PEDIATRIC SURGERY UPDATE ©

Kaposiform Hemangioendothelioma

Kaposiform hemangioendothelioma (KHE) is a rare, locally aggressive vascular tumor that primarily affects infants and young children, though it can occasionally present in adults. First distinguished as a separate entity in 1993, KHE occupies an intermediate position in the spectrum of vascular neoplasms — neither fully benign nor overtly malignant — and is characterized by its capacity for locally invasive and infiltrative growth. Its estimated annual incidence is approximately 0.071 per 100,000 children, though the true prevalence is likely higher, as small or atypical lesions may be misclassified as other vascular anomalies. A slight male predominance has been noted in larger case series. The underlying cause of KHE remains incompletely understood. Most cases arise sporadically without an identifiable trigger, though rare reports describe worsening after trauma, surgery, infection, or vaccination, suggesting that inflammatory stimuli may aggravate the disease. At the molecular level, somatic mutations — including activating variants in the GNA14 gene — have been identified in a subset of specimens, implicating the MAPK/ERK signaling pathway. Whether these mutations are causative or secondary is still debated. Dysregulation of both angiogenesis and lymphangiogenesis are central to KHE's pathology. Elevated vascular endothelial growth factor-C and its receptor (VEGFR-3), along with high angiopoietin-2 levels, have been implicated in driving abnormal vessel formation and contributing to the consumptive coagulopathy that defines the disease's most dangerous complication. On histopathology, KHE is recognized by infiltrating, rounded, confluent nodules composed of spindle-shaped endothelial cells that form malformed lymphatic channels and slit-like vascular lumina. Microthrombi, hemosiderin deposits, and eosinophilic hyaline bodies are frequently observed. Immunohistochemical staining shows positivity for vascular markers CD31 and CD34, and lymphatic markers D2-40, VEGFR-3, and Prox-1, while staining is negative for GLUT-1 — a feature that distinguishes KHE from infantile hemangioma — and for HHV-8. KHE exhibits considerable clinical heterogeneity. Lesions are classified by depth of involvement into three morphological types: superficial (confined to skin and subcutaneous tissue), mixed (involving both superficial and deep structures including muscle, bone, or joint), and deep (no cutaneous involvement, affecting internal organs, retroperitoneum, mediastinum, or bone). A further clinically important subgroup is intracavitary KHE — tumors arising primarily within body cavities such as the thoracic or abdominal cavity, retroperitoneum, or pelvic space, where the bulk of the lesion is contained within the cavity and may involve serosal surfaces, mesentery, or cavity-specific structures. The mixed type is the most common overall, while deep and intracavitary lesions account for a smaller proportion of cases but carry the greatest diagnostic challenge and the most severe clinical burden. Cutaneous KHE typically presents as erythematous, violaceous, or darkened patches, plaques, or firm nodules. When associated with the Kasabach-Merritt phenomenon (KMP), lesions become tense, engorged, purpuric, hot to the touch, and painful. Deep lesions without skin involvement may present with nonspecific symptoms such as abdominal distension, jaundice, respiratory distress, or unexplained thrombocytopenia and coagulopathy, often resulting in significant diagnostic delay. Intracavitary lesions in particular may compress adjacent organs or critical structures as they enlarge, leading to pleural effusion, pericardial effusion, peritoneal effusion, obstructive jaundice, gastrointestinal bleeding, or airway compromise. Approximately 90% of cases become evident within the first year of life, and about half of cutaneous lesions are detectable at birth. Unlike infantile hemangioma, KHE does not undergo spontaneous involution and tends to progress without treatment. The most feared complication of KHE is the Kasabach-Merritt phenomenon, which occurs in 42–71% of patients. KMP is defined by profound thrombocytopenia — with median platelet counts around 21 × 10?/L at presentation — combined with consumptive coagulopathy and hypofibrinogenemia. It is critical to understand that KMP does not occur with infantile hemangioma; it is exclusively associated with KHE and the related tufted angioma. KMP carries a mortality rate estimated between 10–30%, and deaths are most commonly attributable to hemorrhage in vital organs. Intracavitary KHE carries a disproportionately high KMP burden — studies have documented KMP rates approaching 80% in this subgroup, compared to roughly 30% in non-intracavitary cases — a disparity that may reflect the anatomical microenvironment of body cavities, which lack the soft tissue buffering present in superficial or extremity lesions, facilitating early compression of vascular structures, local blood stasis, and amplification of platelet trapping. The rich chylous pools and subserosal lymphatic networks within the thoracic and abdominal cavities may further intensify the local accumulation of coagulant substances and increase susceptibility to KMP. Risk factors for KMP include young age at presentation, large tumor size (particularly greater than 8 cm), and anatomic location — intrathoracic and retroperitoneal lesions are disproportionately associated with KMP. Patients with KMP tend to have larger tumors and present at a younger age than those without. Beyond KMP, KHE causes significant morbidity through musculoskeletal involvement. The tumor's infiltrative and destructive growth can erode bone, invade joints, and alter the mechanical properties of surrounding connective tissue, leading to decreased range of motion, chronic pain, joint contractures, and progressive scoliosis — particularly with thoracic or retroperitoneal lesions. Tumor stimulation, inflammatory cell infiltration, and fibrin deposition near vertebral structures can promote local fibrosis, and during skeletal development, contractures may mechanically pull on bone, eventually driving progressive thoracic deformity. These musculoskeletal complications are more common in older children and can persist even after hematologic parameters normalize. Lymphedema is a recognized long-term sequela, especially with lesions involving the proximal extremities near lymph node basins. Intracavitary KHE is additionally associated with a higher burden of organ dysfunction — including jaundice and abnormal liver function from bile duct or portal vein compression, gastrointestinal hemorrhage from intestinal wall infiltration, and structural deformities such as scoliosis from paraspinal involvement — complications that are far less common in non-intracavitary disease and that can in severe cases impair respiratory and circulatory function and contribute to death. Diagnosis of KHE requires integration of clinical, laboratory, imaging, and pathological data. Ultrasound is useful for superficial or small lesions, typically revealing heterogeneous, ill-defined, hypervascular masses. However, MRI is the preferred modality and provides the most comprehensive assessment of disease extent. On MRI, KHE characteristically demonstrates iso-intensity relative to adjacent muscle on T1-weighted imaging and heterogeneous hyperintensity on T2-weighted imaging, with intense, heterogeneous gadolinium enhancement. Lesions commonly show ill-defined margins, multiplanar involvement, adjacent fat stranding, and bone or joint changes including cortical destruction or remodeling. CT can complement MRI in evaluating bony involvement and is more practical in critically ill patients. Three morphological patterns have been described: well-defined solid mass, solid central mass with surrounding infiltrative regions, and purely infiltrative lesion without a distinct solid core. Biopsy remains the gold standard for diagnosis and should be obtained when clinically safe. In patients with classic KMP and a compatible vascular mass on imaging, histologic confirmation may not always be required before initiating treatment. No FDA-approved therapy exists specifically for KHE. Management must be individualized based on disease severity, the presence or absence of KMP, lesion location, and patient age. For patients with KMP, aggressive combination therapy is required — monotherapy is generally insufficient. The mTOR inhibitor sirolimus, combined with short-term corticosteroids, has emerged as the preferred first-line regimen for KHE with KMP. Sirolimus works by inhibiting the PI3K/AKT/mTOR pathway, which mediates downstream effects of both VEGF-C/VEGFR3 and angiopoietin-2/Tie-2 signaling, and may additionally suppress the proliferation of KHE endothelial cells through effects on autophagy-related pathways. Response rates with sirolimus are high, and angiopoietin-2 levels have been shown to fall significantly with treatment. For patients without KMP, sirolimus monotherapy is effective, and randomized trial evidence demonstrates that low-dose sirolimus (targeting trough concentrations of 5–8 ng/mL) is non-inferior to high-dose sirolimus (10–15 ng/mL) at one year of treatment, with fewer respiratory, skin, and mucosal adverse events. Low-dose sirolimus therefore represents a safer long-term option for non-KMP patients requiring prolonged therapy, though high-dose regimens retain a role for severe cases and those complicated by KMP. Intracavitary KHE, even when treated with sirolimus-based regimens, tends to show lower sustained response rates at 6 and 12 months compared to non-intracavitary disease, underscoring the need for vigilant systemic monitoring and active complication management alongside tumor-directed treatment; outcomes at 24 months, however, appear more comparable between the two groups. Vincristine — alone or combined with corticosteroids or antiplatelet agents such as ticlopidine — remains an alternative first-line option for KMP, with an overall response rate of approximately 72%. Corticosteroids alone yield lower sustained response rates and carry significant long-term side effects. Propranolol and interferon-alpha have been used with variable and generally less reliable results; interferon-alpha in particular carries a risk of serious neurologic complications and is contraindicated in children under one year of age. Topical sirolimus and tacrolimus ointments have shown efficacy for superficial lesions, offering a way to avoid systemic drug exposure in selected patients. Surgical resection is reserved for cases where complete and safe excision is achievable, as the infiltrative nature of most KHE makes curative surgery impractical for the majority. Elective resection during active KMP is generally discouraged due to the risk of worsening coagulopathy and hemorrhage. Arterial embolization can serve as an adjunct in cases with extensive, unresectable lesions or refractory KMP, providing rapid reduction in tumor blood flow. Platelet transfusions should be avoided unless the patient is actively bleeding or being prepared for an invasive procedure. KHE significantly impairs health-related quality of life in affected children and their families. Both physical functioning — particularly in children with activity-limiting musculoskeletal complications — and psychosocial functioning are measurably reduced compared to healthy peers. KMP and activity dysfunction are the strongest risk factors for poor quality of life. Parents of children with KHE consistently report high levels of worry, emotional burden, and disruption to daily activities regardless of lesion location or parental education level. Complete tumor resolution is uncommon. Residual lesions after treatment often persist as vascular staining, telangiectasia, soft tissue fibrosis, or subcutaneous infiltrates. Long-term surveillance is warranted, as untreated residual KHE can continue to infiltrate surrounding tissue and cause progressive fibrosis and joint destruction over time. Early and accurate diagnosis, multidisciplinary management, and individualized treatment remain the cornerstones of improving outcomes in this challenging disease. References: 1- Ryu YJ, Choi YH, Cheon JE, Kim WS, Kim IO, Park JE, Kim YJ. Imaging findings of Kaposiform Hemangioendothelioma in children. Eur J Radiol. 86:198-205, 2017 2- Schmid I, Klenk AK, Sparber-Sauer M, Koscielniak E, Maxwell R, Häberle B. Kaposiform hemangioendothelioma in children: a benign vascular tumor with multiple treatment options. World J Pediatr. 14(4):322-329, 2018 3- Ji Y, Chen S, Li L, Yang K, Xia C, Li L, Yang G, Kong F, Lu G, Liu X. Kaposiform hemangioendothelioma without cutaneous involvement. J Cancer Res Clin Oncol. 144(12):2475-2484, 2018 4- Dai S, Yang K, Qiu T, Zhou J, Zhang X, Chen S, Li L, Ji Y. Health-Related Quality of Life in Children With Kaposiform Hemangioendothelioma. Front Pediatr. 10:720611, 2022 5- Huo J, Chen S, Li J, Liu C. Retroperitoneal kaposiform hemangioendothelioma with kasabach-merritt phenomenon in children: A case report and review of the literature. Front Pediatr. 11:1138689, 2023 6- Zhou J, Lan Y, Qiu T, Zhang Z, Gong X, Zhang X, Yang C, Zhou Z, Zhang Y, Yang M, Fu J, He C, Peng Q, Hu F, Xia C, Kong F, Chen S, Ji Y. Efficacy and safety of high-vs low-dose sirolimus in patients with kaposiform hemangioendothelioma: A randomized clinical trial. J Am Acad Dermatol. 93(1):124-131, 2025 7- Zhou J, Ji Y. Kaposiform hemangioendothelioma. J Am Acad Dermatol. 12:S0190-9622(26)00396-8, 2026

Accessory Breast Tissue

Accessory breast tissue, also termed ectopic or supernumerary breast tissue, refers to mammary tissue located anywhere on the body outside its normal position on the anterior thoracic wall. It is a congenital anomaly that originates during embryonic development. Around the sixth week of gestation, paired mammary ridges, commonly called the "milk lines," appear bilaterally on the ventral surface of the embryo and extend from the axilla to the inguinal and vulvar region. Under normal circumstances these ridges regress almost entirely, leaving only a single pair of buds in the pectoral region that go on to form the adult breasts. When regression fails or is incomplete at any point along this line, residual mammary elements persist and may later develop into accessory breast tissue. Because this represents the reappearance of a structure typical of more primitive mammals, in which multiple paired glands run the length of the trunk, the condition is regarded as atavistic, a reversion to an ancestral pattern. Although the milk line is the usual site, ectopic mammary elements have occasionally been described well beyond it, including the neck, back, face, thigh, and even the sole of the foot. The spectrum of accessory mammary tissue is conventionally described by a classification scheme dating from 1915 that divides it into eight categories according to which components, glandular tissue, nipple, and areola, are present. The most complete form contains all three elements and constitutes a fully formed supernumerary breast. Subsequent categories describe progressively incomplete combinations: glandular tissue with a nipple but no areola; glandular tissue with an areola but no nipple; glandular tissue alone, sometimes called mamma aberrata; a nipple and areola without underlying glandular tissue, known as pseudomamma; a nipple only, which is the classic supernumerary nipple or polythelia; an areola only, termed polythelia areolaris; and finally a patch of hair only, polythelia pilosa. In everyday practice two broad terms dominate: polythelia, denoting supernumerary nipples generally without associated breast tissue, and polymastia, denoting accessory glandular tissue with or without a nipple. The distinction is clinically meaningful because the presence or absence of true glandular tissue determines whether the lesion can undergo the same physiological and pathological changes as a normal breast. Reported prevalence varies considerably depending on the population studied and the definitions used, ranging broadly from about 0.22% to 6% of the general population. Polythelia tends to fall within the lower portion of that range, while accessory glandular tissue is reported in roughly 0.4% to 6% of women and 1% to 3% of men. Geographic and ethnic differences exist, with higher frequencies described among Asian and Japanese women and lower frequencies among those of Caucasian background. Supernumerary nipples have historically been described as somewhat more common in males, yet among patients who actually present for clinical evaluation or excision, the great majority are female and often young, likely because women more frequently seek correction for cosmetic or symptomatic reasons. Lesions are usually solitary and unilateral, though bilateral and multiple lesions occur; when unilateral, a slight predilection for the right side has traditionally been noted, although this is not invariable. By anatomical site, the axilla is by far the most common location for ectopic breast tissue, followed by other regions of the chest, the inframammary fold, and the abdomen. The condition is most often sporadic, but familial clustering is well recognized, including instances of male-to-male transmission. The proposed inheritance patterns are heterogeneous, encompassing autosomal dominant transmission with incomplete penetrance, X-linked dominant, and autosomal recessive modes, and somatic mutations arising early in embryonic life may also contribute. Accessory mammary tissue has been linked to congenital anomalies, most consistently of the renal and urinary tract, and less frequently to cardiovascular malformations, kidney tumors, and chromosomal conditions such as trisomy 21. These associations, however, are inconsistent, and large cohorts composed mainly of adults frequently identify no accompanying congenital anomaly at all. Because most congenital anomalies are detected in early childhood, the apparent rarity of associations in adult series may partly reflect the age at which patients present. Ultrasonographic screening of the kidneys and abdomen is sometimes recommended as part of diagnostic follow-up, particularly in younger patients. Clinically, accessory breast tissue is frequently asymptomatic and may be noticed only as a cosmetic concern or a cutaneous protuberance, often slightly more pigmented than surrounding skin. When functional glandular tissue is present, it responds to the same hormonal stimuli as orthotopic breast tissue, so the lesion may enlarge and become symptomatic at puberty, during pregnancy, or while breastfeeding. Forms consisting of glandular tissue alone, lacking an external nipple or areola, are especially prone to going unrecognized until hormonal stimulation makes them apparent. The characteristic complaint is a soft axillary mass, commonly a few centimeters in size, accompanied by cyclic pain coinciding with menstruation, swelling, tenderness, and fluctuation in volume. Larger lesions may restrict shoulder movement or cause irritation against clothing, and the cosmetic appearance often provokes anxiety. In children and adolescents the diagnosis is uncommon and may be delayed, yet it can occur even before menarche, and a tender, periodically enlarging axillary mass in this age group should raise suspicion. The differential diagnosis is broad and accounts for frequent misidentification. Accessory breast tissue has been mistaken for lipoma, lymphadenopathy, hidradenitis suppurativa, sebaceous cyst, vascular malformation, neurofibroma, lymphoma, and metastatic disease, among others. Ultrasonography is the preferred first-line imaging modality, demonstrating hypoechoic, septate, glandular-appearing tissue analogous to normal breast, sometimes with duct ectasia. Bilateral imaging is advisable to detect contralateral involvement, which may be asynchronous. Mammography and magnetic resonance imaging serve as useful adjuncts when the diagnosis is uncertain or when malignancy or another neoplastic process must be excluded, and fine-needle aspiration or core-needle biopsy can provide definitive confirmation. Histologically, the tissue shows the architecture of normal breast, with mammary lobules and lactiferous ducts in the dermis, surrounding connective tissue stroma, and bundles of nipple-type smooth muscle, often in proximity to cutaneous adnexal glands. Because it is genuine mammary tissue, the ectopic gland is susceptible to the full range of benign and malignant breast disease. Reported benign processes include fibroadenoma, fibrocystic change, ductal hyperplasia, duct ectasia, lactating adenoma, and intraductal or intracystic papilloma, the last being distinctly uncommon in this setting. Malignant transformation, while rare, is documented and includes ductal carcinoma in situ and invasive carcinoma. Importantly, tumors arise within glandular tissue rather than from a supernumerary nipple in isolation; when malignancy or significant proliferative disease is found in association with a supernumerary nipple, it typically reflects underlying accessory glandular tissue. This underscores the principle that wherever ectopic mammary tissue is identified, the possibility of accompanying breast pathology should be considered. Management is largely conservative. Surgical excision is reserved for symptomatic lesions, persistent cosmetic concern, diagnostic uncertainty, or suspicion of neoplasm, and prophylactic removal is not currently recommended. Excision through a small incision placed within a natural axillary fold is generally safe and effective, with liposuction reserved for larger lesions; reported complications include hematoma, seroma, infection, residual tissue, contour irregularity, and hypertrophic scarring. Operating before pregnancy is often favored because reoperation rates are lower and patient satisfaction higher. Overall, accessory breast tissue is a benign, usually innocuous condition whose chief clinical importance lies in correct recognition, distinction from other masses, and awareness of its capacity to develop the same diseases as a normally situated breast. References: 1- De la Torre M, Lorca-García C, de Tomás E, Berenguer B. Axillary ectopic breast tissue in the adolescent. Pediatr Surg Int. 38(10):1445-1451, 2022 2- El Malih S, Ezzahi M, Haloua M, Tahiri L, Akammar A, El Bouardi N, Alami B, Alaoui Lamrani MY, Maaroufi M, Boubbou M. Unusual intracystic papilloma arising from ectopic axillary breast tissue: Case report. Radiol Case Rep. 18(10):3414-3420, 2023 3- Class MM, McCoy K, Melin AA, Hafeez F, Abidi N, Krakowski AC. Bilateral accessory axillary breast tissue in a premenarchal female. Pediatr Dermatol. 41(4):704-706, 2024 4- Al Assaad M, Vulcain DR, Phan A, Boyraz B, Hoda SA. Polythelia (Supernumerary Nipple): Clinicopathological Characterization of an Atavistic Lesion. Int J Surg Pathol. 2025 33(8):1735-1741, 2025 5- Sag S, Sonmez Y, Gungormez EK, Canbaz FA, Gercel G, Yavuzer D, Yasar E, Thomas DT. Pediatric Breast Pathologies: 5-Year Experience and Proposal for a Risk-Based Management Algorithm. J Pediatr Adolesc Gynecol. S1083-3188(26)00309-8, 2026

Endoscopic Functional Luminal Imaging Probe

For most of the history of gastroenterology, the esophagus has been judged by what the eye could see and what a swallow could tell. An endoscope reveals the mucosa; a barium column traces the path of liquid downward; a manometry catheter records the pressures that ripple along the muscular tube as a patient swallows on cue. Each of these tools answers a real question, yet each leaves a gap. None of them measures directly how the esophagus behaves as a mechanical object—how readily its walls yield to stretch, how wide its narrowest point will open under load, how the muscle answers when the lumen is filled rather than when a bolus is swallowed. The functional luminal imaging probe, almost always abbreviated to FLIP, was built to close that gap, and over the past decade it has moved from a research curiosity into a working clinical instrument, including, more recently, in children. The principle behind FLIP is elegant in its simplicity. A catheter carrying a cylindrical balloon is passed transorally and positioned across a region of interest, most often the esophagogastric junction. Inside the balloon sit sixteen impedance-planimetry sensors that measure the electrical voltage between neighboring electrodes as the balloon is filled with a conductive fluid. From those readings the system reconstructs cross-sectional area at multiple points along the balloon and pairing that geometry with a built-in pressure sensor yields the central number of the field: the distensibility index, or DI, calculated as the minimal cross-sectional area divided by the intraballoon pressure at a set fill volume. Two versions of the device exist. EndoFLIP uses a soft balloon for measurement alone, while EsoFLIP carries a stiffer balloon that can dilate a narrowing while reporting diameter changes in real time. The technology is performed during sedated endoscopy, which is part of its appeal—it can be done in the same sitting as the diagnostic exam, without the awake catheter placement that manometry requires. What FLIP can do has expanded well beyond a single measurement. Carlson and colleagues, working from a cohort of more than seven hundred subjects studied alongside high-resolution manometry, showed that the device could be used not just to gauge junction opening but to classify esophageal motility itself. Their approach, FLIP Panometry, watches how the esophageal body contracts in response to sustained distension—an assessment of secondary peristalsis that ordinary manometry, focused on swallow-triggered primary peristalsis, simply does not capture. By combining a contractile-response pattern with a junction-opening category, they built a classification that paralleled the Chicago Classification used for manometry. Patients with normal junction opening and a normal contractile response almost always had normal motility or ineffective motility on manometry, while those with reduced opening and a weak contractile response overwhelmingly carried a disorder of junction outflow, most often achalasia. The message was not that FLIP should replace manometry, but that the two tests illuminate different facets of esophageal function and can confirm, complement, or clarify one another, particularly when an initial manometric impression is inconclusive. The pediatric story is younger and, in some ways, more revealing. EndoFLIP was cleared in the United States in 2019 for the esophagus, pylorus, and anal sphincters in children five years and older, and off-label use has reached infants as young as ten months. Yet the central difficulty in children is the absence of normative data. Benitez and colleagues studied one of the largest pediatric achalasia cohorts reported, measuring junction distensibility before and immediately after balloon dilation and comparing the results to non-achalasia controls. Treatment-naive children had markedly lower distensibility and smaller junction diameters than controls, and dilation produced a clear, immediate rise in DI together with improved symptom scores. But the findings also carried a caution: only half of treatment-naive children fell below the adult diagnostic threshold of 2.0 mm² per mmHg, meaning that adult cutoffs, applied uncritically, could misclassify a substantial fraction of symptomatic children. Pediatric esophagi are not simply smaller adult esophagi, and the reference ranges borrowed from adults may flatter or mislead. Two recent reports show how far the pediatric application now reaches beyond achalasia. In eosinophilic esophagitis, where chronic inflammation can quietly remodel the esophageal wall into fibrosis and stricture, Berson and colleagues found that FLIP detected reduced distensibility even in children who were in clinical and histologic remission. Their cohort's average DI sat below the threshold often used to mark abnormal rigidity, and the histologic eosinophil count did not track with the distensibility number—an argument that biopsy and symptom assessment alone can miss residual mechanical disease that FLIP picks up. In a different vein, Hoskins and colleagues turned the probe toward vascular compression of the esophagus, the kind produced by an aberrant subclavian artery or a vascular ring. There, FLIP detected narrowing more often than endoscopy did, sometimes flagging functional restriction in a normal-looking esophagus, and just as usefully, it helped exclude meaningful obstruction in children whose symptoms turned out to stem from reflux or inflammation rather than the vessel. Paired measurements at the compression site and the lower sphincter showed convincingly reduced diameter and distensibility where the vessel pressed. None of these papers oversells the device. Each returns to the same chorus of limitations: no standardized pediatric protocol, no validated reference values indexed to age and size, balloon and catheter constraints in the smallest patients, cost, and the concentration of expertise in a handful of centers. FLIP does not diagnose by itself; it is described, repeatedly, as a complementary or adjunctive tool, most powerful when its real-time, objective numbers are read alongside endoscopy, imaging, and manometry. Still, the trajectory is clear. A technology that lets a clinician feel the esophagus quantitatively, at the moment of endoscopy, is filling a space the older tools left empty—and as pediatric normative data accumulate, that quiet rise seems likely to continue. References: 1- Benitez AJ, Budhu S, Burger C, Turco R, Ballester L, Shah A, Lynch K, Fiorino K, Menard-Katcher C, Muir AB, Mamula P. Use of the functional luminal imaging probe in pediatrics: A comparison study of patients with achalasia before and after endoscopic dilation and non-achalasia controls. Neurogastroenterol Motil. 33(12):e14133, 2021 2- Krasaelap A, Lerner DG. Advances in Endoscopic Procedures in Pediatric Patients. Pediatr Clin North Am. 68(6):1221-1235, 2021 3- Carlson DA, Gyawali CP, Khan A, Yadlapati R, Chen J, Chokshi RV, Clarke JO, Garza JM, Jain AS, Katz P, Konda V, Lynch K, Schnoll-Sussman FH, Spechler SJ, Vela MF, Prescott JE, Baumann AJ, Donnan EN, Kou W, Kahrilas PJ, Pandolfino JE. Classifying Esophageal Motility by FLIP Panometry: A Study of 722 Subjects With Manometry. Am J Gastroenterol. 116(12):2357-2366, 2021 4- Lerner DG, Mencin A, Novak I, Huang C, Ng K, Lirio RA, Khlevner J, Utterson EC, Harris BR, Pitman RT, Mir S, Gugig R, Walsh CM, Fishman D. Advances in Pediatric Diagnostic Endoscopy: A State-of-the-Art Review. JPGN Rep. 3(3):e224, 2022 5- Berson J, Kota A, Levine J. Endoluminal functional lumen imaging probe: a new modality in the evaluation of esophageal disorders in children and preliminary use in eosinophilic esophagitis. Front Pediatr. 13:1581225, 2025 6- Hoskins BJ, Bose P, Pitman RT. Pediatric vascular compression of the esophagus: Endoluminal functional lumen imaging probe as a complement to imaging and endoscopy. JPGN Rep. 7(2):192-199, 2026

 

Submit!

We are inviting all of you to submit contribution of your own to the newsletter. Credit will be given to the authors keeping his or her name, institution and E-mail address on their work. A list of contributors will appear in the internet homepage. All works should be send to Dr. H. Lugo-Vicente to the e-mail: pediatricsurgerypr@gmail.com