Primary Small Intestine Lymphatic Dilation Syndrome: A Case Report

Primary Small Intestine Lymphatic Dilation Syndrome: A Case Report | 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 Primary Small Intestine Lymphatic Dilation Syndrome: A Case Report Tianpeng He, Yuan Yuan, Qianqian Zhou, Junlong Gao, Dongliang Wang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8548962/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 18 You are reading this latest preprint version Abstract Background Primary intestinal lymphatic dilation (PIL) is a rare disorder that is characterized by abnormal intestinal lymphatic drainage; however, its exact etiology and pathogenesis are yet to be fully elucidated. PIL primarily originates from impaired lymphatic return in the small intestine owing to multiple factors, and leads to increased lymphatic vessel pressure with consequent lymph fluid leakage, malabsorption, and protein loss. The clinical manifestations typically include hypoproteinemia, lymphopenia, diarrhea, and ascites. Case presentation: A 14-year-old female patient was admitted to the hospital because of exertional dyspnea for half a month, nausea and vomiting accompanied by abdominal distension and pain for 10 days, and bilateral lower limb swelling for 3 days. Examination revealed a large amount of fluid accumulation in the abdominal and pelvic cavities, pleural effusion, hypoproteinemia, hypogammaglobulinemia, electrolyte imbalance, decreased lymphocyte count, and a positive result on the chylous test of pleural and abdominal effusions. The CT scan revealed intestinal obstruction, intestinal dilation, and enlargement of the mesenteric lymph nodes. The PET-CT examination ruled out lymphoma. Gastroscopy revealed that the ileal mucosa was edematous, with diffuse patchy changes and granular protrusions on the surface. An ileal biopsy showed dilated lymphatic vessels within the lamina propria, accompanied by infiltration of inflammatory cells. Based on the patient's clinical symptoms and results of the examinations, she was diagnosed with small intestinal lymphatic dilation. After conservative treatment, including albumin supplementation, electrolyte imbalance correction, and nutritional support, the patient's symptoms were alleviated and she was discharged. Conclusion The diagnosis of pediatric small intestinal lymphangiectasia requires a comprehensive consideration of clinical symptoms, laboratory tests, imaging examinations, and endoscopic pathological biopsy results. Pathological histology is key to confirming a diagnosis. The early implementation of targeted conservative treatment can effectively improve patient prognosis. PIL Polyserositis Hypoalbuminemia Case report Prognosis Figures Figure 1 Figure 2 Figure 3 Background Primary intestinal lymphangiectasia (PIL), or Waldmann's disease, is a rare congenital vascular disorder categorized as a protein-losing enteropathy [ 1 ]. The core pathological mechanism is congenital abnormality or dysfunction of the small intestinal lymphatic vessels, which leads to the obstruction of lymphatic drainage and the continuous increase of pressure within the lymphatic vessels. This, in turn, causes lymph fluid to leak into the intestinal and abdominal cavities, resulting in the loss of a large amount of nutrients such as proteins and lymphocytes through the lymph fluid. Eventually, a series of systemic pathological and physiological changes occur. PIL is more common among children and adolescents than in adults [ 2 ]. Its progression is insidious; its clinical manifestations show significant heterogeneity, lacking specific clinical symptoms, which poses significant challenges for early diagnosis. The typical symptoms reported in clinical cases primarily include hypoproteinemia, lymphocyte reduction, generalized edema, and pleural or peritoneal effusion (such as pleural and peritoneal effusion). Diarrhea, as a common manifestation in the gastrointestinal tract, is also frequently reported. As the number of clinical cases reported rises, non-typical symptoms such as limb convulsions, gastrointestinal bleeding, and nutritional anemia have increasingly been identified [ 3 ]. However, intestinal obstruction as the initial presenting symptom remains relatively rare in clinical practice. In recent years, with the advancement of endoscopic technology and growing understanding of the disease, the diagnostic rate has gradually increased [ 4 ]. It retains an extremely low incidence rate, with a prevalence in the population under 1/100,000. In clinical practice, there is generally insufficient vigilance toward this disease, especially for cases presenting atypical symptoms (such as intestinal obstruction), which often result in delayed diagnosis due to the lack of targeted screening, leading to the progression of the disease, an increase in the incidence of complications, and severely affecting the prognosis of patients. Currently, most studies on PIL in both domestic and international fields have focused on summarizing typical cases, exploring diagnostic methods, and optimizing treatment plans. There are relatively few reports on special phenotypes of PIL cases with initial manifestations such as intestinal obstruction, and systematic analyses of relevant clinical characteristics, diagnostic approach, and treatment strategies remain scarce [ 5 ]. In this report, we describe the diagnosis and treatment of a 14-year-old girl with PIL along with a review of relevant literature to systematically explore the clinical characteristics, diagnostic methods, and treatment strategies of PIL to provide a reference for clinical practice. Case presentation Medical history A 14-year-old female patient was admitted to the hospital with shortness of breath on exertion for half a month, nausea and vomiting accompanied by abdominal distension and pain for 10 days, and swelling of both lower extremities for 3 days. The patient experienced exertional dyspnea after long-distance walking without obvious triggers that was relieved upon resting, and, since 10 days, had experienced nausea, vomiting, abdominal distension, and abdominal pain without any obvious cause. An anteroposterior radiograph of the abdomen at the local hospital indicated incomplete intestinal obstruction (Fig. 1 a). After one week of medication treatment, the symptoms of nausea, vomiting, abdominal pain, and abdominal distension improved, but there was still diarrhea. Symmetrical non-pitting edema of both lower extremities occurred 3 days before admission. Throughout the disease course, the patient was conscious, with a listless and dull demeanor, poor sleep and diet, decreased activity tolerance, no fever or chest pain, and normal micturition. In the past month, the patient's weight has increased by 4 kg. The patient had no relevant medical, personal, or family histories. Admission for physical examination At admission, the body temperature was 36.5℃, heart rate was 71 beats/min, breathing rate was 20 cycles/min, and blood pressure was 86/53mmHg; the patient had a listless and dull demeanor. Physical examination revealed bilateral rough breath sounds as well as wet rales at the base of the right lung. The abdomen was bulging with ascites, and with decreased bowel sounds. Bilateral symmetrical non-pitting edema was observed in the lower extremities. Auxiliary examination During the auxiliary examinations, multiple abnormal indices were identified (Table 1 ) as follows: Lymphopenia: Routine blood test showed a lymphocyte count below the normal level. Mild anemia: Red blood cell count and hemoglobin were both decreased. The level of folate and vitamin B₁₂ presenting a downward trend. Serum iron levels, unsaturated iron-binding capacity, and total iron-binding capacity were significantly reduced, whereas serum ferritin levels were normal. These findings indicated that the anemia was associated with folate, vitamin B₁₂, and iron deficiencies. Hypoproteinemia: Total protein, albumin, and globulin levels were all significantly decreased, with an albumin-to-globulin ratio (A/G) of 1.1. The total iron-binding capacity decreased synchronously. The level of immunoglobulin G (IgG) was significantly reduced whereas that of IgA slightly decreased and IgM was at the lower limit of the normal. Complement C3 level decreased. Other abnormalities: Serum calcium level was reduced. The test for fecal fat globules showed a positive result. The serum potassium and sodium levels were 3.06 and 134.84 mmol/L, respectively. Pleural and ascitic fluid tests were positive, and routine examination revealed milky turbid fluid with abnormal biochemical and routine indices. Human rhinovirus nucleic acid test results were positive, whereas all other etiological and serological tests were negative (Table 1 ). Table 1 Results of laboratory examinations Test Category Result Changes Normal Range Test Category Reports Blood routine Fecal examination Positive occult blood Lymphocyte count, 10 9 /L 0.83 ↓ 1.2–3.8 Fecal examination Positive fecal fat globules Red blood cell count, 10 12 /L 3.46 ↓ 4.1–5.3 Pleural and peritoneal effusion chylous test Positive Hemoglobin, g/L 102 ↓ 114–154 Biochemistry of serous fluid Blood biochemistry Total protein in pleural and peritoneal effusion, g/L 8.15 Total protein, g/L 29.47 ↓ 65–85 Albumin in pleural and peritoneal effusion, g/L 4.76 Albumin, g/L 15.44 ↓ 40–55 Chest and abdominal fluid sugar, mmol/L 5.7 Globulin, g/L 14.03 ↓ 20–40 Lactate dehydrogenase in pleural and peritoneal effusion, U/L 150.91 Albumin/Globulin 1.1 ↓ 1.2–2.4 Adenosine deaminase in pleural and peritoneal effusion, U/L 2.55 Glutamic-pyruvic transaminase, U/L 10 - 7–40 Routine examination of pleural and peritoneal effusion Glutamic oxaloacetic transaminase, U/L 17.44 - 13–35 Color Milky white Serum creatinine, µmol/L 35.69 - 41–73 Appearance Turbid K+, mmol/L 3.06 ↓ 3.5–5.3 Coagulation Negative Na+, mmol/L 134.84 ↓ 137–147 Density 1.019 Ca2+, mmol/L 1.8 ↓ 2.1–2.6 Li Fangta experiment Positive Serum iron + total binding capacity Red blood cell count, mm 3 639 Fe, µmol/L 5.74 ↓ 7.8–32.3 Nucleated cell count, mm 3 1281 Unsaturated iron, µmol/L 14.60 ↓ 25–50.1 neutrophil granulocyte% 75 Total iron-binding capacity, µmol/L 20.34 ↓ 45–77 Lymphocyte% 25 Serum transferrin saturation, % 28.22 - 20–55 Human rhinovirus nucleic acid Positive Granulocyte Gonadal complete set Negative Granulocyte, % 4.15 ↑ 0.83–2.24 Hepatitis B three systems + Hepatitis C + HIV + syphilis Negative Granulocyte count, 10 9 /L 162.3 ↑ 35.8–99.6 Antibodies against respiratory pathogens, IgM Negative Ratio of granulocyte 23.7 ↑ 3.2–13.5 Pleural and peritoneal effusion culture Negative Anemia markers Full set of autoantibodies Negative Folate, nmol/L 6.13 ↓ 7–46.4 TORCH5items Negative Vitamin B12, pmol/L 104 ↓ 138–652 Specific cellular immunoassay for tuberculosis bacteria Negative Ferroprotein (FER), ng/mL 42.29 - 4.63–204 24-h urinary protein Negative Immune function IgG, g/L 2.76 ↓ 8.6–17.4 IgA, g/L 0.8 ↓ 1–4.2 IgM, g/L 0.8 - 0.5–2.8 Complement C3, g/L 0.59 ↓ 0.7–1.4 Complement C4, g/L 0.12 0.1–0.4 Imaging examination Computed tomography scanning revealed pleural, abdominal, and pelvic effusions, dilation of the lumen of the small intestine–sigmoid colon, gas accumulation, fluid accumulation, and multiple enlarged mesenteric lymph nodes (Fig. 2 ). The pleural effusion was milky white (Fig. 1 b). Radionuclide lymphatic imaging (ECT) showed an abnormal distribution of imaging agents in the bilateral abdominal cavity and the right lower abdomen, which mostly indicated the possibility of chylothorax and ascites (Fig. 1 c). Positron emission tomography-CT revealed no obvious abnormalities, and lymphoma was ruled out. Colonoscopy revealed edema of the ileal mucosa, which presented as diffuse patchy changes with a Cauley-like surface (Fig. 3 a). A biopsy specimen was obtained from the ileocecal region, and microscopic examination revealed sparse mucosal glands in the intestinal mucosa of the terminal ileum, some dilated lymphatic vessels in the lamina propria, and scattered inflammatory cell infiltration (Fig. 3 b). Final diagnosis The patient was diagnosed with PIL. Treatment Conservative treatment, such as supplementing human albumin, correcting electrolyte imbalance, nutritional support, gastrointestinal decompression, acid suppression, stomach protection, and dietary adjustment, was provided. After 15 days of standardized intervention, the patient's symptoms gradually improved, and eventually he was in good physical condition and was discharged from the hospital smoothly. Outcome and follow-up The patient was instructed to follow a low-fat, high-protein diet plan that was supplemented with oral medium-chain triglyceride (MCT) nutritional powder, calcium, and vitamin D supplements. Follow-up examinations were conducted 1 month and 3 months after discharge. The results of both follow-ups showed that the patient's related clinical symptoms were completely relieved, and all laboratory indicators returned to the normal range, with stable disease condition. Discussion PIL is a protein-losing gastrointestinal disease that is rare in clinical practice. The key pathological mechanism involves an abnormal lymphatic vessel structure, which leads to the leakage of lymph rich in proteins, lymphocytes, and fat from the intestinal mucosal or serosal layer, and results in a series of clinical abnormalities, such as hypoproteinemia, decreased lymphocyte count, hypolipidemia, and luminal effusion [ 5 ]. Among these, PIL is mostly associated with congenital lymphatic dysplasia wherein the pathogenesis is not yet fully understood, and the clinical phenotypes are diverse. Some patients lack the typical symptoms of edema and diarrhea, which can easily lead to misdiagnosis and missed diagnosis [ 6 ]. The clinical characteristics of the patient in this case were consistent with the pathophysiological mechanisms of PIL. The patient presented with incomplete intestinal obstruction, mild anemia, edema, hypokalemia, and hypocalcemia, which are consistent with the typical manifestations of PIL caused by electrolyte imbalance and nutrient absorption disorders secondary to lymphatic loss. The loss of immune components in the lymphatic fluid further weakens the immune function and contributes to the pathological presentation [ 7 ]. On laboratory examination, the deviation from the normal reference range of the absolute count of peripheral blood lymphocytes is a characteristic indicator of PIL, as continuous leakage of lymphatic fluid leads to a large loss of peripheral blood lymphocytes, which is an important diagnostic parameter [ 7 ]. The simultaneous decrease in the patient's plasma albumin and IgG levels constitutes a key laboratory basis for a diagnosis of PIL [ 8 ]. Endoscopy and pathological examinations are the key methods for diagnosing PIL. In this case, colonoscopy and pathological examination clearly confirmed the presence of small intestinal lymphatic vessel dilation, which directly affirmed the anatomical basis of the lesions [ 9 , 10 ]. Routine fecal tests indicated positive occult blood and fat globules, the peritoneal effusion was milky white, ECT suggested possible chylous pleural and peritoneal effusion, and a positive chylous test further completed the closed loop of the diagnostic chain through auxiliary evidence of intestinal protein loss and the leakage indicated on radionuclide angiography [ 11 – 13 ]. The differential diagnosis of PIL should focus on excluding other diseases that can lead to protein loss, lymphocytopenia, and intestinal obstruction and avoid misdiagnosis caused by overlapping symptoms [ 6 ]. When differentiated from nephrotic syndrome, the latter is characterized by massive proteinuria (> 3.5 g/d) and hyperlipidemia as its core features. However, in this case, the patient's urinary protein level was negative and the creatinine level was normal, with no evidence of kidney damage [ 14 ]. For differentiation from liver cirrhosis, the decompensated stage of liver cirrhosis is frequently accompanied by abnormal liver function and signs of portal hypertension (e.g., ascites and esophageal and gastric varices). In this case, the patient's liver function indicators were normal, and there were no related imaging manifestations that met the diagnostic criteria for liver cirrhosis [ 15 ]. PET-CT examination showed no space-occupying lesions, which ruled out small intestinal lymphangiectasia secondary to malignant tumors such as lymphoma [ 16 ]. Negative results from tuberculosis-related laboratory tests, combined with no symptom of tuberculosis, such as low fever and night sweats, ruled out the possibility of tuberculous pleural and peritoneal effusions [ 17 ]. The results of all autoimmune-related tests were negative and did not support the possibility of intestinal mucosal damage or protein loss caused by autoimmune diseases [ 5 ]. Through the above systematic differentiation, the diagnosis of PIL was confirmed. For treatment, Alfano et al. [ 18 ] proposed that the primary goal of PIL treatment is to reduce protein loss, maintain the circulating blood volume, and inhibit excessive tissue fluid production. Therefore, conservative medical treatment is the preferred clinical management. Early treatment in this case mainly focused on symptom-based support as follows: supplementing albumin to correct hypoproteinemia, supplementing fat-soluble vitamins to improve the state of nutritional deficiency, actively correcting electrolyte imbalance to alleviate symptoms related to hypokalemia and hypocalcemia [ 18 ], simultaneously reducing tissue edema through diuresis and resolution of edema, regulating intestinal flora to improve digestive and absorptive functions, and developing a foundation for long-term maintenance treatment [ 19 ]. Octreotide, a natural endogenous somatostatin analog, can aid the reduction of lymphatic leakage through mechanisms such as inhibition of gastrointestinal peristalsis, intestinal blood flow, and lymphatic secretion, and prevention of fatty acid absorption, and thus has become an important adjunctive treatment with internal medicine treatment. Dietary adjustment is at the core of the long-term management of PIL. In this case, a low-fat, high-protein diet supplemented with MCT was adopted [ 20 ]. In the gastrointestinal tract, MCT decomposes into glycerol and medium-chain fatty acids, which is directly absorbed into the portal vein through small intestinal epithelial cells without being transported through the lymphatic vessels, and thereby effectively reduces the pressure within the lymphatic vessels and minimizes lymphatic leakage and protein loss. Although an MCT-based diet cannot reverse the congenital structural abnormalities of lymphatic vessels, many clinical studies have confirmed that it can significantly improve the clinical symptoms of patients with PIL, reduce the long-term mortality rate, and is a key component of disease management [ 21 ]. Surgical treatment is applicable only in specific cases as most PIL cases are caused by congenital diffuse lymphatic dysplasia [ 22 ]. For patients with localized lesions who do not respond to medical treatment, intestinal resection (removal of the diseased intestinal segment) or venolymphatic anastomosis can be considered. However, it is necessary to strictly control the surgical indications, accurately assess the extent of the lesion, and ensure that the diseased tissue is completely removed whereas avoiding short bowel syndrome due to excessive intestinal resection [ 22 , 23 ]. Moreover, it is necessary to adhere to an MCT diet and nutritional support postoperatively to maintain the therapeutic effect [ 23 ]. In conclusion, for patients without a clear medical history or clinical manifestations such as incomplete intestinal obstruction, hypoproteinemia, edema, electrolyte imbalance, and lymphopenia, PIL should be included in the differential diagnosis and confirmed through multidimensional examinations, such as laboratory tests, endoscopic pathology, imaging, and radionuclide angiography, with systematic differentiation to rule out similar diseases. After diagnosis, a comprehensive treatment plan of "symptomatic support + drug assistance + dietary adjustment" should be adopted. As a core intervention measure, the MCT diet can effectively improve the clinical symptoms of patients. Combined with surgical treatment, when necessary, good long-term disease control would improve patient prognosis. Abbreviations MCT medium-chain triglyceride PIL Primary intestinal lymphangiectasia Declarations Ethics approval and consent to participate This article is based on a case report that is exempt from review by an IRB. The patient provided informed consent for the publication of this case report. Consent for publication The publication of this case report and any accompanying images has been approved by the patient with their informed consent. Availability of data and materials The data supporting the findings of this study are available within the article. Competing interests The authors declare that they have no competing interests. Funding This work was supported by the Gansu Province Health Industry Project (Grant number GSWSKY2020-37) and the Joint Scientific Research Project of Science and Technology Department of Gansu Province (Grant number 23JRRA1546). Authors' contributions Junlong Gao and Qianqian Zhou were responsible for collecting patient medical records and assisting in data organization. Tianpeng He was responsible for writing the initial draft of the paper and conducting the review of relevant literature. Yuan Yuan and Dongliang Wang were the attending doctors responsible for diagnosing the patient. All authors made contributions to the paper. All the authors have read and approved the final manuscript. Acknowledgements We would like to thank Editage (www.editage.cn) for English language editing. Clinical trial number not applicable. Additional files Patient Informed Consent Form References Waldmann TA, Steinfeld JL, Dutcher TF, Davidson JD, Gordon RSJ. The role of the gastrointestinal system in idiopathic hypoproteinemia. Gastroenterology. 1961;41:197–207. Ozen A, Lenardo MJ. Protein-losing enteropathy. N Engl J Med. 2023;389:733–48. Cao Y, Feng XH, Ni HX. 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Intestinal lymphangiectasia: A protein-losing enteropathy with hypogammaglobulinemia, lymphocytopenia and impaired homograft rejection. J Clin Investig. 1967;46:1643–56. Freeman HJ. Small intestinal mucosal biopsy for investigation of diarrhea and malabsorption in adults. Gastrointest Endosc Clin N Am. 2000;10:739. Preisich P, Farkas I, Bajnóczy B, Németh L. Duodenoszkóppal és célzott biopsziával diagnosztizált lymphangiectasia intestinalis. Orv Hetil. 1979;120:1387–9. Iida F, Wada R, Sato A, Yamada T. Clinicopathologic consideration of protein-losing enteropathy due to lymphangiectasia of the intestine. Surg Gynecol Obstet. 1980;151:391–5. Zelmanovitz F、Ricardo Masiero P、Leão, Spiro B. Unusual excretion of Tc-99m MDP in regional intestinal lymphangiectasia. Clin Nucl Med. 2003;28:509–10. Castellón Méndez AJ, Bodán Campbell A, Rosales Obregón V, Zahran M. Waldmann's disease: Primary intestinal lymphangiectasia diagnosed by 99mTc-labeled albumin macroaggregate scintigraphy-A case report in an adult patient. Clin Case Rep. 2024;12:e8772. De Sousa JS, Guerreiro O, Cunha A, Araújo J. Association of nephrotic syndrome with intestinal lymphangiectasia. Arch Dis Child. 1968;43:245–8. Miura S, Asakura H, Munakata Y, Kobayashi K, Yoshioka M, Morishita T, et al. Lymphatic role in the pathogenesis of fat malabsorption in liver cirrhosis in rats. Dig Dis Sci. 1982;27:1030–6. Guan W, Wang QS, Wu HB, Zhou WL. 18F-FDG PET/CT findings of primary intestinal lymphoma: Analysis of 23 cases. Nan Fang Yi Ke Da Xue Bao. 2016;36:1175–80. Liu YY, Chen MK, Cao Z, Liu SZ, Ding BJ. Differential diagnosis of intestinal tuberculosis from Crohn's disease and primary intestinal lymphoma in China. Saudi J Gastroenterol: Off J Saudi Gastroenterol Assoc. 2014;20:241–7. Alfano V, Tritto G, Alfonsi L, Cella A, Pasanisi F, Contaldo F. Stable reversal of pathologic signs of primitive intestinal lymphangiectasia with a hypolipidic, MCT-enriched diet. Nutrition. 2000;16:303–4. Klingenberg RD, Homann N, Ludwig D. Type I intestinal lymphangiectasia treated successfully with slow-release octreotide. DIGEST DIS SCI. 2003;48(8):1506–9. Desai AP, Guvenc BH, Carachi R. Evidence for medium chain triglycerides in the treatment of primary intestinal lymphangiectasia. Eur J Pediatr Surg. 2009;19:241–5. Niu Y, Wu Q, Wang Y, Lu L, Feng Y, Cai W, et al. Primary intestinal lymphangiectasia in children: Twelve years of experience in the diagnosis and management. Asia Pac J Clin Nutr. 2021;30:358–64. Kwon Y, Kim MJ. The update of treatment for primary intestinal lymphangiectasia. Pediatr Gastroenterol Hepatol Nutr. 2021;24:413–22. Norman JS, Testa S, Wang CX, Savage T. Milky way: Management of primary intestinal lymphangiectasia. Dig Dis Sci. 2023;68:3872–7. Additional Declarations No competing interests reported. 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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-8548962","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":591690566,"identity":"dee0a4f9-d5fa-440a-831b-a93a53424e8d","order_by":0,"name":"Tianpeng He","email":"","orcid":"","institution":"Gansu Provincial Hospital","correspondingAuthor":false,"prefix":"","firstName":"Tianpeng","middleName":"","lastName":"He","suffix":""},{"id":591690568,"identity":"5fb44dcf-bb30-4352-a30a-6c98fcd114e5","order_by":1,"name":"Yuan Yuan","email":"","orcid":"","institution":"Longhua Hospital Shanghai University of Traditional Chinese Medicine","correspondingAuthor":false,"prefix":"","firstName":"Yuan","middleName":"","lastName":"Yuan","suffix":""},{"id":591690569,"identity":"733f8389-4d0d-4eb8-a809-37b358b3b841","order_by":2,"name":"Qianqian Zhou","email":"","orcid":"","institution":"Gansu Provincial Hospital","correspondingAuthor":false,"prefix":"","firstName":"Qianqian","middleName":"","lastName":"Zhou","suffix":""},{"id":591690571,"identity":"0303c06c-e7ad-42cc-8f56-1edd8aad3548","order_by":3,"name":"Junlong Gao","email":"","orcid":"","institution":"Gansu Provincial Hospital","correspondingAuthor":false,"prefix":"","firstName":"Junlong","middleName":"","lastName":"Gao","suffix":""},{"id":591690573,"identity":"915a06ae-a14d-47ea-ad96-040bac20ad06","order_by":4,"name":"Dongliang Wang","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAyklEQVRIiWNgGAWjYBAC+/nvPz6QqLBhZmNvIFKLAUOCsYHFmTR2fp4DxGsxk6hsO8wvOSOBSC3mDAcSJG6cYZY2uPl44w2GGptoglosGxsOGM6oYDM2uJ1WbMFwLC23gaCew4wNyRJneJINbueYSTA2HCZCyzFmhsN/2yTqN9w8Q6QWgzNsjA2SbQbMkjN4iNQCVMnMIHEmgZmfB+iXBGL8wi/Bw/5DouI/MCoPb7zxocaGCL8gO1IigRTlEC2k6hgFo2AUjIKRAQDAjD6lsLGVjQAAAABJRU5ErkJggg==","orcid":"","institution":"Gansu Provincial Hospital","correspondingAuthor":true,"prefix":"","firstName":"Dongliang","middleName":"","lastName":"Wang","suffix":""}],"badges":[],"createdAt":"2026-01-08 08:38:33","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8548962/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8548962/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":102790776,"identity":"5226ce35-7b07-4492-8a9d-72a0b47c7e5e","added_by":"auto","created_at":"2026-02-16 17:13:09","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":196250,"visible":true,"origin":"","legend":"\u003cp\u003ea) Abdominal X-ray demonstrating incomplete intestinal obstruction; b) Milky white appearance of the drained pleural and ascitic fluid; c) Radionuclide imaging showing abnormal radiotracer accumulation in the bilateral abdominal cavity and right lower abdomen, suggesting chylothorax and chylous ascites.\u003c/p\u003e","description":"","filename":"floatimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8548962/v1/fce33155b7dad9d34d085b4a.jpeg"},{"id":104397281,"identity":"80a90135-d0aa-4e05-afa8-6ce24a445b34","added_by":"auto","created_at":"2026-03-11 11:45:58","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":362812,"visible":true,"origin":"","legend":"\u003cp\u003ea) Enlarged lymph nodes at the mesenteric root; b) Pleural effusion; c) Dilated intestinal loops; d) Pleural effusion; e) Ascitic fluid. f)Expanded intestinal tube\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-8548962/v1/fec6a7b67beb9adee5384926.png"},{"id":102790778,"identity":"dda76a6d-f44a-40bb-873a-961030e022ca","added_by":"auto","created_at":"2026-02-16 17:13:09","extension":"jpeg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":849930,"visible":true,"origin":"","legend":"\u003cp\u003ea) Colonoscopy showing edema of the ileal mucosa with diffuse patchy changes and a waxy surface; b) Pathological findings: Under light microscopy, the ileal mucosal tissue specimens exhibited sparse mucosal glands, dilated lymphatic vessels in the lamina propria, and scattered inflammatory cell infiltration.\u003c/p\u003e\n\u003cp\u003eFig3. a) Colonoscopy showing edema of the ileal mucosa with \u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;diffuse patchy changes and a waxy surface; b) Pathological findings: Under \u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;light microscopy, the ileal mucosal tissue specimens exhibited sparse \u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;mucosal glands, dilated lymphatic vessels in the lamina propria, and \u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;scattered inflammatory cell infiltration.\u003c/p\u003e","description":"","filename":"floatimage3.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8548962/v1/c4bb93e2c38e22faa9cd9daf.jpeg"},{"id":105032979,"identity":"16396351-05c9-4d75-afef-c9ab8b69c870","added_by":"auto","created_at":"2026-03-20 07:09:01","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":2059095,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8548962/v1/eaf7024b-1674-484b-b233-1c9ce96a02d8.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Primary Small Intestine Lymphatic Dilation Syndrome: A Case Report","fulltext":[{"header":"Background","content":"\u003cp\u003ePrimary intestinal lymphangiectasia (PIL), or Waldmann's disease, is a rare congenital vascular disorder categorized as a protein-losing enteropathy [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. The core pathological mechanism is congenital abnormality or dysfunction of the small intestinal lymphatic vessels, which leads to the obstruction of lymphatic drainage and the continuous increase of pressure within the lymphatic vessels. This, in turn, causes lymph fluid to leak into the intestinal and abdominal cavities, resulting in the loss of a large amount of nutrients such as proteins and lymphocytes through the lymph fluid. Eventually, a series of systemic pathological and physiological changes occur. PIL is more common among children and adolescents than in adults [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Its progression is insidious; its clinical manifestations show significant heterogeneity, lacking specific clinical symptoms, which poses significant challenges for early diagnosis. The typical symptoms reported in clinical cases primarily include hypoproteinemia, lymphocyte reduction, generalized edema, and pleural or peritoneal effusion (such as pleural and peritoneal effusion). Diarrhea, as a common manifestation in the gastrointestinal tract, is also frequently reported. As the number of clinical cases reported rises, non-typical symptoms such as limb convulsions, gastrointestinal bleeding, and nutritional anemia have increasingly been identified [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. However, intestinal obstruction as the initial presenting symptom remains relatively rare in clinical practice. In recent years, with the advancement of endoscopic technology and growing understanding of the disease, the diagnostic rate has gradually increased [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. It retains an extremely low incidence rate, with a prevalence in the population under 1/100,000. In clinical practice, there is generally insufficient vigilance toward this disease, especially for cases presenting atypical symptoms (such as intestinal obstruction), which often result in delayed diagnosis due to the lack of targeted screening, leading to the progression of the disease, an increase in the incidence of complications, and severely affecting the prognosis of patients. Currently, most studies on PIL in both domestic and international fields have focused on summarizing typical cases, exploring diagnostic methods, and optimizing treatment plans. There are relatively few reports on special phenotypes of PIL cases with initial manifestations such as intestinal obstruction, and systematic analyses of relevant clinical characteristics, diagnostic approach, and treatment strategies remain scarce [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. In this report, we describe the diagnosis and treatment of a 14-year-old girl with PIL along with a review of relevant literature to systematically explore the clinical characteristics, diagnostic methods, and treatment strategies of PIL to provide a reference for clinical practice.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eMedical history\u003c/h2\u003e \u003cp\u003eA 14-year-old female patient was admitted to the hospital with shortness of breath on exertion for half a month, nausea and vomiting accompanied by abdominal distension and pain for 10 days, and swelling of both lower extremities for 3 days. The patient experienced exertional dyspnea after long-distance walking without obvious triggers that was relieved upon resting, and, since 10 days, had experienced nausea, vomiting, abdominal distension, and abdominal pain without any obvious cause. An anteroposterior radiograph of the abdomen at the local hospital indicated incomplete intestinal obstruction (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003ea). After one week of medication treatment, the symptoms of nausea, vomiting, abdominal pain, and abdominal distension improved, but there was still diarrhea. Symmetrical non-pitting edema of both lower extremities occurred 3 days before admission. Throughout the disease course, the patient was conscious, with a listless and dull demeanor, poor sleep and diet, decreased activity tolerance, no fever or chest pain, and normal micturition. In the past month, the patient's weight has increased by 4 kg. The patient had no relevant medical, personal, or family histories.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eAdmission for physical examination\u003c/h3\u003e\n\u003cp\u003eAt admission, the body temperature was 36.5℃, heart rate was 71 beats/min, breathing rate was 20 cycles/min, and blood pressure was 86/53mmHg; the patient had a listless and dull demeanor. Physical examination revealed bilateral rough breath sounds as well as wet rales at the base of the right lung. The abdomen was bulging with ascites, and with decreased bowel sounds. Bilateral symmetrical non-pitting edema was observed in the lower extremities.\u003c/p\u003e\n\u003ch3\u003eAuxiliary examination\u003c/h3\u003e\n\u003cp\u003eDuring the auxiliary examinations, multiple abnormal indices were identified (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e) as follows: Lymphopenia: Routine blood test showed a lymphocyte count below the normal level. Mild anemia: Red blood cell count and hemoglobin were both decreased. The level of folate and vitamin B₁₂ presenting a downward trend. Serum iron levels, unsaturated iron-binding capacity, and total iron-binding capacity were significantly reduced, whereas serum ferritin levels were normal. These findings indicated that the anemia was associated with folate, vitamin B₁₂, and iron deficiencies. Hypoproteinemia: Total protein, albumin, and globulin levels were all significantly decreased, with an albumin-to-globulin ratio (A/G) of 1.1. The total iron-binding capacity decreased synchronously. The level of immunoglobulin G (IgG) was significantly reduced whereas that of IgA slightly decreased and IgM was at the lower limit of the normal. Complement C3 level decreased. Other abnormalities: Serum calcium level was reduced. The test for fecal fat globules showed a positive result. The serum potassium and sodium levels were 3.06 and 134.84 mmol/L, respectively. Pleural and ascitic fluid tests were positive, and routine examination revealed milky turbid fluid with abnormal biochemical and routine indices. Human rhinovirus nucleic acid test results were positive, whereas all other etiological and serological tests were negative (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eResults of laboratory examinations\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"6\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTest Category\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eResult\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eChanges\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eNormal Range\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eTest Category\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eReports\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eBlood routine\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eFecal examination\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003ePositive occult blood\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLymphocyte count, 10\u003csup\u003e9\u003c/sup\u003e/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.83\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1.2\u0026ndash;3.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eFecal examination\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003ePositive fecal fat globules\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRed blood cell count, 10\u003csup\u003e12\u003c/sup\u003e/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3.46\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.1\u0026ndash;5.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ePleural and peritoneal effusion chylous test\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003ePositive\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHemoglobin, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e102\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e114\u0026ndash;154\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e\u003cb\u003eBiochemistry of serous fluid\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eBlood biochemistry\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eTotal protein in pleural and peritoneal effusion, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e8.15\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal protein, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e29.47\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e65\u0026ndash;85\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eAlbumin in pleural and peritoneal effusion, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e4.76\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAlbumin, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e15.44\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e40\u0026ndash;55\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eChest and abdominal fluid sugar, mmol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e5.7\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlobulin, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e14.03\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e20\u0026ndash;40\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eLactate dehydrogenase in pleural and peritoneal effusion, U/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e150.91\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAlbumin/Globulin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1.2\u0026ndash;2.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eAdenosine deaminase in pleural and peritoneal effusion, U/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e2.55\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlutamic-pyruvic transaminase, U/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e10\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e7\u0026ndash;40\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eRoutine examination of pleural and peritoneal effusion\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGlutamic oxaloacetic transaminase, U/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e17.44\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e13\u0026ndash;35\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eColor\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eMilky white\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum creatinine, \u0026micro;mol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e35.69\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e41\u0026ndash;73\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eAppearance\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eTurbid\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eK+, mmol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e3.06\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e3.5\u0026ndash;5.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eCoagulation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNa+, mmol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e134.84\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e137\u0026ndash;147\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eDensity\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1.019\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCa2+, mmol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e1.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2.1\u0026ndash;2.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eLi Fangta experiment\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003ePositive\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum iron\u0026thinsp;+\u0026thinsp;total binding capacity\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eRed blood cell count, mm\u003csup\u003e3\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e639\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFe, \u0026micro;mol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5.74\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e7.8\u0026ndash;32.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNucleated cell count, mm\u003csup\u003e3\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e1281\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eUnsaturated iron, \u0026micro;mol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e14.60\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e25\u0026ndash;50.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eneutrophil granulocyte%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e75\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal iron-binding capacity, \u0026micro;mol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e20.34\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e45\u0026ndash;77\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eLymphocyte%\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003e25\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum transferrin saturation, %\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e28.22\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e20\u0026ndash;55\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eHuman rhinovirus nucleic acid\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003ePositive\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGranulocyte\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eGonadal complete set\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGranulocyte, %\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4.15\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026uarr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.83\u0026ndash;2.24\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eHepatitis B three systems\u0026thinsp;+\u0026thinsp;Hepatitis C\u0026thinsp;+\u0026thinsp;HIV\u0026thinsp;+\u0026thinsp;syphilis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGranulocyte count, 10\u003csup\u003e9\u003c/sup\u003e/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e162.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026uarr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e35.8\u0026ndash;99.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eAntibodies against respiratory pathogens, IgM\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRatio of granulocyte\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e23.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026uarr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e3.2\u0026ndash;13.5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ePleural and peritoneal effusion culture\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAnemia markers\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eFull set of autoantibodies\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFolate, nmol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6.13\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e7\u0026ndash;46.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eTORCH5items\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eVitamin B12, pmol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e104\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e138\u0026ndash;652\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eSpecific cellular immunoassay for tuberculosis bacteria\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFerroprotein (FER), ng/mL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e42.29\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4.63\u0026ndash;204\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e24-h urinary protein\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eImmune function\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIgG, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2.76\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e8.6\u0026ndash;17.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIgA, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1\u0026ndash;4.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIgM, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e-\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.5\u0026ndash;2.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eComplement C3, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.59\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026darr;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.7\u0026ndash;1.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eComplement C4, g/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0.12\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0.1\u0026ndash;0.4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e\n\u003ch3\u003eImaging examination\u003c/h3\u003e\n\u003cp\u003eComputed tomography scanning revealed pleural, abdominal, and pelvic effusions, dilation of the lumen of the small intestine\u0026ndash;sigmoid colon, gas accumulation, fluid accumulation, and multiple enlarged mesenteric lymph nodes (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The pleural effusion was milky white (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eb). Radionuclide lymphatic imaging (ECT) showed an abnormal distribution of imaging agents in the bilateral abdominal cavity and the right lower abdomen, which mostly indicated the possibility of chylothorax and ascites (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003ec). Positron emission tomography-CT revealed no obvious abnormalities, and lymphoma was ruled out. Colonoscopy revealed edema of the ileal mucosa, which presented as diffuse patchy changes with a Cauley-like surface (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003ea). A biopsy specimen was obtained from the ileocecal region, and microscopic examination revealed sparse mucosal glands in the intestinal mucosa of the terminal ileum, some dilated lymphatic vessels in the lamina propria, and scattered inflammatory cell infiltration (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eb).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e\n\u003ch3\u003eFinal diagnosis\u003c/h3\u003e\n\u003cp\u003eThe patient was diagnosed with PIL.\u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eTreatment\u003c/h2\u003e \u003cp\u003eConservative treatment, such as supplementing human albumin, correcting electrolyte imbalance, nutritional support, gastrointestinal decompression, acid suppression, stomach protection, and dietary adjustment, was provided. After 15 days of standardized intervention, the patient's symptoms gradually improved, and eventually he was in good physical condition and was discharged from the hospital smoothly.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eOutcome and follow-up\u003c/h3\u003e\n\u003cp\u003eThe patient was instructed to follow a low-fat, high-protein diet plan that was supplemented with oral medium-chain triglyceride (MCT) nutritional powder, calcium, and vitamin D supplements. Follow-up examinations were conducted 1 month and 3 months after discharge. The results of both follow-ups showed that the patient's related clinical symptoms were completely relieved, and all laboratory indicators returned to the normal range, with stable disease condition.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003ePIL is a protein-losing gastrointestinal disease that is rare in clinical practice. The key pathological mechanism involves an abnormal lymphatic vessel structure, which leads to the leakage of lymph rich in proteins, lymphocytes, and fat from the intestinal mucosal or serosal layer, and results in a series of clinical abnormalities, such as hypoproteinemia, decreased lymphocyte count, hypolipidemia, and luminal effusion [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Among these, PIL is mostly associated with congenital lymphatic dysplasia wherein the pathogenesis is not yet fully understood, and the clinical phenotypes are diverse. Some patients lack the typical symptoms of edema and diarrhea, which can easily lead to misdiagnosis and missed diagnosis [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. The clinical characteristics of the patient in this case were consistent with the pathophysiological mechanisms of PIL. The patient presented with incomplete intestinal obstruction, mild anemia, edema, hypokalemia, and hypocalcemia, which are consistent with the typical manifestations of PIL caused by electrolyte imbalance and nutrient absorption disorders secondary to lymphatic loss. The loss of immune components in the lymphatic fluid further weakens the immune function and contributes to the pathological presentation [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. On laboratory examination, the deviation from the normal reference range of the absolute count of peripheral blood lymphocytes is a characteristic indicator of PIL, as continuous leakage of lymphatic fluid leads to a large loss of peripheral blood lymphocytes, which is an important diagnostic parameter [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. The simultaneous decrease in the patient's plasma albumin and IgG levels constitutes a key laboratory basis for a diagnosis of PIL [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Endoscopy and pathological examinations are the key methods for diagnosing PIL. In this case, colonoscopy and pathological examination clearly confirmed the presence of small intestinal lymphatic vessel dilation, which directly affirmed the anatomical basis of the lesions [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Routine fecal tests indicated positive occult blood and fat globules, the peritoneal effusion was milky white, ECT suggested possible chylous pleural and peritoneal effusion, and a positive chylous test further completed the closed loop of the diagnostic chain through auxiliary evidence of intestinal protein loss and the leakage indicated on radionuclide angiography [\u003cspan additionalcitationids=\"CR12\" citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. The differential diagnosis of PIL should focus on excluding other diseases that can lead to protein loss, lymphocytopenia, and intestinal obstruction and avoid misdiagnosis caused by overlapping symptoms [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. When differentiated from nephrotic syndrome, the latter is characterized by massive proteinuria (\u0026gt;\u0026thinsp;3.5 g/d) and hyperlipidemia as its core features. However, in this case, the patient's urinary protein level was negative and the creatinine level was normal, with no evidence of kidney damage [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. For differentiation from liver cirrhosis, the decompensated stage of liver cirrhosis is frequently accompanied by abnormal liver function and signs of portal hypertension (e.g., ascites and esophageal and gastric varices). In this case, the patient's liver function indicators were normal, and there were no related imaging manifestations that met the diagnostic criteria for liver cirrhosis [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. PET-CT examination showed no space-occupying lesions, which ruled out small intestinal lymphangiectasia secondary to malignant tumors such as lymphoma [\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Negative results from tuberculosis-related laboratory tests, combined with no symptom of tuberculosis, such as low fever and night sweats, ruled out the possibility of tuberculous pleural and peritoneal effusions [\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]. The results of all autoimmune-related tests were negative and did not support the possibility of intestinal mucosal damage or protein loss caused by autoimmune diseases [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Through the above systematic differentiation, the diagnosis of PIL was confirmed. For treatment, Alfano et al. [\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e] proposed that the primary goal of PIL treatment is to reduce protein loss, maintain the circulating blood volume, and inhibit excessive tissue fluid production. Therefore, conservative medical treatment is the preferred clinical management. Early treatment in this case mainly focused on symptom-based support as follows: supplementing albumin to correct hypoproteinemia, supplementing fat-soluble vitamins to improve the state of nutritional deficiency, actively correcting electrolyte imbalance to alleviate symptoms related to hypokalemia and hypocalcemia [\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e], simultaneously reducing tissue edema through diuresis and resolution of edema, regulating intestinal flora to improve digestive and absorptive functions, and developing a foundation for long-term maintenance treatment [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. Octreotide, a natural endogenous somatostatin analog, can aid the reduction of lymphatic leakage through mechanisms such as inhibition of gastrointestinal peristalsis, intestinal blood flow, and lymphatic secretion, and prevention of fatty acid absorption, and thus has become an important adjunctive treatment with internal medicine treatment. Dietary adjustment is at the core of the long-term management of PIL. In this case, a low-fat, high-protein diet supplemented with MCT was adopted [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. In the gastrointestinal tract, MCT decomposes into glycerol and medium-chain fatty acids, which is directly absorbed into the portal vein through small intestinal epithelial cells without being transported through the lymphatic vessels, and thereby effectively reduces the pressure within the lymphatic vessels and minimizes lymphatic leakage and protein loss. Although an MCT-based diet cannot reverse the congenital structural abnormalities of lymphatic vessels, many clinical studies have confirmed that it can significantly improve the clinical symptoms of patients with PIL, reduce the long-term mortality rate, and is a key component of disease management [\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. Surgical treatment is applicable only in specific cases as most PIL cases are caused by congenital diffuse lymphatic dysplasia [\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e]. For patients with localized lesions who do not respond to medical treatment, intestinal resection (removal of the diseased intestinal segment) or venolymphatic anastomosis can be considered. However, it is necessary to strictly control the surgical indications, accurately assess the extent of the lesion, and ensure that the diseased tissue is completely removed whereas avoiding short bowel syndrome due to excessive intestinal resection [\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e, \u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e]. Moreover, it is necessary to adhere to an MCT diet and nutritional support postoperatively to maintain the therapeutic effect [\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn conclusion, for patients without a clear medical history or clinical manifestations such as incomplete intestinal obstruction, hypoproteinemia, edema, electrolyte imbalance, and lymphopenia, PIL should be included in the differential diagnosis and confirmed through multidimensional examinations, such as laboratory tests, endoscopic pathology, imaging, and radionuclide angiography, with systematic differentiation to rule out similar diseases. After diagnosis, a comprehensive treatment plan of \"symptomatic support\u0026thinsp;+\u0026thinsp;drug assistance\u0026thinsp;+\u0026thinsp;dietary adjustment\" should be adopted. As a core intervention measure, the MCT diet can effectively improve the clinical symptoms of patients. Combined with surgical treatment, when necessary, good long-term disease control would improve patient prognosis.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003e\u003cstrong\u003eMCT\u0026nbsp;\u003c/strong\u003emedium-chain triglyceride\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePIL\u0026nbsp;\u003c/strong\u003ePrimary intestinal lymphangiectasia\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis article is based on a case report that is exempt from review by an IRB. The patient provided informed consent for the publication of this case report.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe publication of this case report and any accompanying images has been approved by the patient with their informed consent.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe data supporting the findings of this study are available within the article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis work was supported by the Gansu Province Health Industry Project (Grant number GSWSKY2020-37) and the Joint Scientific Research Project of Science and Technology Department of Gansu Province (Grant number 23JRRA1546).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors' contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eJunlong Gao and Qianqian Zhou were responsible for collecting patient medical records and assisting in data organization. Tianpeng He was responsible for writing the initial draft of the paper and conducting the review of relevant literature. Yuan Yuan and Dongliang Wang were the attending doctors responsible for diagnosing the patient. All authors made contributions to the paper. All the authors have read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe would like to thank Editage (www.editage.cn) for English language editing.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical trial number\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003enot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAdditional files\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePatient Informed Consent Form\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eWaldmann TA, Steinfeld JL, Dutcher TF, Davidson JD, Gordon RSJ. The role of the gastrointestinal system in idiopathic hypoproteinemia. Gastroenterology. 1961;41:197\u0026ndash;207.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOzen A, Lenardo MJ. Protein-losing enteropathy. N Engl J Med. 2023;389:733\u0026ndash;48.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCao Y, Feng XH, Ni HX. Primary intestinal lymphangiectasia presenting as limb convulsions: A case report. World J Clin Cases. 2022;10:6234\u0026ndash;40.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDong J, Xin J, Shen W, Wen T, Chen X, Sun Y, et al. CT Lymphangiography (CTL) in primary intestinal lymphangiectasia (PIL): A comparative study with intraoperative enteroscopy (IOE). Acad Radiol. 2019;26:275\u0026ndash;81.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eVignes S, Bellanger JM. Primary intestinal lymphangiectasia (Waldmann's disease). Orphanet J Rare Dis. 2008;3:5.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKatsinelos P, Fasoulas K, Beltsis A, Chatzimavroudis G, Paroutoglou G, Maris T, et al. Diagnostic yield and clinical impact of wireless capsule endoscopy in patients with chronic abdominal pain with or without diarrhea: A Greek multicenter study. Eur J Intern Med. 2011;22:e63\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAlshikho MJ, Talas JM, Noureldine SI, Zazou S, Addas A, Kurabi H, et al. Intestinal lymphangiectasia: Insights on management and literature review. Am J Case Rep. 2016;17:512\u0026ndash;22.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eStrober W, Wochner RD, Carbone PP, Waldmann TA. Intestinal lymphangiectasia: A protein-losing enteropathy with hypogammaglobulinemia, lymphocytopenia and impaired homograft rejection. J Clin Investig. 1967;46:1643\u0026ndash;56.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFreeman HJ. Small intestinal mucosal biopsy for investigation of diarrhea and malabsorption in adults. Gastrointest Endosc Clin N Am. 2000;10:739.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePreisich P, Farkas I, Bajn\u0026oacute;czy B, N\u0026eacute;meth L. Duodenoszk\u0026oacute;ppal \u0026eacute;s c\u0026eacute;lzott biopszi\u0026aacute;val diagnosztiz\u0026aacute;lt lymphangiectasia intestinalis. Orv Hetil. 1979;120:1387\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eIida F, Wada R, Sato A, Yamada T. Clinicopathologic consideration of protein-losing enteropathy due to lymphangiectasia of the intestine. Surg Gynecol Obstet. 1980;151:391\u0026ndash;5.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZelmanovitz F、Ricardo Masiero P、Le\u0026atilde;o, Spiro B. Unusual excretion of Tc-99m MDP in regional intestinal lymphangiectasia. Clin Nucl Med. 2003;28:509\u0026ndash;10.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCastell\u0026oacute;n M\u0026eacute;ndez AJ, Bod\u0026aacute;n Campbell A, Rosales Obreg\u0026oacute;n V, Zahran M. Waldmann's disease: Primary intestinal lymphangiectasia diagnosed by 99mTc-labeled albumin macroaggregate scintigraphy-A case report in an adult patient. Clin Case Rep. 2024;12:e8772.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDe Sousa JS, Guerreiro O, Cunha A, Ara\u0026uacute;jo J. Association of nephrotic syndrome with intestinal lymphangiectasia. Arch Dis Child. 1968;43:245\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMiura S, Asakura H, Munakata Y, Kobayashi K, Yoshioka M, Morishita T, et al. Lymphatic role in the pathogenesis of fat malabsorption in liver cirrhosis in rats. Dig Dis Sci. 1982;27:1030\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGuan W, Wang QS, Wu HB, Zhou WL. 18F-FDG PET/CT findings of primary intestinal lymphoma: Analysis of 23 cases. Nan Fang Yi Ke Da Xue Bao. 2016;36:1175\u0026ndash;80.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu YY, Chen MK, Cao Z, Liu SZ, Ding BJ. Differential diagnosis of intestinal tuberculosis from Crohn's disease and primary intestinal lymphoma in China. Saudi J Gastroenterol: Off J Saudi Gastroenterol Assoc. 2014;20:241\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAlfano V, Tritto G, Alfonsi L, Cella A, Pasanisi F, Contaldo F. Stable reversal of pathologic signs of primitive intestinal lymphangiectasia with a hypolipidic, MCT-enriched diet. Nutrition. 2000;16:303\u0026ndash;4.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKlingenberg RD, Homann N, Ludwig D. Type I intestinal lymphangiectasia treated successfully with slow-release octreotide. DIGEST DIS SCI. 2003;48(8):1506\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDesai AP, Guvenc BH, Carachi R. Evidence for medium chain triglycerides in the treatment of primary intestinal lymphangiectasia. Eur J Pediatr Surg. 2009;19:241\u0026ndash;5.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNiu Y, Wu Q, Wang Y, Lu L, Feng Y, Cai W, et al. Primary intestinal lymphangiectasia in children: Twelve years of experience in the diagnosis and management. Asia Pac J Clin Nutr. 2021;30:358\u0026ndash;64.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKwon Y, Kim MJ. The update of treatment for primary intestinal lymphangiectasia. Pediatr Gastroenterol Hepatol Nutr. 2021;24:413\u0026ndash;22.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNorman JS, Testa S, Wang CX, Savage T. Milky way: Management of primary intestinal lymphangiectasia. Dig Dis Sci. 2023;68:3872\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"international-journal-of-emergency-medicine","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"ijem","sideBox":"Learn more about [International Journal of Emergency Medicine](https://intjem.biomedcentral.com/)","snPcode":"12245","submissionUrl":"https://submission.nature.com/new-submission/12245/3","title":"International Journal of Emergency Medicine","twitterHandle":"@IntJEmergMed","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"PIL, Polyserositis, Hypoalbuminemia, Case report, Prognosis","lastPublishedDoi":"10.21203/rs.3.rs-8548962/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8548962/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003ePrimary intestinal lymphatic dilation (PIL) is a rare disorder that is characterized by abnormal intestinal lymphatic drainage; however, its exact etiology and pathogenesis are yet to be fully elucidated. PIL primarily originates from impaired lymphatic return in the small intestine owing to multiple factors, and leads to increased lymphatic vessel pressure with consequent lymph fluid leakage, malabsorption, and protein loss. The clinical manifestations typically include hypoproteinemia, lymphopenia, diarrhea, and ascites.\u003c/p\u003e\u003ch2\u003eCase presentation:\u003c/h2\u003e \u003cp\u003eA 14-year-old female patient was admitted to the hospital because of exertional dyspnea for half a month, nausea and vomiting accompanied by abdominal distension and pain for 10 days, and bilateral lower limb swelling for 3 days. Examination revealed a large amount of fluid accumulation in the abdominal and pelvic cavities, pleural effusion, hypoproteinemia, hypogammaglobulinemia, electrolyte imbalance, decreased lymphocyte count, and a positive result on the chylous test of pleural and abdominal effusions. The CT scan revealed intestinal obstruction, intestinal dilation, and enlargement of the mesenteric lymph nodes. The PET-CT examination ruled out lymphoma. Gastroscopy revealed that the ileal mucosa was edematous, with diffuse patchy changes and granular protrusions on the surface. An ileal biopsy showed dilated lymphatic vessels within the lamina propria, accompanied by infiltration of inflammatory cells. Based on the patient's clinical symptoms and results of the examinations, she was diagnosed with small intestinal lymphatic dilation. After conservative treatment, including albumin supplementation, electrolyte imbalance correction, and nutritional support, the patient's symptoms were alleviated and she was discharged.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThe diagnosis of pediatric small intestinal lymphangiectasia requires a comprehensive consideration of clinical symptoms, laboratory tests, imaging examinations, and endoscopic pathological biopsy results. Pathological histology is key to confirming a diagnosis. The early implementation of targeted conservative treatment can effectively improve patient prognosis.\u003c/p\u003e","manuscriptTitle":"Primary Small Intestine Lymphatic Dilation Syndrome: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-16 17:13:04","doi":"10.21203/rs.3.rs-8548962/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-13T00:32:42+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-12T01:03:30+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"329339866681906969159328546270038141229","date":"2026-03-06T16:29:27+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-02T09:24:31+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"223428607084397571542491199622676584183","date":"2026-02-26T14:10:28+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"9630912237497576025712989768612775472","date":"2026-02-25T01:18:10+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-21T14:40:57+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"339355573356746108621284444150916394648","date":"2026-02-21T07:27:58+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-20T16:47:31+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"103793104751592225297629965690610563680","date":"2026-02-20T16:34:30+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"24400808471897127777205353523891970202","date":"2026-02-20T08:19:29+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-17T21:18:33+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"123847044591780849698714461559729111062","date":"2026-02-17T16:05:00+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"291671149968974875045825542445724025867","date":"2026-02-15T17:00:12+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-02-10T14:02:06+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-13T05:04:35+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-13T05:03:20+00:00","index":"","fulltext":""},{"type":"submitted","content":"International Journal of Emergency Medicine","date":"2026-01-08T08:22:47+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"international-journal-of-emergency-medicine","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"ijem","sideBox":"Learn more about [International Journal of Emergency Medicine](https://intjem.biomedcentral.com/)","snPcode":"12245","submissionUrl":"https://submission.nature.com/new-submission/12245/3","title":"International Journal of Emergency Medicine","twitterHandle":"@IntJEmergMed","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"34aa3bea-585d-4d38-8831-96d941ff2eb5","owner":[],"postedDate":"February 16th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-04-02T11:09:40+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-16 17:13:04","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8548962","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8548962","identity":"rs-8548962","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}