Pulmonary Artery Thrombus in a Growth Faltering Infant with Acinetobacter Sepsis

Pulmonary Artery Thrombus in a Growth Faltering Infant with Acinetobacter Sepsis | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Pulmonary Artery Thrombus in a Growth Faltering Infant with Acinetobacter Sepsis Allison T. Ong, Mariah Zakharia, Julia Green, Vikranth Raja, Natalia Jelen, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7983131/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Primary thromboembolism of the pulmonary artery (PTE) is a rare finding in infant patients. Contributors to infant hypercoagulability include inherited thrombophilias, immature anticoagulation systems, and systemic insults such as septic shock and liver disease. Case Presentation: We present the case of a 7-week-old girl with in-utero HIV exposure diagnosed with a pulmonary artery thromboembolism (PTE). The patient was admitted to the pediatric intensive care unit (PICU) for sepsis in the setting of Acinetobacter nosocomialis bacteremia, growth faltering, and an S4 gallop. Echocardiogram revealed a mass in the pulmonary artery, prompting urgent treatment with thrombectomy. We hypothesize that septic shock, with associated coagulopathy and severe dehydration, contributed to thrombophilia in this critically ill patient. Conclusions This case highlights the rapid, multidisciplinary approach to diagnosing PTE and the underlying factors contributing to thrombophilia in an infant. Early recognition and timely surgical intervention are essential for optimizing patient outcomes. Clinical trial number: not available thromboembolism thrombophilia thrombus sepsis infant critical care HIV case report Figures Figure 1 INTRODUCTION Pulmonary thromboembolism (PTE) is a rare but life-threatening condition in infants, with a mortality rate up to 26% under one year of age. 1 Risk factors in this age group include infection, catheter venous access, congenital heart disease, and thrombophilic states either inherited or acquired. While ultrasound aids in initial evaluation, CT angiography remains the preferred imaging modality for assessment of circulation and surgical planning. We discuss a unique case of PTE in an infant presenting with septic shock, poor weight gain, a heart murmur, and hypoxia. Early recognition and timely multidisciplinary intervention are essential for optimizing patient outcomes and preventing cardiovascular collapse. Further research is needed to improve prevention strategies, and treatment approaches in this age group. PATIENT INFORMATION A 7-week-old female presented to the emergency room with one day of non-bloody diarrhea, feeding intolerance, and weight loss, measuring less than her birth weight of 2.6 kg. Born full-term to an HIV-positive mother with close prenatal care and an undetectable viral load during pregnancy, she had completed a course of AZT at birth and had negative HIV PCR tests at 0 and 14–21 days of life. Her newborn screen showed possible hemoglobin C trait. Until admission she had been ingesting 2 ounces of standard formula every 2 hours without significant reflux or feeding difficulties. Her mother denied fever, sick symptoms, perioral cyanosis, or significant family history. She was hypothermic (35.1°C), tachycardic (HR 155 bpm), and tachypneic (RR 42 br/min). On exam she appeared lethargic, limp, and responsive only to painful stimuli with cachexia, poor skin turgor, and a blood glucose level of 50 mg/dL. While attempting IV access, she became briefly unresponsive, requiring intraosseous access placement, fluid resuscitation with 30 cc/kg normal saline, and initiation of sepsis protocol. Oxygen was administered via nasal cannula for desaturation into the high 80s. Initial labs revealed leukocytosis (WBC 25.6 × 10³/µL, ANC 13.1), bandemia (7%), and elevated CRP (16.8 mg/L). She was started on empiric antibiotics with cefotaxime, vancomycin, and acyclovir and admitted to the PICU for management of sepsis and growth faltering. On day 2, she was noted to have an S3/S4 gallop. Echocardiography revealed an echogenic mass in the right main pulmonary artery causing partial flow obstruction, right atrial dilation, and an ASD with right-to-left shunting (Fig. 1 ). A positive blood culture for Acinetobacter nosocomialis raised concern for infective endocarditis with septic embolization. With high risk for thrombus and massive PE, anticoagulation was also initiated with a heparin drip. She remained subtherapeutic despite titrating the drip to anti-Xa levels per hospital protocol, prompting a switch to bivalirudin. On hospital day 6, she underwent pulmonary thrombectomy, main pulmonary artery and SVC patch plasty, PFO closure, and PDA ligation via median sternotomy. The thrombus was adherent to denuded endothelium, directing the team to manage the patient for infective endocarditis. Postoperatively she was treated with ampicillin/sulbactam (100 mg/kg q6h), later transitioning to oral levofloxacin (10 mg/kg q12h) to complete a 6-week course. Chest tubes were removed on post-op day 3, and she transitioned to enoxaparin for long-term anticoagulation with plans to determine length of treatment as outpatient. Her inpatient hypercoagulability workup was unremarkable (Table 1 ). The thrombotic event was considered multifactorial due to sepsis, dehydration, and endothelial injury. Table 1 Thrombophilia Workup in an Infant Clinical Category Test Name Result Reference Range Interpretation Genetic Mutations Factor V Leiden Mutation Analysis WILD TYPE Negative/Positive Normal Prothrombin G (20120) Mutation Analysis WILD TYPE Negative/Positive Normal Clotting Cascade Derangements Factor VIII 0.77 U/mL 0.54–1.55 U/mL Normal D-dimer 2.49 mcg/mL 0.0-0.49 mcg/mL High Protein C Activity Level 84% 81–140% Normal Protein S Activity Level 59% 62–148% Low Antithrombin III Level 29% 75–110% Low Activated Partial Thromboplastin Time (aPTT) 43 seconds 23–34 seconds Prolonged Antiphospholipid Syndrome Lupus Anticoagulant Negative Negative/Positive Normal Cardiolipin Antibody Negative Negative/Positive Normal Beta 2 Glycoprotein Negative Negative/Positive Normal Polycythemias Hemoglobin 8.4 g/dL 9.5–14.5 g/dL Low Hematocrit 23% 42–66% Low Platelet count 59x10 3 /mcL 150–350 x10 3 /mcL Low Von Willebrand Disease Von Willebrand Factor Activity 190% 43–127% High DISCUSSION Primary thromboembolism of the pulmonary artery (PTE) is a rare and often fatal finding in pediatric patients. We identified a case of PTE in an infant and swiftly intervened to prevent cardiorespiratory collapse. Pediatric thrombotic events follow a bimodal distribution, with a peak during the neonatal period due to central venous catheter use in the NICU and a peak during adolescence when adult thrombotic risk factors emerge. 2 Contributors to infant hypercoagulability include inherited thrombophilias and systemic insults such as septic shock, disseminated intravascular coagulation (DIC), and liver disease. Additional risk factors include maternal lupus, maternal diabetes, chorioamnionitis, and indwelling intravascular catheter use in the NICU. Furthermore, infants may be at increased risk for thrombi due to an immature anticoagulation system, which reaches maturation around 6 months of age. 3 Since the initial thrombophilia workup was normal and there was no evidence of structural cardiac disease, we believe the primary contributing factor was septic shock secondary to Acinetobacter nosocomialis , the subsequent dehydration from feeding and low oral intake contributing to venous stasis. Several reports suggest that in-utero HIV exposure alone may increase the risk of infectious morbidity and hypercoagulability in neonates even when the disease is not transmitted. 4 Inflammatory cytokine responses and antiretroviral therapy in HIV-positive mothers have been shown to affect maternal-fetal transfer of placental antibodies, potentially reducing immune protection against certain opportunistic infections. 5 Impaired immunity in our infant would have predisposed her to systemic infection with Acinetobacter nosocomialis, a bacteria thriving in wet environments that is primarily implicated in nosocomial catheter-based infections, respiratory illness, or urinary tract infections. Acinetobacter species are increasingly implicated in the neonatal population. A newborn’s early microbiome is especially vulnerable to colonization and gut translocation by harmful gram-negative bacteria. 7 , 8 Management of PTE involves anticoagulation, thrombolytics, and/or mechanical thrombectomy to prevent progression to pulmonary embolism and obstructive shock. The 2018 American Society of Hematology Guidelines for pediatric VTE serve a valuable foundation for discussion when selecting from these options. 9 Our patient was managed as a symptomatic DVT and started on anticoagulation without thrombolysis. Initial anticoagulation options include TPA, low molecular weight heparin, and heparin. In cases where tPA is contraindicated, heparin proves ineffective, or when heparin-induced thrombocytopenia (HIT) or antithrombin III deficiency is suspected, direct thrombin inhibitors such as bivalirudin and argatroban should be considered. Direct thrombin inhibitors do not require antithrombin III to be effective, and bivalirudin specifically has shown promising evidence in pediatric populations. 10 In our case, the patient was transitioned to bivalirudin with an aPTT goal of 60–80 after failing to achieve therapeutic goal on heparin. Given the concern for thrombus growth and massive pulmonary embolism, the patient also underwent mechanical thrombectomy, which involved surgical removal of the thrombus along with pulmonary artery plasty and PDA ligation. Since there are reports of an open PDA acting as a nidus for thrombus formation, this combined approach allowed for comprehensive treatment aimed at reducing the thrombotic burden and decreasing the risk of recurrence. This case also highlights the importance of a broad differential and focused examination in the workup of growth faltering. Defined as weight loss exceeding two major percentile lines on an age- and sex-specific growth chart, 11 growth faltering can result from inadequate energy intake, defective energy utilization, or increased energy expenditure. CONCLUSION We present the case of a 7-week infant who developed a PTE in the setting of Acinetobacter spp sepsis. Sepsis, dehydration, and an immature anticoagulation system likely contributed to the formation of a PTE in this patient. Early recognition and timely surgical intervention are essential for optimizing patient outcomes and preventing life-threatening complications. Further research is needed to better understand the underlying risk factors, improve early diagnostic strategies, and enhance treatment approaches for this rare but serious condition. Abbreviations Pulmonary artery thromboembolism (PTE), pediatric intensive care unit (PICU) Declarations Ethics approval and consent to participate: Consent to participate was obtained by the parent of the patient prior to writing of the case report. The parent was informed about our intentions to publish the report in a medical journal for the purpose of educating other healthcare professionals. Consent for publication: Consent for publication has been obtained by a guardian representing the patient in this case. Availability of data and materials: Data published in this case comes from the patient’s medical chart. Competing interests: The authors and co-authors of this publication declare they have no competing interests. Funding: There are no funding sources to declare. Authors’ contributions: AO initiated the draft writing, allocated tasks, and managed the submission as corresponding author. AZ, JG, VR, and NJ contributed to draft writing, figure creation, editing, and formatting. JS supervised the editing of the draft prior to submission. All authors read and approved the final manuscript. Acknowledgments: There are no other acknowledgments to make. References Rajpurkar M, Huang YV, Raffini L. Additional analysis of pediatric pulmonary embolism using the Pediatric. Health Inform Syst database. 2019;3(17):2604–7. 10.1182/bloodadvances.2019000071 . Witmer C, Raffini L. Treatment of venous thromboembolism in pediatric patients. Blood. 2020;135(5):335–43. 10.1182/blood.2019001847 . Laviolette C, Turner J, Lewis L, Yang SG, Pettitt T, Piggott KD. Occlusive Pulmonary Artery Thrombosis in a Healthy Neonate With No Identifiable Risk Factors. JACC Case Rep. 2021;3(9):1216–20. 10.1016/j.jaccas.2021.02.009 . Published 2021 Jun 23. Revel-Vilk S. The conundrum of neonatal coagulopathy. Hematol Am Soc Hematol Educ Program. 2012;2012:450–4. 10.1182/asheducation-2012.1.450 . Slogrove AL, Goetghebuer T, Cotton MF, Singer J, Bettinger JA. Pattern of Infectious Morbidity in HIV-Exposed Uninfected Infants and Children. Front Immunol 7:164, Published 2016 May 6. 10.3389/fimmu.2016.00164 Abu-Raya B, Smolen KK, Willems F, Kollmann TR, Marchant A. Transfer of Maternal Antimicrobial Immunity to HIV-Exposed Uninfected Newborns. Front Immunol. 2016;7:338. 10.3389/fimmu.2016.00338 . Published 2016 Aug 31. Wong D, Nielsen TBBonomo RA, Pantapalangkoor P, Luna B, Spellberg B. Clinical and Pathophysiological Overview of Acinetobacter Infections: a Century of Challenges. Clin Microbiol Rev. 2017;30. https://doi.org/10.1128/cmr.00058-16 . Frontiers |. Acinetobacter spp. in neonatal sepsis: an urgent global threat. Monagle P, Cuello CA, Augustine C, et al. American Society of Hematology 2018 Guidelines for management of venous thromboembolism: treatment of pediatric venous thromboembolism. Blood Adv. 2018;2(22):3292–316. 10.1182/bloodadvances.2018024786 . Buck ML. Bivalirudin as an Alternative to Heparin for Anticoagulation in Infants and Children. J Pediatr Pharmacol Ther. 2015;20(6):408–17. 10.5863/1551-6776-20.6.408 . Tang MN, Adolphe S, Rogers SR, Frank DA. Failure to Thrive or Growth Faltering: Medical, Developmental/Behavioral, Nutritional, and Social Dimensions. Pediatr Rev. 2021;42(11):590–603. 10.1542/pir.2020-001883 . Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7983131","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":545804750,"identity":"449fd411-07d3-4789-b221-a2a2d08f7f73","order_by":0,"name":"Allison T. 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1","display":"","copyAsset":false,"role":"figure","size":812567,"visible":true,"origin":"","legend":"\u003cp\u003e(a) Pre- and post thrombectomy echocardiogram highlighting a thrombus in the left pulmonary artery (LPA) proximal to the bifurcation of the main pulmonary artery (MPA) into the left and right pulmonary arteries (RPA). Also pictured is the aorta (Ao) for reference.\u003c/p\u003e\n\u003cp\u003e(b)\u003cu\u003e \u003c/u\u003ePosterior view of the pre-thrombectomy CTA chest emphasizing significant flow obstruction in the left pulmonary artery.\u003c/p\u003e","description":"","filename":"floatimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7983131/v1/d5c64e249538bef8629f4b87.jpeg"},{"id":102968601,"identity":"e33b8f3c-baca-4f49-8489-5454859cd528","added_by":"auto","created_at":"2026-02-19 05:10:36","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1172586,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7983131/v1/8c701348-166d-4726-ade2-23345830ffcf.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Pulmonary Artery Thrombus in a Growth Faltering Infant with Acinetobacter Sepsis","fulltext":[{"header":"INTRODUCTION","content":"\u003cp\u003ePulmonary thromboembolism (PTE) is a rare but life-threatening condition in infants, with a mortality rate up to 26% under one year of age.\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u003c/sup\u003e Risk factors in this age group include infection, catheter venous access, congenital heart disease, and thrombophilic states either inherited or acquired. While ultrasound aids in initial evaluation, CT angiography remains the preferred imaging modality for assessment of circulation and surgical planning. We discuss a unique case of PTE in an infant presenting with septic shock, poor weight gain, a heart murmur, and hypoxia. Early recognition and timely multidisciplinary intervention are essential for optimizing patient outcomes and preventing cardiovascular collapse. Further research is needed to improve prevention strategies, and treatment approaches in this age group.\u003c/p\u003e"},{"header":"PATIENT INFORMATION","content":"\u003cp\u003eA 7-week-old female presented to the emergency room with one day of non-bloody diarrhea, feeding intolerance, and weight loss, measuring less than her birth weight of 2.6 kg. Born full-term to an HIV-positive mother with close prenatal care and an undetectable viral load during pregnancy, she had completed a course of AZT at birth and had negative HIV PCR tests at 0 and 14\u0026ndash;21 days of life. Her newborn screen showed possible hemoglobin C trait. Until admission she had been ingesting 2 ounces of standard formula every 2 hours without significant reflux or feeding difficulties. Her mother denied fever, sick symptoms, perioral cyanosis, or significant family history.\u003c/p\u003e\n\u003cp\u003eShe was hypothermic (35.1\u0026deg;C), tachycardic (HR 155 bpm), and tachypneic (RR 42 br/min). On exam she appeared lethargic, limp, and responsive only to painful stimuli with cachexia, poor skin turgor, and a blood glucose level of 50 mg/dL. While attempting IV access, she became briefly unresponsive, requiring intraosseous access placement, fluid resuscitation with 30 cc/kg normal saline, and initiation of sepsis protocol. Oxygen was administered via nasal cannula for desaturation into the high 80s. Initial labs revealed leukocytosis (WBC 25.6 \u0026times; 10\u0026sup3;/\u0026micro;L, ANC 13.1), bandemia (7%), and elevated CRP (16.8 mg/L). She was started on empiric antibiotics with cefotaxime, vancomycin, and acyclovir and admitted to the PICU for management of sepsis and growth faltering.\u003c/p\u003e\n\u003cp\u003eOn day 2, she was noted to have an S3/S4 gallop. Echocardiography revealed an echogenic mass in the right main pulmonary artery causing partial flow obstruction, right atrial dilation, and an ASD with right-to-left shunting (Fig. \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e). A positive blood culture for \u003cem\u003eAcinetobacter nosocomialis\u003c/em\u003e raised concern for infective endocarditis with septic embolization. With high risk for thrombus and massive PE, anticoagulation was also initiated with a heparin drip. She remained subtherapeutic despite titrating the drip to anti-Xa levels per hospital protocol, prompting a switch to bivalirudin.\u003c/p\u003e\n\u003cp\u003eOn hospital day 6, she underwent pulmonary thrombectomy, main pulmonary artery and SVC patch plasty, PFO closure, and PDA ligation via median sternotomy. The thrombus was adherent to denuded endothelium, directing the team to manage the patient for infective endocarditis. Postoperatively she was treated with ampicillin/sulbactam (100 mg/kg q6h), later transitioning to oral levofloxacin (10 mg/kg q12h) to complete a 6-week course. Chest tubes were removed on post-op day 3, and she transitioned to enoxaparin for long-term anticoagulation with plans to determine length of treatment as outpatient. Her inpatient hypercoagulability workup was unremarkable (Table \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e). The thrombotic event was considered multifactorial due to sepsis, dehydration, and endothelial injury.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\n \u003ctable id=\"Tab1\" border=\"1\" class=\"fr-table-selection-hover\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eThrombophilia Workup in an Infant\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eClinical Category\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTest Name\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eResult\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eReference Range\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eInterpretation\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eGenetic Mutations\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFactor V Leiden Mutation Analysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eWILD TYPE\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative/Positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eProthrombin G (20120) Mutation Analysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eWILD TYPE\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative/Positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eClotting Cascade Derangements\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFactor VIII\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.77 U/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.54\u0026ndash;1.55 U/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eD-dimer\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.49 mcg/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.0-0.49 mcg/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHigh\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eProtein C Activity Level\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e84%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e81\u0026ndash;140%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eProtein S Activity Level\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e59%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e62\u0026ndash;148%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLow\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAntithrombin III Level\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e29%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e75\u0026ndash;110%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLow\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eActivated Partial Thromboplastin Time (aPTT)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e43 seconds\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e23\u0026ndash;34 seconds\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eProlonged\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAntiphospholipid Syndrome\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLupus Anticoagulant\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative/Positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiolipin Antibody\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative/Positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBeta 2 Glycoprotein\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNegative/Positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNormal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePolycythemias\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHemoglobin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8.4 g/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9.5\u0026ndash;14.5 g/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLow\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHematocrit\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e23%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e42\u0026ndash;66%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLow\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePlatelet count\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e59x10\u003csup\u003e3\u003c/sup\u003e/mcL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e150\u0026ndash;350 x10\u003csup\u003e3\u003c/sup\u003e/mcL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLow\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eVon Willebrand Disease\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eVon Willebrand Factor Activity\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e190%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e43\u0026ndash;127%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHigh\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003ePrimary thromboembolism of the pulmonary artery (PTE) is a rare and often fatal finding in pediatric patients. We identified a case of PTE in an infant and swiftly intervened to prevent cardiorespiratory collapse. Pediatric thrombotic events follow a bimodal distribution, with a peak during the neonatal period due to central venous catheter use in the NICU and a peak during adolescence when adult thrombotic risk factors emerge. \u003csup\u003e2\u003c/sup\u003e Contributors to infant hypercoagulability include inherited thrombophilias and systemic insults such as septic shock, disseminated intravascular coagulation (DIC), and liver disease. Additional risk factors include maternal lupus, maternal diabetes, chorioamnionitis, and indwelling intravascular catheter use in the NICU. Furthermore, infants may be at increased risk for thrombi due to an immature anticoagulation system, which reaches maturation around 6 months of age. \u003csup\u003e3\u003c/sup\u003e\u003c/p\u003e\u003cp\u003eSince the initial thrombophilia workup was normal and there was no evidence of structural cardiac disease, we believe the primary contributing factor was septic shock secondary to \u003cem\u003eAcinetobacter nosocomialis\u003c/em\u003e, the subsequent dehydration from feeding and low oral intake contributing to venous stasis. Several reports suggest that in-utero HIV exposure alone may increase the risk of infectious morbidity and hypercoagulability in neonates even when the disease is not transmitted.\u003csup\u003e\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u003c/sup\u003e Inflammatory cytokine responses and antiretroviral therapy in HIV-positive mothers have been shown to affect maternal-fetal transfer of placental antibodies, potentially reducing immune protection against certain opportunistic infections.\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e Impaired immunity in our infant would have predisposed her to systemic infection with \u003cem\u003eAcinetobacter nosocomialis, a\u003c/em\u003e bacteria thriving in wet environments that is primarily implicated in nosocomial catheter-based infections, respiratory illness, or urinary tract infections. Acinetobacter species are increasingly implicated in the neonatal population. A newborn’s early microbiome is especially vulnerable to colonization and gut translocation by harmful gram-negative bacteria.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e,\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e\u003cp\u003eManagement of PTE involves anticoagulation, thrombolytics, and/or mechanical thrombectomy to prevent progression to pulmonary embolism and obstructive shock. The 2018 American Society of Hematology Guidelines for pediatric VTE serve a valuable foundation for discussion when selecting from these options.\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u003c/sup\u003e Our patient was managed as a symptomatic DVT and started on anticoagulation without thrombolysis. Initial anticoagulation options include TPA, low molecular weight heparin, and heparin. In cases where tPA is contraindicated, heparin proves ineffective, or when heparin-induced thrombocytopenia (HIT) or antithrombin III deficiency is suspected, direct thrombin inhibitors such as bivalirudin and argatroban should be considered. Direct thrombin inhibitors do not require antithrombin III to be effective, and bivalirudin specifically has shown promising evidence in pediatric populations.\u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u003c/sup\u003e In our case, the patient was transitioned to bivalirudin with an aPTT goal of 60–80 after failing to achieve therapeutic goal on heparin. Given the concern for thrombus growth and massive pulmonary embolism, the patient also underwent mechanical thrombectomy, which involved surgical removal of the thrombus along with pulmonary artery plasty and PDA ligation. Since there are reports of an open PDA acting as a nidus for thrombus formation, this combined approach allowed for comprehensive treatment aimed at reducing the thrombotic burden and decreasing the risk of recurrence.\u003c/p\u003e\u003cp\u003eThis case also highlights the importance of a broad differential and focused examination in the workup of growth faltering. Defined as weight loss exceeding two major percentile lines on an age- and sex-specific growth chart,\u003csup\u003e11\u003c/sup\u003e growth faltering can result from inadequate energy intake, defective energy utilization, or increased energy expenditure.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eWe present the case of a 7-week infant who developed a PTE in the setting of \u003cem\u003eAcinetobacter spp\u003c/em\u003e sepsis. Sepsis, dehydration, and an immature anticoagulation system likely contributed to the formation of a PTE in this patient. Early recognition and timely surgical intervention are essential for optimizing patient outcomes and preventing life-threatening complications. Further research is needed to better understand the underlying risk factors, improve early diagnostic strategies, and enhance treatment approaches for this rare but serious condition.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003ePulmonary artery thromboembolism (PTE), pediatric intensive care unit (PICU)\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eEthics approval and consent to participate: Consent to participate was obtained by the parent of the patient prior to writing of the case report. The parent was informed about our intentions to publish the report in a medical journal for the purpose of educating other healthcare professionals.\u003c/p\u003e\n\u003cp\u003eConsent for publication: Consent for publication has been obtained by a guardian representing the patient in this case.\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials: Data published in this case comes from the patient\u0026rsquo;s medical chart.\u003c/p\u003e\n\u003cp\u003eCompeting interests: The authors and co-authors of this publication declare they have no competing interests.\u003c/p\u003e\n\u003cp\u003eFunding: There are no funding sources to declare.\u003c/p\u003e\n\u003cp\u003eAuthors\u0026rsquo; contributions: AO initiated the draft writing, allocated tasks, and managed the submission as corresponding author. AZ, JG, VR, and NJ contributed to draft writing, figure creation, editing, and formatting. JS supervised the editing of the draft prior to submission. All\u0026nbsp; authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003eAcknowledgments: There are no other acknowledgments to make.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eRajpurkar M, Huang YV, Raffini L. Additional analysis of pediatric pulmonary embolism using the Pediatric. Health Inform Syst database. 2019;3(17):2604\u0026ndash;7. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1182/bloodadvances.2019000071\u003c/span\u003e\u003cspan address=\"10.1182/bloodadvances.2019000071\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eWitmer C, Raffini L. Treatment of venous thromboembolism in pediatric patients. 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Pediatr Rev. 2021;42(11):590\u0026ndash;603. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1542/pir.2020-001883\u003c/span\u003e\u003cspan address=\"10.1542/pir.2020-001883\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"thromboembolism, thrombophilia, thrombus, sepsis, infant, critical care, HIV, case report","lastPublishedDoi":"10.21203/rs.3.rs-7983131/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7983131/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePrimary thromboembolism of the pulmonary artery (PTE) is a rare finding in infant patients. Contributors to infant hypercoagulability include inherited thrombophilias, immature anticoagulation systems, and systemic insults such as septic shock and liver disease.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase Presentation:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe present the case of a 7-week-old girl with in-utero HIV exposure diagnosed with a pulmonary artery thromboembolism (PTE). The patient was admitted to the pediatric intensive care unit (PICU) for sepsis in the setting of \u003cem\u003eAcinetobacter nosocomialis\u003c/em\u003e bacteremia, growth faltering, and an S4 gallop. Echocardiogram revealed a mass in the pulmonary artery, prompting urgent treatment with thrombectomy. We hypothesize that septic shock, with associated coagulopathy and severe dehydration, contributed to thrombophilia in this critically ill patient.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis case highlights the rapid, multidisciplinary approach to diagnosing PTE and the underlying factors contributing to thrombophilia in an infant. Early recognition and timely surgical intervention are essential for optimizing patient outcomes.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical trial number:\u003c/strong\u003e not available\u003c/p\u003e","manuscriptTitle":"Pulmonary Artery Thrombus in a Growth Faltering Infant with Acinetobacter Sepsis","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-11-23 11:38:25","doi":"10.21203/rs.3.rs-7983131/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"c97264d2-4f04-4f45-bc33-27913d651210","owner":[],"postedDate":"November 23rd, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-02-19T05:10:18+00:00","versionOfRecord":[],"versionCreatedAt":"2025-11-23 11:38:25","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7983131","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7983131","identity":"rs-7983131","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}