An accessory spleen ("supernumerary spleen", "splenule", or "splenunculus") is a small nodule of splenic tissue found apart from the main body of the spleen. Accessory spleens are found in approximately 10 percent of the population and are typically around 1 centimeter in diameter. They may resemble a lymph node or a small spleen. They form either by the result of developmental anomalies or trauma. They are medically significant in that they may result in interpretation errors in diagnostic imaging or continued symptoms after therapeutic splenectomy.

Accessory spleens may be formed during embryonic development when some of the cells from the developing spleen are deposited along the path from the midline, where the spleen forms, over to its final location on the left side of the abdomen by the 9th–11th ribs. The most common locations for accessory spleens are the hilum of the spleen and adjacent to the tail of the pancreas. They may be found anywhere along the splenic vessels, in the gastrosplenic ligament, the splenorenal ligament, the walls of the stomach or intestines, the pancreatic tail, the greater omentum, the mesentery or the gonads and their path of descent. The typical size is approximately 1 centimeter, but sizes ranging from a few millimeters up to 2–3 centimeters are not uncommon.

Splenogonadal fusion can result in one or more accessory spleens along a path from the abdomen into the pelvis or scrotum. The developing spleen forms near the urogenital ridge from which the gonads develop. The gonads may pick up some tissue from the spleen, and as they descend through the abdomen during development, they can produce either a continuous or a broken line of deposited splenic tissue.

Splenosis is a condition where foci of splenic tissue undergo autotransplantation, most often following physical trauma or splenectomy. Displaced tissue fragments can implant on well vascularized surfaces in the abdominal cavity, or, if the diaphragmatic barrier is broken, the thorax.

Wandering spleen (or Pelvic spleen) is a rare medical disease caused by the loss or weakening of the ligaments that help to hold the spleen stationary.

Wandering spleen is most commonly diagnosed in young children as well as women between the ages of 20 and 40. Even so, the disease is very rare and fewer than 500 occurrences of the disease have been reported as of 2005, of which around 148 (including both children and adult cases) were documented to have been from between 1960 and 1992. Less than 0.5% of all splenectomies, surgical removal of the spleen, are performed due to having this disorder.

Characteristics of the disorder include the loss, weakening, or malformation of the ligaments that help to keep the spleen located in the upper left part of the abdomen. Though not a genetic disease, wandering spleen is often found at birth. It can occur in adults as the result of injuries and other similar conditions that cause the ligaments to weaken, such as connective tissue disease or pregnancy. Wandering spleen (splenoptosis) predisposes the spleen to complications such as torsion, splenic infarction, pancreatic necrosis and rarely pseudocyst formation.

In 1992, the youngest case of the literature of torsion of wandering spleen at two days of birth was reported in Lebanon, by Dr Edouard Sayad.

Enlargement of spleen, ascites, jaundice, and the result of destruction of various blood cells by spleen – anemia, leukopenia, thrombocytopenia, gastrointestinal bleeding – may constitute the presenting symptoms.

Splenomegaly is an enlargement of the spleen. The spleen usually lies in the left upper quadrant (LUQ) of the human abdomen. Splenomegaly is one of the four cardinal signs of "hypersplenism" which include; some reduction in the number of circulating blood cells affecting granulocytes, erythrocytes or platelets in any combination, a compensatory proliferative response in the bone marrow, and the potential for correction of these abnormalities by splenectomy. Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a response to hyperfunction. It is therefore not surprising that splenomegaly is associated with any disease process that involves abnormal red blood cells being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by leukemias and lymphomas. Thus, the finding of an enlarged spleen, along with caput medusa, is an important sign of portal hypertension.

The standard system for classifying splenomegaly on radiography is:

- Normal (not splenomegaly): the largest dimension is less than 11 cm

- Moderate splenomegaly: the largest dimension is between 11–20 cm

- Severe splenomegaly: the largest dimension is greater than 20 cm

Also, a cutoff of a craniocaudal height of 13 cm is also used to define splenomegaly.

Splenomegaly refers strictly to spleen enlargement, and is distinct from hypersplenism, which connotes overactive function by a spleen of any size. Splenomegaly and hypersplenism should not be confused. Each may be found separately, or they may coexist. Clinically if a spleen is palpable, it means it is enlarged as it has to undergo at least twofold enlargement to become palpable. However, the tip of the spleen may be palpable in a newborn baby up to 3 months of age.

For children, the cutoffs for splenomegaly are given in this table, when measuring the greatest length of the spleen between its dome and its tip, in the coronal plane through its hilum while breathing quietly.

In minor injuries with little bleeding, there may be abdominal pain, tenderness in the epigastrium and pain in the left flank. Often there is a sharp pain in the left shoulder, known as Kehr's sign. In larger injuries with more extensive bleeding, signs of hypovolemic shock are most prominent. This might include a rapid pulse, low blood pressure, rapid breathing, paleness, and anxiety.

The basic pathology is some kind of obstructive pathology in the portal, hepatic or splenic vein that causes obstruction of venous blood flow from the spleen towards the heart. The cause of such obstruction may be abnormalities present at birth (congenital) of certain veins, blood clots, or various underlying disorders causing inflammation and obstruction of veins (vascular obstruction) of the liver.

A splenic injury, which includes a ruptured spleen, is any injury to the spleen. The rupture of a normal spleen can be caused by trauma, such as a traffic collision.

The primary symptom, hemorrhage, presents differently depending on the degree of injury, with the symptoms of major hemorrhage, shock, abdominal pain, and distention being clinically obvious. Minor hemorrhage often presents as upper left quadrant pain. Patients with unexplained left upper quadrant pain, particularly if there is evidence of hypovolemia or shock, are generally inquired regarding any recent trauma.

Blunt splenic trauma occurs when a significant impact to the spleen from some outside source (i.e. automobile accident) damages or ruptures the spleen. Treatment varies depending on severity, but often consists of embolism or splenectomy.

Splenic diseases include splenomegaly, where the spleen is enlarged for various reasons. On the other hand, a lack of normal spleen function is called asplenia.

LCAs most often are not clinically detectable. On occasion, their first presentation may be with splenic rupture.

Most patients show no symptoms and the tumours are found incidentally.

Accessory pancreas is a rare condition in which small groups of pancreatic cells are separate from the pancreas. They may occur in the mesentery of the small intestine, the wall of the duodenum, the upper part of the jejunum, or more rarely, in the wall of the stomach, ileum, gallbladder or spleen. The condition was first described by Klob in 1859.

Accessory pancreas is a small cluster of pancreas cells detached from the pancreas and sometimes found in the wall of the stomach or intestines.

Enlargement of the spleen is known as splenomegaly. It may be caused by sickle cell anemia, sarcoidosis, malaria, bacterial endocarditis, leukemia, pernicious anemia, Gaucher's disease, leishmaniasis, Hodgkin's disease, Banti's disease, hereditary spherocytosis, cysts, glandular fever (mononucleosis or 'Mono' caused by the Epstein-Barr Virus), and tumours. Primary tumors of the spleen include hemangiomas and hemangiosarcomas. Marked splenomegaly may result in the spleen occupying a large portion of the left side of the abdomen.

The spleen is the largest collection of lymphoid tissue in the body. It is normally palpable in preterm infants, in 30% of normal, full-term neonates, and in 5% to 10% of infants and toddlers. A spleen easily palpable below the costal margin in any child over the age of 3–4 years should be considered abnormal until proven otherwise.

Splenomegaly can result from antigenic stimulation (e.g., infection), obstruction of blood flow (e.g., portal vein obstruction), underlying functional abnormality (e.g., hemolytic anemia), or infiltration (e.g., leukemia or storage disease, such as Gaucher's disease). The most common cause of acute splenomegaly in children is viral infection, which is transient and usually moderate. Basic work-up for acute splenomegaly includes a complete blood count with differential, platelet count, and reticulocyte and atypical lymphocyte counts to exclude hemolytic anemia and leukemia. Assessment of IgM antibodies to viral capsid antigen (a rising titer) is indicated to confirm Epstein-Barr virus or cytomegalovirus. Other infections should be excluded if these tests are negative.

Littoral cell angioma, abbreviated LCA, and formally known as littoral cell angioma of the spleen, is a benign tumour of the spleen that arises from the cells that line the red pulp.

Asplenia is a form of immunodeficiency, increasing the risk of sepsis from polysaccharide encapsulated bacteria, and can result in overwhelming post splenectomy infection (OPSI), often fatal within a few hours. In particular, patients are at risk from "Streptococcus pneumoniae", "Haemophilus influenzae", and meningococcus. The risk is elevated as much as 350–fold.

The risk to asplenic patients has been expressed as equivalent to an adult dying in a road traffic accident (in every 100 people without spleens, 1 to 5 would develop a severe infection per decade) (reference UK Splenectomy Trust Advice)—hence sensible precautions are advisable. Increased platelet counts can be seen in individuals without a functioning spleen.

Splenogonadal fusion is a rare congenital malformation that results from an abnormal connection between the primitive spleen and gonad during gestation. A portion of the splenic tissue then descends with the gonad. Splenogonadal fusion has been classified into two types: continuous, where there remains a connection between the main spleen and gonad; and discontinuous, where ectopic splenic tissue is attached to the gonad, but there is no connection to the orthotopic spleen. Patients with continuous splenogonadal fusion frequently have additional congenital abnormalities, most commonly cryptorchidism.

The anomaly was first described in 1883 by Bostroem. Since then more than 150 cases of splenogonadal fusion have been documented. The condition is considered benign. A few cases of testicular neoplasm have been reported in association with splenogonadal fusion. The reported cases have occurred in patients with a history of cryptorchidism, which is associated with an elevated risk of neoplasm.

Splenogonadal fusion occurs with a male-to-female ratio of 16:1, and is seen nearly exclusively on the left side. The condition remains a diagnostic challenge, but preoperative consideration of the diagnosis may help avoid unnecessary orchiectomy. On scrotal ultrasound, ectopic splenic tissue may appear as an encapsulated homogeneous extratesticular mass, isoechoic with the normal testis. Subtle hypoechoic nodules may be present in the mass. The presence of splenic tissue may be confirmed with a technetium-99m sulfur colloid scan.

In an effort to preserve some of the spleen's protective roles, attempts are now often made to preserve a small part of the spleen when performing either surgical subtotal (partial) splenectomy, or partial splenic embolization.

This may be particularly important in poorer countries where protective measures for patients with asplenia are not available.

However, it has been advised that preoperative vaccination is advisable until the remnant splenic tissue can reestablish its function.

An autosplenectomy (from" 'auto-' "self," '-splen-' "spleen," '-ectomy' "removal) is a negative outcome of disease and occurs when a disease damages the spleen to such an extent that it becomes shrunken and non-functional. The spleen is an important immunological organ that acts as a filter for red blood cells, triggers phagocytosis of invaders, and mounts an immunological response when necessary. Lack of a spleen, called asplenia, can occur by autosplenectomy or the surgical counterpart, splenectomy. Asplenia can increase susceptibility to infection. Autosplenectomy can occur in cases of sickle-cell disease where the misshapen cells block blood flow to the spleen, causing fibrosis and eventual atrophy of the organ. Autosplenectomy is a rare condition that is linked to certain diseases but is not a common occurrence.

The most frequent cause of autosplenectomy is sickle cell anemia which causes progressive splenic hypofunction over time. Increased deoxygenation causes sickling of red blood cells, which adhere to the spleen wall and splenic macrophages causing ischemia. This ischemia can result in splenic sequestration, where large amounts of blood pool in the spleen but do not flow within vasculature. This lack of blood flow can cause atrophy in the spleen and can lead to autosplenectomy.

Polysplenia or Chaudhrey's disease is a congenital disease manifested by multiple small accessory spleens, rather than a single, full-sized, normal spleen. Polysplenia sometimes occurs alone, but it is often accompanied by other developmental abnormalities. Conditions associated with polysplenia include gastrointestinal abnormalities, such as intestinal malrotation or biliary atresia, as well as cardiac abnormalities, such as dextrocardia.

Ectopic salivary gland tissue which is located in sites other than the normal location is variously described as aberrant, accessory, ectopic, heterotopic or salivary gland choristoma.

Pancreatic disorders are often accompanied by weakness and fatigue. The past Medical history may reveal previous disorders of the biliary tract or duodenum, abdominal trauma or surgery, and metabolic disorders such as diabetes mellitus. The medication history should be detailed and specifically include the use of thiazides, furosemide, estrogens, corticosteroids, sulfonamides, and opiates. Note a family history of pancreatic disorders. In the review of systems, obtain a complete description of any pain in the upper abdomen or epigastric area. Symptoms that may be important in relation to pancreatic disorders are pruritus, abdominal pain, dyspnea, nausea, and vomiting. The functional assessment includes data about the patient’s dietary habits and use of alcohol.

Note any restlessness, flushing, or diaphoresis during the examination. Vital signs may disclose low-grade fever, tachypnea, tachycardia, and hypotension. Inspect the skin for jaundice. Assess the abdomen for distention, tenderness, discoloration, and diminished bowel sounds.

Tests and procedures used to diagnose pancreatic disorders include laboratory analyses of blood, urine, stool, and pancreatic fluid, and imaging studies. Specific blood studies used to assess pancreatic function include measurements of serum amylase, lipase, glucose, calcium, and triglyceride levels. Urine amylase and renal amylase clearance tests may also be ordered. Stool specimens may be analyzed for fat content. The secretin stimulation test measures the bicarbonate concentration of pancreatic fluid after secretin is given intravenously to stimulate the production of pancreatic fluid.