Acute yellow atrophy of the liver, with special reference to its etiology, treatment, and association with pregnancy: with a report of two cases occurring in the puerperium

Abstract

1. Two hitherto unpublished cases of acute yellow atrophy of the liver have been reported. Both occurred in the puerperium, one recovered and one died. These cases have been discussed from an etiological, clinical, diagnostic and therapeutic aspect comparing them with other reported cases.  • 2. The history of the disease has been briefly considered. Its rarity is confirmed and no evidence has been found to support the suggestion that there is a general increase in incidence.  • 3. It has been shown that acute yellow atrophy is not essentially a clinical entity, but a terminal condition which may arise under a variety of different circumstances.  • 4. Our knowledge of the etiology of the disease has been surveyed but no distinct etiological factor common to all cases was found.  • 5. It has been shown that in many cases, as in the new cases presented, the etiology is not a single factor but a combination of factors. The occurrence of unexplained idiopathic cases in which no known etiological factor is discernible, is accepted.  • 6. The toxic theory of the causation of the disease has been considered, and whilst being accepted as possibly correct, it has been shown that it is not necessarily so.  • 7. The suggestion has been made that the disease is more correctly appreciated if regarded as a metabolic disease and a fundamental disturbance of cell metabolism has been postulated as the basis of all cases. It has further been suggested that this disturbance of cell metabolism is probably in the nature of a disturbed carbohydrate metabolism and evidence has been discussed supporting view.  • 8. The possibility of the existence of a hereditary predisposition, and of a hormonic factor in the etiology has been suggested.  • 9. The frequent association of the disease with pregnancy and the puerperium has been discussed and it is believed that this is due to the metabolic instability present in pregnancy. The prevalence of chloroform as a predisposing cause in pregnancy has also been noted, and is regarded as a frequent precipitating agent of acute liver necrosis, indistinguishable from acute yellow atrophy.  • 10. The pathology of the disease has been reviewed and discussed. It has been remarked that the outstanding pathological feature of the disease is necrosis of liver cells and the unsuitability of the nomenclature has been noted. The part played by autolysis in the pathogenesis of the disease has been observed.  • 11. The post mortem report of Case 2 has been compared with the usual pathological appearance. The only discrepancy noticed was the absence of liver shrinkage, which it appears may occur in acute yellow atrophy, though rarely.  • 12. The similarity of the liver changes in acute yello atrophy and pregnancy toxaemia o:C all types has been pointed out, and the association of acute yellow atrophy and pre- eclamptic toxaemia in Case 1 stressed. It is agreed that the difference between the results of these conditions may not be so great as is generally supposed.  • 13. The diagnosis of acute yellow atrophy rests on the association of jaundice, vomiting, severe constitutional and nervous symptoms, with a diminished liver dullness. The. blood chemistry and urine analysis may be of assistance in diagnosis.  • 14. The diagnosis of acute yellow atrophy in Case 1 has been justified, but in Case 2 it has been found impossible to establish a differentiation from delayed chloroform poisoning.  • 15. The symptomatology of the two cases has been found to agree with other recorded cases. It has been noted that the signs and symptoms of pro-eclamptic toxaemia disappeared in a normal manner in spite of the complication of acute yellow atrophy.  • 16. The pulse has been noted as a reliable guide to the condition of the patient, whilst the temperature gave no indication of the severity of the illness.  • 17. A theory has been propounded that death in acute yellow atrophy may occur either from hepatic insufficiency or from auto-intoxication. It has been further suggested that the severe nervous symptoms might also be due in part to autointoxication from the products of necrosed cells. A promising line of research has been suggested on these lines, since some therapeutic indication might become obvious if it was proved that the products of autolysed liver cells cause some of the clinical manifestatidins.  • 18. The prognosis is always grave, but it is believed that prompt, vigorous and continued treatment may be effective, and that contrary to the accepted belief the prognosis is never hopeless.  • 19. It is agreed that the prognosis is worse in pregnancy. Ominous signs in the illness are a progressively decreasing liver in spite of treatment, and persistent vomiting.  • 20. In considering treatment, the importance of prophylaxis has been noted. In this connection, the importance of vomiting, starvation and chloroform especially if present together in pregnancy has been particularly emphasised. It has been suggested that chloroform should be used with greater care and especially in pregnancy should be preceded by routine administration of intravenous glucose. The use of chloroform in eclampsia is regarded as dangerous.  • 21. In treatment, glucose and abundant fluids are the essential elements. It has been pointed out that the provision of fluids is usually inadequate.  • 22. Other useful aids to treatment which should be employed are, calcium, anhaemin, and vitamin B. The provision of efficient nursing is essential to success