Since the spleen is important for protecting against encapsulated organisms, sepsis caused by encapsulated organisms is a possible complication of splenectomy.Additional elective treatments offered: 

Surgical removal of the gallbladder.Experimental treatment:

Bone marrow transplant (heme-oncology intervention): The replacement of the bone marrow with bone marrow from an individual without spherocytosis. The transplanted progenitor cells do not have the genetic mutations found in individuals with hereditary spherocytosis, and therefore do not produce spherocytes. This results in an individual with biconcave-disc-shaped erythrocytes. This treatment is not standard of care, and is not offered as it has only been documented incidentally during treatment for other diseases, such as myelodysplastic sydnrome.Symptomatic treatments:

Folic acid supplementation. Complications
Common Complications
Hemolytic crisis, with more pronounced jaundice due to accelerated hemolysis (may be precipitated by infection). Aplastic crisis with dramatic fall in hemoglobin level and (reticulocyte count)-decompensation, usually due to maturation arrest and often associated with megaloblastic changes; may be precipitated by infection, such as influenza, notably with parvovirus B19. Folate deficiency caused by increased bone marrow requirement. Pigmented gallstones occur in approximately half of untreated patients. Increased hemolysis of red blood cells leads to increased bilirubin levels, because bilirubin is a breakdown product of heme. The high levels of bilirubin must be excreted into the bile by the liver, which may cause the formation of a pigmented gallstone, which is composed of calcium bilirubinate. Since these stones contain high levels of calcium carbonates and phosphate, they are radiopaque and are visible on x-ray. Hyperglycemia with concomitant low hemoglobin A1C levels.
Etiology
Hereditary spherocytosis is an erythrocytic disorder of that affects the following red cell membrane proteins in a congenital fashion:

Spectrin (alpha and beta)
Ankyrin
Band-3 Protein
Protein-4.2
Lesser proteins of significanceHereditary spherocytosis can be an autosomal recessive or autosomal dominant trait. The autosomal recessive inheritance pattern accounts for close to 25% of the clinical cases. The autosomal dominant inheritance patter accounts for over 75% of the clinical cases. Many positive individuals will not present clinically, thus the etiologic data may be artificially skewed towards the more prominent dominant forms. These dominant forms tend to leave a family history that  yields generational splenectomies and black gallstones cholelithiasis. Lastly, an estimated 25% of cases are due to spontaneous mutations. Pathophysiology
Causative Genetic Mutations and Phenotypic Expressions
Hereditary spherocytosis is caused by a variety of molecular defects in the genes that code for the red blood cell proteins spectrin (alpha and beta), ankyrin, band 3 protein, protein 4.2, and other red blood cell membrane proteins:
*Online Mendelian Inheritance in Man (OMIM). The Alpha-1 refers the Alpha-1 Subunit of the Spectrin protein. The Beta refers the Beta Subunit of the Spectrin protein. These genetic mutations are acted upon and executed by erythrocyte progenitor cells within the bone marrow, where red blood cells are normally produced in the non-pathological state (see Extramedullary Hematopoiesis for pathological production outside of the bone marrow). Pathophysiology of Mutated Erythrocytic Membrane Proteins
These proteins are necessary to maintain the normal shape of a red blood cell, which is a biconcave disk.