Infantile Intraventricular Haemorrhage

Last updated by Peer reviewed by Dr Pippa Vincent, MRCGP
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Synonym: periventricular haemorrhage

Intraventricular haemorrhage (IVH) is a significant cause of morbidity and mortality in infants who are born prematurely. Increasing severity of IVH is associated with progressively higher rates of mortality and neurodevelopmental impairment compared with no IVH.[1] Neurological complications include lifelong problems, including seizures, developmental delay and cerebral palsy.

IVH is uncommon in term infants but can be seen in association with trauma and asphyxia. In these cases the bleeding is usually in the choroid plexus. The pathophysiology of IVH is thought to be due to the developmental immaturity of the germinal matrix and impairment of cerebral blood flow autoregulation in the premature neonate.[2]

It is classified according to radiological appearance as follows: [3]

  • Grade I: germinal matrix haemorrhage. Bleeding confined to the germinal matrix/subependymal region. Bleed occupies <10% of ventricle.
  • Grade II: intraventricular blood without distension of the ventricular system. Bleed fills 10-50% of ventricle - approximately 40% of cases.
  • Grade III: blood filling and acutely distending the ventricular system. Dilated ventricles which are >50% full of blood.
  • Grade IV: parenchymal involvement of haemorrhage - venous infarction of the area ipsilateral to the IVH.

Incidence

IVH occurs in 60-70% of neonates weighing 500-750 g and 10-20% of those weighing 1,000-1,500 g.[4] Prematurity and low birth weight are the most important risk factors for grade IV haemorrhage.[5] Research is also underway looking at the role of ventilation in the aetiology of IVH.[6] There is an inverse relationship between the severity of the haemorrhage and the likelihood of survival.

Each additional week of gestation decreases the risk of IVH by 3.5% up to 32 weeks gestation.[7]

Risk factors

  • Prematurity - particularly <32 weeks.
  • Low birth weight.
  • Respiratory distress syndrome.
  • Surfactant use.
  • Endotracheal suctioning.
  • Hypoxia.
  • Sepsis.
  • Hypotension.
  • Hypovolaemia.
  • Hypertension.
  • Altered cerebral blood flow.
  • Positive pressure ventilation.

Symptoms

Most cases present by the third day of life. However, much less commonly there is delayed haemorrhage occurring after the first week. The most common symptoms are:[7]

  • Diminished/absent Moro reflex.
  • Poor muscle tone.
  • Sleepiness.
  • Lethargy.
  • Apnoea.

Premature babies often show sudden deterioration on day two or three, with periods of apnoea, pallor or cyanosis, failure to suck properly, abnormal eye signs, shrill cry, twitching or convulsions, reduced muscle tone or paralysis.

Signs

  • The fontanelle may be tense and bulging with severe IVH.
  • Neurological depression may progress to coma.
  • In mild forms there may be no clinical signs, or there may be alternating symptomatic and asymptomatic periods.
  • Arterial blood gases show metabolic acidosis.
  • Reduced haemoglobin level which may fail to improve on transfusion.
  • Transfontanelle ultrasound; this is the diagnostic tool of choice. All premature babies at less than 30 weeks of gestation have cranial ultrasound at 7-14 days of age.
  • MRI is increasingly used to assess brain injury and its consequences on brain development.[8]

Strategies should be employed to avoid preterm birth, or ensure early administration of corticosteroids and transfer to an appropriate level of neonatal unit when this is unavoidable. There is no specific therapy for preventing extension of a haemorrhage, initial management is mainly supportive and may include the correction of anaemia, acidosis and hypotension. Ventilatory support may also be required for some who deteriorate acutely.

Care bundles may focus on minimal handling (to avoid blood pressure and then cerebral blood flow) changes and nursing with the head in a midline position.[9] Long-term management may be required, such as for neurodevelopmental impairment, seizures and hydrocephalus.

Fluid/volume replacement

  • Packed red blood cells or fresh frozen plasma for anaemia and shock.
  • Sodium bicarbonate infusion (carefully) for metabolic acidosis.

Pharmacological

  • Anticonvulsants for seizures.
  • Acetazolamide can be used to decrease cerebrospinal fluid (CSF) production.[10] This limits late or rapidly progressive hydrocephalus.
  • Intraventricular fibrinolytic therapy with streptokinase has been attempted. However, a 2007 Cochrane review felt it could not be recommended for neonates following IVH.[11]

Surgical

  • Ventriculoperitoneal and ventriculosubgaleal shunts are the definitive treatments for posthaemorrhagic hydrocephalus.
  • There is no evidence that serial lumbar punctures produce any benefit in disability, death rate, or need for a shunt l.[12]
  • Hydrocephalus: approximately 15% of preterm infants with severe IVH will require a permanent shunt for CSF diversion.[14]
  • Infants with massive haemorrhage often rapidly deteriorate and die. Mortality from high-grade IVH may be 27-50%.
  • A significant proportion will show cerebral palsy or motor and cognitive deficits.[15]
  • Infants who have extremely low birth weight with grades I-II IVH have poorer neurodevelopmental outcomes at 20 months than infants with normal cranial ultrasound.[16]
  • Antenatal steroids to the mother and low-dose indometacin to the infant. Indometacin has been shown to decrease the risk of high-grade IVH, without improving developmental outcome.[17]
  • The Department of Health "recommends that all newborn babies are given vitamin K in the newborn period". Optimum timing and method of administration are unsure.
  • Careful timing and management of delivery to avoid birth trauma and immaturity. Choice of tocolytic agent may be important. In a 2020 meta-analysis, magnesium sulfate showed a neuroprotective effect for IVH in premature infants but this effect was not statistically significant.[18] The dose, duration and timing for maximum effect are, as yet, unknown.

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Further reading and references

  • Perlman JM; Periventricular- intraventricular hemorrhage in the premature infant- A historical perspective. Semin Perinatol. 2022 Aug46(5):151591. doi: 10.1016/j.semperi.2022.151591. Epub 2022 Mar 12.

  1. Mukerji A, Shah V, Shah PS; Periventricular/Intraventricular Hemorrhage and Neurodevelopmental Outcomes: A Meta-analysis. Pediatrics. 2015 Dec136(6):1132-43. doi: 10.1542/peds.2015-0944.

  2. Gilard V, Tebani A, Bekri S, et al; Intraventricular Hemorrhage in Very Preterm Infants: A Comprehensive Review. J Clin Med. 2020 Jul 319(8):2447. doi: 10.3390/jcm9082447.

  3. Dorner RA, Burton VJ, Allen MC, et al; Preterm neuroimaging and neurodevelopmental outcome: a focus on intraventricular hemorrhage, post-hemorrhagic hydrocephalus, and associated brain injury. J Perinatol. 2018 Nov38(11):1431-1443. doi: 10.1038/s41372-018-0209-5. Epub 2018 Aug 30.

  4. Koksal N, Baytan B, Bayram Y, et al; Risk factors for intraventricular haemorrhage in very low birth weight infants. Indian J Pediatr. 2002 Jul69(7):561-4.

  5. Sarkar S, Bhagat I, Dechert R, et al; Severe intraventricular hemorrhage in preterm infants: comparison of risk factors and short-term neonatal morbidities between grade 3 and grade 4 intraventricular hemorrhage. Am J Perinatol. 2009 Jun26(6):419-24. Epub 2009 Mar 6.

  6. Aly H, Hammad TA, Essers J, et al; Is mechanical ventilation associated with intraventricular hemorrhage in preterm infants? Brain Dev. 2011 Jun 14.

  7. Starr R, De Jesus O, Shah SD, et al; Periventricular and Intraventricular Hemorrhage.

  8. Kwon SH, Vasung L, Ment LR, et al; The role of neuroimaging in predicting neurodevelopmental outcomes of preterm neonates. Clin Perinatol. 2014 Mar41(1):257-83. doi: 10.1016/j.clp.2013.10.003. Epub 2013 Dec 12.

  9. Romantsik O, Calevo MG, Bruschettini M; Head midline position for preventing the occurrence or extension of germinal matrix-intraventricular haemorrhage in preterm infants. Cochrane Database Syst Rev. 2020 Jul 77(7):CD012362. doi: 10.1002/14651858.CD012362.pub3.

  10. Poca MA, Sahuquillo J; Short-term medical management of hydrocephalus. Expert Opin Pharmacother. 2005 Aug6(9):1525-38.

  11. Whitelaw A, Odd DE; Intraventricular streptokinase after intraventricular hemorrhage in newborn infants. Cochrane Database Syst Rev. 2007 Oct 17(4):CD000498.

  12. Whitelaw A, Lee-Kelland R; Repeated lumbar or ventricular punctures in newborns with intraventricular haemorrhage. Cochrane Database Syst Rev. 2017 Apr 64(4):CD000216. doi: 10.1002/14651858.CD000216.pub2.

  13. Cheng B, Ballabh P; Recovery of the brain after intraventricular hemorrhage. Semin Fetal Neonatal Med. 2022 Feb27(1):101224. doi: 10.1016/j.siny.2021.101224. Epub 2021 Feb 26.

  14. Robinson S; Neonatal posthemorrhagic hydrocephalus from prematurity: pathophysiology and current treatment concepts. J Neurosurg Pediatr. 2012 Mar9(3):242-58. doi: 10.3171/2011.12.PEDS11136.

  15. Gotardo JW, Volkmer NFV, Stangler GP, et al; Impact of peri-intraventricular haemorrhage and periventricular leukomalacia in the neurodevelopment of preterms: A systematic review and meta-analysis. PLoS One. 2019 Oct 1014(10):e0223427. doi: 10.1371/journal.pone.0223427. eCollection 2019.

  16. Patra K, Wilson-Costello D, Taylor HG, et al; Grades I-II intraventricular hemorrhage in extremely low birth weight infants: effects on neurodevelopment. J Pediatr. 2006 Aug149(2):169-73.

  17. McCrea HJ, Ment LR; The diagnosis, management, and postnatal prevention of intraventricular hemorrhage in the preterm neonate. Clin Perinatol. 2008 Dec35(4):777-92, vii.

  18. Moradi Y, Khateri R, Haghighi L, et al; The effect of antenatal magnesium sulfate on intraventricular hemorrhage in premature infants: a systematic review and meta-analysis. Obstet Gynecol Sci. 2020 Jul63(4):395-406. doi: 10.5468/ogs.19210. Epub 2020 Jun 24.

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