no organic, systemic, or metabolic etiology has been determined by endoscopy or other testing. This is the most common cause of chronic dyspepsia, accounting for up to 75% of patients
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
Cephalosporins or extended-spectrum penicillins are commonly used (eg, cephalexin, 0.5 g orally four times daily for 7–10 days; see Table 35–6). Trimethoprim-sulfamethoxazole (two double-strength tablets orally twice daily for 7–10 days) should be considered when there is concern that the pathogen is MRSA (see Tables 35–5 and 35–6). Vancomycin, 15 mg/kg intravenously every 12 hours, is used for patients with signs of a systemic inflammatory response.
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
Urgent treatment for neoplasm consists of (1) cautious use of intravenous diuretics and (2) mediastinal irradiation, starting within 24 hours, with a treatment plan designed to give a high daily dose of radiation but a short total course of therapy to rapidly shrink the local tumor. Intensive radiation therapy combined with chemotherapy will palliate the process in up to 90% of patients. In patients with a subacute presentation, radiation therapy alone usually suffices. Chemotherapy is added if lymphoma or small-cell carcinoma is diagnosed
endovascular stenting emerging as first-line therapy for rapid symptom relief, while definitive treatment targets the underlying cause
transbronchial biopsy, however, is relatively contraindicated because of venous hypertension and the risk of bleeding
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.
Treatment of superficial vein reflux (see Varicose Veins, above) has been shown to decrease the recurrence rate of venous ulcers. Where there is substantial obstruction of the femoral or popliteal deep venous system, superficial varicosities supply the venous return and should not be removed.
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 may occur spontaneously, often in pregnant or postpartum women or in individuals with varicose veins, or it may be associated with trauma, as with a blow to the leg or following intravenous therapy with irritating solutions. It also may be a manifestation of systemic hypercoagulability from abdominal cancer such as carcinoma of the pancreas
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
Superficial thrombophlebitis of varicose veins is uncommon. The typical presentation is acute localized pain with tender, firm veins. The process is usually
The risk of DVT or embolization is very low unless the thrombophlebitis extends into the great saphenous vein in the upper medial thigh
Varicose veins due to primary superficial venous reflux should be differentiated from those secondary to previous or ongoing obstruction of the deep veins (post-thrombotic syndrome
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.
highest incidence occurs in women after pregnancy. Varicosities develop in over 20% of all adults
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
Any patient with chest or back pain with a known or suspected thoracic aorta aneurysm must be brought to the hospital and undergo urgent imaging studies to rule out the aneurysm as a cause of the pain
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
Ascending aortic aneurysms larger than 4.5 cm should be referred to a cardiac surgeon for observation and assessment and considered for repair at 5.5 cm.
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
With the exception of endovascular repair for discrete saccular aneurysms of the descending thoracic aorta, the morbidity and mortality of thoracic aneurysm repair are higher than for infrarenal AAA repair. Paraplegia remains a devastating complication
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
Open surgery is usually required, carrying substantial risk of morbidity (including stroke, diffuse neurologic injury, and intellectual impairment) because interruption of arch blood flow is required
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.
Most thoracic aortic aneurysms are due to atherosclerosis; syphilis is a rare cause
Ehlers-Danlos and Marfan syndromes also are rare causes. Less than 10% of aortic aneurysms occur in the thoracic aorta