Coagulation Defects in Hypoxic Full-term Newborn Infants

Abstract

gross infiltration, those with nodular lesions, and among those with high bacillary density on skin smears.The very detailed monthly assessment of haematological, hepatic, renal, neurological, visual, and cardiac functions failed to show any toxic effects from clofazimine during the period of observation, and thus confirmed the previously gained impression that in the acutely ill, debilitated leprosy patient clofazimine can be safely administered with gratifying therapeutic results. However, the red-brown pigmentation of the skin that was seen in all the patients, coupled with reddish brown urine and sweat and a tendency to development of dry scaly skin, was disturbing to the younger and fairer patients.The study does not show the superiority of clofazimine over dapsone, in the dose used in this trial, in terms of bacterial death and clearance, resolution of skin lesions, and the incidence of erythema nodosum leprosum. While further controlled studies for a longer period are necessary, we suggest that dapsone, which is much cheaper and does not cause significant pigmentation, is preferable to clofazimine in the routine management of untreated lepromatous leprosy. Clofazimine could be reserved for patients who are either sensitive or resistant to dapsone as well as for those who are distressed by recurrent chronic erythema nodosom leprosum or recurrent chronic peripheral neuritis or both.

Blood coagulation status of small-for-dates and postmature infants.

“…Asphyxia was not a predisposing cause of coagulopathies in our cases contrary to the findings of some investigators (Chadd et al, 1971), but in agreement with others (Ekelund and Finnstrom, 1972). Anoxic tissue damage such as that possibly seen in Case 3 (Appendix) may have contributed to intravascular coagulation by releasing tissue thromboplastin into the circulation.…”

Components of the Haemostatic Mechanism at Birth in Pre‐eclampsia With Particular Reference to Fetal Growth Retardation

“…There have been several reports of disseminated intravascular coagulation in intrauterine fetal growth retardation and in cases of perinatal asphyxia (Bryant et al, 1970;Chadd et al, 1971). Howie et al, (1971) were unable to show changes in the haemostatic mechanism in maternal blood when comparing a low birth weight infant group with a normal group.…”

Cardiovascular Alterations and Multiorgan Dysfunction After Birth Asphyxia

“…Coagulation dysfunction in hypoxic infants was reported as early as 1971 in a subset of infants with birth asphyxia, with the cause associated with a consumptive coagulopathy (increased fibrin degradation products) followed by disseminated intravascular coagulation [67, 68]. The effect on coagulation was of short duration and may only play a minor role overall morbidity of birth aphyxia.…”