oratory investigation revealed acidosis: pH7.08, partial pressure of carbon dioxide 8 mm Hg, bicarbonate level2 mmol/L and methanol level 40 mmol/L. There ...
I Case Reports
Neurologic sequelae of methanol poisoning Todd J. Anderson, MD Ashfaq Shuaib, MD Werner J. Becker, MD, FRCPC
A lthough blindness is a common and wellrecognized complication of methanol intoxication, damage to other organ systems is distinctly uncommon.1 We present three patients who had neurologic complications after methanol abuse. These rare but severe complications illustrate the seriousness of this increasingly common form of poisoning. Case reports Case 1 A 55-year-old woman with a long history of depression and suicide attempts presented 18 hours after swallowing 450 ml of methanol. She complained of nausea, behaved abnormally and had decreased visual acuity. Within hours generalized tonic-clonic seizures began, which were treated with phenytoin. She became comatose and had intermittent decerebrate rigidity and generalized hyperreflexia. Her vital signs were normal, and there were no focal neurologic abnormalities. Laboratory investigation revealed acidosis: pH 7.08, partial pressure of carbon dioxide 8 mm Hg, bicarbonate level 2 mmol/L and methanol level 40 mmol/L. There was no hypotension or hypoxia. After 21 hours of continuous ethanol infusion and hemodialysis the methanol level had decreased to zero. Despite normal metabolic features the patient remained comatose, and her flaccid paralysis and hyperreflexia changed to spasticity 15 days after admission. Computed tomograms of her brain showed low-density lesions in the basal ganglia and in the frontal and anterior temporal From the departments of Neurology and Internal Medicine,
University of Calgary
Correspondence to: Dr. Todd J. Anderson, 1403-29 St. NW, Calgary, Alta. T2N 2T9 (reprints not available)
lobes. At the time this paper was written she was still alive. Case 2 A 31-year-old man was admitted to hospital after swallowing an undetermined amount of methanol for several days. He had complained of nausea and had a moderately decreased level of consciousness. Because he was hypotensive a lowdose dopamine infusion was started to keep his blood pressure at 100/60 mm Hg. His respiratory status quickly deteriorated, and endotracheal intubation was required. His level of consciousness was markedly decreased, there were no spontaneous movements and no reflexes in his legs, and the reflexes in his arms were diminished. Laboratory investigations showed a pH of 6.94, an anion gap of 34 mmol/L and a methanol level of 183 mmol/L. The patient was treated with continuous ethanol infusion and hemodialysis for 24 hours. During treatment his partial thromboplastin time was about 3 minutes, but there were no clinical signs of bleeding. His condition improved, and 3 days after admission he regained consciousness. He had flaccid paralysis of both legs, with no sensation below the fourth thoracic vertebra. One month later he regained some vision in his right eye but remained blind on his left side. Pain sensation in his legs returned after 2 months, and at the time of discharge his leg strength had increased to a grade of 3/5.
Case 3 A 30-year-old man who had a history of suicide attempts and recent social stress was found by ambulance attendants at his home with an empty bottle of doxepin hydrochloride. His condiCMAJ, VOL. 136, JUNE 1, 1987
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tion initially improved in hospital but deteriorated after 24 hours. His level of consciousness decreased, and he had metabolic acidosis. The results of screening for toxic substances were positive for methanol, and he was transferred to our hospital 48 hours after presentation. On admission the patient was responsive only to painful stimuli. His pupils were 7 mm in diameter but reactive, and his fundi were pale. Laboratory investigations revealed a pH of 7.28, an anion gap of 21 mmol/L and a methanol level of 4 mmol/L. Despite the low level of methanol he was treated with hemodialysis and ethanol infusion because of his clinical condition. Transient hypophosphatemia and pneumococcal pneumonia developed, but there were no episodes of hypoxia or hypotension. The level of consciousness improved with treatment, but the patient was left with a severe cognitive defect and a transient rest tremor. He could undertake only simple tasks, could not repeat more than two numbers backward and had markedly impaired reading, writing and calculation skills. He also exhibited abnormal thought processes. His snout and glabellar tap reflex was normal. An electroencephalogram showed marked delta-wave activity in the frontal lobes, and a computed tomogram revealed low-density lesions in the lateral basal ganglia and frontal lobes, with hemorrhage in both areas (Fig. 1). The patient's personality and cognitive function improved somewhat over the next several months, but he remained limited intellectually.
Methanol ingestion is becoming recognized as an increasingly common and serious form of poisoning. Although the death rate is high, recovery is usually complete except for the well-known visual defects.1 Over the last decade neurologic sequelae of acute methanol poisoning have rarely been reported, the first being parkinsonism.2 Other sequelae have included pseudobulbar palsy,3'4 intellectual abnormalities and transverse myelitis,5 primitive reflexes3 5 and seizures.' 3,4 The first patient we have reported on did not regain any useful cognitive function and remained in a vegetative state. Her computed tomogram showed signs similar to those of diffuse leukoencephalopathy, with widespread low-density lesions like those seen in other cases of methanol poisoning.6 We believe this is the first reported case of such widespread damage caused by methanol intoxication in a patient who has survived. The second patient had a course similar to one reported by McLean and colleagues.5 Their patient initially had no leg movement and then had spasticity and persistent leg weakness. The autopsy demonstrated bilateral cystic areas of necrosis throughout the subcortical white matter, especially in the anterior frontal lobes. Histologic examina-
Fig. 1 - Case 3: Computed tomogram showing marked leukoencephalopathy and hemorrhage after methanol poisoning.
Fig. 2 - Case 3: Computed tomogram 2 weeks later showing leukoencephalopathy and resolution of hemorrhage.
Another computed tomogram revealed that the bleeding but not the low-density lesions had resolved (Fig. 2). Comments
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tion of the spinal cord revealed descending degeneration through the lateral columns, with swelling of the anterior horn cells. No other cases of myelopathy or myelitis have been reported. Because of the similarity of our case to that of McLean and colleagues, the mechanism of injury may be the same. The third patient we have described had a substantial cognitive deficit after a 48-hour delay in diagnosis. He had primitive reflexes like those of the patient described by McLean and colleagues;5 the only other patient reported to have such reflexes died shortly after presentation.3 We have described the significant damage that may occur to the white matter and basal ganglia in patients who have taken methanol. These sequelae may become increasingly recognized as more patients survive.
References 1. Bennett IL, Cary FH, Mitchell GL et al: Acute methyl alcohol poisoning; a review based on experiences in an outbreak of 323 cases. Medicine 1953; 32: 435-463 2. Riegel H, Wolf G: Schwere neurologische Ausfalle als Folge einer Methylalkoholvergiftung. Fortschr Neurol Psychiatr 1966; 34: 346-351 3. Scrimgeour EM: Outbreak of methanol and isopropanol poisoning in New Britain, Papua New Guinea. Med J Aust 1980; 2: 36-38 4. Naraqui S, Dethlefs R, Slobodnick R et al: An outbreak of acute methyl alcohol intoxication. Aust NZ J Med 1979; 65: 65-68 5. McLean DR, Jacobs H, Mielke BW: Methanol poisoning: a clinical and pathological study. Ann Neurol 1980; 8: 161167 6. Aquilonius SM, Askmark H, Enoksson P et al: Computerised tomography in severe methanol intoxication. Br Med J 1978; 2: 929-930
Combined metronidazole and quinacrine hydrochloride therapy for chronic giardiasis Geoffrey D. Taylor, MD, FRCPC Wanda M. Wenman, MD, FRCPC D. Lorne J. Tyrrell, MD, FRCPC I n the absence of standard methods for performing in-vitro sensitivity testing, the management of symptomatic giardiasis, as for most parasitic infections, is empiric. Treatment is usually not difficult; if the first course is ineffective, then a second course with the original agent or an alternative is usually effective.' Failure of repeated courses has rarely been reported, and no standard approach has been suggested. We describe a case of chronic symptomatic giardiasis in a patient with common variable hypogammaglobulinemia in whom combined treatment with metronidazole and quinacrine hydrochloride was successful after five courses of metronidazole, one of quinacrine, and one of immune globulin and metronidazole had failed. Case report A 47-year-old man had a 25-year history of chronic diarrhea and abdominal cramps. In 1983 From the divisions of Infectious Diseases, the departments of Medicine and Pediatrics, University of Alberta, Edmonton
Reprint requests to: Dr. Geoffrey D. Taylor, Infection Control Unit, 2E3. 14 WC MacKenzie Health Sciences Centre, University of Alberta Hospital, Edmonton, Alta. T6G 2B7
Giardia lamblia cysts and trophozoites were found in stool samples, but results of culture and parasitic studies for bacteria and other common pathogens, including Cryptosporidium, were negative. Between March 1983 and January 1984 he received five courses of metronidazole, 1.5 to 2.5 g/d for 7 to 14 days, and one course of quinacrine, 100 mg three times daily for 10 days. After each course there was an initial response, but the symptoms returned after the medication was stopped, and trophozoites were still present in stool samples. Family members, their dog and the well that supplied their water were found to be free of parasites. The patient had frequently travelled to areas of Alberta in which G. lamblia is endemic but had not drunk untreated water. Further investigations revealed signs of common variable hypogammaglobulinemia: a low serum IgG level, 1.32 (normally 6 to 15) g/L, and no detectable IgA or IgM. The results of barium studies of the small intestine suggested malabsorption. A biopsy specimen showed a distorted villous pattern and lymphoid infiltration of the lamina propria but no Giardia trophozoites. In January 1984 a series of immune globulin infusions, once every 4 weeks for 6 months, combined with continuous oral metronidazole therapy, 750 mg/d, relieved the symptoms until the metronidazole therapy was stopped. After the CMAJ, VOL. 136, JUNE 1, 1987
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