1. 8:40 a.m. The accident involved molten MCA at high temperature of approximately 90℃ and under pressure. It spilled onto the victim’s both legs through an accidentally opened connecting valve. The victim immediately shut the valve. Within a few seconds his co-workers poured water through the fire extinguisher hose as he removed his clothes.
2. 8:45 a.m. The victim was taken to the factory’s medical office and was washed carefully with large amounts of water for 15 minutes.
3. Then for 10 minutes both legs were immersed in an aqueous triethanolamine solution and washed.
4. Next BIAFINE cream (with ethanolamine) was applied on the skin burn and bandage was placed.
5. At this point, the burn appeared to be 1-2 degree burn and was approximately 6-10% of the total body surface area. The burn did not appear to be serious and the victim was in good condition. Therefore, the victim was transported to his home by an ambulance.

1. At midday (3-4 hours after the accident), the victim initially developed gastrointestinal symptoms diarrhea and nausea. Then progressing neurological symptoms developed (alternatively occurring agitation from yesterday and decline). Thereafter the patient developed symptoms of shock on the way to be transported to the hospital (decline of blood pressure and heart sound).
2. 3:00 p.m. The victim arrived at the intensive care unit and was in a state of shock and confusion.
   • Blood pressure: 7 (unit?)
   • Acidosis:  pH=7.22  pO2=116  pCO2=25
   • Alcaline rederve=10.7
   • Hypoglycemia: 8.9
   • Hypokalemia: 3.1
   • Hypokalemia: 8.9
   • Hyperleicocytosis: 28.000/mm3
   • Body temperature: 36.8℃
   • ECG：ischemic signs from V2-V6
   • CPK: 161μ

1. 3 p.m - 6 p.m
   • Oxygen inhalation through nose
   • Infusion of alkaline substance (NaHCO3, THAM)
   However, acidosis did not resolve by 6 p.m.
2. 6 p.m. - 11 a.m. of the following day
   • THAM infusion
   • Alcohol infusion by a tube inserted into his stomach: 95 vol% ethanol (70 ml) was infused at 6 p.m. Thereafter 50 ml was infused at 2-hour intervals until 11 p.m. to maintain the alcohol concentration at 0.5-0.8 g/l. Due to a peak problem, ethanol infusion of 500 ml total was performed continuously by a flow control pump from 11 p.m. to 8 a.m. of the following day.

1. The following day, the victim regained consciousness as blood alcohol level returned to zero (May 8, 1985), and the abnormalities in blood tests started to return to normal. However, his creatinine and CPK levels were high (125 and 1690 μ, respectively).
2. His consciousness was normal two days after the accident (May 9, 1985) (he was able to talk about the circumstances of the accident.).
3. Three days after the accident (May 10, 1985), the victim was moved out of the intensive care unit.

1. The diagnosis at the hospital was second degree burns, involving 10% of the total body surface area.
2. Treatment: Daily treatment included “Flamazine” at first, then “Antibio-tulle,” and finally “Corticotulle.” Thereafter “Eosiu” was used and no other drug was applied.

1. Nine days after the accident, the victim developed gastrointestinal hemorrhage (melena) due to hemorrhaging from a duodenal ulcer. This complication resolved within a few days of conventional treatment.

1. The victim was a 38-year-old male truck driver. An aqueous solution of 80% MCA spilled onto him while he was unloading a cargo. At that time, he was not wearing any special protective equipment. Within 2 minutes of the spillage, he removed his clothes and showered for 20 minutes. When he was admitted to a hospital 1 hour after the accident, his injury of first degree burn involved 25-30% of the total body surface area. Although he was in a slightly irritable mood, there were no other abnormalities. Thereafter, he became unconscious, and ECG showed general cardiac asthenia. The victim was placed on an inhaler and was given intravenous fluid and inotropic drugs (dopamine and dobutamine). To improve (blood) circulation, glucose, and methylprednisolone were administered. In the first 24 hours, his metabolic acidosis was marked despite the administration of a neutralizer. (Basis of deficiency is 10 mOsm/L.)
2. Detoxification treatment was continued for the first 24 hours using ethanol and N-acetyl cysteine.
3. His renal dysfunction progressed, and urinary detoxification occurred the following day. The creatinine kinase level was very high, indicating extensive destruction of the cellular structures. Continuous dialysis of the arterial blood was started.
4. Although the cardiac outflow became normal, the pressure of the pulmonary capillary vessels increased and vascular resistance decreased. These findings were obtained using the catheter of the pulmonary artery and monitoring.
5. Day 4: Since the victim had repeated seizures, he was given sodium barbiturate and diazepam.
6. Day 5: He developed signs of increased intracranial pressure. Inhalation and infusion of sodium barbiturate and manniton were started. However, after 2 days (Day 7), the condition of his brain worsened and he developed signs of cerebral infarction. ECG and angiogram indicated that he was brain dead.
7. Results of serum MCA analysis and autopsy results are not yet published.

A portion of the patient’s first degree burn showed progressing symptoms or signs of histotoxicosis within 2 hours after the contact with MCA. The organs which were markedly affected were the CNS, heart, and kidneys. Despite the most appropriate treatment for his symptoms, the patient died. The chemical injury of the skin from MCA destroys the protective function that the skin has naturally. This destruction of the skin leads to the absorption of a large quantity of MCA into the body. (MCA does not easily dissolve fats and it is not likely to get absorbed through the intact skin.) The effect of histotoxicosis after MCA contacts the skin is similar to that of fluoroacetate. This is because it does not compete with the inhibition of acetate oxidation by the inhibition of aconitase system in the tricarboxylic acid cycle. Reduction of sulphur compounds in the liver and kidneys results from the residue of N-acetylating-SH. Cardiopathy also occurs. This patient showed typical symptoms of MCA poisoning.

Empirical data suggested that Monoacetin (glycerol monoacetate), which was administered as acetated blood, can be an antidote. However, Monoacetin is not used commonly in clinical practice and its alternative, ethanol, is more known. (Ethanol is oxidized to acetic acid.) Our patient was administered ethanol over a 24-hour period. N-acetyl cysteine (SH- as blood) was similarly administered. However, the treatment was not successful.

The patient underwent hemodialysis for his renal disorder. Since hemodialysis facilitates the removal and degradation of MCA, it should have been started earlier.

In this case, the importance of various standards was indicated for increased preparedness for accidents involving chemical products.

For commonly used industrial chemicals, information when the chemicals contact humans is easily available. Such information includes toxicity data, symptoms, and treatment. However, information on chemicals, which are not commonly used, cannot be found or is difficult to find in an emergency. It is absolutely important to upgrade and expand the information, including in the system of poison centers.

1. MCA needs to be carefully noted as a drug with very high toxicity. It should also be carefully noted for its absorption through skin contact.
2. Prompt washing is necessary. Above all, the affected area should be washed immediately with large amounts of water. Contaminated clothes need to be removed. The affected area should be washed with soap after the area is thoroughly washed with water.
3. Studies need to be conducted on the mechanism of poisoning, counteractive effects of Monoacetin, ethanol, and N-acetyl cysteine, and removal technologies (for example: hemodialysis).