Biomedical subjects

G I Martin

Publications and source records attributed to G I Martin.

At least 55 records · Page 3Linked to original sources

PubMed1971

Imipramine pamoate in the treatment of childhood enuresis. A double-blind study.

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Adolescent↗

PubMed1970

The Ehlers-Danlos Syndrome. Report of two cases in monozygous Philippino-American twins.

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Asian People↗

PubMed1970

Oral gentamycin sulfate in treatment of infantile diarrhea due to enteropathogenic E. coli.

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Administration, Oral↗

PubMedDate not supplied

Intrapartum fetal asphyxial brain injury with absent multiorgan system dysfunction.

Current understanding of the physiologic mechanisms of intrapartum fetal asphyxial brain injury has suggested a strong association with multiorgan system injury. Thus the purpose here is to describe 14 cases of severe fetal brain injury with absent multiorgan system dysfunction (MSD). The study population was drawn from a national registry for brain injured infants. MSD was defined by clinical criteria demonstrated to reflect asphyxial injury to the pulmonary, renal, cardiac, hematologic, hepatic, and gastrointestinal systems. Involvement of one other organ in addition to the brain was defined as multiorgan system dysfunction. All infants were diagnosed with hypoxic-ischemic encephalopathy (HIE) in the neonatal period and went on to have permanent central nervous system (CNS) injury and MSD criteria were not met. Of the 292 term, singleton infants with HIE and permanent neurologic injury, 57 (20%) satisfied the entry criteria; of these, 14 (36%) had no MSD. The underlying basis for the fetal brain injury were: uterine rupture, 6 (43%), prolonged FHR deceleration, 5 (36%), fetal exsanguination, 1 (7%), cord prolapse, 1 (7%), and maternal cardiopulmonary arrest, 1 (7%). The mean duration of the prolonged FHR deceleration was 32.1 +/- 9.1 (range 19-51) minutes. All infants were later diagnosed with cerebral palsy. Intrapartum fetal asphyxial brain injury may not necessarily proceed through a physiologic mechanism in which the fetal circulation is centralized and endorgans damaged. These acute injuries, associated with a prolonged FHR deceleration, may be linked to severely decreased cardiac output and hypotension that cause vulnerable portions of the brain to be injured before other organs.

Asphyxia Neonatorum↗

PubMedDate not supplied

Acute fetal asphyxia and permanent brain injury: a retrospective analysis of current indicators.

OBJECTIVE: To determine whether a term neonate who has had sufficient intrapartum asphyxia to produce persistent brain injury will manifest the following four criteria: profound acidemia (arterial pH <7.00), an APGAR score < or =3 for 5 min or longer, seizures within 24 h of birth, and multiorgan system dysfunction. METHODS: Singleton, liveborn, neurologically impaired neonates > or =37 weeks gestation who lived at least 6 days and had sufficient documentation of current intrapartum asphyxia criteria were retrospectively analyzed. Of these infants, solely neonates with acute fetal asphyxia due to a sudden prolonged FHR deceleration that lasted until delivery from a catastrophic event, e.g., uterine rupture, cord prolapse, were included. Organ system dysfunction was defined by separate criteria for each organ system. Dysfunction in one or more was defined as multiorgan system dysfunction. RESULTS: Of the 292 eligible infants in the registry, 47 satisfied the entry criteria. In these 47 neonates, 10 (21%) satisfied all 4 criteria for intrapartum asphyxia. CONCLUSIONS: Our retrospective study suggests that currently used indicators to define permanent fetal brain injury are not valid.

Apgar Score↗

PubMedDate not supplied