Risk Of Splenic Rupture Research Articles

American Medical Society of Sports Medicine Position Statement: Mononucleosis and Athletic Participation.

Infectious mononucleosis (IM) is a common illness in children and young adults caused primarily by the Epstein-Barr Virus (EBV). Transmission occurs primarily through sharing oral secretions, thus IM is known as the "kissing disease." Common clinical manifestations include fever, pharyngitis, posterior cervical lymphadenopathy, and splenomegaly. Atypical lymphocytosis and transaminase elevations are common, and the diagnosis of IM is confirmed with laboratory findings of a positive heterophile antibody ("Monospot"), polymerase chain reaction, or antibodies specific to EBV. Individuals with acute IM may be quite symptomatic and not feel well enough to participate in sports. Splenic enlargement is common, with rupture a relatively rare occurrence, typically occurring within a month of symptom onset, but this risk complicates sports participation, and is often the reason for restricting activity. The management of IM is primarily supportive, with no role for antivirals or corticosteroids. The variability of clinical presentation and the risk of splenic rupture in patients with IM present clinicians with challenging return to play/return to sport (RTS) decisions. This position statement updates the Evidence-Based Subject Review on Mononucleosis by the American Medical Society for Sports Medicine published in 2008 and reviews the epidemiology, clinical manifestations, laboratory assessment, and management including RTS for the athlete with IM. This statement also addresses complications, imaging, special considerations, diversity and equity considerations, and areas for future clinical research. Understanding the evidence regarding IM and sport is essential when communicating with athletes and their families and incorporating shared decision-making in the RTS decision.

Laparoscopic approach in the treatment of splenic angiolipomatous hamartoma: the first report of a case.

Angiolipomatous hamartoma is a benign mesenchymal proliferation of unknown aetiology. Only a few cases have been documented in the published literature. This current case report describes a 57-year-old female patient who was hospitalized for an assessment of a previously radiologically-verified splenic lesion and further treatment. The patient had been surgically treated 10 years previously; a lobectomy of the superior left pulmonary lobe had been performed in order to remove a verified tumour lesion. A complete radiological examination was undertaken, which verified a spleen of a size that was within the physiological range, with a centrally-located lobular tumour lesion. Given the risk of splenic rupture, as well as the fact that the lesion's aetiology was still undetermined, and finally the fact that differential diagnostics indicated the possibility of a metastasis, the patient was treated surgically. Laparoscopic splenectomy, in the treatment of splenic diseases, even rare ones such as this, is not a novelty. Indeed, it needs to be applied as the standard approach, with the well-known benefits that the minimalized approach offers.

Spontaneous splenic rupture as the first clinical manifestation of Niemann-Pick disease type B: A case report and review of the literature

Splenomegaly is the most common phenotype for Niemann-Pick disease type B (NPD-B), an autosomal recessive lipid storage disease caused by deficiency of the lysosomal enzyme acid sphingomyelinase. Although a spleen of massive volume is common in NPD-B, splenic rupture in this disease is rarely reported. We describe a patient with NPD-B who initially presented with spontaneous splenic rupture. Microscopic examination of the spleen specimen revealed expansion of the red pulp by abundant foamy histiocytes. A literature review revealed that splenic rupture resulting from latent splenomegaly may occur in middle adulthood in a mild form of NPD-B associated with SMPD1 variants of lower pathogenicity. We suggest that unexplained splenomegaly or splenic rupture should raise the possibility of a lysosomal storage disease, including NPD. For patients with NPD-B, spleen size should be evaluated periodically, and the risk of splenic rupture should always be considered.

S3520 Epstein-Barr Virus-Induced Acute Hepatitis

INTRODUCTION: Epstein-Barr virus (EBV) is a causative agent of infectious mononucleosis syndrome in young adults. It causes asymptomatic liver-associated enzyme abnormalities in 80 to 90% of cases which are often unrecognized. Jaundice might rarely develop during the clinical course which likely reflects either more severe hepatitis or Epstein-Barr virus infection-associated hemolytic anemia. We report a case of EBV induced acute hepatitis. CASE DESCRIPTION/METHODS: A 28-year-old male with a past medical history of gastroesophageal reflux disease was admitted for yellow skin, nausea, fatigue, fever, and poor oral intake for the last five days. Abdominal exam was benign, but he was noted to have yellow skin and sclera. Blood work showed WBC 9.5 K/uL (lymphocytes 71%), Hb 16.9 g/dL, creatinine 1.0 mg/dL, albumin 3.9 g/dL, AST 541 U/L, ALT 743 U/L, alkaline phosphatase 684 U/L, total bilirubin 12.9 mg/dL with direct bilirubin 10.0 mg/dL. He had acute hepatitis work up like acute hepatitis panel, CMV, Blood culture, COVID-19, HIV, ANA, ASMA which were unremarkable. Ultrasound abdomen did not show gall bladder or biliary etiology. CT abdomen/pelvis showed splenomegaly with mild portal caval lymphadenopathy. He was found to have positive monospot and EBV PCR. He subsequently had a liver biopsy consistent with EBV positive lymphocytes. He was treated conservatively with good clinical improvement. DISCUSSION: Acute viral hepatitis in human can be caused by a variety of viruses with a wide range of clinical manifestations and laboratory findings. EBV is a rare causative agent of acute hepatitis, during the course of infectious mononucleosis. Hepatic manifestations of EBV are usually mild and resolve without serious complications. Treatment in these patients is supportive—namely to remain hydrated with an adequate electrolyte balance. Precautions to avoid contact sports are also important to emphasize, as there is a 0.1%–0.5 % risk of splenic rupture, which is fatal. This case highlights the importance of including EBV in the differential diagnosis of acute hepatitis in adults.

Coexistence of diffuse panbronchiolitis and sarcoidosis revealed during splenectomy: a case report

BackgroundSarcoidosis is a systemic granulomatous disease caused by CD4+ cell-dominant inflammation. Meanwhile, diffuse panbronchiolitis is a chronic inflammatory respiratory disease predominantly caused by CD8+ lymphocytes and neutrophils. Herein, we report a rare case of sarcoidosis in which the clinical presentation had become evident as diffuse panbronchiolitis after splenectomy for sarcoidosis.Case presentationA 23-year-old Japanese woman was referred to our hospital due to splenomegaly of unknown etiology. Upon admission, chest computed tomography scan revealed centrilobular and randomly distributed small nodules in both lungs. Bronchoalveolar lavage revealed a high proportion of lymphocytes and a decreased CD4/CD8 ratio. However, the biopsy specimens obtained from both the liver and lungs revealed noncaseating epithelioid granulomas, which confirmed the diagnosis of sarcoidosis. The patient underwent splenectomy due to progressive cytopenia and high risk of splenic rupture. After the surgery, the condition of the patient was consistently good for 3 months. Then, she gradually developed productive cough and dyspnea. Both sinus and chest computed tomography scan revealed chronic paranasal sinusitis and deterioration of centrilobular nodules in both lung fields, respectively. The second bronchoalveolar lavage revealed a high proportion of neutrophils, and the bronchoalveolar lavage fluid tested positive for Hemophilus influenzae. The titer of cold agglutinin was elevated, thereby confirming the diagnosis of diffuse panbronchiolitis. On the basis of the clinical and radiological findings, the condition of the patient improved with low-dose macrolide therapy for 3 months.ConclusionsThe coexistence of sarcoidosis and diffuse panbronchiolitis has not been previously reported, and the hidden profiles of diffuse panbronchiolitis may have been revealed by splenectomy.

Splenic Lesions in a Patient With Crohn’s Disease

Question: A 35-year-old woman with severe Crohn’s disease presented for evaluation of a persistent continuous low-grade fever and asthenia for few days. She was treated at that time with thalidomide (100 mg/d) and oral prednisone (20 mg/d) Physical examination was unremarkable. Her past medical history was significant for a colonic and perianal Crohn’s disease refractory to medical therapy including corticoids, azathioprine, infliximab, and adalimumab. She underwent total proctocolectomy with definitive ileostomy. Laboratory tests showed elevated white blood cells (14,700/μL) and C-reactive protein (57 mg/L; normal, <5). Liver function tests, amylase, and lipase levels were normal. All microbiological samples were negative. Abdominal CT (Figure A) demonstrated splenic hypodense and multiloculated lesions suggestive of splenic abscesses. Follow-up MRI (Figure B) showed progression of these splenic lesions with heterogeneous high signal on T2-weighted images and peripheral contrast enhancement. Ultrasound-guided needle puncture of the cysts showed hemorrhagic liquid with damaged neutrophils and macrophages; bacteriologic, mycologic, and parasitologic examinations were negative. Because of persistent fever and risk of splenic rupture, the patient underwent diagnostic and therapeutic splenectomy. Postoperative recovery was uneventful. Macroscopically (Figure C), there were round masses (the largest was 6 cm) into the spleen, filled with a white-grayish fluid and thick wall. Figure D shows a low-power view of microscopic sections (H&E staining). What is the diagnosis? Look on page 716 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Microscopically, the lesions were characterized by a necrotic center, containing damaged neutrophils and a peripheral area containing histiocytes and macrophages. Gram, Ziehl-Neelsen, periodic acid Schiff, and Groccott stains did not identify pathogenic microorganisms. Aseptic abscesses syndrome is a systemic disorder of unknown etiology. Aseptic abscesses are characterized by deep, sterile, round lesions consisting of neutrophils that do not respond to antibiotics, but usually improve with corticosteroids. Typical presentation of aseptic abscesses syndrome includes fever, abdominal pain, leukocytosis, and presence of intraabdominal aseptic lesions.1André M.F. Piette J.C. Kémény J.L. et al.Aseptic abscesses: a study of 30 patients with or without inflammatory bowel disease and review of the literature.Medicine. 2007; 84: 145-161Crossref Scopus (111) Google Scholar The abscesses involve the spleen in 90% of patients.2Coat N. Le Berre-Heresbach N. Poinsignon Y. et al.Crohn’s disease complicated by multiple and recurrent aseptic splenic abscesses.Gastroenterol Clin Biol. 2001; 25: 425-428PubMed Google Scholar Rarely, abscesses can be extraabdominal, such as pulmonary, cerebral, or cutaneous. Aseptic abscesses have been described in inflammatory bowel disease, especially in Crohn’s disease and in other inflammatory diseases.3Zakout R. Fonseca M. Santos J.M. et al.Multiple aseptic liver abscesses as the initial manifestation of Crohn’s disease: report of a case.Dis Colon Rectum. 2009; 52: 343-345Crossref PubMed Scopus (14) Google Scholar Diagnosis relies on a combination of a typical clinical and radiological presentation (ie, deep abscesses), the pathologic findings with neutrophilic features, and the exclusion of alternative diagnosis, especially infectious disease. All the infectious investigations have to be negative. Antibiotics are inefficient but there is marked improvement with corticosteroids (1 mg/kg of prednisone or equivalent recommended).1André M.F. Piette J.C. Kémény J.L. et al.Aseptic abscesses: a study of 30 patients with or without inflammatory bowel disease and review of the literature.Medicine. 2007; 84: 145-161Crossref Scopus (111) Google Scholar It is often a relapsing condition (within the spleen or in other locations after splenectomy) and additional immunosuppressive therapy is required in almost one-half of the patients.1André M.F. Piette J.C. Kémény J.L. et al.Aseptic abscesses: a study of 30 patients with or without inflammatory bowel disease and review of the literature.Medicine. 2007; 84: 145-161Crossref Scopus (111) Google Scholar

English

BACKGROUND: Splenomegaly with an incidence of about 2-5% is a challenging medical problem. Splenomegaly during pregnancy presents a further testing situation for the obstetrician. The diagnosis especially during advanced gestation becomes difficult by clinical examination. Further the risk of splenic rupture may increase in pregnancy due to several physiological and mechanical reasons. It is noteworthy that anemia which is a frequent association with splenomegaly is also an important medical condition of pregnancy. CASE REPORT: We report three cases of massive splenomegaly with pregnancy (all with different etiology and presentation) first with severe anemia, second with dragging pain and third with recurrent fever and its adverse effects on pregnancy outcomes. Though none of our patient had the life threatening splenic rupture but we found association of massive splenomegaly with fetal growth restriction and aggravation of preexisting anemia requiring blood components. To the best of our knowledge, there are no published reports indicating adverse effects of massive splenomegaly on pregnancy outcome.

Liver Transplantation for Massive Hepatic Lymphangiomatosis in a Child

Liver Transplantation for Massive Hepatic Lymphangiomatosis in a Child

Mobilization of Hematopoietic Stem Cells in a Thalassemic Mouse Model: Implications for Human Gene Therapy of Thalassemia

Granulocyte colony-stimulating factor (G-CSF)-mobilized blood stem cells may become the preferable source of hematopoietic stem cells (HSCs) for gene therapy because of the higher yield of cells compared with conventional bone marrow harvesting. A G-CSF-associated risk of splenic rupture has been recognized in normal donors of HSCs, but limited information is available about the G-CSF effect in the presence of splenomegaly and extramedullary hematopoiesis. We investigated the G-CSF effect in a thalassemic mouse model (HBB(th-3)) as compared with a normal strain (C57BL/6), in terms of safety, mobilization efficacy, and distribution of stem cells among hematopoietic compartments. There was no death or clinical sequelae of splenic rupture in G-CSF-treated animals of either strain; however, hemorrhagic infarcts in the spleen were detected with low frequency in G-CSF-treated HBB(th-3) mice (12.5%). HBB(th-3) mice mobilized less effectively than C57BL/6 mice (Lin(-)Sca-1(+)c-Kit(+) cells/microl of peripheral blood mononuclear cells [PBMCs]: 90 +/- 55 vs. 255 +/- 174, respectively, p = 0.01; CFU-GM/ml PBMCs: 390 +/- 262 vs. 1131 +/- 875, p = 0.01) because of increased splenic trapping of hematopoietic stem and progenitor cells (Lin(-)Sca-1(+)c-Kit(+) cells per spleen (x10(5)): 487 +/- 35 vs. 109 +/- 19.6, p = 0.01; CFU-GM per spleen (x10(2)): 1470 +/- 347 vs. 530 +/- 425, p = 0.0006). Splenectomy restored the mobilization proficiency of thalassemic mice at comparable levels to normal mice and resulted in the development of a hematopoietic compensatory mechanism in the thalassemic liver that protected splenectomized mice from severe anemia. Our data imply that, in view of human gene therapy for thalassemia, either multiple cycles or alternative ways of mobilization may be required for a sufficient yield of transplantable HSCs. In addition, strategies to minimize the risk of G-CSF-induced splenic infarcts should be explored in a clinical setting.

Spontaneous Splenic Rupture in Infectious Mononucleosis

Abdominal complaints in patients with infectious mononucleosis should alert the surgeon to the potential, and possibly fatal, risk of splenic rupture. Radiologic evaluation by ultrasonography and computed tomography is indicated for appropriate management. We describe a case in which a diagnosis of splenic rupture occurring spontaneously on a background of infectious mononucleosis was made as a result of a high index of suspicion. The patient was treated conservatively.

G-CSF-induced spleen size changes in peripheral blood progenitor cell donors.

PBPC donors given G-CSF experience splenic enlargement and, rarely, spontaneous rupture of the spleen. This study evaluated the incidence and time course of splenic enlargement in PBPC concentrate donors and assessed factors affecting size changes. Twenty healthy adults were given G-CSF (10 microg/kg/day) for 5 days and a PBPC concentrate was collected by apheresis. Ultrasound was used to assess craniocaudal spleen length before giving G-CSF, on the day of apheresis and 3 or 4 days after apheresis. The effects of donor age, gender, race, and changes in blood chemistries, blood counts, and CD34+ cell counts on spleen length change were assessed. Spleen length increased in 19 of 20 donors. Mean length changed from 10.9 +/- 2.0 cm before G-CSF to 12.3 +/- 2.1 cm on the day of apheresis (p < 0.001). The mean increase in length was 1.5 +/- 0.9 cm or 13.8 +/- 9.1 percent. Spleen length increased 20 percent or more in six subjects. The spleen length fell to 11.3 +/- 1.8 cm (p < 0.001) 3 or 4 days after apheresis, but it remained greater than baseline levels (p = 0.03). Spleen length change was not affected by donor gender, race, or age. There was no relationship between changes in spleen length and 1) baseline and apheresis-day blood counts and chemistries, or 2) changes in blood counts and chemistries. Spleen size increases in almost all PBPC donors. Enlargement is transient but may be marked in some donors and may place them at risk for splenic rupture.

Splenic infarction: sonographic patterns, diagnosis, follow-up, and complications.

Forty splenic infarcts in 23 patients were examined with ultrasound (US). At clinical presentation, splenic infarction was associated with severe left upper quadrant pain (n = 10) or diffuse abdominal pain (n = 4) or was asymptomatic (n = 9). In this retrospective study, predominantly wedge-shaped (n = 17) or round (n = 23), irregularly delineated (n = 33) or smooth (n = 7), hypoechoic (n = 40) and anechoic (n = 5) lesions were found at first examination. During follow-up observation, four patients died because of complications unrelated to infarct, and five patients underwent splenectomy as a consequence of US findings. Expanding intralienal liquefaction, increasing subcapsular hemorrhage, free peritoneal blood (even in spleens shown to have an intact surface at sonography), and flow phenomena in the area of infarction demonstrated at B-mode pulsed Doppler US were identified as infarct-related complications associated with the risk of splenic rupture. Despite the high self-healing tendency in splenic infarction, short-term follow-up with US is recommended for early recognition of these possible complications.