This document provides information on intraventricular hemorrhage (IVH), a common complication in preterm infants. It discusses the anatomy of the ventricular system and germinal matrix, where bleeding typically occurs. Risk factors for IVH include lack of blood flow autoregulation and a highly vascular germinal matrix in preterms. Grading systems for IVH are described. Management involves supportive care, monitoring for progression, and addressing complications like posthemorrhagic ventricular dilatation. While grades 1-2 IVH often resolve without sequelae, higher grades carry increased risks of neurodevelopmental impairment or mortality. Preventive strategies discussed include antenatal steroids, avoiding blood pressure fluctuations, and synchronized ventilation.
5. This includes the hemorrhagic oedema that is observed
most commonly after vaginal deliveries.
The edema is soft, superficial and pitting and crosses the
sites of suture lines.
Usual site of caput formation is the vertex and steadily
resolves over the first few days of life.
Compression of the presenting part exerted by the uterus or
the cervix on the is the most common pathogenesis & seen
in 20 – 40% of vaccuum deliveries.
No intervention is needed.
CAPUT SUCCEDANEUM
6. Cephalhematoma refers to a circumscribed region of hemorrhage
overlying the skull ( subperiosteal)and confined by the cranial
sutures.
Highest incidence found with use of vaccum (10.8%) followed
closely by midforcep delivery(9.5%) and less by low forceps(7.2%)
An underlying linear skull fracture is seen in 10 – 20 % cases with
cephalhematoma.
The lesion usually seen increasing in size after birth and presents
as a firm, tense mass that does not transilluminate.
Common complications include severe hyperbilirubinemia,
anaemia, osteomyelitis.
No specific therapy is indicated. Evacuation of the lesion is
contraindicated.
CEPHALHEMATOMA
7. Subgaleal hemorrhage refers to the hemorrhage beneath
the aponeurosis covering the scalp and connecting the
frontal and occipital components of the occipitofrontalis
muscle.
Blood may spread beneath the entire scalp and may even
dissect into the subcutaneous tissues of the neck.
The infants generally present at 1 hr of age and manifests
as a firm, fluctuant mass, increasing in size postnatally,
and may present at the subcut tissue on the posterior part
of neck.
SUBGALEAL HEMATOMA
8. These infants have a relatively high incidence of :
1. Hypovolemic shock (10%)
2. Requirement of volume expansion or ionotropic
support (35%)
3. Need for transfusion for anaemia (35%)
4. Secondary coagulopathy (50 %)
5. Hyperbilirubinemia (35%)
After the acute phase, the lesion usualy resolves in 2
– 3 wks.
SUBGALEAL HEMATOMA
9.
10. INTRACRANIAL HEMORRHAGE
• Intracranial hemorrhage is a collective term
encompassing many different conditions characterised
by the extravascular accumulation of blood within
different intracranial spaces.
Term Infant Preterm Infant
Commonest are subdural,
subarachnoid or
subtentorial.
Mostly related to Birth
trauma, HIE, coagulopathies
and undetermined causes
Commonest is bleeding from
the subependymal germinal
matrix and may result in
intraventricular or
periventricular hemorrhage.
White matter injury due to
hypoxic ischaemia and
infections.
11. An Epidural hemorrhage is a collection of blood between the inner
skull and the dura.
Usually caused by injury to the middle meningeal artery, which is less
susceptible to injury as it is freely movable in the space.
Causes include TRAUMA.
Affected infants usually have a skull fracture and cephalhematoma
and the treatment is supportive with possible surgical / needle
aspirations.
EPIDURAL HEMORRHAGES
12. Subdural hemorrhage refers to the hemorrhage in the plane between
the dura and the arachnoid membrane and involves tears of bridging
veins of the subdural compartment.
Usually follows a traumatic delivery of a near term / term infant.
Signs may include lethargy ± irritability, asymmetric hypotonia,
impaired third cranial nervy function ipsilateral to lesion, focal seizures,
signs of raised icp.
Other clinical clues can be decreased feeding, failure to thrive,
intermittent vomiting – often related to late post SDH neuropathic
effects.
CT / MRI (esp for posterior fossa lesions) are modalities of choice.
Management involoves a proper and repeated neurologic followup and
sos interventions.
SUBDURAL HEMORRHAGE
13. A subarachnoid hemorrhage is an accumulation of blood
between the arachnoid mater and the pia mater.
Infant SAH is venous , as opposed to arterial in adults.
SAH may be primary , coming from the vessels of the
subarachnoid space, or secondary occurring when the blood
extends from existing intraventricular, cerebral or cerebellar
hemorrhages.
Close observation and repeated neurologic assessments are
mainstay of management.
Anticonvulsant medications and IV fluid therapy are needed if
lethargy / seizures are present.
Serum electrolyte and urine output monitoring to be done for
possible SIADH , if significant SAH has been identified.
SUB-ARACHNOID HEMORRHAGES
14. An Intracerebral parenchymal hemorrhage occurs deep within the brain
tissue after venous infarction and is commonly referred as
PERIVENTRICULAR HEMORRHAGIC INFARCTION.
The most common complications of PVHI is Periventricular leukomalacia
in preterm infants and porencephalic cysts in term infants.
Clinical signs of PVHI follow those of severe neonatal encephalopathy
and overlap with clinical signs as seen with SDH, SAH or IVH.
CT is the modality of choice.
Management requires observation and supportive care. If imaging
studies show a midline shift, neurosurgical consultation needed.
Developmental studies of preterm infants with PVHI have shown that
significant cognitive and/or motor delays complicate the overall recovery
in atleast 2/3 rd of the survivors.
Careful follow up is therefore indicated in every case.
CEREBRAL HEMORRHAGE
15. An Intracerebellar parenchymal hemorrhage is most often
seen in preterm infants with complications of labor and
delivery and in whom intense respiratory management is
required.
Incidences have been found approx 10% in preterms
<34wks, by MRI studies & is almost always associated
with birth injury in terms.
Clinically, an ICPH is unique in causing unexplained
motor agitation, in addition to respiratory compromise,
apnea and breathing irregularities. Other general
symptoms of ICH are also present.
CT and MRI are preferable over Ultrasound.
Management is usually conservative.
CEREBELLAR HEMORRHAGE
16. I N T R A V E N T R I C U L A R
H E M O R R H A G E
19. INTRODUCTION
• Intraventricular hemorrhage is the most common CNS complication of a preterm birth.
• The overall incidence of IVH in preterm infants <1500gm is approx 13 – 15 %.
• Because IVH is rarely seen in term infants, their incidence rates are exceptionally low and
associated with birth related injury and / or asphyxia.
• The germinal matrix begins to involute after 34 wks postconceptional age, and thus the
peculiar vulnerability decreases, but is not totally eliminated.
• By 36 wks gestation, the germinal matrix has involuted in most infants, although sopme
residual may persists.
20. WHY PRETERMS….???
1. Lack of cerebral blood flow autoregulation.
Therefore, a PRESSURE PASSIVE state exists.
2. Highly vascularized subependymal germinal matrix, lack of supporting
basement membrane in blood vessels, and increased amount of fibrinolytic
activity in germinal matrix.
3. Pathologic increased fluctuations in the cerebral blood flow velocity.
(Eg. RDS, Pneumothorax, PDA, Hypothermia, hyperosmolarity, etc.)
4. Isolated hypertension associated with seizures, intubations and
suctionings also predisposes these babies to IVH.
21. • The occurrence of preterm IVH is greatly associated with the immaturity of the germinal
matrix of the lateral ventricles
• The cortical neuronal and glial cell precursors develop from the germinal matrix and the
adjacent ventricular germinal zone during the late 2nd and 3rd trimester.
• This ependymal germinal matrix is highly vascularized region with arterial supply from
the anterior and the middle cerebral arteries and the anterior choroidal vessels.
• Bleed in this region, thus may be confined to the germinal matrix or it may rupture into
either lateral ventricles and may thereby become a unilateral or bilateral GM / IVH.
PATHOPHYSIOLOGY
22. Increased cerebral blood flow
Fluctuations in the cerebral blood flow.
Increased Central venous pressure.
Endothelial Injury.
Vulnerable germinal matrix capillaries.
Coagulation disturbances.
Increased Fibrinolysis.
PATHOGENETIC FACTORS LEADING TO IVH.
23. CLINICAL PRESENTATION
• Asymptomatic (sometimes).
• Sudden & catastrophic deterioration in form of
neurologic signs like stupor, coma, seizures, posturing
or apneas.
• Full fontanel with sudden drop in hematocrit.
• Can be accompanied by hyperglycemia, hyperkalemia,
hypotension, bradycardia.
• SIADH may be seen.
• Sometimes, IVH can present as a gradual clinical
deterioration with altered levels of consciousness,
hypotonia, abnormal extremity or eye movements.
25. CRANIAL ULTRASOUND
• Cranial Ultrasound is the procedure of choice for Screening and Diagnosis of Intraventricular
hemorrhage.
• CT and MRI are acceptable alternatives but are more expensive and require transport to the
imaging service.
• 2 systems for classifying GM / IVH have been started for clinical use – Papille & Volpe systems.
• Papille was initially CT based system but was further adapted for the interpretation of USG. Volpe
system is ultrasound based.
• The utility of the classification schema resides in the ability of the clinicians to communicate
degrees of severity and to have a source of information for comparison of lesions as well as
having means to follow progression or regression and recovery of the initial insult of IVH.
26. CRANIAL ULTRASOUND
Grade Papille Grading system Volpe Grading syytem
1 Subependymal hemorrhage
with minimal or no /ivh
Germinal matrix hemorrhage
< 10% IVH
2 IVH without Ventricular
dilatation
IVH 10 – 50 %
3 Enlargement of ventricles
secondary to distension
with blood
IVH > 50 % with lateral
ventricle dilatation
4 Extension of hemorrhage
into the parenchyma along
with IVH and enlargement.
-
There is no Grade 4 in volpe classification. Final stage is Periventricular echodensity signifying parenchymal lesion
27. CRANIAL ULTRASOUND SCREENING
Age USG Indication
1 day Perinatal asphyxia ,
In utero drug
exposure
3 days Unstable clinical
course
7 days All infants ≤32 wks
gestation
36 wks PMA or
before discharge
All NICU babies
• A cranial ultrasound is indicated for screening sick
preterm infants for IVH from the first day of life ,
throughout hospitalization.
• Typically a Neurosonography is done between day 1
and 7, depending on clinical presentation and
institutional protocols.
• Approx 50 % GM/IVH may occur on Day1.
• Approx 90 % GM/IVH have occurred by Day4.
• Of all GM/IVH identified by Day 4 of life, 20 – 40 % will
progress to more extensive hemorrhage.
28. M A N A G E M E N T O F
I N T R A V E N T R I C U L A R
H E M O R R H A G E
29. M A N A G E M E N T O F
I N T R A V E N T R I C U L A R
H E M O R R H A G E
P R E V E N T I O N A C U T E
M A N A G E M E N T
P O S T N A T A L
P R E V E N T I O N
P R E N A T A L
P R E V E N T I O N
F O L L O W U P
30. IVH PREVENTION
Prenatal strategies
• Avoidance of Premature deliveries.
• Transportation in utero.
• Antenatal steroid therapy.
Postnatal strategies
• Avoid Birth asphyxia.
• Avoid blood pressure fluctuations
• Avoid rapid infusions of volume
expanders or hypertonic solutions.
• Prompt & cautious CVS support to
prevent hypotension.
• Correct acid –base abnormalities
• Correct coagulopathies.
• Synchronized mechanical ventilation.
31. ACUTE STAGE MANAGEMENT
• General supportive care to maintain normal blood volume.
• Maintain electrolyte and acid- base status.
• Blood transfusion to maintain hematocrit , in large bleeds.
• Thrombocytopenia or coagulation disturbances should be corrected.
• In case of Posthemorrhagic ventricular dilatation, careful monitoring of ventricular size by serial
ultrasounds and appropriate interventions ( Therapeutic lumbar punctures,VP shunts/ medical
decompressiosn) .
• Follow up serial imaging to detect progression of IVH and later progressive hydrocephalus.
32. OUTCOME
• Grade 1 & 2 IVH - Spontaneous Resolution
• Grade 3 IVH - Evolves over 1 – 3 wks.
After this it produces fibrotic reaction that
obliterates subarachnoid space & leads to
ventricular dilatation and hydrocephalus.
• Intraparenchymal Hemorrhage - Mortality / Followed in 1 – 8
wks by tissue destruction
and formation of
porencephalic cyst.
33. PROGNOSIS
• Grade 1 & 2 IVH – No significant neurologic dysfunction.
• Grade 3 IVH – neurologic abnormality in 35 % of infants.
• Grade 4 IVH – Neurologic abnormality in 55 % of infants.
• Mortality seen in approximately 50 % of neonates with hemorrhagic infarct.
2008, Browser et al.
34. EVIDENCES
• 1. Metaanalysis performed in 1996 by P. crowley ,regarding the benefits of antenatal steroid use in preterm delivery
have concluded that Corticosteroid treatment is associated with a substantial reduction in the risk of intraventricular
haemorrhage, regardless of the criteria used for diagnosis.
• 2. A metaanalysis performed by smit,od,whitlaw in 2013 had concluded that Postnatal administration of
phenobarbital cannot be recommended as prophylaxis to prevent IVH in preterm infants and is associated with an
increased need for mechanical ventilation.
• 3. A metaanalysis performed by Peter w. fowlie (1996, 2003) have concluded that prophylactic indomethacin has a
number of short term benefits for the preterm infant but there is no evidence to suggest that it results in an
improvement in the rate of survival free of disability
• 4. Jeffrey M. Perlman, M.B., Steven Goodman, M.D., Katherine L. Kreusser, M.D., and Joseph J. Volpe, M.D;
Reduction in Intraventricular Hemorrhage by Elimination of Fluctuating Cerebral Blood-Flow Velocity in Preterm
Infants with Respiratory Distress Syndrome; N Engl J Med 1985; 312:1353-1357 which concluded that elimination of
fluctuating cerebral blood-flow velocity in preterm infants with respiratory distress syndrome markedly reduces the
incidence and severity of intraventricular hemorrhage.
35. EVIDENCES
5 . The other preventive strategies studied and found not to be useful are vitamin A, ethanmsylate, antenatal vitamin
k administration to mother for imminent preterm delivery.
6. Lynn J. Groome, PhD, MD1, , Robert L. Goldenberg, MD1, Suzanne P. Cliver, BA1, Richard O. Davis, MD1,
Rachel L. Copper, RN1,March of Dimes Multicenter Study Group; Neonatal periventricular-intraventricular
hemorrhage after maternal β-sympathomimetic tocolysis concluded that β-Sympathomimetic tocolytic therapy
may be associated with a more than two fold increase in the incidence of neonatal periventricular-intraventricular
hemorrhage.
7. Caldas JP, Braghini CA, Mazzola TN, Vilela MM, Marba ST. Peri-intraventricular hemorrhage and oxidative and inflammatory stress
markers in very-low birth weight newborns. J Pediatr (Rio J). 2015;91:373---9
This study has not found any association between ROI, GSH, and IL‐6 levels with the occurrence of PIVH in very‐low birth weight
infants.
36. EVIDENCES
5. Studies regarding the neurodevelopmental outcomes:
Allison H. Payne, MD, MS; Susan R. Hintz, MD, MS; Anna Maria Hibbs, MD, MS; Michele C. Walsh, MD,
MS; Betty R. Vohr, MD; Carla M. Bann, PhD; Deanne E. Wilson-Costello, MD ; for the Eunice Kennedy
Shriver National Institute of Child Health and Human Development Neonatal Research Network ;
Neurodevelopmental Outcomes of Extremely Low-Gestational-Age Neonates With Low-Grade
Periventricular-Intraventricular Hemorrhage; JAMA Pediatr. 2013;167(5):451-459.
doi:10.1001/jamapediatrics.2013.866.
• Results = Low-grade hemorrhage was not associated with significant differences in unadjusted or adjusted risk of
any adverse neurodevelopmental outcome compared with infants without hemorrhage. Compared with low-grade
hemorrhage, severe hemorrhage was associated with decreased adjusted continuous cognitive (β, −3.91 [95% CI,
−6.41 to −1.42]) and language (β, −3.19 [−6.19 to −0.19]) scores as well as increased odds of each adjusted
categorical outcome except severe cognitive impairment (odds ratio [OR], 1.46 [0.74 to 2.88]) and mild language
impairment (OR, 1.35 [0.88 to 2.06]).
• Conclusion = The authors concluded that at 18 to 22 months, the neurodevelopmental outcomes of extremely low-
gestational-age infants with low-grade periventricular-intraventricular hemorrhage are not significantly different
from those without hemorrhage. Additional study at school age and beyond would be informative.
37. TO
CONCLUDE………. Cranial hemorrhage in infants can be 1. Extracranial 2. Intracranial
The extracranial hemorrhages include – caput, cephalhematoma & subgaleal
hematoma.
The intracranial hemorrhages can further be – Extradural, subdural, subarachnoid,
cerebral, intracerebellar, intraventricular hemorrhage.
Vaccum delivery has been implicated in etiogenesis of ICH .esp term neonates, closely
followed by high and mid forceps followed by low forceps extraction.
Intraventricular hemorrhage is the most common CNS complication of a preterm birth.
38. Germinal matrix bleed and resulting intraventricular hemorrhage is more commonly
seen with preterm babies & is greatly associated with the immaturity of the germinal
matrix.
A cranial ultrasound is indicated for screening sick preterm infants for IVH from the first
day of life throughout hospitalization.
IVH grading is performed as per the Papille & Volpe grading systems. ( Cranial ultrasound
based)
Prognosis of Grade 1 & 2 IVH has been found the best and nearly equivalent to a normal
neonate.
Strict neurologic follow up is a must in all the cases of IVH for long term morbidity
corrections.
TO
CONCLUDE……….