Spontaneous Splenic Rupture in a Vivax Malaria Case Treated with Transcatheter Coil Embolization of the Splenic Artery

An enlarged spleen is considered one of the most common signs of malaria, and splenic rupture rarely occurs as an important life-threatening complication. Splenectomy has been recommended as the treatment of choice for hemodynamically unstable patients. However, a very limited number of splenic rupture patients have been treated with transcatheter coil embolization. Here we report a 38-year-old Korean vivax malaria patient with ruptured spleen who was treated successfully by embolization of the splenic artery. The present study showed that angiographic embolization of the splenic artery may be an appropriate option to avoid perioperative harmful effects of splenectomy in malaria patients.     

Spontaneous splenic rupture in infectious mononucleosis: a review.

Spontaneous rupture of the spleen is a rare complication of infectious mononucleosis (IM) occurring in 0.1-0.5 percent of patients with proven IM [1]. Although splenectomy has been advocated as the definitive therapy in the past, numerous recent reports have documented favorable outcomes with non-operative management. A review of the literature suggests that non-operative management can be successful if appropriate criteria, such as hemodynamic stability and transfusion requirements are applied in patient selection. We report the case of a 36 year old man with infectious mononucleosis who had a spontaneous splenic rupture and who was successfully managed by splenectomy. Based on review of the literature, an approach to management of a spontaneously ruptured spleen secondary to IM is suggested.     

Splenomegaly induced by recombinant human granulocyte-colony stimulating factor in rats

Spontaneous ruptures of the spleen have been observed in donors and patients with malignancy during mobilization of peripheral blood stem cells. Thus, we investigated the morphological and histological alteration of the spleen, and mRNA expression levels and activities of the DNA-synthesizing enzymes thymidylate synthase (TS) and thymidine kinase (TK) in the splenic cells, of rats treated with recombinant human granulocyte-colony stimulating factor (rhG-CSF). Daily injections of rhG-CSF for 5 or 7 days slightly enhanced the splenic weight. Single or 3-day treatment with rhG-CSF markedly enhanced the number of granulocytes in peripheral blood. Expression levels of TS and TK mRNA in the splenic cells were significantly increased 6 hours after rhG-CSF treatment. Early expression of TS and TK mRNA in the splenic cells may indicate a reseeding of hematopoietic cells from the bone marrow. Daily injections with rhG-CSF enhanced the TS and TK activities in the splenic cells. As continuous elevations of DNA-synthesizing enzyme activity and spleno-megaly are suggestive of a possible splenic rupture, the monitoring of peripheral granulocytes and splenic size is necessary during the rhG-CSF treatment.     

Spontaneous splenic rupture in two patients with hematologic malignancy

BACKGROUND: Spontaneous splenic rupture (SSR) is a very rare complication described in several hundred patients, mainly as case reports. It is defined as a splenic rupture without antecedent injury. The authors of the present paper describe the only two SSR cases diagnosed at the Hemato-oncology department, coincidentally in one year. PATIENTS: The first patient was admitted to hospital because of planned chemotherapy for relapsed hairy cell leukemia. The second was directed to the Hemato-oncology outpatient department because of anemia and painful splenomegaly diagnosed by a physician. The diagnose of hematologic malignancy (diffuse large B-cell lymphoma) was determined subsequently on the basis of histological examination of the spleen. CONCLUSION: It is necessary to consider SSR not only in patients with known diagnosis of malignant disease but in the patients with negative anamnesis, too. The aim of the paper is to draw attention to the existence of this complication.     

Physiological clearance of Aβ by spleen and splenectomy aggravates Alzheimer‐type pathogenesis

BackgroundA previous study demonstrated that nearly 40%–60% of brain Aβ flows out into the peripheral system for clearance. However, where and how circulating Aβ is cleared in the periphery remains unclear. The spleen acts as a blood filter and an immune organ. The aim of the present study was to investigate the role of the spleen in the clearance of Aβ in the periphery.MethodsWe investigated the physiological clearance of Aβ by the spleen and established a mouse model of AD and spleen excision by removing the spleens of APP/PS1 mice to investigate the effect of splenectomy on AD mice.ResultsWe found that Aβ levels in the splenic artery were higher than those in the splenic vein, suggesting that circulating Aβ is cleared when blood flows through the spleen. Next, we found that splenic monocytes/macrophages could take up Aβ directly in vivo and in vitro. Splenectomy aggravated behaviour deficits, brain Aβ burden and AD‐related pathologies in AD mice.ConclusionOur study reveals for the first time that the spleen exerts a physiological function of clearing circulating Aβ in the periphery. Our study also suggests that splenectomy, which is a routine treatment for splenic rupture and hypersplenism, might accelerate the development of AD.     

Splenic hematoma as a first manifestation of cytomegalovirus infection

Splenic rupture is rare but life threatening complication of mononucleosis syndrome. It has been suggested that subcapsular splenic hematoma formation precedes rupture. The case of 44-year-old, previously healthy, male with splenic hematoma occurring after rising of heavy cargo is reported. Mononucleosis syndrome was suggested based on routine laboratory tests (elevated white blood cell count with predominance of lymphocytes and raised serum transaminases) and CMV infection was confirmed by serological test. Nonoperative management was used since the patient was hemodynamically stable with no further signs of splenic rupture. The same approach has been used in growing number of cases of patients with spontaneous splenic rupture in mononucleosis syndrome. Importance of considering splenic hematoma and/or rupture if abdominal pain occurs in the course of mononucleosis syndrome is outlined as well as importance of routine laboratory tests in suspecting mononucleosis syndrome in otherwise clinically silent patient.     

Spontaneous splenic rupture due to falciparum malaria successfully treated with a conservative approach

Malaria is frequently associated with splenomegaly. However, spontaneous splenic rupture is a rare and life-threatening complication. It is mostly seen in acute infection in non-immune adults and Plasmodium vivax and Plasmodium falciparum have been associated with the majority of cases.We describe a case of splenic rupture in an adult with complicated malaria by Plasmodium falciparum in which a conservative approach was used.     

Splenic hemodynamics and decreased endothelial nitric oxide synthase in the spleen of rats with liver cirrhosis

The enlarged spleen in liver cirrhosis is considered to play a role in the pathogenesis of portal hypertension, but the splenic hemodynamics and molecular mechanisms behind the phenomenon have not been elucidated. The present study aimed to examine the splenic hemodynamics associated with splenic microcirculation and congestion, and to determine the status of the endothelial nitric oxide synthase (eNOS) signaling pathway in the spleen of rats with liver cirrhosis. Liver cirrhosis was induced by bile duct ligation. In rats with bile duct ligation (BDL rats) and control rats, splenic blood flow was measured using a laser Doppler flowmeter, and splenic blood volume was measured using a near-infrared spectrophotometer. The expressions of eNOS and its upstream effectors, Akt, TNF-alpha and VEGF, in the spleen were also determined. Specific splenic blood flow was significantly decreased in BDL rats compared with control rats. Specific splenic blood volume was also decreased in BDL rats, while their total splenic blood volume, especially the deoxygenated volume, was significantly increased. The expressions of phosphorylated and total eNOS, and the eNOS phosphorylation ratio, were all significantly decreased in the spleen of BDL rats. The Akt phosphorylation ratio and TNF-alpha concentration were also decreased in the spleen of BDL rats although the expression of VEGF was increased. These findings suggest that the eNOS signaling pathway is suppressed in the spleen of cirrhotic rats, and may contribute to the measured decreases in specific blood flow and volume in the spleen of liver cirrhosis. Determination of the factors influencing the suppression of eNOS in the spleen may shed light on how liver cirrhosis results in hypodynamic intrasplenic circulation.     

脾全切除术与脾部分切除术治疗外伤性脾破裂的临床疗效对比

目的:比较脾全切除术和脾部分切除术治疗外伤性脾破裂的临床疗效和安全性。方法:选择我院2013年3月~2016年3月收治的84例外伤性脾破裂患者并平均分为两组,脾全切除组42例采用脾全切除术治疗,脾部分切除组42例采用脾部分切除术治疗,比较两组的手术效果、治疗前后血小板计数、血清Ig A、Ig G、Ig M、CD3~+、CD4~+、CD8~+及CD4~+/CD8~+水平的变化以及术后并发症的发生情况。结果:部分切除组术中失血量、排气时间、住院时间均短于全切除组,但部分切除组手术时间显著长于全切除组,差异有统计学意义(P0.05)。部分切除组血小板计数、Ig M、CD8~+水平明显低于对照组,Ig A、Ig G、CD3~+、CD4~+、CD8~+、CD4~+/CD8~+显著高于全切除组(P0.05)。部分切除组并发症发生率显著低于全切除组(P0.05)。结论:脾部分切除术治疗外伤性脾裂的手术效果优于脾全切除术,且对患者血小板及免疫功能的影响较小。     

Fine needle aspiration of thoracic splenosis. A case report.

BACKGROUND: Thoracic splenosis is a rare event, and fine needle aspiration (FNA) of a pleural implant of splenic tissue can be a pitfall when previous anamnestic data are ignored. CASE: A 53-year-old male underwent FNA of a left thoracic subpleural nodule highly suggestive of a metastatic lesion. The presence of a population of small and medium-sized lymphocytes suggested the possibility of lymphoproliferative disease; frozen sections confirmed this possibility. The final diagnosis was normal splenic tissue. Twenty-five years earlier the patient sustained a gunshot wound in the left side of the upper abdomen followed by splenectomy and drainage of the left pleural cavity because of mild, concomitant hemothorax. CONCLUSION: A left pleural thoracic nodule in subjects with a previous history of traumatic rupture of the spleen must be considered highly suggestive of thoracic splenosis. Scintigraphy with Tc 99 m and magnetic resonance imaging are diagnostic, while FNA, especially in the absence of anamnestic data, can create a pitfall that can induce inappropriate removal of ectopic, normally functioning splenic tissue.     

Cardiopulmonary effects of hemorrhagic shock in splenic autotransplanted pigs: a new surgical model

The spleen is an important organ for hemodynamic compensation during hemorrhagic shock. The aim of the study was to compare the hemodynamic and metabolic responses of sham-operated pigs with intact spleen, splenectomized pigs, and splenic autotransplanted pigs during hemorrhagic shock. Hemorrhagic shock was induced by 30% total blood volume bleed in sham-operated, splenectomized and splenic autotransplanted pigs (n = 20). Cardiopulmonary and metabolic variables were measured before, immediately after, and at 20, 60 and 100 minutes after hemorrhage. Upon hemorrhagic shock induction, body temperature, mean arterial pressure, mean pulmonary arterial pressure, cardiac output, cardiac index and oxygen delivery decreased, while lactate and shock index increased. Hemoglobin and hematocrit were significantly lower in the splenectomized and splenic autotransplant groups as compared with the control group at 60 and 100 minutes after hemorrhage (p < 0.05). Unlike intact spleen, splenic autotransplant could not improve hemodynamic parameters in hemorrhagic shock in pigs. In comparison to mice, rats or dogs, this species could be an interesting investigation model to test new surgical procedures during splenic related hemorrhagic shock, with potential applications in human medicine.     

B lymphocyte subpopulations separated by velocity sedimentation. II. Characterization of tolerance susceptibility.

Neonatal and adult splenic B lymphocyte subpopulations, separated by velocity sedimentation, were tested in an in vitro splenic focus assay for their susceptibility to tolerance induction with hapten-protein conjugates. At least two tolerizable B cell subsets have been defined in the neonatal spleen; one comprising the slowly sedimenting, small lymphocytes and the other comprising the very rapidly sedimenting, large lymphocytes. In addition, a rapidly sedimenting large B cell subset in the adult spleen was found to be highly susceptible to tolerance induction. It was suggested that the inability to detect this susceptibility in unfractionated adult spleen was due to the low proportion of these very large lymphocytes in the total spleen cell population. The tolerizable B cell subsets presently defined probably represent the least mature B lymphocytes detectable in the splenic focus assay.     

Heroin-induced alterations in leukocyte numbers and apoptosis in the rat spleen

The present study assessed the effects of acute heroin treatment on the cellularity of the rat spleen and the rate of splenocyte death by necrosis or apoptosis. The results showed that 1 h after a single injection of heroin, the total number of leukocytes in the spleen was decreased in a dose-dependent manner. Prior injection of naltrexone completely blocked heroin's effect, and the heroin-induced decrease in splenic leukocytes was not associated with a heroin-induced increase in circulating leukocytes. A 1-h exposure to heroin did not increase levels of lactate dehydrogenase, a cytosolic enzyme, in supernatants of splenic mononuclear cells cultured for 45 min or 24 h, suggesting that heroin does not increase necrotic death in the spleen. In contrast, a 1-h heroin treatment did increase the percentage of Annexin V(+) cells in 0- and 24-h cultures of splenic mononuclear cells, indicating that heroin increases apoptotic death in the spleen. A 3-h exposure to heroin also produced a significant increase in apoptosis in the spleen. DNA fragmentation, a marker of cells in late stages of apoptosis, could not be detected in fresh splenocytes, but was evident in 24-h cultures of splenic mononuclear cells from saline- and heroin-treated rats. These results demonstrate that a single administration of heroin produces a decrease in the number of splenic leukocytes and an increase in the apoptotic death of splenic mononuclear cells.     

Splenic phagocytes promote responses to nucleosomes in (NZB x NZW) F1 mice

Autoantigen presentation to T cells is crucial for the development of autoimmune disease. However, the mechanisms of autoantigen presentation are poorly understood. In this study, we show that splenic phagocytes play an important role in autoantigen presentation in murine lupus. Nucleosomes are major autoantigens in systemic lupus erythematosus. We found that nucleosome-specific T cells were stimulated dominantly in the spleen, compared with lymph nodes, lung, and thymus. Among splenic APCs, F4/80(+) macrophages and CD11b(+)CD11c(+) dendritic cells were strong stimulators for nucleosome-specific T cells. When splenic phagocytes were depleted in (NZB x NZW) F(1) (NZB/W F(1)) mice, nucleosome presentation in the spleen was dramatically suppressed. Moreover, depletion of splenic phagocytes significantly suppressed anti-nucleosome Ab and anti-dsDNA Ab production. Proteinuria progression was delayed and survival was prolonged in phagocyte-depleted mice. The numbers of autoantibody- secreting cells were decreased in the spleen from phagocyte-depleted mice. Multiple injections of splenic F4/80(+) macrophages, not those of splenic CD11c(+) dendritic cells, induced autoantibody production and proteinuria progression in NZB/W F(1) mice. These results indicate that autoantigen presentation by splenic phagocytes including macrophages significantly contributes to autoantibody production and disease progression in lupus-prone mice.     

Ectopic splenic nodules in the olive baboon (Papio cynocephalus anubis)

Post-mortem evaluation of a female sub-adult olive baboon (Papio cynocephalus anubis) revealed a case of ectopic spleen anomaly. Three spherical masses characterized the spleen anomaly. The splenic nodules were located on the left upper quadrant of the stomach, at the distal end of the pancreas. The anterior nodule measures 1.2 cm, the middle nodule 1.9 cm and the posterior nodule 1.3 cm in diameter. Normal spleen was not observed in this case. All the three ectopic splenic nodules showed normal histological architecture. A case of ectopic splenic nodules in baboon is important in that the spleen malformation can readily be mistaken for a pathological process.     

Plasmodium chabaudi AS: erythropoietic responses during infection in resistant and susceptible mice.

The course of anemia and the erythropoietic response in the bone marrow, spleen, and blood were studied during Plasmodium chabaudi AS infection in resistant C57BL/6 (B6) and susceptible A/J (A) mice. Infections in B6 mice were characterized by moderate levels of both parasitemia and anemia and survival. In contrast, A mice experienced high parasitemia, severe anemia, and high mortality rates. During the period of anemia, erythropoiesis, as measured by in vivo 59Fe incorporation, was significantly more depressed in bone marrow and more increased in the spleen in resistant B6 mice. The increase in splenic 59Fe incorporation was a function of the size of the spleen. Bone marrow CFU-E were decreased to 50% of control in both strains, while splenic CFU-E were increased twofold greater in B6 mice compared to those in A mice. However, the absolute numbers of CFU-E per spleen in the two strains were not significantly different during peak parasitemia. Bone marrow BFU-E were transiently increased before peak parasitemia whereas splenic BFU-E peaked during peak parasitemia. A mice had significantly lower numbers of BFU-E per spleen on all days except at peak parasitemia. The frequency of blood-borne BFU-E and plasma erythropoietin titers was increased earlier and to a greater extent in A mice. These results suggest that an impaired amplification of late-stage splenic erythropoiesis may be an important determinant in the severity of anemia and lethality of infection with P. chabaudi AS in A mice. Moreover, these results demonstrate that the defective amplification of splenic erythropoiesis in A mice is neither caused by a defect in the mobilization of BFU-E from the bone marrow to the spleen nor caused by a defect in erythropoietin production.     

Site of action of a soluble immune response suppressor (SIRS) produced by concanavalin A-activated spleen cells.

The cellular site of action of SIRS, a soluble immune response suppressor released by Con A-activated spleen cells which suppresses antibody responses to heterologous erythrocytes by murine spleen cells in vitro, was investigated. Exposure of spleen cells to SIRS for 2 hr at 37 degrees C or 1 hr at 4 degrees C was sufficient to suppress 5-day antibody responses in vitro. Similar exposure of splenic or peritoneal exudate macrophages to SIRS also suppressed antibody responses by untreated splenic lymphoid cells; exposure of splenic lymphoid cells to SIRS was without effect. SIRS did not act via T cells which might have contaminated the macrophage preparations. SIRS-mediated suppression could be partially overcome by an excess of normal peritoneal exudate macrophages, but not by an excess of T or B cells. These data indicate that the target cell of SIRS activity is the macrophage. The results are discussed in the context of macrophage functions that could be affected by SIRS.     

脾脏保留手术对外伤性脾破裂患者免疫功能的影响

目的:探究脾脏保留手术对外伤性脾破裂患者免疫功能的影响。方法:选取2015年8月~2018年9月我院收治的外伤性脾破裂患者83例进行回顾性分析,根据手术方式不同分为两组,对照组(41例)患者给予脾脏切除术,观察组(42例)患者给予脾脏保留手术。比较两组患者的手术时间、术中出血量、下床活动时间、术后1d引流量、抢救成功率及治疗前后CD3~+、CD4~+、CD8~+和Tuftsin因子水平和并发症的发生情况。结果:治疗后,观察组患者的手术时间、术中出血量、术后下床时间和术后1d引流量均显著短于或低于对照组,而救治成功率显著高于对照组(P0.05)。两组患者治疗后的CD3~+、CD4~+和CD4~+/CD8~+水平均较治疗前显著下降,且观察组以上指标均显著高于对照组(P0.05)。对照组治疗后血清Tuftsin因子水平较治疗前显著下降,而观察组血清Tuftsin因子水平较治疗前显著升高,并显著高于对照组(P0.05)。观察组患者的总并发症发生率为7.14%,较对照组(24.39%)显著降低(P0.05)。结论:与脾脏切除术相比,脾脏保留手术可显著改善外伤性脾破裂患者的免疫功能,且手术效果更好,安全性更高。     

Neuropeptide Y-, substance P- and VIP-immunoreactive nerves in cat spleen in relation to autonomic vascular and volume control

Summary Neuropeptide Y (NPY)-immunoreactive (IR) nerve fibres were found around both arteries and veins and in smooth muscle trabeculae of the cat spleen with the highest density on the arterial side. Considerably more tyrosine hydroxylase (TH)- and dopamine--hydroxylase (DBH)-positive than NPY-IR nerves were seen in the trabeculae and splenic capsule. The NPY-IR nerves in the spleen most likely originated in the coeliac ganglion, since (1) splanchnic nerve sectioning did not change the splenic NPY-IR nerves, (2) most neurones in the coeliac ganglion were NPY-IR, as well as DBH- and TH-positive, and (3) NPY-IR was transported axonally from the coeliac ganglion towards the spleen via the splenic nerve. Local NPY infusion in the isolated, blood-perfused cat spleen caused a marked increase in splenic vascular resistance and a small volume reduction. NA caused a comparatively larger reduction in splenic volume than NPY in addition to vasoconstriction. VIP-IR cell bodies in the coeliac ganglion were NPY- and TH-negative. VIP-IR nerves were seen both around the splenic artery and vein as well as around arterioles and within venous trabeculae of the spleen. VIP infusion caused reduction of splenic perfusion pressure (i.e. vasodilation) as well as an increase in splenic volume. Substance P-IR nerves, most likely of splanchnic afferent origin, were present in the coeliac ganglion around the splenic artery and arterioles of the spleen. Infusion of substance P induced marked reduction in perfusion pressure and a reduction in splenic volume. Enkephalin-immunoreactive nerves of splanchnic origin surrounded some TH- and NPY-positive, coeliac ganglion cells.It is concluded that several vasoactive peptides are located in splenic nerves. NPY is present in noradrenergic neurones and causes mainly increased vascular resistance. VIP occurs in non-adrenergic neurones of sympathetic origin and induces vasodilation and relaxation of the capsule. Finally, substance P is present in peripheral branches of spinal afferent nerves and causes vasodilation and capsule contraction. Stimulation of the splenic nerves may thus release several vasoactive substances in addition to noradrenaline, exerting a variety of actions.