Delayed splenic hematoma rupture

Delayed Splenic Hematoma Rupture CARY C. MCDONALD, MD The diagnosis of splenic hematoma can be clinically challenging. A case of delayed rupture of an atraumaUc splenic hematoma is described, illustrating how unusual the presentation of this entity can be. (Am J Emerg Med 1995;13:540-542. Copyright © 1995 by W.B. Saunders Company) The e m e r g e n c y d e p a r t m e n t (ED) p r e s e n t a t i o n o f a patient c o m p l a i n i n g o f flank o r c h e s t pain is c o m m o n . Diagnosing the life-threatening c o n d i t i o n o f d e l a y e d r u p t u r e o f a splenic h e m a t o m a can be challenging b e c a u s e the differential diagn o s i s o f a p a t i e n t w i t h u n c l e a r s y m p t o m a t o l o g y c a n be lengthy. This c a s e e x e m p l i f i e s the challenge in diagnosing this entity.

CASE REPORT A 50-year-old man summoned paramedics for a complaint of left flank pain. He was found by Emergency Medical Services personnel to be in no distress with normal vital signs. He stated that his symptoms had resolved and refused further care. The patient was deemed competent and signed a refusal of service document. One hour later he activated the 911 system again because of recurring pain and was evaluated by the same paramedic crew. The patient complained of intermittent left flank and left abdominal pain associated with some nausea and no vomiting. His vital signs remained within normal limits, and his pain was determined to be reproducible with palpation and change of position. He was transported to the ED without incident. On arrival in the ED, the patient complained of acute left-sided thorocoabdominal pain (3 to 4 on a 10-point scale) radiating down his left arm associated with shortness of breath and nausea. The pain was sharp and intermittent, developing over the previous 2 hours. He denied any trauma, fever, diarrhea, upper respiratory, or urinary symptoms. There was a past medical history of diet-controlled diabetes mellitus and hypercholesterolemia. He denied any history of hypertension, heart disease, or renal stones and was taking no regular medication. His social history revealed a former two-pack-perday smoking habit as well as heavy alcohol use. The patient abstained from tobacco and alcohol for the previous 6 weeks, after a New Year's resolution. Physical examination showed an alert, well-developed, wellnourished normothermic man with a blood pressure (BP) of 137/73 mm Hg, pulse of 124 beats per minute, and 24 respirations per minute. Head and neck examination was unremarkable. The chest wall was nontender, and the lungs were clear to auscultation. The heart examination was normal with no murmur, gallop, or rub. The abdomen was soft, nondistended, and nontender without palpable masses. Normal, active bowel sounds were present. Rectal exami-

From the Department of Emergency Services, Wake Medical Center, Raleigh, and the Department of Emergency Medicine, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Manuscript received October 19, 1994; accepted December 1, 1994. Reprints are not available. Key Words: Spleen, splenic hematoma, ruptured spleen, delayed splenic rupture. Copyright © 1995 by W.B. Saunders Company 0735-6757/95/1305-001355.00/0 540

nation was nontender and negative for blood. The back was unremarkable in appearance, and there was no costovertebral angle tenderness. Extremities had symmetric equal pulses and normal capillary refill. Neurological examination was nonfocal. The skin was pale, but warm and dry. During the patient's assessment, he was placed on a cardiac monitor that showed a sinus tachycardia of 120 beats/min. Pulse oximetry on room air was 96%, and oxygen was administered by face mask at 15 L/min. An intravenous line of normal saline was initiated to keep vein open and a rapid blood glucose was 20.9 mmol/L (376 mg/dL). A 12-lead electrocardiogram (ECG) showed a sinus tachycardia of 137 beats/min without any ST-T chanses (Figure 1). Immediately after completion of the ECG the patient stated, " I don't feel so good," and became unresponsive with agonal respirations. The cardiac monitor showed a sinus bradycardia at a rate of 26 (Figure 2). Respirations were supported with a bag-valve-mask device; atropine 1 mg was administered intravenously as well as a 300 mL saline fluid bolus. He became conscious and complained of worsening chest pain. Blood pressure was 137/73 mm Hg. A repeat ECG showed new 1 to 2 mm ST segment depression in leads V2 and V3. A cardiologist was consulted by telephone to attend to this patient for a presumed cardiac event. A nitroglycerine drip was started at 20 ~g per minute. A portable chest radiograph was normal (Figure 3). Laboratory results included arterial blood gases of pH 7.41, Pco2 33, Po2 295 and HCO3- 21. The white blood cell count was 10.1 106/L. The hemoglobin and hematocrit were 144 g/L (14.4 g/dL) and 0.43 (43%) respectively. Platelet count and coagulation studies were within normal limits. Chemistries, including amylase and cardiac enzymes, were normal except for a serum glucose of 20.9 mmol/L (376 mg/dL). The cardiologist arrived and performed a bedside echocardiogram showing normal left ventricular function without evidence of pericardial effusion. The thoracic aorta appeared normal. The patient complained of worsening chest pain as well as left upper quadrant abdominal pain. The BP dropped to 58/26, and the pulse was 106. The abdominal examination remained unremarkable. The nitroglycerine was discontinued, another 300 mL saline bolus was given, and a dopamine infusion was established at 5 p~g/kg/min. Computed tomography (CT) of the chest and abdomen were requested as well as type and cross-match for four units of packed red blood cells. The patient complained of worsening abdominal pain and developed some mild left upper quadrant tenderness. The BP improved to 141/ 50, but he became rate sensitive to the dopamine with a pulse as high as 159. A norepinephrine infusion was initiated, and the dopamine was reduced with eventual improvement in hemodynamics on both medications. Chest CT (Figure 4) showed small bilateral pleural effusions and no evidence of aortic aneurysm or dissection. The abdominal CT (Figure 5) showed a large perisplenic hematoma with active extravasation of blood. Blood was seen extending into the pericolic gutters (Figure 6). There was no evidence of injury or laceration to the spleen. The aorta, kidneys, liver, pancreas, and gall bladder were all unremarkable. A general surgeon was immediately consulted. Transfusion of packed red blood cells was initiated and a repeat hematocrit had decreased to 0.28 (28%). The patient was taken to the operating room for a laparotomy, which showed a splenic subcapsular hematoma and complete disruption of the spleen. Two thousand milliliters of free blood was in the abdominal cavity. A splenectomy was performed uneventfully, and the patient was discharged on the third postoperative day without further incident.

CARY C, McDONALD • DELAYED SPLENIC HEMATOMA RUPTURE

541

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AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 13, Number 5 • September 1995

FIGURE 5. Abdominal CT showing a large perisplenic hematoma (arrow).

DISCUSSION The etiology of splenic hematomas is usually secondary to trauma to the chest or abdomen from blunt trauma such as falls, altercations, sports injuries, or motor vehicle accidents. ~ Rib fractures are associated in only 10% of cases. 2 Associated risk factors include substance abuse and splenomegaly. Delayed rupture can occur in splenic hematomas without any history of trauma. The overall incidence of delayed splenic rupture in 1943 was 14%. In 1976 the incidence had decreased to 0.3%, This is attributed to improved methods of detection including CT scanning and diagnostic peritoneal lavage. 3 Delayed rupture occurs in 15% of splenic hematomas. 4 The initial injury often goes unnoticed, especially in substance abusers who are less likely to recall the event. Only 20% of patients complain of left upper quadrant pain. Many cases are precipitated by minor stress such as bending, twisting, or stretching. The interval between injury and subsequent hemorrhage is within 1 week in 50% of patients, within 2 weeks in 25%, and beyond 4 weeks in 10%.2 Mortality has improved tremendously over the years. In a 1932 series, mortality was 39%, in a 1966 series it was 10%, and in a 1974 series it was 2.8%. This improvement is attributed to increased availability of emergency care and more aggressive approach to volume resuscitation and surgery. 2 An ED patient presenting with chest, abdominal, or flank pain in the presence of cardiovascular instability, an otherwise equivocal physical examination, and essentially normal laboratory work can be diagnostically challenging in identifying the underlying life threat. Patients with underlying Conditions such as cirrhosis, mononucleosis, lymphoma, and

FIGURE 6. Abdominal CT showing extension of blood into the pericolic gutters (arrows). leukemia may have splenomegaly. The differential diagnosis includes myocardial infarction, pericardial effusion or tamponade, aortic dissection or aneurysm, tension pneumothorax, pulmonary embolus or edema, renal or mesenteric vascular occlusion, gastrointestinal bleeding, bowel obstruction or perforation, pancreatitis, hepatitis, and sepsis. In female patients the differential diagnosis includes ectopic pregnancy and ovarian cyst. 5 Deteriorating patients obviously require aggressive management and frequent or continuous reevaluation. Early thorocoabdominal CT scanning would supersede diagnostic peritoneal lavage in patients with progressing symptomatology in the absence of trauma, because peritoneal lavage can be negative in the presence of retroperitoneal bleeding. Serial hematocrits, blood bank type and crossmatching, and early surgical intervention may diminish morbidity. The ED presentation of a patient with delayed rupture of splenic hematoma is reviewed with emphasis on the unusual presentation and difficult diagnosis of this condition.

REFERENCES 1. Dang C, Schlater T, Bui H, et al: Delayed rupture of the spleen. Ann Emerg Med 1990;19:399-403 2. Durston W, Bivins H: Delayed splenic rupture in a cirrhotic. Ann Emerg Med 1983;12:91-93 3. Albu E, Parikh V, Abugaida AM, et al: Delayed splenic rupture in a drug addict. Ann Emerg Med 1993;22:861-862 4. Benjamin CI, Engrav LH, Perry JF: Delayed rupture of delayed diagnosis of rupture of the spleen. Surg Gynecol Obstet 1976;142:171-172 5. Petri RW, O'Brien PD, Vukich DJ: Delayed splenic rupture. Ann Emerg Med 1990;19:1302-1305