All newly detected solitary gastric polyps should be resected at the time of index endoscopy to achieve both diagnostic and therapeutic goals

For polyps exceeding 20 mm, referral to an endoscopist with experience in advanced resection techniques is advised

Surveillance Recommendations for Gastric Polyps

Surveillance plans should be formulated based on the histopathological type of the polyps and surrounding gastric mucosa: [1]

Fundic gland polyps (FGPs): Non-syndromic FGPs without dysplasia do not require surveillance endoscopy. However, watchful follow-up is advised for syndromic patients with dysplastic FGPs, large polyps (>10 mm), or mucosal carpeting by polyps. [1] Hyperplastic polyps: Endoscopic resection is advised for large polyps (>10 mm). If dysplasia is noted on biopsy, periodic (yearly) surveillance is advised. Helicobacter pylori eradication can lead to regression of hyperplastic polyps. [1] Gastric adenomas: After complete resection, follow-up surveillance endoscopy should be completed at 1 year for low-grade dysplasia and 6 months for high-grade dysplasia. If the polyp is biopsied or resection is incomplete, follow-up endoscopy is advised within 3 months for high-grade dysplasia and 6 months for low-grade dysplasia. Subsequent annual follow-up is recommended to monitor for malignant changes. [1] Surrounding mucosa: Endoscopic surveillance is advised when histopathology of adjacent mucosa confirms gastric intestinal metaplasia (GIM) and/or atrophic gastritis. Biopsies from the gastric antrum and corpus should be obtained at minimum

The majority are fundic gland polyps or hyperplastic polyps, which usually are small, single or multiple. Fundic gland polyps have no malignant potential and do not usually require removal or endoscopic surveillance

20) fundic gland polyps are found or concomitant duodenal adenomas are present, the possibility of familial polyposis should be considered. Large hyperplastic polyps (> 1.0 cm) should be removed at endoscopy as they may rarely cause chronic blood loss.

Adenomatous polyps account for 10–20% of gastric polyps. They are usually solitary lesions that usually arise in a background of chronic atrophic gastritis associated with H pylori infection, which should be treated

Submucosal gastric polypoid lesions include benign gastric stromal tumors (commonly misclassified as leiomyomas) and pancreatic rests

Hyperplastic polyps are associated with chronic gastritis and Helicobacter pylori infection. Fundic gland polyps are often multiple and associated with proton pump inhibitor use or familial adenomatous polyposis

Submucosal tumors present as polypoid lesions beneath intact mucosa and require differentiation from malignant entities:

Leiomyomas: Well-circumscribed, hypodense lesions commonly in the cardia; slow-growing tumors from smooth muscle cells [1-2] Lipomas: Well-circumscribed, low-attenuation lesions composed of adipose tissue with characteristic yellowish appearance on endoscopy [1][7] Schwannomas: Rare, well-defined tumors that may show progressive enhancement; more common in females and elderly patients (age 50-60 years) [1][3] Glomus tumors: Hypervascular solitary lesions typically in the antrum [1][7] Heterotopic pancreas: Developmental anomaly appearing as polypoid lesion, commonly in the antrum

For submucosal tumors, surface biopsy may be non-diagnostic as the overlying mucosa is typically intact. [5] Endoscopic ultrasound (EUS) is valuable for characterizing submucosal lesions, determining the layer of origin, assessing size, and differentiating benign from malignant features. EUS shows characteristic patterns: lipomas appear hyperechoic in the submucosa, while leiomyomas appear hypoechoic.

Specific CT features help differentiate tumor types

MRI may be used as an adjunct, particularly for characterizing larger lesions or when CT findings are equivocal.

Malignant transformation potential varies: adenomas are precancerous and require complete removal, while hyperplastic polyps have low malignant potential except when showing dysplasia

https://www.openevidence.com/ask/d2f05f86-65a4-4a21-8227-0b1054f92b14

Other esophagus motility disorders

Dysphagia for liquids as well as solids tends to be intermittent and nonprogressive. DY

Manometry is not routinely used for mild to moderate symptoms because the findings seldom influence medical management

Barium esophagography is useful to exclude mechanical obstruction and to evaluate esophageal motility

Upper endoscopy also is performed to exclude a mechanical obstruction (as a cause of dysphagia) and to look for evidence of erosive refl traders ux esophagitis (a common cause of chest pain) or eosinophilic esophagitis (confirmed by esophageal biopsy)

The most common cause of ascites is portal hypertension secondary to chronic liver disease, which accounts for over 80% of patients with ascites

injection drug use, a history of viral hepatitis or jaundice, and birth in an area endemic for hepatitis. A history of cancer or marked weight loss arouses suspicion of malignant ascites. Fevers may suggest

nonportal hypertensive ascites include infections (tuberculous peritonitis), intra-abdominal malignancy, inflammatory disorders of the peritoneum, and ductal disruptions (chylous, pancreatic, biliary

pericarditis. A large tender liver is characteristic of acute alcoholic hepatitis or Budd-Chiari syndrome (thrombosis of the hepatic veins). Large abdominal wall veins with cephalad flow suggest portal hypertension; inferiorly directed flow implies hepatic vein obstruction The physical examination is relatively insensitive for detecting ascitic fluid. In general, patients must have at least 1500 mL of fluid to be detected reliably by this method

A PMN count of > 250/mcL (0.25 × 109/L) (neutrocytic ascites) with a PMN percentage of > 75% of all white cells is highly suggestive of bacterial peritonitis, either spontaneous primary peritonitis or secondary peritonitis (due to an intra-abdominal source of infection, eg, a perforated viscus or appendicitis

complex interaction of increased visceral afferent sensitivity, gastric delayed emptying or impaired accommodation to food or psychosocial stressors. Or Peptic ulcer disease is present in 5–15% and GERD is present in up to 20% of patients with dyspepsia, even without significant heartburn

Multiple antibiotic classes are effective against both streptococci and staphylococci, with the optimal choice depending on whether methicillin-resistant Staphylococcus aureus (MRSA) is suspected and the severity of infection.

For methicillin-susceptible strains, beta-lactam antibiotics remain the mainstay of treatment. These include penicillinase-resistant penicillins (dicloxacillin, oxacillin, nafcillin), first-generation cephalosporins (cephalexin, cefazolin), and amoxicillin-clavulanate, all of which provide excellent coverage against both streptococci and methicillin-susceptible staphylococci (MSSA). [1-4]

Clindamycin is particularly valuable as it demonstrates activity against approximately 80% or more of community-associated MRSA strains while maintaining excellent activity against group A streptococcus, making it an attractive single-agent option for skin and soft tissue infections. [5] However, clindamycin resistance appears to be increasing. [5]

For MRSA coverage with dual activity, several options exist. Linezolid and tedizolid (oxazolidinones) have activity against both MRSA and streptococci. [2][6-7] Vancomycin provides coverage against both organisms and has been the traditional mainstay for MRSA infections. [2][7] When MRSA is suspected but streptococcal coverage is also needed, combination therapy with trimethoprim-sulfamethoxazole (TMP-SMX) plus a beta-lactam (such as cephalexin or penicillin) is recommended, as TMP-SMX alone has poorly defined activity against streptococci. [1][5]

Doxycycline and minocycycline are effective against most MRSA isolates but have less well-defined activity against group A streptococcus, so they may require combination with a beta-lactam when streptococcal infection cannot be excluded. [1][5]

Would you like me to provide specific dosing recommendations for any of these antibiotics or discuss treatment duration for particular infections?

1

cephalexin, dicloxacillin, penicillin VK, amoxicillin/clavulanate, or clindamycin (for penicillin-allergic patients). [1-2] These beta-lactam antibiotics provide excellent coverage against streptococci and methicillin-susceptible S. aureus (MSSA

endovascular stenting emerging as first-line therapy for rapid symptom relief, while definitive treatment targets the underlying cause

Brachial venography or radionuclide scanning following intravenous injection of technetium (Tc-99m) pertechnetate demonstrates a block to the flow of contrast material into the right heart and enlarged collateral veins. These techniques also allow estimation of blood flow around the occlusion as well as serial evaluation of the response to therapy.

Failure of venous insufficiency ulcerations to heal is most often due to inconsistent use of first-line treatment methods. Ongoing control of edema is essential to prevent recurrent ulceration; the use of compression stockings following ulcer healing is critical, with recurrence rates 2–20 times higher if compression stockings are not used

Primary varicose veins result from a complex multifactorial process involving genetic predisposition and environmental factors. The pathophysiology involves initial structural weakness within the vein wall leading to vein dilation, or valve incompetence causing blood pooling and subsequent vein dilation. [1][3] Risk factors include family history (autosomal dominant inheritance with variable penetrance), female sex, multiparity, pregnancy, prolonged standing, obesity, and advanced age. [2-3] If both parents have varicose veins, offspring have a 90% chance of developing them. [2]

Secondary varicose veins develop through a distinct mechanism involving inflammation, thrombosis, and recanalization that results in venous wall damage, dilation, and valve insufficiency. [3] The clinical picture manifests as post-thrombotic syndrome, which can include pain, edema, skin changes, and venous leg ulcers. [3] The 2020 CEAP classification further subdivides secondary causes into intravenous (Esi) and extravenous (Ese) etiologies. [4] Intravenous causes include any condition causing venous wall or valve damage from within the lumen, such as DVT, traumatic arteriovenous fistulas, or primary intravenous sarcoma. Extravenous causes involve conditions affecting venous hemodynamics without direct wall or valve damage, such as central venous hypertension from obesity or heart failure, extrinsic compression from tumors or retroperitoneal fibrosis, or muscle pump dysfunction from paraplegia or arthritis

Superficial thrombophlebitis related to a PICC may be associated with occult DVT in about 20% of cases, but occult DVT is much less commonly associated with spontaneous superficial thrombophlebitis of the saphenous vein (about 5% of cases). Pulmonary emboli are exceedingly rare and occur from an associated DVT

Anatomic contraindications: Aneurysmal dilation of the GSV near the saphenofemoral junction, extreme tortuosity precluding catheter delivery, subcutaneous location above the saphenous fascia, and active superficial thrombophlebitis with partial obstruction are relative contraindications to endovenous procedures

Venoactive drugs (diosmin, hesperidin, horse chestnut seed extract) may be considered as adjuncts to compression for symptomatic relief in countries where available

Endovenous ablation is contraindicated or relatively unsuitable when venous anatomy precludes catheter-based treatment, specifically: aneurysmal dilation of the GSV close to the saphenofemoral junction, subcutaneous location of truncal veins above the saphenous fascia and close to the skin, and significant tortuosity of the GSV or SSV. [1] In these scenarios, high ligation and stripping is recommended as the preferred alternative (grade 1 strong recommendation

Endovenous Thermal Ablation (RFA/EVLA)

Relative contraindications include inappropriate vein size, with veins <2 mm and >15 mm representing potential contraindications for RFA specifically. [1] A history of superficial thrombophlebitis resulting in a partially obstructed saphenous vein may preclude thermal ablation. [1] Significant tortuosity of the GSV on duplex examination can make catheter delivery difficult.

Endovenous ablation is the preferred treatment for symptomatic varicose veins with axial reflux, offering less postprocedure pain, reduced morbidity, and earlier return to activity

Endovenous thermal ablation (radiofrequency ablation [RFA] and endovenous laser ablation [EVLA]) has largely replaced surgery as the standard of care

Ultrasound-guided foam sclerotherapy (UGFS) represents a less invasive option but has higher recurrence rates

The risk of DVT or embolization is very low unless the thrombophlebitis extends into the great saphenous vein in the upper medial thigh

imaging of the deep venous system is obligatory to exclude a congenital malformation or atresia of the deep veins. Surgical treatment of varicose veins in these patients is contraindicated because the varicosities may play a significant role in venous drainage of the limb.

involved, typically the great saphenous vein and its tributaries, but the short saphenous vein (posterior lower leg) may also be affected

Aortic dissection typically presents acutely with sudden, severe tearing chest or back pain, often described as lancinating in quality. [5-6] Approximately 50% of patients with thoracic aortic aneurysm may progress to dissection without timely intervention. [5] In contrast, thoracic aortic aneurysm is usually asymptomatic and discovered incidentally during physical examination or imaging for other indications. [5]

Additional Risk Factors and Mortality Data

Preoperative cardiac evaluation is critical, as coronary artery disease significantly impacts outcomes. Patients with unstable CAD, left main stenosis, or 3-vessel disease generally warrant revascularization prior to or concomitant with thoracic aortic procedures. [2]

Preoperative renal dysfunction is the most important predictor of acute renal failure after thoracic aortic operations. Preoperative hydration and avoidance of hypotension, low cardiac output, and hypovolemia in the perioperative period may reduce this complication. [2]

Chronic pulmonary disease and smoking history are important predictors of postoperative respiratory complications. Pulmonary function tests and arterial blood gas analyses help risk-stratify these patients. Smoking cessation is advisable preoperatively

Absolute size thresholds for degenerative aneurysms: [1][3][5]

Ascending aorta/aortic root: ≥5.5 cm

Descending thoracic aorta: ≥6.0 cm (or 5.5 cm if favorable anatomy for TEVAR)

Thoracoabdominal aorta: ≥6.0 cm

Lower thresholds apply for: [3]

Marfan syndrome or genetic conditions: 4.0-5.0 cm depending on condition

Bicuspid aortic valve: 5.0-5.5 cm

Rapid growth: >0.5 cm/year

Concomitant cardiac surgery: >4.5 cm if undergoing aortic valve surgery

Immediate surgical evaluation: [5]

Any symptomatic aneurysm regardless of size (chest/back pain, dysphagia, hoarseness, hemoptysis)

Acute complications (dissection, rupture, malperfusion)

Post-Repair Surveillance

After TEVAR: CT at 1 month, 12 months, then annually if stable. [1]

After open repair: CT or MRI within 1 year, then every 5 years if no residual aortopathy. Annual imaging if residual disease or abnormal findings.

Selection

Initial Assessment: Transthoracic echocardiography (TTE) is recommended at diagnosis to assess aortic valve anatomy, valve function, and thoracic aortic diameters. CT or MRI is reasonable for comprehensive anatomic assessment. [1]

Surveillance Imaging: The choice depends on aneurysm location: [2]

Aortic root/proximal ascending aorta: TTE can be used if measurements correlate well with CT/MRI

Mid-ascending, arch, or descending thoracic aorta: CT or MRI is recommended

MRI is preferred for long-term surveillance to avoid cumulative radiation exposure from serial CT scans [1][3]

Surveillance Intervals

Size-Based Recommendations: [2-4]

<4.0 cm: Every 2-3 years if stable

4.0-4.4 cm: Every 2 years

4.5-4.9 cm: Annually

5.0-5.4 cm: Every 6-12 months (consider optimization for repair)

≥5.5 cm: Surgical evaluation indicated

Initial surveillance: Obtain follow-up imaging at 6-12 months after diagnosis to establish the growth rate. If stable, adjust interval based on size. [1]

Growth rate considerations: Descending thoracic aneurysms grow faster than ascending aneurysms (mean 2.76 mm/year vs 1 mm/year overall). Growth accelerates exponentially above 4.5 cm diameter. [3-4]

Earlier intervention is reasonable when high-risk features are present, including rapid growth (≥0.5 cm/year), symptomatic aneurysm, saccular morphology, or penetrating atherosclerotic ulcers

elective surgical repair is suggested at 5.5 cm in patients without underlying connective tissue disorders, with earlier intervention at 4.5-5.0 cm in patients with connective tissue disorders or bicuspid aortic valve

Descending thoracic aortic aneurysm should be referred to a vascular specialist when they reach 5 cm for observation and assessment and considered for repair at 5.5 cm

Generally, degenerative aneurysms of the thoracic aorta will enlarge (on average 0.1 cm/year) and require repair to prevent death from rupture. Endovascular repair of saccular aneurysms, particularly those distal to the left subclavian artery and the descending thoracic aorta, have good results

Descending thoracic aneurysms measuring 5.5 cm or larger should be considered for repair, since the 5-year survival is 54% in untreated patients. Aneurysms of the descending thoracic aorta are treated routinely by endovascular grafting.

Ehlers-Danlos and Marfan syndromes also are rare causes. Less than 10% of aortic aneurysms occur in the thoracic aorta