Diverticulitis-Associated Mesenteric Venous Thrombophlebitis: A Case Report and Systematic Review of Diagnosis, Management, and Outcomes

Abstract

Diverticulitis can rarely seed the portal‑mesenteric venous system, causing septic thrombophlebitis with morbidity and management uncertainty. This study systematically reviewed diverticulitis‑associated mesenteric venous thrombophlebitis to summarize its presentation, diagnostics, treatment, and outcomes. Twenty‑eight single‑patient reports met the selection criteria. The mean age was 54 years; fever and abdominal pain predominated. Contrast‑enhanced CT established the diagnosis in most patients, usually showing sigmoid diverticulitis with inferior mesenteric or portal‑mesenteric vein thrombus. Sigmoid involvement predominated, and inferior mesenteric vein involvement was common. Blood cultures were positive in 53.6% (common organisms: Bacteroides, Escherichia coli, and Klebsiella). Abscess, venous gas, and perforation were frequent. Broad‑spectrum antibiotics were universal, and anticoagulation was given in 82.1%, and surgery was performed in 53.6% for deterioration or complications. In a complete‑case comparison of 23 anticoagulated versus five non‑anticoagulated patients, times to symptom resolution, radiographic clearance, and length of stay were similar, with venous recanalization documented in 30.4% versus 20.0% and adverse events in 26.1% versus 0%, respectively. Overall, the length of stay averaged 19 days. Radiographic resolution occurred at approximately three months with venous recanalization in 28.6% of cases, and no deaths or recurrences. In conclusion, early CT, prompt antibiotics, consideration of anticoagulation for extensive or occlusive thrombosis, and selective drainage or resection appear prudent, but prospective data will be needed.

INTRODUCTION

Diverticulitis is a common cause of acute abdominal pain, but septic thrombosis of the portal-mesenteric venous system that arises from a diverticular infection is uncommon and frequently underrecognized.¹ Mesenteric venous thrombophlebitis, also termed pylephlebitis or portal-mesenteric venous thrombosis, develops when an intra-abdominal infection seeds the draining veins, producing endothelial injury, local inflammation, and thrombus formation. The clinical features are nonspecific and often overlap with uncomplicated diverticulitis, while biochemical abnormalities may be subtle.^2,3 Therefore, early diagnosis depends on a high index of suspicion and timely imaging. Contrast-enhanced computed tomography is the principal modality for identifying inflamed diverticula and venous filling defects, and blood cultures may reveal enteric gram-negative and anaerobic organisms.^4-6

Optimal management is not standardized. Broad-spectrum antibiotics directed at enteric flora are universally recommended, but the indications for anticoagulation, the choice of agent, and treatment duration, and the role of operative intervention or image-guided drainage vary across reports.^7,8 The anatomic distribution of thrombus within the portal-mesenteric system is heterogeneous, and associated complications, such as abscess, venous gas, or bowel ischemia, can occur, which further complicates decision-making.^9-11

A systematic review of diverticulitis-associated mesenteric venous thrombophlebitis was conducted to address these gaps. The objectives were to assess the patient characteristics, presentation, laboratory and microbiologic findings, imaging pathways, anatomic patterns of venous involvement, therapeutic strategies including antibiotics and anticoagulation, surgical indications, and clinical and radiographic outcomes.^12,13 This study aimed to provide practical guidance for clinicians and highlight priorities for prospective study by consolidating the available evidence from published cases.^14,15

CASE

1. Patient presentation

A 51-year-old man with a remote childhood heart murmur and diverticulosis diagnosed approximately seven years earlier presented to the emergency department after referral by his primary care physician for six days of malaise and elevated liver function tests. He reported the following: fatigue and generalized weakness requiring bed rest, intermittent fever with shaking chills and rigors beginning five days prior, mild intermittent left lower quadrant (LLQ) pain, night sweats, nausea without vomiting, diarrhea that began the night before presentation, dark urine approximately three times daily, poor tolerance of fluids, and headache without neck stiffness or confusion. He had taken Tylenol for fever; chronic medications included minoxidil for hair loss and ibuprofen four to six doses per week. On arrival, he was febrile at 101.5 °F but otherwise hemodynamically stable. The examination was notable only for LLQ tenderness without rebound or guarding.

Laboratory tests showed WBC 10.6 thousand/μL (normal 5–10) with absolute neutrophils 8.45 thousand/μL (normal 1.5–8). Abnormal or borderline comprehensive metabolic panel values included sodium 134 mmol/L (normal 135–145), chloride 96 mmol/L (normal 96–106), bicarbonate 22 mmol/L (normal 22–28), anion gap 16 mmol/L (normal 4– 12), ALT 107 U/L (normal 7–56), AST 64 U/L (normal 8–48), alkaline phosphatase 185 IU/L (normal 40–130), albumin 3.1 g/dL (normal 3.5–5.5), and total bilirubin 3.13 mg/dL (normal 0.2–1.2). Lactate was normal at 0.63 mmol/L (normal 0.5– 2.2). Contrast CT of the abdomen and pelvis revealed an inflamed sigmoid diverticulum with adjacent mural thickening and pericolonic fat stranding compatible with acute sigmoid diverticulitis without abscess or free perforation. An occlusion of the inferior mesenteric vein with surrounding fat stranding was noted, suggestive of thrombophlebitis (Figs. 1, 2). The thrombus closely followed the course of the inferior mesenteric vein draining the inflamed sigmoid colon, without imaging evidence of alternative intra‑abdominal sources such as appendicitis, pancreatitis, or biliary infection. Blood cultures were obtained, and he was discharged with a prescription of Augmentin.

Fig. 1.

Contrast-enhanced computed tomography shows sigmoid diverticulitis with mural thickening and pericolonic fat stranding adjacent to an occlusive inferior mesenteric vein thrombus. Coronal reformats reveal cranial extension toward the portal system without pneumoperitoneum or a drainable abscess.

Fig. 2.

Axial contrast-enhanced computed tomography at the level of the pelvis confirms sigmoid diverticulitis with pericolonic fat stranding and an adjacent occlusive inferior mesenteric vein thrombus (curved arrows), without pneumoperitoneum, portal venous gas, or a drainable abscess.

He returned the next day after the recovery of Proteus mirabilis, a typical colonic gram‑negative rod, from blood cultures, further supporting sigmoid diverticulitis as the primary infectious focus. He was admitted and treated with intravenous ceftriaxone plus metronidazole, then transitioned to ertapenem because of the rising liver function tests. Repeat blood cultures on hospital day 2 grew Staphylococcus hominis, a presumed contaminant, with no further growth. Considering the occlusive inferior mesenteric vein thrombus with cranial extension toward the portal system, ongoing Proteus mirabilis bacteremia, cholestatic liver abnormalities, and the absence of major bleeding risk factors, anticoagulation was initiated with enoxaparin (Lovenox^®) at a therapeutic dose and changed to rivaroxaban (Xarelto^®) on day 5.

The goal of anticoagulation was to prevent thrombus propagation into the portal system and promote venous recanalization. By day 6, he was afebrile without leukocytosis, and blood cultures had been negative for more than 72 hours. He was discharged with a PICC line for four weeks of ertapenem and rivaroxaban (Xarelto^®) for three months, with outpatient plans for repeat CT venography to reassess inferior mesenteric vein thrombophlebitis and for colonoscopy in the following weeks.

2. Systematic review methods

The reports for this systematic review were identified through a structured search of the published literature and are summarized in the PRISMA 2020 flow diagram (Fig. 3). Single‑patient case reports were included in which diverticulitis was the presumed source of portal‑mesenteric or mesenteric venous thrombophlebitis and sufficient individual‑level clinical data could be abstracted. Non‑English reports and articles without extractable outcomes were excluded. The following were extracted each eligible case: patient demographics and comorbidities; presenting symptoms and physical findings; inflammatory and cholestatic laboratory tests; microbiologic data; imaging modality and anatomic distribution of venous thrombosis; antimicrobial and anticoagulant regimens (agent or class, timing of initiation, and duration); hypercoagulable evaluation; surgical or percutaneous interventions; and clinical and radiographic outcomes including symptom resolution, length of stay, recurrence, adverse events, and venous recanalization. Variables that were not reported in the source publication were coded as missing rather than assumed absent.

Fig. 3.

PRISMA 2020 flow diagram of study selection: 198 records identified, 111 duplicates removed, 87 records screened, 31 full-text reports assessed, 3 excluded (2 not in English; 1 erroneous outcomes), and 28 studies included.

STATA/BE 19.5 (StataCorp LLC, College Station, TX, USA) was used for all statistical analyses. The data were summarized descriptively, with the counts and percentages for the categorical variables and medians with interquartile ranges for continuous variables. The binary outcomes were compared between groups using risk differences with exact 95% confidence intervals. A Fisher’s exact test was used as a sensitivity analysis when the expected cell counts were <5. Continuous outcomes were compared using the two‑sample Wilcoxon rank‑sum (Mann–Whitney) test, with exact p-values for small samples. All analyses were conducted on a complete‑case basis for each outcome, with no imputation of missing data. No multiplicity adjustments were made for multiple comparisons, and no regression or survival modeling was performed. The statistical significance was defined as p<0.05.

3. Systematic review findings

1) Literature overview

Twenty-eight publications met the inclusion criteria, and all were single-patient case reports (Fig. 3). The reports appeared across 25 journals, led by Cureus (3/28, 10.7%) and BMJ Case Reports (2/28, 7.1%). Most patients were reported from the United States (9/28, 32.1%), with additional cases from France (2/28, 7.1%), Italy (2/28, 7.1%), and Spain (2/28, 7.1%), among others.

2) Patient demographics

The mean patient age was 54 years (SD 13.4; range 19 to 74). Ethnicity was usually not reported, but African-American (1/28, 3.6%), Japanese (1/28, 3.6%), and Korean (1/28, 3.6%) patients were included. Obesity was noted in two cases (2/28, 7.1%). Two patients were postpartum at nine days and two months, respectively (2/28, 7.1%). Two patients were smokers (2/28, 7.1%), one with a 20 pack-year history, and one patient was a non-smoker (1/28, 3.6%). Alcohol use was reported in two patients (2/28, 7.1%), including one with alcohol use disorder and one consuming approximately 1,000 mL of beer daily. Two patients were immunosuppressed, one with alcoholic liver cirrhosis (Child-Pugh A) and one with HIV on HAART, while three were explicitly immunocompetent (3/28, 10.7%). The common comorbidities included diabetes mellitus (4/28, 14.3%), hypertension (4/28, 14.3%), hypercholesterolemia (2/28, 7.1%), and benign prostatic hyperplasia (2/28, 7.1%). Five patients had a history of diverticulitis (5/28, 17.9%). One patient had an incidental small cecal adenocarcinoma on colectomy pathology (1/28, 3.6%). One patient was heterozygous for thrombophilia-associated mutations in MTHFR A1298C and PAI-1 4G/5G (1/28, 3.6%). Reported studies and patient characteristics, including source journals, reporting countries, and baseline demographics, are summarized (Table 1).

Table 1.

Study and Patient Characteristics: Sources, Geography, and Baseline Demographics for 28 Single-Patient Reports Included in the Review

Study/Patient feature	Result
Total included cases	28 (100)
Article type
Case reports	28 (100)
Top journals (n)
Cureus	3
BMJ Case Reports	2
Others	23
Reporting country
United States	9 (32.1)
France	2 (7.1)
Italy	2 (7.1)
Spain	2 (7.1)
Others	13 (46.4)
Age, years	Mean 54 (SD 13.4; range 19–74)
Sex	Not consistently reported
Ethnicity reported, rare
African-American	1
Japanese	1
Korean	1
Selected comorbidities
Diabetes	4 (14.3)
Hypertension	4 (14.3)
Hypercholesterolemia	2 (7.1)
BPH	2 (7.1)
Special states
Obesity	2 (7.1)
Postpartum	2 (7.1)
Immunosuppressed	2 (7.1)
History of diverticulitis	5 (17.9)

Values are presented as number (%).

BPH, benign prostatic hyperplasia.

3) Symptom presentation

The patients presented a mean of six days after symptom onset (SD 4). Abdominal pain was reported in 25 out of 28 cases (89.3%), with one case explicitly without pain (1/28, 3.6%). Abdominal tenderness upon examination was described in 20 cases (20/28, 71.4%). Fever occurred in 26 cases (26/28, 92.9%), with a mean reported temperature of 38.4°C (SD 1.1). Nausea was reported in four cases (4/28, 14.3%), diarrhea in 11 (11/28, 39.3%), constipation in one (1/28, 3.6%), and jaundice in three (3/28, 10.7%). Tachycardia was present in six cases (6/28, 21.4%), with a mean reported heart rate of approximately 104 beats per minute (SD 21).

4) Laboratory testing

Leukocytosis occurred in 18/28 (64.3%), with a mean WBC of 13.7×10⁹/L (SD 3.1). Neutrophilia was reported in 5/28 (17.9%), with a mean of 88.5% (SD 5.4). Thrombocytopenia occurred in 5/28 (17.9%) and thrombocytosis in 1/28 (3.6%). The platelet counts were otherwise within the normal range. C-reactive protein was elevated in 14/28 (50.0%), with a mean level of 19.2 mg/L (SD 10.1). Liver tests were frequently abnormal: AST elevated in 7/28 (25.0%), mean 232.2 U/L (SD 325.6); ALT elevated in 8/28 (28.6%), mean 126.1 U/L (SD 81.9); ALP elevated in 6/28 (21.4%), mean 312.7 U/L (SD 232.9); GGT elevated in 4/28 (14.3%), mean 387.2 U/L (SD 163.7). The total bilirubin was elevated in 7/28 (25.0%), mean 5.3 mg/dL (SD 4.8); direct bilirubin in 3/28 (10.7%), mean 3.0 mg/dL (SD 1.8). INR was 1.3 in 1/28 (3.6%). Lactate was elevated in two patients, with a mean of 4.4 mmol/L (SD 1.3). Blood cultures were obtained in 19/28 (67.9%) and were positive in 15/28 (53.6%). The common organisms included Bacteroides spp. (4/28, 14.3%), E. coli (3/28, 10.7%), and Klebsiella spp. (3/28, 10.7%). The presenting symptoms, inflammatory and cholestatic laboratory abnormalities, and bloodstream microbiology are summarized (Table 2).

Table 2.

Presentation, Laboratory Findings, and Microbiology: Symptoms, Inflammation Markers, Liver Tests, and Bloodstream Pathogens

Domain	Result
Symptom-to-presentation interval	Mean 6 days (SD 4)
Key symptoms/signs
Abdominal pain	25 (89.3)
Fever	26 (92.9)
Abdominal tenderness	20 (71.4)
Diarrhea	11 (39.3)
Nausea	4 (14.3)
Jaundice	3 (10.7)
Tachycardia	6 (21.4%; mean HR approximately 104 bpm)
Leukocytosis	18 (64.3); mean WBC 13.7×109/L (SD 3.1)
CRP elevated	14 (50.0); mean 19.2 mg/L
Liver tests elevated
AST	7 (25.0), mean 232.2 U/L
ALT	8 (28.6), mean 126.1 U/L
ALP	6 (21.4), mean 312.7 U/L
GGT	4 (14.3), mean 387.2 U/L
Bilirubin elevated
Total	7 (25.0), mean 5.3 mg/dL
Direct	3 (10.7), mean 3.0 mg/dL
Coagulation/Lactate
INR	1.3 (reported in 1)
Lactate elevated	2 (mean 4.4 mmol/L)
Blood cultures positive	15/28 (53.6); common organisms: Bacteroides spp. (4), Escherichia coli (3), Klebsiella spp. (3)

Values are presented as number (%).

HR, heart rate; GGT, gamma-glutamyl transferase; WBC, white blood cell.

5) Diagnostic results

First-line imaging was contrast-enhanced CT of the abdomen and pelvis in 18/28 (64.3%), followed by non-contrast CT in 3/28 (10.7%), abdominal radiography in 3/28 (10.7%), and ultrasound in 3/28 (10.7%). Ultimately, 20/28 (71.4%) were diagnosed via contrast-enhanced CT. Diverticulitis most commonly involved the sigmoid colon (20/28, 71.4%), with other sites including the cecum (3/28, 10.7%), jejunum (1/28, 3.6%), and terminal ileum (1/28, 3.6%). All patients (28/28, 100.0%) had mesenteric venous thrombophlebitis. Additional complications included abscess (6/28, 21.4%), venous gas (13/28, 46.4%), perforation (4/28, 14.3%), and ascites (1/28, 3.6%). Venous involvement included the portal vein system (main trunk 12/28, 42.9%; right branch 4/28, 14.3%; left branch 6/28, 21.4%), superior mesenteric vein (11/28, 39.3%), inferior mesenteric vein (21/28, 75.0%), and splenic vein (7/28, 25.0%); other sites were the ileocolic vein (2/28, 7.1%), superior rectal vein (1/28, 3.6%), and tributaries (2/28, 7.1%). The thrombus was completely occlusive in 6/28 (21.4%) and partial or non-occlusive in 12/28 (42.9%). Doppler flow was absent in 1/28 (3.6%) in the left portal branch. The liver findings included hepatomegaly (3/28, 10.7%), cirrhosis (2/28, 7.1%), nonspecific attenuation changes such as periportal edema (2/28, 7.1%), and steatosis (1/28, 3.6%); splenomegaly occurred in 2/28 (7.1%). The imaging pathways, anatomic site of diverticulitis, associated complications, and venous territories involved are detailed (Table 3).

Table 3.

Imaging Findings and Venous Involvement: Initial Imaging Pathways, Site of Diverticulitis, Complications, and Portal-Mesenteric Venous Anatomy Involved

Domain	Result
First-line imaging
Contrast CT	18 (64.3)
Non-contrast CT	3 (10.7)
Abd. radiography	3 (10.7)
Ultrasound	3 (10.7)
Final diagnostic test
Contrast CT	20 (71.4)
Diverticulitis location
Sigmoid	20 (71.4)
Cecum	3 (10.7)
Jejunum	1 (3.6)
Terminal ileum	1 (3.6)
Complications on imaging
Venous gas	13 (46.4)
Abscess	6 (21.4)
Perforation	4 (14.3)
Ascites	1 (3.6)
Veins involved (any)
Inferior mesenteric vein	21 (75.0)
Superior mesenteric vein	11 (39.3)
Portal vein main trunk	12 (42.9)
Right PV branch	4 (14.3)
Left PV branch	6 (21.4)
Splenic vein	7 (25.0)
Ileocolic	2 (7.1)
Superior rectal	1 (3.6)
Thrombus character
Complete occlusion	6 (21.4)
Partial/non-occlusive	12 (42.9)
Follow-up imaging obtained	9 (32.1)

Values are presented as number (%).

PV, portal vein.

6) Treatment

Antibiotics were started at presentation in 21/28 (75.0%). The remaining starts occurred after positive blood cultures, post-operatively, or at outpatient follow-up (each 1/28, 3.6%). The empiric regimens varied and are summarized in Supplementary Table 1. The most commonly reported explicit regimens were piperacillin–tazobactam (4/28, 14.3%) and either metronidazole plus ciprofloxacin or amoxicillin–clavulanate (each 2/28, 7.1%); an additional 5/28 (17.9%) received unspecified broad-spectrum therapy. Therapy was narrowed or otherwise adjusted in 7/28 (25.0%), including step-down to oral agents at discharge (3/28, 10.7%) and culture- guided changes (3/28, 10.7%); single cases reflected changes for toxicity and C. difficile (each 1/28, 3.6%). When the antibiotic duration was reported (10/28, 35.7%), the mean antibiotic duration was 31 days (SD 10.1).

Anticoagulation was used in 23/28 patients (82.1%), initiated at presentation in 13/28 (46.4%) or after additional diagnostics or surgery in 3/28 (10.7%). Five patients (17.9%) were managed without systemic anticoagulation. In these reports, either anticoagulation was not mentioned, or the authors explicitly chose antibiotics and source control alone. The initial anticoagulant regimens included unfractionated heparin in eight patients, low‑molecular‑weight heparin in six, a direct oral anticoagulant in one, and agents not specified in eight. Where specified, direct oral anticoagulants included dabigatran 150 mg twice daily for six months and rivaroxaban dosed according to venous thromboembolism regimens. Transitions between classes were common: 12/28 patients (42.9%) were ultimately switched to warfarin or phenprocoumon (6/28, 21.4%) or to a direct oral anticoagulant (8/28, 28.6%). Anticoagulation was started on the day of mesenteric venous thrombophlebitis diagnosis in 13/23 anticoagulated patients (56.5%). Among the 10 cases with a reported duration, the median planned course was six months (interquartile range 3–6); one patient was treated indefinitely. Hypercoagulable testing was performed in 8/28 (28.6%) without clinically significant inherited thrombophilia. Image‑guided drainage was reported in 1/28 (3.6%). Surgery was required in 15/28 cases (53.6%), including bowel resection (13/28, 46.4%), diverting ostomy (8/28, 28.6%), and venous excision or ligation (3/28, 10.7%), most often for deterioration despite medical therapy (8/28, 28.6%) or diverticulitis‑related complications (6/28, 21.4%).

7) Outcomes

Hospital courses were prolonged, but the overall outcomes were favorable. The mean length of stay was 19.1 days (SD 14.5); 4/28 patients (14.3%) required ICU care, and the mean follow‑up was 4.7 months (SD 4.5). In the complete‑case comparison of 23 anticoagulated and five non‑anticoagulated patients (Table 4), the median time to symptom resolution was seven days (interquartile range [IQR] 2–22; n=9) with anticoagulation versus four days (IQR 1–7; n=2) without (p=0.40). The median time to radiographic resolution was 56 days (IQR 39–98.5; n=8) compared to 35 days (n=1) (p=0.25), and the median length of stay was 17 days (IQR 8–30; n=10) versus 10 days (IQR 9–22; n=3), respectively (p=0.87). No deaths or recurrences were reported in either group (risk difference 0.00, 95% CI 0.00–0.15 for both). Adverse events occurred exclusively among the anticoagulated patients―6/23 (26.1%) versus 0/5 (0%)―with a risk difference of 0.26 (95% CI 0.10– 0.48). They included anemia with pleural effusion, hypotension requiring intensive care, Clostridioides difficile infection, drug-induced liver injury, sepsis with acute kidney injury, and a pulmonary embolism. Follow‑up imaging was obtained in 9/28 (32.1%) cases. Complete or partial venous recanalization was documented in 7/23 (30.4%) patients receiving anticoagulation and 1/5 (20.0%) without anticoagulation (risk difference 0.10, 95% CI 0.07–0.15), for an overall recanalization rate of 28.6% (8/28). Through the initial anticoagulant class, recanalization was reported in 4/8 (50.0%) patients treated with unfractionated heparin, 2/6 (33.3%) with low‑molecular‑weight heparin, 0/1 with a direct oral anticoagulant, and 1/8 (12.5%) receiving regimens not otherwise specified. Adverse events occurred in 4/8 (50.0%), 1/6 (16.7%), 0/1 (0%), and 1/8 (12.5%) patients in these groups, respectively.

Table 4.

Management and Outcomes: Antimicrobial, Anticoagulation, and Procedural Strategies; Hospital Course and Follow-Up Outcomes

Domain	Result
Antibiotics	Initiated for all; at presentation in 21 (75.0%); typical empirics: piperacillin-tazobactam (4), metronidazole+ciprofloxacin (2), amoxicillin-clavulanate (2), metronidazole+ceftriaxone (1), meropenem (1), others/unspecified (5)
Antibiotic duration	Mean 31 days (reported in 10 cases)
Anticoagulation used	23 (82.1%); initial agents: UFH 8 (28.6%), LMWH 6 (21.4%), DOACs 1 (3.6%), and unspecified agents 8 (28.6%); transitions to warfarin/phenprocoumon 6 (21.4%) or DOACs 8 (28.6%)
Anticoagulation duration	Mean 5.24 months (reported in 10 cases); one indefinite plan
Procedures	Image-guided drainage 1 (3.6%); Surgery 15 (53.6%) - bowel resection 13 (46.4%); diverting ostomy 8 (28.6%); venous excision/ligation 3 (10.7%); indications: deterioration 8 (28.6%), diverticulitis complications 6 (21.4%), elective/diagnostic 3 (10.7%)
Hospital course	Length of stay: mean 19.1 days (SD 14.5); ICU in 4 (14.3%)
Follow-up & outcomes	Symptom resolution: mean 12.6 days; Radiographic resolution: mean 90.6 days; Venous recanalization: 8/28 (28.6%); Mortality 0/25 reported; Recurrence 0/7; AEs in 6 anticoagulated cases (26.1%): anemia with pleural effusion, hypotension requiring intensive care, Clostridioides difficile infection, DILI, sepsis with acute kidney injury, and pulmonary embolism

UFH, unfractionated heparin; LMWH, low-molecular-weight heparin; DOACs, direct oral anticoagulants; ICU, intensive care unit; AEs, adverse events; DILI, drug-induced liver injury.

DISCUSSION

This study reviewed 28 single-patient reports of diverticulitis- associated mesenteric venous thrombophlebitis and underscores consistent diagnostic and therapeutic patterns. Patients typically presented after almost a week of symptoms, most often with fever (92.9%) and abdominal pain, and with frequent inflammatory or cholestatic abnormalities; bacteremia was common (53.6%).

The cholestatic liver test abnormalities observed in approximately one quarter of patients likely reflected a combination of sepsis‑associated cholestasis and impaired portal venous outflow due to thrombosis, rather than primary biliary obstruction in most cases. This pattern is consistent with a larger pylephlebitis series, in which hyperbilirubinemia and elevated cholestatic enzymes are common despite the absence of structural biliary disease on imaging.¹⁶ In this review, drug‑induced liver injury from broad‑spectrum antibiotics and concomitant hepatobiliary infections were rare but important additional contributors, as illustrated by one case of piperacillin– tazobactam-associated liver injury.

Imaging usually revealed sigmoid diverticulitis with thrombosis, most often involving the inferior mesenteric vein (75.0%) and less often extending to the portal-mesenteric system.^17,18 In most reports, including the present case, venous thrombus was anatomically contiguous with the inflamed diverticular segment and blood cultures yielded enteric organisms, while other intra‑abdominal sources were not identified, supporting diverticulitis as the primary driver of infection‑related thrombosis.

From a diagnostic perspective, the differential diagnosis for portal‑mesenteric venous thrombosis in a patient with abdominal pain and sepsis includes other intra‑abdominal infections (appendicitis, pancreatitis, acute cholecystitis/cholangitis, and inflammatory bowel disease), underlying cirrhosis with non‑malignant portal vein thrombosis, malignancy‑related thrombosis, and primary hypercoagulable states or myeloproliferative neoplasms. In this review, hypercoagulable testing was performed in only 28.6% of patients and did not reveal clinically significant inherited thrombophilia. Chronic liver disease was uncommon, supporting infection‑driven thrombosis in most diverticulitis‑associated cases rather than primary thrombophilia.

Because the clinical features overlap with uncomplicated diverticulitis, early vascular imaging is critical when systemic inflammation, cholestatic liver tests, bacteremia, or persistent pain are present. The index case shows that venous thrombophlebitis can arise even when the colonic inflammation itself appears radiologically ‘uncomplicated,’ without an abscess or free perforation. Transmural microperforation and pericolonic phlebitis likely allow septic thrombus to form when the inferior mesenteric vein is draining, so the overall clinical episode should be regarded as complicated diverticulitis despite the absence of gross perforation on CT. Contrast-enhanced CT established the diagnosis in 71.4% and delineated the expected anatomic pattern. Portal venous gas, observed in 46.4%, should be interpreted as a marker of severe infection rather than an automatic indication for surgery in the absence of peritonitis.

Management hinged on prompt broad‑spectrum antibiotics with anaerobic and gram‑negative coverage, followed by culture‑guided narrowing; the reported courses averaged approximately 31 days in the 10 cases that specified a duration. Anticoagulation was used in 82.1% of cases and was usually continued for several months. In the complete‑case analysis, 13/23 anticoagulated patients (56.5%) started therapy on the day of diagnosis, and the median planned duration among 10 patients with available data was six months (IQR 3–6), with one treated indefinitely. Recanalization was documented in approximately one third of the anticoagulated patients (30.4%) and in 20% of those managed without anticoagulation, but wide confidence intervals and incomplete imaging follow‑up limit the inference about the effect of anticoagulation on recanalization. Hypercoagulable evaluations were infrequent and unrevealing, supporting infection‑driven thrombosis in most cases. Surgery, required in 53.6% of patients, was typically reserved for clinical deterioration or complications such as perforation or a non‑drainable abscess.^19-23

The optimal anticoagulant agent in diverticulitis‑associated mesenteric venous thrombophlebitis is unclear. Most reported patients received heparin‑based regimens with a transition to warfarin or phenprocoumon, whereas a minority were treated with direct oral anticoagulants such as rivaroxaban or dabigatran. In broader cohorts of non‑cirrhotic portal and splanchnic vein thrombosis, direct oral anticoagulants have shown recanalization rates at least comparable to, and in some analyses higher than, those with vitamin K antagonists, with similar or reduced major bleeding. Nevertheless, this evidence is observational and not specific to pylephlebitis. Overall, these data support direct oral anticoagulants as a reasonable option in carefully selected patients without advanced liver disease or a high gastrointestinal bleeding risk, while underscoring the need for prospective comparative studies.^24-26

The outcomes were generally favorable: survival was 100%, but the hospital stays were prolonged, and radiographic improvement lagged clinical recovery by weeks to months.^27-31 These data support a staged approach: obtain blood cultures and contrast-enhanced CT early; start broad-spectrum therapy and tailor to cultures; consider systemic anticoagulation when the thrombus is occlusive or clearly propagating, when it extends into the main portal or superior mesenteric veins, or when there is persistent bacteremia or systemic inflammation despite the appropriate antibiotics and the bleeding risk is acceptable. This approach is consistent with broader pylephlebitis reviews, which recommend anticoagulation in patients with thrombosis progression on imaging, persistent fever, or extensive splanchnic vein involvement; pursue source control when indicated; and schedule interval cross-sectional imaging to document stability or recanalization before expecting radiographic normalization.^16,32-35 The observational data in non‑cirrhotic portal and splanchnic vein thrombosis also suggest that anticoagulation therapy improves recanalization and may reduce progression and mortality compared to no treatment.^16,24,25

The evidence base is limited by the case-report design, heterogeneous reporting, selection and publication bias, and variable follow-up.^36-38 Prospective multicenter registries will be needed to define the predictors of thrombosis, clarify indications and duration for anticoagulation (including direct oral agents), standardize imaging follow-up, and quantify the long-term outcomes such as recurrent thrombosis or portal hypertension.^39,40

Diverticulitis-associated mesenteric venous thrombophlebitis is an uncommon but serious complication that can mimic routine diverticulitis. Across 28 cases, early contrast-enhanced CT with blood cultures enabled diagnosis, and management centered on prompt broad-spectrum antibiotics with culture-guided narrowing, selective anticoagulation for extensive or occlusive thrombus, and surgery for complications.^41,42 Short-term survival was favorable, but the hospital stays were prolonged, and radiographic resolution lagged clinical recovery, underscoring the need for coordinated care and clear expectations for follow- up. Prospective studies should refine the indications and anticoagulation duration, standardize imaging follow-up, and quantify long-term outcomes.^43-45

SUPPLEMENTARY MATERIAL

Supplementary material is available at the Korean Journal of Gastroenterology website (https://www.kjg.or.kr/).