Acute Severe Flare-up of Ulcerative Colitis Complicated by Acute Deep Venous Thrombosis in a Rural Kenyan Hospital

Introduction

Patients with inflammatory bowel disease (IBD), which include Crohn’s disease (CD) and ulcerative colitis (UC), have a 2-to-3-fold increased risk of developing deep venous thrombosis (DVT) and pulmonary embolism (PE) compared with the general population (1). DVT and PE are collectively known as venous thromboembolism (VTE). This risk seems to be specific to IBD as opposed to other autoimmune diseases with direct and indirect chronic bowel involvement, including rheumatoid arthritis and celiac disease, as demonstrated by Miehsler et al. in their study of 618 patients with IBD, 243 with rheumatoid arthritis, and 207 with celiac disease (2). In UC, the risk factors and mechanisms for VTE induce a state of Virchow’s triad (vascular injury, hemostasis, and hypercoagulation) (3). These include: i) chronic inflammation of UC that can trigger the release of pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha (TNF-α) that promote a hypercoagulable state and can activate the endothelium, thereby increasing thrombosis (4, 5); ii) during flare-ups of UC, patients may experience prolonged moments of immobility (a known risk factor of VTE) due to diarrhea, abdominal pain, and fatigue (4); iii) medications like corticosteroids used in the management of UC and abdominal surgical interventions (including the use of central venous catheters) for severe UC can increase the risk of VTE by creating a hypercoagulable state, endothelial injury, and immobility (3, 4, 6); iv) in severe UC, poor feeding can lead to malnutrition and deficiencies of key nutrients involved in coagulation pathways, thus increasing a prothrombotic state (4). Other studies of VTE risk in UC have identified patients aged over 45 years as being more than three times predisposed to VTE after hospital discharge compared to younger patients (7). These are in addition to the traditional risk factors for VTE found in the general population (8). The management of VTE in UC involves the use of thromboprophylaxis (both pharmacologic and non-pharmacologic) to prevent VTE and the active management of VTE in UC. Nonpharmacologic measures include adequate hydration, using graded compression stockings or pneumatic devices, vitamin B6 and B12 supplementation to lower homocysteine levels, and post-surgery early mobilization (9). Both the American College of Gastroenterology and the British Society of Gastroenterology recommend pharmacologic DVT prophylaxis to forestall VTE in patients admitted with flare-ups of UC (10, 11). The risk of bleeding with the use of anticoagulants for VTE thromboprophylaxis remains a clinical concern in these patients, although several studies have demonstrated very low risks of minor or major bleeding, even after major surgery related to UC (12, 13). The treatment of VTE in active UC is the same as in patients without IBD, provided there is no hemodynamically significant bleeding or indications for thrombolysis (14). These include the use of low molecular weight heparin, warfarin, direct oral anticoagulants, use of catheter-directed thrombolysis in selected cases, and placement of inferior vena cava filters in patients with recurrent VTE despite anticoagulation (14-16). The duration of anticoagulation (6 months vs. extended period) is based on individualized risks for recurrent VTE. Nguyen et al. demonstrated that among IBD patients who have had unprovoked VTE, the benefits of long-term anticoagulation in reducing recurrent VTE outweigh the risks of the possible associated bleeding (17).

Case Summary

History and physical examination

A 74-year-old retired civil servant, a married father of 10 adult children, from Nakuru township, Nakuru County, Kenya, presented to us in November 2025 with acute extensive deep venous thrombosis of the left leg involving the common femoral, femoral, popliteal, and calf veins as seen on Doppler ultrasound scan. He had well-controlled hypertension on losartan, dyslipidemia, and osteoarthritis of the lumbosacral spine and both knees on analgesics. At the time, he was also in an acute, severe flare-up of ulcerative colitis, having defaulted on his treatment (sulfasalazine) for over 5 months. He had been diagnosed with ulcerative colitis in 2006 on the clinical basis of recurrent hematochezia, abdominal pains, and loss of weight. The diagnosis was confirmed by colonoscopy with biopsy and histological analysis, and he had been on follow-up at various gastroenterology and general medical outpatient clinics in public and private health centers. Over the years, he had variously used oral 5-aminosalicylate acid (5-ASA)/sulfasalazine, oral prednisone, and methotrexate. He was on sulfasalazine 500 mg daily at the time of presentation but admitted to poor compliance due to financial reasons. He recalled at least 4 prior admissions related to flare-ups of UC and needing blood transfusions at least twice, intravenous steroids, and supportive care. We had first seen him in our hospital in December 2020 with a 1-month history of recurrent hematochezia and did a colonoscopy, which showed uniform pancolitis, with histology showing mucosal and submucosal inflammation with granulocytic infiltrates, consistent with UC. He had responded rapidly to oral prednisone, sulfasalazine, and supportive care, with cessation of hematochezia within 3 days. He was subsequently lost to follow-up during the COVID-19 era. He reappeared at our medical clinic in late 2024 for matters unrelated to UC and reported that his gastroenterologist had maintained him on sulfasalazine (due to affordability and availability issues) and that he was in clinical remission from the UC. He would sporadically come for reviews since then. Presently, he had clinical features of severe UC that developed 1 week prior. He was passing 6-8 loose bloody stools daily associated with cramping abdominal pains and fevers (peak temperature of 38.2^oC), tachycardic at 108 bpm, anemic with an Hb of 10 g/dL, and had an ESR of 45 mm/hr. He had developed swelling and pain in his left lower limb 3 days before presenting to the hospital. He had no history of trauma to the leg or recent surgery. During the 1-week flare-up of UC, he stayed indoors. He had defaulted on all his medications 5 months prior to the current presentation. His physical examination was significant for fever, tachycardia, mild pallor, and dehydration. His BP was 108/56 mmHg. His abdomen was diffusely tender but with no peritonism or organomegaly. He had normal S1 and S2 heart sounds and normal chest auscultation bilaterally; he was corpus mentis with no focal neurology, and he had no skin rashes or pretibial nodules to suggest erythema nodosum. The left lower limb was swollen and tender at the calf but had a normal neurovascular examination.

Work-up and Diagnosis

His complete blood count showed an Hb of 10 g/dL with an MCV of 91 fL, WBC of 12.4 x 10³/µL, and platelets of 224 x 10³/µL; the ESR was 45 mm/hr.; a random glucose of 135 mg/dL; the stool was loose and bloody with 3+ leucocytes, 2+ mucus, and numerous trophozoites of Entamoeba histolytica seen; he had a mild acute kidney injury with a serum creatinine of 1.6 mg/dL, Na+ of 128 mmol/L, and K+ of 2.9 mmol/L; the liver panel was normal; a blood smear for malaria parasites was negative; urinalysis was normal; a chest and an erect abdominal X-ray were normal; a Doppler ultrasound of the left leg showed extensive deep venous thrombosis involving the common femoral, femoral, popliteal, and calf veins, while an abdominopelvic ultrasound was unremarkable.

We made a clinical diagnosis of a severe flare-up of UC based on the Truelove and Witts Severity Index for Ulcerative Colitis scoring calculator (18) precipitated by nonadherence to treatment and E. histolytica enterocolitis and complicated by acute left lower limb extensive DVT and prerenal acute kidney injury with mild hyponatremia and hypokalemia.

Management and Follow-up

We recommended inpatient management at our facility or a facility of his choice, but he and the family declined. We therefore treated him pragmatically as an outpatient with the available resources as follows: we stopped his active hematochezia with intravenous (IV) tranexamic acid, 1 gm 3x daily for 3 days (he got the other doses in a nearby health center). The hematochezia subsided by the second day of treatment. To suppress the flare-up of severe acute UC, we administered IV hydrocortisone 100 mg 3x daily for 3 days, then switched him to oral prednisone tapered over a 7-day period and oral sulfasalazine 500 mg 2x daily. To treat the amoebiasis, we administered IV metronidazole 500 mg 3x daily for 2 days and then switched him to the oral form for a total of 7 days. Additionally, we administered IV ceftriaxone, 1 gm daily for 2 days, followed by a 5-day oral course of ciprofloxacin to cover bacillary dysentery. To manage the acute left leg DVT, we put him on bilateral compression stockings and started him on anticoagulation therapy at the end of the 3-day course of tranexamic acid. We administered oral rivaroxaban at 15 mg 2x daily for 21 days, followed by 20 mg daily for an initial 6 months, then 10 mg daily long-term. Other supportive care included IV fluid resuscitation with electrolyte replacement followed by oral rehydration salt solution, IV then oral hyoscine butyl bromide, paracetamol, omeprazole, metoclopramide, ferrous sulfate, and multivitamins. By the end of the second day of treatment, the hematochezia and abdominal pains had subsided; he was passing normal stool by the third day, and his vital signs were normal. When we administered rivaroxaban, he had no recurrence of hematochezia and no further bleeding diatheses since then. His follow-up laboratory tests were normal 2 weeks after we started his treatment. We did health education on prevention of amebic infections. A follow-up colonoscopy is pending due to financial constraints. He is currently irregularly attending our medical outpatient clinic on sulfasalazine 500 mg daily and rivaroxaban 10 mg daily, together with losartan and atorvastatin, and is in clinical remission.

Discussion

Our patient presented with an acute severe flare-up of UC based on the Truelove and Witts Severity Index for Ulcerative Colitis (18) complicated by an acute extensive DVT of the left leg in the absence of the traditional risk factors for DVT. The poorly controlled UC, coupled with his age, was his most likely risk factor for developing DVT. The risk of VTE in IBD (UC and CD) increases 3-fold during acute flare-ups (12). Patients with UC have a 2-to-3-fold increased risk of DVT and VTE (1). The 2025 American College of Gastroenterology guidelines for the management of moderate-to-severely active UC strongly recommend inducing remission by the use of oral systemic corticosteroids, sphingosine-1-phosphate (S1P) receptor modulators (ozanimod and etrasimod), interleukin (IL)-12/23p40 antibody ustekinumab, anti-tumor necrosis factor (TNF) therapy (using infliximab, adalimumab, or golimumab), and Janus kinase (JAK) inhibitors (tofacitinib and upadacitinib). The same drugs, together with methotrexate, 5-ASA/sulfasalazine, are recommended to maintain remission, albeit in specific individualized clinical scenarios (10). These guidelines, together with other similar society guidelines, also provide guidance on the general management of UC (10). In our resource-limited clinical setting, we are only able to access and use corticosteroids, 5-ASA/sulfasalazine, and methotrexate; hence, their use in our patient. At any rate, our treatment objectives of inducing and maintaining remission, treating concurrent infections, and optimizing the patient’s overall health were all achieved in a pragmatic approach. Our main concern was how to manage the acute extensive left DVT to forestall VTE with therapeutic anticoagulation in the face of severe active gross hematochezia and dehydration. Studies have consistently shown that it is safe to administer therapeutic anticoagulation even in patients with severe flare-ups of UC, provided that there are no hemodynamically significant bleeding or indications for thrombolysis (14). Other studies on the use of anticoagulation in active UC have demonstrated very low risks of minor or major bleeding, even after major surgery related to UC (12, 13). In our case, we exercised clinical discretion by first stopping the active hematochezia using an antifibrinolytic agent (tranexamic acid) and then administering rivaroxaban (a direct oral anticoagulant) at therapeutic doses without any bleeding complications. We elected to keep him on long-term anticoagulation in view of the unprovoked nature of the DVT. This is consistent with evidence in such scenarios (17).

Conclusion

Patients with IBD (UC and Crohn’s disease) have a 2-to-3-fold increased risk of DVT and VTE. In UC flare-ups, the chronic inflammation burden, immobility, prothrombotic medications like steroids, and surgical procedures induce a state of Virchow’s triad (vascular injury, hemostasis, and hypercoagulation) that promotes VTE. UC patients with acute moderate-to-severe flare-ups need both pharmacologic and non-pharmacologic thromboprophylaxis. IBD patients with VTE should be treated with therapeutic anticoagulation as they have very low risks of minor and major bleeding, even after major abdominal surgery related to the IBD.

Acknowledgement

The authors acknowledge Mr. Seth Manera (administrator) and the staff in the medical clinic of St. Joseph Rift Valley Hospital, Gilgil, for their help with managing this patient.

Ethical consideration

Informed consent was obtained from the patient to publish this case study.

Funding

The authors have no funding sources to declare.