Neurohypophyseal dysfunction following perinatal asphyxia

Khare, Santosh

doi:10.1016/s0022-3476(77)80386-7

Cited by 18 publications

(6 citation statements)

References 6 publications

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“…Therefore, hypoxia during birth is obviously one of the nonosmotic stimuli for AVP release [2, 3,14,15]. The degree of asphyxia is correlated with high AVP serum concentrations [6] and some in fants develop the syndrome of inappropriate AVP secretion [10], Additionally, increased intracranial pres sure stimulates AVP secretion [4]. The vagi nally delivered infants in our study had in deed higher U-AVP values than those born by cesarean section.…”

Section: Discussionmentioning

confidence: 66%

The Role of Arginine-Vasopressin in the Regulation of Water Metabolism in Preterm Infants in the First Days of Life

Stegner¹,

Henkel²,

Commentz³

1987

Horm Res

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We studied the role of arginine-vasopressin (AVP) in the regulation of fluid homeostasis in preterm infants. Group 1 was fed orally, groups 2 and 3 received fluids parenterally, and group 3 developed respiratory distress syndrome (RDS) and had to be ventilated. The infants of group 3 were not able to excrete the administered fluid, gained weight and consecutively developed hyponatremia. 1 -min Apgar scores as well as log FiO₂ correlated significantly with urinary AVP excretion on day 1. We conclude that nonosmotic stimuli are involved in the release of AVP and therefore disturb fluid homeostasis in severely ill infants with RDS.

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Section: Discussionmentioning

confidence: 66%

The Role of Arginine-Vasopressin in the Regulation of Water Metabolism in Preterm Infants in the First Days of Life

Stegner¹,

Henkel²,

Commentz³

1987

Horm Res

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“…Khare et al reported one case of neurohypophyseal dusyfunction following perinatal asphyxia. Although progress of their case was the same as ours, they did not have the detailed examination including head MRI and measurement of plasma ADH [7].…”

Section: Discussionmentioning

confidence: 84%

“…There should be more CDI cases caused by severe perinatal asphyxia and are not only recognized, because severe perinatal asphyxia does not often become a target of the aggressive diagnosis and treatment. However, to the best of our knowledge, there are a few reports of neonatal CDI caused by severe perinatal asphyxia [7]. Khare et al reported one case of neurohypophyseal dusyfunction following perinatal asphyxia.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Central Diabetes Insipidus Caused by Severe Perinatal Asphyxia

Ueda¹,

Numoto²,

Kakita³

et al. 2016

Pediat Therapeut

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We describe three rare cases of neonatal central diabetes inspidus (CDI) caused by severe perinatal asphyxia. In these cases, hypernatremia, high plasma osmolality and hyposthenuria, with polyuria occurred after one week of age. CDI in one case might be due to the temporal dysfunction of hypothalamic-neurohypophyseal axis and the other two cases to permanent dysfunction. Although these cases are rare, early diagnosis and treatment of CDI are indispensable. Follow-up of serum sodium, serum and urine osmolality is necessary after acute phase to maintain water and electrocyte homeostasis in severe perinatal asphyxia.

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“…Transient DI has been related to disseminated intravascular coagulation (DIC) in an infant who had listeriosis [23]. Feldman et al [24], Kaplan and Feigin [25], and Kahre [8] reported cases of inappropriate secretion of ADH following neonatal asphyxia. In the latter report the patient experienced a gradual transition to DI.…”

Section: Central Diabetes Insipidusmentioning

confidence: 99%

“…Idiopathic hypothalamic dysfunction with dilated unresponsive pupils has been reported as part of the spectrum of hypothalamic dysfunction [29]. Pitressin-sensitive DI is a difficult diagnosis and management in the perinatal period and even in infancy [8,23].…”

Section: Central Diabetes Insipidusmentioning

confidence: 99%

Empty Sella Syndrome, Panhypopituitarism, and Diabetes Insipidus

Jones

Drut

Valencia

et al. 2005

Fetal and Pediatric Pathology

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We present an 18-month-old girl with short stature, obesity, panhypopituitarism, diabetes insipidus, and visual defects. Postmortem examination revealed brain atrophy due to a diffuse encephalopathy, numerous calcified neurons in cerebral cortex, deep telencephalic and diencephalic nuclei, diffuse neuronal necrosis in hypothalamic nuclei, moderate atrophy of optic nerves, very thin hypophyseal stalk, and empty sella with the hypophysis compressed to the dorsal aspect of the concavity. Our hypothesis is that the presence of an empty sella in a child with hypophyseal-hypothalamic abnormalities should alert physicians to the existence of hypothalamic lesions secondary to a perinatal insult. We discuss the possible pathogenesis of these findings as well as lines of evidence available in the literature.

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Neurohypophyseal dysfunction following perinatal asphyxia

Cited by 18 publications

References 6 publications

The Role of Arginine-Vasopressin in the Regulation of Water Metabolism in Preterm Infants in the First Days of Life

The Role of Arginine-Vasopressin in the Regulation of Water Metabolism in Preterm Infants in the First Days of Life

Neonatal Central Diabetes Insipidus Caused by Severe Perinatal Asphyxia

Empty Sella Syndrome, Panhypopituitarism, and Diabetes Insipidus

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