軽度の低血圧，正常動脈血酸素分圧，代謝性アシドーシスを伴った一酸化炭素中毒の白質病変について

A CASE OF CARBON MONOXIDE LEUKO-ENCEPHALOPATHY WITH MILD HYPOTENSION,NORMAL PaO2 AND METABOLIC ACIDOSIS

I．はじめに

　一酸化炭素中毒は大脳皮質にくらべ白質病変が著明なため多くの研究者の注目をうけてきた。しかし白質病変の生成機序についてはなお不明の点が多く，諸家の意見も一致しない。

　私どもは都市ガス自殺を企てて低血圧，代謝性アシドーシスをきたし動脈血酸素分圧が来院時に既に正常であつた症例の剖検で大脳白質の際立つた病変を認めたので報告し考察を行なうこととする。

A 25-year-old woman was admitted to the Asahikawa City Hospital after attempting suicide by gas.

On admission, she was comatose. Her blood pressure was 80/50 mmHg, puls rate 90/min, and respiration was 28/min and regular. Arterial blood gas was as follows: Pa0₂; 138 mmHg, S0₂; 98.4%, PaCO₂; 22.7 mmHg, HCO₃ ; 11.5 mEq/L, pH ; 7.329, anion gap ; 24.6 mEq/L and computed base excess; -12.4 mEq/L.

One month later, she became apallic, and died of acute pneumonia after being hospitalized for 18 months.

The general autopsy showed severe acute lobar pneumonia and chronic adhesive pleuritis.

The brain was small and weighed 1,140 grams. Coronal section of the cerebrum showed cysticnecrosis and sponginess of the white matter of the frontal, parietal, occipital and temporal lobes, bi-laterally. The centrum semiovale was most severely affected and had web like formations in the cavities. The lesions were soft, discolored and had distinct margins. There was a cystic lesion in the para-hippocampal gyrus on each side, measuring 1 cm in diameter. The cerebral and cerebellar cortex, and subcortical U-fibers were minimally affected.

Microscopic examination showed symmetric necrosis of the centrum semiovale. Lesions were also found in the internal capsules, the left globus pallidus and in subcortical U-fibers. The peripheral areas of the necrotic zone were spongy, with moderate to large amount of gemistocytes and gitter cells. The neuronal loss was minimal in the cerebral cortex, however, it was severe in the Sommer sectors. The brain stem and the cerebellum were normal except for mild atrophy of the pyrami-dal tract.

The clinico-pathological correlation in this case was thoght of as follows:

Systemic hypotension which is a common com-plication of carbon monoxide intoxication involved in hypoperfusion of oxygen, nutrient and buffers in the endarterial zone, the cerebral white matter. In addition, histotoxic action of carbon monoxide induced anemic anoxia due to Hb deprivation, even though Pa0₂ was sufficient. On the basis of these tissue anoxia and buffer deprivation, lactic acidosis developed in the endarterial zone and damaged the cerebral white matter except for subcortical U-fibers.