pyloric stenosis in adults

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Treatment of Pyloric Stenosis in AdultsWarning: The NCBI website requires JavaScript to operate. Idiopathic stenosis of adult pyloric - a common presentation with uncommon diagnosis Syed Moin HassanaInternal Medicine Residency, Oak Hill Hospital, Brooksville, FL, USAAteeq MubarikbInternal Medicine Resident, Oak Hill Hospital, Brooksville, FL, USASalman MuddassirbInternal Medicine Resident, Oak Hill Hospital, Brooksville, FLCT West Methods and results: The patient presented acute abdominal pain at the top of the start associated with nausea, vomiting, black tar feces of scent and anorexia. In the Esophagogastroduodenoscopia (EGD), the pylorus showed a single "cervix sign". The patient had multiple endoscopic dilations with minimal relief. He then suffered a partial gastronomy distal with a Billroth 1 gastroduodenostomy with a considerable improvement in his symptoms in follow-up. Conclusion: Adult idiopathic hypertrophic pediatric stenosis (AIHPS) is a rare disease that is also reported due to a difficulty in diagnosis. The most common symptoms of AIHPS are post-prandial nausea, vomiting, early blood and epigastric pain as seen in our patient. Does endoscopy usually show? Cervix? a unique sign that shows a fixed, markedly narrow, pylore with a smooth border. Multiple treatments have been proposed for AIHPS, including endoscopic dilation, pyloromyotomy with or without pyloroplasty, gastrectomy with a Billroth 1 gastroduodenostomy or without pyloroplasty. Currently, there is no evidence that a surgical technique is superior to another. Further research on AIHPS is required before a technique can be standardized as the standard of care.1. Introduction Hypertrophic hypertrophic idiopathic stenosis (HPS) is a rare but well-defined entity in adults with only 200–300 cases reported so far in literature [–]. AIHPS pathological anatomy was first described in 1842 [], and Maier et al. later confirmed it as a specific disease in 1885 []. We report a case to highlight this disease difficult to diagnose but potentially curable.2. Case presentation Caucasian woman of 50 years with medical history of past hypertension entered the emergency department with the main complaint of abdominal pain. He reported severe upper left upper abdominal pain that began two weeks ago, progressively worsened, rated a 10/10 in intensity, not irritating and described as acute, burning and stabbing. He was associated with nausea, vomiting, black tar stools that swell, and anorexia. She reported chronic abdominal pain, vomiting and diarrhea since she was 13. He saw 6-8 doctors a month in his youth, with most doctors ascribed their symptoms to a sensitive stomach or food poisoning. His first esophagogastroduodenoscopia (EGD) in 2013 showed a hiatal hernia. In April 2017 an EGD repetition was performed, which, according to the patient, was not conclusive in the clarification of a cause of his symptoms. In the current admission, a study of gastric emptied was performed, which showed delayed gastric emptied. The pelvis of the CT abdomen showed thickening of the distal gastric antrum (). In the later EGD, 300 ml of residual oatmeal was appreciated in the stomach, and the pylore showed a 'sign of the neck'. A stenotic pylore was found, dilated at 15 mm (, ). At this time, our main differential diagnosis included AIHPS, peptic ulcer disease, malignant and gastrointestinal estromal tumors (GISTs). The definitive diagnosis can only be done in the final report of pathology. The patient was discharged and had multiple endoscopic dilations during the coming months with minimal relief in the symptoms. After discussing with gastroenterology, general surgery and the patient who wanted a more permanent treatment for their underlying condition, a distal partial gastronomy was subjected to a Billroth 1 gastroduodenostomy. The pathology was significant for the clinically hyperplastic gastric musculature. There was no evidence of superficial gastric metaplasia or increase of polymorphonuclear leukocytes (). After the pathology report, the patient was diagnosed with AIHPS as any evidence of malignancy or GISTs had been discarded. Postoperatively, the patient had a gradual and slow recovery, and in her follow-up visit of 3 months, she reported a considerable improvement in her symptoms. TC abdomen pelvis that shows the thickening of the distal gastric antrum (yellow arrow). Full color available online. Portable endoscopy (a) 300 ml of residual oatmeal (b) " (c) Pylorus showing "cervix signal" d) Serial Balloon Dilator inserted into the small pylore opening. Endoscopy showing (a) Serial Balloon Dilator by expanding in series the stenotic pyloric opening from 12 mm to 15 mm with a bloody response; (b) in the retreat after dilation is seen a defect of division of at least 5 mm. Cross section of the pylorus that shows (a) greater thickness of the pylorus muscle, (b) focally hyperplastic gastric musculature propria (c) magnification 10× and layer of hyperplastic musculature reaching up to lamina propria.3. Discussion Hypertrophic idiopathic stenosis (HPS) is a rare disease that is not reported due to a difficulty in diagnosis. This challenge in the diagnosis is evident by our patient, who consulted several doctors and subjected to procedures over the years before the diagnosis of AIHPS was made. AIHPS is most commonly reported in middle-aged men while our case was a middle-aged woman [,]. Hypertrophic Pyloric stenosis (HPS) has been classified in several ways by several authors. The most universally accepted classifications are by Danikas et al. and Zarineh et al. Danikas et al. HPS divided into three types: Type 1, which is childhood HPS diagnosed in a late stage; Type 2, which is the most common type, and which occurs during adult life and is likely secondary to underlying pathologies of GI, such as peptic ulcer disease, malignity, and certain inflammatory diseases; and Type 3, which is adult initiation idiopathic HPS []. Zarineh et al. divided HPS in primary, which has no underlying cause and under which AIHPS would be classified, and secondary, caused by an underlying disorder such as excessive healing of gastric or duodal ulcers, malignancy, GISTs, postoperative intraabdominal adhesions, bezoars, and greater vague activity that causes pylore hypertrophy []. The secondary type of HPS has no or mild hypertrophy of the hair muscle compared to the primary type. The exact etiology of AIHPS is unclear, with genetic and environmental factors involved. Most researchers believe that it is the persistence of the mild form of HPS [–], which is further reinforced by the fact that both childhood IHPS and adult have similar histological and anatomical changes []. However, it is still unclear as to the reason for the prolonged asymptomatic period up to the age of 30 to 60 years. Some researchers postulate edema, spasm, or inflammation triggers piloric occlusion in a predisposed individual []. Other possible etiologies include prolonged pylorospasm, vague hyperactivity, and changes in the Auerbach plexus. Our patient has had multiple symptoms since she was 13 years old, which gives credibility to this theory. The most common symptoms of AIHPS are post-prandial nausea, vomiting, early blood and epigastric pain as seen in our patient. An abdominal mass rarely feels compared to the juvenile form of HPS []. The differential diagnosis includes malignant and diabetic gastroparesis, both of which can occur similarly to AIHPS. In pathology, GISTs can be difficult to differentiate from AIHPS []. The diagnosis of AIHPS in the image is difficult, as some cases may have completely normal studies without pathogenic signs []. "The sign of Kirklin" or "shower" describes the protrusion of the piloric muscle in the duodenal layer in the upper GI series. This sign has been widely studied in the juvenile HSH and it has been found to occur in 50% of pediatric patients [], but its frequency is not clear in the HPS. The sign can also be caused by manual pressure on the stomach [–]. Abdominal CT scan shows non-specific gastric wall thickening in some cases, as seen in our patient. However, it is mainly used to rule out the secondary causes of HPS including malignancy. Endoscopy usually shows a unique sign of cervix, which is a fixed pylore, markedly narrowed with a smooth border, and which persists after anticolinergic therapy. You can differentiate from pylorospasm when the pressure is applied through the endoscope. The cervix sign was present in our patient and was the main clue that helped us diagnose AIHPS [,]. So far, no studies have been conducted that describe the sensitivity and specificity of any radiological test or endoscopy findings in the diagnosis of AIHPS. The diagnosis of AIHPS is based on a high rate of clinical suspicion and suggestive radiological and endoscopic signs with the definitive diagnosis of the pathologist. The pathology shows a thick, elongated pylorus. In the microscopy, there is marked hypertrophy and hyperplasia of the gastric muscle propria without marked inflammatory cells or seen malignancy []. Multiple treatments have been proposed for AIHPS, including endoscopic dilation, pyloromyotomy with or without pyloroplasty, gastrectomy with a Billroth 1 gastroduodenostomy or without pyloroplasty. Laparoscopic pyloroplasty is a less invasive option. Endoscopic dilation has a high rate of recurrence and provides only temporary relief of symptoms. It is an option in high-risk surgical patients. Currently, there is no evidence that a surgical technique is superior to another. Further research on AIHPS is justified before a method such as the standard of care can be finalized [,]. Statement of disclosure This research was supported (in whole or in part) by HCA and/or an affiliate of HCA. The views expressed in this publication represent those of the author or authors and do not necessarily represent the official opinions of HCA or any of its affiliates. ReferencesFormats: Share , 8600 Rockville Pike, Bethesda MD, 20894 USA

Pathology Research International On this pageCase Silent Report Open AccessAlireza Zarineh, Marino E. Leon, Reda S. Saad, Jan F. Silverman, "Hyrophic idiopathic pilric stenosis in an adult, a possible gastric carcinoma mimic", Pathology Research International, vol. 2010, Article ID 614280, 4 pages, 2010. https://doi.org/10.4061/2010/614280Idiopathic Hypertrophic pathology in an adult, a possible mymic of gastric carcinomaAlireza Zarineh1Department of Medical Pathology and Laboratory Medicine, Allegheny Hospital General/Drexel University College of Medicine, 320 East North Avenue, Pittsburgh, 71 PA 15212, USA2 Images studies showed gastric distention with air fluid levels and without evidence of extrinsic compression. In the upper endoscopy, massive gastric distention and no evidence of any ulcer or other mucous defects was observed. Microscopically, hypertrophy marked muscle mucosa with smooth muscle cells arranged in waxes and fascicles was present that gradually transferred to normal areas. Muscle fibers stained with smooth muscle actin and triroma stain highlighted the fibrosis between muscle fibers. Although rare, IHPM can clinically and histologically imitate other proliferations in the gastric wall, such as gastrointestinal stroma tumor or spinal cell neoplasm. Recent progress in understanding the pathogenesis of IHPM is discussed.1. IntroductionPrimitive or idiopathic hypertrophy of the piloric muscle (IHPM) in adults is a relatively rare but well established entity [, ]. The incidence of congenital hypertrophic piloric stenosis is reported between 0.25% and 0.5% of all live births in literature [, ]. The adult variant, however, is even more rare with less than 200 cases reported in English literature []. Although it is not clear what causes this condition, theories have been proposed such as the persistence of a slight manifestation of a juvenile form in adulthood [, ]. IHPM seems to be much more common in middle-aged men [, ].Let's report a case in an older man without previous history of gastrointestinal symptoms and no apparent precipitant factor.2. Report a Case A 71-year-old Caucasian man had been experiencing abdominal strain, nausea and vomiting for three months. His symptoms gradually worsened during the previous two weeks when he was referred to our institution for further evaluation. Abdominal damping and vomiting seemed to be mostly postprandial, and vomiting consisted mainly of non-digested and non-bile foods. Their symptoms were independent of the type and consistency of the type of food ingested. His past medical history was significant for cardiovascular disease, end-stage kidney disease and diabetes mellitus without history of gastrointestinal problems. Abdominal films obtained prior to admission showed massive gastric distention. The physical examination revealed a mild and slightly neglected abdomen. No tenderness, mass and/or hernia was discovered. The rest of the test was not noticeable except for his dialysis fistula in the upper right extremity. He was admitted with diagnosis of gástric outlet obstruction. Abdominal films after admission demonstrated once again gastric disstraint with air fluid levels. A computed tomography showed no evidence of extrinsic compression. A higher endoscopy (EGD) demonstrated a massive gastric strain with a large collection of partially digested foods. There was no evidence of an ulcer or other mucous defect in the piloric canal, but the canal did not seem to relax and dilate (Figure ). The endoscope passed the channel with light resistance, which was interpreted as pyloric stenosis. The duodenum was not remarkable. The patient did not improve, and surgery was recommended. An enormously dilated stomach was found in the exploratory laparotomy. During this procedure, a minigastrotomy was performed on the largest curvature of the stomach, and more than 3 litres of gastric content of bad odour particle matter, consisting of long-standing food retention, were eliminated. The origin of this retention seemed to be due to pyloric stenosis with an associated thick gastric wall. A Roux-en-Y gastrojejunostomy anthretomy was performed, and a Witzel feeding jejunostomy tube was placed.3. The specimen consisted of a segment of stomach, antrum and pylore of cm. The wall of the stomach thickened evenly on the proximal part of the specimen involving the entire circumference of the gastric wall. A very prominent gastric fold of 1,5 cm thick and situated at 1 cm of the distal margin was observed in the pylorus. There were focal areas of congestion in the mucosa, but there were no masses or ulcers. Microscopically, hypertrophy of the musculature was observed marked with smooth muscle cells arranged in the rods and fascicles in the pylore, while the remaining stomach also showed a thick musculature propria (Figures and ). The transition between thick and normal areas was gradual. The maximum thickness of the hair muscle measured at 1.3 cm. There were also focal changes in mucosa consisting of reactive gastropathy (chemical) and a single hyperplastic polyp was present. Lymphoid aggregates consisting of mild chronic gastritis were present in gastric mucosa. There was no evidence of diabetic gastropathy, including hydrographic neuron degeneration, vasculopathy or smooth muscle degeneration. The immunohistochemical stain for smooth muscle actin (near 1A4, Dako cytomation, Carpenteria, CA; ) confirmed the thick layer of smooth muscle (Figure ). Triroma stain showed the presence of fibrosis between muscle fibers.4. Discussion The adult IHPM has been described above in the literature [–]. Patients with adult hypertrophic pilric stenosis tend to have a history of epigastric pain or vomiting with occasional relief after vomiting []. The radiology test can be normal in many cases [, ], and endoscopy is often needed to make the diagnosis of IHPS and exclude other causes. Schuster defined a unique endoscopic sign called the "neck sign" to describe the narrowing of the pylore []. This sign is consistent and persists after anticholinergic therapy, and the pressure by the endoscope differentiates it from the much more common pylorospasm []. The microscopic examination shows a marked hypertrophy of hairy muscles that may be associated with reactive mucous gastropathy. However, no other significant pathological process, such as inflammation or neoplasia, should be seen in the propria musculature. The transition of the hypertrophy section is generally gradual from normal areas [, ]. The presence of fibrosis in addition to smooth muscle hypertrophy can often be present, as was observed in our case. The exact etiology of adult IHPM is unclear. The most accepted etiological classification includes a primary type without apparent underlying disease and a secondary type. The secondary type may have many causes including exuberant healing of a previous gastric or duodenal ulcer, carcinoma, gastrointestinal stroma tumor, extrinsic postoperative adhesions, bezoars and vague hyperactivity leading to muscle hypertrophy [, , , , ]. The secondary type usually shows a predominantly fibrous tissue-located replacement with hyperphyll. Other rare causes reported are post-inflammatory complication in Crohn's disease [] and mucosal diaphragm []. The ulcer of stress in pyloro has been proposed as the cause of hypertrophic childhood pilric stenosis [], although it does not seem to have a role in adult form. The only explanation proposed for the primary type is the persistence of the youth form that later presents in adult life [, , ]. However, given the early age of 30 to 60 years [], it is not clear why most patients remain asymptomatic until the middle age, although it is speculated that the condition may be aggravated by another gastric pathology []. Finally, as with a child form, a family trend of occurrence for adults with hypertrophic piloric stenosis has been documented, and both forms can occur in the same family. However, some cases seem to arise from novo at a more advanced age []. The differential diagnosis includes the most common neoplastic processes and diabetic gastropathy both can have the similar clinical presentation. While recognizing carcinoma is often direct, spine cell neoplasms such as gastrointestinal stroma tumor may be more difficult to differentiate from IHPMs. Diabetic gastropathy shows the characteristic hydrographic degeneration with severe reduction in the density of unparalleled axons, vasculopathy with the thickening of the walls of the vessel, and smooth muscle degeneration and fibrosis, with eosinophilic inclusion bodies (M-bodies) that appear to be unique in this condition. The preferred treatment is gastric resection surgery and Billroth I anastomosis, as was done in our patient. Although pyloroplasty and vagotomy have also been performed with successful results [], recurrence has been reported with this [] approach. We present this relatively unusual presentation of gastric outlet obstruction to raise awareness of the existence of this lesion and not to confuse histological findings with other proliferations in the gastric wall as a gastrointestinal entromal tumor or other spinal cell neoplasms. Attention to clinical and histological characteristics should allow for correct interpretation and prevent misinterpretation of a neoplasia, especially at the time of the frozen section. ReferencesCopyrightCopyright © 2010 Alireza Zarineh et al. This is an open access article distributed under the , which allows unrestricted use, distribution and reproduction in any medium, provided that the original work is duly cited. More related articles Share Related articles

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