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Aggressive treatment, outcome and long time neurologic and pulmonary complications of lethal hydrogen sulphide (H2S) intoxication


Hydrogen sulphide poisoning can occur in industrial/occupational (oil refining, viscose rayon manufacturing, vulcanization of rubber, hydrochloric acid in farm wells, leather industry, sewage cleaning, roofing asphalt tanks, etc), recreational (cleaning of hot spring reservoirs, caves, sulfur springs, etc), or hospital (plaster of Paris, etc) settings. The first reports date from the 17th century where city sewage cleaners were found dead in the vicinity of the sewers. At a concentration of 0–25 ppm H2S has a specific odour of rotten eggs. This odour is an unreliable marker since at higher concentrations (> 100 ppm) the gas rapidly causes paralysis of (the olfactory system resulting in anosmia. At concentrations > 50 ppm symptoms are characterized by mucositis (conjunctivitis, upper airway irritation), nausea and dizziness, at > 200 ppm pulmonary edema can occur, at > 500 ppm neurologic problems arise (agitation, seizures followed by coma), at > 1000 ppm sudden death can occur. Main target organs are the central nervous system (CNS) and the respiratory system. Acute high dose intoxication mainly results in CNS problems whereas chronic lower dose intoxication results in acute lung injury (ALI) or acute pulmonary edema, the latter carrying a worse prognosis. There is still a great controversy in the literature about the best treatment and little is known about long time CNS and pulmonary complications in survivors.

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Five male patients, mean age 39 ± 11 years, working in the petroleum refining industry were admitted to the ICU of a 600 bed teaching hospital with acute H2S poisoning. Two patients were exposed to concentrations of 9000 ppm (nine times the lethal dose), three others to > 1000 ppm. The following parameters were obtained on admission in the ICU: Glasgow Coma Score (GCS), arterial blood gases, LDH, lactate, anion gap (AG), hemoglobin, white blood cell (WBC) count, platelet count, and chest X-ray. Treatment consisted of intubation (ETT) and mechanical ventilation (MV) if GCS < 6, antidotes: sodium nitrite (NaNO2) 3% (10 ml iv/15'; = 300 mg), sodium thiosulfate (NaS2O3) 25% (50 ml iv/30'; = 12.5 g), and steroids iv (methylprednisolone 2 g on admission followed by tapering dose over 7–14 days) in all patients. In cases of ALI euphylline (250 mg iv), broad spectrum antibiotics (with coverage of anaerobics) with prostaglandin E1 (continuous infusion starting at 5 up to 30 ng/kg/min) were added. Bronchoscopy with broncho-alveolar lavage (BAL) and peripheral biopsies were done in the MV patients. End-points were mortality treatment related morbidity and long-term complications (CNS, pulmonary). Values are mean ± standard deviation.


The GCS was 6.6 ± 5, the GCS was 3/15 in three patients and these were intubated and mechanically ventilated. pH was 7.32 ± 0.11, pO2 151 ± 90 mmHg (with an FiO2 of 84 ± 17%), pCO2 was 43.2 ± 11.7 mmHg, LDH 599.6 ± 585.7 IU/l, lactate 14.06 ± 19.46, AG 17 ± 3 mEq/l, hemoglobin 14.4 ± 0.8 g/dl, WBC 9.7 ± 3.6 × 109/l, platelets 220 ± 39 × 106/l. Carboxyhemoglobin and methemoglobin levels (performed in two) were normal. Chest X-ray showed bilateral nodular opacities in two patients (with GCS 3/15 and MV) and unilateral involvement in one. CT scan confirmed the presence of large airway disease in two but showed no evidence of roundglass opacities or bronchieetasis. BAL fluid showed raised WBC: mainly polymorphonuclears (PMN) in two during the early phase and mainly macrophages in one (after 24 h), RBC were raised in the BAL-fluid after 24 h. Side-effects of the antidote treatment were minor and transient nausea, agitation sweats, fall in blood pressure. One patient died on day 6 (GCS 3/15 on the spot, immediate CPR, acute fulminant pulmonary edema developed on day 1 as well as a central diabetes insipidus, MODS developed on day 3). Neurologic sequelae in form of a Claude Bernard Horner syndrome were noted in one case. Pulmonary sequelae were seen in three cases: bronchial hyper-reactivity in two (one of which had reactive airway disturbance syndrome), and chemical pneumonitis with bronchiolitis obliterans and fibrosis in the third. Lung function tests showed an FEV of 77 ± 22.7%, FEV/VC 73 ± 7.3%. TLC 83 ± 15%, DLco 86.5 ± 12.5. Under treatment with beta-2-mimetics and inhalation steroids lung function tests returned to normal in all except one (fibrosis) patient. All patients could go back to work after 5 ± 5.4 months.


Hydrogen sulphide intoxication at concentrations of > 1000 ppm are rarely seen. On the basis of our findings we recommend aggressive treatment in these cases with oxygen supplements by face mask or via ETT + MV (if GCS < 6), antidotes (Na-nitrite, Na-thiosulfate) in appropriate doses, and steroids iv. In the MV patients with opacities on chest X-ray or CT scan euphylline, broad spectrum antibiotics and prostaglandin E1 iv should be added. This treatment resulted in a mortality of only 20% in five cases of lethal dose intoxication. Neurologic sequelae are rare. A worse prognosis (mortality and pulmonary complications) can be expected in those cases presenting with acute pulmonary edema. With appropriate treatment (beta-2-mimetics, inhalation steroids) quality of life and lung function tests returned to normal in the majority of survivors.

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Malbrain, M., Bomans, P., Rappoort, G. et al. Aggressive treatment, outcome and long time neurologic and pulmonary complications of lethal hydrogen sulphide (H2S) intoxication. Crit Care 1 (Suppl 1), P132 (1997).

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