thrombocytopenic purpura ITP, chronic myeloproliferative neoplasm CMPN, non-Hodgkin’s lymphoma NHL and pancytopenia).

As per final diagnoses (Table 1) indications included I] Therapeutic (113,90.4%) – laceration 67, diffuse splenomegaly 25, hypersplenism 7, repeated blood transfusion 5, splenitis 4, infarction 3, ITP  2 II] Diagnostic (10,8.0%) –   cyst 7, abscess 1, NHL 2. III] Incidental (2,1.6%) – pancreatic neoplasms.

Traumatic splenic laceration was significantly higher (p 2.90 E-06) in males (61,66.3%). Dominant indications in 0-10 age were hemolytic anemia (66.7%), 10-19 age were hemolytic anemia and trauma (45.5%, 27.3%), 20-49 age was trauma (62.8 %), 50-59 years was fibrocongestion (50%) and 60-69 age was CMPN and NHL (28.6% each) (p 0.00066)

The mean splenic weight was 480.9 overall, 903 gm in diffuse splenomegaly and 1390 gm in hypersplenism. Beef-red color in 115 and hemosiderosis (Fig1a) were seen in 10 cases. Solid nodules included G.G. bodies 5, NHL 2 and abscess 1 (Fig1b, 1c).

Causes of splenic laceration (Fig 1d) included vehicular accident 60, physical assault five and iatrogenic 2. Hemolytic anemia had beta-Thalassemia 12, sickle-thalassemia one and hereditary spherocytosis 6. Microscopy showed atrophic white pulp, congested red pulp with siderophages 11, EMH 6 and sickled RBC 1. Fibrocongestion showed congested red pulp 13, G.G. bodies 10, siderophages four and EMH 2. Splenic cyst included primary cyst 2 (Figure 2a, 2b), pseudocyst 3 (Figure 2c, 2d). Hydatid cyst 2 showed fibrous pericyst and tender-coconut-like ectocyst. ITP showed foamy macrophages, siderophages and fibrocongested red pulp. Figures 3a, 3b show perisplenitis and figures 3c,3d show NHL. CMPN included Chronic myeloid leukemia, myelofibrosis (Figure 4a) and polycythemia vera. Infarcts (Fig 1b) were caused by splenic thrombosis, splenic artery aneurysm, microfilarial abscess (Fig 4b) and CMPN.

Spleniculi and hilar vessels: Hilar brown nodules were assumed to be spleniculi. Microscopy showed siderophages three and EMH 2. Six spleniculi were reclassified as lymph nodes (L.N.) due to the microscopic absence of splenic arterioles. L.N.

K value for agreement:  <0.2 poor, 0.2-0.4 fair, 0.4-0.6 moderate, 0.6-0.8 good,

0.8-1.0 excellent agreement.

P-value < 0.05 is statistically significant.

Additional microscopic nodules included one tubercle and 5 Gamna Gandy bodies.

Figure 1a: Spleen shows golden brown hemosiderosis (blue star) confirmed by Prussian blue stain (white star). Figure 1b: Spleen shows multiple grey-brown Gamna Gandy bodies (white arrows) and wedge-shaped pale infarct (black arrow). Figure 1c: Spleen with large ragged cavitatory abscess. Figure 1d: Spleen with the traumatic capsular breach (white arrows).

Figure 2a: Primary cyst shows pearly-white inner surface and trabeculations. Figure 2b: Photomicrograph of primary cyst shows cuboidal to the squamous epithelial lining, Hematoxylin Eosin (HE) 100 x. Figure 2c: Pseudocyst shows a ragged cyst wall with hemorrhagic contents. Fig 2d: Photomicrograph of pseudocyst shows hemorrhages and calcification. Epithelial lining absent, HE, 100 x.

linked with speed driving, vehicular accidents and splenic laceration. Splenic hilar injury, pulverized parenchyma and hemoperitoneum mandate splenectomy. [2,3].  In hemolytic anemia, splenectomy is advisable if infarction or transfusion exceeds 200 ml/kg/year.[3]. Massive splenomegaly with hypersplenism warrants splenectomy [3]. Splenic cysts need splenectomy, while marsupialization or sclerosant injections have a high recurrence risk. [4]. ITP needs splenectomy if refractory to medical therapy. [3].

Common clinical presentations include anemia, fever, abdominal discomfort, jaundice and bleeding.[5]. Shetty et al. [6] concluded USG is an ideal screening modality. Their spectrum included 60.8% benign lesions (cyst, abscess, infarct). Microscopic findings hemosiderosis, EMH, G.G. bodies, infarcts were similar to our study [2,7]. Spleen, being an in-utero hemopoietic organ, can undergo EMH when marrow shows myelofibrosis or metastasis. Awamleh et al. [8] found 2.1% splenic metastases, while we found none. The phagocytic function makes it a rare metastatic site.

Multipronged investigations like hemogram, serotests for malaria, blood culture, bone marrow, gastroscopy and electrophoresis are essential to investigate splenomegaly.[5]. Our study showed optimum gross-microscopy agreement for capsular breach, cyst, infarct and hilar vessel lesions (Table 2). Spleniculi may cause disease recurrence if not resected. Conversely, retained spleniculi can maintain functions and reduce post-splenectomy complications.[9].