Seminars in Fetal & Neonatal Medicine xxx (2015) 1e6

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Seminars in Fetal & Neonatal Medicine

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Review

The bleeding newborn: A review of presentation, diagnosis, and

management
Julie Jaffray a, b, Guy Young a, b, Richard H. Ko a, b, *
a
Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, CA, USA
b
Keck School of Medicine, University of Southern California, Los Angeles, CA, USA

s u m m a r y
Keywords: The neonatal hemostatic system is continuously developing with rapidly changing concentrations of
Hemorrhage many coagulation proteins. Thus, determining the etiology of bleeding in a newborn has additional
Hemostasis
challenges beyond those seen in older children or adults. Bleeding can be seen in both well and sick
Infant
Newborn
newborns due to congenital causes, such as hemophilia or von Willebrand disease, and acquired causes,
such as liver failure or disseminated intravascular coagulation. Traditional coagulation testing should be
interpreted with caution and with the help of a hematologist, if possible, due to the greatly different
normal ranges between neonates as compared with older children and adults. However, despite these
challenges, both clinical and laboratory clues can guide physicians appropriately to diagnose and treat
the bleeding newborn.
© 2015 Elsevier Ltd. All rights reserved.

1. Introduction known as developmental hemostasis [2]. Figure 1 illustrates the

fetal development of the pro- and anticoagulant proteins [3e5].
Bleeding in healthy neonates is rare, but in sick neonates, it is Procoagulants present at adult levels at birth include fibrinogen,
often serious and can be fatal. The clinical presentation of bleeding factor V (FV), factor VIII (FVIII) and von Willebrand factor (VWF),
in neonates includes intracranial hemorrhage (ICH), cepha- whereas factors II (FII), VII (FVII), IX (FIX) and X (FX) (vitamin K-
lohematoma, bleeding after a procedure or venepuncture, or dependent factors), and factors XI (FXI), XII (FXII), prekallikrein and
mucocutaneous bleeding such as bruising or gastrointestinal high-molecular-weight kininogen (contact factors) are present at
bleeding [1]. The etiology of such bleeding may arise from about 50% of adult levels at birth [6,7]. To balance lower levels of
congenital issues, such as hemophilia, or from acquired issues procoagulants, most of the anticoagulants (antithrombin, heparin
including liver failure. Determining the cause of bleeding is a cofactor II, protein C and protein S) are also lower at birth, though as
clinical challenge for both primary treating practitioners as well as a compensatory mechanism, the anticoagulant a-2-macroglobulin
hematology consultants due to the continuously evolving coagu- is actually higher at birth than adult levels [6,7].
lation system in neonates. As a result of lower levels of the procoagulant proteins, the
The coagulation system is comprised of cellular elements activated partial thromboplastin time (aPTT) and prothrombin time
(platelets being the most important) and plasma proteins, all of (PT) are prolonged in neonates when compared to the adult range.
which work in concert to protect from both hemorrhage and Previous studies reported reference ranges for the aPTT, PT and the
thrombosis. The concentrations of the plasma proteins are different pro- and anticoagulant protein levels, in term and premature ne-
in neonates when compared to older children and adults, and un- onates [6e8]. Unfortunately these reference ranges must be inter-
dergo rapid maturation over the first six months of life in a process preted with caution due to the significant laboratory variability of
reagents and instruments used. The Scientific and Standardization
Committee of the International Society on Thrombosis and Hae-
mostasis (ISTH) recommends creating pediatric reference ranges in
each hospital, although this is quite time-consuming and costly [9].
* Corresponding author. Address: Children's Center for Cancer and Blood Dis- This review discusses the various causes of bleeding in neonates
eases, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Mailstop #54, Los and provides guidance on how to arrive at the appropriate diag-
Angeles, CA 90027, USA. Tel.: þ1 (323) 361 5600; fax: þ1 (323) 361 7128.
nosis and suggest different treatment options. Bleeding disorders
E-mail address: rko@chla.usc.edu (R.H. Ko).

http://dx.doi.org/10.1016/j.siny.2015.12.002
1744-165X/© 2015 Elsevier Ltd. All rights reserved.

Please cite this article in press as: Jaffray J, et al., The bleeding newborn: A review of presentation, diagnosis, and management, Seminars in Fetal
& Neonatal Medicine (2015), http://dx.doi.org/10.1016/j.siny.2015.12.002
2 J. Jaffray et al. / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e6

Fig. 1. Fetal development of the coagulation system. FV, factor V; FVII, factor VII; FVIII, factor VIII; FIX, factor X; AT, antithrombin; HCII, heparin cofactor II. Reproduced with
permission from Jaffray J, Young G. Developmental hemostasis clinical implications from the fetus to the adolescent. Pediatr Clin N Am 2013; 60:1407e17.

caused by thrombocytopenia or platelet dysfunction will be 2.2. von Willebrand disease

addressed in another article.
von Willebrand Disease (VWD) is the most frequently inherited
bleeding disorder, affecting ~1% of the population, and is trans-
2. Congenital causes of bleeding mitted in autosomal dominant or recessive patterns [16,17]. There
are three main categories of VWD based on the quantitative level or
2.1. Hemophilia function of von Willebrand factor (VWF): type 1, 2, or 3.
Most patients with VWD have type I, which is due to a partial
Deficiencies of FVIII and FIX are known as hemophilia A and B, quantitative deficiency of VWF and is usually associated with a mild
respectively, and are inherited in an X-linked recessive pattern. phenotypic bleeding presentation [18]. Type 2 VWD is a qualitative
Female relatives are known as hemophilia carriers. The incidence of dysfunction of VWF and is typically associated with a more severe
hemophilia is 1 per 5000 males (FVIII) and 1 in 20,000 males (FIX) bleeding phenotype. Type 2 is further divided into four separate
[10]. Persons with hemophilia are classified based on their plasma subtypes, 2A, 2B, 2M, and 2N, which are based on the functional
factor activity [severe (<1%), moderate (1e5%) or mild (>5 to 40%)]. and structural interactions between VWF and platelets or FVIII.
Bleeding in hemophilia (mostly the severe type) may present in Type 3 is the rarest form of VWD in which patients have complete
neonates as either post-procedural bleeding (e.g. circumcision or or almost complete deficiency of VWF and have the most severe
heel sticks) or even as ICH. Newborns with hemophilia are 44 times bleeding phenotype [18,19]. Typically only patients with type 3 or
more likely to have symptomatic ICH compared to normal new- some type 2 VWD present with bleeding as neonates [20]. Muco-
borns, and it is more likely to occur after an assisted vaginal de- cutaneous bleeding is the hallmark of VWD; patients can have
livery [11,12]. The mean age of patients with hemophilia having epistaxis, bruising, gum bleeding, and gastrointestinal bleeding, but
their first bleed is 28.5 days [13]. also bleeding after trauma or surgery.
Although diagnosing hemophilia in neonates is usually The diagnosis of VWD is based on three main laboratory assays:
straightforward, issues of developmental hemostasis can make it (i) a quantitative measure of VWF in the plasma, (ii) the activity of
more challenging than in older children. Up to 70% of patients are VWF and its ability to bind platelets (iii) and FVIII activity [21]. High
diagnosed in the first month of life [14]. Any newborn with unex- molecular weight multimer analysis can also be performed to help
pected or excessive bleeding should have an aPTT, and, though differentiate type 2 varieties. Table 1 shows the laboratory values
many normal infants have a prolonged aPTT, this should not pre- that are consistent with each type of VWD. At birth, neonates have
clude an evaluation of factor levels in the above situation. As the normal to increased levels of VWF activity and high-molecular
FVIII activity in neonates approximates that of a normal adult, weight VWF multimers compared to adult levels, which is why
making the diagnosis of severe or moderate hemophilia A is most patients with type 1 and 2 VWD do not present with bleeding
straightforward. The diagnosis of mild hemophilia can be more until later in life [7,8].
difficult due to increased FVIII activity resulting from the stress of The management of bleeding in a neonate with VWD is typically
delivery, thus levels should be repeated at six to 12 months of age if with plasma-derived FVIII (pdFVIII) products that contain VWF, and
mild FVIII deficiency is suspected [15]. When evaluating FIX levels, consultation with a pediatric hematologist is suggested to assist in
however, as stated previously, FIX activity is about 50% of adult management.
levels at birth, which overlaps with the range of mild hemophilia,
making the diagnosis of mild hemophilia B difficult, and, as above,
testing should be repeated at six to 12 months. 2.3. Rare inherited bleeding disorders
Treatment of hemophilia is based on replacing the missing
protein with factor concentrates; if needed, consultation with a Patients with rare factor deficiencies represent 3e5% of all
pediatric hematologist is suggested to assist in management. coagulation disorders, with an incidence of 1:500,000 to

Please cite this article in press as: Jaffray J, et al., The bleeding newborn: A review of presentation, diagnosis, and management, Seminars in Fetal
& Neonatal Medicine (2015), http://dx.doi.org/10.1016/j.siny.2015.12.002
 J. Jaffray et al. / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e6 3

Table 1
Typical laboratory values for the main types of von Willebrand disease.

Type 1 Type 2A Type 2B Type 2M Type 2N Type3

VWF antigen Low Low Low Low Low Absent

VWF activity Low Very low Very low Very low Normal or low Absent
FVIII activity Low Normal or low Normal or low Normal or low Very low Extremely low
Platelet count Normal Normal Low Normal Normal Normal
VWF multimers Normal or mildly Loss of high and Decreased high molecular Normal Normal Absent
decreased expression intermediate weight weight multimers
in all sizes multimers

VWF, von Willebrand factor; FVIII, factor VIII.

1:2,000,000 [22,23]. Deficiencies in fibrinogen, FII, FV, FVII, FX, FXI, (50e70% of cases), ICH, and prolonged bleeding after procedures or
or FXIII may present in neonates, and each will be discussed briefly trauma [27e29].
below. Low levels of FXIII do not prolong the PT or aPTT. Thus if both the
PT and aPTT are within the normal range for age, and a bleeding
2.3.1. Disorders of fibrinogen disorder is suspected, then a quantitative FXIII assay should be
Fibrinogen is converted to fibrin and, along with platelets, forms performed. The clot solubility assay previously used to diagnose
the structure of blood clots. Patients with disorders of fibrinogen FXIII deficiency lacks sensitivity for very low levels of FXIII. Plasma-
may have either decreased or complete absence of fibrinogen levels derived and recombinant FXIII products are available, although the
(hypofibrinogenemia, afibrinogenemia), or dysfunctional fibrin- recombinant form can only be used for A-subunit deletions. Cry-
ogen (dysfibrinogenemia). Afibrinogenemia is inherited in an oprecipitate should be used if FXIII concentrate is unavailable.
autosomal recessive pattern, whereas the heterozygous form is
hypofibrinogenemia. Neonates may present with prolonged 3. Acquired causes of bleeding
bleeding from the umbilical cord stump, post circumcision, ICH, or
mucocutaneous bleeding [24]. 3.1. Liver failure
Patients with disorders of fibrinogen will have a prolonged PT
and aPTT. Decreased functional or antigenic fibrinogen assays are The liver is responsible for the synthesis of most pro- and
the confirmatory tests. Normal term neonates have fibrinogen anticoagulant proteins (except FVIII and VWF) and thrombopoetin,
levels equal to adult normal values at birth [7,8]. which stimulates platelet production. A disruption in liver function
Fibrinogen concentrates are the ideal treatment for bleeding may have a significant impact on the coagulation system, exacer-
episodes. Fresh frozen plasma (FFP) or cryoprecipitate may also be bating the effects in neonates whose systems are already delicately
used for bleeding when fibrinogen concentrates are unavailable. balanced. Patients with liver failure may present with both
bleeding and thrombosis, and the etiology, diagnosis, and treat-
2.3.2. Prothrombin (FII), FV, FVII, FX, and FXI deficiency ment are all challenging. Neonates with liver disease may present
Patients with FII, FV, FVII, FX, and FXI deficiency are inherited in with any manner of bleeding. Coagulation laboratory abnormalities
an autosomal recessive pattern, and there is a higher incidence of seen in liver failure are elevated PT, aPTT and D-dimer, decreased
FXI deficiency in those of Ashkenazi Jewish descent [25]. Most fibrinogen activity, and decreased platelet count.
factor deficiencies in neonates can lead to mucocutaneous The treatment for bleeding in liver failure is difficult due to the
bleeding, ICH, prolonged umbilical stump bleeding, or bleeding risks of fluid overload and thrombosis. FFP has historically been
after procedures or trauma. FVII and FXI levels do not correlate well the first line of treatment for bleeding due to liver failure in ne-
with bleeding phenotype; some patients with very low factor levels onates since it replaces all coagulation proteins. Studies have
do not have any bleeding, and those with higher factor levels may shown that large volumes of FFP are required to correct the
have profuse bleeding [25,26]. coagulation abnormalities [30]. Off-label use of rFVIIa has been
Diagnosing rare factor deficiencies should begin with a PT and used and resulted in excellent control of bleeding due to liver
aPTT. Isolated prolongation of the PT is seen with FVII deficiency, disease in neonates; however, this medication carries with it a risk
and isolated prolongation of the aPTT is seen with FXI deficiency. for thrombosis [31]. Cryoprecipitate to correct low fibrinogen, and
Patients with FII, FV and FX deficiency will result in a prolonga- prothrombin complex concentrates (PCCs) to correct deficiencies
tion of both the PT and aPTT. When a specific factor deficiency is of factors II, VII, IX, and X can be used for bleeding due to liver
suspected, confirmatory factor-specific assays should be per- disease.
formed. As above, diagnosing these factor deficiencies in a
newborn is challenging due to the issues of developmental he- 3.2. Vitamin K deficiency bleeding
mostasis [7,8].
Factor concentrates are available for the replacement of FVII Vitamin K is a crucial cofactor in the production of procoagu-
(rFVIIa) and FII, FVII, FIX, and FX (prothrombin complex concen- lant proteins factors II, VII, IX and X, and of natural coagulation
trates). FXI concentrate is available in some countries but not in the inhibitors, proteins C and S. Vitamin K is essential for the g-
USA currently. FFP is the only treatment for patients with de- carboxylation of these clotting factors which is required for their
ficiencies of FV and FXI. functionality. Vitamin K deficiency bleeding (VKDB) is classified as
early, classical, or late (see Table 2). Early onset VKDB is due to
2.3.3. FXIII deficiency cross-placental transfer of compounds that interfere with vitamin
FXIII, composed of two A and two B subunits, cross-links fibrin K metabolism. Classical VKDB is due to a physiologic deficiency in
and stabilizes clots. FXIII deficiency is inherited in an autosomal vitamin K at birth combined with either a lack of vitamin K in
recessive pattern and clinical manifestations may occur in neo- breast milk or inadequate feeding. Late onset VKDB is again due to
nates, most commonly with umbilical cord stump bleeding inadequate vitamin K content in breast milk and is thus found

Please cite this article in press as: Jaffray J, et al., The bleeding newborn: A review of presentation, diagnosis, and management, Seminars in Fetal
& Neonatal Medicine (2015), http://dx.doi.org/10.1016/j.siny.2015.12.002
4 J. Jaffray et al. / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e6

Table 2
Vitamin K deficiency classification.a

Early Classical Late

Age <24 h 1e7 days 2 weeks

Risk factors Maternal medications (vitamin K antagonists, Lack of prophylactic vitamin K treatment, Exclusive breastfeeding, poor feeding,
anticonvulsants, antituberculin drugs) poor feeding (particularly if breastfed) gastrointestinal disorders, liver disease,
pancreatic disease, antibiotic therapy
Sites of bleeding Cephalohematoma, umbilical stump, intracranial Gastrointestinal, umbilicus, mucocutaneous, Intracranial, mucocutaneous, gastrointestinal
circumcision, intracranial
Frequency Less than 5% in at-risk population With prophylactic vitamin K: extremely rare, Variable depending on age and conditions
Without prophylactic vitamin K (0.01e1%) listed above
Treatment Prothrombin complex concentrates, vitamin K Parenteral vitamin K (intravenous preferred) Vitamin K
(may not be effective) Prothrombin complex concentrates for active Prothrombin complex concentrates for
bleeding active bleeding, recombinant factor VIIa
(for mild cases where only the prothrombin
time is prolonged)
Prevention Avoidance of above medications during pregnancy Vitamin K prophylaxis at birth Adequate vitamin K replacement (in many
cases will need to be parenteral)
a
Table adapted with permission from Jaffray J, Young G. Developmental hemostasis clinical implications from the fetus to the adolescent. Pediatr Clin N Am 2013;
60:1407e17.

almost universally in exclusively breastfed infants. Prior to the hemorrhagic and/or thrombotic complications. In some patients
widespread use of vitamin K prophylaxis, the incidence of classical significant hemorrhage and thrombosis may occur simultaneously.
VKDB was reported to be as high as 1.5%; however, the condition is DIC is always caused by an underlying medical disorder. In neo-
only rarely seen today, and is almost always associated with sit- nates, the most frequent etiology is sepsis.
uations where vitamin K was not administered in the immediate The pathophysiology of DIC is complex and not completely
newborn period. understood. Briefly, an inciting event triggers the release of pro-
The clinical features of VKDB are similar to other bleeding di- inflammatory cytokines, especially interleukin-6 (IL-6) and tumor
atheses and include bruising, mucus membrane bleeding, bleeding necrosis factor-a (TNF-a). IL-6 leads to tissue factor-mediated
after trauma or invasive procedures, ICH, or signs of internal activation of the coagulation system that in turn leads to
bleeding such as hematuria. enhanced fibrin formation, mostly in the microvasculature. TNF-a
The diagnostic evaluation for VKDB is straightforward as the PT leads to inhibition of both the natural anticoagulants (anti-
is always prolonged and the aPTT is nearly always prolonged. In thrombin, proteins C and S) and fibrinolysis by increasing levels of
the typical scenario, the PT is prolonged out of proportion to the plasminogen activator inhibitor-1. The sum of these effects is
aPTT. In a newborn with the above clinical and laboratory findings, microvascular thrombosis, which often leads to organ dysfunction
eliciting a history in which vitamin K was not administered is and consumption of procoagulant proteins and platelets, which
sufficient to make a presumptive diagnosis, and the administra- may lead to hemorrhage.
tion of parenteral vitamin K should be undertaken immediately. Bleeding may occur at any site but frequently involves the skin
Improvement, if not complete correction, of the PT and aPTT (at vascular access sites) and mucus membranes. Severe internal
several hours after the administration of parenteral vitamin K hemorrhage is less frequent, but ICH may occur and be
serves as confirmation of the diagnosis. Whereas measuring factor catastrophic.
levels (specifically FII, FVII, FIX, and FX) may assist in the diagnosis, When a patient at risk for DIC presents with hemorrhage, spe-
they are not necessary and delays in instituting appropriate cific laboratory abnormalities can only provide supportive evi-
therapy could lead to severe, even catastrophic, bleeding dence, not confirm the diagnosis of DIC. Routine laboratory assays
complications. such as the CBC, PT, aPTT, and fibrinogen are often abnormal as a
Without question, the most effective management for VKDB is result of fibrin formation and degradation as well as consumption
prevention, and all newborns should receive vitamin K immedi- of coagulation proteins. Thrombocytopenia is often present, and e
ately after birth. Although the recommended route of administra- depending on the etiology e leukocytosis, leukopenia, and anemia.
tion varies between countries (intramuscular in the USA and oral in When DIC is suspected, measurement of fibrin degradation prod-
the UK, for example), both approaches are effective. Currently ucts (FDP) or D-dimers is helpful. The combination of thrombocy-
available treatment is generally in the form of vitamin K1 (also topenia, hypofibrinogenemia, prolonged PT and aPTT and elevated
known as phytonadione), which can be administered parenterally FDP or D-dimer is strongly suggestive for the presence of DIC. A
via intravenous, intramuscular, and subcutaneous injection, and scoring system has been developed by the ISTH which incorporates
orally; however, intravenous administration is recommended in the results of the above assays [33].
the acute setting. The management of DIC most importantly requires treatment of
It is important to note that whereas the effect of parenteral the underlying condition causing the DIC. Correcting the coagul-
vitamin K is rapid, it is not instantaneous and may take several opathy will be impossible if the underlying disorder cannot be
hours. Thus, in a patient presenting with severe hemorrhage such controlled. Since DIC is a derangement of all aspects of the coagu-
as ICH, additional therapy with PCCs aimed at immediate correction lation system, both FFP (coagulant protein replacement) and cry-
of factor deficiencies is required. oprecipitate (fibrinogen replacement) are usually first-line therapy.
Importantly, FFP should be given to manage bleeding complica-
3.3. Disseminated intravascular coagulation tions, not to improve laboratory values. In one study in neonates
with DIC, FFP did not have an impact on survival or resolution of
Disseminated intravascular coagulation (DIC) is a disorder DIC [34]. For severe bleeding in patients with DIC, PCCs and rFVIIa
characterized by consumption of procoagulant, anticoagulant, can be used, but with caution due to the risk of thrombotic
fibrinolytic proteins, and platelets [32]. Patients may develop complications.

Please cite this article in press as: Jaffray J, et al., The bleeding newborn: A review of presentation, diagnosis, and management, Seminars in Fetal
& Neonatal Medicine (2015), http://dx.doi.org/10.1016/j.siny.2015.12.002
 J. Jaffray et al. / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e6 5

Sick or acƟvely bleeding? No

Isolated
ated PT
P Isolated
ated aPTT
a PT and aPTT
aP Normal
ormal PT
prolongaƟon prolongaƟon prolonged /aPTT

Yes
eck FV
Check FVII Check
ck FVIII,
FVI FIX, Check MulƟpl
MulƟple Check
Chheck
eck EvaluaƟo
EvaluaƟon
acƟvity FXI, FXII acƟvity fibrinogen, factor quanƟtaƟve for VWD
FII, FV, FX deficiencies FXIII level
Check CBC, PT, aPTT, and fibrinogen. acƟvity
Consider
nside
rFVIIa Low
ow FXI
FXIII VWD
Single
ingle ffactor Liver diagnosed
No deficiency failure
Give vitamin K Vitamin
tamin K given? FVIIII or FIX F
FXI pdFXIII
dFXIII oor
deficiency deficiency rFXIII pdFVI
pdFVIII
products

Specific
cific fa
factor
Treat the products FFP orr
underlying Yes Is the paƟent in cryoprecipitate
disorder. DIC?
FFP as needed.
No

Yes
May need Thrombocytopenic
ombo
platelets or
further evaluaƟon.

Fig. 2. Algorithm for the approach to a bleeding neonate. aPTT, activated partial thromboplastin time; CBC, complete blood count; DIC, disseminated intravascular coagulation; FFP,
fresh frozen plasma; FII, factor II; FV, factor V; FVII, factor VII; FVIII, factor VIII; FIX, factor IX; FXI, factor XI; FXII, factor XII; FXIII, factor XIII; pdFVIII, plasma-derived factor VIII;
pdFXIII, plasma-derived factor XIII; PT, prothrombin time; rVIIa, activated recombinant factor VII; rXIII, recombinant factor XIII; VWD, von Willebrand disease.

3.4. Therapeutic hypothermia diagnosis and institute appropriate treatment. We have provided
here a framework (see Fig. 2) to diagnose and treat neonates who
Recently, therapeutic hypothermia has been used as a treatment are actively bleeding. Often initial care is supportive until confir-
for severe asphyxia to prevent the neurologic sequelae of hypo- matory testing results return. A thorough history and physical can
xiceischemic events (such as neonatal ICH) and to improve out- be key in making the proper diagnosis.
comes [35,36]. However, hypothermia may further increase the risk
of ICH by causing changes in cerebral blood flow, increased fragility
of injured tissues, hypotension, changes in the function of the
Practice points
coagulation system, thrombocytopenia, and metabolic de-
rangements [37]. Current evidence suggests that coagulopathy,
 Neonates are in a continuous state of developmental
thrombocytopenia and bleeding may not be significantly increased
hemostasis.
with hypothermia [35,36,38]. Close attention should be paid to
 Bleeding in neonates can be challenging to diagnose and
platelet count, coagulation measures (PT, aPTT, fibrinogen), and
treat.
clinical signs of bleeding when neonates undergo hypothermic
 With systematic evaluation of various coagulation tests,
cooling protocols. If derangements in the coagulation measures are
the appropriate diagnosis can be made and treatment can
found and bleeding is present, they should be replaced with FFP or
be initiated.
cryoprecipitate as indicated.
 Initially, treatment is often supportive, but once a diag-
nosis is made, it can and should be tailored to specific
3.5. Extracorporeal life support etiologies.

Neonates requiring extracorporeal life support (including car-

diopulmonary bypass surgery or extracorporeal membrane
oxygenation) are at risk for significant bleeding. These patients Conflict of interest statement
often undergo large, complicated surgical procedures that stress
the coagulation system. A discussion of all the issues related to None declared.
bleeding related to extracorporeal life support is beyond the scope
of this review, but in summary, treatment is based on supportive Funding sources
care with FFP, cryoprecipitate, platelet transfusions, and
monitoring. None.

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Please cite this article in press as: Jaffray J, et al., The bleeding newborn: A review of presentation, diagnosis, and management, Seminars in Fetal
& Neonatal Medicine (2015), http://dx.doi.org/10.1016/j.siny.2015.12.002
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Please cite this article in press as: Jaffray J, et al., The bleeding newborn: A review of presentation, diagnosis, and management, Seminars in Fetal
& Neonatal Medicine (2015), http://dx.doi.org/10.1016/j.siny.2015.12.002