Skip to main content
Download PDF

Epidemiology, risk factors, diagnosis, and treatment of intra-abdominal traumatic neuromas - a narrative review

BMC Gastroenterology volume 23, Article number: 416 (2023) Cite this article

Highlights

This is the largest case series and case review of traumatic neuroma in the abdominal cavity.

We conclude and update the clinical and epidemiological characteristics of TN in the abdominal cavity.

We assessed and discussed the management of TN in the abdominal cavity, especially TBN.

Abstract

Traumatic neuroma (TN) is a disorganized proliferation of injured nerves arising from the axons and Schwann cells. Although TN rarely occurs in the abdominal cavity, the incidence of TN may be underestimated because of the large number of asymptomatic patients. TN can cause persistent pain, which seriously affects quality of life. TN of the biliary system can cause bile duct obstruction, leading to acute cholangitis. It is difficult to differentiate TN from malignancies or recurrence of malignancy, which results in a number of patients receiving aggressive treatment. We collected cases reports of intra-abdominal TN over the past 30 years form PubMed and cases diagnosed in our medical center over the past 20 years, which is the largest case series of intra-abdominal TN to the best of our knowledge. In this review, we discuss the epidemiology, pathophysiology, risk factors, classification, diagnosis, and management of intra-abdominal TN.

Peer Review reports

Introduction

Traumatic neuroma (TN) is not a true neoplasm but an abnormal proliferation of injured nerves with scar tissues resulting from trauma, surgery, bleeding, or ischemia [1]. It may occur anywhere but is most common in the lower extremities, followed by the head and neck [2]. The first TN was reported by Odier in 1811 with veterans suffering from disabling pain in their amputated limbs [3, 4]. TN in the digestive system is rare and mostly occurs in the biliary tree after cholecystectomy or liver transplantation, known as traumatic biliary neuroma (TBN), because of the abundant nerve supply to the gallbladder, cystic duct, and hepatic ducts [5]. The first case involving the digestive system was described in 1928 by Husseinoff [6]. Most intra-abdominal TNs are asymptomatic [7, 8]. Some TBNs in cystic duct after cholecystectomy may cause biliary-type pain and result in post cholecystectomy syndrome [9, 10]. Only a few patients develop acute cholangitis or fatal graft dysfunction due to obstruction by a neuroma, presenting with jaundice [11,12,13,14,15]. Other sites reported including celiac trunk, ampulla of Vater, pancreas, inferior mesenteric artery stump and rectal wall, etc. [2, 7, 8, 16, 17]. Although TN is a benign lesion, it is sometimes difficult to differentiate it from a malignant tumor, and some patients receive aggressive treatment. In this review, we collected a total of 93 cases of intra-abdominal TNs reported in the past 30 years in the literature and those diagnosed in our medical center in the past 20 years and determined the clinical and pathological characteristics and diagnostic and therapeutic approaches for intra-abdominal traumatic neuroma.

Epidemiology

Owing to the lack of effective methods for preoperative diagnosis and the large proportion of asymptomatic patients, the incidence of TN may be underestimated [9]. Only a few European studies have reported the incidence of TBN after cholecystectomy or liver transplantation; the rest of the TNs in the abdomen are sporadic cases [2, 8, 17, 18].

One study reported that TBN was found in approximately 10% post cholecystectomy patients during autopsy [19]. Another postmortem study suggested that remarkable nerve proliferation in the remnant cystic duct was observed in almost 40% post cholecystectomy patients, 28% of whom had TBN [20]. In this review, we collected 32 cases of TBN after cholecystectomy (Table 1), including 4 patients who underwent laparoscopic cholecystectomy and 4 patients who underwent common bile duct exploration. The ratio of men to women was nearly 3:1 (23 males, 8 females and 1 unknown). The incidence is higher in males than females, which is in contrast to the fact that women develop cholecystolithiasis more often than men [21]. The incidence of TBN increases with age, nearly 70% patients are > 60 years of age. The median age at diagnosis was 64 years (range:39–81 years). The interval between cholecystectomy and the diagnosis varied from 2 months to 56 years. The median interval between the open cholecystectomy and TBN was 17 years. Over 65% patients diagnosed above 10 years after open cholecystectomy, which is consistent with another study’s result that the median time from surgery to diagnosis is more than 12 years in the subgroup of patients who underwent open cholecystectomy [12]. Compared with open cholecystectomy, rare cases have been reported after laparoscopic cholecystectomy. On the one hand, patients who receive open cholecystectomy usually suffer from severe cholecystitis or other complications, which may increase the difficulty of the surgery and risk of damaging bile ducts, nerves and arteries. However, given the long time from TBN formation to symptom onset, it is premature to conclude that the incidence of TBN after laparoscopic cholecystectomy is lower than that after open cholecystectomy.

Table 1 Published case reports of TBN over the past 30 years and cases in our medical center over the past 20 years
Full size table

Nine patients from our center were included in this study (8 males and 1 female). Patients who undergo cholecystectomy in our hospital receive regular follow-up, and the maximum follow-up time for asymptomatic patients is 10 years. Among these nine patients, five had TN during follow-up. Four patients showed no changes during the follow-up period, but were found to have TN after more than 10 years of follow-up and were treated again in our hospital. The patients ranged in age from 51 to 75 years, with a minimum onset time of 4 months and a maximum of 21 years after surgery. Seven patients had previously undergone open cholecystectomy, one had previously undergone laparoscopic cholecystectomy, and one had previously undergone resection of a congenital choledochal cyst. Abdominal pain was the main clinical manifestation in six patients, 2 patients, abdominal pain in two patients, and abnormal liver function in one patient.(Table 1).

Biliary stenosis is one of a common complication of liver transplantation (LT), with an incidence of 5% ~ 28% after deceased-donor transplant and 28% ~ 37% after living-donor transplant [22, 23]. A study from France reported that symptomatic and histologically proven TBN accounted for 9.6% of anastomotic biliary stenosis [24], which is similar to the study from Croatia on TBN, representing 6.1% of liver re-transplantation [15]. As for the incidence of TBN after LT, the results vary from 0.6 to 9.2% in different studies (Table 2) [9, 15, 25, 26]. When it comes to the symptomatic TBN, the incidence is even lower from 0.5% ~ 2.8% [9, 25]. There are totally 56 cases in this review (Table 2). Similar to TBN after cholecystectomy, the incidence was much higher in male than female with a ratio at 4 of 1. The interval between the diagnosis of TBN and first transplantation ranged from 1 to 239 months. Although the time span is quite long, more than 50% TBN diagnosed within one year of the first transplantation. The median time to diagnosis of TBN varies from 6 to 69 months [15, 24, 25]. There is discrepancy in the median time from surgery to diagnosis after liver transplantation of different studies, but it’s notably shorter than neuromas diagnosed after cholecystectomy [9, 15]. Among the 30 patients with certain types of biliary reconstruction, only one underwent hepaticojejunostomy and the rest underwent duct-to-duct anastomosis.

Table 2 Published case reports of TN following LT over the past 30 years
Full size table

TN also occurres after other abdominal surgeries, including gastrectomy, polypectomy and, rectal cancer surgery(Table 3) [2, 7, 8, 27]. One patient did not have a history of surgery, but suffered from blunt abdominal trauma [18].

Table 3 Published case reports of TN with other sites intra-abdominal
Full size table

Pathophysiology mechanism & risk factors

Normally, the continuity between the two ends of a severed nerve is re-established by the orderly growth of axons from the proximal to the distal stump through tubes of proliferative Schwann cells. When the nerve ends are far apart or missing stumps, which prevent the reestablishment of neural continuity, hyperplastic proliferation of axons mixing with Schwann cells in a fibrocollagenous stroma develops into TN at the proximal end of the injured nerve [26]. The mechanism of this dysregulating growth pattern still remains unclear, athough a few studies have reported increasing levels of fibroblast growth factor and its receptor in TN [19, 28]. Targeting the pathophysiology of TN, He et al. found that chondroitin sulfate proteoglycans (CSPGs) can inhibit the formation of TN by blocking irregular axon regeneration in the proximal nerve stump. Kryger et al. found that trkA-IgG (an inhibitor of nerve growth factor) can reduce the information of TN in a rat model, but further research is still needed [29, 30].

Surgery is the primary risk factor for TN. Surgical manipulations, including excessive exploration, thermocoagulation, and vascular ligation, which may damage the surrounding nerves or arteries, can increase the risk of TN [1]. As many sympathetic and parasympathetic nerves are located outside the wall of the bile ducts, most TBN are extraluminal. However, if the common duct or hepatic duct is damaged during a careless or difficult surgery, intraluminal proliferation of nerves associated with an inflammatory scar can occur [31, 32], which may cause bile duct obstruction at the early stage after surgery. Three patients (two with laparoscopic cholecystectomy and one with open cholecystectomy) had bile duct injury during cholecystectomy and were diagnosed with TBN within 3 months, which was significantly different from the long interval time of cholecystectomy. With progress in laparoscopic techniques, laparoscopic cholecystectomy has been applied to a wider range of patients. When performing difficult laparoscopic cholecystectomy for acute cholecystitis, bailout procedures could be helpful in preventing bile duct injury, which theoretically decreases the incidence of TBN [33].

The situation is much more complicated with regard to TBN after LT. The origin of TBN after transplantation is still controversial, with some suggesting that it arises from the recipient bile ducts because most TBNs reported after LT occurred in patients who had duct-to-duct biliary reconstructions and less frequently occurred after bilioenteric reconstruction, since nerve regeneration originated from the proximal nerve ending [5, 24]. Others considered that it may arise from the recipient, or from the donors’ nervous tissue, on account of the small bifurcating nerve trunks seen in the perihilar intrahepatic septa during histological examinations of allografts with hilar neuromas, which indicates the survival of donors’ innervation [9, 26].

A few studies found that the number of nerve fibers decreased immediately after severing of the main hilar trunks; then, it increased due to proliferation and reinnervation in the post-transplant period [34, 35]. This result is consistent with the fact that the incidence of TBN is much higher in patients more than 3 months after transplantation [9]. Immunosuppressors may play an important role in accelerating nerve proliferation and reinnervation. Tacrolimus was found that could improve neurologic recovery and enhance axon regeneration by its neurotrophic and immunosuppressive actions after peripheral nerve injures [36], what’s more, the another common immunosuppressor, cyclosporine, was also found that had a promotion in axon growth of the recipient proximal nerve endings into nerve allografts in rats [37]. Therefore, immunosuppressants may be risk factors for TBN.

Besides surgical manipulations and immunosuppressants, infections, foreign bodies, trauma, ischemia, and scarring may also contribute to the formation of TBN [18, 38]. The continuity of the nerve can also be inhibited by granulation and fibrous tissue arising from the surrounding blood vessels and adjacent soft tissues [26]. There are also a few neuromas in the bile duct without any history of surgery or trauma; it might be postulated that bile or cholesterol are the inciting stimuli for fibrous and neural proliferation [31, 38].

Classification

There are several classification methods that are based on various factors. Nerve continuity is the most commonly used method. End-bulb neuroma (EBN), also known as terminal neuroma or stump neuroma, is a bulbous enlargement from the end of a completely disrupted nerve. Neuroma-in-continuity (NIC), also called spindle neuroma, results from partial nerve transection [39,40,41,42,43], and is divided into two pathological types: spindle neuromas with intact perineurium or lateral neuromas that occur after partial disruption of the perineurium and after nerve repairs [44]. This is similar to the results of Colina et al. that if the perineurial continuity of injured axons is preserved, encapsulated neuroma occurs macroscopically as small white-gray nodules macroscopically [9, 10] If the continuity of the perineurium is interrupted, branching axons would invade the mesenchyme, resulting in uneven thickening of duct walls [9]. Herrera et al. classified TBN into two types according to its pathological characteristics and location: type I originates from and is located in the main biliary tract wall, while type II originates from the surrounding tissues next to the main biliary tract [25]. They suggested that this type of classification is useful for treatment decision making.

Diagnosis

Clinical manifestation

When the intraluminal TBNs occur or extraluminal TBNs cause obstruction in common bile duct, the most common presentation is jaundice [5, 27, 45,46,47,48,49,50]. Several of patients are more likely to present with right upper quadrant pain, elevated transaminase levels and anorexia [2, 19]. Several studies have suggested that TBNs may be blamed for post cholecystectomy syndrome because of the relief of symptoms after surgical resection in most cases [10]. Given that many nerves normally surround the extrahepatic bile duct, the number of symptomatic patients was lower than that expected. Some patients are asymptomatic, and lesions can be detected accidentally on radiological examinations [7, 51].

Accessory examination

Laboratory examination

Patients with TBN may have abnormal laboratory results due to biliary obstructions, such as elevated bilirubin and transaminase levels. Patients sometimes present with elevated levels of carbohydrate antigen 19 − 9 (CA19-9) due to cholangitis [28]. Nevertheless, the magnitude of CA19-9 elevation cannot be used as a specific indicator to differentiate biliary malignancies from TBN [52]. A previous study suggested that patients with benign tumors had a lower elevated level of CA19-9, which returned to normal after the relief of obstruction compared to malignant diseases [53], which may aid in the differential diagnosis.

Imaging examination

Although it is difficult to diagnose TN preoperatively, imaging remains an indispensable component of the diagnosis. This method requires further treatment. Few studies have described the imaging characteristics of TN in the abdominal cavity; hence, in addition to summarizing cases in our center, we learned from TN located in the limbs, head, and neck. The imaging characteristics of the TN are shown in Table 4.

Table 4 Imaging characteristics for TN.
Full size table
Ultrasonography

Several studies have analyzed the characteristics of TN on ultrasonography to aid in the differential diagnosis between TN and recurrent lymphadenopathy after neck dissection. All concluded that TN had smaller short-axis diameters and shorter to long-axis ratios than recurrent lymphadenopathy [54, 55]. Moreover, the absence of vascular flow is another important characteristic of TN compared with recurrent lymphadenopathy. Most of TNs were fusiform, the rest were oval [55, 56]. As for the margin, one study suggested that TN had well-defined margins [56], while another study considered that TN had ill-defined margins [55]. Different types of TN may account for these differing results. When a capsule occurs, it may have a well-defined margin; otherwise, it may have an ill-defined one. The presence of central hyperechogenicity, which results from dense collagenous tissue, is also considered one of the sonographic features of TN [54, 56]. The nerve from which a TN originates may exhibit internal linear hypoechogenicity [55].

Computed tomography (CT)

TBNs can be contrast-enhanced on CT imaging [5, 10, 57, 58], which is consistent with the results of our study (Fig. 1). TNs after neck dissection could also appear as nodules with central hypoattenuation and a hyperattenuating rim [54, 59]. This suggests that the appearance of TN on CT can vary and may be location-related. Neither contrast enhancement nor a hyperattenuating rim can be used as a differentiating characteristic because they are also observed in malignancy and recurrent lymphadenopathy. A previous case of TN around the stump of the inferior mesenteric artery described the dynamic process from an irregular-margin lesion to a well-circumscribed nodule with enlargement of the diameter [2], which is not typical for TN and usually remains stable over the years [59].

Fig. 1
figure 1

Portal-venous phase CT shows dilation of the bile ducts and an enhanced mass with central hypoattenuation and hyperattenuating rim

Full size image
Magnetic resonance imaging (MRI)

TNs in the limbs or neck appear as homogeneous nodules isointense to muscles on T1-weighted images, high-intensity with hypointense rims on T2-weighted images, and heterogeneous contrast enhancement [42, 54, 60]. Few studies have described the characteristics of intra-abdominal TN on MRI. It is difficult to detect TNs located in the biliary tree because of the same signal intensity between the nerves, soft tissues, and pancreatic head [31]. Some studies found only bile duct dilatation on MRI without a compressive mass [11, 31]. Several studies detected markedly homogeneous or heterogeneously enhanced nodules with low-intensity capsules on T2-weighted images [2, 5, 24]. Some authors have suggested that the surrounding fibrous scar tissues of TN correspond to the hypointense rim, mimicking a capsule, which was observed by histopathologic examination of the specimen [54, 61].

Damage to the nerve blood barrier during prior injury could result in increased vascular permeability, which may cause passive diffusion of contrast agents, accounting for the enhancement of TNs [62,63,64]. In our center, five TN patients with TN underwent cholecystectomy with preoperative MRI images, and none of them had distinct margins. MRI showed heterogeneous thickening of the common bile ducts with contrast enhancement (Fig. 2).

Fig. 2
figure 2

Heterogeneous thicken of the common bile ducts with contrast enhancement on T1-weighted images

Full size image
Positron emission tomography/computed tomography (PET/CT)

PET/CT has been widely used for the detection and staging of many cancers [65]. It also helps distinguish benign tumors from malignancies. However, this was not a cancer specific examination. Active inflammation often results in false-positive results, and false-negative results have been observed in malignancies with low metabolic activity [66]. Only two cases of TN were reported with PET/CT results, which were reversed. One exhibited no increase in uptake [7], whereas the other exhibited increased uptake [2]. Therefore, the diagnosis of TN cannot be excluded based on positive PET/CT results.

Endoscopic examinations

With recent progress in endoscopic technology, endoscopic ultrasonography (EUS), endoscopic retrograde cholangiopancreatoscopy (ERCP), and endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) have been increasingly used in the diagnosis of ampullary and extrahepatic bile duct tumors. Compared to conventional examinations, endoscopic examinations have great advantages in the diagnosis of TN in the bile duct. Several authors have described TN as a homogeneous hypoechoic mass with a clear margin on EUS [57, 58, 67,68,69]. Intraductal ultrasonography (IDUS) could get much clearer views of the TN located at cystic stump [57, 70].

Pathological biopsy

Some patients with TN can be diagnosed on the basis of their past history, clinical manifestations, and imaging examinations. However, patients with severe symptoms that are difficult to distinguish from malignant tumors require pathological examination to confirm their diagnosis. ERCP enables doctors to observe lesions under direct vision [71, 72]. Yasuda et al. and Toyonaga et al. reported that TNs were covered by normal bile duct mucosa during endoscopic cholangioscopy [58, 67]. Hence, superficial biopsy of the tumor may fail to confirm the diagnosis of TN, and EUS-FNA is useful for obtaining deep tumor tissues, which could improve the accuracy of diagnosis. Microscopically, it is a disorganized proliferation of axons with Schwann cells and fibroblasts in collagenous stoma, which stains positive on immunohistochemistry for S-100 protein (Fig. 3).

Fig. 3
figure 3

Proliferation of nerve fiber stained by immunohistochemistry of S-100 protein

Full size image

Management

A flow chart of the diagnostic and management options for TN is shown in Fig. 4. The management of TNs should differ according to their location and symptoms. Regular follow-up is recommended [58, 67]. Regarding patients who only developed abdominal pain without biliary obstruction, Topazian et al. reported that patients experienced temporary relief of pain after injection of bupivacaine and triamcinolone under EUS-guided, but the security and effectiveness still need further confirmation [73]. Surgery is not recommended because pain can recur after resection of TBNs [73,74,75].

Fig. 4
figure 4

Flow chart of diagnostic and management options for TN.

Full size image

Surgery and interventional management are the most common treatments for patients with biliary obstructions. Several authors suggested that surgery was optimal choice for symptomatic patients of TBN [15, 16, 24]. Among all cases reviewed in this article, resection of the lesion with hepaticojejunostomy was the most common surgical procedure, accounting for 47.1%. Resection followed by duct-to-duct anastomosis occurred in the second place, accounting for approximately 20% patients. Navez et al. considered hepaticojejunostomy to be the best type of biliary reconstruction, based on the fact that the incidence of TBN was higher in patients who underwent duct-to-duct anastomosis during the first liver transplantation, and as a result, it seemed more likely for TBN to recur after duct-to-duct anastomosis [24]. None of the patients who underwent duct-to-duct anastomosis experienced recurrence during the follow-up. The best method for biliary reconstruction requires further study and more precise evidence. Some patients underwent much more aggressive surgeries, including periportal lymphadenectomy, pancreaticoduodenectomy, and hemihepatectomy, owing to difficulties in distinguishing them from biliary malignancies [1, 16, 28, 76]. Frozen section examination during surgery is useful for confirming diagnoses to avoid unnecessary extensive resections [5, 7, 77]. In addition, almost 20% of patients with TBNs after liver transplantation receive retransplantation for reasons of liver failure or rejection [15, 25].

Interventional management consists of two parts. One is preoperative drainage to relieve jaundice, including endoscopic drainage and percutaneous transhepatic drainage under ultrasound or radiologic guidance. The second part aimed to solve the stricture of the bile ducts, including balloon dilatation and stent placement. However, the effects of the interventional treatments did not improve. Multiple cases reported failure of biliary stenting or balloon dilatation for relieving biliary obstruction in the long term [12, 15, 24,25,26, 28, 78]. Fibrotic nature and poor compressibility may account for these unsuccessful outcomes. In addition, repetitive invasive interventions may accelerate the formation, resulting in an early biliary structure [78]. As for TN located in the gastrointestinal tract, a few authors considered that it was effective to achieve en bloc resection by endoscopic mucosal resection [8, 69].

Conclusion

Although TN is a benign lesion, it is sometimes difficult to differentiate it from a malignant tumor. TN lacks the typical clinical characteristics. Therefore, it is necessary to make a comprehensive judgment based on the patient’s medical history, clinical manifestations, and imaging findings. If necessary, needle biopsy can be performed to confirm the diagnosis. Conservative treatment is recommended for patients with TN without biliary obstruction. If biliary obstruction occurs, surgical or interventional treatment is necessary.

Data Availability

The manuscript contains all data from this study.

References

  1. Choi SB, Park YN, Kim KS. Traumatic neuroma of the right hepatic duct undertaken right hemihepatectomy. ANZ J Surg. 2009;79(1–2):91–2.

    Article  PubMed  Google Scholar 

  2. Jeon SM, Lee JY, Byeon SJ. Traumatic neuroma at the Inferior Mesenteric Artery stump after rectal Cancer Surgery: a Case Report and Literature Review. Korean J Gastroenterol. 2016;68(5):279–83.

    Article  PubMed  Google Scholar 

  3. Swanson HH. Traumatic neuromas. A review of the literature. Oral Surg Oral Med Oral Pathol. 1961;14:317–26.

    Article  CAS  PubMed  Google Scholar 

  4. Brogan DM, Kakar S. Management of neuromas of the upper extremity. Hand Clin. 2013;29(3):409–20.

    Article  PubMed  Google Scholar 

  5. Ueno Y, et al. Traumatic neuroma of the bile duct. Abdom Imaging. 2008;33(5):560–2.

    Article  PubMed  Google Scholar 

  6. Ueber DH. Einem fall Von Wucherung Des Nervengewebes Nach Wiederholten Operationen Der Gallenga: nge. Zbl Allg Path. 1928;43:344–8.

    Google Scholar 

  7. Kwon JH, Ryu SW, Kang YN. Traumatic neuroma around the celiac trunk after gastrectomy mimicking a nodal Metastasis: a case report. Korean J Radiol. 2007;8(3):242–5.

    Article  PubMed  PubMed Central  Google Scholar 

  8. Curran T, et al. Case report of a traumatic rectal neuroma. Gastroenterol Rep (Oxf). 2016;4(4):331–3.

    PubMed  Google Scholar 

  9. Colina F, et al. Amputation neuroma of the hepatic hilum after orthotopic liver transplantation. Histopathology. 1994;25(2):151–7.

    Article  CAS  PubMed  Google Scholar 

  10. Kim HH, et al. Education and imaging. Hepatobiliary and pancreatic: traumatic bile duct neuroma. J Gastroenterol Hepatol. 2011;26(9):1465.

    Article  PubMed  Google Scholar 

  11. Hotta T, et al. A traumatic neuroma of the bile duct: a case report. Hepatogastroenterology. 2004;51(55):39–42.

    PubMed  Google Scholar 

  12. Lalchandani P, et al. Traumatic bile duct neuroma presenting with acute cholangitis: a case report and review of literature. Ann Hepatobiliary Pancreat Surg. 2019;23(3):282–5.

    Article  PubMed  PubMed Central  Google Scholar 

  13. Iannelli A, et al. Traumatic neuroma of the cystic duct with biliary obstruction. Report of a case. Acta Gastroenterol Belg. 2003;66(1):28–9.

    CAS  PubMed  Google Scholar 

  14. Larson DM, Storsteen KA. Traumatic neuroma of the bile ducts with intrahepatic extension causing obstructive Jaundice. Hum Pathol. 1984;15(3):287–9.

    Article  CAS  PubMed  Google Scholar 

  15. Mrzljak A, et al. Traumatic neuroma and liver retransplant. Exp Clin Transplant. 2020;18(6):749–50.

    Article  PubMed  Google Scholar 

  16. Cheng Y, et al. Hepatobiliary and pancreatic: traumatic neuroma of the ampulla of Vater. J Gastroenterol Hepatol. 2014;29(7):1342.

    Article  CAS  PubMed  Google Scholar 

  17. Geddy PM, Venables CW. Traumatic neuroma at the tail of the pancreas following splenectomy. Postgrad Med J. 1991;67(783):90–1.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Katsinelos P, et al. Biliary stricture due to neuroma after an innocent blunt abdominal trauma. Surg Endosc. 2002;16(10):1494.

    CAS  PubMed  Google Scholar 

  19. Pickens A, et al. An unusual etiology of biliary hilar obstruction and the potential role of acidic fibroblast growth factor in the development of a biliary neuroma. Am Surg. 1999;65(1):47–51.

    Article  CAS  PubMed  Google Scholar 

  20. Berge T, Haeger K. Clinical significance of the amputation neuroma and length of the cystic duct remnant. Acta Chir Scand. 1967;133(1):55–60.

    CAS  PubMed  Google Scholar 

  21. Littlefield A, Lenahan C. Cholelithiasis: presentation and management. J Midwifery Womens Health. 2019;64(3):289–97.

    Article  PubMed  Google Scholar 

  22. Sharma S, Gurakar A, Jabbour N. Biliary strictures following liver transplantation: past, present and preventive strategies. Liver Transpl. 2008;14(6):759–69.

    Article  PubMed  Google Scholar 

  23. Yildirim S, et al. Treatment of biliary Complications after liver transplant: results of a single center. Exp Clin Transplant. 2015;13(Suppl 1):71–4.

    PubMed  Google Scholar 

  24. Navez J, et al. Traumatic biliary neuroma after orthotopic liver transplantation: a possible cause of unexplained anastomotic biliary stricture. Clin Transpl. 2016;30(10):1366–9.

    Article  Google Scholar 

  25. Herrera L, et al. Traumatic neuroma of extrahepatic bile ducts after orthotopic liver transplantation. Transpl Proc. 2009;41(3):1054–6.

    Article  CAS  Google Scholar 

  26. Mentha G, et al. Traumatic neuroma with biliary duct obstruction after orthotopic liver transplantation. Transplantation. 1999;67(1):177–9.

    Article  CAS  PubMed  Google Scholar 

  27. Yang SS, et al. Jaundice 8years after left hemi-hepatectomy for hepatocellular carcinoma. Clin Res Hepatol Gastroenterol. 2020;44(5):622–4.

    Article  PubMed  Google Scholar 

  28. Paquette IM, et al. Neuroma of the bile duct: a late complication after cholecystectomy. J Gastrointest Surg. 2009;13(8):1517–9.

    Article  PubMed  Google Scholar 

  29. He FL, et al. Covering the proximal nerve stump with chondroitin sulfate proteoglycans prevents traumatic painful neuroma formation by blocking axon regeneration after neurotomy in Sprague Dawley rats. J Neurosurg. 2020;134(5):1599–609.

    Article  PubMed  Google Scholar 

  30. Kryger GS, et al. Nerve growth factor inhibition prevents traumatic neuroma formation in the rat. J Hand Surg Am. 2001;26(4):635–44.

    Article  CAS  PubMed  Google Scholar 

  31. Tsitouridis J, et al. Non traumatic neuroma of the bile Duct: report of a case. Dig Endosc. 1998;10(4):323–6.

    Article  PubMed  Google Scholar 

  32. Shumate CR, et al. Traumatic neuroma of the bile duct causing cholangitis and atrophy of the right hepatic lobe. South Med J. 1992;85(4):425–7.

    Article  CAS  PubMed  Google Scholar 

  33. Wakabayashi G, et al. Tokyo guidelines 2018: surgical management of acute cholecystitis: safe steps in laparoscopic cholecystectomy for acute cholecystitis (with videos). J Hepatobiliary Pancreat Sci. 2018;25(1):73–86.

    Article  PubMed  Google Scholar 

  34. Dhillon AP, et al. Immunohistochemical studies on the innervation of human transplanted liver. J Pathol. 1992;167(2):211–6.

    Article  CAS  PubMed  Google Scholar 

  35. Boon AP, et al. Hepatic reinnervation following orthotopic liver transplantation in man. J Pathol. 1992;167(2):217–22.

    Article  CAS  PubMed  Google Scholar 

  36. Sosa I, Reyes O, Kuffler DP. Immunosuppressants: neuroprotection and promoting neurological recovery following peripheral nerve and spinal cord lesions. Exp Neurol. 2005;195(1):7–15.

    Article  CAS  PubMed  Google Scholar 

  37. Zalewski AA, Gulati AK. Survival of nerve allografts in sensitized rats treated with cyclosporin A. J Neurosurg. 1984;60(4):828–34.

    Article  CAS  PubMed  Google Scholar 

  38. Peison B, Benisch B. Traumatic neuroma of the cystic duct in the absence of previous Surgery. Hum Pathol. 1985;16(11):1168–9.

    Article  CAS  PubMed  Google Scholar 

  39. Henrot P et al. Imaging of the painful lower limb stump. Radiographics, 2000. 20 Spec No: p. S219-35.

  40. Chhabra A, et al. MR neurography of neuromas related to nerve injury and entrapment with surgical correlation. AJNR Am J Neuroradiol. 2010;31(8):1363–8.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Murphey MD, et al. From the archives of the AFIP. Imaging of musculoskeletal neurogenic tumors: radiologic-pathologic correlation. Radiographics. 1999;19(5):1253–80.

    Article  CAS  PubMed  Google Scholar 

  42. Ahlawat S, et al. MRI features of peripheral traumatic neuromas. Eur Radiol. 2016;26(4):1204–12.

    Article  PubMed  Google Scholar 

  43. Wadhwa V, et al. Spectrum of superficial nerve-related Tumor and tumor-like lesions: MRI features. Acta Radiol. 2014;55(3):345–58.

    Article  PubMed  Google Scholar 

  44. Mavrogenis AF, et al. Current treatment concepts for neuromas-in-continuity. Injury. 2008;39(Suppl 3):S43–8.

    Article  PubMed  Google Scholar 

  45. Capovilla M, et al. [Post-cholecystectomy amputation neuroma of the common bile duct with obstructive Jaundice]. Gastroenterol Clin Biol. 2005;29(1):79–81.

    PubMed  Google Scholar 

  46. Wysocki A, Papla B, Budzynski P. Neuromas of the extrahepatic bile ducts as a cause of obstructive Jaundice. Eur J Gastroenterol Hepatol. 2002;14(5):573–6.

    Article  PubMed  Google Scholar 

  47. Chantranuwat C, Shuangshoti S. Traumatic neuroma as a cause of obstructive Jaundice. J Med Assoc Thai. 1999;82(6):619–22.

    CAS  PubMed  Google Scholar 

  48. Nagata Y, et al. Traumatic neuroma of the common hepatic duct after laparoscopic cholecystectomy. Am J Gastroenterol. 1995;90(10):1887–8.

    CAS  PubMed  Google Scholar 

  49. Nagafuchi Y, et al. A traumatic neuroma associated with obstructive Jaundice after laparoscopic cholecystectomy. Hepatogastroenterology. 1998;45(20):424–7.

    CAS  PubMed  Google Scholar 

  50. Saint-Paul MC, et al. [Neuroma of the common bile duct]. Ann Gastroenterol Hepatol (Paris). 1993;29(2):65–7.

    CAS  PubMed  Google Scholar 

  51. Furukawa K, et al. Amputation neuroma mimicking lymph node Metastasis of remnant gastric cancer: a case report. Surg Case Rep. 2017;3(1):123.

    Article  PubMed  PubMed Central  Google Scholar 

  52. Hyman J, Wilczynski SP, Schwarz RE. Extrahepatic bile duct stricture and elevated CA 19 – 9: malignant or benign? South Med J. 2003;96(1):89–92.

    Article  PubMed  Google Scholar 

  53. Mann DV, et al. Elevated tumour marker CA19-9: clinical interpretation and influence of obstructive Jaundice. Eur J Surg Oncol. 2000;26(5):474–9.

    Article  CAS  PubMed  Google Scholar 

  54. Yabuuchi H, et al. Traumatic neuroma and recurrent lymphadenopathy after neck dissection: comparison of radiologic features. Radiology. 2004;233(2):523–9.

    Article  PubMed  Google Scholar 

  55. Ha EJ, et al. Characteristic ultrasound feature of traumatic neuromas after neck dissection: direct continuity with the cervical plexus. Thyroid. 2012;22(8):820–6.

    Article  PubMed  Google Scholar 

  56. Kwak JY, et al. Sonographic features of traumatic neuromas after neck dissection. J Clin Ultrasound. 2009;37(4):189–93.

    Article  PubMed  Google Scholar 

  57. Shimura K, et al. Intraductal ultrasonography of traumatic neuroma of the bile duct. Abdom Imaging. 2001;26(6):632–4.

    Article  CAS  PubMed  Google Scholar 

  58. Toyonaga H, et al. Traumatic bile duct neuroma diagnosed by boring biopsy with cholangioscopy. Gastrointest Endosc. 2018;87(5):1361–2.

    Article  PubMed  Google Scholar 

  59. Huang LF, Weissman JL, Fan C. Traumatic neuroma after neck dissection: CT characteristics in four cases. AJNR Am J Neuroradiol. 2000;21(9):1676–80.

    CAS  PubMed  PubMed Central  Google Scholar 

  60. Abreu E, et al. Peripheral Tumor and tumor-like neurogenic lesions. Eur J Radiol. 2013;82(1):38–50.

    Article  PubMed  Google Scholar 

  61. Singson RD, et al. MRI of postamputation neuromas. Skeletal Radiol. 1990;19(4):259–62.

    Article  CAS  PubMed  Google Scholar 

  62. Pindrik J, Chhabra A, Belzberg AJ. Update on peripheral nerve Surgery. Neurosurgery. 2013;60(Suppl 1):70–7.

    Article  PubMed  Google Scholar 

  63. Aagaard BD, et al. High-resolution magnetic resonance imaging is a noninvasive method of observing injury and recovery in the peripheral nervous system. Neurosurgery. 2003;53(1):199–203. discussion 203-4.

    Article  PubMed  Google Scholar 

  64. Liao CD, et al. Peripheral nerve repair: monitoring by using gadofluorine M-enhanced MR imaging with chitosan nerve conduits with cultured mesenchymal stem cells in rat model of neurotmesis. Radiology. 2012;262(1):161–71.

    Article  PubMed  Google Scholar 

  65. Chen J, et al. Improvement in preoperative staging of gastric adenocarcinoma with positron emission tomography. Cancer. 2005;103(11):2383–90.

    Article  PubMed  Google Scholar 

  66. Chang JM, et al. False positive and false negative FDG-PET scans in various thoracic Diseases. Korean J Radiol. 2006;7(1):57–69.

    Article  PubMed  PubMed Central  Google Scholar 

  67. Yasuda I, et al. Endoscopic images of amputation neuroma at the cystic duct stump. Gastrointest Endosc. 2019;90(6):986–7.

    Article  PubMed  Google Scholar 

  68. Kim DH, et al. Traumatic neuroma of remnant cystic duct mimicking duodenal subepithelial Tumor: a case report. World J Clin Cases. 2020;8(17):3821–7.

    Article  PubMed  PubMed Central  Google Scholar 

  69. Estifan E, Patel V, Grossman M. Cap-Assisted Endoscopic Mucosal Resection of an Incidental Rectal Traumatic Neuroma. Case Rep Gastrointest Med, 2019. 2019: p. 8328456.

  70. Menzel J, et al. Preoperative diagnosis of bile duct strictures–comparison of intraductal ultrasonography with conventional endosonography. Scand J Gastroenterol. 2000;35(1):77–82.

    Article  CAS  PubMed  Google Scholar 

  71. Bisogni D et al. Lights of cholangioscopy by SpyGlass DS in detecting indeterminate biliary strictures: is it time to definitely discard the traditional endoscopic retrograde cholangiopancreatography (ERCP)- based sampling techniques? Minerva Med, 2020.

  72. Gornals JB, Consiglieri C, Redondo S. SpyGlass DS-guided conversion of transmural pancreaticogastrostomy drainage to transpapillary drainage by rendezvous via a lumen-apposing metal stent. Endoscopy. 2017;49:01.

    Google Scholar 

  73. Topazian M, Salem RR, Robert ME. Painful cystic duct remnant diagnosed by endoscopic ultrasound. Am J Gastroenterol. 2005;100(2):491–5.

    Article  PubMed  Google Scholar 

  74. Stamatis ED, Myerson MS. Treatment of recurrence of symptoms after excision of an interdigital neuroma. A retrospective review. J Bone Joint Surg Br. 2004;86(1):48–53.

    Article  CAS  PubMed  Google Scholar 

  75. Barbera J, Albert-Pamplo R. Centrocentral anastomosis of the proximal nerve stump in the treatment of painful amputation neuromas of major nerves. J Neurosurg. 1993;79(3):331–4.

    Article  CAS  PubMed  Google Scholar 

  76. Koh DW, et al. [Amputation neuroma mimicking common bile duct cancer: a case report]. Korean J Gastroenterol. 2008;52(1):32–6.

    PubMed  Google Scholar 

  77. Cheng Y, et al. Traumatic bile duct neuroma after resection of hilar cholangiocarcinoma. Clin Res Hepatol Gastroenterol. 2014;38(2):127–8.

    Article  PubMed  Google Scholar 

  78. Terzi A, et al. Traumatic neuroma causing biliary stricture after Orthotopic Liver Transplant, treated with hepaticojejunostomy: a Case Report. Exp Clin Transplant. 2017;15(Suppl 1):175–7.

    PubMed  Google Scholar 

Download references

Acknowledgements

None.

Funding

This work was supported by the National Natural Science Foundation of China (Grant No.82002578) and the Sichuan Science and Technology Program (Grant No.2022YSF0060, 2022YSF0114, 2022NSFSC0680, and 2023YFS0094)0.1·3·5 project for disciplines of excellence–Clinical Research Incubation Project, West China Hospital, Sichuan University (20HXFH021); 1·3·5 project for disciplines of excellence, West China Hospital,Sichuan University (ZYJC21049).

Author information

Author notes

  1. Yaoqun Wang and Sishu Yang contributed equally to this work.

Authors and Affiliations

  1. Division of Biliary Tract Surgery, Department of General Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, China

    Yaoqun Wang, Sishu Yang, Bei Li, Xianze Xiong & Jiong Lu

  2. Research Center for Biliary Diseases, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, China

    Yaoqun Wang, Bei Li, Xianze Xiong & Jiong Lu

  3. Department of Hepatobiliary Surgery, Sichuan Provincial Corps Hospital, Chinese People’s Armed Police Forces, Leshan, China

    Cunyong Shuai

Authors
  1. Yaoqun Wang
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Sishu Yang
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Bei Li
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Cunyong Shuai
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Xianze Xiong
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Jiong Lu
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

Yaoqun Wang, Yang SS and Shuai CY analyzed the data and wrote the manuscript; Yaoqun Wang, Li B helped with data collection; Lu Jiong and Xiong XZ designed, organized, and supervised the writing of the manuscript; all authors approved the final manuscript as submitted.

Corresponding authors

Correspondence to Cunyong Shuai, Xianze Xiong or Jiong Lu.

Ethics declarations

Ethics approval and consent to participate

All patients in our center signed an informed consent form upon admission and agreed to the collection of their clinical information for clinical research.

Consent for publication

Not applicable.

Conflict of interest

The authors declare that they have no competing interest.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Wang, Y., Yang, S., Li, B. et al. Epidemiology, risk factors, diagnosis, and treatment of intra-abdominal traumatic neuromas - a narrative review. BMC Gastroenterol 23, 416 (2023). https://doi.org/10.1186/s12876-023-03049-y

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12876-023-03049-y

Keywords

BMC Gastroenterology

ISSN: 1471-230X

Contact us