On the pathogenesis of germinal layer hemorrhage in the neonate.
The paper describes the sequence of events typical in the pathogenesis of germinal layer hemorrhage (GLH): An initial, often prenatal, severe asphyxic event, leading to abolishment of autoregulation of cerebral perfusion, and, most likely, to hypoxic-ischemic lesions in the endothelium of the large capillaries of the germinal matrix. The hypoxia is accompanied by exhaustion of myocardial energy reserves with circulatory failure, hypotension and aggravation of cerebral ischemia. In the period immediately after birth, circulation failure proceeds with cardiac insufficiency, hypotension, cerebral ischemia, and possibly venous hypertension. Following resuscitation, arterial blood pressure gradually increases (type 3) with increased strain on the damaged germinal matrix capillary walls in the absence of autoregulation. This effect is further aggravated by arterial blood pressure increments of type 1 and 2 leading to GLH, possibly with increments of venous pressure as a contributing factor.
Lou
H C
HC
John F. Kennedy Institute, Glostrup, Denmark.
D001794:Blood Pressure; D001921:Brain / Q000033:anatomy & histology / Q000098:blood supply*; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D002543:Cerebral Hemorrhage / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000473:pathology* / Q000503:physiopathology; D014661:Vasoconstriction; D014699:Venules / Q000503:physiopathology
D002245:Carbon Dioxide