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This paper describes two patients who were exposed to toxic substances in the workplace, but for whom diagnosis proved difficult, particularly in case 2. Case 1 was exposed to methyl iodide and case 2 to manganese. Poisoning was characterised by delayed onset of symptoms following exposure and symptom progression after cessation of exposure. The clinical consequences of exposure to these substances include cerebellar and Parkinsonian symptoms followed by the development of cognitive impairment and the late appearance of psychiatric disturbances. Both cases were evaluated by physicians with little training in toxicology. Apart from abnormal liver function in case 1 and decreased power, coordination and proprioception in case 2, results of most routine medical investigations were normal. Both cases were referred for MRI brain scan and neuropsychological assessment. Abnormalities were noted on MRI but reported as being absent initially in case 1and of unknown significance in case 2. There was evidence of cognitive impairment in both and personality change in case 1 of sufficient severity to prevent both cases from returning to work and to impact on family life. There is no antidote to methyl iodide or manganese poisoning. Successful treatment requires early diagnosis and cessation of exposure, but neurotoxic syndromes are difficult to diagnose when a time lag exists between exposure and symptom onset and there is no biomarker of exposure. These syndromes may initially be confused with other neurodegenerative conditions, infectious processes, and psychiatric disorders. Clinician's lack of familiarity with the potential toxicity of environmental and industrial chemicals can lead to misdiagnosis and mismanagement, and this lack of recognition can lead to continued exposure. These cases highlight the importance of taking a detailed occupational history in patients who present with atypical neurological symptoms.

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BACKGROUND: Bismuth iodoform paraffin paste (BIPP) is used for the packing of wound and surgical cavities. Features of both bismuth and iodoform toxicities have been associated with the use of BIPP, but there are no previous reports of 2,3-dimercaptopropane-1-sulphonate (DMPS) chelation therapy for bismuth poisoning secondary to its use. CASE REPORT: A 67-year-old man presented with a pelvic tumor requiring extensive surgical resection. BIPP packing was required post-operatively for surgical wound breakdown. A few days after insertion, the patient developed neurological features of bismuth toxicity (blood and urine bismuth concentrations were 340 microg/L and 2800 microg/L, respectively), which was treated with removal of the BIPP packing and DMPS chelation [27 days of intravenous DMPS (5 mg/kg 4 times daily for 5 days, 5 mg/kg three times daily for 5 days followed by 5 mg/kg twice a day for 17 days) followed by 24 days of oral DMPS (200 mg three times a day for 10 days, followed 200 mg twice daily for 14 days)]. This resulted in improvement in his symptoms and a decline in his pre-chelation bismuth concentration of 480 microg/L to 5 microg/L following chelation. There were no adverse effects during chelation. CONCLUSIONS: DMPS chelation appears to be a potentially effective chelating agent in bismuth toxicity.

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This report describes a case in which a consciousness disturbance was associated with a high plasma iodine level and which improved after the removal of iodoform gauze that had been applied to infected wounds. A 71-year-old male with poorly controlled diabetes underwent a laminectomy for an epidural abscess. On the 6th and 8th postoperative days, he underwent debridement for fasciitis in the both arms and iodoform gauze was applied to the wounds (both arms and lumbar region) at the end of the first debridement and then changed every day. His consciousness then gradually deteriorated after the debridement. His plasma iodine level was measured and was shown to be remarkably high (6,280 microg/dl) 19 days after the laminectomy (13 days after the beginning of iodoform application). His consciousness recovered gradually with a concomitant decrease in the plasma iodine level. Three months after the removal of the iodoform he became almost alert. Caution should be exercised in using iodoform gauze because of the possibility that it could affect consciousness.

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A 76-year-old man with supranuclear palsy, developed consciousness disturbance followed by the treatment of decubitus ulcer in the sacral region using iodoform-gauze. He was semicoma and tachycardia. His pupils were miotic and light reflexes were absent. EEG demonstrated diffuse and random slow activities. Plasma concentration of free iodine was high (151 micrograms/dl), but the other laboratory findings including thyroid functions were normal. He was diagnosed as suffering from iodoform poisoning. The symptoms and laboratory abnormalities of the patient recovered soon after the removal of iodoform-gauze. Although iodoform has been widely used for the treatment of wounds, there are few case reports of its side effects, such as consciousness disturbance, delirium, headache and tachycardia.

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Two workers were poisoned following exposure to methyl iodide with inadequate protective devices. Their cases are presented together with a review of literature. Both patients developed symptoms and signs of cerebellar lesions and damage of the third, fourth, or sixth cranial nerve pathways. Spinal cord lesions producing motor and sensory disturbances were present in one. Late psychiatric disorders were observed in both patients. Although these symptoms were very similar to those reported in the nine published cases of methyl iodide poisoning, the toxicological diagnosis was delayed in one case: as repeated overexposure produced recurrent attacks of multifocal neurological dysfunction, multiple sclerosis was initially diagnosed, although several of the features observed are unusual in this disease. The manifestations of methyl iodide poisoning are similar to those of intoxication with other monohalomethanes. All these compounds probably share the same mechanisms of action. This mechanism and its therapeutic consequences are discussed.

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A case of iodoform toxicity caused by use of 5% iodoformed bandage in occlusive surgical dressings for tamponing of diffuse hemorrhage in pelvic cavity, following amputation for treatment of rectum adenocarcinoma. Despite the frequent use of iodoformed dressings following surgical procedures, the signs and symptoms of iodoform toxicity syndrome can be easily mistook for other syndromes. A revision of the published observations suggest that this syndrome is not as rare as thought but probably has been underdiagnosed.

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Three cases of iodoform poisoning are described following dressings with 10% iodoform gauze (0.10 x 5 m) on extended wounds. Five, ten and sixteen days after the beginning of dressings, the patients became confuse, hallucinated, and one of them was subsequently comatose. Vomiting, fever, tachycardia with premature ventricular beats and shortening of P-R interval, slight increase of transaminases and proteinuria were observed. Within a few days (3 to 8) after the iodoform dressings were discontinued, the signs of iodoform toxicity disappeared. The toxicity of iodoform is probably unrecognized if the rarity of the observations published and the amount of iodoform gauzes annually sold are compared.

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A 19-year-old patient intending to commit suicide gave himself an intravenous injection of about 14 g methyliodide. The patient was admitted to our hospital in a state of somnolence and agitation followed by a cerebral convulsion and severe hypotension. The serum concentration of methyl iodide was measured by mass spectroscopy. In addition to an antidote therapy with acetylcysteine, haemoperfusion was performed followed by a remarkable decrease of the methyliodide concentration. The patient survived this severe intoxication and was discharged from the hospital after a week.

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A 20-month-old girl ingested a maximum of 25 mL of pure methylene iodide. Within two hours, the patient exhibited lethargy and incoordination and vomited. An abdominal radiograph demonstrated the radiopaque material in the gut. In vivo conversion to carbon monoxide was documented with a peak carboxyhemoglobin level of 14.2% reached at 11 hours after ingestion. Two days after ingestion, evidence of hepatotoxicity was apparent, and fulminant hepatic failure quickly ensued. Despite aggressive supportive care and transfer to a liver transplant center, the patient died nine days after ingestion. Methylene iodide ingestion has not been previously reported in human beings. This case verifies that this substance is a potent hepatotoxin, is metabolized to carbon monoxide in vivo, is radiopaque, and may cause bone marrow suppression.

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A 41-year-old chemist developed methyl iodide intoxication. His case is presented with a review of pertinent literature. Characteristics of the poisoning include a delay between exposure and onset of symptoms; early systemic toxicity with congestive changes in the lungs and oliguric renal failure; prominent cerebellar and Parkinsonian neurologic symptoms as well as seizures and coma in severe cases; and psychiatric disturbances that can last from months to years. Although methyl iodide is a rare form of intoxicant, its manifestations are similar to that of poisoning with the other monohalomethanes that are not uncommon.

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