A rare cause of left upper quadrant abdominal pain

Abstract

Dr. Fiorentino: A 44-year-old black woman from Cuba was admitted to the Emergency Department (ED) because of stabbing abdominal pain in the left upper quadrant, which had begun suddenly after she finished working. During the week prior to admission, she had no fever, no symptoms or signs of gastroenteritis, no dysuria, and no change in bowel habit. The patient said that she had the same symptoms 2 years prior to this episode after an airplane flight. On that occasion, she was admitted to a hospital, but she did not remember the diagnosis and no records were available. The patient also had no recollection of previous diagnosis of hemoglobinopathies, was not aware of previous health problems or diseases and had no recollection of childhood hospitalization. On admission to the ED, she presented symptomatic with mild tenderness in the left upper quadrant of the abdomen. The vital signs were: pulse 93 beats/min, respiratory rate (RR) 16 breaths/min, blood pressure (BP) 130/85 mmHg, body temperature 36.7 C. The finger stick glucose was 91 mg%. The 12-lead ECG showed a sinus rhythm with a normal QRS shape. Physical examination revealed a soft abdomen that was mildly tender in the left upper quadrant. There were no pulsating masses, no splenomegaly, no asymmetrical peripheral pulses nor detectable bruits. The liver was slightly enlarged on palpation. The remainder of the examination was unremarkable. The results of routine laboratory findings, including b-HCG, ALT, AST, pancreatic amylase, bilirubin, creatinine, coagulation parameters were within normal range, except for a mild anemia (Hb = 11.2 g/dl; Htc = 33.4%; VCM = 80.5 fl), mild LDH (903 U/L) and PCR increase (3.29 mg/dl) [1, 2]. The ultrasound (US) abdominal examination [3] revealed an abnormal and inhomogeneous splenic echostructure because of multiple lesions, with the characteristics of ischemic infarctions and scarring (Fig. 1, see white arrows); there were no other pathological findings in the liver, kidneys, pancreas, abdominal aorta and pelvic organs. Acute splenic infarctions appear as more or less echogenic lesions, without Doppler signal (Fig. 2; see white arrows), with variable dimensions, that extend to the surface. Their characteristic pyramidal shape allows us to distinguish splenic infarction from abscesses or tumoral infiltration. The chronic relapsing infarction is typical of sickle cell anemia. In this case, the spleen has multiple echogenic or hypoechoic focal lesions that led to a progressive splenic capsule retraction because of fibrous scars. During recovery there is an increase in echogenicity and the retraction of the infarcted area. The complications (20% of all cases) are [4]: gradual colliquation (degeneration of splenic tissue to a liquid state after a necrotic process), sub-capsular bleedings, pseudoaneurysms or arterio-venous fistulae and hemoperitoneum. The possible evolutions are: