Peritoneal carcinomatosis (PC) refers to malignant epithelial cells that spread to the peritoneum, principally from abdominal malignancies. Until recently, PC prognosis has been considered ill-fated, with palliative therapies serving as the only treatment option. New locoregional treatments are changing the outcome of PC, and imaging modalities have a critical role in early diagnosis and disease staging, determining treatment decision making strategies. The aim of this review is to provide a practical approach for detecting and characterizing peritoneal deposits in cross-sectional imaging modalities, taking into account their appearances, including the secondary complications, the anatomical characteristics of the peritoneal cavity, together with the differential diagnosis with other benign and malignant peritoneal conditions. Among the cross-sectional imaging modalities, computed tomography (CT) is widely available and fast; however, magnetic resonance (MR) performs better in terms of sensitivity (92% vs. 68%), due to its higher contrast resolution. The appearance of peritoneal deposits on CT and MR mainly depends on the primary tumour histology; in case of unknown primary tumour (3–5% of cases), their behaviour at imaging may provide insights into the tumour origin. The timepoint of tumour evolution, previous or ongoing treatments, and the peritoneal spaces in which they occur also play an important role in determining the appearance of peritoneal deposits. Thus, knowledge of peritoneal anatomy and fluid circulation is essential in the detection and characterisation of peritoneal deposits. Several benign and malignant conditions show similar imaging features that overlap those of PC, making differential diagnosis challenging. Knowledge of peritoneal anatomy and primary tumour histology is crucial, but one must also consider clinical history, laboratory findings, and previous imaging examinations to achieve a correct diagnosis. In conclusion, to correctly diagnose PC in cross-sectional imaging modalities, knowledge of peritoneal anatomy and peritoneal fluid flow characteristics are mandatory. Peritoneal deposit features reflect the primary tumour characteristics, and this specificity may be helpful in its identification when it is unknown. Moreover, several benign and malignant peritoneal conditions may mimic PC, which need to be considered even in oncologic patients. The peritoneum is the second most common metastatic location for abdominal tumours, only surpassed by the liver.Only 10% of the cases of peritoneal carcinomatosis (PC) are related to extra abdominal tumours .Traditionally, PC implied an ill-fated prognosis and only palliative treatments were applied. However, the introduction of new surgical techniques and regional therapies have changed this scenario, and palliative systemic treatment is no longer the only therapeutic option. A combination of systemic chemotherapy, cytoreductive surgery (CRS), and hyperthermic intraperitoneal chemotherapy (HIPEC) achieves promising results in selected PC cases from colorectal, ovarian, and gastric cancers ,4,5. TheThus, despite its difficulty, the early diagnosis of PC based on imaging findings is essential for disease staging, for the subsequent management of primary tumours and for patient prognosis. Given the aggressiveness of cytoreductive surgery, it is mandatory to adequately select patients in whom the potential benefits will prevail as surgical candidates, distinguishing them from those who should be treated with systemic chemotherapy, either neoadjuvant or palliative. The peritoneal carcinomatosis index (PCI) serves to quantify the extent of the peritoneal involvement and serves as a predictor of incomplete CRS .The aim of this review is to provide a practical approach when encountering a peritoneal carcinomatosis case using cross-sectional imaging, and to establish where to look for deposits, the possible appearances they may show, and the main complications. In the event of no prior known primary tumour, this review also aims to depict the deposits characteristics that may be helpful in suggesting the origin and to describe differential diagnosis.The gold standard for the assessment of PC is explorative laparoscopy, which is a minimally invasive procedure that allows for direct visualization and biopsy. However, as an initial approach, cross-sectional imaging modalities are preferred, and the most common and widespread imaging technique used is intravenous contrast-enhanced (CE) computed tomography (CT) thanks to its availability, fast acquisition time, and the possibility of multiplanar reconstructions ,8. The aMagnetic resonance (MR), including diffusion-weighted imaging (DWI) and contrast-enhanced T1-weighted sequences, is a promising diagnostic modality, as it provides a higher sensitivity 91%) and similar specificity (85%) to CE-CT -2-deoxy-2-fluoro-D-glucose). It improves the diagnostic performance of CT but shows slightly lower sensitivity 87%) than MR, probably due to its lower spatial resolution, with limited depiction of small nodules. On the other hand, its specificity is slightly higher (92%) [F-2-deoxy% than MRRadiologists need to be aware of clinical and laboratory findings.The clinical presentation of PC is variable, nonspecific, and depends on its extension. Patients may present with characteristic symptoms of the primary tumour and nonspecific symptoms. Abdominal pain and ascites occur in 85% of patients . ComplicSerum tumour markers are measurable indicators associated with malignancy, produced either by the tumour or by the body in response to the tumour. They do not serve as a main tool for cancer diagnosis but are useful in supporting diagnosis and treatment response . For insHow to proceed? CT is a very useful first-line modality . HoweverPET-CT should be considered when encountering equivocal imaging findings, when tumour marker levels rise with no identifiable cause upon imaging, and to detect nodal or extra-abdominal metastases.In our clinical practice, CT images are acquired on the axial plane at the portal venous after intravenous administration of iodine contrast medium, with a flow rate of 3 mL/s. Multiplane reconstruction can be obtained on coronal and sagittal planes. No oral contrast is required. When using a dual-source scanner, virtual, unenhanced images can be generated.2. Following intravenous injection of 0.2 mmol/kg of gadolinium-based contrast agents, fat-suppressed 3D T1-weighted sequences are obtained upon breath hold at the arterial and portal phases covering the upper abdomen and after a 3 min late phase of the whole abdomen.MR images can be obtained using 1.5 T or 3.0 T field-strength MR scanners with a surface-phased array coil covering the abdomen and the pelvis. The acquisition protocol includes coronal and axial T2-weighted images and diffusion-weighted imaging (respiratory-triggered for the upper abdomen and on breath hold for the inferior abdomen) with 3 b values of 0, 150, and 800 s/mmThe term peritoneal carcinomatosis refers to the spread of malignant epithelial cells as tumour deposits to the peritoneum .PC represents a very complex condition at imaging, more than any other metastatic site.The appearance of the peritoneal deposits is determined not only by the histological characteristics of the primary tumour, the timepoint of the tumour’s evolution, and the treatment  but alsoSome anatomic knowledge is required in the quest for deposits. The aim of this review is not to offer a comprehensive description of peritoneal anatomy but to establish sufficient certainty that all locations are thoroughly investigated.The peritoneal cavity is the virtual space that exists between the parietal and visceral peritoneum  and, undCranially, it covers the diaphragm  .Caudally, it descends into the pelvis. Its complex anatomy in this location is shown in more detail later.Anterolaterally, it is separated from the abdominal wall by the fat from the preperitoneal space, that is, the space between the peritoneum and the transversalis fascia .Posteriorly, it is distanced from the posterior abdominal wall by the retroperitoneal space. It forms the anterior boundary of the retroperitoneal space .The parietal peritoneum delineates the periphery of the peritoneal cavity:The peritoneum invaginates to fully cover most of the abdominal viscera, anteriorly and posteriorly, becoming the visceral peritoneum. It is organised into a folded disposition as ligaments, folds, and mesenteries to nurture, innervate, and support the intraperitoneal organs, connecting them to the posterior parietal peritoneum.As a common rule, the abnormal thickening and pathological enhancement of surfaces covered by the peritoneum may be the only initial imaging finding in PC.It may be difficult, in the absence of ascites, to differentiate parietal peritoneal deposits from their visceral counterparts at locations where the two leaves are adjacent . For the sake of simplicity, some examples of parietal peritoneal deposits are shown; the rest are included within their peritoneal space .If the deposit lies within a fat-containing peritoneal space, the spectrum of presentation ranges from nodular focal fat stranding to irregular haziness, evolving towards solid lesions. These solid lesions may initially be millimetric, appearing as either solitary or multiple soft-tissue nodules that eventually grow and merge to form plaques or sheets, and then masses. Most commonly, PC appears as a combination of all these findings.Peritoneal spaces are classified as supra- or inframesocolic ,30. The Deposits within the transverse mesocolon appear either on its mesentery  or/and oImaging features of serosal bowel deposits include nodular lesions, segmental parietal thickening, and diffuse infiltration. Their detection may be an arduous task, more so if bowel is not sufficiently distended. In addition, it is important to note that layered implants blend in with the bowel contour, whereas nodular deposits alter it and are thus easier to detect .This description of serosal bowel deposits has the same validity for the rest of the gastrointestinal tract.Next, we use a cranial-to-caudal and lateral-to-medial approach to review the peritoneal spaces.Supramesocolic cavity comprehends the subphrenic, perihepatic, and perisplenic spaces; periportal space, lesser omentum, lesser sac, and right subhepatic space. These locations need to be carefully assessed using multiplanar reconstructions, as deposits within them may require complex surgery or, in some cases, may be considered unresectable.Imaging features include the thickening and pathological enhancement of the diaphragm, nodules, and masses .Deposits can be identified as a continuum from abnormal peritoneal enhancement to subtle nodularity and well-defined nodules, often showing a biconvex morphology.Perihepatic deposits may occur on the superficial visceral peritoneum that surrounds most of the liver surface  and/or underneath the Glisson capsule, within the subcapsular space. Glisson’s capsule is a thick fibrous membrane that lies deep in the visceral peritoneum. It is assumed that deposits infiltrate the liver capsule upon deposition on the visceral peritoneum. The liver capsule covers the entire hepatic surface, including the periportal space, and is in communication with the lesser omentum, thus becoming another route for deposits to reach the subcapsular space. Both the periportal space and the lesser omentum are reviewed next.In the event of subcapsular deposits, secondary parenchymal invasion may occur, resulting in a characteristic scalloping of the underlying parenchyma . DespitePeriportal deposits need to be differentiated from parenchymal metastases. Deposits within the periportal space appear as nodular or plaque-like lesions, predominantly at the porta hepatis and along the left branch of the portal vein; they are usually ill defined and not circumferentially surrounded by hepatic parenchyma, unlike their intraparenchymal counterparts .A proven useful tip is the distention of the periportal space over time due to the presence of deposits. As with any radiological examination, comparison with prior images in the setting of peritoneal carcinomatosis is mandatory .Deposits within this location may cause biliary obstruction, which usually presents at a late stage. Dilatation of the intrahepatic biliary ducts  with no identifiable cause should raise the possibility of deposits within the periportal spaces. Another secondary finding may be a progressive compressive effect on the portal vein over time .This portion of the peritoneum suspends the liver and the lesser curvature of the stomach and separates the first two centimetres of the duodenum from the liver. It is formed by the gastrohepatic and hepatoduodenal ligaments.Deposits within this space show features that are common to any fat-containing space. Furthermore, since the porta hepatis runs in the hepatoduodenal ligament, biliary obstruction or portal vein compression may be found to be indirect signs of PC .As previously seen, once the disease is in the lesser omentum it can easily spread to the periportal space thanks to the surrounding connective tissue of the Glisson sheath, which makes them continuous. This is a particularly important route for the spread of pancreatic and gastrointestinal tumours.Potential space between the pancreas and the stomach. Its distention, either by a solid lesion or by ascites, as is reviewed later, is a sign of its involvement by PC . It commPouch inferior to segment VI of the liver. It communicates with the right subphrenic space, the right paracolic gutter and the lesser sac. Deposits within this space tend to be more subtle, partly due to small size of this space, and range from an ill-defined outer hepatic contour to focal fat stranding and nodules .Inframesocolic spaces are also described using the same cranial-to-caudal and lateral-to-medial approach: greater omentum, paracolic gutters, small bowel mesentery, sigmoid mesocolon, and pelvis recesses.The greater omentum is the main peritoneal fold. It connects the stomach to the anterior surface of the transverse colon and then extends caudally into the pelvis covering the small bowel loops. It lies mainly inferior to the transverse colon mesocolon, although its smaller cranial portion (the gastrocolic ligament) is within the supramesocolic space.The uniqueness of the imaging features of deposits in this location is the omental cake, which occurs when nodular deposits collide  and blenA helpful diagnostic sign as the infiltration progresses is the subsequent displacement of the bowel loops. Enlargement of the fatty content and mass effect due to omental seeding may be more apparent than the actual deposits .Omental deposits are more easily detected using MR. However, in the early stages and especially in thin patients, CT appears to perform better, although the scarce fatty content in thin patients may negatively contribute to the identification of peritoneal deposits .The small-bowel mesentery is a fan-shaped peritoneal double layer that surrounds the small bowel and then extends diagonally from the ligament of Treitz in the left upper quadrant to the ileocecal junction, anchoring at these two locations and at the posterior parietal peritoneum.Within the mesenteric fat: as in the rest of the fat-containing peritoneal spaces, they may range from focal nodular fat stranding to irregular haziness to nodules and masses .Mesenteric deposits show a rather unique and more complex appearance when compared to deposits elsewhere in the abdominal cavity. Deposits may be found in the following locations:Within the SB and caecal serosa: deposits may also lie within the serosa covering the small bowel and the caecum .Involving both the mesentery and the serosa: as in the transverse mesocolon, deposits may appear both within the mesentery and the serosa covering the small bowel loops and the caecum .Within the mesenteric leaves: Deposits within the mesenteric leaves may go unperceived. The nodular thickening and enhancement of the mesenteric leaves is usually more conspicuous using MR but can be also spotted using CT and becomes more noticeable when accompanied by ascites .Stellate mesentery: Diffuse mesenteric infiltration leads to a stellate appearance, which is commonly associated with breast  , gastricAs a result of tumour infiltration, the mesentery becomes rigid and loses its usual free wavering. SB loops appear thickened, with restricted distensibility, looking initially separated and angulated and, finally, clustered . Over tiThe main complication of deposits lying within this space is bowel obstruction, which usually occurs at a late stage, and its diagnosis is not challenging. However, it may also be the presenting sign. It typically involves more than one small bowel loop, and the degree of occlusion may vary. Another, less frequent, complication is bowel ischaemia due to perivascular infiltration .Peritoneal recesses occur between the colon, partially covered by the posterior parietal peritoneum  and the lateral parietal peritoneum on each side. They constitute the attachments of the ascending and descending colon to the posterior parietal peritoneum.Both are in continuity with the peritoneal spaces in the pelvis. Superiorly, the right paracolic gutter communicates with the right subphrenic and right subhepatic spaces, whereas the left paracolic gutter, which is much smaller, is partially separated from the left subphrenic space by the phrenicocolic ligament b.The infiltrated peritoneum typically appears to be nodularly thickened, showing pathological enhancement .The oblique orientation of the small bowel mesentery described earlier divides the inframesocolic compartment into two compartments, right and left, with the latter being larger. The only structure standing in the way of free communication between the left inframesocolic space and the pelvis is the sigmoid mesocolon, thus the reason why it constitutes a common site of deposits, as it is an area of arrested flow. Deposits within the sigmoid mesocolon lie on its fat and/or on the serosa, and differentiation between them may not always be feasible. Sigmoid luminal stenosis with/without signs of obstruction is a frequent consequence of the seeding .The mesentery of the appendix is anchored to the lower end of the small bowel mesentery, close to the ileocecal junction and the tip of the appendix. Despite its small size, it may be an important site in appendiceal neoplasms: in case of rupture, deposits will likely appear there first.Deposits within the pelvis may be quite tricky to find, as the anatomy is rather complex and there are several structures that fit in a small cavity; therefore, careful exploration using multiplanar reconstructions is recommended.The parietal peritoneum that covers the abdominal wall goes down to the pelvis, where it does not reach the pelvis floor, as it reflects on the pelvis organs . The peritoneal reflexion covers the dome of the urinary bladder, then descends along its posterior wall and laterally forms paravesical spaces, a fold over the ureters; in men, it also covers the deferent ducts and the seminal vesicles. It continues towards the rectum and then ascends, partially cloaking the upper and middle rectum  and the lateral pelvic walls . In womeTwo blind-end pouches are found in women—the uterovesical, anteriorly, and the rectouterine, posteriorly—while there is only one in men, the rectovesical .Pelvic organs, except for the tubes, which are intraperitoneal, are only superiorly and laterally covered by the peritoneum. Thus, deposits can be identified as enhancing nodular peritoneal thickenings on the pelvic walls  or withiAs ureters are in close contact with the peritoneum at the paravesical spaces, pelvis deposits may be the cause of ureterohydronephrosis, and this is frequently overlooked, especially as the only sign of PC. Any deposit along the posterior parietal peritoneum in the proximity of the course of the ureter may also be the cause of a urinary obstruction, but the pelvis is a very frequent location .Occlusion may occur as a result of pelvis deposits within the peritonealised portion of the rectum.Another common site of PC in the pelvis is the ovaries. As seen previously, these are extraperitoneal organs, but are considered intraperitoneal, as they communicate with the peritoneal cavity. This is the reason why ovaries are included among the PC locations.Compared to primary ovarian tumours, ovarian metastases seem to be smaller and more frequently bilateral, showing more uniform cysts and more moderate enhancement of the solid portions . HoweverThe term Krukenberg tumour is sometimes misused in the setting of ovarian metastases from a gastrointestinal tumour, as its use should be limited to ovarian metastasis from a poorly differentiated adenocarcinoma with signet ring cell features . KrukenbNow that the peritoneal anatomy has been revised, the focus is placed on the fluid contained in the peritoneal cavity, as it plays a determinant role in the seeding of the deposits.Peritoneal fluid circulates following the path determined by ligaments and mesenteries, under the influence of the abdominal pressure fluctuations caused by respiration and intestinal peristalsis.In the case of tumour spread to the peritoneum, the quantity of the peritoneal liquid rises due to two conditions: the obstruction of the lymphatics in charge of the resorption and the overproduction of fluid caused by the vascular permeability factor secreted by the tumour cells ,38.Fluid in the inframesocolic space naturally goes down on the right of the small bowel mesentery  through Ascites may be one of the first signs of PC. Its appearance correlates closely with its volume: if minimal, is only be found in the pelvic recesses, surrounding the liver and the spleen, or between the small bowel loops, in a triangle-shaped fashion . If quanSuspicious signs may be ascites with rounded or bulging contours, or concomitantly present in the greater and lesser sacs .Another important clue is how SB loops behave in peritoneal liquid: in nonneoplastic ascites or in the early stages of PC, they float freely, with an anterior location, whereas in advanced PC, as the mesentery becomes fibrotic and rigid, SB loops are pulled back centrally and posteriorly (the tethered bowel sign) . CharactIn the setting of portal hypertension and non-malignant ascites, collateral vessels within the parietal peritoneum should be cautiously noted, so as not to misdiagnose them as deposits .With regard to signal, the deposit does not fall far from the primary tumour; that is, deposits will usually show a density/signal intensity and enhancement pattern resembling the primary tumour, as extraperitoneal metastases do.Thus, one should always bear in mind the underlying histology and imaging features of the primary tumour and contemplate the possibility of a second primary tumour if a discrepancy is found.In addition, in the event of no known primary tumour, which occurs in about 3–5% of cases of PC , the behIndeed, knowledge of the underlying deposit content responsible for the appearance of high signal intensity in T1- and T2-weighted images of peritoneal deposits is an important diagnostic criterion that can contribute to the diagnosis of the primary tumour.T1 hyperintensity may be observed within a deposit due to three contents: melanin, blood, and calcium.Melanin-containing deposits: from melanoma .Calcium-containing deposits: mucinous tumours of different origins  may calcify .Blood-containing deposits: blood content is frequently found in peritoneal deposits from hypervascular tumours of different origins  .T2 hyperintensity can reflect different contents within deposits: myxoid, non-mineralised cartilage, or mucin. This may also be due to keratin in the setting of a squamous differentiation.Myxoid-containing deposits: as in myxoid liposarcoma .Non-mineralised cartilage-containing deposits: from chondrosarcoma .Mucin-containing deposits: from mucinous tumours arising on different organs, namely ovary, stomach, colon, pancreas, appendix, gallbladder, and the urachus .Keratin-containing deposits: from tumours showing squamous differentiation .CT hyperdensity can be due to calcium  or bloodThe vascular pattern of deposits also correlates with the characteristics of the primary tumour and may impact the differential diagnosis  dependinIt is worth underlining that, in oncologic patients, not all peritoneal abnormalities correspond to carcinomatosis; hence, PC needs to be differentiated from other neoplastic and nonneoplastic conditions  . This maOmental infarction is a rare cause of acute abdomen, usually self-limiting, that presents with nonspecific symptoms. The right omentum is more commonly affected, as it moves more freely, and its vascularization is longer and more tortuous. It can be primary or secondary to other processes such as tumour, hernia, or postoperative adhesions .It is usually a straightforward diagnosis of CT: striking fat stranding of the infarcted omentum with minimal or no involvement of the adjacent bowel  .Omental infarction may mimic PC at first glance, but the clinical setting and the inflamed aspect of the omental fat usually reveal the diagnosis. The importance of the correct diagnosis upon imaging relies on its conservative management unless superinfection occurs.Amyloidosis is a rare disease consisting of abnormal protein deposition throughout the body, which more frequently occurs in the gastrointestinal tract, kidneys, and heart. Peritoneal deposition is very rare and can mimic PC .Two forms of peritoneal involvement have been described : diffuseSarcoidosis is a systemic granulomatous disease of unknown aetiology. The most common location is the lung . ExtrapuThis is a hereditary condition characterised by recurrent episodes of fever and systemic serosal inflammation, which mainly occurs in the abdomen. It especially affects patients of Mediterranean heritage. Imaging features are nonspecific; if it presents with ascites and peritonitis, it may strongly mimic PC . The mosThis is a rare but serious condition. It can be idiopathic or secondary, either to peritoneal dialysis or other causes, benign  and malignant  . It presM. tuberculosis complex) [Peritoneal tuberculosis may be a challenging entity to diagnose, given its insidious onset, its vague clinical presentation , and the difficult isolation of the agents (complex) .It is important to achieve a prompt diagnosis, as a delay in treatment may cause a worse outcome.Wet (the most common), where the salient feature is ascites, either free or loculated, which may show high attenuation on CT due to the high protein contents.Dry, where cellular content is predominant.Fibrotic fixed, where the main features are fibrotic changes, causing clustered SB loops.An in-between state may also be found (fibrotic mixed).Imaging classification includes three main types :Wet  or congenital (accessory spleen).Splenosis is usually a consequence of spleen injury, either from trauma or surgery, resulting in splenic fragments that acquire a vascular supply and may grow. They may seed on the liver, as in the case shown in the figure, although they most frequently seed in the left lobe, with a subcapsular location. Intrahepatic splenosis usually shows increased enhancement on the arterial phase and may be a potential pitfall for hepatocarcinoma, neuroendocrine metastases, or adenoma ,58,59. DAccessory spleens enhance similar to the spleen, although this may be difficult to evaluate due to their small size. As a rule, these nodules are well-defined and homogeneous, whereas peritoneal deposits may tend to be more irregular and heterogeneous.Inflammatory–phlegmonous changes secondary to bowel perforation caused by a foreign body may mimic peritoneal carcinomatosis in oncologic patients.Either spontaneous or secondary to inflammation or trauma, it is usually asymptomatic and its presentation on imaging depends on the time of evolution. Using CT, if acute, it appears as an omental or mesenteric focal fat stranding that may have a discrete mass effect on the adjacent organs; over time, it shrinks and becomes well-defined and peripherally calcified. Initially, it may mimic a liposarcoma and, when it becomes fibrotic , it can be misdiagnosed as a deposit, especially in oncologic patients. Clinical history and previous imaging examinations are essential to achieve a correct diagnosis.This is a benign condition characterised by the implantation of endometrial tissue outside the uterine cavity. Peritoneal endometriosis is usually accompanied by other imaging findings that suggest the diagnosis; however, peritoneal involvement may appear as the sole finding. Endometriotic deposits will likely show areas of high signal intensity in T1WI due to blood content and/or low signal intensity in T2WI due to fibrosis.This is a rare condition that occurs in women of reproductive age, characterised by the development of multiple leiomyomas within the peritoneum. Potential risk factors are increased levels of endogenous/exogenous oestrogens  and prioMalignant transformation is a rare complication . PeritonDesmoid tumours (DT) belong to a heterogeneous group of locally aggressive fibromatosis, although non-metastasising, that may arise throughout the body, most commonly extra-abdominally. In 30% of patients, there is an association with familial adenomatous polyposis and, in this setting, tumours are most frequently multiple and intra-abdominal  .There is also an association with pregnancy and prior trauma and surgery have been described as possible risk factors . In the DTs are soft-tissue masses that may show either well-demarcated or ill-defined margins that extend into the adjacent mesenteric fat. They are usually isodense to muscle; their signal intensity on MR depends on the predominant content . Enhancement ranges from moderate to intense. As infiltrating mesenteric soft-tissue masses, they can mimic PC.It occurs in women, predominantly postmenopausal, and is challenging to diagnose as it resembles advanced epithelial ovarian carcinoma (AEOC), both in imaging and in the histological exam. It occurs less frequently than AEOC and has a worse prognosis . The disThis clinical term refers to a syndrome characterised by the presence of mucinous loculated ascites within the peritoneum .These mucinous septated collections disseminate along the peritoneal surface and their mass effect causes a scalloped appearance of adjacent organs. Pseudomyxoma cells lack adherence molecules on their surface, so they spread by a redistribution phenomenon, which means they follow the current of the intraperitoneal fluid and tend to accumulate at the gravity-dependent and resorption sites described at the beginning of this review . Thus, tThis entity has been classically associated with a perforated epithelial neoplasm of the appendix; although less frequently, it can originate from mucinous tumours arising from other organs . It shouThis very rare and fatal primary malignancy of the peritoneum shows features that overlap those of PC; thus, it is difficult to distinguish these entities using imaging alone. The link with asbestos exposure is weaker than in pleural mesothelioma but remains its best-defined risk factor : a histoA rare mesenchymal malignancy that arises from peritoneal surfaces as multiple soft-tissue masses. This occurs most frequently in young male patients. Imaging features overlap with other peritoneal malignant tumours. Calcification may occur on 30% of the cases .As described at the beginning of this review, the term peritoneal carcinomatosis is used when the disease is caused by epithelial cells. The peritoneum may also be the soil of malignant nonepithelial cellular lines, mesenchymal or lymphoid, and thus refer to sarcomatosis and lymphomatosis, respectively .In the setting of an unknown primary tumour, the differential diagnosis should always include the possibility of another cell line being the origin of the peritoneal deposits.Peritoneal lymphomatosis (PL) is a rare condition but important to suspect, as it responds favourably to chemotherapy. It is uncommon, as the peritoneum lacks lymphoid tissue, and the underlying mechanism is unknown. It is associated most frequently with diffuse large B-cell lymphoma, although it can occur in many subtypes .Imaging features include homogeneous soft-tissue diffuse infiltration of peritoneal leaves , associaAscites, which can be massive in PC, is rather mild in PL, and hepatosplenomegaly occurs more frequently.Isolated peritoneal disease with no bowel or lymph node involvement is rare .Bowel obstruction is uncommon, even in extensive lymphomatous infiltration of small bowel, due to its lack of desmoplastic reaction .Peritoneal sarcomatosis (PS) is defined as a disseminated intraperitoneal spread either from an intra-abdominal primary sarcoma or from extremity sarcomas . SarcomaBowel obstruction and hydronephrosis tend to be more common in PC .Despite these differences, the diagnosis of PL/PS based on imaging can be difficult to achieve as PC is much more frequent; thus, the diagnosis should be confirmed using histology.To correctly diagnose PC, a systematic approach to the abdominal cavity is highly recommended. The knowledge of peritoneal anatomy and peritoneal fluid flow characteristics substantially contribute to an understanding of where to look for deposits and their appearance on cross-sectional imaging.Indeed, in CT and MR, features of peritoneal deposits and their behaviour on contrast-enhanced cross-sectional images are related to the histologic characteristics of the primary tumour. Therefore, in the event of peritoneal carcinomatosis with unknown primary tumour, signal intensity/density characteristics of the peritoneal deposits, together with their vascular properties, may be helpful in the identification of the primary tumour.Moreover, it can occur that the sole presenting sign of peritoneal carcinomatosis is intra-abdominal complications, such as bowel obstruction or ureterohydronephrosis, which should be considered suspicious in oncologic patients, even in the absence of clear radiological evidence of peritoneal deposits.Furthermore, there are several benign and malignant peritoneal conditions that may mimic peritoneal carcinomatosis. Thus, even in oncologic patients, it is important to consider these conditions in the differential diagnosis with peritoneal carcinomatosis. However, when relying solely on imaging, it remains difficult to conduct a differential diagnosis, since the imaging features overlap between benign/other malignant conditions.


Focal cortical dysplasia (FCD) represents a heterogeneous group of morphological changes in the brain tissue that can predispose the development of pharmacoresistant epilepsy . This group of neurological disorders affects not only the cerebral cortex but also the subjacent white matter. This work reviews the literature describing the morphological substrate of pharmacoresistant epilepsy. All illustrations presented in this study are obtained from brain biopsies from refractory epilepsy patients investigated by the authors. Regarding classification, there are three main FCD types, all of which involve cortical dyslamination. The 2022 revision of the International League Against Epilepsy (ILAE) FCD classification includes new histologically defined pathological entities: mild malformation of cortical development (mMCD), mild malformation of cortical development with oligodendroglial hyperplasia in frontal lobe epilepsy (MOGHE), and “no FCD on histopathology”. Although the pathomorphological characteristics of the various forms of focal cortical dysplasias are well known, their aetiologic and pathogenetic features remain elusive. The identification of genetic variants in FCD opens an avenue for novel treatment strategies, which are of particular utility in cases where total resection of the epileptogenic area is impossible. The morbidity of active epilepsy is similar for countries with different economic development; it is 2.3–5.9/1000 for high-income countries, 3.7–13.3/1000 for high-income to middle-income economies, 2.4–2.8/1000 for countries with low-income to middle-income economies, and 3.6–15.4/1000 for low-income economies . A. A45]. AConventional GG corresponds to grade 1 according to the WHO classification of CNS tumours . In termThe majority of GG (>80%) contain ramified cells either within the tumour or in the adjacent cortex that express the oncofoetal epitope CD34, which is not normally expressed outside of vascular endothelial cells in the mature brain B 49]. F. F49]. FConventional GG and GC are well-differentiated, clinically indolent tumours with excellent prognosis . FollowiAnaplastic ganglioglioma (AGG) is a glioneuronal tumour composed of dysplastic neurones and an anaplastic glial component with increased mitotic activity . AGG corThe anaplastic changes in AGG predominantly affect the glial cells E,F 48]..48]. TumA rare GG variant is desmoplastic infantile ganglioglioma (DIGG). It is characterised by desmoplastic stroma and mature neuronal cell component G,H. DIGGDysembryoplastic neuroepithelial tumour (DNET), first described in 1988 by Daumas-Duport et al. , is a slAccording to the literature, in patients with recurrent unprovoked epileptic seizures, in the context of pharmacoresistant epilepsy, DNET represents 18% of tumours in adulthood and 23% of neoplasms in children .Neuroradiological findings are important in distinguishing DNET from tumour glial proliferations, especially oligodendrogliomas. Most DNETs are well-defined formations in the cerebral cortex. MRI imaging demonstrates a T1-hypointense lesion with an intratumoural nodular character. T2-weighted imaging reveals a well-demarcated hyperintense lesion, usually found in the temporal lobe. The majority of DNETs are non-contrasting formations, they are very rarely contrast, and extremely rarely even show peripheral (ring-) contrast ,68.Pathomorphologically, DNET can be divided into “simple” and “complex” histological variants. Common to both forms are the presence of specific glioneuronal elements—oligodendrocyte-like cellular elements, “floating” mature neurones without dysplastic changes, and intracortical, mucin-like spaces with microcystic characteristics  is a rare neoplasm, accounting for less than 1% of all CNS tumours. It is found in children and young individuals, and is often associated with focal epilepsy, but with a relatively good prognosis ,76.PXA is primarily diagnosed during the first two decades of life. Most often, it develops in the cortex of the cerebral hemispheres, particularly in the temporal lobe, and invades the overlying leptomeninges .Imaging studies  show a solitary supratentorial mass, often involving the leptomeninges. Cystic and contrast-enhancing lesions are common. The classic tumour configuration is demonstrated by a cyst and a contrasting mural nodule .Macroscopically, PXAs are well-demarcated formations, usually with a yellowish cut surface, which is explained by the lipidised astrocyte cellular composition. A cystic component is present, sometimes with calcifications .Histologically, large pleomorphic cells with astrocytic- or mesenchymal-like morphology are found. Bizarre nuclei with multinucleated cell shapes and abundant eosinophilic cytoplasm are characteristic. Smaller polygonal or spindle-shaped cells are also found, often forming bundles . ImportaConventional PXA corresponds to second grade, while anaplastic forms correspond to third grade tumour classification according to the WHO . An inteDifferential diagnosis is made with giant cell glioblastoma, gliosarcoma, epithelioid glioblastoma, and pleomorphic sarcoma. An important point here is the proof of various genetic aberrations—IDH mutations, gain of chromosome 7, EGFR amplifications, and loss of chromosome 10, which are typical for glioblastoma or high-grade astrocytomas. BRAF mutations are common for both PXA and epithelioid glioblastoma, but the latter is immunohistochemically negative for intracellular reticulin ,48.The Ki-67 proliferative index is usually less than 3% in conventional PXA, corresponding to the WHO’s grade 2, while more than 10% proliferative activity points to anaplastic PXA, which are WHO grade 3 tumours .PXA is associated with a good prognosis, as in the majority of the cases complete surgical removal is the definitive treatment. In anaplastic PXAs, as well as in cases with partially removed conventional PXAs, radio- and chemotherapy are considered. In the rare cases of proven MGMT promoter methylation, treatment with temozolomide is also introduced , and in Rosette-forming glioneuronal tumour (RFGNT) is a rare, slow-growing WHO first grade tumour affecting young individuals. It develops in the posterior fossa, with involvement of the fourth ventricle. The tumour manifests clinically much more often with headache and ataxia than with seizures. The average age at diagnosis is 27 years, and it is slightly more common in women .MRI reveals a circumscribed, solid mass, sometimes with a cystic component, which often shows peripheral contrast .Histologically, RFGNT has biphasic nature. The neurocytic component contains a monomorphic population of small cells with eosinophilic cytoplasm, forming rosettes around eosinophilic neuropil, as well as pseudorosettes formed around small-calibre blood vessels A. NeurocThe complete surgical removal of the tumour is evidenced to be its definitive treatment. In the literature, there are single reports of malignant transformation with dissemination in the CNS .Papillary glioneuronal tumour (PGNT) is a low-grade neoplasm, WHO grade 1  composedPGNTs are extremely rare, accounting for less than 0.02% of all CNS tumours. The mean age at diagnosis is 23 years .The clinical manifestation of PGNT includes epileptic seizures, headaches, visual disturbances, etc. The majority of PGNTs are supratentorial lesions, primarily involving the temporal lobe. Imaging data are non-specific .A definitive diagnosis is made only after histological examination, which is illustrated by pseudopapillary structures containing hyalinised vessel walls surrounded by a biphasic neoplastic cell population. Immediately adjacent to the fibrovascular axes  are spindle-shaped to cuboidal glial cells that are positive for GFAP by immunohistochemistry. NeuN- and synaptophysin-positive neuronal cells are found between the pseudopapillary structures. Very rarely, PGNTs show signs of transformation to a high-grade tumour such as increased mitotic activity , manifestations of vascular proliferation, and areas of necrosis .Differential diagnosis is made between extraventricular neurocytoma, astroblastoma, ependymoma, and RFGNT. A major distinguishable feature of PGNT is its characteristic immunohistochemical profile, verifying the condition’s biphasic nature. In addition, a specific translocation has been demonstrated in the tumour—t   .A case series on 71 patients pathomorphologically diagnosed with PGNTs demonstrated a real possibility of total surgical resection correlating with definitive treatment of the patients .Hypothalamic hamartoma (HH) is a tumour-like lesion with minimal growth potential, developing in the hypothalamus tuber cinereum or from the floor of the third ventricle. Although HH can be asymptomatic, in some cases, there are manifestations in the form of epileptic seizures with sudden onset of uncontrollable laughter (gelastic epilepsy) or premature puberty . Its freMacroscopically, HH resemble the grey matter of the brain. Histologically, they are represented by collections of mature, small neurones and glia C,D. The Currently, the choice of treatment for HH is their disconnection rather than their complete surgical removal due to the presence of significant risks associated with their resection .Angiocentric glioma is a WHO grade 1, slow-growing supratentorial tumour observed in children that is strongly associated with seizures . The incHistologically, angiocentric glioma is composed of monomorphic bipolar tumour cells. They are spindle-shaped, with oval or elongated nuclei and eosinophilic cytoplasm. There is a tendency for perpendicular arrangement of tumour cells around the pia mater and vessel walls. Similarly to other low-grade epilepsy-associated tumours, hallmarks of FCD may be seen adjacent to angiocentric gliomas .Differential diagnosis is made with ependymoma, pilocytic astrocytoma, and low-grade astrocytoma. The first two tumours show a tendency to form a tumour mass, and the third demonstrates a diffuse growth, similarly to the angiocentric glioma, but without a tendency for perivasal arrangement of proliferating glial cells .Tumour cells in angiocentric glioma show positive immunohistochemical reaction for GFAP, S-100 proteins, and vimentin, and exhibit a “dot-like” cytoplasmic reaction for EMA. The proliferative index (Ki-67) is low, ranging from 1% to 5% ,96.Complete surgical removal of these tumours leads to complete seizure control. There is a case description of a patient with initially histologically verified low-grade angiocentric glioma, who relapsed after 21 months, exhibited morphological signs of anaplastic transformation, and subsequently suffered a lethal outcome ,97.Isomorphic diffuse astrocytoma (IDA) was first described in 2004 in patients with early-onset pharmacoresistant focal epilepsy corresponding to the first degree tumours of the WHO ,99. To dCavernomas are vascular malformations with nodular character composed of cavernous spaces lined with endothelial cells but lacking the typical histological structure of “mature” blood vessel wall A. MRI reAround 4–6% of cases with pharmacoresistant epilepsy are caused by cavernous vascular malformations. The seizures are typically associated with blood products that induce reactive perilesional gliosis. The recurrent microhaemorrhages, and consequently the hemosiderin deposits in the cortical tissue, likely cause hyperexcitability through ferrous ions and subsequent oxidative damage and lipid peroxide formation causing proliferation of epileptogenic glial cells .AVMs can be found in all parts of the CNS; however, they predominantly affect the middle cerebral artery pool. MRI findings include a limited lesion with hemosiderin deposits. Angiography reveals arteriovenous shunting. Histological examination allows visualisation of vessels with different calibre and thickness of the tunica media. Typical features in the vicinity of the lesion include signs of gliosis and clusters of hemosiderophages, which are indicative of recurrent haemorrhages. Although AVMs can manifest at all stages of life, most of them present between the ages of 20 and 40. This type of malformation “steals” a significant portion of the blood supply from adjacent brain regions, which may be the underlying cause of seizures in patients with AVM. Hemosiderin deposits may also contribute to epileptogenesis .Focal epilepsy has been reported in around 80% of Sturge–Weber syndrome patients. The prevalence of the condition is about 1/50,000. Its inheritance pattern remains elusive .Typical diagnostic imaging and macroscopic findings include extensive unilateral leptomeningeal angioma, cortical “railway” calcifications, and less frequently atrophy of the subjacent neocortex. The white matter presents signs of chronic ischemia and reactive gliosis. Functional MRI examination reveals reduced glucose metabolic activity and hypoperfusion of the affected cortical region. Microscopically, large curved venous structures among thickened leptomeninges  are found B,C. SignThe epileptogenic substrate in Sturge–Weber syndrome is cellular damage caused by excessive vascular proliferation which disrupts the normal blood supply to the brain tissue and leads to atrophy and focal calcification of the adjacent brain parenchyma .Meningioangiomatosis (MA) is a rare tumour-like meningovascular hamartomatous lesion . The majThe MA is benign and surgically treatable, although resection can be complicated by the invasive character of the lesion ,110,111.FCD type IIIc is histopathologically defined by the ILAE Classification, 2022, as abnormal cortical organisation adjacent to epilepsy-associated vascular malformations . In a reEpileptic seizures are commonly observed in encephalitis patients. Cytotoxic T-lymphocytes and antibody-mediated complement activation are the most important components of the adaptive immune system, inducing neurodegenerative changes that can subsequently lead to epileptogenic encephalitis. On the other hand, the innate immune system acts through interleukin-1 and Toll-like receptor-associated mechanisms, playing a direct role in epileptogenesis ,114,115.In 1958, the Canadian neurosurgeon Theodore Rasmussen published a scientific report entitled: “Focal seizures due to chronic localised encephalitis” in three childhood patients. Rasmussen’s encephalitis involves one hemisphere. It begins with a “prodromal period” that sometimes lasts for years, during which mild hemiparesis or rare seizures may be observed. This is followed by the “acute phase” of the disease, characterised by more frequent pharmacoresistant unilateral simple partial seizures or secondary generalised seizures. Over the course of the disease, the inflammatory manifestations spread through the hemisphere, which determines the appearance of new epileptogenic zones. A few months after the onset of the epileptic seizures, neurological deficits in one hemisphere follow, including hemiparesis, hemianopia, impairment of cognitive function, and aphasia . The neuThe second group of encephalitis in which epileptic seizures are observed are antibody-associated; these are classified as paraneoplastic and non-paraneoplastic limbic encephalitis . Many paIn the limbic encephalitis, histologically in the temporal neocortex and in the hippocampus, there are pronounced signs of astrogliosis, microglial activation with a tendency to form nodules, and infiltration of T-lymphocytes in the brain parenchyma ,122.After a longer period of time, the only biopsy finding in patients with encephalitis may be marked “cellular” gliosis.FCD IIId is most prominent in regions of pre- or perinatal stroke and adjacent to the resulting porencephalic cyst. Another clinico-pathological FCD IIId subtype is that of neocortical layer 4 loss in the occipital lobe associated with perinatal hypoxemic disturbances occurring predominately in male children . FCD III2 in the cerebral white matter using the IHC markers MAP2 or NeuN . Ano. Ano2) aSLC35A2 somatic mutations are demonstrated in 45–100% of MOGHE patients ,126. BonIn 2 to 26% of patients operated on due to pharmacoresistant epilepsy, the pathomorphological examination does not allow a definite histological diagnosis (“no FCD on histopathology”). In some of these patients, preoperative imaging showed an abnormal finding that was not confirmed morphologically ,5.Principal epileptogenic lesions comprise any morphological lesion with aetiologically defined pathogenesis of either neoplastic, genetic, infectious, traumatic, or metabolic origin. Principal lesions include different epilepsy-associated tumours, vascular malformations, encephalitis, malformations of cortical development, traumatic scars, etc. .“Dual Pathology” refers to patients with HS, who have a second principal lesion other than FCD type I, i.e., tumour, glial scar, encephalitis, vascular malformation, FCD type IIa, or FDC type IIb . Histolo“Double Pathology” refers to two independent lesions affecting one or multiple lobes, but not including HS. Both lesions evolve from an independent pathogenesis, e.g., cavernous hemangioma in one cerebral hemisphere and a GG in the other .The complete surgical resection of all the various principal lesions is crucial in cases with Dual and Double Pathology as each lesion itself represents an epileptogenic focus.Targeted imaging and molecular genetic studies provide important clues in the diagnosis of different histopathological variant of FCD. MRI data is an essential cornerstone in the workup of patients with focal epilepsy . CertainGenetic testing of somatic and germline mutations for FCD is currently not available in most pathology laboratories. It is an important diagnostic tool for determining whether patients with FCD carry pathogenetic variants. Different genes  have been reported to cause canonical FCD IIa . SLC35A2The genetic panel needs to be expanded, especially in histopathologically proven cases of FCD type Ib and Ic, where the exact aberrations are not yet known. The leptomeningeal vascular malformations also represent an area where more genetic studies are needed.In summary, the diverse spectrum of FCD includes isolated forms , forms associated with other principal epileptogenic lesions (FCD type III), as well as cases with predilection for white matter involvement . Although the pathomorphological characteristics of individual forms are well known, their aetiological and pathogenetic features are not fully understood and need to be explored further. The adult group of patients with medically refractory epilepsy is dominated by HS. In the pediatric group most cases present with isolated forms of FCD—types I and II. Glioneuronal tumours are a very common finding in both groups. The most common long-term epilepsy associated tumours are GG and DNET which are typically benign, low-grade tumours. Malignant transformation may be observed exceedingly rarely. Additional immunohistochemistry analyses prove invaluable in the diagnosis of FCD. NeuN staining allows visualisation of the abnormal histoarchitectronics of the neocortex in FCD type I cases. In addition, it enables the detection of heterotropic neurones which are a defining feature of mMCD and MOGHE. Of particular utility for the diagnosis of FCD type II are the markers SMI32 Neurofilament (staining dysmorphic neurones in FCD IIa) and vimentin . The neuronal loss and fibrillary gliosis in HS can be proved with the IHC markers NeuN and GFAP, respectively. Useful markers in cases with LEAT are CD34 (for GG cases), Alcian blue , Reticulin (illustrating increased number of reticular fibres in PXA and DIGG). Although high-grade transformation of LEAT is extremely rare, it can be IHC verified by Ki-67 revealing increased proliferation index.In terms of management of pharmacoresistant epilepsy, targeted MRI investigation of epileptogenic lesions, their complete surgical removal and correct histological diagnosis seem to be the most effective approach. Moreover, imaging and genetic examination may provide further insight into the mechanisms underlying these conditions thereby opening novel therapeutic avenues as has been the case with FCD type II (mTOR inhibitors) and MOGHE .


Pancreatic pseudocysts are rare in pediatrics . They caA 13-year-old girl was admitted for chronic epigastric pain with a distended abdomen. There was a history of abdominal trauma by beef kick 8 months earlier requiring 4 days of hospitalization but without specific exploration. There was no particular personal or familial history including pancreatitis or hyperlipidemia. The clinical examination showed a distended abdomen with collateral venous circulation, dull to percussion with the sensation of a soft mass. There were no clinical and biological inflammatory signs. Standard tests as blood sugar, creatinine, blood and urine ionogram, amylasemia, and lipasemia were normal at the time of diagnosis. The tumor markers as lactate dehydrogenase, alpha-fetoprotein, and beta-human chorionic gonadotropin were normal. Abdominal ultrasound revealed a large anechoic cystic mass not clearly attached. The abdominopelvic computed tomography exam confirmed the bulky cystic mass with homogeneous hypodense content surrounded by a thin and regular wall measuring 190 × 172 × 125 mm in size at the anterior face of the body of the pancreas (Fig. Pancreatic pseudocysts are rare benign conditions ,2. It isThe child’s pancreatic pseudocyst can be large and difficult to diagnose. The history of abdominal trauma and the dilation of the main pancreatic duct communicating with the cyst are decisive clinical and morphological factors. The cystogastric bypass by laparotomy remains the appropriate treatment in the absence of endoscopic and radiological treatment.


Uterine fibroids incarcerated in abdominal wall hernias during pregnancy are rare, with only six cases reported in umbilical hernias. This case report presents the first reported case of an incarcerated uterine fibroid in an epigastric hernia.A 31-year-old primigravid Caucasian woman at 28 weeks gestational age presented with sudden onset abdominal pain and vomiting. Physical examination revealed an incarcerated epigastric hernia containing a non-reducible firm mass. Ultrasound showed a healthy fetus, and during surgery, a subserosal and sessile fibroid originating from the anterior uterine wall was found in the hernia sac. It was easily reduced, and the hernia was repaired with no complications. The patient proceeded to deliver a healthy baby boy by cesarean section at full term.Uterine fibroids incarcerated in abdominal wall hernias during pregnancy are rare and affect mostly primigravid women in the third trimester. Abdominal ultrasound may facilitate the diagnosis, and pedunculated fibroids may be resected while sessile fibroids should be simply reduced. Clinicians should consider incarcerated fibroid as a differential diagnosis in pregnant women with irreducible ventral abdominal wall hernias. This case report aims to contribute to the literature and optimize the management of abdominal wall hernias in pregnant women. Epigastric hernias are a protrusion of the omentum or an abdominal organ through a fascia defect in the Linea Alba above the umbilicus. The uterus is located in the pelvis and is far from the umbilicus. Due to pregnancy, the uterus is enlarged and the anterior wall can reach the umbilicus. There have been six reported cases of uterine fibroids incarcerated in an umbilical hernia during pregnancy. This is the first case of an incarcerated uterine fibroid in an epigastric hernia.A 31-year-old primigravid Caucasian woman at 28 weeks gestational age was admitted for sudden onset abdominal pain with vomiting during the last 24 h. Up to this point, she had an uncomplicated pregnancy. She reported an asymptomatic epigastric hernia that had been present for years. She had no other medical or surgical history. Physical examination showed a non-reducible epigastric firm mass indicating an incarcerated epigastric hernia. Fetal ultrasound revealed a healthy fetus with no abnormality. Given the sudden onset of her pain and our inability to reduce the hernia, she was brought emergently to the operating room with the diagnosis of an incarcerated epigastric hernia. No abdominal ultrasound was made due to the unavailability of a radiologist.The patient received no tocolytics preoperatively due to absence of contractions and she was monitored by a gynecologist during the surgical intervention.A supraumbilical incision was made under general anesthesia to perform the procedure. Upon exploration, a hernia sac measuring 3 cm in diameter was identified. Upon opening the sac, an omental fragment was discovered adhering to a sessile fibroid that originated from the anterior uterine wall Fig. . It was The incarceration of a uterine fibroid in an umbilical or epigastric hernia is very rare and have been reported mostly in pregnant women. The uterus is typically located in the pelvis and doesn’t reach the umbilicus or the epigastric region and fibroids are typically too small to reach the umbilicus. Due to pregnancy, the uterus is enlarged and can reach the epigastric abdominal wall.There have been six reported cases of a uterine fibroid incarcerated in an umbilical hernia during pregnancy Table . All hapThe first case was reported by Ehigiegba in 1999, a 31-year-old primigravid woman at 28 weeks’ gestation presenting a pedunculated fibroid incarcerated in an umbilical hernia, which was treated by myomectomy and hernia repair.Five out of the six reported cases were primigravid pregnancies. Only one case happened in the third pregnancy. Five out of the six happened in the third trimester. Only one case happened in the second trimester. None in the first trimester.In our case, the patient was primigravid and the incarceration of the fibroid happened in the third trimester.Three cases were diagnosed via abdominal ultrasound. The rest relied only on physical examination, and the diagnosis of the incarcerated fibroid was made during the surgery. In our case we relied only on examination. No abdominal ultrasound was performed, which could have helped make the diagnosis pre-operatively. We suggest that every pregnant woman in the second or third trimester presenting an abdominal hernia should be explored by an abdominal ultrasound and consider an incarcerated fibroid as a differential diagnosis.Four pedunculated fibroids were reported; three were treated by myomectomy with no further complications. The fourth case was treated by simple reduction of the fibroid and hernia repair.Two cases of sessile fibroids were treated by hernia reduction and repair.In our case, the fibroid was sessile with a large base of implantation so a simple reduction was performed. No myomectomy was performed due to the large base of implantation of the fibroid with a high risk of hemorrhage, miscarriage, and preterm labor.Uterine fibroid incarcerated in an abdominal wall hernia is very rare. It affects mostly primigravid pregnant women during the third trimester. Abdominal ultrasound may facilitate the diagnosis. Pedunculated fibroids may be resected while sessile fibroids should be simply reduced.The diagnosis of incarcerated fibroid should be considered as a differential diagnosis in pregnant women presenting with known uterine fibroids and an irreducible ventral abdominal wall hernia. Meticulous examination in cooperation with ultrasound evaluation are important adjunctive tools to optimize the diagnosis and decision-making toward surgical treatment.In writing this case report, we aim to contribute to the literature by detailing what we believe to be the first reported case of fibroid incarceration in an epigastric hernia during pregnancy and to further optimize and standardize the management of abdominal wall hernias in pregnant women.


Stercoral perforation is a rare sequela of poorly controlled constipation that is more commonly seen in older, bedridden patients than in pediatric patients. We present the case of a 13-year-old patient requiring a divided sigmoid colostomy following rectal perforation, one of the few examples in the pediatric literature of stercoral perforation from chronic constipation. The current report highlights the importance of appropriate treatment of functional constipation at onset and the life-threatening complications that can occur without appropriate follow-up. Chronic idiopathic constipation affects up to 30% of the pediatric population -3. Also A 13-year-old female with no significant past medical history except for chronic constipation presented to the emergency room with severe right lower quadrant (RLQ) pain and obstipation. On arrival, she was hypotensive at 70/30 mmHg and was tachycardic at 110 beats per minute. She had a normal respiratory rate and saturation on room air. The patient was alert but appeared paler than typical according to her mother. The abdominal examination was notable for firmness and tenderness to palpation at the RLQ area. There was no tenderness to palpation in other areas of her abdomen but stool burden was palpable. Bowel sounds were also present throughout. Cardiac, lung, and skin examinations were unremarkable. Complete blood count and metabolic panels were unremarkable with a white blood cell count (WBC) of 10,300 WBCs per microliter. She was administered 3 L of normal saline boluses and started on a norepinephrine drip and a piperacillin and tazobactam infusion. Computed tomography (CT) imaging from the referring institution demonstrated rectal wall discontinuity at the 2 o’clock position with stool leakage and a large stool burden in the descending colon, sigmoid colon, and rectum (Figures The patient was urgently taken to the operating room for rectal examination under anesthesia, diagnostic laparoscopy, rectal biopsy, repair of rectal perforation, and creation of a sigmoid ostomy. The rectum was initially examined with a digital rectal examination and anoscopy which demonstrated a 5 mm × 3 cm perforation at the 2 o’clock position on the rectal wall and a 1 cm × 0.5 cm defect of the mucosa at the 6 o’clock position. Given an enlarged abscess cavity seen outside of the 2 o’clock perforation, a red rubber catheter was placed at the site for drainage and secured to the rectal wall with an absorbable suture. On diagnostic laparoscopy, the catheter was not visible inside the peritoneum, confirming that this site was an extraperitoneal perforation. In addition, no intraperitoneal stool contamination was seen. A biopsy of the rectum was then obtained 2 cm proximal to the dentate line, adjacent to the 6 o’clock position. A laparoscopic-assisted diverting sigmoid colostomy was created at the descending sigmoid junction in the standard fashion. There were no complications during the procedure. Biopsy results showed necrotic colorectal mucosa likely from pressure and the presence of normal ganglion cells with no other pertinent findings.The patient did well post-surgery and her bowel function normalized by postoperative day three. She was discharged on postoperative day four on a bowel regimen. The drain fell out on its own three weeks after discharge. A follow-up examination under anesthesia and contrast enema two months after the index procedure demonstrated a well-healed rectal wall without stricture. A colostomy takedown was planned after an interval of nutritional optimization.Six months after examination under anesthesia, she underwent a scheduled colonoscopy and motility evaluation in preparation for an ostomy takedown that demonstrated colitis in the rectosigmoid region. However, the workup for inflammatory bowel disease, including biopsy, was unremarkable and the inflammation was thought to be due to diversion colitis. A laparoscopic sigmoidectomy during colostomy takedown was performed to prevent recurrence by resecting the redundant colon. She recovered well postoperatively and was discharged home.According to the American College of Gastroenterology, constipation accounts for at least 2.5 million doctor visits per year . ChronicManagement of patients with uncomplicated bowel obstruction and absent signs of peritonitis is often nonoperative, including manual or endoscopic removal of fecal impaction, aggressive bowel regimen, and observation . In caseStercoral perforation is a rare but serious complication of poorly controlled constipation that can result in sepsis and potentially lead to a lethal outcome. Our presented case involves a stercoral rectal perforation in a pediatric patient due to chronic constipation. This case emphasizes the significance of implementing appropriate treatment for functional constipation, performing a full workup to rule out pathological etiologies of constipation such as Hirschsprung’s disease, and conducting an early evaluation of possible perforation.


A giant cell tumor of the tendon sheath (GCTTS) presents as a rare neoplasm demanding a heightened index of suspicion for precise diagnostic evaluation, especially when manifesting in the digital phalanges, as it is part of a group of neoplasms known as tenosynovial giant cell tumors (TCGTs). An accurate and timely diagnosis is crucial, as it significantly enhances treatment outcomes for this heterogeneous group of lesions. We describe the case of a male patient who presented with multiple nodules in the fourth finger of his left hand and was ultimately diagnosed with a localized form of a GCTTS, an unusual presentation for localized forms of this entity. Our objective is to outline the diagnostic and therapeutic approach, discussing options for differential diagnosis and treatment modalities. To achieve this, we conducted a literature review and compared our findings and the observed evolution in our patient. Early recognition of hand tumors allows for timely diagnosis, facilitating optimal resections during surgical procedures. This, in turn, reduces morbidity and enhances the functionality of the affected extremity, as detailed in the current case. The term tenosynovial giant cell tumor (TCGT) encompasses a group of neoplasms primarily originating in the synovial membrane of joints, bursae, or tendon sheaths, displaying synovial differentiation. These lesions typically manifest either in extremities or in large joints. Localized forms usually appear as a single nodule on the hands, while diffuse forms, seen in large joints such as the knee, often display multiple masses . The estA 69-year-old male patient, with a medical history of type 2 diabetes and hypertension, was referred to our outpatient clinic. He presented with multiple nodules on the fourth finger of his left hand that showed progressive and slow growth over the past four years. His main complaint was limited finger mobility, particularly during finger flexion.Physical examination revealed diminished mobility of the fourth finger during flexion of the metacarpophalangeal joint. He reported no pain during finger movement, and his left hand exhibited normal color, capillary refill, and no sensory deficits. Limitation in flexion of the affected joint was due to the presence of multiple firm, lobulated, and non-tender masses located on the palmar and ulnar aspects of the proximal phalanx of the affected finger, which measured approximately 15 x 10 mm each, they did not coalesce and were partially mobile (Figure A plain X-ray examination of the patient's left hand in two projections revealed radiopaque tumors within the soft tissue regions, precisely at the head of the proximal phalanx of the fourth finger and near the proximal interphalangeal joint Figure .An elective digital exploration was scheduled under local-regional anesthesia based on our clinical and radiological suspicion of a hand tumor, likely a giant cell tumor. The procedure was successfully performed without complications, revealing a multilobulated, firm, and amber-colored tumor. Notably, the tumor extended from the palmar aspect of the hand in flexor zone II to the ulnar and dorsal aspects of extensor zones III and IV. Importantly, the tumor displayed no significant adhesions to digital anatomical structures, and we exercised great care in preserving the integrity of neurovascular bundles, as well as the flexor and extensor apparatus of the finger Figure .We performed a complete resection Figure  followedIn the post-operative follow-up, sutures were removed, revealing satisfactory wound healing and good digital mobility. Subsequent histopathological analysis categorized the specimen as localized GCTTS Figure . The posTGCTs are a group of neoplasms that primarily affect individuals between the ages of 20 and 50. They can manifest as either a single nodule, referred to as a localized TGCT, or as multiple nodules, known as diffuse TGCTs, along a synovial layer, bursa, or tendon sheath. While the TGCT predominantly involves large joints like the knee and hip, it can also affect fingers, and, on rare occasions, the temporomandibular joint or the spine . Unlike Conventional radiography is often employed as an initial diagnostic tool; however, it may not always detect abnormalities but is used to rule out calcifications, which are infrequently observed in TGCTs but may be present in other potential diagnoses. MRI is the preferred method for detecting and characterizing TGCTs ,6. In ouSeveral factors have been associated with recurrence, such as proximity to the distal interphalangeal joints, the presence of degenerative joint disease, pressure erosions in radiographs, increased mitotic activity, and type 2 lesions. However, the one consistent observation made by multiple authors in preventing recurrence is the complete surgical excision, including the removal of all satellite nodules when present ,7. The lResection serves as the initial treatment choice for TGCTs. The most suitable surgical approach remains a subject of debate and hinges on the tumor's specific location. Additionally, treatment options encompass radiosynovectomy, external beam radiotherapy, chemotherapy, and the use of tyrosine-kinase inhibitors, either in conjunction with surgery or as standalone methods. The localized-type TGCT carries a 10-year recurrence risk of up to 9.8% and a lifetime recurrence risk of up to 15%. In the case of a localized-type TGCT, a simple surgical excision as a standalone treatment is typically sufficient for a cure and can be confirmed during the surgical procedure [This case report underscores the importance of clinical suspicion, thorough evaluation, and surgical management in the approach to GCTTS of the hand. Furthermore, it highlights the need for further research to better understand the pathogenesis and associated risk factors of this rare neoplastic entity. Achieving complete resection through timely diagnosis and appropriate surgical treatment in patients with GCTTS not only preserves hand function but also reduces the risk of recurrence, much like what occurred in this patient. Histopathological analysis is essential to differentiate giant cell tumors from entities with malignant potential and other forms of TCGTs.


The traditional indications for lobectomy for resectable Non‐small Cell Lung Cancer (NSCLC) may be set to change. Recently, anatomical segmentectomy (AS) versus lobectomy as an approach for early‐stage NSCLC has been described in phase 3 randomised controlled trials. The demand for methods to facilitate AS may increase as a consequence. We describe three cases of AS using the combination of endobronchial infiltration of indocyanine green (ICG) to identify the intersegmental plane , and Computed Tomography (CT) guided methylene blue injection for lesion localisation. The operations were completed successfully demonstrating satisfactory post‐operative outcomes including lesion resection with clear surgical margins and acceptable length of stay. We believe that endobronchial instillation of ICG and CT‐guided methylene blue injection for lesion localisation show promise as a technique to complement parenchymal sparing thoracic oncological surgery. We describe three cases of anatomical segmentectomy (AS) using the combination of endobronchial infiltration of indocyanine green (ICG) to identify the intersegmental plane , and Computed Tomography (CT) guided methylene blue injection for lesion localisation. The operations were completed successfully demonstrating satisfactory post‐operative outcomes including lesion resection with clear surgical margins and acceptable length of stay. We believe that endobronchial instillation of ICG and CT‐guided methylene blue injection for lesion localisation show promise as a technique to complement parenchymal sparing thoracic oncological surgery. Lung cancer is the most common cancer diagnosis worldwide and results in over a quarter of all cancer deaths.An increase in mortality and higher recurrence rates in patients treated with sublobar resections compared with lobectomy was noted in the 1990s.More recently, the surgical management for early‐stage NSCLC has been re‐examined. Overall survival was analogous to those ‘intentionally selected’ for sublobar resection versus lobectomy in one systematic review.The increase in survival from NSCLC has led to a rise in patients with metachronous tumours. These patients, who have already undergone a lobectomy, are often appropriate candidates for parenchymal sparing strategies. These factors have generated opportunities for more sophisticated, targeted approaches to parenchymal sparing surgical resection.Of note, a phase 3 randomised controlled trial (RCT) published this year demonstrated AS compared with lobectomy in early‐stage non‐small cell lung cancers to have similar outcomes, promoting AS for consideration in this population.The intersegmental plane is critical for the accurate performance of AS.A 74‐year‐old man with a history of childhood passive cigarette smoke exposure and paternal family history of leukaemia presented with a four‐month history of abdominal pain. Investigations revealed an incidental ground glass nodule measuring 7 × 6 × 12 mm abutting the horizontal fissure posteriorly in the right upper lobe. No distant metastatic disease or mediastinal/hilar lymph nodal involvement was detected on subsequent PET/CT imaging. Pre‐operative lung function testing demonstrated an FEV1 of 107% at 2.71L, FVC of 109%, normal volumes and normal DLCO.A multidisciplinary decision was made to perform an AS. 1 mL of methylene blue was injected via CT guidance with a 22‐gauge spinal needle, followed by endoscopic ICG injection under flexible bronchoscopy. Blue dye was identified at RB2 consistent with a recent methylene blue injection. An Olympus B5‐2C balloon was placed and inflated inside RB2b to prevent spillage. 2.5 mLs of ICG was instilled into the segmental airway (RB2). Anatomical right upper lobe posterior segmentectomy was conducted under four‐port robotic surgery (Da Vinci system).The patient was successfully discharged on day three post‐operation. Histopathology confirmed an 8 mm adenocarcinoma in situ with clear surgical margins. The three lymph nodes sampled were not involved. Stage TisN0 was confirmed.An 84‐year‐old male smoker with a 30‐pack‐year history of exposure presented a two‐month non‐productive cough history. He had a past history of renal cell carcinoma treated with nephrectomy and prostate cancer for which he underwent combined brachytherapy and radiotherapy. A CT chest found a spiculated 12 × 12 mm lesion in the right upper lobe. PET/CT scan demonstrated no metastatic disease. CT‐guided biopsy confirmed lung adenocarcinoma with ERBB2 mutation.Pre‐operative lung function testing demonstrated FEV1 of 106%, FVC of 138%, normal lung volumes and normal DLCO. The multidisciplinary decision was for AS. 10 mLs of ICG was instilled endobronchially via Olympus TH190 flexible bronchoscope into RB2, followed by 40 mLs of saline flush. The right upper lobe posterior segment was successfully resected robotically (Da Vinci system).Post‐operatively, there was a small apical pneumothorax that settled on serial imaging. Histopathology confirmed mucinous adenocarcinoma with clear surgical margins. He was discharged on day five post‐operation. All five lymph nodes sampled were not involved. StageT1bN0 was confirmed. Post‐operative spirometry demonstrated unchanged values.A 69‐year‐old man with a history of a left lower lobectomy in 2017 for stage I adenocarcinoma underwent routine surveillance CT chest, which identified a new 7 mm ground‐glass nodule in his right lower lobe in 2020. Subsequent PET/CT scan demonstrated no metastatic disease. His other significant background was a previous right nephrectomy for clear cell renal carcinoma.A multidisciplinary decision recommended AS. 1 mL of methylene blue was injected into the lesion under CT guidance with a 22‐gauge spinal needle , and better preservation of lung function. Successful surgical margins were achieved in all three cases.Small nodules are often not palpable. It is difficult to confirm that the correct tissue is in the resected specimen, frozen section is similarly problematic. Having the correlational accuracy of CT‐guided methylene blue target lesion injection and a tract to the pleural surface of the lung combined with segmental bronchi ICG delineating the segmental border may increase the accuracy of lung nodule resection.Retrospective and case‐control studies of lobectomy versus segmentectomy demonstrate comparable results for small (Stage 1A <2 cm or 3 cm) tumours.A recently published systematic review compared patients treated with sublobar resection versus lobectomy. In an ‘intentionally selected’ cohort of patients with peripheral, less than 2 cm parenchymal lesions, sublobar resection had similar outcomes to lobectomy in terms of disease‐free and overall survival.Andolfi et al. published on the various methods of identification of the intersegmental plane during thoracoscopic segmentectomy.n = 245). A combination of ICG instilled endobronchially and intravenous ICG injection via injection in the segmental pulmonary artery was performed. In addition to using this method, lesion localization was facilitated by electromagnetic navigational bronchoscopy (ENB) in 38% of cases. Geraci et al. quote 80/93 (86%) patients were found to have the lesion accurately identified using their method. In their cohort, segmentectomy was largely confined to lesions <2 cm, N0/N1 disease and resections that were deemed to be likely to achieve satisfactory surgical margins. Failure of localisation was caused by the inaccurate injection of ICG, failure of the navigational bronchoscopy software or pleural perforation of the dye.Several thoracic surgeons have adopted intravenous injection of ICG via the segmental pulmonary artery. A retrospective cohort study published in 2019 looked at data from a single surgeon at a single facility  final approval of the version to be published.All authors have no conflicts of interest to declare.The authors declare that appropriate written informed consent was obtained for the publication of this manuscript and accompanying images.


Oropharyngeal teratomas are an extremely rare congenital tumor. They are often diagnosed prenatally and can cause significant airway obstruction and feeding difficulties at birth. We present a five-month-old female that was diagnosed with a palatal teratoma that presented with failure to thrive, difficulty feeding, and eventually with severe obstructive sleep apnea.We present a five-month-old term, otherwise healthy female who became stridulous after an episode of the respiratory syncytial virus at one month old. At three months old, an otolaryngologist diagnosed mild laryngomalacia with no mass identified, and no surgical intervention was recommended. Due to continued poor weight gain, at four months old, a nasogastric tube was placed. She was subsequently admitted for further workup. She had severe stridor, a failure to thrive, and was in the 0.07th percentile for weight. Workup revealed severe obstructive sleep apnea and a palatal mass obstructing her left oropharynx. A biopsy and debulking of the mass was performed in the operating room. Pathology resulted as a mature teratoma with evidence of glial and intestinal tissue.There are no pathognomonic characteristics found on imaging to diagnose teratomas, and diagnosis is made with pathologic identification of two of the three germ cell layers. Although most teratomas are benign, there is potential for malignant transformation involving any of the represented germ cell layers. Many teratomas are diagnosed prenatally and can be quite large, often requiring Ex Utero Intrapartum Treatment (EXIT) procedure at birth to establish a safe airway.Overall, this case highlights the importance of a thorough head and neck exam, including a bilateral flexible laryngoscopy, when evaluating an infant with airway obstruction. Providers evaluating these patients should consider oropharyngeal masses, such as teratoma, as part of the differential to ensure accurate and timely diagnosis. This article was previously presented as a meeting abstract at the 2022 Children's Mercy Hospital Research Symposium on May 2nd, 2022. Oropharyngeal teratomas are a rare congenital tumor. They are often diagnosed prenatally and can cause significant airway obstruction and feeding difficulties at birth. The patient prognosis is dependent on the respiratory distress of the newborn, as well as the potential risk for malignant transformation and extension of the mass. Teratomas occur in one in 4,000 births and display a female predominance. The head and neck region only represents 5-15% of these tumors, and only 2% are in the oropharynx . IdentifThe patient is a five-month-old term, otherwise healthy female who initially was breastfeeding well. After an episode of respiratory syncytial virus at one month old, she became stridulous and had difficulties with feeding. She was seen by an otolaryngologist at three months of age who performed both an awake and sedated airway evaluation. Findings showed only mild laryngomalacia, and no surgical intervention was recommended. No masses or lesions were visualized at that time. Due to continued poor weight gain, at four months old, a nasogastric tube was placed. Despite enteral feeds, working with a lactation consultant and a feeding specialist, she failed to gain weight, and her breathing became increasingly noisy. She was subsequently admitted to a tertiary care children's hospital for further work-up at age five months. At the time of admission she had severe stridor, FTT, and was in the 0.07th percentile for weight. A sleep study showed severe obstructive sleep apnea with an apnea-hypopnea index of 172.5 events per hour and an oxygen nadir of 74%. Further evaluation by a pediatric otolaryngologist revealed a palatal mass obstructing the entire left oropharynx. Flexible nasopharyngoscopy showed a patent right nasal passage and a large mass obstructing the left nasopharynx. She was taken to the operating room (OR) for a biopsy and debulking of the visible intraoral portion of the mass Figure .The patient's status significantly improved with debulking of the tumor. She had a stable airway with reduced obstructive symptoms, her feeding improved, and she was discharged home with close follow-up from otolaryngology and hematology/oncology. Although she did require another operative intervention as part of her treatment, the goal in sending her home was to improve weight gain and nutrition prior to completing a definitive tumor excision.Seven weeks following her diagnosis, she was then taken to OR for excision of the remaining tumor located within the soft palate. Prior to the final surgical decisions, the medical team and family had a long discussion regarding surgical options, risks, and benefits. An en bloc excision of the left soft palate lesion with margins would ensure complete excision; however, this would require the loss of half the soft palate and would likely create substantial long-term feeding and speech implications. Another alternative discussed was to essentially dissect and peel the tumor out of the soft palate by elevating it off the oral and nasal mucosal layers. This would hopefully offer preservation of the palatal function; however, a more conservative approach for resection could also result in a potentially higher risk for recurrence or persistence of tumor. Ultimately the family and medical team decided to move forward with the palatal preservation surgical approach. The case was performed successfully with all gross tumor removed, and the soft palate was closed primarily without residual defect. Post-operatively she had significant improvement in her breathing, feeding, and sleeping. Her soft palate incisions healed well. She had a three-month post-operative MRI showing post-surgical changes and no residual mass. Since surgery, she has improved her weight-for-age percentile from 0.07th (z-score: -4.10) to 7.10th (z-score: -1.47), gaining 3.82kg. The patient continues to follow closely with otolaryngology and hematology/oncology, with plans for a repeat MRI in four months. If her next MRI shows no residual mass, then we will increase serial imaging increments to six months. Oropharyngeal teratomas are extremely rare tumors most often diagnosed in the prenatal/neonatal period. Interestingly, the presented patient was initially seen by a medical professional at three months old, which was the origin of multiple consultations, including lactation, feeding, ear, nose, and throat (ENT), and her pediatrician. Her FTT persisted despite seeing these specialists and undergoing appropriate work-up. FTT is a common problem, representing 5% to 10% of patients seen in the primary care outpatient setting . This reIn this case, a bilateral flexible nasopharyngoscopy exam was completed during her evaluation with pediatric otolaryngology. It is unclear if her initial endoscopy by an outside otolaryngologist was completed unilaterally or bilaterally. Interestingly, with the bilateral endoscopy, the initial pass through the right nare did not identify any signs of obstruction. It was not until passing the scope through the left nare that the tumor was seen. This was surprising that such a large lesion could be missed when an endoscopy was performed on the contralateral side, and speaks to the importance of bilateral endoscopy exams. When evaluating a patient for FTT, it is important to rule out airway obstruction. One study found that in pediatric patients with FTT, the prevalence of OSA was 5.5%, compared to the general population, which is between 0.7% and 4.3% . AdditioThe final treatment plan for this patient resulted from a multidisciplinary discussion of risks and benefits with the family and medical team. One consideration explored was a large palatal resection with mucosal margins and full resection of the tumor. This specific treatment would place her at risk of inability to breastfeed, severe velopharyngeal insufficiency, potential need for speech surgery, and long-standing nasal regurgitation. Given these risks, in addition to the benign pathology, the medical team and family elected for the less invasive approach. To date, no obvious signs of recurrent/residual disease are present; however, she will require close monitoring. Postoperatively, mom was very excited that she was able to resume breast-feeding, and she has not had any evidence of nasal regurgitation. This case demonstrates the need for a personalized decision with caregivers and family, including oncology, surgeon, and family.In conclusion, this case highlights the importance of a thorough head and neck exam, including a bilateral flexible laryngoscopy, when evaluating an infant with FTT and airway obstruction. Providers evaluating these patients should consider oropharyngeal masses, such as teratoma, as part of the differential to ensure accurate and timely diagnosis. Treatment for teratomas is surgical excision; however, it should be tailored to the individual patient with a shared decision-making model involving the family and medical team.


Traumatic abdominal wall hernia (TAWH) following blunt injury is a rare clinical entity, induced by traumatic disruption of the abdominal wall's muscle and fascia, alongside abdominal organ herniation. A thorough clinical examination and a high level of suspicion are necessary for the diagnosis. We present the case of a 45-year-old individual who presented to the surgical outpatient clinic with a left lateral bulge in his belly caused by a mountaineering accident. After obtaining a thorough history of the mechanism of injury and clinical assessment, abdominal ultrasonography and computed tomography (CT) scan revealed a significant traumatic left lateral abdominal wall hernia. The patient subsequently underwent an open surgical mesh repair, followed by anatomical and functional restoration of the muscular deficit over the mesh, with an uneventful postoperative course. TAWH constitutes a diagnostic challenge, and in many cases remains untreated for long periods of time. Considering that TAWH occurs in less than 1% of all blunt abdominal trauma, many surgeons are unaware of this rare manifestation. Here we suggest that elective surgery with an open, tension-free polypropylene mesh repair appears to be an appropriate therapeutic option. Traumatic abdominal wall hernia (TAWH) has been described in the literature for over a century, with Selby being the first to report such a case in 1906 . While iA 45-year-old man presented to our surgical outpatient clinic complaining about an immense left lateral mass in his abdomen, induced by falling onto a boulder while mountaineering a few months ago Figure . After aThe patient underwent elective open surgical mesh repair. He was placed in a left lateral decubitus (nephrectomy) position and a transverse incision over the hernia protrusion was made Figure . A compl TAWH is considered a rare sequela of blunt trauma with only a few cases having been described in the current literature. This infrequent type of hernia is defined by disruption of the abdominal wall musculature while the skin remains intact . A propoTAWH is more prevalent in younger individuals, usually under the age of 50, since they're more likely to be involved in automobile accidents. A thorough history and clinical examination are essential in the diagnosis of TAWH. Abdominal discomfort, abrasions, ecchymosis, or hematoma may be the only clinical findings, while the differential diagnosis should always include pre-existing hernias, abdominal wall hematomas, and tumors . NonetheEarly diagnosis and surgical intervention for TAWH are critical aspects to the outcome of these patients as they minimize the risk of entrapment of the bowel in the defect, which in turn can lead to strangulation or perforation. Surgical exploration, typically through a midline incision, aids in the identification of related injuries or those missed by the CT scan and allows for prompt treatment . IndividThe surgical treatment of TAWH includes the primary closure of the defect in layers, with or without the use of a prosthetic mesh repair. When a tension-free repair is possible and there is no underlying hollow viscus injury, the mesh may be employed as an on-lay graft (as in our case), below or over the sutured repair. Laparoscopic repair of TAWH has also been reported as it utilizes the advantages of laparoscopy in preventing negative laparotomies and revealing any underlying condition . In our case, the choice of an open transverse incision over the hernia protrusion was made in order to achieve better access to the hernia sac and the disrupted musculature of the left lateral abdominal wall. There was no underlying hollow viscus injury and thus a tension-free repair of the defect with the use of a prosthetic polypropylene was performed. In addition, an anatomic restoration of the muscular deficit over the mesh was established, by suture fixation of the origin of the three lateral abdominal muscles on the periosteum of the iliac crest . The above-mentioned approach was utilized to achieve functional abdominal wall restoration. In trauma patients, TAWH is a rare clinical entity that requires a high level of clinical suspicion. In addition to a thorough clinical assessment, CT appears to be the gold standard for confirming the diagnosis, screening for concomitant intra-abdominal injuries, and classifying the hernia. In terms of surgical treatment, both an open surgical approach via a transverse incision and laparoscopic repair of TAWH are viable options. Nevertheless, since TAWH are associated with significant morbidity and mortality, the timing of diagnosis and surgical intervention determines the outcome of these patients.