(2024) 24:564
Jansen et al. BMC Pediatrics
https://doi.org/10.1186/s12887-024-05002-8

BMC Pediatrics

CASE REPORTOpen Access

Neonatal cardiorespiratory failure causedby splenic hemorrhages: a case report on a fatal
and a rescued case
Nadieh A. Jansen1, Anne T M Dittrich2, Manouk Backes3, Benno Kusters4, Willemijn M Klein5 andTim Hundscheid1*

Abstract
Two cases of neonatal splenic hemorrhage with acute cardiorespiratory failure are described in this report. The firstcase involves a full-term neonate who was found unresponsive without any witnesses and could not be successfully resuscitated. A postmortem diagnosis revealed a splenic hemorrhage. Second case is an extremely premature
neonate who experienced a witnessed cardiovascular collapse on the 14th day of life. Rapid cardiovascular support
was administered, resulting in a positive outcome. While splenic hemorrhage is commonly associated with traumatic
events, these cases highlight the need of considering spontaneous splenic hemorrhages as a potential cause of acuteneonatal compromise, even in the absence of birth-related trauma (e.g., asphyxia, prolonged labor, clavicle fractures,
brachial plexus injuries). This report emphasizes the importance of including splenic hemorrhage timely in the differential diagnosis of neonatal cardiorespiratory instability, especially in the absence of more common diagnoses,
and discusses the challenges associated with its recognition and treatment.
Keywords Splenic hemorrhage, Splenic bleeding, Neonate, Case report, Birth trauma*Correspondence:
Tim Hundscheid
tim.hundscheid@radboudumc.nl
1
Department of Pediatrics, Division of Neonatology, Radboud University
Medical Center, Amalia Children’s Hospital, Nijmegen, The Netherlands
2
Department of Pediatrics, Radboud University Medical Center Radboud
University Medical Center, Amalia Children’s Hospital, Nijmegen, The
Netherlands
3
Department of Pediatric Surgery, Radboud University Medical Center
Radboud University Medical Center, Amalia Children’s Hospital, Nijmegen,
The Netherlands
4
Department of Pathology, Radboud University Medical Center,
Nijmegen, The Netherlands
5
Department of Medical Imaging, Radboud University Medical Center,
Nijmegen, The Netherlands

Background
Cardiorespiratory failure in newborns can be regarded
as a final common pathway, with a broad spectrum ofpotential underlying diagnoses. The primary considerations encompass sepsis, pulmonary hypertension,
abdominal problems (e.g., obstruction, or necrotizing
enterocolitis (NEC) in premature cases), blood loss (e.g.,
due to birth trauma or coagulation disorders, with cerebral bleeding being the most common), a (congenital)
cardiac disorder or an inborn error of metabolism [1].
The diagnostic assessment involves the initial eliminationand preemptive treatment of these most prevalent and/or life-threatening causes. However, when the cause of
cardiorespiratory failure remains unknown after rulingout the most common causes, this article aims to demonstrate the importance of timely considering splenic hemorrhage in the differential diagnosis.

© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which
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Jansen et al. BMC Pediatrics(2024) 24:564

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In children, a splenic hemorrhage most often resultsfrom blunt trauma [2, 3]. As the spleen is a highly vascular organ, there is a high risk of cardiorespiratory failure
due to hypovolemic shock when a splenic hemorrhage
occurs [4]. The clinical presentation of neonatal splenic
hemorrhage is often nonspecific and may include pallor,anemia, abdominal distention, and eventually cardiorespiratory failure [1].
This report describes two cases of splenic hemorrhage
in neonates as primary cause of cardiorespiratory failure,including a description of symptoms, diagnostics tests,
management and outcome.

Case description
Case 1This case involves a full-term male neonate who was bornafter an uncomplicated pregnancy and delivery, with abirth weight of 4400 g (p98). After clinical observation
due to being large for gestational age with adequate glucose levels, he was discharged home. After intermittent
non-alarming feeding difficulties within the first few
days, on the third day, he was found unresponsive, pale,and floppy in his bed. The emergency services noticed atense abdomen and asystole. Resuscitation was started
according to current advanced life support guidelines,
which involves the administration of fluid boluses (totalof 20 ml/kg isotonic saline) and adrenaline (every 5 min
10 mcg/kg). As the cause of asystole remained unclear
after forty minutes, resuscitation was discontinued as nofurther recovery was anticipated, after which the patient
deceased.
Post-mortem diagnostics were performed with parental consent to determine the cause of death. The mostremarkable finding was a hemoglobin (Hb) level of 0,8mmol/L. There were no signs of infection, with a C-reactive protein (CRP) of 9 mg/L, negative blood and spinal
fluid cultures, as well as fecal and nasopharyngeal polymerase chain reaction tests. Magnetic resonance imaging(MRI) and computed tomography (CT) showed massive
hemorrhage in and around the spleen (Fig. 1). Differential
diagnostic causes included a spontaneous hematoma of
the spleen or pathological mass (e.g., congenital hemangioma or another tumor). There were no fractures or(other) traumatic injuries visible, and no congenital malformations were observed.
At autopsy, the most remarkable findings included
a very pale skin color, few corpse stains and a slightly
bulging abdomen, all indicative of a large hemorrhage.
Furthermore, macroscopic examination revealed enlargement of all organs, along with the presence of a partly friable and partly solid blood clot weighing 56 g, adhered
to the spleen. A ruptured capsule on the spleen’s edge,
with accompanying blood clot and fragments of spleenFig. 1 coronal T2 MR image of patient 1, performed postmortem.
There is diffuse intra-abdominal blood. The arrow indicatesthe enlarged and inhomogeneous spleen. The image is indicative
for a large splenic hemorrhage with capsular rupture

tissue indicated that the blood originated from the spleen.
There was no evidence of trauma to the inner thoracic or
abdominal walls, tumors, or vascular malformations, nor
was there any sign of non-accidental injury. In the casehistory, there were no individuals in the family with coagulation problems, cardiovascular diseases at a young age,or acute cardiac death. Whole exome sequencing did notindicate any underlying hematological or metabolic disease. The probable cause of death was identified as a neonatal splenic hemorrhage, possibly after a birth trauma,considering the infant’s birth weight.
Case 2

An extremely premature male infant, born after
24 + 5/7 weeks gestation with a birth weight of 650 g(p15), presented with acute cardiorespiratory failure

Jansen et al. BMC Pediatrics(2024) 24:564

at the postnatal age of two weeks. His medical history includes infant respiratory distress syndrome andapnea of prematurity. He received non-invasive respiratory support and caffeine. Two days before his clinical deterioration, he was extubated after the initiationof dexamethasone. Because of a suspected nosocomial
infection, he received flucloxacillin and gentamicin
until last evening. Antibiotics were discontinued after
low inflammatory markers and negative blood culture.
Echoencephalography showed an intraventricular hemorrhage grade 2 on the left side and periventricularechogenicity grade 1 on both sides of the brain.
His cardiorespiratory failure presented with a drop in
his basal heart rate to 110 beats/minute without variation with numerous bradycardias. Clinical assessment
showed a pale child, peripherally poorly circulated withincreased work of breathing and tachypnea. Apart froma somewhat swollen abdomen, there were no indications of an abdominal problem. His arterial bloodpressure measured 44/26 mmHg, with a mean of 35
mmHg. Despite the relatively low systolic pressure forhis age, the mean blood pressure remained relatively
normal. Arterial blood gas analysis showed a pH of
6.56, ­pCO2 8.5 kPa, and remarkably, a hyperlactatemiaof 13 mmol/L. The differential diagnoses included primary respiratory failure, primary cardiac failure, sepsis,
abdominal focus, or blood loss.
He was intubated with low respiratory settings andFraction of Inspired Oxygen ­(FiO2) of 0.4, making a primary respiratory problem less likely. Echocardiography
showed a biventricular dysfunction with left ventricular
dilatation, without primary cardiac pathology. The poor
myocardial function was attributed to the metabolic
dysregulation of the patient and was supported with
dobutamine and a fluid bolus. Despite these interventions, the lactate levels rose to 17 mmol/L with a pH
below the measurable threshold. Therefore, noradrenaline was administered, and dexamethasone was substituted for hydrocortisone. Sodium bicarbonate wasadministered to correct the metabolic acidosis. An
overview of the most important blood results over 24 h
is presented in Fig. 2.
Despite the recent discontinuation of gentamicin andflucloxacillin, the onset of severe cardiorespiratory failureand colonization with Enterobacter cloacae and Serratia
marcescens prompted the initiation of high dose meropenem. Blood cultures did not grow a pathogen, which led
to the discontinuation of antibiotics after four days.
Prior to the clinical deterioration, feeding was well tolerated, and defecation was normal. Despite some abdominal distension, no other features of NEC were seen on
clinical examination by the pediatric surgeon and an
abdominal X-ray revealed no abnormalities. Due to the

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significant clinical decline, enteral nutrition was halted
and substituted for total parenteral feeding.
As the hemoglobin rate dropped from 6.6 to 6 mmol/L
in 24 h, an echoencephalography was performed, showing no signs of bleeding. In absence of a clear diagnosis,
an abdominal ultrasound was performed by the pediatricradiologist. A capsulated fluid collection with an amorphous structure was found in the left upper abdomen.
The structure caused compression on the spleen andstomach caudally, measuring 28 × 26 × 37 mm, estimatedvolume of 14 ml. Therefore, the ultrasound diagnosis wasconsistent with a subcapsular hemorrhage of the spleen(Fig. 3). As the hemorrhage of the spleen was confined tothe subcapsular space and the symptoms were stabilizing,a surgical intervention was not indicated, and conservative management including repeated evaluation by thepediatric surgeon continued.
After the first fluid bolus (10 mL/kg), two erythrocytetransfusions (total 30 mL/kg), fresh frozen plasma (15 ml/kg), vitamin K 0.5 mg and circulatory support with dobutamine (maximum of 5.0 mcg/kg/min), hydrocortisone(5 mg/kg/day) and noradrenaline (maximum of 0.2 mcg/
kg/min), cardiorespiratory stabilization was achieved, as
depicted in Fig. 2. Within 24 h after the deterioration,
dobutamine could be stopped and the noradrenaline wasweaned. Four days later, the infant could be extubated to
non-invasive respiratory support.
After hematological examination, no evidence wasfound for a coagulation disorder. On the acute moment
there was prolongation of clotting times which was likely
secondary to consumption during bleeding. Follow-up
indicated normalization of clotting times.
There were no signs of organ dysfunction following
the period of cardiorespiratory distress. Echoencephalographic follow up and MRI of the brain at term equivalent
age showed no abnormalities. A follow-up abdominal
ultrasound four weeks later showed a decreased volumeof the splenic hemorrhage. Clinically, he recovered wellfrom the incident and actual functions within the normal
spectrum of an extremely preterm infant.

Discussion
This report elucidates the potential implications of neonatal splenic hemorrhage leading to acute and severe cardiorespiratory failure.
Since the description of neonatal splenic rupture in1967 [5], additional cases have been described and linked
to birth trauma [4, 6]. The clinical presentation of neonatal splenic hemorrhage is often non-specific, with symptoms ranging from pallor, anemia, abdominal distention
to cardiorespiratory failure [4]. A few case reports haveeven mentioned scrotal abnormalities as the sole symptom of a splenic rupture [7]. Most splenic hemorrhages

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Fig. 2 A L-lactate levels over time since the onset of cardiorespiratory insufficiency. B pH value over time since the onset of cardiorespiratory
insufficiency. C Blood count values at the day of the cardiorespiratory insufficiency

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Fig. 3 A. Transversal and B. sagittal ultrasound of case 2. The arrow indicates the fluid (hemorrhage) in the left upper abdomen. The arrowhead
indicates the splenic parenchyma forming a border of the hemorrhage

occur within hours to several days after birth [4, 6, 8],
supporting the primary hypothesis that birth trauma
plays an important role in the occurrence of splenic hemorrhages. Increased intrathoracic pressure during birth
may force the liver and spleen out of the diaphragmatic
hollow. The pressure on the supporting ligament could
potentially lead to splenic rupture by forming a subcapsular hematoma, followed by rupture of the capsule
which leads to a hemodynamic instable patient [9]. Thiswas possible the cause of the splenic hemorrhage in our
first case considering the clinically notable swollen abdomen at presentation. In that case, the hematoma shouldhave occurred during birth, and the capsule rupture threedays later, after which his clinical condition deteriorated
acutely.
Chang et al. presented a spectrum in the outcome after
splenic hemorrhage. Notably the outcome ranged frommortality to complication-free survival irrespective ofhemoglobin levels and traumatic or non-traumatic birth[4]. However, neonatal non-traumatic splenic hemorrhages are exceptionally rare and, consequently, theyreceive less consideration in the absence of anticipatedbirth trauma [4, 9]. Due to the low incidence of splenic
rupture, systematic ultrasound screening of the spleen
has not been conducted after traumatic or non-traumaticbirth.
In our second case, the occurrence of a splenic capsularhemorrhage at the age of two weeks renders a traumatic
hemorrhage due to a traumatic event at birth unlikely
and emphasizes the lack of clarity regarding the precise
pathophysiology of splenic hemorrhage [9].
Our second patient was an extremely premature neonate, a condition for which there are limited cases ofsplenic hemorrhage reported in the literature. One suchcase involved a neonate born after 27 weeks’ gestation[11]. In this case, clinical signs of hypovolemic shock,accompanied by metabolic acidosis and a decreased
hemoglobin level 20 h postnatally, prompted urgent
intervention. Surgical exploration revealed a subcapsularsplenic hemorrhage, successfully managed without splenectomy, albeit with postoperative complications such asa subcapsular hematoma of the liver, acute renal failure,and disseminated intravascular coagulation [10].
In another case, a preterm neonate delivered at 32
weeks’ gestation, the challenges in managing cardiorespiratory failure attributed to splenic hemorrhage were
evident. An emergency caesarean section was performed
due to abnormal fetal heart rhythms, with a difficult
extraction. The Apgar score was 3/3/3, with a venous pHof 7.31 and a cord hemoglobin level of 8.7 mmol/L The
neonate required intubation at 10 min postpartum. At
three hours of age, an acute episode of cardiorespiratory
failure transpired, accompanied by disseminated intravascular coagulation and severe anemia (Hb 2.7 mmol/L).
Nine hours later an abdominal ultrasound revealed a substantial subcapsular splenic hematoma with associatedhemoperitoneum. Despite judicious fluid management,
the prognosis remained unfavorable due to multi-visceralfailure, hepatocellular insufficiency, and pulmonary arterial hypertension treated with nitric oxide. Additionally,
there was severe neurological impairment. Considering
the unfavorable prognosis and hemodynamic instability,
surgical intervention was considered impractical, resulting in the discontinuation of intensive care treatment [8].
In the described cases, the question arises as to whether
earlier consideration of splenic hemorrhage could have
prevented severe complications or, more critically, a fatal
outcome.
Currently, conservative management is the primary
treatment for (blunt) splenic injuries in children. With
conservative management splenic function might bepreserved [2, 3, 11, 12]. Recent data also indicate that

Jansen et al. BMC Pediatrics(2024) 24:564

the degree of cardiac insufficiency and, in particular,
response to fluid resuscitation determine whether surgery is necessary [2, 11]. Given the eventual favorable
response observed after fluid resuscitation, the subcapsular splenic hemorrhage was managed conservatively
in the second case. In case of an ongoing splenic hemorrhage with persistent cardiorespiratory insufficiency,
surgical therapy would have been indicated, which considering the patient’s weight and age, would have meant
splenectomy rather than embolization.
This report elucidates the potential implicationsof neonatal splenic hemorrhage leading to acute andsevere cardiorespiratory failure. In both cases, extensive
diagnostics were conducted, and empirical treatment
initiated prior to the final diagnosis. Notably, splenic
hemorrhage was not initially considered in the differential diagnosis by the attending pediatricians or neonatologists, underscoring the challenge in early identificationand treatment. Given the rarity of the condition, thesetwo cases provide relevant new insights into the clinicalaspects and outcomes of splenic hemorrhage. As splenic
hemorrhage can present in various ways, we underscorethe significance of incorporating splenic hemorrhage asa pertinent consideration among potential diagnoses forneonatal acute cardiorespiratory failure.
Abbreviations
CRP	C-reactive protein
CT	Computed tomography
Hb	Hemoglobin
kg	Kilogrammcg	Microgrammg	Milligram
MRI	Magnetic resonance imaging
NEC	Necrotizing enterocolitis
Acknowledgements
In both cases, we obtained Informed consent of the patients’ parents topublish this article. At the request of Boet’s parents, this case report is written
in memory of Boet (Case 1).
Authors’ contributions
NJ was a major contributor in writing the manuscript and analyzed the dataof the patient files. AD interpreted the patient data of case 1 and revised themanuscript. MB interpreted the patient data of case 2 regarding the surgicalopinion and also reviewed the manuscript. BK performed the pathologicalexamination of the patient in case 1 and reviewed the description of theexamination in the manuscript. WK performed the radiological evaluationof the patient images and collected the images for the manuscript andprepared the documentation of the radiological images. She also reviewed
the manuscript. TH made a significant contribution to writing the manuscript
and provided additional information from the neonatology perspective. All
authors read and approved the final manuscript.
Funding
Not applicable.
Availability of data and materials
No datasets were generated or analysed during the current study.

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Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
In both cases, we obtained Informed consent of the patients’ parents topublish this article. At the request of Boet’s parents, this case report is written
in memory of Boet (Case 1).
Competing interests
The authors declare no competing interests.
Received: 3 April 2024 Accepted: 8 August 2024

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