Hypercoagulation and Pediatric Inflammatory Bowel Disease: A Case Report

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Inflammatory bowel disease (IBD) is associated with hypercoagulability. The exact pathophysiology is not well known. However, it has been demonstrated in adult IBD studies that there is an increased risk for venous and arterial thrombosis and pulmonary embolism. This risk is significantly increased during times of disease flare (1,2). Currently, there are consensus practice guidelines including prophylactic anticoagulation in hospitalized adult but not pediatric IBD patients. We present a case of a girl with ulcerative colitis (UC) who developed toe ischemia while hospitalized for an acute flare in order the demonstrate the importance of 1) considering the presence of hypercoagulability in a hospitalized pediatric IBD patient 2) need for further pediatric studies in hypercoagulation and IBD and 3) considering surgical options earlier for hypercoagulability secondary to severe inflammation in UC. An 11-year-old girl with UC presented to Children's Medical Center Dallas in March 2015 with 2 weeks of increased bloody stools (7–8 per day) and nocturnal stools (4 per night). Two days prior, she had 2 episodes of nonbloody nonbilious emesis associated with decreased oral intake. She denied having any fevers, abdominal/joint pain, weight loss, vision changes, or new lesions.
Her past medical history is significant for UC diagnosed in 2006, before the widespread adoption of early onset IBD workup (3), and not significant for metabolic disease. Her UC was initially refractory to steroids but was in remission with sulfasalazine until she presented with multiple acute flares secondary to medication noncompliance. Her medications included mesalamine enemas and suppositories, oral mesalamine, oral prednisone (started 09/2014, weaned off 02/2015), and VSL 3. Before readmission, she was only on VSL 3 due to mom's concern about side effects and not on any other medications including oral contraceptives. There were discussions about starting a biologic versus immunomodulatory medication as maintenance therapy; however, mom refused. Her past surgical history was significant for multiple esophagogastroduodenoscopies and colonoscopies, last being in September 2014, which were visually normal. Biopsies showed mild active colonic inflammation. Family and social history were noncontributory.
Her physical examination was significant for obesity (body mass index was 26.94 kg/m2, 97th percentile). Initial labs included normal electrolytes and urinalysis, albumin of 3.1 g/dL (nl 3.6–5.1 g/dL), white blood cell count of 13.1 × 103/mm3, hemoglobin of 10 g/dL (roughly around her baseline), hematocrit of 33.1% (nl 36%–46%), platelets of 392 × 103/mm3, erythrocyte sedimentation rate of 28 mm/h (nl 0–15 mm/h), C-reactive protein of 3.97 mg/dL (nl 0–1 mg/dL), fecal calprotectin of 329 μg/g (nl <50 μg/g), and negative stool studies including Clostridium difficile polymerase chain reaction, culture, cryptosporidium, and giardia. Two days after admission, she got an esophagogastroduodenoscopy, which was grossly normal, and a colonoscopy which showed significant colonic ulceration and erythema. Biopsies showed mild-moderate colonic crypt changes with dense lymphoplasmacytic infiltrates. IV solu-medrol and budesonide SR daily were started but with no improvement in her pediatric ulcerative colitis activity index score (65 majority of the time). Surgery was consulted and colectomy was recommended. Budesonide was held in preparation for surgery. Approximately 2 weeks postadmission, the patient's left great toe became swollen and discolored with tenderness upon palpation with good perfusion (Fig. 1). The differential included ischemia, thromboembolism, septic emboli, clotting, or rheumatologic disorder so multiple subspecialties were consulted. Vancomycin and ondansetron were started given concern for infectious vegetations. An echocardiogram showed no evidence of thrombus or vegetations. Computed tomography angiogram of the bilateral lower extremities was negative for venous or arterial occlusion. Hematology workup was significant for elevated factor 8 activity, fibrinogen, protein S activity, and D dimer; these are nonspecific and are elevated during times of inflammation. Negative workup included factor V Leiden, prothrombin mutation, antiphospholipid antibodies, and protein C activity.

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