Simon C. Body, MBChB, MPH

• Associate Professor of Anesthesia
• Harvard Medical School
• Brigham and Women's Hospital
• Boston, Massachusetts

The clinical onset of radia tion pericarditis is usually within the first year but may be delayed for many years; often a full decade or more may pass before constriction becomes evident medications gabapentin buy generic arava online. I ncessant Recurrent Pericard itis lasting longer than 4-6 weeks but less than 3 months without remission Recu rrence after a documented first espisode and a symptom-free i nterva l of 4-6 weeks or longer medicine 1975 cost of arava. It results from direct lymphatic or hematogenous spread; clinical pulmonary involvement may be absent or minor medicine disposal buy discount arava 10mg, although associated pleural effusions are common treatment high blood pressure arava 10mg without prescription. Bacterial pericarditis is equally rare and usually results from direct extension from pulmonary infections medicine zoloft cheap 20 mg arava mastercard. Borrelia burgdorferi treatment xyy arava 20mg mastercard, the organism responsible for Lyme disease, can also cause myopericarditis (and occa sionally heart block). The pathogenesis is uncertain; it occurs both with untreated uremia and in otherwise stable dialysis patients. Spread of adj acent lung cancer as well as invasion by breast cancer, renal cell carci noma, Hodgkin disease, and lymphomas are the most common neoplastic processes involving the pericardium and have become the most frequent causes of pericardia! Pericarditis may occur 2-5 days after infarction due to an inflammatory reaction to trans mural myocardial necrosis (postmyocardial infarction or postcardiotomy pericarditis [Dressler syndrome]). Radiation can initiate a fibrinous and fibrotic process in the pericardium, presenting as subacute pericarditis or constriction. Radiation pericarditis usually follows treat ments of more than 4000 cGy delivered to ports including more than 30% of the heart. Other causes of pericarditis include connective tissue diseases, such as lupus erythematosus and rheumatoid arthritis, drug-induced pericarditis (minoxidil, penicillins, clozapine), and myxedema. Laboratory Findings and Diagnostic Studies the diagnosis of viral pericarditis is usually clinical, and leukocytosis is often present. Rising viral titers in paired sera may be obtained for confirmation but are rarely done. Cardiac enzymes may be slightly elevated, reflecting an epicardial myocarditis component. Studies support ini tial treatment of the acute episode with colchicine to pre vent recurrences. Tapering of colchicine is not mandatory; however, in the last week of treatment, the dosage can be reduced every other day for patients less than 70 kg or once a day for those more than 70 kg. Aspirin and colchicine should be used instead of nonsteroidal anti-inflammatory medica tions in postmyocardial infarction pericarditis (Dressler syndrome), since nonsteroidal anti-inflammatory medica tions and corticosteroids may have an adverse effect on myocardial healing. Aspirin in doses of 7 50- 1 000 mg three times daily for 1 -2 weeks plus 3 months of colchicine is the recommended treatment. Colchicine should be used for at least 6 months as therapy in all refractory cases and in recurrent pericarditis. Indomethacin in doses of 25-50 mg every 8 hours can also be considered in recur rent pericarditis in place of ibuprofen. Systemic corticoste roids can be added in patients with severe symptoms, in refractory cases, or in patients with immune-mediated etiologies, but such therapy may entail a higher risk of recurrence and may actually prolong the illness. Colchicine is recommended in addition to corticosteroids, again for at least 3 months, to help prevent recurrences. The major early complication is tamponade, which occurs in less than 5% of patients. Rarely, when colchicine therapy alone fails or cannot be tolerated (usually do to gastrointes tinal symptoms), the pericarditis may require more signifi cant immunosuppression, such as cyclophosphamide, azathioprine, intravenous human immunoglobulins, inter leukin- 1 receptor antagonists (anakinra), or methotrexate. Standard antituberculous drug therapy is usually suc cessful for tuberculous pericarditis (see Chapter 9), but constrictive pericarditis can occur. Uremic pericarditis usually resolves with the institution of-or with more aggressive-dialysis. Whereas anti-inflammatory agents may relieve the pain and fever associated with uremic pericarditis, indomethacin and systemic corticosteroids do not affect its natural history. The prognosis with neoplastic effu sion is poor, with only a small minority surviving 1 year. If it is compromising the clinical comfort of the patient, the effusion is initially drained percutaneously. The diagnosis of tuberculous pericarditis can be inferred if acid-fast bacilli are found elsewhere. If bacte rial pericarditis is suspected on clinical grounds, diagnos tic pericardiocentesis can be confirmatory. The pericardium is characteristically "shaggy" in uremic pericarditis, and the effusion is hemor rhagic and exudative. The diagnosis of neoplastic pericar ditis can occasionally be made by cytologic examination of the effusion or by pericardia! The sedimentation rate is high in postmyocardial infarction or postcardiot omy pericarditis and can help confirm the diagnosis. The chest radiograph is frequently normal but may show cardiac enlargement (if pericardia! Treatment For acute pericarditis, experts suggest a restriction in activ ity until symptom resolution. For athletes the duration of exercise restriction should be until resolution of symp toms and normalization of all laboratory tests (generally 3 months). Symptomatic therapy is the initial approach to radiation pericarditis, but recurrent effusions and constriction often require surgery. Tamponade is characterized by elevated intrapericardial pressure (greater than 1 5 mm Hg), which restricts venous return and ventricular filling. As a result, the stroke volume and arterial pulse pressure fall, and the heart rate and venous pressure rise. When to Refer Patients who do not respond initially to conservative man agement, who have recurrences, or who appear to be devel oping constrictive pericarditis should be referred to a cardiologist for further assessment. Large idiopathic chronic effusions (over 3 months) have a 30-35% risk of progression to car diac tamponade. In cardiac tamponade, tachycardia, tachy pnea, a narrow pulse pressure, and a relatively preserved systolic pressure are characteristic. Pulsus paradoxus is defined as a decline of greater than 10 mm Hg in systolic pressure during inspiration. Edema or ascites are rarely present in tamponade; these signs favor a more chronic process. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardia! Laboratory Findings Laboratory tests tend to reflect the underlying processes (see causes of pericarditis above). Because the pericardium covers the ascending aorta and arch, aortic dissection and/or rupture can lead to tamponade as well. Conversely, smaller effusions that appear rapidly can cause tamponade due to the curvilinear relationship between the volume of fluid and the Chest radiograph can suggest chronic effusion by an enlarged cardiac silhouette with a globular configuration but may appear normal in acute situations. Electrical alternans is present only occasionally but is pathognomonic and is believed to be due to the heart swinging within the large effusion. Diagnostic pericardiocentesis or biopsy is often indicated for micro biologic and cytologic studies; a pericardia! Effusions due to hypothyroidism or lymphatic obstruction may contain cholesterol or be chylous in nature, respectively. Serial echocardiograms are indicated if no intervention is immediately contemplated. When tamponade is pres ent, urgent pericardiocentesis or cardiac surgery is required. Effusions related to recurrent inflammatory pericarditis can be treated as noted above (see Acute Inflammatory Pericarditis). Recurrent effusion in neoplastic dis ease and uremia, in p articular, may require partial pericardiectomy. General Considerations Inflammation can lead to a thickened, fibrotic, adherent pericardium that restricts diastolic filling and produces chronically elevated venous pressures. In the past, tubercu losis was the most common cause of constrictive pericardi tis, but while it remains so in underdeveloped countries, it is otherwise rare now. The risk of con strictive pericarditis due to viral or idiopathic pericarditis is less than l %. Its occurrence increases following immune mediated or neoplastic pericarditis (2-5%) and is highest after purulent bacterial pericarditis (20-30%). Other causes include post cardiac surgery, radiation therapy, and connective tissue disorders. A small number of cases are drug-induced or secondary to trauma, asbestosis, sarcoid osis, or uremia. The only definitive way to diagnose this condition is to reveal the underlying constrictive physiology once the pericardia! Symptoms and Signs the principal symptoms are slowly progressive dyspnea, fatigue, and weakness. The exami nation reveals these signs and a characteristically elevated jugular venous pressure with a rapid y descent. This can be detected at bedside by careful observation of the jugular pulse and noting an apparent increased pulse wave at the end of ventricular systole (due to the relative accentuation of the v wave by the rapid y descent). Diagnostic Studies At times constrictive pericarditis is extremely difficult to differentiate from restrictive cardiomyopathy and the two may coexist. When unclear, the use of both noninvasive testing and cardiac catheterization is required to sort out the difference. Radiographic fi ndi ngs-The chest radiograph may show normal heart size or cardiomegaly. Pericardiectomy removes only the pericardium between the phrenic nerve pathways, however, and most patients still require diuretics after the procedure, though symptoms are usually dramatically improved. Morbidity and mortality after pericardiectomy are high (up to 15%) and are greatest in those with the most disability prior to the procedure. When to Refer If the diagnosis of constrictive pericarditis is unclear or the symptoms of fluid retention resist medical therapy, then referral to a cardiologist is warranted to both establish the diagnosis and recommend therapy. Cardiac catheterization-This procedure is often con firmatory or can be diagnostic in difficult cases where the echocardiographic features are unclear or mixed. As a generality, the pulmonary pressure is low in constriction (as opposed to restrictive cardiomyopathy). If there is laboratory evidence of ongoing inflammation, then anti-inflammatory medications may have a role. As in other disorders of right heart failure, the diuresis should be aggressive, using loop diuretics (oral torsemide or bumetanide if bowel edema is suspected or intravenous furosemide), thiazides, and aldosterone antag onists (especially in the presence of ascites and liver con gestion). General Considerations the normal pulmonary bed offers about one-tenth as much resistance to blood flow as the systemic arterial sys tem. The clinical classification of pulmonary hypertension by the Fourth World Symposium on Pulmonary Hyperten sion is outlined in Table 1 0-2 1. In rare instances, obstruction of the pulmo nary venous circulation may occur (pulmonary vena occlusive disease and capillary hemangiomatosis). Group 3 includes cases due to parenchymal lung disease, impaired control of breathing, or living at high altitude. These guidelines cover persistent pulmonary hypertension in the newborn, diaphragmatic hernia in the young child, and bronchopulmonary dyplasia in children. Idiopathic pulmonary hypertension is not cov ered because it is uncommon in children. Because of the complexity of treating pulmonary hypertension in children, a multi-disciplinary team approach is critical. Pul monary hypertension due to left heart d isease Systolic dysfu nction Diastolic dysfu nction Ill. Chronic lung disease, especially sleep apnea, often is overlooked as a cause for pulmonary hypertension as is chronic thromboembolic disease. Patients with idiopathic pulmonary hypertension are characteristically young women who have evidence of right heart failure that is usually progressive, leading to death in 2-8 years without therapy. This is a decidedly dif ferent prognosis than patients with Eisenmenger physiol ogy due to a left-to-right shunt; 40% of patients with Eisenmenger physiology are alive 25 years after the diagno sis has been made. Patients have manifestations of low cardiac output, with weakness and fatigue, as well as edema and ascites as right heart failure advances. Drug and toxic pulmonary hypertension have been described as associated with the use of anorexigenic agents that increase serotonin release and block its uptake. In some cases, there is epidemiologic linkage to ingestion of rapeseed oil or L-tryptophan and use of illicit drugs, such as amphetamines. Pulmonary hypertension associated with connective tissue disease includes cases associated with scleroderma-up to 8 - 1 2% of patients with B. Diagnostic Studies the laboratory evaluation of idiopathic pulmonary hyper tension must exclude a secondary cause. A hypercoagulable state should be sought by measuring protein C and S levels, the presence of a lupus anticoagulant, the level of factor V Leiden, prothrombin gene mutations, and D-dimer. Septal flattening seen on the echocardiogram is consistent with pulmonary hypertension. Catheter ization allows measurement of pulmonary pressures and testing for vasoreactivity using a variety of agents, including 1 00% oxygen, adenosine, epoprostenol, and nitric oxide. More and more, a 6-minute walk test is done to provide both clinical assessment of dis ease progression and prognosis. Treatment & Prognosis the testing results described can be used to help define low- and high-risk patients. Aerobic exercise is recommended but no heavy physical exertion or isometic exercise. Pregancy should be strongly discouraged and pre ventive measures taken to ensure it does not occur. Diuretics are useful for the management of right-sided heart failure; clinical experience suggests loop diuretics (torsemide or butmetanide), which are absorbed if bowel edema is pres ent, plus spironolactone are preferable.

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Major complications occur in 5% (mainly ischemic colitis) and rebleeding occurs in up to 25% medicine hat weather arava 20mg sale. Surgical Treatment Emergency surgery is required in less than 5% of patients with acute lower gastrointestinal bleeding due to the effi cacy of colonoscopic and angiographic therapies medicine express discount arava 20 mg. It is indicated in patients with ongoing bleeding that requires more than 6 units of blood within 24 hours or more than 10 total units in whom attempts at endoscopic or angio graphic therapy failed medications known to cause miscarriage cheap arava 20 mg free shipping. Laparotomy is warranted if a small bowel tumor is identified by capsule endoscopy or radiographic studies medicine 0829085 trusted arava 10 mg. Most other lesions identified by capsule imaging can be further evaluated with enteroscopes that use over tubes with balloons to advance the scope through most of the small intestine in a forward and retrograde direction medicine and manicures order arava 10 mg otc. For massive or hemodynamically sig nificant acute bleeding medicine dispenser generic arava 20mg on line, angiography may be superior to enteroscopy for localization and embolization of a bleeding vascular abnormality. A nuclear scan for Meckel diverticulum should be obtained in patients under age 30. With the advent of capsule imaging and advanced endo scopic technologies for evaluating and treating bleeding lesions in the small intestine, intraoperative enteroscopy of the small bowel is seldom required. Chronic gastrointestinal blood loss of less than 1 00 mL/day may cause no appreciable change in stool appearance. In the United States, 2% of men and 5% of women have iron deficiency anemia (serum ferritin less than 30-45 mcg/L). Among men and postmenopausal women, a potential gastrointestinal cause of blood loss can be identified in the colon in 1 5-30% and in the upper gastrointestinal tract in 35-55%; a malig nancy is present in 10%. Iron deficiency on rare occasions is caused by malabsorption (especially celiac disease) or mal nutrition. Patients with iron deficiency ane mia should be evaluated for possible celiac disease with either IgA anti-tissue transglutaminase or duodenal biopsy. After evaluation of the upper and lower gastrointestinal tract with upper endoscopy and colonoscopy, the origin of occult bleeding remains unexplained in 30-50% of patients. In patients younger than 60 years with unexplained occult bleeding or iron deficiency, it is recommended to pursue further evaluation of the small intestine for a source of obscure-occult bleeding (as described above) in order to exclude a small intestinal neoplasm or inflammatory bowel disease. Patients over age 60 with occult bleeding who have a normal initial endoscopic evaluation and no other worri some symptoms or signs (eg, abdominal pain, weight loss) most commonly have blood loss from angioectasias, which may be clinically unimportant. Therefore, it is reasonable to give an empiric trial of iron supplementation and observe the patient for evidence of clinically significant bleeding. For anemia that responds poorly to iron supple mentation or recurrent or persistent chronic occult gastro intestinal blood loss, further evaluation is pursued for a source of obscure-occult bleeding (as described above). Etiology of Ascites the term "ascites" denotes the pathologic accumulation of fluid in the peritoneal cavity. Healthy men have little or no intraperitoneal fluid, but women normally may have up to 20 mL depending on the phase of the menstrual cycle. The causes of ascites may be classified into two broad patho physiologic categories: that which is associated with a normal peritoneum and that which occurs due to a dis eased peritoneum (Table 1 5-7). The most common cause of ascites is portal hypertension secondary to chronic liver disease, which accounts for over 80% of patients with asci tes. The most common causes of nonportal hypertensive ascites include infections (tubercu lous peritonitis), intra-abdominal malignancy, inflamma tory disorders of the peritoneum, and ductal disruptions (chylous, pancreatic, biliary). Fevers may sug gest infected peritoneal fluid, including bacterial peritonitis (spontaneous or secondary). Patients with chronic liver disease and ascites are at greatest risk for developing spon taneous bacterial peritonitis. In immigrants, immunocom promised hosts, or severely malnourished alcoholics, tuberculous peritonitis should be considered. Physical examination should emphasize signs of portal hypertension and chronic liver disease. Elevated jugular venous pressure may suggest right-sided heart failure or constrictive pericarditis. A large tender liver is characteris tic of acute alcoholic hepatitis or Budd-Chiari syndrome (thrombosis of the hepatic veins). The presence of large abdominal wall veins with cephalad flow also suggests portal hypertension; inferiorly directed flow implies hepatic vein obstruction. Signs of chronic liver disease include palmar erythema, cutaneous spider angiomas, gynecomastia, and muscle wasting. Anasarca results from cardiac failure or nephrotic syndrome with hypoalbu minemia. Finally, firm lymph nodes in the left supracla vicular region or umbilicus may suggest intra-abdominal malignancy. In general, patients must have at least 1 500 mL of fluid to be detected reliably by this method. Even the experienced clinician may find it difficult to dis tinguish between obesity and small-volume ascites. Abdominal paracentesis-Abdominal paracentesis is performed as part of the diagnostic evaluation in all patients with new onset of ascites to help determine the cause. It also is recommended for patients admitted to the hospital with cirrhosis and ascites (in whom the prevalence of bacterial peritonitis is 1 0-20%) and when patients with known ascites deteriorate clinically (development of fever, abdominal pain, rapid worsening of renal function, or worsened hepatic encephalopathy) to exclude bacterial peritonitis. Bloody fluid is most commonly attributable to a traumatic paracentesis, but up to 20% of cases of malignant ascites are bloody. Sym ptoms and Signs the history usually is one of increasing abdominal girth, with the presence of abdominal pain depending on the cause. Because most ascites is secondary to chronic liver (1) Cell count-A white blood cell count with differen tial is the most important test. An elevated white count with a predominance of lymphocytes arouses suspicion of tub erculosis or p eritoneal carcinomatosis. Calculated by subtract ing the ascitic fluid albumin from the serum albumin, the gradient correlates directly with the portal pressure. However, an increased ascitic fluid pro tein is also found in up to 20% of cases of uncomplicated cirrhosis. Two-thirds of patients with malignant ascites have a total protein level more than 2. In patients with nonportal hypertensive ascites, these studies are useful in detecting lymphadenopathy and masses of the mesentery and of solid organs such as the liver, ovaries, and pancreas. Fur thermore, they permit directed percutaneous needle biop sies of these lesions. It permits direct visualization and biopsy of the peritoneum, liver, and some intra-abdominal lymph nodes. An elevated amylase may suggest pancreatic ascites or a perforation of the gastrointestinal tract with leakage of pancreatic secre tions into the ascitic fluid. Perforation of the biliary tree is suspected with an ascitic bilirubin concentration that is greater than the serum bilirubin. An elevated ascitic creati nine suggests leakage of urine from the bladder or ureters. Ascitic fluid cytologic examination is ordered if peritoneal carcinomatosis is suspected. General Considerations "Spontaneous" bacterial infection of ascitic fluid occurs in the absence of an apparent intra-abdominal source of infection. It is seen with few exceptions in patients with ascites caused by chronic liver disease. Translocation of enteric bacteria across the gut wall or mesenteric lymphat ics leads to seeding of the ascitic fluid, as may bacteremia from other sites. Approximately 20-30% of cirrhotic patients with ascites develop spontaneous peritonitis; how ever, the incidence is greater than 40% in patients with ascitic fluid total protein less than 1 g/ dL, probably due to decreased ascitic fluid opsonic activity. Virtually all cases of spontaneous bacterial peritonitis are caused by a monomicrobial infection. The most common pathogens are enteric gram-negative bacteria (E coli, Klebsiella pneumoniae) or gram-positive bacteria (Streptococ cus pneumoniae, viridans strepto cocci, Enterococcus sp ecies). Imaging Ab dominal ultrasound is useful in confirming the presence of ascites and in the guidance of paracentesis. Sym ptoms and Signs Eighty to ninety percent of patients with spontaneous bac terial peritonitis are symptomatic; in many cases the pre sentation is subtle. Spontaneous bacterial peritonitis may be present in 10-20% of patients hospitalized with chronic liver disease, sometimes in the absence of any suggestive symptoms or signs. The most common symptoms are fever and abdominal pain, present in two-thirds of patients. Spontaneous bacte rial peritonitis may also present with a change in mental status due to exacerbation or precipitation of hepatic encephalopathy, or sudden worsening of renal function. Physical examination typically demonstrates signs of chronic liver disease with ascites. Abdominal tenderness is present in less than 50% of patients, and its presence sug gests other processes. Neutrocytic ascites may also be seen in some patients with peritoneal carcinomatosis, pancreatic ascites, or tuberculous ascites. Prevention Up to 70% of patients who survive an episode of spontane ous bacterial peritonitis will have another episode within 1 year. Oral once-daily prophylactic therapy-with nor floxacin, 400 mg, ciprofloxacin, 250-500 mg, or trime thoprim -sulfamethoxazole, one double-strength tablet -has been shown to reduce the rate of recurrent infections to less than 20% and is recommended. Prophylaxis should be considered also in patients who have not had prior bacte rial peritonitis but are at increased risk of infection due to low-protein ascites (total ascitic protein less than 1 g/dL). Although improvement in survival in cirrhotic patients with ascites treated with prophylactic antibiotics has not been shown, decision analytic modeling suggests that in patients with prior bacterial peritonitis or low ascitic fluid protein, the use of prophylactic antibiotics is a cost effective strategy. Laboratory Findings the most important diagnostic test is abdominal paracen tesis. Ascitic fluid should be sent for cell count with dif ferential, and blood culture bottles should be inoculated at the bedside; Gram stain and reagent strips are insensitive. Patients with neutrocytic ascites are presumed to be infected and should be started-regardless of symptoms on antibiotics. Although 1 0-30% of patients with neutro cytic ascites have negative ascitic bacterial cultures ("culture-negative neutrocytic ascites"), it is presumed that these patients have bacterial peritonitis and should be treated empirically. Occasionally, a positive blood culture identifies the organism when ascitic fluid is sterile. Treatment Empiric therapy for spontaneous bacterial peritonitis should be initiated with a third-generation cephalosporin (such as cefotaxime, 2 g intravenously every 8 - 1 2 hours, or ceftriaxone, 1 - 2 g intravenously every 24 hours) or a com bination beta-lactam/beta-lactamase agent (such as ampi cillin/sulbactam, 2 g/ 1 g intravenously every 6 hours). B ecause of a high risk of nephrotoxicity in patients with chronic liver disease, aminoglycosides should not be used. A repeat paracentesis is recommended after 48 hours of treatment in patients without clinical improvement. If the ascitic neutrophil count has not decreased by 25%, antibi otic coverage should be adjusted (guided by culture and sensitivity results, if available) and secondary causes of peritonitis excluded. Intravenous albumin increases effective arterial circulating volume and renal perfusion, decreasing the incidence of kidney injury and mortality. Differential Diagnosis Spontaneous bacterial peritonitis must be distinguished from secondary bacterial peritonitis, in which ascitic fluid has become secondarily infected by an intra-abdominal infection. Even in the presence of perforation, clinical symptoms and signs of peritonitis may be lacking owing to the separation of the visceral and parietal peritoneum by the ascitic fluid. Causes of secondary bacterial peritonitis include appendicitis, diverticulitis, perforated peptic ulcer, and perforated gallbladder. Ascitic neutrophil counts greater than 10,000/ meL also are suspicious; however, most patients with sec ondary peritonitis have neutrophil counts within the range of spontaneous peritonitis. Nonselective beta blockers increase the risk of hepatorenal syndrome in patients with bacterial peritonitis and should be discontin ued permanently due to their adverse impact on cardiac output and renal perfusion in advanced cirrhosis which is associated with decreased long-term survival. Patients with suspected secondary bacterial peritonitis should be given broad-spectrum coverage for enteric aerobic and anaerobic flora with a third-generation cephalosporin and metroni dazole pending identification and definitive (usually surgi cal) treatment of the cause. However, if the disease is recognized and treated early, the rate is less than 10%. As the majority of patients have underlying severe liver disease, many may die of liver failure, hepatorenal syndrome, or bleeding compli cations from portal hypertension. The most effective treat ment for recurrent spontaneous bacterial peritonitis is liver transplant. Nonselective blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites. Albumin infusion improves outcomes of patients with spontaneous bacterial peritonitis: a meta-analysis of randomized trials. Renal dysfunction is the most important inde pendent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis. Cytology is positive in over 95%, but laparoscopy may be required in patients with negative cytology to confirm the diagnosis and to exclude tuberculous peritonitis, with which it may be confused. Malignant ascites attributable to portal hypertension usually is associated with an increased serum ascites-albumin gradient (greater than 1. Patients may be treated with periodic large-volume paracentesis for symptomatic relief. Indwelling catheters can be left in place for patients approaching the end of life who require periodic paracentesis for symptomatic relief. Intraperitoneal chemotherapy is sometimes used to shrink the tumor, but the overall prognosis is extremely poor, with only 10% survival at 6 months. With newer treatments consisting of surgical debulking and intraperitoneal che motherapy, long-term survival from ovarian cancer is possible. It is character ized by episodic bouts of acute peritonitis that may be associated with serositis involving the joints and pleura. Peritoneal attacks are marked by the sudden onset of fever, severe abdominal pain, and abdominal tenderness with guarding or rebound tenderness. Because symptoms resemble those of surgical peritonitis, patients may undergo unnec essary exploratory laparotomy. The most common tumors causing carcinomatosis are primary adenocarcinomas of the ovary, uterus, pancreas, stomach, colon, lung, or breast.

Nystatin powder (1 00 symptoms 10 weeks pregnant cheap arava 20 mg on line,000 units/g) applied to dentures three or four times daily and rinsed off for several weeks may help denture wearers symptoms 5 days before your missed period order arava 20 mg without prescription. Clinically treatment synonym arava 10mg without a prescription, there is painful acute gingival inflammation and necrosis treatment ketoacidosis 10 mg arava otc, often with bleeding symptoms 2dpo arava 20 mg without prescription, halitosis treatment for hemorrhoids generic arava 10 mg without prescription, fever, and cervical lymphadenopathy. Warm half strength peroxide rinses and oral penicillin (250 mg three times daily for 10 days) may help. Rarely painful, it may be secondary to nutritional deficiencies (eg, niacin, riboflavin, iron, or vitamin E), drug reactions, dehydration, irritants, or foods and liquids, and possibly to autoimmune reactions or psoriasis. If the primary cause cannot be identified and corrected, empiric nutritional replacement therapy may be of value. Glossodynia is burning and pain of the tongue, which may occur with or without glossitis. Their cause remains uncertain, although an association with human herpesvirus 6 has been suggested. Minor aph thous ulcers are less than 1 em in diameter and generally heal in 1 0 - 1 4 days. Major aphthous ulcers are greater than 1 em in diameter and can be disabling due to the degree of associated oral pain. Stress seems to be a major predispos ing factor to the eruptions of aphthous ulcers. A study found that the frequency of viral rhinitis and bedtime after 1 1 pm were independent predictors of aphthous ulcer fre quency and severity in college students. Clinically, there is initial burning, followed by typical small vesicles that rupture and form scabs. Lesions are most commonly found on the attached gingiva and mucocuta neous junction of the lip, but lesions can also form on the tongue, buccal mucosa, and soft palate. Acyclovir (200-800 mg orally five times daily for 7 -l 0 days) or valacyclovir (1 000 mg orally twice daily for 7- 1 0 days) may shorten the course and reduce postherpetic pain. These treatments may be effective only when started within 24-48 hours of the onset of initial symptoms (pain, itching, burning) and are not effective once vesicles have erupted. Differential diagnosis includes aphthous stomatitis, erythema multi forme, syphilitic chancre, and carcinoma. Coxsackievirus caused lesions (grayish-white tonsillar plaques and palatal ulcers of herpangina or buccal and lip ulcers in hand-foot and-mouth disease) are seen more commonly in children under age 6. Other topical therapies shown to be effective in controlled studies include diclofenac 3% in hyaluronan 2. A l -week tapering course of prednisone (40-60 mg/day) has also been used successfully. Cimetidine maintenance therapy may be useful in patients with recurrent aphthous ulcers. Large or persistent areas of ulcerative stomatitis may be secondary to erythema multiforme or drug allergies, acute herpes simplex, pemphigus, pemphigoid, epidermolysis bullosa acquisita, bullous lichen planus, Beh<;et disease, or inflammatory bowel disease. Focus is to treat group A beta-hemolytic strepto coccus infection to prevent rheu matic sequelae. General Considerations Pharyngitis and tonsillitis account for over 10% of all office visits to primary care clinicians and 50% of outpatient anti biotic use. A second public health policy concern is reducing the extraordinary cost (both in dollars and in the development of antibiotic resistant S pneumoniae) in the United States associated with unnecessary antibiotic use. Questions being asked: Have the rapid antigen tests supplanted the need to culture a throat under most circumstances Are clinical criteria alone a sufficient basis for decisions about which patients should be given antibiotics Should any patient receive any antibiotic other than penicillin (or erythromycin if penicil lin-allergic) Numerous well-done studies and experience with rapid laboratory tests for detection of streptococci (eliminating the delay caused by culturing) informed a consensus experience. Herpes Stomatitis Herpes gingivostomatitis is common, mild, and short-lived and requires no intervention in most adults. However, about one-third of patients with infectious mononucleosis have secondary streptococcal tonsillitis, requiring treatment. Ampicillin should routinely be avoided if mononucleosis is suspected because it induces a rash that might be misinterpreted by the patient as a penicillin allergy. Diphtheria (extremely rare but described in the alcoholic population) presents with low-grade fever and an ill patient with a gray tonsillar pseudomembrane. Sore throat may be severe, with odyno phagia, tender adenopathy, and a scarlatiniform rash. Treatment Given the availability of many well-documented studies in recent years, one would think that a consensus might develop as to the most appropriate way to treat a sore throat. Pharyngeal i nflammation and petechiae of the soft palate caused by group A streptococcus. Forty years ago, a single intramuscular inj ection ofben zathine penicillin or procaine penicillin, 1. Antibi otic choice aims to reduce the already low (1 0-20%) inci dence of treatment failures (positive culture after treatment despite symptomatic resolution) and recurrences. Penicil lin V potassium (250 mg orally three times daily or 500 mg twice daily for 10 days) or cefuroxime axetil (250 mg orally twice daily for 5 - 1 0 days) are both effective. The efficacy of a 5-day regimen of penicillin V potassium appears to be similar to that of a 1 0-day course, with a 94% clinical response rate and an 84% streptococcal eradication rate. Erythromycin (also active against Mycoplasma and Chlamydia) is a reasonable alternative to penicillin in aller gic patients. Cephalosporins are somewhat more effective than penicillin in producing bacteriologic cures; 5 -day administration has been successful for cefpodoxime and cefuroxime. The macrolide antibiotics have also been reported to be successful in shorter-duration regimens. Azithromycin (500 mg once daily), because of its long half life, need be taken for only 3 days. Adequate antibiotic treatment usually avoids the strep tococcal complications of scarlet fever, glomerulonephritis, rheumatic myocarditis, and local abscess formation. Surprisingly, penicillin-tolerant strains are not isolated more frequently in those who fail treatment than in those treated successfully with penicillin. The reasons for failure appear to be complex, and a second course of treatment with the same drug is reasonable. Alternatives to penicillin include cefuroxime and other cephalosporins, dicloxacillin (which is beta-lactamase resistant), and amoxicillin with clavulanate. When there is a history of penicillin allergy, alternatives should be used, such as erythromycin. Erythromycin resistance with failure rates of about 25% -is an increasing problem in many areas. In cases of severe penicillin allergy, cepha losporins should be avoided as the cross-reaction is com mon (8% or more). Ancillary treatment of pharyngitis includes analgesics and anti-inflammatory agents, such as aspirin, acetamino phen, and corticosteroids. In meta-analysis, corticosteroids increased the likelihood of complete pain resolution at 24 hours by threefold without an increase in recurrence or adverse events. In severe cases, anesthetic gargles and lozenges (eg, benzocaine) may provide additional symptomatic relief. Occasionally, odynophagia is so intense that hospi talization for intravenous hydration and antibiotics is nec essary. Evidence-based evaluation and management of patients with pharyngitis in the emergency department. Peri tonsillar abscess (quinsy) and cellulitis present with severe sore throat, odynophagia, trismus, medial deviation of the soft palate and peritonsillar fold, and an abnormal muffled ("hot potato") voice. Following therapy, peritonsillar celluli this usually either resolves over several days or evolves into peritonsillar abscess. The existence of an abscess may be confirmed by aspirating pus from the peritonsillar fold just superior and medial to the upper pole of the tonsil. A 1 9-gauge or 2 1 -gauge needle should be passed medial to the molar and no deeper than 1 em, because the internal carotid artery may lie more medially than its usual location and pass posterior and deep to the tonsillar fossa. Most com monly, patients with peritonsillar abscess present to the emergency department and receive a dose of parenteral amoxicillin (1 g), amoxicillin-sulbactam (3 g), or clindamy cin (600-900 mg). Less severe cases and patients who are able to tolerate oral intake may be treated for 7- 1 0 days with oral antibiotics, including amoxicillin, 500 mg three times a day; amoxicillin-clavulanate, 875 mg twice a day; or clindamycin, 300 mg four times daily. Although antibiotic treatment is generally undisputed, there is controversy regarding the surgical management of peritonsillar abscess. Some clinicians incise and drain the area and continue with parenteral antibiotics, whereas others aspirate only and monitor as an outpatient. To drain the abscess and avoid recurrence, it may be appropriate to con sider immediate tonsillectomy (quinsy tonsillectomy). About 10% of patients with peritonsillar abscess exhibit relative indications for tonsillectomy. Regardless of the method used, one must be sure the abscess is adequately treated, since complications such as extension to the retro pharyngeal, deep neck, and posterior mediastinal spaces are possible. There is controversy about whether a single abscess is a sufficient indication for tonsillectomy; about 30% of patients aged 1 7-30 who do not undergo early planned tonsillectomy following peritonsillar abscess ulti mately undergo surgery, and only about 1 3 % of those over 30 have their tonsils removed. External drainage via bilateral submental incisions is required if the airway is threat ened or when medical therapy has not reversed the process. Treatment of deep neck abscesses includes securing the airway, intravenous antibiotics, and incision and drainage. When the infection involves the floor of the mouth, base of the tongue, or the supraglottic or paraglottic space, the airway may be secured either by intubation or tracheot omy. Tracheotomy is preferable in the patients with sub stantial pharyngeal edema, since attempts at intubation may precipitate acute airway obstruction. Bleeding in association with a deep neck abscess is very rare but sug gests carotid artery or internal jugular vein involvement and requires prompt neck exploration both for drainage of pus and for vascular control. Patients with Lemierre syndrome require prompt institution of antibiotics appropriate for Fusobacterium necrophorum as well as the more usual upper airway patho gens. General Considerations Ludwig angina is the most commonly encountered neck space infection. It is a cellulitis of the sublingual and sub maxillary spaces, often arising from infection of the man dibular dentition. Other causes include suppurative lymphadenitis, direct spread of pha ryngeal infection, penetrating trauma, pharyngoesopha geal foreign bodies, cervical osteomyelitis, and intravenous inj ection of the internal jugular vein, especially in drug abusers. Recurrent deep neck infection may suggest an underlying congenital lesion, such as a branchial cleft cyst. Suppurative lymphadenopathy in middle-aged persons who smoke and drink alcohol regularly should be consid ered a manifestation of malignancy (typically metastatic squamous cell carcinoma) until proven otherwise. Clin ical Findings Patients with Ludwig angina have edema and erythema of the upper neck under the chin and often of the floor of the mouth. The tongue may be displaced upward and backward by the posterior spread of cellulitis, and coalescence of pus is often present in the floor of mouth. Microbiologic isolates include strepto cocci, staphylococci, Bacteroides, and Fusobacterium. Patients with deep neck abscesses usually present with marked neck pain and swelling. Deep neck abscesses are emergencies because they may rapidly compromise the airway. Untreated or inad equately treated, they may spread to the mediastinum or cause sepsis. It often will distinguish inflammation and phlegmon (requiring antibiotics) from abscess (requiring drainage) and define for the surgeon the extent of an abscess. This condition, known as Lemierre syndrome, is rare and usually associated with severe headache. The presence of pulmonary infiltrates consistent with septic emboli in the setting of a neck abscess should lead one to suspect Lemierre syndrome. Severe neck infections that require wide external drainage: clinical analysis of 17 consecutive cases. In general, sleep-disordered breathing problems are attributed to nar rowing of the upper aerodigestive tract during sleep due to changes in position, muscle tone, and soft tissue hypertro phy or laxity. The most common sites of obstruction are the oropharynx and the base of the tongue. Clinical examination should include examination of the nasal cavity, nasopharynx, oro pharynx, and larynx to help exclude other causes of dynamic airway obstruction. In many cases of isolated snoring, the palate and uvula appear enlarged and elon gated with excessive mucosa hanging below the muscular portion of the soft palate. Persistent symptoms may occur following initial treatment necessitating costly (and sometimes painful) repeat proce dures. The durability of these procedures in alleviating symptoms is also poorly understood, and late failures can lead to patient and clinician frustration. Obstructive sleep apnea and its effects on cardio vascular diseases: a narrative review. Imaging and Diagnostic Testing Sleep examination with polysomnography is strongly advised in the evaluation of a patient with complaints of snoring. Radiographic imaging of the head or neck is gen erally not necessary for management of primary snoring. Treatment Expeditious and inexpensive management solutions of snoring are sought, often with little or no benefit.

They rarely symptoms white tongue arava 20mg overnight delivery, if ever medicine 6469 purchase arava from india, resolve completely and may leave behind a sulcus medications erectile dysfunction proven arava 20 mg, or vocal fold scar medicine zocor discount 20 mg arava mastercard, if they decompress or are marsupialized medications that interact with grapefruit buy generic arava 10 mg on-line. Polypoid corditis is different from vocal fold polyps and may form from loss of elastin fibers and loosening of the intracellular junctions within the lamina propria medicine vicodin cheap arava online visa. This loss allows swelling of the gelatinous matrix of the superfi cial lamina propria (called Reinke edema). These changes in the vocal folds are strongly associated with smoking, but also with vocal abuse, chemical industrial irritants, and hypothyroidism. While this problem is common in both male and female smokers, women seem more troubled by the characteristic decline in modal pitch caused by the increased mass of the vocal folds. If the patient stops smok ing or the lesions cause stridor and airway obstruction, surgical resection of the hyperplastic vocal fold mucosa may be indicated to improve the voice or airway, or both. A common but often unrecognized cause of hoarseness and odynophonia are contact ulcers or their close relatives, granulomas. Both lesions form on the vocal processes of the arytenoid cartilages, and patients often can correctly inform the clinician which side is affected. The cause of these ulcers and granulomas is disputed, but they are clearly related to trauma and may be related to exposure of the underlying perichondrium. Epiglottitis Epiglottitis (or, more correctly, supraglottitis) should be suspected when a patient presents with a rapidly develop ing sore throat or when odynophagia (pain on swallowing) is out of proportion to apparently minimal oropharyngeal findings on examination. Rarely in the era of H influenzae type b vaccine is this bacterium isolated in adults. Unlike in children, indirect laryngoscopy is generally safe and may demonstrate a swollen, erythema tous epiglottis. Lateral plain radiographs may demonstrate an enlarged epiglottis (the epiglottis "thumb sign"). Initial treatment is hospitalization for intravenous antibiotics eg, ceftizoxime, 1-2 g intravenously every 8 - 1 2 hours; or cefuroxime, 750- 1 500 mg intravenously every 8 hours; and dexamethasone, usually 4- 1 0 mg as initial bolus, then 4 mg intravenously every 6 hours-and observation of the air way. Similarly, substitution of oral antibiotics may be appropriate to complete a 10-day course. Chronic ulceration or granuloma formation has been asso ciated with gastroesophageal reflux but is also common in patients with muscle tension dysphonia. Treatment is often multimodal, and an inhaled corticosteroid (eg, fluticasone 440 meg twice daily) may be the most effective pharmaco logic therapy. Adjunct treatment measures include proton pump inhibitor therapy (omeprazole 40 mg orally twice daily, or equivalent) and voice therapy with special atten tion to vocal hygiene. Laryngeal cancer is very treatable and early detection is the key to maximizing posttreatment voice, swallowing, and breathing function. Symptoms and Signs A change in voice quality is most often the presenting com plaint, although throat or ear pain, hemoptysis, dysphagia, weight loss, and airway compromise may occur. B ecause of their early impact on vocal quality, glottic cancers are among the smallest detectable human malignancies and treatment success is very high with early lesions. Neck metastases are not common in early glottic (true vocal fold) cancer in which the vocal folds are mobile, but a third of patients in whom there is impaired fold mobility will also have involved lymph nodes at neck dissection. Supra glottic carcinoma (false vocal folds, aryepiglottic folds, epiglottis), on the other hand, often metastasizes to both sides of the neck early in the disease. Complete head and neck examination, including laryngoscopy, by an experi enced clinician is mandated for any person with the con cerning symptoms listed under Essentials of Diagnosis. La ryngeal Leu koplakia Leukoplakia of the vocal folds is commonly found in asso ciation with hoarseness in smokers. In some cases, invasive squamous cell carcinoma is present in the initial biopsy specimen. Some patients-estimated to be less than 5% of those with mild dysplasia and about 35-60% of those with severe dysplasia-will subsequently develop squamous cell carci noma. Treatment options include close follow-up with laryngovideostroboscopy, serial resection, and external beam radiation therapy. Despite their cost and the lack of any evidence for their use in the treatment of leukoplakia, proton pump inhibitors have become the mainstay of treat ment for these lesions. Imaging evaluates neck nodes, tumor volume, and cartilage sclerosis or destruction. Formal cardio pulmonary evaluation may be indicated, especially if partial laryngeal surgery is being considered. All partial laryngectomy candidates should have good to excellent lung function and exercise tolerance because chronic microaspiration may be expected following the procedure. Biopsy Diagnosis is made by biopsy at the time of laryngoscopy when true fold mobility and arytenoid fixation, as well as surface tumor extent, can be evaluated. Most otolaryngolo gists recommend esophagoscopy and bronchoscopy at the same time to exclude synchronous primary tumor. General Considerations Squamous cell carcinoma of the larynx, the most common malignancy of the larynx, o ccurs almost exclusively in patients with a history of significant tobacco use. In addition to the late complications, clinicians have noted that the over all success in the treatment of larynx cancer has declined in parallel with the increase in organ preservation chemora diation therapy over the past 20 years. Some experts have proposed that this decline is the direct result of the shift in management of advanced laryngeal cancer away from sur gery. Organ preservation surgery should be considered and discussed as an alternative to chemoradiation but may require referral to an appropriate regional center where such techniques are offered. After thorough evaluation of candidacy and discussion of the treatment options, patient choice plays a critical role in the ultimate decision to pur sue surgery or chemoradiation as a definitive treatment modality. The patient and treating clinicians must carefully consider different early and late side effects and complica tions associated with different treatment modalities. Supraglottic tumors metasta size early and bilaterally to the neck, and this must be included in the treatment plans even when the neck is apparently uninvolved. Glottic tumors in which the true vocal folds are mobile (T1 or T2) have less than a 5% rate of nodal involvement; when a fold is immobile, the rate of ipsilateral nodal involvement climbs to about 30%. This decision will depend on the treatment chosen for the larynx and the extent of neck involvement. Total laryngectomy is largely reserved for patients with advanced resectable tumors with extralaryngeal spread or cartilage involvement, for those with persistent tumor fol lowing chemoradiation, and for patients with recurrent or second primary tumor following previous radiation therapy. Voice rehabilitation via a primary (or at times secondary) tracheoesophageal puncture produces intelligible and serviceable speech in about 75-85% of patients. Indwelling prostheses that are changed every 3-6 months are a com mon alternative to patient-inserted prostheses, which need changing more frequently. In addition to the 3-4% annual rate of second tumors and monitoring for recurrence, psychosocial aspects of treatment are common. Dysphagia, impaired communication, and altered appearance may result in patient difficulties adapting to the workplace and to social interactions. Nevertheless, about 65% of patients with larynx cancer are cured, most have useful speech, and many resume their prior livelihoods with adaptations. Radiotherapy plus cetuximab for locoregionally advanced head and neck cancer: 5 -year survival data from a phase 3 randomised trial, and relation between cetuximab induced rash and survival. Open biopsies of nodal metastases should be discour aged because they may lead to higher rates of tumor treatment failure. T3 and T4 lesions may involve multiple laryngeal subsites with limitation of laryn geal mobility. Treatment Treatment of laryngeal carcinoma has four goals: cure, preservation of safe and effective swallowing, preservation of useful voice, and avoidance of a permanent tracheos toma. For early glottic and supraglottic cancers, radiation therapy is the standard of care since cure rates are greater than 95% and 80%, respectively. That said, radiation therapy carries substantial morbidity, and many early tumors (T1 and T2 lesions, without involved nodes) and selected advanced tumors (T3 and T4) may be treated with partial laryngectomy if at least one cricoarytenoid unit can be preserved. Five-year locoregional cure rates exceed 80-90% with surgery, and patient-reported satisfaction is excellent. Twenty-five years ago, total laryngectomy was often recommended for such patients. Cisplatin-based chemo therapy concomitant with radiation therapy has been shown to be superior to either irradiation alone or induc tion chemotherapy followed by radiation. The same bene fits have been demonstrated with the epidermal growth factor receptor blocker cetuximab with lower overall sys temic toxicity and better patient tolerance. However, chemoradiation using either cetuximab or cisplatin is asso ciated with prolonged gastrostomy-dependent dysphagia. Com mon causes of unilateral recurrent laryngeal nerve involvement include thyroid surgery (and occasionally thyroid cancer), other neck surgery (anterior discectomy and carotid endarterectomy), and mediastinal or apical involvement by lung cancer. Skull base tumors often involve or abut upon lower cranial nerves and may affect the vagus nerve directly, or the vagus nerve may be dam aged during surgical management of the lesion. While iat rogenic injury is the most common cause of unilateral vocal fold paralysis, the second most common cause is idiopathic. However, before deciding whether the paralysis is due to iatrogenic injury or is idiopathic, the clinician must exclude other causes, such as malignancy. Unlike unilateral fold paralysis, bilateral fold paralysis usually causes inspiratory stridor with deep inspiration. If the onset of bilateral fold paralysis is insidious, it may be asymptomatic at rest, and the patient may have a normal voice. However, the acute onset of bilateral vocal fold paralysis with inspiratory stridor at rest should be managed by a specialist immediately in a critical care environment. Causes of bilateral fold paralysis include thyroid surgery, esophageal cancer, and ventricular shunt malfunction. Unilateral or bilateral fold immobility may also be seen in cricoarytenoid arthritis secondary to advanced rheumatoid arthritis, intubation injuries, glottic and subglottic stenosis, and, of course, laryngeal cancer. The goal of intervention is the creation of a safe airway with minimal reduction in voice quality and airway protection from aspiration. A number of fold lateralization procedures for bilateral paralysis have been advocated as a means of removing the tracheotomy tube. Unilateral vocal fold paralysis is occasionally temporary and may take over a year to resolve spontaneously. Surgical management of persistent or irrecoverable symptomatic unilateral vocal fold paralysis has evolved over the last several decades. The primary goal is medialization of the paralyzed fold in order to create a stable platform for vocal fold vibration. Additional goals include improving pulmo nary toilet by facilitating of cough and advancing diet. Suc cess has been reported for years with inj ection laryngoplasty using Teflon, Gelfoam, fat, and collagen. Teflon is the only permanent injectable material, but its use is discouraged because of granuloma formation within the vocal folds of some patients. Temporary injectable materials, such as col lagen or fat, provide excellent temporary restoration of voice and can be placed under local or general anesthesia. Once the paralysis is determined to be permanent, formal medialization thyroplasty may be performed by creating a small window in the thyroid cartilage and placing an implant between the thyroarytenoid muscle and inner table of the thyroid cartilage. This procedure moves the vocal fold medially and creates a stable platform for bilat eral, symmetric mucosal vibration. Evidence-based practice: evaluation and manage ment of unilateral vocal fold paralysis. In an acute emergency, cricothyrotomy secures an airway more rapidly than tracheotomy, with fewer potential immediate complications, such as pneumothorax and hemorrhage. Percutaneous dilatational tracheotomy as an elective bedside (or intensive care unit) procedure has undergone scrutiny in recent years as an alternative to tracheotomy. In experienced hands, the various methods of percutaneous tracheotomy have been documented to be safe in carefully selected patients. B edside tracheotomy (in the intensive care unit) achieves similar cost reduction and is advocated by some experts as slightly less costly than the percutaneous procedures. The most common indication for elective tracheotomy is the need for prolonged mechanical ventilation. There is no firm rule about how many days a patient must be intu bated before conversion to tracheotomy should be advised. The incidence of serious complications, such as subglottic stenosis increases with extended endotracheal intubation. As soon as it is apparent that the patient will require pro tracted ventilatory support, tracheotomy should replace the endotracheal tube. Less frequent indications for trache ostomy are life-threatening aspiration pneumonia, the need to improve pulmonary toilet to correct problems related to insufficient clearing of tracheobronchial secre tions, and sleep apnea. Posttracheotomy care requires humidified air to pre vent secretions from crusting and occluding the inner can nula of the tracheotomy tube. The most frequent early complication of tracheotomy is dislodgment of the tracheotomy tube. Surgical creation of an inferiorly based tracheal flap sutured to the inferior neck skin may make reinsertion of a dislodged tube easier. It should be recalled that the act of swallowing requires elevation of the larynx, which is limited by tracheotomy. Care of the skin around the stoma is important to prevent maceration and secondary infection. Detec tion of radiolucent foreign bodies may be aided by inspira tion-expiration films that demonstrate air trapping distal to the obstructed segment. Tracheal and bronchial foreign bodies should be removed under general anesthesia with rigid bronchoscopy by a skilled endoscopist working with an experienced anesthesiologist. Rapid growth and tenderness suggest an inflammatory process, while firm, painless, and slowly enlarging masses are often neo plastic. In young adults, most neck masses are benign (branchial cleft cyst, thyroglossal duct cyst, reactive lymph adenitis), although malignancy should always be consid ered (lymphoma, metastatic thyroid carcinoma).

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