Vitamin K Deficiency Presenting in an Infant with an Anterior Mediastinal Mass: A Case Report and Review of the Literature


Case Report
Vitamin K Deficiency Presenting in an Infant with an Anterior
Mediastinal Mass: A Case Report and Review of the Literature

Mauricio A. Palau, Amanda Winters, Xiayuan Liang, Rachelle Nuss, Susan Niermeyer,
Megan Gossling, and Clyde Wright

School of Medicine, University of Colorado, Boulder, CO, USA

Correspondence should be addressed to Mauricio A. Palau; mauricio.palau@childrenscolorado.org

Received 2 November 2016; Accepted 19 January 2017; Published 9 February 2017

Academic Editor: Roland Broadbent

Copyright © 2017 Mauricio A. Palau et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.

We report a case of a 1-month-old infant with spontaneous thymic hemorrhage secondary to severe vitamin K deficiency. He was
brought to medical attention due to scrotal bruising and during evaluation was noted to be tachypneic and hypoxemic. Chest X-
ray revealed an enlarged cardiothymic silhouette, and a follow-up echocardiogram revealed a mass in the anterior mediastinum.
Routine laboratory work-up revealed severe coagulopathy. Further questioning revealed the patient had not received prophylactic
vitamin K at birth. The coagulopathy resolved with administration of vitamin K, and a biopsy confirmed the anterior mediastinal
mass was due to spontaneous thymic hemorrhage.

1. Introduction

Vitamin K deficiency bleeding (VKDB), formerly known
as hemorrhagic disease of the newborn, is a coagulopathy
infants acquire due to insufficient vitamin K stores. Vitamin K
is necessary for the synthesis of functional forms of coagula-
tion factors II, VII, IX, and X in the liver [1]. These proteins are
secreted into the blood and ultimately assist in the conversion
of fibrinogen to fibrin and the formation of a hemostatic
thrombus. Therefore, infants who accumulate inactive vita-
min K-dependent coagulation factors have an increased
bleeding tendency [2]. Herein, we report the case of a 1-
month-old infant whose VKDB presented as scrotal bruising
and respiratory distress due to an anterior mediastinal mass
that was ultimately determined to be spontaneous thymic
hemorrhage, representing an unusual clinical manifestation
of VKDB.

2. Case Presentation

A term 28-day-old male, born at home, was referred by the
family midwife to the emergency department for ecchymosis
of his left hemiscrotum. This exclusively breastfed infant,
without significant family history, had been thriving at home

when the parents noted acute discoloration of his right testicle
at 26 days of age. In the 24 hours prior to admission, the
discoloration of his right testicle migrated to the left testicle.
His parents reported that he had become progressively fussy
with decreased oral intake and appeared more pale. The
parents denied increased work of breathing, fevers, apnea,
cyanosis, emesis, or rash.

The parents stated that he had been previously healthy.
Prenatal care was provided by a midwife, and prenatal labs
were reported as negative. A prenatal ultrasound performed
at home by the midwife at mid-gestation was reported as nor-
mal. Pregnancy was uncomplicated, as was his spontaneous
vaginal delivery. The infant did not receive vitamin K pro-
phylaxis at birth, though his mother was taking oral vitamin
K, a prenatal vitamin, and herbal supplements daily. The
baby was taken care of by his parents, who were Mennonite.
There was no consanguinity. The baby’s father had flu-like
symptoms the week of his admission; otherwise there had
been no known sick contacts.

On arrival to the newborn intensive care unit, the infant
appeared lethargic, pale, and jaundiced and had evidence of
oozing from peripheral IV attempts. His left hemiscrotum
was purpuric; otherwise, there was no evidence of bruising
or petechiae. He had increased work of breathing with

Hindawi Publishing Corporation
Case Reports in Pediatrics
Volume 2017, Article ID 7628946, 5 pages
http://dx.doi.org/10.1155/2017/7628946

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2 Case Reports in Pediatrics

Figure 1: Anterior-posterior (AP) chest x-ray demonstrating
marked enlargement of the cardiothymic silhouette.

retractions and had a normal cardiac and abdominal exam.
He had no dysmorphic features and other than lethargy
had an appropriate neurological exam. An anterior-posterior
(AP) chest X-ray (Figure 1) performed in the emergency
department demonstrated marked enlargement of the car-
diothymic silhouette, which prompted further evaluation. An
echocardiogram revealed a large anterior mediastinal mass
with bilateral pleural effusions. A complete metabolic panel
was positive for a mild indirect hyperbilirubinemia (TSB 10.1,
DB 0.4; normal range TSB<11.5 mg/dL, DB 0–0.6 mg/dL) and
negative for metabolic acidosis or transaminitis. A complete
blood count and coagulopathy studies were significant for
anemia (Hgb 8.4, Hct 24.2, normal range Hgb 10.5–14.8 g/dL,
Hct 30.0–40.9%), mildly low platelets (143,000, normal range
150–500 103/𝜇L), a markedly abnormal prothrombin time
(greater than 80, normal range 13.2–16.5 seconds), a pro-
foundly abnormal partial thromboplastin time (greater than
250, normal range 29–48 seconds), and a normal fibrinogen
(376, normal range 150–400 mgs/dL). Based on the severely
abnormal coagulation studies, the patient was treated acutely
for suspected vitamin K deficiency related bleeding. The
patient received three IV doses of vitamin K, packed red
blood cells (60 mL/kg total), fresh frozen plasma (15 mL/kg),
and platelets (15 mL/kg). Within 6 hours, the infant’s hema-
tologic indices normalized and his clinical bleeding resolved.

Despite resolution of the coagulopathy, the anterior medi-
astinal mass remained. The differential diagnosis included
venous or lymphatic malformations, thymic enlargement,
or rarer tumors. Therefore, further diagnostic imaging of
the anterior mediastinal mass was pursued. A chest ultra-
sound revealed a solid mass without cystic components,
making an infantile lymphangioma unlikely. A CT of chest/
abdomen/pelvis (Figure 2) demonstrated a homogeneously
enhancing anterior mediastinal mass which maintained
thymic contour, with mass effect upon the vessels and airway.
The homogeneity of the mass was thought to be inconsistent
with the typical appearance of a germ cell tumor. While
the infant’s coagulopathy and borderline thrombocytopenia
initially raised concern for Kasabach-Merritt phenomenon

Figure 2: CT of chest/abdomen/pelvis demonstrated a homoge-
neously enhancing anterior mediastinal mass which maintained
thymic contour, with mass effect upon the vessels and airway.

(KMP), no significant vascularity was demonstrated on the
CT imaging, making the diagnosis of kaposiform heman-
gioendothelioma with associated KMP less likely.

The infant underwent ultrasound-guided biopsy of his
mediastinal mass on the hospital day following admission
once his coagulopathy had resolved. This biopsy was critical
in making the diagnosis of spontaneous thymic hemorrhage.
Representative histology of the mass is shown in Figure 3. The
patient’s tissue was consistent with normal thymic ultrastruc-
ture with Hassall’s corpuscles noted and slightly increased in
number compared to normal tissue. Cytokeratin staining was
performed and showed no increase in intensity or aberrant
distribution, ruling out the differential diagnosis of thymoma.
Many red blood cells were noted in the tissue sample, and
the biopsy specimen was grossly bloody as noted by the pro-
ceduralist. Flow cytometry revealed immunophenotype of
immature T cells consistent with normal cortical thymocytes.
In light of these pathologic findings as well as the medical
history and clinical response to vitamin K and FFP, the final
diagnosis for this patient was thymic hemorrhage secondary
to vitamin K deficiency, with possible component of thymic
hyperplasia. The patient’s respiratory distress resolved over a
few days and he was discharged home on hospital day #7 with
follow-up by his general pediatrician.

3. Discussion

Newborns, in particular those who are exclusively breastfed,
have multiple risk factors for VKDB. First, placental transfer
of vitamin K is limited with extremely low cord concentra-
tions (<0.05𝜇g/L) compared to adult levels [1]. Second, infant
liver reserve levels are substantially lower than adult levels [2].
Third, infant production of vitamin K is reduced secondary
to immature or altered gut flora [3]. Lastly, vitamin K content
in breast milk (1𝜇g/L) is significantly lower (60𝜇g/L) than
found in formula [4].

These risk factors predispose infants to develop VKDB,
classified by the age of onset. Early VKDB occurs in the
first 24 hours of life but typically only is seen in infants
whose mothers take medications that interfere with vitamin
K metabolism (e.g., anticoagulants, anticonvulsants, or anti-
tuberculosis drugs). Classic VKDB occurs between 2 and 7
days of life and is primarily secondary to inadequate feed-
ing. Late VKDB arises between day 8 and 6 months of



Case Reports in Pediatrics 3

∗

2x 40x Cytokeratin
N

or
m

al
 th

ym
us

Pa
tie

nt
 A

.M
.

Figure 3: Representative histology. Comparison of core biopsy specimen from the patient’s mediastinal mass with histology of normal thymus.
The 2x view demonstrates overall preservation of cortical and medullary regions, with the suggestion of increased RBC’s in the patient sample
compared to the normal specimen. This is better seen on the 40x view (arrows) and is consistent with hemorrhage into the thymic tissue.
Asterisks mark normal Hassall’s corpuscles, which can be seen in normal tissue and in cases of thymic hyperplasia. Cytokeratin staining in
the patient is of normal intensity and distribution, ruling out the differential diagnosis of thymoma.

life, with peak incidence between 3 and 8 weeks. This form
nearly always occurs in exclusively breast-fed infants and is
often associated with undiagnosed hepatobiliary dysfunction
impairing absorption of vitamin K [1].

To prevent all forms of VKDB, administration of intra-
muscular vitamin K at birth has been a standard practice in
the United States since 1961 when the American Academy of
Pediatrics’ recommended the injection for all newborns [5].
Without prophylaxis, early and classical VKDB have an inci-
dence as high as 6% and 2% of live births, respectively [3, 6].
The relative risk for developing late VKDB was estimated at 81
times greater among infants who did not receive prophylaxis
[7]. However, authors speculate these estimates are lower
than the actual figures because the number of exclusively
breastfed infants who do not receive intramuscular vitamin
K are unknown. Surveillance programs in different coun-
tries, including the British Isles, Sweden, Switzerland, and
Germany, demonstrate that the IM injection of 1 mg of vit-
amin K is more effective at preventing late VKDB than when
given by the oral route [8].

The clinical presentation of early and classic VKDB is
variable, with bleeding most commonly occurring from the
gastrointestinal tract (53%) and umbilicus (23%) [9]. The
main distinguishing feature of the late syndrome is the higher
frequency of intracranial hemorrhage (ICH). An analysis of
131 published cases of late VKDB revealed 63% had presented
with severe ICH, with 14% mortality and 40% long-term
neurological morbidity among surviving infants [10]. In 2013,
4 cases of late VKDB were reported at a children’s hospital in
Tennessee, of which 3 suffered ICH [11]. Three of the infants

were born at major area hospitals and one was born at home.
In each case, parents had declined intramuscular vitamin K
prophylaxis.

Given the potential catastrophic consequences of VKDB
and the attenuation of the disease with treatment, rapid diag-
nosis is paramount. A confirmed case fulfills the following
diagnostic criteria [8]: (1) elevation of the prothrombin time
(PT)≥4 times the laboratory limit of normal; (2) normal or
elevated platelet count, normal fibrinogen, and absent fibrin
degradation products (excludes disseminated intravascular
coagulation); and (3) PT returning to normal after vitamin K
administration. Once diagnosed, infants who present with a
non-life-threatening bleeding should receive a single 1-2 mg
intravenous dose of vitamin K

1
(synonyms include phyllo-

quinone and phytonadione) [8]. For life-threatening bleeding
presentations, additional treatment with fresh frozen plasma
(at a dose of 10–15 mL/kg) may be necessary [12].

Despite the most common manifestations of VKDB
outlined above, our patient’s thymic hemorrhage is an exceed-
ingly rare clinical presentation. Our literature review identi-
fied four case reports of neonatal thymic hemorrhage [13–16].
Three of the infants did not receive Vitamin K prophylaxis at
birth. Additionally, one infant with both true thymic hyper-
plasia and spontaneous thymic bleeding was described [17].
In all of these infants, respiratory distress in the context of
imaging revealing an anterior mediastinal mass were shared
features. The combination of the ultrasound and CT find-
ings for the neonate in our case helped deter the team from
performing a thoracotomy given how it narrowed the dif-
ferential diagnosis.



4 Case Reports in Pediatrics

In the present case, the overwhelming concern was the
anterior mediastinal mass. Although the vitamin K deficiency
was diagnosed and corrected early in the infant’s hospitaliza-
tion, the work-up of the anterior mediastinal mass continued.
While the differential diagnosis included spontaneous hem-
orrhage into normal thymic tissue, malignancy or vitamin K
associated bleeding into benign or malignant tissue could not
be ruled out.

Anterior mediastinal masses in neonates and infants
could represent venous or lymphatic malformations and
thymic enlargement (whether due to thymic hyperplasia,
thymic cysts, thymoma, or thymic hemorrhage). Rarer possi-
bilities include germ cell tumors (primarily teratomas), neu-
roblastoma, rhabdomyosarcoma, lymphoma, Langerhans cell
histiocytosis, or Wilm’s tumor [18]. However, coagulopathy
as an additional clinical feature narrows the spectrum of
possibilities to primarily venous/lymphatic malformations
and (less likely) lymphomas [19–21].

Venous and lymphatic malformations represent a diverse
category of rare lesions that are nevertheless most commonly
described in neonates and infants. The most common of
these are infantile lymphangiomas (formerly known as cystic
hygromas) and kaposiform hemangioendotheliomas (KHE).
Lymphangiomas are benign congenital malformations char-
acterized by proliferation of normal lymphatic tissue and are
frequently cystic in nature [22]. They are commonly diag-
nosed in children less than 2 years of age and most frequently
arise in the head/neck or axillae; only 1-2% are found in the
mediastinum. They can be incidentally found or diagnosed
due to respiratory compromise or recurrent superinfection
of the abnormal cystic tissue. Kaposiform hemangioendo-
thelioma is an aggressive vascular tumor with incidence of
approximately 1 in 100,000 children, with 93% of cases diag-
nosed before the age of one year [20]. It can arise anywhere
in the body. While intrathoracic lesions are among the rarest,
this location dramatically increases (∼18-fold) the risk of
the major complication of KHE, which is termed Kasabach-
Merritt phenomenon (KMP) [20]. KMP is thought to arise
from tortuosity of the abnormal vessels in the tumor, causing
trapping of platelets and secondary thrombocytopenia. Asso-
ciated platelet activation then causes secondary elevation in
D-dimer and hypofibrinogenemia, mimicking disseminated
intravascular coagulation (DIC), often with abnormalities in
PT and PTT values. Amelioration of the KMP is achieved by
targeted therapy designed to cause regression of the tumor
itself. Pathologically, KHE is diagnosed by its characteris-
tic infiltrative nature, presence of spindled epithelial cells,
microthrombi, and lymphatic endothelial markers such as
CD34 and (variably) factor VIII-related antigen [23]. Our
patient’s platelet count was low normal and the fibrinogen
level was in the normal range, ruling out DIC and KMP.

Primary thymic enlargement represents about 2–4% of
all pediatric mediastinal masses and can occur secondary to
a variety of etiologies [18]. Thymic hyperplasia is among the
most common cause of enlarged thymus in younger children
and is defined as increase in size and weight of the gland with-
out change in its normal histology [24]. The true incidence is
unknown, as many cases are diagnosed incidentally without
associated symptoms [17]. Lymphofollicular hyperplasia is

another potential cause of an abnormally large thymus and
is characterized histologically by increased number and size
of germinal centers. It is often associated with autoimmune
disease, particularly myasthenia gravis [17, 24]. In addition to
histologic examination, flow cytometry can help differentiate
these two etiologies, as well as evaluating T-lymphoblastic
lymphoma [24]. Thymic cysts can arise as remnants of the
thymopharyngeal duct or can be acquired via degeneration
of Hassall’s corpuscles [17]. Finally, thymomas are indolent
tumors of the thymic epithelium, most commonly seen in
middle age and very rare in children [25]. Only 50 cases
have been described in the pediatric literature, with patients
diagnosed at a variety of ages and tumor stages [25]. Prolif-
eration of epithelial cells, as demonstrated pathologically by
cytokeratin staining, is diagnostic [25].

While lymphoma is a common cause of mediastinal mass
in older pediatric patients [18], it is exceedingly rare in infants
less than one year of age, with estimated incidence of 2.5
cases per million or less [26, 27]. Those case reports that
exist typically describe aggressive disease with leukemic and
other organ-system involvement and suggest that rare cancer
predisposition syndromes such as ataxia-telangiectasia may
be responsible for the young age at presentation [19, 28, 29].

4. Conclusion

It is crucial as a medical provider to be aware of the varied pre-
sentation of VKDB in the neonatal period. Although they are
a relatively rare constellation of signs and symptoms, a non-
consumptive coagulopathy, respiratory distress, and an ante-
rior mediastinal mass should prompt the work-up of acute
thymic hemorrhage. Vitamin K deficiency bleeding should
be suspected and treated as an emergency in this situation.
As in our reported patient, prompt recognition and diagnosis
can lead to rapid clinical resolution and avoidance of thora-
cotomy. Our case also led to an educational opportunity on
the critical importance of vitamin K prophylaxis at birth.

Competing Interests

The authors declare that there is no conflict of interests
regarding the publication of this paper.

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