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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.

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Presentation on theme: "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."— Presentation transcript:

1 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  Two otherwise healthy, Filipino workers from a poultry meat-processing factory suffered sudden loss of consciousness while cleaning pig slotted floors.

4 Case 1 (28 y/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 1 V 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 87001/µL Hemoglob in 13.4g/dL MCV91.6fL Platelets289K1/µL Segment70% Lymphocy te 22% Eosinophil4% PT (INR)1.0 APTT23.8sec 生化 Fasting sugar 133mg/dL ALT96U/L BUN22.1mg/dL Creatinine1.50mg/dL eGFR53 mL/min/1.73 ㎡ Na149mEq/L K6.4mEq/L Cl103mEq/L Ca8.1mg/dL P2.4mg/dL Mg1.7mEq/L CK-MB3.9ng/mL Troponin-I0.01ng/mL Lactate24.2mg/dL Free-T41.38ng/dL TSH0.77µIU/mL Cortisol22.3µg/dL O2HB63.6% COHB1.2% METHB0.3% O2CT64.9% 動脈血 PH PCO290.0mmHg PO269.3mmHg HCO313.7mm/L SBE- 20.9mm/L Sa%60.5% Lab data (28 y/o male)

6 Course (28 y/o male)  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 2 V 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 95001/µL Hemoglobi n 14.4g/dL MCV83.8fL Platelets162K1/µL Segment57.9% Lymphocyt e 37.6% Eosinophil1.8% PT (INR)1.0 APTT23.8sec 生化 Fasting sugar 119mg/dL ALT41U/L BUN18.1mg/dL Creatinine1.54mg/dL eGFR52 mL/min/1.73 ㎡ Na138mEq/L K3.1mEq/L Cl101mEq/L Ca8.7mg/dL P3.1mg/dL Mg1.7mEq/L CK-MB5.1ng/mL Troponin-I0.017ng/mL Lactate23.8mg/dL Free-T41.36ng/dL TSH0.69µIU/mL Cortisol50.3µg/dL O2 HB %70.3% CO HB %0.9% MET HB %7.2% O2 CT78.3% 動脈血 PH PCO284.1mmHg PO251.9mmHg HCO319.3mm/L SBE-12.3mm/L Sa%73.8% Lab data (34 y/o male)

9 CXR (34 y/o male) EKG (34 y/o male)

10 Course (34 y/o male) 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 GaGa

11 Course (34 y/o male) 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 ~ Woodall GM et al, Inhal Toxicol. 2005;17:

13 Source  Organic 1. Incomplete oxidation 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 of Toxicology. 2010, 29:

14 Knock down !! Apnea !! ~ Doujaiji B et al, Ann Saudi Med. 2010;30:76-80

15 Symptoms 0.05 ppm (airbone concentration) Pungent smell mimicking “rotten egg” 0.1 ppmAnosmia ppmParalysis, conjunctivitis 250 ppmPhotophobia, pulmonary edema ppmHeadache, nausea, vomiting, confusion, tachycardia, hypotension ppmRespiratory arrest ppmKnocked down (central neurotoxicity) > 1000 ppmDying immediately within a breath ~ Tee L. Guidotti, International Journal of Toxicology. 2010, 29:

16 Diagnosis Measurement of blood 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, American Journal of Industrial Medicine. 1999, 35:

17 Treatment ~ Gregorakos L et al, Angiology. 1995, 46:

18 Antidote – Nitrite Salt  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 Oxy-Hb Met-Hb Sulfa-MetHb Oxy-Hb + SO2 H2S Amyl nitrite, Sodium nitrite cyt c 2+ cyt c 3+ cyt a 2+ cyt a 3+ cyt a 3 2+ cyt a 3 3+ H2O2 + 2H + 2H2O ~ Smith RP et al, Ann Rev Toxicol. 1976, 16:189 Mitochondria Blood

19 Nitrite Kit Amyl nitrite If spontaneous 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 and Toxicology. 2010, 5:28

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21 Highlights  Hydrogen sulfide poisoning 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

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23 Investigation of death Autopsy findings : pulmonary edema and greenish discoloration of viscera. The presence of sulfide ion in blood or major organs at toxic concentrations (usually in excess of 1.0 mg/L or mg/kg) the demonstration of potentially lethal levels of sulfide (1 – 5 mg/L or mg/kg) in blood, lung, and skeletal muscle will provide the best corroboration of a ruling of death due to acute hydrogen sulfide intoxication.

24 Conclusion Certain neurotoxic effects of exposure are probably due to a direct toxic effect on the brain, while others are almost certainly a result of hypoxia secondary to H2S-induced respiratory insuffıciency. pulmonary edema is a common consequence of poisoning and there is suggestive evidence of hyperactive airway responses in some individuals following brief H2S-induced unconsciousness (knockdown)

25 criteria for acceptable community levels are very different than those governing occupational standards urinary thiosulfate determinations can be useful for monitoring occupational exposure. determination of sulfide ion concentrations in blood or major organs can be useful in corroborating a diagnosis of fatal H2S toxicity, but there are many pitfalls in collecting, storing, and analyzing tissue and fluid samples.

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29 LABORATORY TESTING Biological Monitoring for Chronic Industrial Exposure. Diagnosis of Acute Poisoning

30 Chronic Industrial Exposure measurement of urinary thiosulfate one study : 29 unexposed healthy men had urinary thiosulfate values of 0.4 – 5.4 umol/mmol creatinine a volunteer exposed to 18 ppm hydrogen sulfide for 30 minutes exhibited urinary thiosulfate concentrations that increased to a peak of 30 umol/mmol creatinine at 15 hours, before declining to a normal value by 17 hours. Ingestion of food or water high in sulfur content can dramatically increase urinary thiosulfate concentration.

31 Chronic Industrial Exposure not routinely performed : paucity of studies correlating air concentrations with urinary excretion data, as well as the potential complications in interpretation of such data.

32 Special concern Paramedics and caregivers were also reported to have become injured secondarily Undressing, dry decontamination, water decontamination in an airy space Mouth-to-mouth resuscitation is not indicated When transferring a patient with H2S poisoning by an ambulance, all windows should be opened

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34 Clarification  1) Certain neurotoxic effects of exposure are probably due to a direct toxic effect on the brain, while others are almost certainly a result of hypoxia secondary to H2S-induced respiratory insufficiency  2) pulmonary edema is a common consequence of poisoning and there is suggestive evidence of hyperactive airway responses in some individuals following brief H2S-induced unconsciousness (knockdown);

35 Clarification  3) criteria for acceptable community levels are very different than those governing occupational standards;  4) urinary thiosulfate determinations can be useful for monitoring occupational exposure;  5) determination of sulfide ion concentrations in blood or major organs can be useful in corroborating a diagnosis of fatal H2S toxicity, but there are many pitfalls in collecting, storing, and analyzing tissue and fluid samples.

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