Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 7202988

[Breech presentation (author's transl)].

E Hochuli·O Käch
View original source ↗Export metadata ↓

Abstract

The perinatal mortality and morbidity of 303 breech deliveries was investigated. In 80 newborn the acidosis (pH less than 7.20) was due to positional variations such as footling, knee and mixed breech presentations in vaginal deliveries. Our results are incorporated in a new concept of triage which permits continuing vaginal breech deliveries as a calculable risk.

Explore related subjects

AcidosisAdolescentAdultBreech PresentationCesarean SectionFemaleHumansInfant MortalityInfant, NewbornInfant, Newborn, DiseasesInfant, PrematureLabor PresentationPregnancySwitzerlandEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E Hochuli, O Käch. 1981. [Breech presentation (author's transl)].. https://doi.org/10.1055/s-2008-1036836

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1998

Metabolic acidosis and protein catabolism: mechanisms and clinical implications.

Metabolic acidosis increases protein degradation resulting in muscle wasting and a negative nitrogen balance. The branched-chain amino acids serve as useful markers of these changes and their catabolism is increased in acidosis, particularly for the spontaneous acidosis associated with renal failure. As a result, the neutral nitrogen balance is compromised and malnutrition results. Glucocorticoids mediate these changes through the recently discovered ATP-dependent ubiquitin-proteasome pathway. Therapy necessitates correction of the underlying acidosis either through adjustment of the alkalinity of the dialysate for the patient on dialysis or through dietary protein restriction and sodium bicarbonate supplements for the predialysis patient.

Acidosis↗
PubMed1998

Factors contributing to catabolism in end-stage renal disease patients.

End-stage renal disease (ESRD) patients, whether they are treated with hemodialysis or continuous ambulatory peritoneal dialysis, frequently suffer from protein-energy malnutrition, which is associated with increased morbidity and mortality. The protein requirements in dialysis patients are increased compared to those of healthy individuals and nondialyzed patients with chronic renal failure. The intake of protein and energy is frequently reduced because of the underlying disease, comorbidity, psychosocial factors, and uremic anorexia (underdialysis). There are several factors in ESRD patients that may enhance protein catabolism and increase protein requirements, such as low energy intake, amino acid abnormalities, metabolic acidosis, endocrine abnormalities (insulin resistance, hyperglucagonemia, hyperparathyroidism, insensitivity to growth hormone and insulin-like growth factor-1, cardiac failure, infection and inflammation, anemia, and physical inactivity. The dialytic procedures per se may enhance protein catabolism due to dialytic losses of protein and amino acids and, in hemodialysis, an inflammatory response to blood-dialyzer interaction. The relative importance of the various factors which cause anorexia and stimulate protein catabolism is still not well understood.

Acidosis↗