mmHg GENERAL APPEARANCE: pale and cyanotic, foul odor CONSCIOUSNESS: E 1V 1 M 1 HEENT: sclera: anicteric, conjunctiva: not pale pupil size L/R: 6/6 (mm), cyanotic lips NECK: supple, no jugular vein engorgement CHEST: no breathing sounds HEART: no heart sounds ABDOMEN: soft and flat, hypoactive bowel sounds EXTREMITIES: freely movable, no pitting edema
- 5. 血液 WBC 8700 1/µL Hemoglobin13.4 g/dL MCV 91.6 fL Platelets 289K 1/µL Segment 70 % Lymphocyte 22 % Eosinophil 4 % PT (INR) 1.0 APTT 23.8 sec 生化 Fasting sugar 133 mg/dL ALT 96 U/L BUN 22.1 mg/dL Creatinine 1.50 mg/dL eGFR 53 mL/min/1.73㎡ Na 149 mEq/L K 6.4 mEq/L Cl 103 mEq/L Ca 8.1 mg/dL P 2.4 mg/dL Mg 1.7 mEq/L CK-MB 3.9 ng/mL Troponin-I 0.01 ng/mL Lactate 24.2 mg/dL Free-T4 1.38 ng/dL TSH 0.77 µIU/mL Cortisol 22.3 µg/dL O2HB 63.6 % COHB 1.2 % METHB 0.3 % O2CT 64.9 % 動脈血 PH 6.799 PCO2 90.0 mmHg PO2 69.3 mmHg HCO3 13.7 mm/L SBE - 20.9 mm/L Sa% 60.5 % Lab data (28 y/o male)
- 6. Course (28 y/omale) An out-of-hospital cardiac arrest victim Blood tests revealed hypoxemia, hypercapnia, acute renal failure, lactate acidosis and hyperkalemia Electrocardiogram showed asystole CPCR failure
- 7. Vital signs:T: 33.0 ℃ P: 131 bpm R: 6 cpm BP: 77/51 mmHg GENERAL APPEARANCE: acute-ill looking, foul odor CONSCIOUSNESS: E 2V 1 M 4 HEENT: sclera: anicteric, conjunctiva: not pale pupil size L/R: 3/3 (mm), throat: not injected NECK: supple, no jugular vein engorgement CHEST: respiratory pattern: slow and shallow breathing sound: clear HEART: rapid heart beat without murmurs ABDOMEN: Soft and flat, normoactive bowel sounds, no local tenderness, no rebounding pain EXTREMITIES: freely movable, symmetric peripheral pulse Case 2 (34 y/o male) -- Physical examination
- 8. 血液 WBC 9500 1/µL Hemoglobin14.4 g/dL MCV 83.8 fL Platelets 162K 1/µL Segment 57.9 % Lymphocyte 37.6 % Eosinophil 1.8 % PT (INR) 1.0 APTT 23.8 sec 生化 Fasting sugar 119 mg/dL ALT 41 U/L BUN 18.1 mg/dL Creatinine 1.54 mg/dL eGFR 52 mL/min/1.73㎡ Na 138 mEq/L K 3.1 mEq/L Cl 101 mEq/L Ca 8.7 mg/dL P 3.1 mg/dL Mg 1.7 mEq/L CK-MB 5.1 ng/mL Troponin-I 0.017 ng/mL Lactate 23.8 mg/dL Free-T4 1.36 ng/dL TSH 0.69 µIU/mL Cortisol 50.3 µg/dL O2 HB % 70.3 % CO HB % 0.9 % MET HB % 7.2 % O2 CT 78.3 % 動脈血 PH 6.979 PCO2 84.1 mmHg PO2 51.9 mmHg HCO3 19.3 mm/L SBE -12.3 mm/L Sa% 73.8 % Lab data (34 y/o male)
- 9. CXR (34 y/omale) EKG (34 y/o male)
- 10. Course (34 y/omale) Day 1, at ER Day 1, in ICU Intubation with mechanical ventilator support N/S challenge, Norepinephrine run 30 µg/min Give amyl nitrite 1pc inhalation and 3% sodium nitrite 10ml iv drip for 20 mins Brain CT: no evidence of ICH or structural lesions Day 2, in ICU Consciousness: confused and disoriented G a
- 11. Course (34 y/omale) Day 4, in ICU Day 5, at ordinary ward Aspiration pneumonia => give empiric antibiotics: Ceftazidime 2g q8h Day 16, at ordinary ward Consciousness clear Discharge Extubation EEG: diffuse cortical dysfunction
- 12. Introduction Hydrogen sulfide(H2S) is a colorless toxic gas that has strong odor of “rotten eggs” H2S poisoning usually occurs by inhalation Discussion ~WoodallGM et al, InhalToxicol. 2005;17:593-639
- 13. Source Organic 1. Incompleteoxidation of sulfur compounds 2. Bacterial degradation of sulfur compounds Inorganic, mainly industrial 1. Petroleum industry -- contamination or by-product 2. Chemical industry -- reactant for production of chemicals 3. Production of heavy water 4. Metal refining ~Tee L. Guidotti , International Journal ofToxicology. 2010, 29:569-581
- 14. Knock down !! Apnea !! ~ DoujaijiB et al, Ann Saudi Med. 2010;30:76-80
- 15. Symptoms 0.05 ppm (airbone concentration) Pungentsmell mimicking “rotten egg” 0.1 ppm Anosmia 50-150 ppm Paralysis, conjunctivitis 250 ppm Photophobia, pulmonary edema 250-500 ppm Headache, nausea, vomiting, confusion, tachycardia, hypotension 500-750 ppm Respiratory arrest 750-1000 ppm Knocked down (central neurotoxicity) > 1000 ppm Dying immediately within a breath ~Tee L. Guidotti , International Journal ofToxicology. 2010, 29:569-581
- 16. Diagnosis Measurement ofblood sulfide in acute emergencies is of little clinical value. History of hydrogen sulfide exposure Odor of hydrogen sulfide Serum BUN, Cr, electrolyte, glucose, CPK, blood gas & serum lactate ECG & Chest X-ray CT scan ~ Milby HT et al, AmericanJournal of Industrial Medicine. 1999, 35:192-195
- 17. Treatment ~ Gregorakos Let al, Angiology. 1995, 46:1123-1131
- 18. Antidote – NitriteSalt Nitrite salt oxidizes the Fe2+ of hemoglobin to Fe3+, deriving Met-Hb Met-Hb competes with the Fe3+ of cytochrome oxidase and protects it from oxidization by H2S Keep the Met-Hb level < 25% with a concern of hypoxemia from methemoglobinemia Met-Hb Sulfa-MetHb Oxy-Hb + SO2 ~ Smith RP et al, Ann RevToxicol. 1976, 16:189 Mitochondria Blood
- 19. Nitrite Kit Amyl nitrite • Ifspontaneous breathing remains, give amyl nitrite inhalation every 3 min until sodium nitrite is ready Sodium nitrite • Dissolve 0.6g sodium nitrite to 20 ml of water ( 3% solution) • IV 10ml of the 3% sodium nitrite solution > 20 mins ~ Morii et al,Journal of Occupational Medicine andToxicology. 2010, 5:28
- 21. Highlights Hydrogen sulfidepoisoning is a relatively uncommon and frequently lethal hazard Toxidrome： 1. odor perception followed by olfactory paralysis 2. burning eyes 3. pulmonary edema 4. knock down Foul odor Keep Airway, breath, circulation, O2 100% Antidote：Amyl nitrite、Sodium nitrite
- 22.
Editor's Notes
- #4 The 34 y/o male had no systemic disease before. According to his boss. He was working at 病死豬處理場. Since today, when his frend and him was working there, 有一些紙屑掉入槽內, then his freind jump in and wanted to picked them up. But he did not go out for a while. Then the patient also jump in then collapse. Both of them was sent to our ER where his friend died without ROSC. When he was transferred to our ER, conscious change with air hunger pattern, then intubation was done. Due to highly suspected H2S intoxication, amyl nitrite and sodium nitrite were given and he was transferred to our ICU for further care.
- #14 汽油石化 氣體工廠 下水道 冷凍食品加工廠
- #15 H2S inhibits oxidative phosphorylation in mitochondria by binding with Fe3+ of cytochrome oxidase a3 Interferes with oxygen utilization at the cellular level. As a cellular poison, H2S affects all organs, particularly the CNS and pulmonary system (“Knock down” and apnea ) H2S inhibits enzymes in mitochondria by binding with Fe3+ of cytochrome oxidase a3. like Cyanogen compounds : block cellular respiration, and interferes with oxygen utilization at the cellular level. rapid “Knock down” : inhibiting neuronal cytochrome C oxidase and carbonic anhydrase in CNS.
- #16 mild dizziness, headaches or nausea to severe lactic acidosis via its inhibition of oxidative phosphorylation, and moreover, leading to cardiac arrhythmias and sudden death.
- #17 * Sulfide and thisfulfate => for chronic exposure. Environmental sulfide by electrochemical sensor History: Darkening of jewelry or silver coins in the vicinity of the victim should also heighten suspicion for hydrogen sulfide exposure. coin in package ECG: inshemia or infraction CXR: r/o pulmonary edema, 20 % ALI ABG: r/o carboxyhemoblobin or methemohemoglobin, Vein gas O2 elevation CT scan: white matter demyelination and degeneration of the basal ganglia lesions in patients with severe poisoning
- #19 Nitrite salt oxidizes the Fe2+ of hemoglobin to Fe3+, deriving Met-Hb, which competes with the Fe3+ of cytochrome oxidase and protects it from oxidization by sulfide. nitrites can induce hypotension and hypoxia and excessive methemoglobin formation can worsen tissue hypoxia in an unstable patient
- #20 * 2安瓿亞硝酸鈉(Sodium Nitrite)注射劑，每支10毫升注射溶液含300毫克亞硝酸鈉 2小瓶硫代硫酸鈉(Sodium Thiosulfate)注射劑，每支50毫升注射溶液含12.5公克硫代硫酸鈉(Sodium Thiosulfate)，在製造過程中加入Boric acid 及/或Sodium Borate來調節酸鹼值 12安瓿亞硝酸戊酯(Amyl Nitrite)吸入劑，每瓶0.3毫升可使用3-5分鐘 1支22號針頭滅菌且可丟棄式10毫升塑膠注射器，1支可丟棄式60毫升塑膠注射器， 1支滅菌可丟棄式20號針頭，1條胃管，1支非滅菌60毫升注射器，1包止血袋，1套治療氰化物中毒的使用說明書 Sodium thiosulfate is not efficacious, it is used to treat cyanogen poisoning Hyperbaric oxygen therapy and nitrite therapy should only be instituted after maximum supportive measures have been instituted for severely ill patients Patient with persistent neurologic findings who are unresponsive to nitrites => HBO