The main factors contributing to the development of secondary osteonecrosis are trauma, the habitual use of alcohol and steroid drugs, and medical conditions such as diabetes mellitus and hyperlipidemia1,2. Osteonecrosis is frequently seen in association with pancreatitis complicated by the alcohol factor but is rarely associated with uncomplicated pancreatitis1-4. We are aware of only one report of symptomatic osteonecrosis secondary to trauma-induced pancreatitis4.
We treated a child in whom multifocal osteonecrosis developed following traumatic pancreatitis. The patient's family was informed that data concerning the case would be submitted for publication and they consented.
A ten-year-old girl was injured in a fall from an iron fence surrounding a swing set. She sustained a severe impact to the abdomen and was taken to our hospital. Her family history and medical history were unremarkable. On admission, the blood pressure was 120/87 mm Hg, the pulse was 82 beats/min, and the body temperature was 36.7°C. She reported intense abdominal pain and nausea. Upper abdominal muscle guarding was observed, and an abdominal computed tomography scan showed pancreatic trauma. The serum amylase level was 296 IU/L, and the white blood-cell count was 14,200/µL (14.2 × 109/L). She was diagnosed with traumatic pancreatitis. Peripancreatic drainage was performed, and conservative treatment consisting of fasting (including water), fluid management, administration of FOY (gabexate mesilate), and administration of antibiotics was initiated.
Approximately ten days after the injury, polyarthralgia developed in both elbow joints, both knees, and the right ankle joint and gradually intensified. The patient had intermittent fevers of between 39°C and 40°C, but no heat or swelling was detected locally in the painful joints. The radiographic findings were unremarkable, but Tc99m bone scintigraphy showed high levels of tracer accumulation in the distal parts of both femora, in the proximal parts of both tibiae, and in the distal part of the right tibia. Magnetic resonance imaging showed a mixture of (1) extensive band-shaped area(s) with low signal intensity on both T1 and T2-weighted images encompassing large areas of both femora and both tibiae and (2) slightly high-intensity region(s) containing multiple nodular or macular lesions, which, in part, suggested the possibility of fatty marrow being replaced by osteonecrosis (Figs. 1-A and 1-B). Fat-suppressed T2-weighted (short tau inversion recovery [STIR]) images showed lesions with high signal intensity in the bone marrow, suggesting bone marrow edema and inflammation in response to osteonecrosis.
Even with the conservative care described above, the patient continued to experience high fever and abdominal pain. The serum amylase level rose to 8140 IU/L, and the P-amylase level, to 5117 IU/L. Diagnostic imaging revealed gradual enlargement of a pancreatic pseudocyst, which reached a diameter of 13 cm, and two months after the initial trauma a gastropancreatic pseudocyst was decompressed endoscopically. Immediately after the surgery, the abdominal pain and fever were reduced, and the amylase values decreased in parallel to a reduction in the size of the pseudocyst. Because of the patient's severe condition and the need for fluid management, including intravenous hyperalimentation, the bone lesions were treated with symptomatic therapy and in-bed muscle-strengthening training for the limbs. Subsequently, radiographs showed radiolucent lesions and sclerotic areas around both the knee and the elbow joints and in the metacarpal bones, which gradually became more pronounced (Figs. 2-A and 2-B). Periosteal callus formation was also noted. The musculoskeletal symptoms decreased gradually with the reduction in the amylase levels. One year after the accident, the patient was able to run without pain and experienced no interference with daily activities.