[Splenic rupture--splenic hematoma].
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We present a case of spontaneous splenic rupture in a man with splenic vein thrombosis. The splenic vein thrombosis appears to have been caused by protein S deficiency. We are not aware of this having been described before.
Among the methods of early diagnosis of rupture and trauma of the spleen, fixation of radioactive isotopes is one of the most interesting. An experimental study in the dog of B.M.H.P. metabolism, using B.M.H.P. labelled with Hg-203 and its rate of elimination by the kidney, gives information on lesions of the spleen, in particular, sub-capsular rupture. Splenic trauma reduces the capacity of uptake of mercury by this organ. Excretion in the urine then increases very definitely. This simple and inoffensive method should be used in man.
Delayed splenic rupture is a rare but life threatening complication of abdominal trauma. A case is reported in which initial evaluation by CT did not show hemoperitoneum or splenic laceration in a patient who ruptured his spleen 10 days following the initial injury. The limitations of current diagnostic methods are reviewed.
Spontaneous splenic rupture in hemophilia A is an uncommon occurrence which is difficult to diagnose. We have reported a case of hemophilic rupture of the spleen unaccompanied by thrombocytosis, which has been emphasized as a diagnostic clue to hemophilic splenic rupture. Hence, splenic rupture should still be considered in any hemophilic patient with pain in the left upper quadrant and a normal platelet count. Splenic rupture in hemophilia must be recognized because its treatment requires not only clotting factor infusion but also surgical intervention.
Splenic rupture is a common injury associated with blunt abdominal trauma. In contrast, delayed splenic rupture is less frequent and comprises about 8--28% of cases of splenic rupture. The symptom free period can last for days or weeks. The mechanism is explained as follows. A rupture of the parenchyma occurs but the spleen capsula remains intact. A hematoma forms below the capsule and causes a strong overdistension of the capsule so that a bursting and release of blood into the abdominal cavity results. The mortality rate with splenic ruptures in 6--55% and with delayed splenic ruptures 14.6%. Our experiences are reviewed. After commencement of the hemorrhage therapy must consist of treatment for shock and immediate laparotomy and splenectomy.
A 27-year-old white man was admitted in shock with a tender distended abdomen 5 years following significant thoraco-abdominal trauma. Immediately following resuscitation he had an emergency exploratory laparotomy because of his critical condition. At operation 3 liters of old and fresh blood were present intraperitoneally and the spleen was ruptured. The spleen was surrounded by and adherent to the omentum and adjacent viscera. Splenectomy was performed and recovery was uneventful. Histologic examination of the spleen confirmed the 5-year interval between injury and rupture. Delayed splenic rupture accounts for 14% of all splenic injuries and has a high mortality. This case represents the longest reported delay between splenic trauma and delayed rupture.
Although splenic injury is the most frequent abdominal injury resulting from blunt trauma, delayed splenic rupture is a rare event. From 1981 to 1990, 75 patients treated at St. Elizabeth Hospital Medical Center (Youngstown, OH) had blunt splenic injury. Splenic rupture was delayed in six of these patients (8%). More severe trauma, such as occurs with motor vehicle accidents, is more likely to lead to immediate rupture. Lesser trauma resulting from minor falls or fights is more likely to lead to delayed rupture. Subcapsular hematoma is the most common etiology for delayed splenic rupture. Although there is no reliable symptom or sign during the latent period, abdominal pain occurs almost uniformly and Kehr's sign is quite common. Peritoneal lavage and abdominal computerized axial tomography scan are accurate in diagnosing splenic rupture. Unfortunately, they are not always reliable in predicting delayed rupture.
Splenic rupture in blunt and penetrating trauma is well documented. Other etiologies include hematologic and inflammatory disorders. The case presented documents occult splenic rupture. There was no history of trauma. Furthermore, no evidence of systemic disease or pathology could be found. Occult, spontaneous splenic rupture is rarely diagnosed, although the associated mortality/morbidity is high. The astute clinician must have a high index of suspicion relying on clinical and roentgenographic study for rapid diagnosis and management.
Four cases of spontaneous splenic rupture after infectious mononucleosis (IM) have been treated at this institution since 1978. The condition is rare, occurring in 0.1-0.5 per cent of patients with proven infectious mononucleosis. Splenectomy is considered the treatment of choice for these patients. However, because recent trends in the management of traumatic splenic rupture are moving towards nonoperative treatment with selected patients, a similar approach has been considered for the patient with spontaneous splenic rupture following IM. The major reason for avoiding splenectomy is the increased incidence of sepsis in splenectomized patients. Yet, splenic rupture is accompanied by hemorrhage and the risks associated with blood transfusion for ongoing hemorrhage are of similar magnitude as those of sepsis following splenectomy. In addition, the grossly abnormal spleens seen at operation tend to include large, contained hematomas that may also be prone to rupture. Therefore, operative management still appears to be the preferred treatment for spontaneous splenic rupture following IM. Splenectomy is curative, safe, and obviates the need for transfusion, extended hospitalization, and activity restriction.
Spontaneous splenic rupture occurs in association with infectious mononucleosis. Three cases of serologically proven infectious mononucleosis complicated by spontaneous splenic rupture are described. In two, the diagnosis was confirmed preoperatively by abdominal computerized tomographic (CT) scan. Treatment by splenectomy was curative in all three patients. Infectious mononucleosis patients who have acute abdominal pain must be considered for potential splenic hemorrhage.
A recent case of posttraumatic splenic abscess in a young man following nonoperative management of his splenic rupture is reported. With the recent trend toward nonoperative management of hemodynamically stable splenic rupture, the potential complications of splenic abscess may become more common. In view of the high mortality associated with unrecognized splenic abscess, it is important for the clinician to be aware of this entity.
"Conservative" management of splenic rupture in patients with mononucleosis has not been adequately evaluated because of its infrequent occurrence. Splenic rupture can be lethal in this setting and is the most common cause of death from mononucleosis. We report a case of spontaneous splenic rupture in a young girl with mononucleosis. The initial management was nonoperative but because of recurrent pain and rebleeding, a splenectomy was later performed. We do not recommend observation of splenic rupture in patients with mononucleosis because of the danger of delayed hemorrhage.
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Fatal chemotherapy splenic rupture is a rare event in acute leukemia. We report on a patient with acute monoblastic leukemia who developed splenic rupture 13 hours after the initiation of aggressive chemotherapy. Histologic studies of the spleen showed diffuse capsular infiltration and disseminated areas of subcapsular necrosis. Lysis of the leukemic cells and release of their enzymatic content, induced by the chemotherapy, probably led to proteolytic injury of the splenic capsule. We suggest that this mechanism may be an important pathogenetic factor in the occurrence of splenic rupture in patients with acute leukemia.
We report splenic rupture a few hours after a colonoscopy. Even though the patient had no previous history of splenic injury or symptoms attributable to splenocolonic adhesions, exploration revealed adhesions between the spleen and the colon at the level of the splenic flexure. Pathological examination revealed capsular thickening and fibrosis. Splenocolonic adhesions may lead to potentially lethal rupture of the spleen. A careful history prior to endoscopy should rule out pathological conditions that may lead to formation of adhesions between the spleen and the colon. In addition, the endoscopist should consider splenic rupture after colonoscopy in the patient who develops abdominal pain and acute anemia without evidence of intestinal perforation or external bleeding.
Retroperitoneal bleeding from splenic rupture occurred after initially uneventful arthroscopy. The diagnosis was finally set up in CT-scan, whilst peritoneal lavage was negative. Since there was no incidence of previous abdominal trauma and no abnormal findings in histology, spontaneous perioperative splenic rupture has been discussed.
Spontaneous splenic rupture is a rare but life-threatening complication of infectious mononucleosis. Patients typically present with acute abdominal pain most marked in the left lower abdomen. Occasionally the pain is referred to the left shoulder and preceded by "flu-like" symptoms. Palor, orthostasis, and tachycardia can also be observed. Because abdominal pain and tachycardia are unusual in uncomplicated cases of infectious mononucleosis, the possibility of spontaneous splenic hematoma or rupture must be considered. The case presented here typifies the clinical manifestations of this entity and illustrates appropriate management.