Inferior mesenteric vein thrombophlebitis secondary to acute diverticulitis

Abstract

Inferior mesenteric vein thrombophlebitis is an uncommon condition. Most cases of portal-mesenteric thrombophlebitis affect either the portal vein or superior mesenteric vein; it is not known why the inferior mesenteric vein is less affected. Thrombophlebitis typically occurs following inflammatory intra-abdominal processes, such as diverticulitis. Diverticulitis is a common condition in the Western world, with several common complications, such as fistula formation and bowel wall perforation. However, although diverticulitis is a common cause of portal-mesenteric thrombophlebitis, thrombophlebitis is still a rare complication of diverticulitis. We present a case of diverticulitis complicated with interior mesenteric vein thrombophlebitis with gas extension into the portal vein.

Introduction

The inferior mesenteric vein (IMV) drains the large intestine from the distal transverse colon to the superior rectum. The IMV drains into the splenic vein behind the body of the pancreas. The superior mesenteric vein (SMV) joins with the splenic vein behind the neck of the pancreas to form the hepatic portal vein. The hepatic portal vein drains the nutrient-rich blood from the splenic vein, IMV and SMV to the liver; this comprises the “portal-mesenteric circulation.”

Thrombophlebitis of the IMV is rare; only 6% of cases of portal-mesenteric thrombophlebitis affect the IMV exclusively [1]. IMV thrombophlebitis may occur secondary to inflammatory intra-abdominal processes, such as diverticulitis [1,2]. Radiological evaluation plays a critical role in the diagnosis of IMV thrombophlebitis. Imaging can demonstrate the thrombus and associated inflammatory changes [1,3,4]. It is widely agreed upon that the treatment of IMV thrombophlebitis includes antibiotics and potentially surgery. However, there is considerable debate in the literature regarding the use of anticoagulation.

Diverticulitis is a common inflammatory condition in the Western world, and it is often complicated by hemorrhage, obstruction and the formation of abscesses and fistulas [2]. Thrombophlebitis, however, is an uncommon complication of diverticulitis [1]. We present a case of diverticulitis complicated by IMV thrombophlebitis.

Case presentation

A 28 year old male presented to the Emergency Department with complaints of loose stools and progressive abdominal and pubic pain over the past several days. Pertinent medical history included obesity, gastroesophageal reflux disease, hypercholesterolemia, and diverticulitis. He reported that the pain reminded him of a prior episode of diverticulitis. The patient was afebrile, and physical exam revealed a soft abdomen with bilateral tenderness. Abnormal CBC values were as follows: hemoglobin 13.8 (L; Normal 14.0-18.0 g/dL), platelet 64 (L; Normal 130-400 K/cmm), and lymphocytes 7.0 (L; Normal 10.0-40.0%). Abnormal chemistry panel was as follows: serum calcium 8.0 (L; Normal 8.5-10.5 mg/dL), albumin 2.2 (L; Normal 3.4-4.8 g/dL), globulin 4.4 (H; Normal 2.3-3.5 g/dL), A/G ratio 0.5 (L; Normal1.0-2.0 ratio), mean plasma glucose 186 (H; Normal 68-105 mg/dL), total bilirubin 2.2 (H; Normal 0.0-1.2 mg/dL), direct bilirubin 1.8 (H; Normal 0.1-0.5 mg/dL), AST 179 (H; Normal 3-48 IU/L), ALT 141 (H; Normal 15-71 IU/L) and phosphorus 1.9 (L; Normal 2.8-4.5 mg/dL).

Supine and upright abdominal radiography revealed an unremarkable gas pattern. No free intraperitoneal air was demonstrated. Subsequent contrast enhanced computed tomographic (CT) imaging of the abdomen and pelvis revealed diverticulosis in the sigmoid colon, with abnormal wall thickening, pericolonic fat stranding and thickening of the mesocolic fascia. The findings were consistent with acute diverticulitis (Fig. 1, Fig. 2, Fig. 3, Fig. 4). The diverticulitis was complicated by an abscess measuring 2.4 cm. Additionally, inflammation and air pockets were demonstrated in the IMV, suggesting septic IMV thrombophlebitis. An air pocket was also visualized at the confluence of the IMV and splenic vein. Except for fatty infiltration of the liver, all other CT imaging findings were unremarkable. Diffuse increased and coarsened echotexture of the liver was demonstrated on ultrasonography.

Fig. 1.

(A)Axial contrast enhanced CT image demonstrating an abscess adjacent to the sigmoid colon (white arrow) and inflammation within the sigmoid mesocolon (yellow arrow). (B) Axial contrast enhanced CT image demonstrating inflammation within the sigmoid mesocolon (yellow oval).

Fig. 2.

Axial contrast enhanced CT image demonstrating air located at the confluence of the inferior mesenteric vein and splenic vein (red arrow).

Fig. 3.

Coronal curved planar reformatted contrast enhanced CT image demonstrating an abscess adjacent to the sigmoid colon (white arrow), air in the inferior mesenteric vein and origin of the portal vein (red arrows), and a thrombus in the inferior mesenteric vein (blue arrow).

Fig. 4.

Sagittal curved planar reformatted contrast enhanced CT image demonstrating an abscess adjacent to the sigmoid colon (white arrow), air within the inferior mesenteric vein (red arrows), and inflammation surrounding the inferior mesenteric vein (yellow arrows).

The patient was subsequently admitted for inpatient care. He was placed on empiric piperacillin and tazobactam following a positive blood culture. General surgery was consulted for evaluation, but the patient did not undergo surgical intervention. The patient stayed in the hospital for 10 days and was continued on intravenous piperacillin and tazobactam therapy for the duration of his admission. He was discharged with a 10 day course of amoxicillin and clavulanate.

Discussion

Thrombophlebitis of the mesenteric veins and portal vein can occur as a sequelae of intra-abdominal inflammation [5,6]. Of the portal-mesenteric veins, the SMV is the most commonly affected by thrombophlebitis, and the IMV is the least commonly affected [7]. It is not known why the IMV is the least commonly affected [8]. Isolated IMV thrombophlebitis accounts for only 6% of portal-mesenteric thrombophlebitis [1]. Thrombophlebitis can occur as a sequela of intra-abdominal infectious processes, including diverticulitis, appendicitis, IBD, pancreatitis, biliary tree infection and cancer [4,5,9]. Thrombophlebitis occurs as a sequelae of 0.2%-0.6% of intra-abdominal infections [5,6].

Diverticular disease is very common in the Western world, affecting approximately 60% of individuals over the age of 60 years [2]. Diverticulitis is the inflammation of colonic diverticula. Diverticulitis is often accompanied with bowel wall perforations, microperforations, abscesses, obstructions, and fistulas [2]. Pylephlebitis is an uncommon sequela of diverticulitis, arising in only 3% of cases of diverticulitis [1]. It is thought that diverticulitis creates an inflammatory and infectious milieu that induces a hypercoagulable state; this induces thrombosis at focal sites of infection in small mesenteric veins that extend into the larger portal-mesenteric mesenteric veins [1]. Additionally, concurrent obesity and smoking also predispose to thrombosis [3].

Complications of diverticulitis-induced thrombophlebitis include bacteremia, sepsis, ischemia, venous hemorrhage, and hepatic abscess [1]. Bacteremia is often polymicrobial and commonly includes Viridans streptococci and colonic Gram negative bacilli, such as Eschericha Coli, Bacteroides fragilis, Proteus mirabilis, and Klebsiella pneumoniae [1,4]. B fragilis is the most common bacterium implicated in bacteremia, and, interestingly, it can activate the coagulation cascade and possibly contribute to the pro-coagulative state [3].

Diverticulitis-induced portal-mesenteric thrombophlebitis has a high mortality rate of 25% [1,5,9]. As such, prompt diagnosis and treatment are imperative to avoiding poor outcomes [9]. However, the clinical presentation is relatively nonspecific. Common signs and symptoms include fever, chills, nausea, elevated inflammatory markers, and colicky abdominal pain that is out of proportion to physical exam [1,8,9]. Fever and abdominal pain are the most commonly reported symptoms [4]. Laboratory findings are often equivocal. Leukocytosis and elevated liver enzymes may or may not be elevated, and blood cultures are positive 44%-88% of the time [4].

Because of the vague signs and symptoms, a high suspicion is necessary for the diagnosis of diverticulitis-induced portal-mesenteric thrombophlebitis [3,4]. Classically, definitive diagnosis requires the drainage of purulent material out of the portal tree; however, in clinical practice, radiological evidence of thrombophlebitis is sufficient for diagnosis [3,5]. Abdominal radiography may reveal intraluminal air, a nonspecific finding; additionally, radiography will not demonstrate portal-mesenteric inflammatory changes [1]. Thus, subsequent imaging modalities are required. Color duplex sonography can be used to measure flow defects [1]. Portal venous phase contrast-enhanced CT imaging is considered the “gold standard” imaging modality because it allows for the direct visualization of the thrombus and surrounding venous inflammatory changes [1,3]. The thrombus appears as a hypointense flow defect [1,3]. CT imaging also allows for the visualization of concomitant intra-abdominal inflammatory processes, such as diverticulitis or appendicitis [4]. It is recommended to investigate for precipitating inflammatory conditions in cases of thrombophlebitis [10]. Lastly, magnetic resonance imaging may be useful in confirming the diagnosis of thrombophlebitis if CT findings are equivocal [3].

Treatment includes empiric antibiotic therapy, as well as surgery in select cases. Anticoagulation therapy is a controversial topic, on which there is no consensus in the literature. It is widely agreed upon that patients should be started on empiric broad spectrum antibiotics, regardless of whether a positive culture was yielded. Several empiric antibiotic protocols have been described, with all ensuring adequate Gram-negative anaerobe coverage [4,5]. The antibiotic therapy should later be narrowed following the results of culture [4,5]. Liver abscesses may need to be drained [4], and surgical intervention may need to be considered in cases of suppurative thrombophlebitis [1,4].

The use of anticoagulants is controversial. No randomized controlled trials have been conducted to demonstrate the utility anticoagulation therapy [5]. Baril et al. [11] conducted a retrospective chart review of thrombophlebitis cases at their institution; the group concluded that anticoagulation is indicated in hypercoagulable states, such as cancer, and clotting factor deficiencies, while isolated portal vein thrombophlebitis in the absence of coagulation disorders does not require anticoagulation therapy. As noted by Pradka et al. [12], however, the indications for anticoagulant use in thrombophlebitis are expanding beyond hypercoagulable states. In a retrospective chart review coupled with a literature review, Plemmons et al. [13] demonstrated superior results when coupling antibiotic therapy with heparin, as compared to antibiotics alone. Kanellopoulou et al. [14], in an analysis of published case reports, demonstrated similar findings to Plemmons et al. [13] and concluded that anticoagulation has an overall beneficial effect. Naymagon et al. [15] confidently endorse the use of anticoagulation whenever possible. Additionally, Choudhry et al. [16] conducted a retrospective review of 95 cases of thrombophlebitis at their institution and endorse the use of anticoagulation. However, the group emphasizes utilizing caution in anticoagulant administration [16]. Similarly, Pinto et al. [3] do not endorse the widespread use of anticoagulation; instead, they recommend careful consideration of the risks and benefits of anticoagulation in each individual case. There is even less data regarding the use of thrombolytics [5].

We present the case of an obese male with a prior history of diverticulitis presenting to the Emergency Department with flare up of diverticulitis, with IMV thrombophlebitis revealed on imaging.

Patient consent

Written consent was obtained directly from the patient.