Intracranial haemorrhage associated with hyaline membrane disease.

Harrison, V. C.; Heese, H. De V.; Klein, Max

doi:10.1136/adc.43.227.116

Cited by 49 publications

(22 citation statements)

References 8 publications

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“…Deficiencies in clotting factors and fibrinogen, increased levels of fibrinogenlfibrin degradation products and thrombocytopenia (2,4,19,22,23) have been reported to be caused by DIC. These coagulation abnormalities are associated with clinical symptoms of bleeding (7,8,16,25,29) particularly IVH and fibrin thrombi at autopsy (3,7, 16,3 1) suggesting that DIC contributes to the fatal outcome of this disease. Decreased levels of AT-I11 have been described in early stages of DIC in adult patients (6,26).…”

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confidence: 99%

Low Antithrombin III Levels in Neonates with Idiopathic Respiratory Distress Syndrome: Poor Prognosis

Peters¹,

Cate²,

Breederveld³

et al. 1984

Pediatr Res

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SummaryAutomated microanalytic chromogenic coagulation assays allow serial monitoring of critically ill newborn infants. In this study 84 premature infants 126 healthy prematures and 58 neonates with idiopathic respiratory distress syndrome (IRDS)] were studied daily during the first week of life, to investigate the possible significance of hemostatic abnormalities in IRDS.In neonates with IRDS, coagulation factors I1 and X, antithrombin I11 (AT-111), plasminogen, and a2-antiplasmin were significantly lower than control values. Recovery of the initially low AT-111 levels was delayed relative to the other coagulation parameters measured. An AT-I11 r 0.15 U/ml was present within the first 6 h of life in eight patients who developed IRDS, seven of whom died within 48 h. Autopsy of these neonates showed widespread fibrin deposition and hemorrhage in vital organs consistent with intravascular coagulation. These findings indicate that very low levels of AT-I11 are associated with disseminated intravascular coagulation in neonates with IRDS and suggest that a deficiency of AT-I11 is predictive of a poor outcome. AbbreviationsAT-111, antithrombin 111 DIC, disseminated intravascular coagulation IRDS, idiopathic respiratory distress syndrome IVH, intraventricular hemorrhage DIC is frequently encountered in premature newborn infants suffering from IRDS. Deficiencies in clotting factors and fibrinogen, increased levels of fibrinogenlfibrin degradation products and thrombocytopenia (2,4,19,22,23) have been reported to be caused by DIC. These coagulation abnormalities are associated with clinical symptoms of bleeding (7,8,16,25,29) particularly IVH and fibrin thrombi at autopsy (3,7, 16,3 1) suggesting that DIC contributes to the fatal outcome of this disease. Decreased levels of AT-I11 have been described in early stages of DIC in adult patients (6,26). In cord blood samples of premature infants who developed IRDS, reduced AT-I11 levels have been reported (1 8, 2 1, 34); however, the relationship between AT-I11 activity and the clinical course of IRDS has not yet been thoroughly investigated. The availability of automated chromogenic coagulation assays enables the serial study of several coagulation parameters, and of AT-I11 in particular, in premature neonates with IRDS. These results are correlated with clinical signs and autopsy findings.

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confidence: 99%

Low Antithrombin III Levels in Neonates with Idiopathic Respiratory Distress Syndrome: Poor Prognosis

Peters¹,

Cate²,

Breederveld³

et al. 1984

Pediatr Res

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“…This is critically dependent on whether the drugs were mainly given before or after the development of IVH. Unfortunately, retrospective diagnosis of the occurrence of an IVH is extremely difficult though pinpointing the probable time to within a brief period may be possible if frequent haematocrit readings or special investigations have been done (Harrison, Heese, and Klein, 1968;Tsiantos et al, 1974). In the absence of such methods descriptions of episodes of sudden collapse recorded in the clinical notes have to be relied upon.…”

Section: Discussionmentioning

confidence: 99%

“…A widely held belief is that infants with IVH are distinctive in having a severe metabolic acidosis which is resistant to alkali therapy (Harrison et al, 1968 Roberton and Howat (1975) and Anderson et al (1976) believe that alkali was given, in their respective series, mainly after IVH had occurred. The alternative explanation is that excessive alkali therapy when given to babies with HMD has caused or contributed to the development of IVH.…”

Section: Discussionmentioning

confidence: 99%

Hyaline membrane disease, alkali, and intraventricular haemorrhage.

Wigglesworth¹,

Keith²,

Girling³

et al. 1976

Archives of Disease in Childhood

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. (1976). Archives of Disease in Childhood, 51, 755. Hyaline membrane disease, alkali, and intraventricular haemorrhage. The relation between intraventricular haemorrhage (IVH) and hyaline membrane disease (HMD) was studied in singletons that came to necropsy at Hammersmith Hospital over the years 1966-73. The incidence of IVH in singleton live births was 3 -22/1000 and of HMD 4-44/1000. Although the high figures were partly due to the large number of low birthweight infants born at this hospital, the incidence of IVH in babies weighing 1001-1500 g was three times as great as that reported in the 1958 British Perinatal Mortality Survey. Most IVH deaths were in babies with HMD, but the higher frequency of IVH was not associated with any prolongation of survival time of babies who died with HMD as compared with the 1958 survey. IVH was seen frequently at gestations of up to 36 weeks in babies with HMD but was rare above 30 weeks' gestation in babies without HMD. This indicated that factors associated with HMD must cause most cases of IVH seen at gestations above 30 weeks.Comparison of clinical details in infants with HMD who died with or without IVH (at gestations of 30-37 weeks) showed no significant differences between the groups other than a high incidence of fits and greater use of alkali therapy in the babies with IVH. During the 12 hours when most alkali therapy was given, babies dying with IVH received a mean total alkali dosage of 10 21 mmol/kg and those dying without IVH 6 34 mmol/kg (P <0-001). There was no difference in severity of hypoxia or of metabolic acidosis between the 2 groups. Babies who died with HMD and germinal layer haemorrhage (GLH) without IVH had received significantly more alkali than those who died with HMD alone, whereas survivors of severe respiratory distress syndrome had received lower alkali doses than other groups.It is suggested that the greatly increased death rate from IVH in babies with HMD indicates some alteration of management of HMD (since 1958) as a causative factor. Liberal use of hypertonic alkali solutions is the common factor which distinguishes babies dying with GLH and IVH from other groups of babies with HMD. Although the causal nature of this association remains unproved, it seems justifiable to urge caution in alkali usage.

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“…It is also of in terest that in one study, ventricular fluid of preterm infants in the new born period contained a high concentration of protein, whether or not in traventricular hemorrhage was present [1]. Several studies have con firmed that trauma is not a factor in these instances of intraventricular hemorrhage [3,4], Intraventricular hemorrhage in premature infants tends to occur more frequently in infants with respiratory distress syn drome [2,5], In general, the smaller the premature infant and lower the gestation age, the higher the incidence of intraventricular hemorrhage [2,4], It appears to be twice as common in males as compared to females…”

Section: Discussionmentioning

confidence: 99%

“…Intraventricular hemorrhage has been a common finding in autopsies of premature infants, along with hyaline membrane disease and respirato ry distress syndrome [1,2,5]. In the past, most of these infants did not survive, so that posthemorrhagic hydrocephalus was relatively uncommon W ise/Bai.lard 235 as a cause of hydrocephalus in infants, and when it did occur, it was usually secondary to the intracranial bleeding associated with birth trau ma in full-term infants [7], The significant improvement in the care of preterm infants in recent years is resulting in the survival of some of these infants with intraventricular hemorrhage.…”

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Hydrocephalus Secondary to Intracranial Hemorrhage in Premature Infants

Wise¹,

Ballard²

1976

Pediatr Neurosurg

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Premature (low birth weight) infants are particularly susceptible to intracranial hemorrhage. This frequently arises from the subependymal area and may dissect into the brain or into the ventricles. If the infant survives, hydrocephalus is a frequent sequela. Because of major improvements in the care of premature infants in recent years and the proliferation of intensive care nurseries, increasing numbers of low birth weight infants are surviving and developing hydrocephalus. Seven cases are described of infants who developed hydrocephalus following intracranial bleeding. Initially, ventricular and lumbar punctures were done to attempt to control head growth but this was unsuccessful. Two were treated with temporary external ventriculostomy which did not permanently control the hydrocephalus. Definitive treatment included ventriculoatrial shunts using an expandable ‘telescopic’ cardiac catheter in two and ventriculoperitoneal shunts in five. The pathogenesis and management of the condition are discussed.

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Intracranial haemorrhage associated with hyaline membrane disease.

Cited by 49 publications

References 8 publications

Low Antithrombin III Levels in Neonates with Idiopathic Respiratory Distress Syndrome: Poor Prognosis

Low Antithrombin III Levels in Neonates with Idiopathic Respiratory Distress Syndrome: Poor Prognosis

Hyaline membrane disease, alkali, and intraventricular haemorrhage.

Hydrocephalus Secondary to Intracranial Hemorrhage in Premature Infants

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