Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Management and outcome

Authors:: Linda S de Vries, MD, PhD; Lara M Leijser, MD, PhD, MSc
Section Editors:: Richard Martin, MD; Douglas R Nordli, Jr, MD
Deputy Editor:: Carrie Armsby, MD, MPH

Literature review current through: Jan 2024.

This topic last updated: Jun 15, 2023.

INTRODUCTION — Germinal matrix and intraventricular hemorrhage (GMH-IVH; also referred to as simply IVH) is an important cause of brain injury in preterm infants. The negative impact of GMH-IVH on neurodevelopmental outcome is due not only to the direct consequences of GMH-IVH, but also to the associated complications, including posthemorrhagic ventricular dilatation (PHVD) and white matter injury (WMI).

The management, complications, outcome, and prevention of GMH-IVH in the preterm infant are discussed in this topic review. The risk factors, clinical features, and diagnosis of GMH-IVH are discussed separately. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis".)

SEVERITY AND GRADING — The severity of GMH-IVH is based upon the findings on cranial ultrasonography (table 1) (see "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Cranial ultrasound'):

●Grade I – Either:

•Bleeding that is confined to the germinal matrix (ie, GMH only) (image 1), or

•GMH plus IVH occupying <10 percent of the lateral ventricular area

●Grade II – IVH that occupies 10 to 50 percent of the lateral ventricle area (image 2)

●Grade III – IVH that occupies >50 percent of the lateral ventricle area and is associated with acute ventricular dilatation (image 3)

●Periventricular hemorrhagic infarction (PVHI; previously referred to as grade IV IVH) – Hemorrhagic infarction in periventricular white matter ipsilateral to large IVH (image 4 and image 5)

"Low-grade" or "mild" GMH-IVH refers to grades I and II and "severe" refers to grades III and PVHI (grade IV). Infants with severe GMH-IVH are at considerably higher risk of neurodevelopmental disabilities than infants with milder GMH-IVH. (See 'Outcome' below.)

MANAGEMENT — Treatment of preterm infants with GMH-IVH is supportive and directed towards limiting fluctuations in cerebral perfusion, avoiding further brain injury, and early detection of complications [1].

Supportive care — Supportive care for infants with GMH-IVH includes:

●Blood pressure management – This includes maintaining normal blood pressure to preserve cerebral blood flow. The goal is to avoid significant or sudden perturbations and to avoid significant hypo- or hypertension. (See "Assessment and management of low blood pressure in extremely preterm infants", section on 'Management approach'.)

●Respiratory support – The goal is to provide adequate oxygenation and ventilation with specific avoidance of hypocarbia, hypercarbia, and acidosis. (See "Respiratory support, oxygen delivery, and oxygen monitoring in the newborn" and "Respiratory distress syndrome (RDS) in preterm infants: Management" and "Approach to mechanical ventilation in very preterm neonates" and "Neonatal target oxygen levels for preterm infants".)

●Fluid and nutritional support – Provision of appropriate fluid, metabolic, and nutritional support plays a key role in supporting the neonate. (See "Fluid and electrolyte therapy in newborns" and "Approach to enteral nutrition in the premature infant".)

●Address thrombocytopenia and/or coagulopathy – Significant thrombocytopenia and/or coagulopathy may increase the likelihood of progressive hemorrhage in preterm neonates with established GMH-IVH. If severe GMH-IVH is present on the admission cranial ultrasound, we suggest measuring the platelet count, prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR). If the aPTT and/or INR are significantly prolonged (table 2), we suggest administration of fresh frozen plasma (FFP) to prevent extension of the bleed [2]. However, there is no convincing evidence to support prophylactic administration of FFP for prevention in the absence of an established GMH-IVH.

Indications for platelet transfusion in preterm neonates are discussed in detail separately. (See "Neonatal thrombocytopenia: Clinical manifestations, evaluation, and management", section on 'Platelet transfusion'.)

Limited data are available on the use of recombinant-activated Factor VII in neonates with IVH [3,4]. Routine use of this agent is not recommended until there are more data on its safety and efficacy in this population.

●Seizure management – Seizures should be treated to avoid any associated impairment of cerebral oxygenation and cerebral perfusion, or elevations of systemic blood pressure. (See "Clinical features, evaluation, and diagnosis of neonatal seizures" and "Treatment of neonatal seizures".)

Monitoring

●Serial ultrasound monitoring – For neonates with an established diagnosis of severe GMH-IVH (ie, grade III or PVHI (table 1)), we suggest monitoring with twice weekly cranial ultrasound for four weeks after its onset to detect development of posthemorrhagic ventricular dilatation (PHVD; also referred to as posthemorrhagic hydrocephalus [PHH]), the major complication of severe IVH (algorithm 1). Details of serial ultrasound monitoring for PHVD are provided separately. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Serial monitoring'.)

●Clinical monitoring – Cranial ultrasound monitoring does not obviate the need for clinical monitoring. All affected neonates should be monitored for increasing head circumference and/or signs and symptoms of increased intracranial pressure (ICP); however, these are late findings of PHVD. Signs of elevated ICP in preterm neonates include apnea, bradycardia, irritability, sunsetting, and feeding difficulties.

●Investigational monitoring techniques – Ongoing research is focused on using noninvasive neurophysiological assessments and biomarkers to identify neonates who may benefit from early intervention for PHVD. These monitoring tools include [5-10]:

•Flash visual evoked potentials and amplitude integrated electroencephalography (aEEG)

•Near-infrared spectroscopy (NIRS)

•Diffuse correlation spectroscopy (DSC)

•Various possible biomarkers of IVH and PHVD (eg, activin or S100B, chemokines and cytokines, amyloid precursor protein [APP] in the cerebrospinal fluid [CSF])

While these tools hold promise for future clinical application, they are currently used primarily for research purposes.

Management of PHVD — PHVD is the major acute complication of severe GMH-IVH (ie, grade III or PVHI (table 1)) [11]. PHVD usually begins within one to three weeks after the onset of severe IVH. The early stages of PHVD can be detected by routine ultrasound surveillance, as discussed separately. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Posthemorrhagic ventricular dilatation (PHVD)'.)

Our approach to managing PHVD is based on early detection of asymptomatic cases identified by findings of lateral ventricular dilatation on serial ultrasound examinations (algorithm 1) [12]. We suggest an early treatment approach (ie, initiating treatment if cranial ultrasound demonstrates progressive ventricular dilatation) rather than waiting until clinical signs of elevated ICP are evident.

Moderate-risk infants — Moderate-risk infants are those who develop moderate ventricular dilation on serial ultrasonography (ie, ventricular index [VI] >97^th percentile to ≤4 mm above the 97^th percentile, and anterior horn width [AHW] >6 to 10 mm). (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Serial monitoring'.)

Infants with moderate-risk ventricular dilation are monitored with daily physical examination and twice weekly cranial ultrasounds (algorithm 1):

●If the ventricular dilatation stops or stabilizes, the infant does not require treatment. Twice weekly cranial ultrasounds are continued up to four weeks and the infant should undergo neuroimaging at term-equivalent age, as discussed separately. (See "Long-term neurodevelopmental impairment in infants born preterm: Risk assessment, follow-up care, and early intervention", section on 'Selective MRI imaging'.)

●If there is progressive dilatation, intervention is started with initial serial lumbar punctures (LPs) followed by CSF drainage using temporary ventricular access device (VAD) and, if needed, a permanent ventriculo-peritoneal shunt (VPS). The management approach is the same as for high-risk patients. (See 'High-risk infants' below.)

High-risk infants — High-risk infants are those with significant and persistent lateral ventricular dilatation (VI >4 mm above the97^th percentile and anterior horn width [AHW] >10 mm or thalamo-occipital distance [TOD] >25 mm) [12-16]. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Serial monitoring'.)

Our approach to management of high-risk patients is as follows (algorithm 1):

●Initial management (serial LPs) – Serial LPs to drain CSF are initially performed to maintain a VI <4 mm above the 97^th percentile for postmenstrual age (PMA). Cranial ultrasonography is performed the next day, and the decision to perform a subsequent LP is based on the findings of persistent dilatation on the follow-up study. LPs are performed no more often than once daily and restricted to 10 mL/kg per LP. (See 'Temporary CSF drainage' below.)

●Subsequent management – Subsequent management depends upon whether the dilation resolves or persists.

•Resolution of PHVD – If there is no further dilatation, monitoring with cranial ultrasound is continued twice a week up to four weeks. If there is no sign of progressive dilatation during this time period and ventricular indices remain in acceptable range (VI <97^th percentile and AHW <6 mm), the infant does not require treatment or further ultrasound monitoring. They should undergo neuroimaging at term-equivalent age, as discussed separately. (See "Long-term neurodevelopmental impairment in infants born preterm: Risk assessment, follow-up care, and early intervention", section on 'Selective MRI imaging'.)

•Persistent PHVD – If VI and AHW remain well above normal values and the neonate requires more than three to five serial LPs or if LPs fail to adequately decrease VI and AHW or if serial LPs are not well tolerated, we suggest placing a temporary VAD. (See 'Temporary CSF drainage' below.)

Over the course of 7 to 10 days following VAD placement, drainage is performed once or twice a day with an initial aliquot of 10 mL/kg, with a goal of keeping the VI well below 4 mm above the 97^th percentile for PMA and AHW <10 mm. The frequency and volume of the drainage is modified based on daily ultrasound measurements.

●Indications for permanent shunting – Placement of a permanent CSF shunt is generally warranted for infants with persistent need for VAD drainage after four to six weeks. To be certain that the infant needs a permanent shunt, a challenge can be performed wherein VAD drainage is discontinued for 24 to 48 hours. Observing increases in VI and AHW during this period confirms the need for permanent shunt placement. (See 'Permanent ventricular shunt' below.)

Additional criteria that are generally required prior to placement of a VPS include:

•The infant's weight is approximately 2 kg or higher, and

•CSF protein is <1.5 g/L, and

•CSF red blood cell count is <100/mm³

Symptomatic infants — In our center, it is rare for infants with PHVD to present with clinical signs or symptoms of increased ICP (eg, bulging fontanelle, splayed cranial sutures, increasing head circumference by >2 cm/week, apneas, feeding problems) because these are late findings in the course of PHVD, and we generally intervene at an earlier stage.

Nevertheless, for the rare infant with symptomatic PHVD, we suggest initiating CSF drainage by immediate insertion and tapping from a temporary VADs rather than starting with serial lumbar punctures. CSF drainage may be increased to 15 mL/kg day (divided in two separate taps), but care should be taken not to reduce the ventricular size too rapidly because this may cause hemodynamic changes and may increase the risk of rebleeding [17]. (See 'Interventions for CSF drainage' below.)

Interventions for CSF drainage

Temporary CSF drainage — Management of progressive PHVD may include the following interventions for temporary CSF drainage [1,18]. The rationale for deferring permanent CSF shunt placement is to avoid shunt obstruction, which can occur in the acute setting immediately after a severe IVH due to high levels of protein in CSF. In addition, older infants are usually better candidates for surgery and sometimes the progression of PHVD arrests such that placement of a permanent VPS can be avoided. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Clinical presentation and course'.)

●Serial LPs – Serial LPs can be used as a temporizing measure in neonates with progressive PHVD to reduce the likelihood of developing clinically significant elevations in intracranial pressure. Success rates are higher if the LP is performed with the infant in a sitting position rather than lying [19]. In a 2017 meta-analysis of three clinical trials involving 233 infants with IVH, serial LPs did not appear to reduce the need for permanent CSF shunting [20]. However, in a subsequent clinical trial not included in the meta-analysis, nearly one-third of enrolled infants with PHVD were successfully managed with serial LPs alone [16]. These data are described in greater detail below. (See 'Evidence supporting early treatment of PHVD' below.)

Additional details about performing LPs in infants, including risks associated with the procedure, are provided separately. (See "Lumbar puncture in children".)

●VADs – VADs are often used as a temporizing means to drain CSF to avoid or delay the need for a permanent shunt [21-23].

In our center, when a VAD is required, we typically use a tunneled ventricular drain with a subcutaneous reservoir, which can be tapped for CSF removal. In variations of this system, the tunneled catheter drains into an external drip chamber, surgically prepared pouch in the supraclavicular region, or the subgaleal space [24-26]. Subgaleal shunts drain continuously and do not require tapping unless drainage is inadequate or the shunt obstructs distally. Subgaleal shunts, as compared with ventricular reservoirs, reduce the need for daily CSF aspiration [11] and prolong the time period before permanent shunt placement [27]. There appears to be no difference in eventual need for permanent shunting when comparing ventricular reservoir patients and subgaleal shunt patients [23,27,28]. VAD placement can result in penetrating injury to the corpus callosum [29].

Permanent ventricular shunt — Placement of a permanent ventricular shunt for continuous CSF drainage may be required for some infants with persistent PHVD [11,30]. This most commonly consists of a ventriculoperitoneal shunt (VPS). However, VPS placement usually cannot be performed in the acute phase because the amount of blood and protein in the CSF tends to cause shunt obstruction.

VPSs can be associated with significant morbidity, especially in extremely preterm and low birth weight infants. Complications with shunts include infection and shunt malfunction. Many infants with VPSs require repeated revisions, which are thought to contribute to reduced cognitive function in this population [31]. The use of VPSs for management of hydrocephalus in infants and children is discussed in greater detail separately. (See "Hydrocephalus in children: Management and prognosis", section on 'CSF shunt'.)

Neuroendoscopic procedures — Neuroendoscopic procedures that are sometimes performed in infants with PHVD include endoscopic third ventriculostomy (ETV) and neuroendoscopic lavage [32,33]. The success of ETV is higher in infants >6 months compared with young infants [34]. ETV is discussed in detail separately. (See "Hydrocephalus in children: Management and prognosis", section on 'Endoscopic third ventriculostomy'.)

No role for diuretic therapy — Diuretic agents such as acetazolamide or furosemide do not play a role in the management of PHVD. The available data suggest that these agents neither decrease the need for shunting nor reduce mortality risk and they are associated with known adverse effects (eg, nephrocalcinosis) [11,18,35].

Evidence supporting early treatment of PHVD — The practice of early intervention for high-risk PHVD (ie, prior to the onset of signs and symptoms) is supported by observational studies and limited clinical trial data [16,36-41].

The ELVIS trial (early versus late ventricular intervention study) was a multicenter clinical trial involving 126 preterm infants with PHVD who were randomly assigned to a lower or higher threshold for intervention (using the moderate- and high-risk criteria described above) [16]. The study did not detect a significant difference in the need for permanent CSF shunting in the two groups (19 percent in the early intervention group versus 23 percent in the later intervention group). A two-year follow-up study of the ELVIS trial reported on rates of severe neurodevelopmental impairment (NDI, defined as cerebral palsy [CP] or a score >2 standard deviations below the mean on standardized cognitive or motor assessment [ie, Bayley Scales of Infant Development]) for 113 of the 126 infants enrolled in the trial [39]. At two years, fewer infants in the early intervention group had adverse outcome (defined as death or severe NDI) compared with the later intervention group (35 versus 51 percent; adjusted odds ratio [OR] 0.24, 95% CI, 0.07-0.87). In addition, magnetic resonance imaging at term equivalent showed less brain injury and smaller ventricular volumes for the early treatment group [40].

Similar findings were noted in an observational study that compared outcomes for infants with PHVD managed at three different institutions; two centers used an early intervention approach (similar to the approach described above) while the approach at the third center consisted of later neurosurgical intervention based upon clinical signs of elevated ICP [36]. Two-year outcomes were available for the 120 infants (73 from early intervention centers and 47 from the later intervention center). More infants managed at the early intervention centers were alive without CP at two years compared with infants managed at the later intervention center (62 versus 19 percent). In addition, more of the surviving infants in the early intervention centers had normal cognitive and motor scores at two years compared with infants managed at the later intervention center (89 versus 37 percent).

In a meta-analysis of 66 studies (2 randomized trials [including ELVIS], 16 prospective observational studies, and 48 retrospective studies) reporting outcomes on >2500 preterm infants with PHVD who underwent temporizing neurosurgical intervention, older age at time of intervention was strongly correlated with increased risk of requiring permanent shunting and increased risk of NDI [41].

FOLLOW-UP — All neonates with severe GMH-IVH require long-term neurodevelopmental follow-up. This issue is discussed in detail separately. (See "Long-term neurodevelopmental impairment in infants born preterm: Risk assessment, follow-up care, and early intervention".)

OUTCOME

Acute complications — The main complications of GMH-IVH are posthemorrhagic ventricular dilatation (PHVD) and white matter injury (WMI). These occur predominantly in infants with severe IVH (ie, grade III or PVHI). The risk of these complications is discussed separately. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Acute complications'.)

Permanent shunt placement — Approximately 5 to 15 percent of neonates with severe IVH (ie, grade III or PVHI) ultimately require placement of a permanent ventricular shunt [23,27,30,42]. Endoscopic third ventriculostomy (ETV) is an alternative surgical procedure that is performed in a small subset of infants with PHVD. (See 'Permanent ventricular shunt' above and 'Neuroendoscopic procedures' above.)

Infants who require permanent shunt placement generally have higher risk of neurodevelopmental disabilities compared with those who do not require permanent shunting [43]. However, as discussed above, the timing of intervention also impacts the risk of neurodevelopmental disability. (See 'Evidence supporting early treatment of PHVD' above.)

Mortality — The risk of mortality in infants with GMH-IVH increases with the severity of the hemorrhage. In the available studies, reported mortality rates according to GMH-IVH severity were [42,44-46]:

●Grade I – 4 to 7 percent

●Grade II – 10 to 18 percent

●Grade III – 18 to 30 percent

●PVHI (grade IV) – 40 to 50 percent

However, it is important to recognize that infants with severe IVH often have other comorbidities that likely contribute to the high mortality risk in this population. (See "Preterm birth: Definitions of prematurity, epidemiology, and risk factors for infant mortality", section on 'Risk factors for mortality'.)

Long-term neurodevelopmental outcomes — For surviving infants, the risk of long-term neurodevelopmental disabilities (eg, cerebral palsy [CP], cognitive impairment) is highest for extremely preterm infants (EPT; gestational age <28 weeks) with severe IVH (ie, grade III or PVHI), especially those who develop PHVD requiring permanent shunt placement [47-49]. Infants with low-grade GMH-IVH (ie, grades I and II) have a modestly increased risk of long-term sequelae compared with those without GMH-IVH [49-55].

Low-grade GMH-IVH — Studies are somewhat inconsistent as to whether infants with low-grade GMH-IVH (grades I and II) are at increased risk of neurodevelopmental impairment. Taken together, the available data suggest that infants with low grade GMH-IVH have a modestly higher risk of neurodevelopmental impairment (NDI) compared with infants of similar gestational age without GMH-IVH [49-54].

In a meta-analysis of eight studies including >11,000 preterm infants, the risk of severe NDI (defined as CP, severe cognitive impairment, or sensory impairment [visual impairment or hearing loss]) at age 18 to 36 months was higher in infants with low grade GMH-IVH versus those without (21 versus 17 percent; odds ratio [OR] 1.32, 95% CI 1.1-1.58) [54].

The risks specifically for CP and severe cognitive impairment among infants with and without low-grade GMH-IVH in these studies were as follows:

●CP – 12 versus 7.7 percent (OR 1.76, 95% CI 1.39-2.24; 10 studies, 11,018 infants); the difference was smaller in an analysis limited to studies including infants born after 2000 (10 versus 7.3 percent (OR 1.53, 95% CI 1.22-1.9; 5 studies, 5345 infants) [54].

●Cognitive impairment (ie, BSID-II score <70) – 25 versus 20 percent (OR 1.79, 95% CI 1.09-2.95; 4 studies 3646 infants) [54].

Severe IVH — Infants with severe IVH (grade III or PVHI) have substantially higher rates of severe NDI compared with infants without IVH born at the same gestational age [30,42,47-50,54].

In a meta-analysis of seven studies, the risk of moderate to severe NDI at age 18 to 36 months was three- to four-fold higher in infants with versus without severe IVH (unadjusted OR 3.27 [95% CI 2.44-4.39]; adjusted OR 4.26 [95% CI 3.25-5.59]) [54]. In the individual studies, reported rates of severe NDI among EPT infants with severe IVH ranged from approximately 30 to 60 percent [30,42,48-50]. This is considerably higher than the baseline risk of severe NDI in EPT infants, which is approximately 15 to 25 percent. (See "Long-term neurodevelopmental impairment in infants born preterm: Epidemiology and risk factors", section on 'Extremely preterm infant'.)

The risks specifically for CP and severe cognitive impairment were also considerably higher:

●CP – OR 4.98 (95% CI 4.13-6.0; 10 studies) [54]. In the individual studies, the risk of CP among EPT infants with grade III IVH was approximately 20 to 50 percent; the risk in infants with PVHI was 40 to 80 percent [47-50]. This is considerably higher than the baseline risk of CP in EPT infants, which is approximately 6 to 12 percent. (See "Long-term neurodevelopmental impairment in infants born preterm: Epidemiology and risk factors", section on 'Extremely preterm infant'.)

●Cognitive impairment – OR 2.83 (95% CI 1.54-5.2; 3 studies using BSID-II) and OR 2.3 (95% CI 1.67-3.15; 2 studies using Bayley-III) [54].

For infants with severe IVH, the risk of long-term NDI is increased if there is bilateral involvement or if there is associated cystic periventricular leukomalacia (c-PVL) [56]. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'White matter injury'.)

PREVENTION

Prevention of GMH-IVH — The most effective strategy for prevention of GMH-IVH is to reduce the incidence of preterm birth. This issue is discussed separately. (See "Spontaneous preterm birth: Overview of interventions for risk reduction".)

●Obstetric care – Other obstetric practices that reduce the risk of GMH-IVH in the offspring include:

•Antenatal glucocorticoids for patients at risk for preterm delivery, as discussed separately (see "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery")

•Prompt recognition and appropriate treatment of intrauterine infection (clinical chorioamnionitis) (see "Clinical chorioamnionitis", section on 'Maternal management')

●Neonatal care – From the neonatologist's perspective, postnatal interventions to reduce the risk of GMH-IVH generally consist of providing high-quality delivery room and postnatal care for very preterm (VPT) and extremely preterm (EPT) neonates. The goals are to provide adequate respiratory and cardiovascular support while avoiding abrupt physiologic fluctuations (eg, severe hypoxemia, hypo- or hypercapnia, hypo- or hypertension) that could contribute to reduced cerebral blood flow and increased risk of GMH-IVH. Specific postnatal risk factors for GMH-IVH are discussed in detail separately. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Postnatal factors'.)

Key aspects of neonatal care that may impact the risk of GMH-IVH are discussed in separate topic reviews [57-59]:

•Delivery room resuscitation (see "Neonatal resuscitation in the delivery room")

•Respiratory support (see "Respiratory support, oxygen delivery, and oxygen monitoring in the newborn" and "Respiratory distress syndrome (RDS) in preterm infants: Management" and "Approach to mechanical ventilation in very preterm neonates" and "Neonatal target oxygen levels for preterm infants")

•Hemodynamic support (see "Assessment and management of low blood pressure in extremely preterm infants" and "Neonatal shock: Management" and "Management of hypertension in neonates and infants")

•Restrictive red blood cell (RBC) transfusion practice (see "Red blood cell (RBC) transfusions in the neonate", section on 'Restrictive versus liberal strategy' and "Anemia of prematurity (AOP)", section on 'Management')

•Treatment of severe thrombocytopenia (algorithm 2) (see "Neonatal thrombocytopenia: Clinical manifestations, evaluation, and management", section on 'Management')

•Management of patent ductus arteriosus (see "Patent ductus arteriosus (PDA) in preterm infants: Management and outcome")

•In addition, we use a bundle of nursing care that includes optimal positioning (midline head position), minimal and gentle handling, avoidance of sudden leg elevation, and avoidance of rapid flushing or withdrawal of blood from intravenous lines [58]. Although it is uncertain based on the available evidence whether maintaining elevated supine midline head position reduces the risk of GMH-IVH, we continue to include this as part of routine care for preterm infants [58-62].

●Interventions with uncertain or unproven efficacy – The following interventions have been studied for the prevention of GMH-IVH in preterm neonates and have been found to be ineffective or harmful, or the data are inconclusive. These interventions generally do not play a role in routine practice:

•Phenobarbital (antenatal maternal or postnatal neonatal administration) [63,64]

•Maternal vitamin K [65]

•Neonatal vitamin E supplementation [66]

•Ethamsylate (not available in the United States) [67]

•Antithrombin [68]

Prevention of PHVD — Efforts to prevent posthemorrhagic ventricular dilatation (PHVD) should focus primarily on preventing severe IVH as well as promptly recognizing severe IVH when it does occur and instituting appropriate monitoring for the neonate. (See 'Prevention of GMH-IVH' above and 'Monitoring' above.)

Other interventions aimed at preventing PHVD once severe IVH has occurred have generally not been effective. Strategies that have been studied include prophylactic CSF drainage and use of fibrinolytic agents. The rationale for these interventions is based on the assumption that PHVD is primarily due to inflammatory response of the subarachnoid villi to the presence of blood. It was hypothesized that removing inflammatory blood products from the CSF might reduce the risk of PHVD. However, these interventions have not been shown to be effective in preventing PHVD, and as a result, they are not recommended [11].

●Prophylactic CSF drainage – In a meta-analysis of three trials (233 infants) comparing prophylactic CSF drainage (with serial LPs or ventricular traps) versus no CSF drainage, the likelihood of needing a permanent shunt was similar in both groups (47 versus 45 percent; RR 0.96, 95% CI 0.73-1.26). Rates of mortality and major disability among survivors were also similar in both groups [20]. Ventricular taps should be avoided, as these will result in multiple needle tracks within the brain.

●Fibrinolytic agents – Studies reporting on intraventricular injection of fibrinolytic agents for prevention of PHVD have reported variable findings [11,37,38,69,70]. Based on the available data, it appears to be associated with substantial risk of adverse events, and it is unclear whether there is any benefit. As a result, fibrinolytic therapy for PHVD is not recommended for routine administration and should continue to be viewed as experimental.

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SUMMARY AND RECOMMENDATIONS

●Clinical significance ‒ Germinal matrix and intraventricular hemorrhage (GMH-IVH) is an important cause of brain injury in preterm infants. The severity of GMH-IVH is based upon the findings on cranial ultrasonography (table 1). The negative impact of GMH-IVH on neurodevelopmental outcome is due not only to the direct consequences of GMH-IVH, but also to the associated complications, including posthemorrhagic ventricular dilatation (PHVD) and white matter injury (WMI). (See 'Severity and grading' above and 'Outcome' above and "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Acute complications'.)

●Management – Treatment of GMH-IVH is supportive and directed towards preserving cerebral perfusion, avoiding further brain injury, and early detection of complications. (See 'Management' above.)

•Supportive care – Supportive care includes blood pressure management, respiratory support, fluid and nutritional support, seizure management, and addressing clinically significant thrombocytopenia and coagulopathy. (See 'Supportive care' above.)

•Monitoring

-Serial ultrasound monitoring – For neonates with an established diagnosis of severe GMH-IVH (ie, grade III or PVHI), we suggest monitoring with twice weekly cranial ultrasounds for four weeks after its onset to detect PHVD (algorithm 1). (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Serial monitoring'.)

-Clinical monitoring – In addition, all neonates with GMH-IVH should be monitored for increasing head circumference and/or signs and symptoms of increased intracranial pressure (ICP), which are late findings of PHVD. Signs of elevated ICP in preterm neonates include apnea, bradycardia, irritability, sunsetting, and feeding difficulties. (See 'Monitoring' above.)

●Management of PHVD ‒ Our approach to managing PHVD consists of detection of asymptomatic cases using serial ultrasonography and early intervention based upon progressive ventricular dilatation rather than waiting until clinical signs of elevated ICP are evident (algorithm 1). (See 'Management of PHVD' above.)

•Risk assessment – The first step is to assess the neonate's risk of progressing to severe symptomatic PHVD by trending ultrasound measurements over time. Infants with moderate ventricular dilation (ie, ventricular index [VI] >97^th percentile to ≤4 mm above the 97^th percentile and anterior horn width [AHW] >6 to ≤10 mm) are at moderate risk of developing symptomatic PHVD. Infants with more severe ventricular dilatation (ie, VI >4 mm above the 97^th percentile and AHW >10 mm or thalamo-occipital distance [TOD] >25 mm) are at high risk. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis", section on 'Serial monitoring'.)

•Moderate-risk infants – Infants at moderate risk are monitored with daily physical examination and twice weekly cranial ultrasounds. If the ventricular dilatation resolves or stabilizes, they do not require treatment (algorithm 1). (See 'Moderate-risk infants' above.)

•High-risk infants – For most asymptomatic high-risk infants, we suggest initiating cerebrospinal fluid (CSF) drainage rather than deferring intervention until signs and symptoms of elevated intracranial pressure develop (Grade 2C). Intervention consists of temporizing procedures such as serial lumbar punctures (LPs) or ventricular access device (VAD) (algorithm 1). (See 'High-risk infants' above and 'Interventions for CSF drainage' above and 'Evidence supporting early treatment of PHVD' above.)

•Symptomatic infants – We also suggest initiating CSF drainage for infants with symptomatic PHVD (eg, bulging fontanelle, splayed cranial sutures, increasing head circumference by >2 cm/week, apneas, feeding problems) (Grade 2C). VADs are typically used for CSF drainage in this setting. (See 'Symptomatic infants' above.)

•Indications for permanent shunting – For infants who continue to require VAD drainage beyond four to six weeks, we suggest ventriculoperitoneal shunt (VPS) placement (algorithm 1) (Grade 2C). Endoscopic third ventriculostomy is an alternative procedure that is performed in a small subset of patients at some centers. VPS usually cannot be placed in the acute phase due to the neonate's small size and because the amount of blood in the CSF can cause shunt obstruction. Thus, temporary CSF drainage techniques are used until the infant is approximately 2 kg, CSF protein is <1.5 g/L, and CSF red blood cell count is <100/mm³. (See 'Permanent ventricular shunt' above and "Hydrocephalus in children: Management and prognosis", section on 'CSF diversion procedures'.)

●Follow-up – All neonates with severe GMH-IVH require long-term neurodevelopmental follow-up, as discussed separately. (See "Long-term neurodevelopmental impairment in infants born preterm: Risk assessment, follow-up care, and early intervention".)

●Outcome ‒ The risk of mortality in infants with GMH-IVH increases with the severity of the hemorrhage, ranging from approximately 5 percent in infants with grade I GMH-IVH to as high as 40 to 50 percent in infants with PVHI (grade IV IVH). Surviving infants are at increased risk of long-term neurodevelopmental disabilities (eg, cerebral palsy [CP], cognitive impairment). The risk is highest for extremely preterm infants (gestational age <28 weeks) with severe IVH (ie, grade III or PVHI), especially those who develop PHVD requiring permanent shunt placement. (See 'Outcome' above.)

●Prevention ‒ The most effective strategy to prevent GMH-IVH is to reduce the risk of preterm birth. When preterm birth cannot be avoided, appropriate prenatal and delivery room care should be provided to the mother and neonate. This includes antenatal glucocorticoid administration, prompt resuscitative efforts, and respiratory and hemodynamic support as needed. The goals are to provide balanced respiratory and cardiovascular support while avoiding abrupt physiologic fluctuations (eg, severe hypoxemia, hypo- or hypercapnia, hypo- or hypertension). (See 'Prevention' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Lisa M Adcock, MD, who contributed to an earlier version of this topic review.

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Topic 5000 Version 57.0

References

1 : Inder TE, Perlman JM, Volpe JJ. Preterm Intraventricular Hemorrhage/Posthemorrhagic hydrocephalus. In: Volpe's Neurology of the Newborn, 6th, Volpe JJ (Ed), Elsevier, Philadelphia 2018. p.637.

2 : Coagulopathy screening and early plasma treatment for the prevention of intraventricular hemorrhage in preterm infants.

3 : IVH in VLBW Preterm Babies - Therapy with Recombinant Activated F VII?

4 : A prospective pilot study of prophylactic treatment of preterm neonates with recombinant activated factor VII during the first 72 hours of life.

5 : Can neurophysiological assessment improve timing of intervention in posthaemorrhagic ventricular dilatation?

6 : Biomarkers of brain injury in the premature infant.

7 : Decompressing posthaemorrhagic ventricular dilatation significantly improves regional cerebral oxygen saturation in preterm infants.

8 : Lumbar Cerebrospinal Fluid Biomarkers of Posthemorrhagic Hydrocephalus of Prematurity: Amyloid Precursor Protein, Soluble Amyloid Precursor Proteinα, and L1 Cell Adhesion Molecule.

9 : Chemokine and cytokine levels in the lumbar cerebrospinal fluid of preterm infants with post-hemorrhagic hydrocephalus.

10 : Diffuse correlation spectroscopy blood flow monitoring for intraventricular hemorrhage vulnerability in extremely low gestational age newborns.

11 : Pediatric hydrocephalus: systematic literature review and evidence-based guidelines. Part 2: Management of posthemorrhagic hydrocephalus in premature infants.

12 : Management of Post-hemorrhagic Ventricular Dilatation in the Infant Born Preterm.

13 : New reference values for the neonatal cerebral ventricles.

14 : Measurement of the growth of the lateral ventricles in preterm infants with real-time ultrasound.

15 : A longitudinal study of post-haemorrhagic ventricular dilatation in the newborn.

16 : Treatment thresholds for intervention in posthaemorrhagic ventricular dilation: a randomised controlled trial.

17 : Intraparenchymal hemorrhage after serial ventricular reservoir taps in neonates with hydrocephalus and association with neurodevelopmental outcome at 2 years of age.

18 : A review of the current treatment methods for posthaemorrhagic hydrocephalus of infants.

19 : Assessment of infant position and timing of stylet removal to improve lumbar puncture success in neonates (NeoCLEAR): an open-label, 2 × 2 factorial, randomised, controlled trial.

20 : Repeated lumbar or ventricular punctures in newborns with intraventricular haemorrhage.

21 : Long-term experience with subcutaneously tunneled external ventricular drainage in preterm infants.

22 : Treatment of posthemorrhagic hydrocephalus in the preterm infant with a ventricular access device.

23 : Shunting outcomes in posthemorrhagic hydrocephalus: results of a Hydrocephalus Clinical Research Network prospective cohort study.

24 : Neonatal ventriculosubgaleal shunts.

25 : The initial neurosurgical interventions for the treatment of posthaemorrhagic hydrocephalus in preterm infants: A focused review.

26 : Treatment of posthemorrhagic ventricular dilation in preterm infants: a systematic review and meta-analysis of outcomes and complications.

27 : Ventricular reservoir versus ventriculosubgaleal shunt for posthemorrhagic hydrocephalus in preterm infants: infection risks and ventriculoperitoneal shunt rate.

28 : Neonatal posthemorrhagic hydrocephalus from prematurity: pathophysiology and current treatment concepts.

29 : Corpus callosum injury after neurosurgical intervention for posthemorrhagic ventricular dilatation and association with neurodevelopmental outcome at 2 years.

30 : Outcomes of extremely preterm infants following severe intracranial hemorrhage.

31 : Are Shunt Revisions Associated with IQ in Congenital Hydrocephalus? A Meta -Analysis.

32 : Neuroendoscopic surgery in neonates - indication and results over a 10-year practice.

33 : Is ventricular lavage a novel treatment of neonatal posthemorrhagic hydrocephalus? a meta analysis.

34 : The efficacy of endoscopic third ventriculostomy in children 1 year of age or younger: A systematic review and meta-analysis.

35 : Diuretic therapy for newborn infants with posthemorrhagic ventricular dilatation.

36 : Posthemorrhagic ventricular dilatation in preterm infants: When best to intervene?

37 : Randomized clinical trial of prevention of hydrocephalus after intraventricular hemorrhage in preterm infants: brain-washing versus tapping fluid.

38 : Drainage, irrigation and fibrinolytic therapy (DRIFT) for posthaemorrhagic ventricular dilatation: 10-year follow-up of a randomised controlled trial.

39 : Randomized Controlled Early versus Late Ventricular Intervention Study in Posthemorrhagic Ventricular Dilatation: Outcome at 2 Years.

40 : Assessment of Brain Injury and Brain Volumes after Posthemorrhagic Ventricular Dilatation: A Nested Substudy of the Randomized Controlled ELVIS Trial.

41 : Timing of Temporizing Neurosurgical Treatment in Relation to Shunting and Neurodevelopmental Outcomes in Posthemorrhagic Ventricular Dilatation of Prematurity: A Meta-analysis.

42 : Outcomes of intraventricular hemorrhage and posthemorrhagic hydrocephalus in a population-based cohort of very preterm infants born to residents of Nova Scotia from 1993 to 2010.

43 : Neurodevelopmental outcome of extremely low birth weight infants with posthemorrhagic hydrocephalus requiring shunt insertion.

44 : Trends in hospitalization of preterm infants with intraventricular hemorrhage and hydrocephalus in the United States, 2000-2010.

45 : Neurodevelopmental outcome of preterm infants with severe intraventricular hemorrhage and therapy for post-hemorrhagic ventricular dilatation.

46 : Periventricular Hemorrhagic Infarction in Very Preterm Infants: Characteristic Sonographic Findings and Association with Neurodevelopmental Outcome at Age 2 Years.

47 : Predictors of cerebral palsy in very preterm infants: the EPIPAGE prospective population-based cohort study.

48 : Intracranial Hemorrhage and 2-Year Neurodevelopmental Outcomes in Infants Born Extremely Preterm.

49 : School-age outcomes following intraventricular haemorrhage in infants born extremely preterm.

50 : Intraventricular hemorrhage and neurodevelopmental outcomes in extreme preterm infants.

51 : Impact of intraventricular hemorrhage on cognitive and behavioral outcomes at 18 years of age in low birth weight preterm infants.

52 : Neurodevelopmental outcomes of extremely low-gestational-age neonates with low-grade periventricular-intraventricular hemorrhage.

53 : Low-Grade Intraventricular Hemorrhage and Neurodevelopmental Outcomes at 24-42 Months of Age.

54 : Preterm Brain Injury and Neurodevelopmental Outcomes: A Meta-analysis.

55 : Influence of isolated low-grade intracranial haemorrhages on the neurodevelopmental outcome of infants born very low birthweight.

56 : Outcome of Preterm Infants with Transient Cystic Periventricular Leukomalacia on Serial Cranial Imaging Up to Term Equivalent Age.

57 : Successful implementation of an intracranial hemorrhage (ICH) bundle in reducing severe ICH: a quality improvement project.

58 : Neonatal care bundles are associated with a reduction in the incidence of intraventricular haemorrhage in preterm infants: a multicentre cohort study.

59 : Neuroprotection Care Bundle Implementation to Decrease Acute Brain Injury in Preterm Infants.

60 : Head midline position for preventing the occurrence or extension of germinal matrix-intraventricular haemorrhage in preterm infants.

61 : Elevated supine midline head position for prevention of intraventricular hemorrhage in VLBW and ELBW infants: a retrospective multicenter study.

62 : Reduction of Severe Intraventricular Hemorrhage in Preterm Infants: A Quality Improvement Project.

63 : Phenobarbital prior to preterm birth for preventing neonatal periventricular haemorrhage.

64 : Postnatal phenobarbital for the prevention of intraventricular haemorrhage in preterm infants.

65 : Vitamin K prior to preterm birth for preventing neonatal periventricular haemorrhage.

66 : Vitamin E supplementation for prevention of morbidity and mortality in preterm infants.

67 : Ethamsylate for the prevention of morbidity and mortality in preterm or very low birth weight infants.

68 : Antithrombin for the prevention of intraventricular hemorrhage in very preterm infants.

69 : Failure of fibrinolytic endoventricular treatment to prevent neonatal post-haemorrhagic hydrocephalus. A case-control trial.

70 : Efficacy and safety of intraventricular fibrinolytic therapy for post-intraventricular hemorrhagic hydrocephalus in extreme low birth weight infants: a preliminary clinical study.

خرید پکیج

Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Management and outcome

References