The spleen is a hematopoietic organ that filters and removes aging blood products and aids in immunity against incapsulated bacterial organisms. Splenic infarction occurs when blood flow to the spleen is compromised causing tissue ischemia and eventual necrosis. Splenic infarction may be the result of arterial or venous occlusion. Occlusion is usually caused by bland or septic emboli as well as venous congestion by abnormal cells. Infarction may involve a small segmental area of the spleen or may be global depending on which vessel is occluded. This occurrence is caused by a wide variety of underlying disease states with prognosis dependent on the causative illness. The most typical presentation includes left sided abdominal pain in a patient with underlying hematologic disorder, blood borne malignancy, blunt abdominal trauma, hypercoagulable state or embolic illness. Treatment of splenic infarct ranges from supportive care to splenectomy. 
Therapeutic splenic infarction via splenic embolization has been used to treat hemorrhage from traumatic splenic injuries. Splenic embolization has also been used in the treatment of severe portal hypertension and in the pre-operative phase of splenectomy to reduce intra-operative blood loss.
The two most common causes of splenic infarct are thromboembolic disease and infiltrative hematologic diseases. In patients under 40 years of age, the most common cause is a hematologic disease. Causes of splenic infarction may be categorized as follows:
Additionally, broad categories of autoimmune and collagen vascular diseases, as well as the "wandering spleen," have been noted in case reports of the splenic infarct.
Splenic infarcts are considered a rare cause of abdominal pain although the exact prevalance is unclear. The diagnosis of splenic infarct is thought to be rising due to increased abdominal imaging, increased use of splenic embolization and increased nonoperative management of traumatic splenic injuries. This disease may affect patients of all ages. Patient 4o years of age and younger are more likey to have underlying hematologic illness while patients 40 years of age and older are more likely to suffer splenic infarct due to thromboembolic diseases.
The splenic artery (branching off the celiac artery) supplies blood flow to the spleen in combination with the short gastric arteries (branches off of the left gastroepiploic artery).
One of the most common causes of splenic infarction sickle hemoglobinopathies. In patients with sickle cell disease, episodes of hypoxia or acidosis cause red blood cells to transform into an abnormal shape leading to crystallization and occlusion of the vasculature. This process can lead to multiple infarctions beginning in childhood. Over time, multiple infarctions cause scarring and contraction of the spleen. This may ultimately result in complete splenic autoinfection by the time of adulthood.
Diseases which cause splenomegaly may place patients at risk for splenic infarction. These diseases include chronic myelogenous leukemia, myelofibrosis, Gaucher disease, Malarial splenomegaly syndrome, AIDS with mycobacterium avium complex, Lymphoma.
Rarely, abnormal splenic vascular anatomy may cause infarction. An anatomical variant known as the wandering spleen has been identified in which the spleen has an abnormal vascular attachment that predisposes to torsion.
Splenic infarction is a rare cause of abdominal pain. Diagnosis is often suspected based on the presence of underlying disease states most likely to cause splenic infarction. A study published in 2010 set out to better characterize the modern experience of splenic infarction. This study performed chart reviews of 26 patients admitted to the hospital with diagnosis of splenic infarction. Their observations were as follows:
Interestingly, authors noted that in 21 of 26 patients, the diagnosis of splenic infarct led to the diagnosis of a previously unrecognized underlying illness.
Abdominal pain remains the leading chief complaint in patients diagnosed with a splenic infarct. Evaluation of patients who present with abdominal pain requires a broad differential approach.
Lab evaluation my help rule in other causes of abdominal pain. Elevated liver function tests, bilirubin or lipase, may suggest a hepatobiliary or pancreatic source for pain. Leukocytosis and elevated lactate dehydrogenase (LDH) may be found in splenic infarction. However, these results lack specificity to splenic infarct.
Radiographic testing is required to detect this rare illness. In the hyperacute phase of infarction, abdominal CT scan performed with intravenous contrast is the imaging modality of choice in suspected splenic infarction. Splenic infarct appears as a wedge-shaped area of splenic tissue with the apex pointed toward the helium and the base of the splenic capsule. As the infarction matures, the affected tissue may normalize, liquefy or become contracted or scarred. Abdominal ultrasound has also been used to detect splenic infarction. Ultrasound findings of the hypoechoic wedge-shaped region of splenic tissue indicate infarction. Evolution of infarction may appear as hyperechoic with retraction of the splenic capsule.
Treatment of splenic infarct is based primarily on the underlying causative disease state. Splenic infarct in the non-infectious setting may be treated with analgesics, hydration, anti-emetics and other means of supportive care. Hospital admission may be required to provide supportive treatment, monitoring, and further diagnostic testing if the underlying cause is not established. In patients with sickle cell hemoglobinopathies, treatment to correct hypoxia and acidosis may be required. In the case of septic emboli, patients may require intravenous antibiotics and further cardiac evaluation. In patients with the underlying hematologic disease or autoimmune disease, consultation with hematology, oncology or rheumatology may be indicated. Abdominal pain due to uncomplicated cases of splenic infarction resolve without intervention in 7-14 days.
In the case of traumatic splenic injury, abnormal vasculature or hemodynamic instability, the surgical evaluation may be required. Dangerous complications of splenic infarct include pseudocyst formation, abscess, hemorrhage, splenic rupture, and aneurysm. In some instances, the infarcted splenic tissue may become infected and lead to abscess formation. Infarcted tissue may also undergo a hemorrhagic transformation. These complications warrant emergent surgical consultation.
Splenic infarcts are a rare cause of abdominal pain. The patients often present to the emergency department physician, primary care provider, nurse practitioner or the internist. The pathology is easily identified with imaging studies but its management requires an interprofessional team.
Treatment of splenic infarct is based primarily on the underlying causative disease state. Splenic infarct in the non-infectious setting may be treated with analgesics, hydration, anti-emetics and other means of supportive care. In the case of traumatic splenic injury, abnormal vasculature or hemodynamic instability, the surgical evaluation may be required. Dangerous complications of splenic infarct include pseudocyst formation, abscess, hemorrhage, splenic rupture, and aneurysm. In some instances, the infarcted splenic tissue may become infected and lead to abscess formation. Infarcted tissue may also undergo a hemorrhagic transformation. These complications warrant emergent surgical consultation.
In patients undergoing surgery, it is important to ensure that the patient does get vaccinated against encapsulated organisms. For traumatic cases, the outlook is excellent but in patients with sickle cell disease or a chronic hematolgocial disorder, repeated episodes may occur.
|||Kato K,Gleeson TA, Splenic necrosis requiring ultrasound-guided drainage following meningococcal septicaemia. Oxford medical case reports. 2019 Mar; [PubMed PMID: 30949357]|
|||Mamoun C,Houda F, [Splenic infarction revealing infectious endocarditis in a pregnant woman: about a case and brief literature review]. The Pan African medical journal. 2018; [PubMed PMID: 30455813]|
|||Niccoli Asabella A,Altini C,Nappi AG,Lavelli V,Ferrari C,Marzullo A,Loiodice A,Rubini G, Sickle cell diseases: What can nuclear medicine offer? Hellenic journal of nuclear medicine. 2019 Mar 5; [PubMed PMID: 30843001]|
|||Wand O,Tayer-Shifman OE,Khoury S,Hershko AY, A practical approach to infarction of the spleen as a rare manifestation of multiple common diseases. Annals of medicine. 2018 Sep; [PubMed PMID: 29929401]|
|||Smalls N,Obirieze A,Ehanire I, The impact of coagulopathy on traumatic splenic injuries. American journal of surgery. 2015 Oct; [PubMed PMID: 26384795]|
|||Bender MA, Sickle Cell Disease 1993; [PubMed PMID: 20301551]|
|||el Barzouhi A,van Buren M,van Nieuwkoop C, Renal and Splenic Infarction in a Patient with Familial Hypercholesterolemia and Previous Cerebral Infarction. The American journal of case reports. 2018 Dec 10; [PubMed PMID: 30531677]|
|||Nofal R,Zeinali L,Sawaf H, Splenic infarction induced by epstein-barr virus infection in a patient with sickle cell trait. Journal of paediatrics and child health. 2019 Feb; [PubMed PMID: 30746887]|
|||Pereda MA,Isaac J,Zhang Y,Jayakumar R,Gupta R,Miller ST, Massive Splenic Infarction in a Child With Sickle Cell Disease on Chronic Transfusion Therapy. Journal of pediatric hematology/oncology. 2019 Mar; [PubMed PMID: 30499910]|
|||Blackwood B,Binder W, Unusual Complications From Babesia Infection: Splenic Infarction and Splenic Rupture in Two Separate Patients. The Journal of emergency medicine. 2018 Nov; [PubMed PMID: 30253953]|
|||Fernando C,Mendis S,Upasena AP,Costa YJ,Williams HS,Moratuwagama D, Splenic Syndrome in a Young Man at High Altitude with Undetected Sickle Cell Trait. Journal of patient experience. 2018 Jun; [PubMed PMID: 29978033]|