Tekle et al.
Malaria Journal (2025) 24:146 Malaria Journal
https://doi.org/10.1186/s12936-025-05386-7
CASE REPORT Open Access
Splenic infarction in a paediatric patient
with Plasmodium vivax malaria from Ethiopia:
a case report
Alemayehu Beharu Tekle1*, Tamirat T. Bekele2, Alemu B. Solbamo2, Molla A. Kebede3, Melaku T. Berhanu4 and
Dereje D. Baramo5
Abstract
Background Splenic infarction is an uncommon but serious side effect of Plasmodium vivax malaria, especially
in young patients. Prompt diagnosis and effective treatment are essential to avoid serious consequences. Though
there are few report of splenic infarction following P. vivax from different endemic country, PubMed and Google-
based literature search found that it was the first case report of this type from Ethiopia.
Case presentation The patient was an 11-year-old girl, from Wolaita Sodo, Ethiopia, who had a high-grade fever,
chills, rigors, headache, vomiting, and abdominal pain in the left upper quadrant. Upon examination, hepatomegaly,
splenomegaly, and extreme pallor were found. Laboratory tests revealed acute kidney injury (creatinine 1.63 mg/
dL), acute liver injury (AST 323 U/L, ALT 129 U/L), and severe anaemia (haemoglobin 3.4 g/dL, haematocrit 10.2%).
A peripheral blood smear showed a trophozoite stage of P. vivax and was negative for Plasmodium falciparum.
An abdominal ultrasound revealed hepatosplenomegaly along with a wedge-shaped, multifocal, hypoechoic splenic
region that was consistent with an infarction.
Management and outcome The patient had blood transfusions, NSAIDs for pain, and intravenous artesunate
as treatment. Primaquine was used in radical therapy. After three days, her abdominal pain had considerably subsided
and she became afebrile. Complete symptom relief, normalized abdominal ultrasound findings, and better laboratory
results—including normal haemoglobin and liver enzymes—were all observed at the two-month follow-up.
Conclusion This case underscores the importance of considering splenic infarction in paediatric patients with P.
vivax malaria presenting with abdominal pain. Early recognition through imaging and laboratory investigations,
along with prompt antimalarial therapy, is critical for favourable outcomes.
Keywords Plasmodium vivax, Splenic infarction, Ethiopia, Pediatric malaria
*Correspondence:
Alemayehu Beharu Tekle
alemayehub.tekle@wsu.edu.et
Full list of author information is available at the end of the article
© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0
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Tekle et al. Malaria Journal (2025) 24:146 Page 2 of 5
Background Case presentation
Malaria is still a major global health issue, especially An 11-year-old girl from Wolaita Sodo, Ethiopia, pre-
in tropical and subtropical areas. It is estimated that sented with a four-day history of high-grade, inter-
627,000 people died from malaria worldwide in 2020, mittent fever accompanied by chills, rigors, headache,
out of an estimated 241 million who were infected and two episodes of non-bloody, non-bilious vomiting.
with the disease. Humans contract these protozoans She also reported left upper quadrant abdominal pain
from infected Anopheles mosquito vectors [1–3]. Plas- that had been present for two days and worsened sig-
modium vivax is the second most important parasite nificantly over the past 24 h. There was no history of
of human malaria widely perceived as causing mild jaundice, dark-colored urine, diarrhoea, or abdominal
and self-limited illness [4]. Almost all severe forms of trauma.
malaria are caused by Plasmodium falciparum, but On examination, her vital signs were stable: temper-
recently there have been reports of serious complica- ature 38.2 °C, pulse rate 80 beats/min, blood pressure
tions such as myocardial infarction, severe anaemia, 110/60 mmHg, and respiratory rate 14 breaths/min.
respiratory distress, splenic complications, shock, She weighed 31 kg, measured 143 cm in height, and had
and multiple organ dysfunction also develop with P. a BMI of 15.5 kg/m2 (within the normal range on the
vivax infection among children from endemic regions Z-score). She appeared pale but was anicteric. Abdomi-
such as Indonesia, India and Brazil [5–9]. nal examination revealed a tender spleen palpable 6 cm
Anaemia, leucopenia, and thrombocytopenia are below the left costal margin and a soft, non-tender liver
known haematological changes that occur in malaria palpable 4 cm below the right costal margin. Other sys-
[10]. Splenic complications identified in cases of temic examinations were unremarkable.
malaria are splenic infarction, spontaneous splenic Laboratory studies showed severe anaemia (haemo-
rupture, hyperreactive malarial syndrome, hypersplen- globin 3.4 g/dL, haematocrit 10.2%), acute liver injury
ism, ectopic spleen and splenic torsion, and splenic (AST 323 U/L, ALT 129 U/L), and acute kidney injury
cysts. Splenic infarction is not usually noted and is (creatinine 1.63 mg/dL). Peripheral blood smear con-
likely underdiagnosed in many cases of complicated firmed the trophozoite stage of P. vivax and was nega-
malaria [9, 11–13]. tive for P. falciparum (Table 1).
Blood filtering and pathogen removal depend on the Abdominal ultrasound revealed hepatomegaly with a
spleen. The sequestration of parasitized red blood cells homogenous echo pattern and splenomegaly (16.3 cm)
in malaria results in splenic enlargement and dysfunc- with peripheral, multifocal, wedge-shaped hypoechoic
tion. Splenic infarction may develop from the conges- areas, the largest measuring 4.2 × 2.6 cm, indicative of
tion that results from underlying vascular dysfunction. splenic infarction (Fig. 1). Doppler imaging showed no
Children who are dehydrated, anaemic, or co-infected blood flow in these areas.
with various infections are at risk for splenic infarc- The patient was treated with intravenous artesunate
tion [14, 15]. Splenic infarction patients frequently and NSAIDs for pain relief. She received two whole
experience fever, splenomegaly, and abdominal pain. blood transfusions at 20 mL/kg each and was initiated
Children’s symptoms can be ambiguous and could be on radical therapy with primaquine. Her condition
confused with those of other conditions like appen- improved steadily; she became afebrile three days after
dicitis or gastroenteritis. Because they often reveal starting anti-malarial treatment, and the abdominal
splenic necrosis, imaging tests—particularly CT and pain gradually subsided.
ultrasound scans—are essential for the diagnosis [15, At discharge, on the tenth day of admission, follow-
16]. up investigations showed significant improvement, with
In their assessment of severe sequelae linked to P. haemoglobin levels rising to 11.6 g/dL and normaliza-
vivax malaria, Rizvi et al. [17] pointed out that splenic tion of liver and kidney function tests. The patient was
infarction was underreported but that, if not identified closely monitored for complications, including splenic
promptly, could result in serious morbidity. The neces- rupture, abscess formation, and sepsis.
sity of doctors being more cognizant of this possible At a two-month follow-up, the patient was asymp-
consequence was underlined. tomatic. Abdominal pain had completely resolved, the
This report describes the case of a young girl present- spleen and liver were no longer palpable, and repeat
ing with splenic infarction in acute vivax malaria. ultrasound findings were normal.
Tekle et al. Malaria Journal (2025) 24:146 Page 3 of 5
Table 1 Relevant investigations of patient
S. No Investigation done Parameters Normal reference On admission (Day 1) On Discharge (Day 10)
value for her age
1 CBC WBC 4–10.5 µm3 4500 cells/mm3 4600 cells/mm3
Lymphocytes 25–33% 32% 31%
Granulocytes 54–62% 56.3% 52%
Haemoglobin 12.5–16.1 g/dl 3.4 g/dl 11.6 g/dl
Haematocrit 36–47% 10.2% 39.8%
Platelet 150–450 × 103 µL 436,000 400 × 103 µL
2 Peripheral blood film Thin and thick No hemo parasite Trophozoite stage of P. vivax
blood smear
3 Serum bilirubin Total < 1 mg/dl 0.8 mg/dl
Direct < 1 mg/dl 0.2
4 Liver enzyme test AST 10-40U/L 323U/L 39 U/L
ALT 5-45U/L 129U/L 30 U/L
5 Serum electrolyte Potassium 3.5–5.5 meq/l 3.5 meq/l
Sodium 135-145 meq/l 139 meq/l
Calcium total 8.8–10.8 mg/dL 10 mg/dl
6 Renal function test Creatinine 0.31–0.88 mg/dl 1.63 mg/dl
BUN 7-18 mg/dl 14
7 Urine analysis Blood Negative +3 Negative
Protein Negative Negative Negative
Discussion Abdominal pain can result from a number of malar-
A young patient with splenic infarction—a rare but ial consequences, including pancreatitis, hepatitis/
dangerous side effect of P. vivax malaria—is depicted in hepatomegaly, acalculous cholecystitis, acute surgical
the case study. Plasmodium vivax was once believed to abdomen, splenic rupture, splenic infarction, splenic
be a benign species that mostly caused mild infections, torsion, and acute renal failure [19, 20].
but it has recently been connected to severe side effects Clinically, splenic infarction is difficult to diagnose
such splenic infarction, acute kidney injury (AKI), since symptoms, such as fever and abdominal pain, are
and anaemia, particularly in endemic areas like Brazil, vague and can be mistaken for other illnesses such as
Indonesia, and India [4–6]. appendicitis or gastroenteritis [15]. In this instance,
Only a few cases of splenic infarction following P. abdominal ultrasonography indicated splenic infarction
vivax infection have been reported in the English litera- due to splenomegaly and pain in the left upper quad-
ture, and this is the first documented case from Ethio- rant. Imaging tests are still essential for detecting this
pia. This is likely not due to the rarity of the condition, issue; ultrasound reveals hypoechoic, wedge-shaped
given that Ethiopia is a malaria-endemic country, but lesions that are suggestive of an infarction. The lack of
may rather be due to underreporting [10, 18]. blood flow in the afflicted areas was further verified by
Splenic infarction in malaria has a complicated aeti- Doppler imaging [16].
ology. The spleen, an essential organ for blood filtration In this instance, treatment focused on using intrave-
and immunological response, expands and becomes nous artesunate to treat the underlying P. vivax malaria,
obstructed as a result of immune cell invasion and par- primaquine for radical therapy to avoid relapse, and
asitized red blood cell sequestration. This splenic con- NSAIDs and blood transfusions to manage symptoms.
gestion, which is made worse by vascular dysfunction, Over a two-month follow-up period, the youngster
dehydration, anaemia, and other co-infections, puts reacted nicely, with all symptoms completely resolved
patients at risk for infarction [14, 15]. and haematological, renal, and hepatic values returning
Severe anaemia (haemoglobin 3.4 g/dL, haematocrit to normal. This highlights the need of early diagnosis
10.2%) and AKI (creatinine 1.63 mg/dL) were clearly and appropriate treatment in achieving optimal out-
contributing factors in this patient, aggravating splenic comes in patients of splenic infarction.
hypoxia and vascular stasis. This case confirms findings in the literature that P.
vivax malaria sequelae are underreported and can
Tekle et al. Malaria Journal (2025) 24:146 Page 4 of 5
Fig. 1 Abdominal ultrasound showing splenic infarct
cause severe morbidity if not detected promptly, even AST Aspartate transaminase
BUN Blood urea nitrogen
though they are rare. As emphasized by Rizvi et al. [17], AKI Acute kidney injury
greater clinician awareness is essential for the timely NSAIDS Non steroidal anti inflammatory drugs
diagnosis of splenic infarction, especially in endemic
Author contributions
areas where P. vivax is prevalent. ABT, TTB, and ABS were involved in the conception and design of the study,
drafting and revising of the article, and final approval of the version to be sub-
mitted and also involved in direct patient management. MAK, MTB, and DDB
were involved in the conception and design of the study, drafting and revising
Conclusion the article, and final approval of the version to be submitted.
As demonstrated by this example, P. vivax malaria can
no longer be considered consistently benign. Despite Funding
The case report, authorship, and/or publication of this work did not receive
their rarity, complications like splenic infarction call any specific grant from funding agencies in the public, commercial, or not-for-
for caution, particularly in children who exhibit sple- profit sectors.
nomegaly and abdominal pain. Adequate anti-malarial
Data availability
treatment, early imaging, and careful monitoring are On a valid request, the corresponding author will provide access to the data-
essential for guaranteeing recovery and averting nega- sets that were gathered and used to conduct this article.
tive consequences.
Abbreviations
CBC Complete blood count
ALT Alanine transaminase
Tekle et al. Malaria Journal (2025) 24:146 Page 5 of 5
Declarations 17. Rizvi I, Tripathi DK, Chughtai AM, Beg M, Zaman S, Zaidi N. Complications
associated with Plasmodium vivax malaria: a retrospective study from a
Ethics approval and consent to participate tertiary care hospital based in Western Uttar Pradesh. India Ann Afr Med.
The need for ethical approval was waived. 2013;12:155–9.
18. Aggarwal V, Nagpal A, Agrawal Y, Kumar V, Kanwal SK, Dhingra B. Plas-
Informed consent modium vivax malaria complicated by splenic infarct. Paediatr Int Child
Before preparing the case report, the patient’s family provided written Health. 2014;34:63–5.
informed consent to write the case and be published. 19. Singh J, Dinkar A, Atam V, Atam I. An uncommon presentation of severe
falciparum malaria: acute pancreatitis. Int Res J Med Sci. 2014;2:1–5.
Competing interest 20. Seshadri P, Dev AV, Viggeswarpu S, Sathyendra S, Peter JV. Acute pancrea-
The authors declare no competing interests. titis and subdural haematoma in a patient with severe falciparum malaria:
case report and review of literature. Malar J. 2008;7:97.
Author details
1
Department of Emergency and Critical Care Medicine, School of Medicine,
Wolaita Sodo University, Wolaita Sodo, Ethiopia. 2 Department of Pediatrics
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in pub-
and Child Health, School of Medicine, Wolaita Sodo University, Wolaita Sodo,
lished maps and institutional affiliations.
Ethiopia. 3 Department of Internal Medicine, School of Medicine, Mizan-Tepi
University, Mizan‑Teferi, Ethiopia. 4 Department of Emergency and Critical Care
Medicine, School of Medicine, Asrat Woldeyes Health Science College, Debre
Berhan University, Debre Berhan, Ethiopia. 5 Department of Radiology, School Alemayehu Beharu. Tekle is an Assistant Professor of Emergency
of Medicine, Yirgalem Hospital Medical College, Yirgalem, Ethiopia. and Critical care medicine, Department of Emergency and critical
care medicine, School of Medicine, College of Medicine and Health
Received: 27 January 2025 Accepted: 26 April 2025 Sciences at Wolaita Sodo University, Ethiopia. AB is Medical Doctor
and has Specialty Certificate in Emergency and critical care medicine
Tamirat T. Bekele is an Assistant Professor of Pediatrics and Child
health, Department of Pediatrics and Child health, School of Medi-
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