A diagnostic dilemma: a rare case of falciform ligament abscess from gallbladder perforation masquerading as pancreatitis and subsequent abdominal wall cellulitis

Abstract

Introduction and importance:

Pathology of the falciform ligament is rare in adulthood due to the closure of the communication of the umbilicus with the external environment during embryological development. Compared to the pediatric population, where pathologies arise from external communication, falciform ligament abscesses in adults occur as a sequelae of hepatopancreaticobiliary pathology through an unclear mechanism. Falciform ligament abscess in adults is an exceedingly rare complication, with only 19 cases published in English literature.

Case presentation:

A 77-year-old male presented with right upper quadrant and epigastric pain and fevers in the setting of deranged liver function tests, elevated lipase, and no radiological evidence of cholecystitis, pancreatitis, or liver pathology. Gallbladder perforation, communication, and falciform ligament abscess formation were confirmed on interval computerized tomography during admission. They were initially managed with antibiotics, cholecystectomy, and intraoperative drainage of the abscess. Re-accumulation of the abscess required further antimicrobial therapy and wound drainage. They made a full recovery without complications.

Clinical discussion:

We present 1 of 2 published cases of gallbladder perforation into the falciform ligament with subsequent abscess formation. Our case demonstrates a pathologic communication between gallbladder and falciform ligament, contrary to the current hypothesis of abscess formation. Moreover, there was absence of a demonstratable cause of portal venous reflux as a mode of bacterial transit.

Conclusion:

Definitive management of the causative pathology and drainage of a non-loculated abscess is reasonable, and prompt diagnosis and management are required to prevent further complications, such as sepsis or cholecysto-umbilical fistula formation.

Introduction

The falciform ligament is formed by peritoneal reflections that occur during embryology. Its course traverses from the umbilicus toward the xiphisternum deep to linea alba, delivering the ligamentum teres in its free margin, the embryological remnant of the left umbilical vein. The falciform ligament then continues along the anterior and superior surface of the liver before separating (being a reflection) and attaching to the diaphragm, with the space created housing the bare area of the liver and communicating posteriorly with the porta hepatis, a potential route of bacterial transit.

HIGHLIGHTS

• Falciform ligament abscess is a rare complication of cholecystitis.

• We present a case of falciform ligament abscess from a perforated gallbladder.

• Laparoscopic cholecystectomy and falciform ligament drain placement was undertaken.

• Further percutaneous drainage and wound packing was needed after re-accumulation.

Pathology of the falciform ligament in the neonatal population is a relatively common complication of umbilical pathologies due to the communication of the umbilicus with the external environment. This communication is usually obliterated by three months of age, making falciform ligament pathology scarce in adulthood.

A comprehensive literature review yielded only 19 English case reports of falciform ligament abscess published in the adult population, with etiologies including cholecystitis^[1,2^], hepatic abscess^[3^], and obstructive cholangitis^[4–7^]. Notably, there is only one case secondary to gallbladder perforation^[8^]. Other pathologies of the falciform ligament, such as necrosis^[9^], thrombosis^[10^], and cholecysto-umbilical fistula formation^[11^] have been previously described in association with hepatopancreaticobiliary pathologies.

We present a case of falciform ligament abscess secondary to gallbladder perforation without radiographic evidence of cholecystitis, masquerading as acute clinical and biochemical pancreatitis and subsequent abdominal wall cellulitis. This work has been conducted in line with SCARE criteria^[12^]. No Artificial Intelligence was used in the research or preparation of this manuscript.

Presentation of case

A timeline of progression of care accompanies the following summary in Figure 1. A 77-year-old male presented to Northeast Health Wangaratta with a 1-day history of sudden onset, sharp epigastric pain radiating to the right upper quadrant, and fevers. This was on a background medical history of hypertension, two previous transient ischemic attacks, and an episode of alcoholic pancreatitis 8 years prior to presentation, at which time he abstained from alcohol consumption completely. He was febrile at presentation without any hemodynamic compromise, with mildly elevated inflammation markers, mixed derangement of liver function tests and elevated lipase triple the upper normal limit (Table 1). Computed tomography of the abdomen and pelvis, and ultrasound scan of the abdomen on presentation showed no radiological evidence of pancreatitis or a/calculous cholecystitis. He was provisionally diagnosed with acute pancreatitis, admitted for observation, and conservatively managed with supportive therapy, including intravenous crystalloid fluids, analgesia, proton-pump inhibitor for stress ulcer prophylaxis, and light diet as tolerated. A workup for medical causes of pancreatitis was negative. Blood cultures were also negative.

Figure 1.

Timeline of significant events and progression of care.

Table 1.

Biochemical marker trends during inpatient admission

Day	WCC (×109/l)	CRP (mg/l)	Bilirubin (mmol/l)	AST (U/l)	ALT (U/l)	ALP (U/l)	GGT (U/l)	Lipase (U/l)
Admission 1
0	6.7	5	23	348	215	185	182	4845
1	7.6	30	-	-	-	-	-	-
2	12.0	-	-	-	-	-	-	-
3 (Cefazolin commenced)	9.4	239	21	42	123	166	162	26
4	7.1	211	-	-	-	-	-	-
5	7.2	196	-	-	-	-	-	-
6	5.6	167	-	-	-	-	-	-
7 (Surgery)	8.7	144	16	286	228	585	616	-
8	7.9	80	9	121	173	456	494	-
9	6.6	65	9	91	165	414	460	-
10	7.8	55	8	60	136	417	490	-
11 (Oral amoxicillin + clavulanic acid)	7.1	-	-	-	-	-	-	-
Admission 2
0 (Antibiotics recommenced)	16.6	11	25	27	37	212	190	-
1	13.7	104	-	-	-	-	-	-
2	7.5	105	-	-	-	-	-	-
3	5.6	53	-	-	-	-	-	-
4	4.4	28	-	-	-	-	-	-
5 (Oral cotrimoxazole)	4.6	14	-	-	-	-	-	-
Follow up
1	5.0	5	11	21	33	136	92	-
2	4.2	8	11	20	23	128	64	-

ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CRP, C-reactive protein; GGT, gamma-glutamyl transferase; WCC, white cell count.

On Day 3 of admission, the patient reported worsening epigastric pain radiating inferiorly towards his umbilicus, associated with progressive paraumbilical cellulitis within this distribution and high-grade fevers. This was despite an improvement in appetite, nausea and vomiting, and mobility restrictions due to pain. A magnetic resonance cholangiopancreatogram was performed to rule out hepatobiliary duct pathology and occult gallstone disease which could not be identified on initial computed tomography and ultrasound. This demonstrated a T2 hyperintense region tracking along the falciform ligament into the anterior abdominal wall alongside a recanalized umbilical vein without portal vein thrombosis or pylephlebitis (Fig. 2). There was no radiological evidence of pancreatitis or cholelithiasis, with only mild gallbladder wall edema noted.

Figure 2.

Magnetic resonance cholangiopancreatogram. (A) Axial view shows contact (red circle) between the gallbladder neck (red arrow) with the falciform ligament and an area of T2 hyperintense signal along the ligament into the anterior abdominal wall (blue arrow) representing an early abscess. Note that the gallbladder has not yet decompressed. (B) Sagittal 3D reconstruction shows the hyperintense signal tracking from the gallbladder (red arrow) along the anterior abdominal wall (blue arrow).

Intravenous cefazolin for empirical antimicrobial coverage for cellulitis was commenced; however, the patient had persistent high-grade fevers despite biochemical improvement in inflammatory markers and liver function test derangement, and normalization of lipase. On Day 5, a repeat computed tomography of the abdomen and pelvis with portal venous contrast showed decompression of the gallbladder and heterogenous fluid throughout the falciform ligament into the abdominal wall, suggesting that the gallbladder had ruptured into the falciform ligament (Fig. 3). The patient’s antimicrobial regime was escalated to amoxicillin and clavulanic acid to adequately cover biliary sepsis. An emergent diagnostic laparoscopy and proceed cholecystectomy was performed showing grossly normal gallbladder tissue with a focal area of necrosis in gallbladder neck. The omentum was adherent to both the gallbladder and falciform ligament and showed an inflamed ligament on mobilization. Upon supraumbilical Hasson port site removal, bile-stained purulent discharge was noted and readily expressed from the port site. A drain was placed into the falciform ligament, with the distal fenestrated tip sitting at the superior aspect of the falciform at the point of suspected fistulation, exiting at the supraumbilical port site. The patient recovered well postoperatively with no new febrile episodes or postoperative complications during index admission. The drain was removed on postoperative Day 4 (Day 11 of admission) and he was discharged home on oral amoxicillin + clavulanic acid to complete a 14-day total course. Histopathology of the gallbladder revealed mild chronic cholecystitis without cholelithiasis. There was no evidence of underlying malignancy or ischemia in the sectioned specimen.

Figure 3.

Computed tomography of the abdomen and pelvis in the portal venous phase. (A) Axial view identifying the falciform ligament abscess (blue arrow), which is communicating with the gallbladder neck (green arrow) and tracks anteriorly within the falciform ligament between the anatomical left and right lobes of the liver. Note the defect within the gallbladder wall (green arrow) and decompression of the gallbladder in comparison to Figure 2. (B) A collection is seen (circled) on axial slice within the falciform ligament and shown tracking along its course into the anterior abdominal wall (C and D) to the level of the umbilicus. Note the tubular appearance of the collection that has been described in other published cases.

Despite adherence to post-operative advice, the patient re-presented for an outpatient clinic appointment 10 days following discharge with fevers and rigors, with repeat computed tomography of the abdomen and pelvis demonstrating a re-accumulation of the falciform ligament collection. Readmission, intravenous antibiotics and subsequent bedside drainage of this purulent collection was performed. A sample of the pus was sent for microscopy and culture, and grew Enterobacter cloacae complex resistant to amoxicillin, clavulanic acid, and ceftriaxone. The cavity was irrigated and packed with a self-debriding dressing to promote tissue granulation. Early clinical response negated the need for more invasive intervention. On Day 5, the patient was stepped on to oral cotrimoxazole and discharged with the hospital in the home service for daily wound irrigation and packing. In subsequent follow up appointment reviews, the patient’s collection had resolved, and inflammatory markers normalized, and was discharged from the surgical service.

Discussion

Falciform ligament abscesses are a rare entity and occur secondary to various hepatopancreaticobiliary pathologies. It has been posited that the transit of bacteria may occur through retrograde biliary tract or gallbladder infection via trangression into the cholecystic and pericholedochal venous system, draining into the poral vein and the via retrograde flow to the patent umbilical vein with eventual egress into the free margin of the falciform ligament, a potential space, producing an abscess^[7^]. In our case, there was pathologic communication between the gallbladder and adjacent falciform ligament, as evidenced by omental patching of both the focus of necrotic gallbladder and falciform ligament, radiological evidence of gallbladder decompression and communication, absence of free bile in the peritoneal cavity; and bilious, purulent discharge on entry into the falciform ligament. This is similarly described by Sones et al in 1981, the only other published case of falciform ligament abscess formation from gallbladder perforation (Table 2)^[8^]. This abnormal communication has also been seen in cholecysto-umbilical fistulae, which is likely a natural progression of these early abscesses contained in the ligament^[11^] and shares the same pathophysiological mechanism as the more well described complications of cholecystitis, such a gallstone ileus or other biliary fistulae.

Table 2.

Summary of published cases (English) of falciform ligament abscesses in adults

Author	Age (Sex)	Time from symptoms to formation	Etiology	Management	Complications
Fang & Huang (2021)	33(M)	14 days	Acute calculous cholecystitis and cholangitis	Surgical resection of the gallbladder and falciform ligament mass, antibiotics	-
Ji, Wang, & Li (2022)	68(M)	41 days	Acute pancreatitis, obstructive choledocholithiasis, and cholelithiasis	ERCP, cholecystectomy, antibiotics, incision and drainage of falciform abscess	Need for subsequent percutaneous aspiration of falciform ligament abscess
Arakura et al (2009)	63(M)	-	Cholelithiasis, cholangitis and stenosis of the distal bile duct	ERCP, antibiotics, antithrombotic therapy	Left portal thrombosis
Warren et al (2012)	73(M)	14 days	Obstructing ampullary carcinoma	ERCP, antibiotics, pancreaticoduodenectomy, incision and drainage and partial excision of falciform ligament	Portal venous thrombosis
Bhattacharya, Reddy, & Bhutia (2022)	69(F)	7 days	Calculous cholecystitis	Cholecystectomy, antibiotics	-
Kuribara et al (2022)	69(M)	5 days	Unclear (hypothesized to be bile stasis)	Antibiotics (failed)	Progression of abscess with multiple subsequent liver abscesses treated with antibiotics and left hepatectomy
Sen et al (2016)	40(M)	10 days	Cholelithiasis and obstructive choledocholithiasis with cholangitis	Antibiotics, percutaneous drainage, ERCP, cholecystectomy and abscess cavity excision	Left portal vein thrombosis
Doklestić et al (2022)	67 F	3 days	Calculous cholecystitis, portal vein thrombophlebitis without thrombosis	Antibiotics	-
Tsukuda et al (2008)	70 F	28 days	Choledocholithiasis, ERCP	Antibiotics, ERCP, cholecystectomy	-
Fujikawa & Araki M	86 F	3 days	-	Percutaneous drainage, antibiotics	-
Mori et al (1989)	59 F	-	Hepatic abscess and cholecystitis (primary aetiology not noted)	Percutaneous drainage	-
	66 F			Cholecystectomy
	66 M			Antibiotics
Atif & Khalq (2015)	40 M	6 months	Paraduodenal abscess	Ligamentectomy	-
Sones, Thomas & Masand (1981)	71 M	21 days	Gallbladder perforation	Percutaneous drainage	-

Our case is unique for a few reasons. Firstly, this patient had no convincing radiological evidence of cholecystitis or pancreatitis and was provisionally diagnosed on a biochemical and clinical basis. Furthermore, no gallstones were demonstrated radiologically or surgically. This complicated the diagnosis and resulted in a delay in definitive management. Secondly, on diagnostic laparoscopy, the gallbladder appeared grossly normal, with only a focal patch of necrosis adjacent to the falciform ligament and histopathology demonstrating only mild chronic cholecystitis. The etiology and significance of this is not clear. Considering an elevated lipase and radiological and pathological absence of a gallstone, choledocholithiasis with spontaneous passage of the gallstone may be a unifying antecedent diagnosis and is supported by other published cases as an etiology of abscess formation, mechanistically explained in the above paragraph. However, we acknowledge that the radiologic absence of pylephlebitis would be unusual if this were the case. Moreover, gallbladder perforation could have resulted from contact of the inflamed falciform ligament with a normal gallbladder.

Portal vein pylephlebitis and/or thrombosis, either causative or co-existing, appears to be a relatively common complication of this pathology, evident in 16% of published cases^[2,5–7^]. This should prompt clinicians to review the portal vasculature on imaging carefully and consider treating these complications. Our patient demonstrated a recanalized left umbilical vein without a history or portal hypertension or evidence of portal vein thrombosis/pylephlebitis. The significance of this is unknown but may represent underlying portal reflux and a potential route of bacterial transit from the gallbladder or common bile duct, reversal of flow through the recanalized umbilical vein, and transgression to the potential space within the falciform ligament, therefore forming an abscess.

The likely etiology of recurrence in our case was natural closure of the lanced abscess and re-accumulation of infection with poor oral antibiotic penetration to the collection and an organism resistant to the chosen agent. Given the rarity of such a case, management of the re-accumulation was empiric and extrapolated from first principles in the management of abscesses. On retrospective review of the literature, summarized in Table 2, others have treated this pathology similarly with percutaneous drainage, source control (i.e., cholecystectomy or endoscopic retrograde cholangiopancreatography), and antibiotics^[1–5,8,13,14^]. Moreover, recurrence has also been seen and successfully treated with the same approach to us – with percutaneous drainage and antimicrobial therapy^[4,15^]. However, other studies have proven ligamentectomy as a reasonable alternative, particularly in recurrent or recalcitrant cases, particularly if there are concerns with associated malignancy^[7,16,17^].

Conclusion

Cholecystectomy and drainage of the falciform collection in conjunction with antimicrobial therapy without falciform ligament excision is a reasonable initial approach to this pathology, as demonstrated by other published cases. However, progression or recurrence of the abscess, as in our case, has been demonstrated after initial drainage. Like our case of recurrence, others have responded well to further antimicrobial therapy and percutaneous drainage.

Ethical approval

Approval was sought and provided.

Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Sources of funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Conflicts of interest disclosure

the authors have no conflicts of interest to disclose.

Author contributions

J.A.W. and H.T. contributed equally to this work as co-first authors. J.W., H.T., M.R., and M.S.: conceptualization; J.W., H.T., and M.R.: data curation; J.W., H.T., and M.R.: formal analysis; H.T. and M.R.: investigation; J.W., H.T., and M.R.: methodology; J.W. and H.T.: project administration; M.R. and M.S.: supervision; M.R. and M.S.: validation; J.W., H.T., and M.R.: visualization; J.W. and H.T.: roles/writing – original draft; J.W., H.T., and M.R.: writing – review & editing.

Research registration unique identifying number (UIN)

No applicable.

Guarantor

Jayden A. Wearne and Hannah T.T.H Truong.

Provenance and peer review

This work was not commisioned and was peer reviewed by at least two external reviewers.

Data availability statement

The deidentified data that support the findings of this case are available from the corresponding author, J.W., upon reasonable request.