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M Villard

Publications and source records attributed to M Villard.

7 recordsLinked to original sources
PubMed1984

An epidemic of "childbed fever".

Postpartum infection remains a cause of considerable maternal morbidity and occasional maternal mortality. Puerperal sepsis mediated by what is now known as group A beta-hemolytic streptococci or Streptococcus pyogenes was once a common and lethal nosocomial scourge. Fortunately, multiple developments have decreased the incidence and ameliorated the clinical course of group A beta-hemolytic streptococcal postpartum sepsis. Despite these developments, epidemic group A streptococcal sepsis still jeopardizes modern mothers. We describe an epidemic of five women with group A beta-hemolytic streptococci-mediated postpartum infections which occurred at Mather Air Force Base Hospital, Sacramento, California. The remarkable, yet characteristic signs, symptoms, and clinical course of these patients are briefly reviewed along with the epidemiologic methods which led to the discovery of the common nosocomial source. Familiarization of the clinical aspects of these patients and the methods used to eradicate this epidemic will facilitate the protection and care of other women. Unfortunately, modern mothers still remain in jeopardy from "childbed fever."

California↗
PubMed1983

[Functional spontaneous splenorenal anastomosis in portal hypertension due to cavernoma. Apropos of 5 cases reports].

Natural splenorenal shunts were observed in 5 children with portal vein obstruction. In all 5 cases, 1 or several criteria were found suggesting that such anastomoses were functional. For a better understanding of the spontaneous improvement of some children with portal vein obstruction, it would be advisable repeat radiologic, fiberoptic and ultrasonographic investigations at regular intervals in such children.

Child↗
PubMedDate not supplied

[Pulmonary arterial hypertension and systemic lupus erythematosus. Apropos of 2 cases. Review of the literature].

Pulmonary arterial hypertension may develop in patients with systemic lupus erythematosus (SLE) in the absence of lung tissue lesion or embolism in the pulmonary circulation. Its mechanisms and prognosis are imperfectly known, although various suggestions have been made concerning the possible role of pulmonary arterial spasm, immune complex arteritis or arterial wall fibrosis. We report two cases of SLE in female patients who presented with clinical signs of pulmonary arterial hypertension. The fact that pulmonary arterial hypertension regressed completely in one patient and resulted in death in the other points to different pathogenic mechanisms. In the first patient the dramatic therapeutic effectiveness of a calcium inhibitor suggests that an arterial spasm was involved, whereas the anatomical lesions found in the second patient are in favour of a fibrotic inflammatory arteritis. This pathogenic heterogeneity of pulmonary arterial hypertension in SLE, which may correspond to different evolutive stages of the disease, is documented by a review of the literature with special attention to the frequency and to the clinical biochemical, haemodynamic and histological aspects of this complication of SLE.

Adult↗