اصغر قطه اصغر كلب اصغر حصان
اكبر ماطور بالعالم اكبر كلب اكنر كيكه فراوله
الخميس، 26 مارس 2009
الاثنين، 23 مارس 2009
. Techniques of Varicocelectomy
Refers ence
1. Goldstein M., Gilbert BR, Dicker AP, Dwosh J, Gnecco C: Microsurgical inguinal varicocelectomy with delivery of the testis: An artery and lymphatic sparing technique. J. Urol 148:1808-1811, 19922. Mattews, GJ., Matthews, ED., Goldstein, M: Induction of spermatogenesis and achievement of pregnancy after microsurgical varicocelectomy in men with azoospermia and severe oligoasthenospermia
الجمعة، 13 مارس 2009
lasix
LASIX®
Furosemide
Diuretic
Action And Clinical Pharmacology: Animal experiments using stop-flow and micropuncture techniques have demonstrated that furosemide inhibits sodium reabsorption in the ascending limb of Henle's loop as well as in both proximal and distal tubules. The action of furosemide on the distal tubule is independent of any inhibitory effect on carbonic anhydrase or aldosterone. Furosemide may promote diuresis in cases which have previously proved resistant to other diuretics. Furosemide has no significant pharmacological effects other than on renal function. Absorption, Metabolism and Excretion: In man, furosemide is rapidly absorbed from the gastrointestinal tract. The diuretic effect of furosemide is apparent within 1 hour following oral administration and the peak effect occurs in the first or second hour. The duration of action is 4 to 6 hours but may continue up to 8 hours. Following i.v. administration of the drug, the diuresis occurs within 30 minutes and the duration of action is about 2 hours. Urinary excretion is accomplished both by glomerular filtration and proximal tubular secretion, together this accounts for roughly only 2/3 of the ingested dose, the remainder being excreted in the feces. A small fraction is metabolized by cleavage of the side chain. Indications And Clinical Uses: The treatment of edema associated with congestive heart failure, cirrhosis of the liver and renal disease, including nephrotic syndrome as well as other edematous states amenable to diuretic therapy. Furosemide can also be used alone in the control of mild to moderate hypertension or in combination with other antihypertensive agents in the treatment of more severe cases. Hypertensive patients who cannot be adequately controlled with thiazides will probably also not be adequately controllable with furosemide alone. Parenteral furosemide is indicated when a rapid onset and an intense diuresis is desired e.g., acute pulmonary edema, cerebral edema. Parenteral furosemide is also indicated when oral therapy is precluded because of interference with intestinal absorption or for other reasons. Parenteral furosemide, by virtue of its therapeutic indications, will be generally administered to patients in hospital or outpatient clinics. However, in case of emergency where parenteral furosemide is administered outside this setting, the recommended dosage should be closely adhered to and the patient kept under close observation. Contra-Indications: Complete renal shutdown. If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, the drug should be discontinued. Therapy with furosemide should not be initiated in patients with hepatic coma and precoma or in states of electrolyte depletion until the basic condition is improved or corrected. Severe hyponatremia, hypokalemia, hypovolemia or hypotension must be regarded as contraindications until serum electrolytes and fluid balance and blood pressure have been restored to normal levels. Furosemide is also contraindicated in patients with a known history of hypersensitivity to this compound. As furosemide may be capable of displacing bilirubin from albumin at least in vitro, it should not be administered to jaundiced newborn infants or to infants suffering from diseases (e.g., Rh incompatibility, familial non-hemolytic jaundice, etc.) with the potential of causing hyperbilirubinemia and possibly kernicterus. Manufacturers' Warnings In Clinical States: Furosemide is a potent diuretic which if given in excessive amounts can lead to a profound diuresis with water and electrolyte depletion. Therefore, careful medical supervision is required, and dose and dose schedule have to be adjusted to the individual patient's needs (see Dosage). Cases of tinnitus and reversible deafness have been reported. There have also been some reports of cases, the majority in children undergoing renal transplantation, in which permanent deafness has occurred. In these latter cases, the onset of deafness was usually insidious and gradually progressive up to 6 months after furosemide therapy. Hearing impairment is more likely to occur in patients with severely reduced renal function who are given large doses of furosemide parenterally, at a rate exceeding 4 mg/min or in patients who are also receiving drugs known to be ototoxic. Sulfonamide diuretics have been reported to decrease arterial responsiveness to pressor amines and to enhance the effect of tubocurarine. Great caution should be exercised in administering curare or its derivatives to patients undergoing therapy with furosemide and it is advisable to discontinue furosemide for 1 week prior to any elective surgery. Pregnancy: The teratogenic and embryotoxic potential of furosemide in humans is unknown. The drug should not be used in pregnant women or in women of childbearing potential unless in the opinion of the attending physician the benefits to the patient outweigh the possible risk to the fetus. Lactation: It should be noted that diuretics may partially inhibit lactation and that furosemide passes into the breast milk. Precautions: General: During long-term therapy a high-potassium diet is recommended. Potassium supplements may be required especially when high doses are used for prolonged periods. Particular caution with potassium levels is necessary when the patient is on digitalis glycosides, potassium-depleting steroids, or in the case of infants and children. Potassium supplementation, diminution in dose, or discontinuation of furosemide therapy may be required. Since rigid sodium restriction is conducive to both hyponatremia and hypokalemia, strict restriction in sodium intake is not advisable in patients receiving furosemide therapy. Furosemide parenteral administered in doses up to 100 mg should be injected slowly (1 to 2 minutes) when the i.v. route is used. Furosemide may lower the state of patient alertness and/or reactivity particularly at the start of treatment, as a result of a reduction in blood pressure and of other adverse reactions. (see Adverse Effects). Geriatrics: Excessive diuresis induced by furosemide may result in dehydration and reduction of blood volume, with circulatory collapse and with the possibility of vascular thrombosis and embolism particularly in elderly patients. Furosemide may cause electrolyte depletion. Children: In children, urge to defecate, complaints of abdominal pain and cramping have been reported after i.v. furosemide. An association of these symptoms with a low serum calcium and/or a low calcium:protein ratio is possible. Calcium levels should be monitored when children are to receive i.v. furosemide for durations longer than a few days. Furosemide may lower serum calcium levels, and rare cases of tetany have been reported. Accordingly, periodic serum calcium concentrations should be obtained. Special Diseases and Conditions: Increases in blood glucose and alterations in glucose tolerance tests with abnormalities of the fasting and 2-hour postprandial blood sugar levels have been observed. Rare cases of precipitation of diabetes mellitus have been reported. Asymptomatic hyperuricemia can occur and gout may rarely be precipitated. It may be advisable to hospitalize patients with hepatic cirrhosis and ascites prior to initiating therapy. Sudden alterations of fluid and electrolyte balance in patients with cirrhosis may precipitate hepatic coma; therefore, strict observation is necessary during the period of diuresis. Supplemental potassium chloride and, if required, an aldosterone antagonist, are helpful in preventing hypokalemia and metabolic alkalosis. Laboratory Tests: Frequent serum electrolyte and CO2 content determinations should be performed during the first few months of therapy and periodically thereafter. It is essential to replace electrolyte losses and to maintain fluid balance so as to avoid any risk of electrolyte depletion (hyponatremia, hypochloremia, hypokalemia, hypomagnesemia or hypocalcemia), hypovolemia, or hypotension. Checks on urine and blood glucose should be made at regular intervals especially in diabetics and in those suspected of latent diabetes when receiving furosemide. Increases in blood glucose and alterations in glucose tolerance tests with abnormalities of the fasting and 2-hour postprandial blood sugar levels have been observed. Frequent BUN determinations during the first few months of therapy and periodically thereafter, as well as regular observations for possible occurrences of blood dyscrasias, liver damage or idiosyncratic reactions are advisable. Drug Interactions: Sulfonamide diuretics have been reported to decrease arterial responsiveness to pressor amines and to enhance the effect of tubocurarine or curare-type muscle relaxants. In edematous hypertensive patients being treated with antihypertensive agents, care should be taken to reduce the dose of these drugs when furosemide is administered, since furosemide potentiates their hypotensive effect. Especially in combination with ACE inhibitors, a marked hypotension may be seen sometimes progressing to shock. The concomitant administration of furosemide with ACE inhibitors may lead to deterioration in renal function and, in isolated cases, to acute renal failure. Since furosemide is a sulfonamide derivative, it should be used with caution in patients with known sulfonamide sensitivity. In case of concomitant abuse of laxatives, the risk of an increased potassium loss should be considered. Glucocorticoids, carbenoxolone and licorice may also increase potassium loss. It has been reported in the literature that diuretics such as furosemide may enhance the nephrotoxicity of cephaloridine. Therefore the simultaneous administration of both drugs is not advisable. Administration of furosemide to diabetic patients may result in possible decrease of diabetic control. Dosage adjustments of the anti-diabetic agent may be needed. Renal clearance of lithium is decreased in patients receiving furosemide, and lithium toxicity may result. Concurrent administration of furosemide and sucralfate should be avoided, as sucralfate reduces the absorption of furosemide and hence weakens its effect. Patients receiving high doses of salicylates in conjunction with furosemide may experience salicylate toxicity at lower doses because of competition for renal excretory sites. Nonsteroidal anti-inflammatory drugs (e.g., indomethacin, acetylsalicylic acid) may attenuate the effect of furosemide and may cause renal failure in case of pre-existing hypovolemia. Probenecid and anticonvulsant drugs (phenytoin, carbamazepine, phenobarbital) may also attenuate the effect of furosemide. Clinical studies have shown that the administration of indomethacin can reduce the natriuretic and antihypertensive effect of furosemide in some patients. This response has been attributed to inhibition of prostaglandin synthesis by indomethacin. Therefore, when indomethacin is added to the treatment of a patient receiving furosemide or furosemide is added to the treatment of a patient receiving indomethacin, the patient should be closely observed to determine if the desired effect of furosemide is obtained. Indomethacin blocks the furosemide-induced increase in plasma-renin activity. This fact should be kept in mind when evaluating plasma-renin activity in hypertensive patients. Hearing impairment is more likely to occur in patients who are also receiving drugs known to be ototoxic (e.g., aminoglycosides antibiotics, ethacrynic acid and cisplatin) (see Warnings). Administration of furosemide i.v. within 24 hours after the ingestion of chloral hydrate has caused the sensation of heat, sweating, restlessness, nausea, rise in blood pressure and tachycardia in isolated cases. Pediatrics: Renal calcifications (nephrolithiasis and nephrocalcinosis), from barely visible on x-ray to staghorn, have occurred in some severely premature infants treated with furosemide i.v. for edema due to patent ductus arteriosus and hyaline membrane disease. The concurrent use of chlorothiazide has been reported to decrease hypercalciuria and to dissolve some calculi. When administered to premature infants with respiratory distress syndrome in the first few weeks of life, diuretic treatment with furosemide may accentuate the risk of a patent ductus arteriosus. Adverse Reactions: Adverse reactions are categorized by body system: Metabolic: Electrolyte depletion has occurred during therapy with furosemide, especially in patients receiving higher doses with a restricted salt intake. Electrolyte depletion manifests itself by adverse reactions attributed to various body systems: weakness, dizziness, drowsiness, polyuria, polydipsia, orthostatic hypotension, lethargy, leg cramps, sweating, bladder spasms, anorexia, vomiting, mental confusion and meteorism (see Precautions). Transient elevations of BUN have been observed, especially in patients with renal insufficiency. As with other diuretics, there may be a transient rise in serum creatinine, uric acid (this may lead to gout attack in predisposed patients), cholesterol and triglyceride levels during furosemide treatment. Treatment with furosemide has occasionally caused some deterioration in cases of manifest diabetes, or has made latent diabetes manifest. Pre-existing metabolic alkalosis (e.g., in decompensated cirrhosis of the liver) may be aggravated. Cardiovascular: Too vigorous diuresis may induce orthostatic hypotension or acute hypotensive episodes. In extreme cases, hypovolemia may lead to dehydration, circulatory collapse and thrombophilia. Thrombophlebitis and emboli have been reported. CNS and Special Senses: At the commencement of treatment, excessive diuresis may give rise, especially in elderly patients, to a feeling of pressure in the head, dizziness, dryness of the mouth or blurring of vision. Paresthesia, vertigo, and xanthopsia have been reported. Cases of tinnitus and reversible deafness have been reported. There have also been some reports of cases, the majority in children undergoing renal transplantation, in which permanent deafness has occurred. In these latter cases, the onset of deafness is usually insidious and gradually progressive up to 6 months after furosemide therapy. Hearing impairment is more likely to occur in patients with severely reduced renal function who are given large doses of furosemide parenterally, at a rate exceeding 4 mg/min or in patients who are also receiving drugs known to be ototoxic (see Warnings). Dermatologic and Hypersensitivity: Various forms of dermatitis, including urticaria, erythema multiforme, exfoliative dermatitis, pruritus and epidermolysis bullosa have occurred. Dermatologic and hypersensitivity reactions to furosemide also include purpura, photosensitivity, rash. Systemic hypersensitivity reactions include vasculitis, interstitial nephritis and necrotizing angiitis. Anaphylactic shock is rare and can occur with the i.v. administration of furosemide. Hematologic: Anemia, eosinophilia, leukopenia and thrombocytopenia (with purpura) have occurred, as well as agranulocytosis, aplastic anemia and hemolytic anemia. Urogenital: Symptoms of obstructed micturition (e.g., in hydronephrosis, prostatic hypertrophy, ureterostenosis) may become manifest or may be aggravated during medication with diuretics. Gastrointestinal: In children, urge to defecate, complaints of abdominal pain and cramping have been reported after furosemide i.v. (see Precautions). Pancreatitis, anorexia, jaundice (intrahepatic cholestatic jaundice) oral and gastric burning, diarrhea, nausea, vomiting and constipation have been reported. Rare occurrences of sweet taste have been reported. Other: In addition, the following adverse reactions have been reported: transient pain at injection site following i.m. injection and paradoxical swelling. Symptoms And Treatment Of Overdose: Symptoms: Dehydration, electrolyte depletion and hypotension may be caused by overdosage or accidental ingestion. In cirrhotic patients, overdosage may precipitate hepatic coma. tag_Treatment Treatment: The drug should be discontinued and appropriate corrective treatment applied: replacement of excessive fluid and electrolyte losses; serum electrolytes, carbon dioxide level and blood pressure should be determined frequently. Adequate drainage must be assured in patients with urinary bladder outlet obstruction (such as prostatic hypertrophy). Dosage And Administration: Adults: Oral: Edema: The usual initial dose is 40 to 80 mg. Ordinarily a prompt diuresis ensues and the starting dose can then be maintained or even reduced. If a satisfactory diuresis has not occurred within 6 hours, succeeding doses should be increased by increments of 20 to 40 mg, if necessary. Maximum daily dose: 200 mg. Once the effective single dose has been determined, it may be repeated 1 to 3 times a day. The mobilization of edema may be most efficiently and safely accomplished by utilizing an intermittent dosage schedule in which furosemide is given for 2 to 4 consecutive days each week. With doses exceeding 120 mg/day, careful clinical and laboratory observations are particularly advisable. Hypertension: A dosage schedule of 20 to 40 mg twice daily is recommended. Individualized therapy is of great importance. Careful observations for changes in blood pressure must be made when furosemide is used with other antihypertensive drugs, especially during initial therapy. The dosage of other agents must be reduced by at least 50% as soon as furosemide is added to the regimen to prevent an excessive drop in blood pressure. As the blood pressure falls under the potentiating effect of furosemide, a further reduction in dosage, or even discontinuation of other antihypertensive drugs may be necessary. It is further recommended, if 40 mg twice daily does not lead to a clinically satisfactory response, to add other antihypertensive agents, rather than an increase in the dose of furosemide. Parenteral: Parenteral furosemide should not be added into the tubing of a running infusion solution. Edema: Usual initial dose is 20 to 40 mg injected as a single dose i.m. or i.v. I.V. injections should be given slowly over a period of 1 to 2 minutes. Ordinarily, a prompt diuresis ensues. If the diuretic response with a single dose of 20 to 40 mg is not satisfactory it may be increased by increments of 20 mg not sooner than 2 hours after the previous dose until the desired diuretic effect has been obtained. Maximum daily dose: 100 mg. Once the effective single dose has been determined, it should then be given once or twice daily. Parenteral therapy should be replaced by treatment with furosemide tablets as soon as this is practical. Acute Pulmonary Edema: The following schedule is recommended: 40 mg are to be slowly injected i.v. followed by another 40 mg i.v. 1 to 1.5 hours later if indicated by the patient's condition. Children: Oral and Parenteral: Therapy should be instituted in the hospital, in carefully selected patients, under close observation with frequent monitoring of serum electrolytes. Parenteral furosemide should not be added into the tubing of a running infusion solution. Orally or parenterally, the initial dose should be in the range of 0.5 to 1.0 mg/kg body weight. The total daily dose (given in divided doses of 6 to 12 hours apart) should not exceed 2 mg/kg orally or 1 mg/kg parenterally. In the newborn and in premature babies, the daily dose should not exceed 1 mg/kg. An intermittent dosage schedule should be adopted as soon as possible using the minimum effective dose at the longest possible intervals. Particular caution with regard to potassium levels is always desirable when furosemide is used in infants and children. Availability And Storage: Oral Solution: Each mL of clear, yellowish-orange solution contains: furosemide 10 mg. Bottles of 25 mL (with calibrated dropper) and 120 mL (with calibrated spoon). Protect from light. Parenteral: Each mL of injectable sterile solution contains: 10 mg of furosemide pH: 9.1. Ampuls of 2 mL, boxes of 5 and 50; ampuls of 4 mL, boxes of 5 and 50. Multidose vials of 30 mL (nonmedicinal ingredients: benzyl alcohol 9.0 mg/mL, edetate disodium, sodium chloride for isotonicity and sodium hydroxide for pH adjustment), cartons of 10. Tablets: 20 mg: Each white, round tablet (Code DLF) contains: furosemide 20 mg. Amber bottles of 300, boxes of 30. 40 mg: Each yellow, round, scored tablet (Code Lasix 40) contains: furosemide 40 mg. Amber bottles of 500, boxes of 30. 80 mg: Each yellow, flat, oblong tablet, scored both sides (Code DKF) contains: furosemide 80 mg. Amber bottles of 30 and 300. (Shown in Product Recognition Section
الأربعاء، 11 مارس 2009
body temp.
Body Temperature
What is body temperature?
Body temperature is a measure of the body's ability to generate and get rid of heat. The body is very good at keeping its temperature within a narrow, safe range in spite of large variations in temperatures outside the body.
When you are too hot, the blood vessels in your skin expand (dilate) to carry the excess heat to your skin's surface. You may begin to sweat, and as the sweat evaporates, it helps cool your body. When you are too cold, your blood vessels narrow (contract) so that blood flow to your skin is reduced to conserve body heat. You may start shivering, which is an involuntary, rapid contraction of the muscles. This extra muscle activity helps generate more heat. Under normal conditions, this keeps your body temperature within a narrow, safe range.
Where is body temperature measured?
Your body temperature can be measured in many locations on your body. The mouth, ear, armpit, and rectum are the most commonly used places. Temperature can also be measured on your forehead.
What are Fahrenheit and Celsius?
Thermometers are calibrated in either degrees Fahrenheit (°F) or degrees Celsius (°C), depending on the custom of the region. Temperatures in the United States are often measured in degrees Fahrenheit, but the standard in most other countries is degrees Celsius.
What is normal body temperature?
Most people think of a "normal" body temperature as an oral temperature of 98.6F. This is an average of normal body temperatures. Your temperature may actually be 1°F (0.6°C) or more above or below 98.6F. Also, your normal body temperature changes by as much as 1°F (0.6°C) throughout the day, depending on how active you are and the time of day. Body temperature is very sensitive to hormone levels and may be higher or lower when a woman is ovulating or having her menstrual period.
A rectal or ear (tympanic membrane) temperature reading is 0.5 to 1°F (0.3 to 0.6°C) higher than an oral temperature reading. A temperature taken in the armpit is 0.5 to 1°F (0.3 to 0.6°C) lower than an oral temperature reading.
What is a fever?
In most adults, an oral temperature above 100F or a rectal or ear temperature above 101F is considered a fever. A child has a fever when his or her rectal temperature is 100.4F or higher.
What can cause a fever?
A fever may occur as a reaction to:
Infection. This is the most common cause of a fever. Infections may affect the whole body or a specific body part (localized infection).
Medicines, such as antibiotics, narcotics, barbiturates, antihistamines, and many others. These are called drug fevers. Some medicines, such as antibiotics, raise the body temperature directly; others interfere with the body's ability to readjust its temperature when other factors cause the temperature to rise.
Severe trauma or injury, such as a heart attack, stroke, heat exhaustion or heatstroke, or burns.
Other medical conditions, such as arthritis, hyperthyroidism, and even some cancers, such as leukemia, Hodgkin's lymphoma, and liver and lung cancer
What is body temperature?
Body temperature is a measure of the body's ability to generate and get rid of heat. The body is very good at keeping its temperature within a narrow, safe range in spite of large variations in temperatures outside the body.
When you are too hot, the blood vessels in your skin expand (dilate) to carry the excess heat to your skin's surface. You may begin to sweat, and as the sweat evaporates, it helps cool your body. When you are too cold, your blood vessels narrow (contract) so that blood flow to your skin is reduced to conserve body heat. You may start shivering, which is an involuntary, rapid contraction of the muscles. This extra muscle activity helps generate more heat. Under normal conditions, this keeps your body temperature within a narrow, safe range.
Where is body temperature measured?
Your body temperature can be measured in many locations on your body. The mouth, ear, armpit, and rectum are the most commonly used places. Temperature can also be measured on your forehead.
What are Fahrenheit and Celsius?
Thermometers are calibrated in either degrees Fahrenheit (°F) or degrees Celsius (°C), depending on the custom of the region. Temperatures in the United States are often measured in degrees Fahrenheit, but the standard in most other countries is degrees Celsius.
What is normal body temperature?
Most people think of a "normal" body temperature as an oral temperature of 98.6F. This is an average of normal body temperatures. Your temperature may actually be 1°F (0.6°C) or more above or below 98.6F. Also, your normal body temperature changes by as much as 1°F (0.6°C) throughout the day, depending on how active you are and the time of day. Body temperature is very sensitive to hormone levels and may be higher or lower when a woman is ovulating or having her menstrual period.
A rectal or ear (tympanic membrane) temperature reading is 0.5 to 1°F (0.3 to 0.6°C) higher than an oral temperature reading. A temperature taken in the armpit is 0.5 to 1°F (0.3 to 0.6°C) lower than an oral temperature reading.
What is a fever?
In most adults, an oral temperature above 100F or a rectal or ear temperature above 101F is considered a fever. A child has a fever when his or her rectal temperature is 100.4F or higher.
What can cause a fever?
A fever may occur as a reaction to:
Infection. This is the most common cause of a fever. Infections may affect the whole body or a specific body part (localized infection).
Medicines, such as antibiotics, narcotics, barbiturates, antihistamines, and many others. These are called drug fevers. Some medicines, such as antibiotics, raise the body temperature directly; others interfere with the body's ability to readjust its temperature when other factors cause the temperature to rise.
Severe trauma or injury, such as a heart attack, stroke, heat exhaustion or heatstroke, or burns.
Other medical conditions, such as arthritis, hyperthyroidism, and even some cancers, such as leukemia, Hodgkin's lymphoma, and liver and lung cancer
الاثنين، 9 مارس 2009
dysphagia
Swallowing
Swallowing is a complex process. Some 50 pairs of muscles and many nerves work to move food from the mouth to the stomach. This happens in three stages. First, the tongue moves the food around in the mouth for chewing. Chewing makes the food the right size to swallow and helps mix the food with saliva. Saliva softens and moistens the food to make swallowing easier. During this first stage, the tongue collects the prepared food or liquid, making it ready for swallowing.
The second stage begins when the tongue pushes the food or liquid to the back of the mouth, which triggers a swallowing reflex that passes the food through the pharynx (the canal that connects the mouth with the esophagus). During this stage, the larynx (voice box) closes tightly and breathing stops to prevent food or liquid from entering the lungs.
The third stage begins when food or liquid enters the esophagus, the canal that carries food and liquid to the stomach. This passage through the esophagus usually occurs in about 3 seconds, depending on the texture or consistency of the food
Evaluation of Dysphagia
History:
In taking the history it is important to note the duration of the dysphagia. Also important is whether the problem is difficulty swallowing or pain on swallowing (odynophagia). Odynophagia suggests inflammatory or malignant neoplastic processes. The level of sensation of the difficulty in swallowing (“the catch”) should be sought. Suprasternal pain suggests a hypopharyngeal location of disease. A substernal or subxyphoid location of symptoms suggests an esophageal source. These locators can be misleading, though, as distal esophageal problems can occasionally present with suprasternal discomfort. Dysphagia to solids suggest esophageal or other structural obstruction. Dysphagia to liquids suggests pharyngeal disorders, including neuromuscular disease. Weight loss in a patient with dysphagia is an indicator of the significance and duration of the disease. Dietary changes in response to the dysphagia give insight into the nature and severity of disease. History of voice changes, hemoptysis, regurgitation of food, nasal leakage of liquids, and otalgia are all important to elicit. Previous surgery or trauma of the pharynx, chest, or abdomen should be sought. Patients should be probed about ingestion of caustic substances.
Review of Systems:
Review of systems often reveals systemic diseases that cause dysphagia. These include spinal osteoarthritis, tuberculosis, and thyroid enlargement. Systemic neuromuscular or autoimmune disorders may cause problems with esophageal motility. Otalgia may indicate upper digestive tract malignancy. Use of alcohol or tobacco raises suspicion of malignancy. A family history of digestive disease should be sought, such as history of oculopharyngeal dysphagia and muscular dystrophy. Use of certain medications such as antihistamines, anticholinergics, antidepressants, and antihypertensives can affect salivary gland function or the neurology of swallowing.
Physical Examination:
General factors such as body habitus, drooling, and mental status should be noted. Voice quality (e.g. a wet sounding voice suggesting pooling of secretions), Wheezing or labored breathing, and any cranial nerve weakness should be noted. Gurgling noise in the neck or crepitus in the neck may indicate the presence of Zenker’s diverticulum. Inspection or palpation of the tongue and tongue strength may unmask fibrillation or fasciculation of one or both sides. The oropharynx should be inspected for palatal elevation and posterior pharyngeal motion on phonation. Lateral movement of the mucosa of the posterior pharynx indicates weakness on the opposite side. Nasopharyngoscopy and hypopharyngoscopy can check for symmetry of the pharyngeal constrictors. Laryngeal examination is important but can be made difficult by the presence of pooled secretions. However, the nature of secretions gives clues to the nature of the disorder. Thick mucoid secretions are from standing accumulation such as paralysis or adynamic motor dysfunction. Foamy secretions in the piriform sinus or laryngeal vestibule indicate turbulence secondary to anatomic obstruction such as a nonrelaxing cricopharyngeal muscle or stricture. Vocal fold movement during variable pitch phonation, whispering, loud voicing, and during inspiration should be observed. Arytenoids should be inspected for immobility. The interarytenoid mucosa is erythematous and edematous in gastroesophageal reflux disease.
Imaging Studies for Evaluation of Dysphagia
Imaging studies for dysphagia should be chosen based on the history associated with the dysphagia.
Plain Films:
Plain films are indicated in diagnosing specific causes of dysphagia, such as inflammatory (epiglottitis, retropharyngeal abscess) or radio-opaque foreign bodies. The advantages of this modality are that it is cheap and quick. The disadvantages are its inability to detect mechanics of the swallow and inability to resolve mucosal surfaces.
Barium Esophagram
The barium esophagram involves the use of a cup of liquid barium that is swallowed, then followed fluoroscopically to the stomach. Because the study is documented only on plain film, it is not considered a dynamic swallow study. The air contrast esophagram uses effervescent granules followed by administration of barium to provide better anatomic detail. The advantages of the study are that it is widely available, and with air contrast it provides better anatomic detail. The disadvantages are that the study involves radiation exposure, the logistics are difficult in bedridden patients, and the study is not a dynamic one so it cannot adequately detect dynamic dysfunction. The study is indicated in patients in whom structural disorders are suspected (e.g. dysphagia to solid foods and not to liquids) because of its relatively good level of anatomic detail.
Manometry:
Manometry uses a catheter that measures pressures at various intervals along the length of the esophagus. With each swallow, data on strength, timing, and sequencing of pressure events are obtained. The advantage of the study is that it is an actual test of pressure wave physiology. The disadvantages of the study are that it is not widely available, cannot diagnose visible lesions, is unpleasant, and is a technically demanding study to perform. For these reasons this study is rarely used except in cases where elevated intraluminal pressures must be followed (e.g. achalasia). The study may be indicated for patients who need recurrent intraluminal pressure assessment for achalasia or diffuse esophageal spasm.
Bolus Scintigraphy:
Bolus Scintigraphy is a study in which a short-lived radioactive isotope is mixed with a single swallowed bolus. A gamma camera images the radiation field and counts the number of radiation particles present. The advantages of this study are that it uses less radiation than standard radiography and it allows quantitative measurement of the fraction of the bolus aspirated. Disadvantages are that the study provides no anatomic detail. It uses only a single bolus-different consistencies of boluses are not tested. Also, the test is not widely available. Scintigraphy may be indicated to follow improvement in a patient with a history of aspiration or to follow esophageal emptying in achalasia.
Ultrasound:
Ultrasound can image the upper digestive tract, assess mobility and bolus transit, and identify vallecular stasis. The advantages of the study are that it uses no radiation, is portable, and normal food can be used. The disadvantages are that it is not widely available and the study is segmental in nature so that anatomic detail is poor.
Flexible Endoscopic Evaluation of Swallowing (FEES):
The flexible endoscopic evaluation of swallowing utilizes commonly available and portable equipment to evaluate swallowing. In this study, the flexible nasopharyngoscope is passed thought the nose to the nasopharynx in order to view the upper aerodigestive tract. Anatomy and function of the upper aerodigestive tract are assessed (palate, pharynx, larynx function, salivary pooling, and sensation). Then swallowing is assessed with boluses of varying consistencies. A description of the study follows: First, the flexible scope is passed through he anesthetized nasal fossa with the tip in the posterior part of the nasal fossa. The palate is checked from the nasopharyngeal surface. Subtle palate weakness can be detected. Oral sounds, e.g. “k,k,k,” “ss,” and spontaneous speech are observed as part of palate function testing. Even mild unilateral weakness can be detected with this test. After checking the palate, the tip of the scope is moved beyond the edge of the palate and is turned downward. This allows a panoramic assessment of the laryngopharynx and observation of pooling of secretions in the piriform sinuses, vallecula, and laryngeal vestibule. Next, the tip of the fiberscope is positioned parallel to the posterior pharyngeal wall opposite to the epiglottis to obtain a larynx view. Vocal cord mobility and closure are assessed in this view. Sensory testing can be performed at this point by touching the tip of the fiberscope to various points on the hypopharynx and larynx to assess symmetry of reaction.
A more quantitative sensory testing modality involves the use of controlled pulses of air in set pressures to determine sensory threshold of laryngeal closure. After this structural assessment the tip of the endoscope is pulled back to the level of the soft palate and food of various consistencies is administered. This is often followed by administration of methylene blue dye. This allows visualization of leakage during the oral phase, visualization of overflow aspiration from the hypopharynx and visualization of tell-tale signs of aspiration with blue dye staining the laryngeal vestibule. Overall, the advantages of the FEES are that the equipment is simple, widely available, portable, does not expose the patient to radiation, can be used to train the patient in speech therapy via biofeedback. It allows a better assessment of neurologic status (including sensation) and gives a more detailed rendering of the anatomy than is available from other methodologies. The disadvantages of the FEES include the "blind spot" that occurs during the swallow, which prevents direct visualization of aspiration and penetration, and the fact that the cricopharyngeus and esophagus cannot be assessed. FEES is indicated in evaluation of oral and pharyngeal sources of dysphagia.
Causes of Dysphagia
Foreign Bodies:
In the pharynx, fish and chicken bones are the usual foreign body culprits. Foreign bodies of the pharynx usually lodge themselves in the pharyngeal or lingual tonsils or in the piriform sinuses. The patient has a globus sensation or sharp pain when attempting to swallow. Patients usually present within a few hours, but foreign bodies are actually identified on endoscopy in only 25% of patients who complain of their presence. Most of the time the foreign body passes, and mucosal trauma from the passage of the body produces symptoms for several days. In most cases, radiography is not necessary. Simple examination with a head mirror and/or a nasopharyngoscope should be performed. Usually, the pharyngeal foreign body can be identified and removed all at the same time. In rare cases, general anesthesia may be required. If complete examination reveals no foreign body but suspicion is high, then repeat exam should be performed in 24 hours. If symptoms persist, radiographs or endoscopy may be considered. Serious complications can result from persistent foreign bodies. The include retropharyngeal abscess (the most common cause of which is a fish bone in the retropharyngeal space), perforation, and cellulitis. In the face of these complications, the patient will present with the foreign body complaint in addition to fever, dysphagia, and odynophagia.
The most common esophageal foreign bodies in adults are meat impactions and bones. Coins and button batteries are not uncommon in children. Most adults have other esophageal pathology contributing to the impaction of the foreign body. Denture use is a common predisposing factor as dentures decrease sensation on the palate leading to misjudging of the size of the bolus. Impaction usually occurs at areas of physiologic narrowing. These include the cricopharyngeus, the point where the esophagus is compressed by the aortic arch, the left main-stem bronchus, and the lower esophageal sphincter. They may also lodge at areas of pathologic narrowing such as a peptic stricture or a Schatzki's ring. Symptoms vary from none to complete obstruction with drooling. Other symptoms include dysphagia, odynophagia, foreign body sensation, excessive salivation, vomiting, chest pain and rarely wheezing (secondary to tracheal displacement). Physical exam is usually normal. Evidence of emphysema in the neck or chest may be a sign of perforation. Fever may be evidence of mediastinitis. All patients with esophageal foreign bodies should undergo radiography, usually a PA and lateral chest and neck film. Failure to detect a foreign body does not rule it out-esophagoscopy should be performed in such cases.
In management of esophageal foreign bodies, airway protection is critical as esophageal foreign bodies may become airway foreign bodies. Asymptomatic coins in the distal esophagus should be given 12 hours to pass, whereas coins in the mid to upper esophagus should be removed as soon as possible to avoid regurgitation of the coin into the airway. Rigid and flexible endoscopy are equally efficacious for most foreign bodies. Flexible endoscopy does not require general anesthesia, but it also does not protect the trachea. Sharp or pointed objects may cause significant trauma and should be removed via rigid endoscopy. After removal of a foreign body, a chest X-ray should be obtained and the patient should be observed for 24 hours for signs and symptoms of mediastinitis. Button batteries are particularly dangerous and should be removed immediately because their ability to cause direct corrosion, low voltage burns, and direct pressure necrosis, leading to complications such as perforation, and tracheal and aortic fistulas. They can be distinguished from coins because button batteries have a halo on PA films because of their bilaminar structure. Careful endoscopy should be performed at the time of removal, minding the fact that the battery may have corroded the esophageal wall. Barium esophagrams should be performed 24 hours after removal of a button battery and again 14 days later to check for fistulization. Alternative methods to address foreign bodies includes the use of Balloon catheters to remove foreign bodies, but they do not provide for control of the foreign body. Glucagon has been shown to relax the lower esophageal sphincter, but it is not successful in foreign body treatment when other pathology is present.
Cricopharyngeal Achalasia:
A prominent cricopharyngeus can cause dysphagia by failure of adequate opening of the pharyngoesophageal segment. This failure to open occurs secondary to failure of pharyngeal and laryngeal elevation during swallowing, abnormal cricopharyngeal contraction, or inflammatory (e.g. gastroesophageal reflux disease, GERD) or neoplastic process. Symptoms range from a "globus" sensation to significant dysphagia with pooling of secretions and aspiration. Medical therapy includes treatment of GERD and Botox injection into the cricopharyngeus for temporary relief. If Botox works to correct dysphagia, cricopharyngeal myotomy may provide more permanent relief. In this somewhat controversial procedure, a careful releasing scalpel incision is made in the cricopharyngeal muscle avoiding mucosal damage. In properly chosen patients, this procedure has a high success rate. Patients with clear signs of cricopharyngeal spasm/hypertrophy on radiology and manometry are most likely to benefit.
Zenker's Diverticulum:
The Zenker's diverticulum is an acquired mucosal herniation through a posterior portion of the cricopharyngeus in an area of congenital weakness in the muscle known as Killian's dehiscence. Symptoms caused by the diverticulum include coughing up undigested food, aspiration, and chronic mucus production. Small diverticula can be treated by cricopharyngeal myotomy alone. Larger diverticula require dissection off of the rest of the esophagus and transection with the defect sutured in layers. Diverticulopexy, or suspension of the diverticulum vertically in pre-vertebral fascia is used to shorten the procedure and reduce risk in high risk elderly patients. Endoscopic techniques use a variation of the Van Overbeek's diverticuloscope and the CO2 laser to perform the diverticulotomy. The GIA stapler can also be used to divide and secure the pouch endoscopically.
Lateral Pharyngeal Pouches and Diverticula:
Lateral pharyngeal pouches are transient or persistent protrusions of the upper lateral pharyngeal wall in an area of weakness of the unsupported thyrohyoid membrane. They usually do not require surgical treatment, but can be treated in a similar fashion to Zenker's diverticula.
Cervical Spine Disease:
Large osteoarthritic spurs may develop on the cervical spines of patients with long-standing osteoarthritis. These spurs are a common finding in patients with diffuse idiopathic hyperostosis. The spurs are usually asymptomatic, but they may affect swallowing. Surgical resection of the spurs has been shown to help in some patients.
Anterior surgical approaches to the spine that require dissection and retraction of the larynx and pharynx can cause temporary or prolonged dysphagia secondary to interruption of the motor or sensory innervation.
Tracheostomy:
Tracheostomy affects swallowing in several ways. First, by tethering the trachea to the anterior neck skin (especially with use of the Bjork flap), the tracheostomy prevents proper laryngeal elevation during the pharyngeal phase of swallowing. Direct pressure from the trachea with or without the cuff increases extrinsic esophageal pressure and leads to regurgitation and even aspiration. Tracheostomy may decrease sensitivity of the glottic closure reflex, resulting in increased risk of aspiration. To minimize these complications the smallest sized tracheostomy possible should be used and the airway should be closely monitored and frequently suctioned.
Strictures/Caustic Ingestion:
Strictures most often result from reflux of gastric acid into the esophagus, but also can result from ingestion of caustic substances. Rarely, strictures are caused by medications such as doxycycline, oral potassium chloride, and quinidine. Alkali ingestion occurs most frequently in children and causes rapid liquefaction necrosis and penetrates deeper than acid. Acid causes coagulation necrosis and creates an eschar that prevents deep burns. The acute reaction in the ingestion of caustic substances includes odynophagia, dysphagia, and inflammatory edema. Supraglottic edema can cause stridor and airway distress. Deep burns, especially with alkali, can cause perforation. Initial endoscopic evaluation is necessary within 24-48 hours of ingestion. If the injury is deep enough, stricture formation is noted 3-6 weeks later. Radiographic studies should be performed after three weeks to assess for the formation of strictures. The treatment for strictures, should they occur is dilatation or even excision.
Achalasia:
Achalasia is characterized by distal esophageal flaccidity associated with failure of the distal esophageal sphincter to relax. Patients present with dysphagia for solids greater than liquids. Radiology reveals a bird's beak deformity. Manometric studies confirm increased intraluminal pressure. Therapies include nitrates and calcium channel blockers, injection of botulinum toxin into the lower esophagus, endoscopic balloon dilation or, usually as a last resort, myotomy.
Diffuse Esophageal Spasm:
Patients with diffuse esophageal spasm suffer substernal cramp-like pain that may mimic myocardial infarction. Contrast and manometric studies demonstrate diffuse spastic activity. Treatment includes medical and surgical options similar to achalasia with referral to GI medicine.
Gastro-esophageal Reflux Disease (GERD):
GERD is recognized in about 10-15% of the population. The disease does not typically cause dysphagia, so other causes should be explored. The cause of GERD is related to incompetence of the lower esophageal sphincter. Regurgitation of stomach contents may cause sensation of subxyphoid pressure. Severe disease may lead to stricture formation, Barrett's esophagus, and increased risk of esophageal cancer. Radiography shows evidence of lower esophageal sphincter incompetence or sliding hiatal hernia in 1/3 of patients. Indirect laryngoscopy may show interarytenoid erythema or edema. Manometry shows decreased lower esophageal sphincter tone. The gold standard for diagnosis is the 24 hour pH probe. Treatment is with anti-reflux medications such as H2 blockers and proton pump inhibitors along with life-style modifications.
Cancer of the Larynx or Pharynx:
Cancer of the upper aerodigestive tract is often associated with odynophagia. Patients usually have a history of heavy smoking and/or drinking and unilateral throat pain on swallowing radiating to the ipsilateral ear or to the angle of the mandible. Careful physical exam usually identifies the lesion.
Cancer of the Esophagus:
Cancer of the esophagus carries a very vague symptom complex and is usually diagnosed late in its course, accounting for the poor survival rate. A chief symptom is dysphagia to solids more than liquids.
Stroke:
Swallowing difficulty after stroke may occur in up to 47% of cases. Most patients recover within one week. However, there is a high rate of aspiration pneumonia in these patients. Causes for dysphagia after stroke include delayed triggering of the swallow reflex, cricopharyngeal dysfunction, reduced lingual and pharyngeal control, and weak cough. With brain stem strokes, direct cranial nerve deficits can lead to further impairment of glottis closure and coordination of phases of swallowing. Treatment consists of rehabilitative speech therapy and placement of a nasoduodenal feeding tube or gastric feeding tube to avoid aspiration. Also frequent pulmonary toilet is required. If laryngeal impairment is permanent, vocal cord medialization procedures, narrow field laryngectomy, or other procedures may be useful.
Laryngeal Nerve Injury:
Isolated recurrent laryngeal nerve injuries result in dysphagia and aspiration secondary to decreased glottic closure pressures and neurogenic dysfunction of the inferior constrictor and cricopharyngeus muscles. Treatment is often by true vocal fold gelfoam injection for temporary medialization of the paralyzed vocal fold, followed later by medialization thyroplasty.
Parkinson's Disease:
Affecting 1% of people over age 50, Parkinson's disease is a progressive disorder of the CNS marked by the classic triad of resting tremor, bradykinesia and rigidity. Dysphagia in Parkinson's disease is addressed by dietary modification and gastric feeding tube placement for end-stage disease.
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Muscular Dystrophy:
Muscular dystrophy can result in spasm of the SCM, masticator, or cricopharyngeus muscles. An oculopharyngeal form of muscular dystrophy also exists.
Myasthenia Gravis:
Dysphagia may be the presenting symptom in this disorder of acetylcholine receptors and aspiration pneumonia may be the terminal event. Dysphagia and fatigue are typically worse later in the day.
Autoimmune Disorders:
Autoimmune disorders that carry a high incidence of dysphagia include systemic sclerosis, system lupus erythematosis, dermatomyositis, mixed connective tissue disease, mucosal pemphigoid, epidermolysis bullosa, Sjogren's syndrome (xerostomia) and Rheumatoid arthritis (cricoarytenoid joint fixation).
Aging:
Dysphagia affects 2% of the population over the age of 65. Oral preparatory phase problems result from poor dentition, and oral phase problems result from loss of tongue connective tissue. Pharyngeal phase changes include increased pharyngeal transit time and prolonged upper esophageal sphincter relaxation time. With these physiologic changes, any superimposed pathology is easily noticed in the otherwise healthy elderly individual.
Children:
In children and infants, nasal obstruction may present with feeding difficulties. Nasal masses, choanal atresia, and choanal stenosis fall in this category. Oral lesions such as cleft lip or palate, mucoceles, ranulas, and Warthin's duct stenosis may cause dysphagia. Upper aerodigestive tract anomalies such as laryngomalacia, vocal cord paralysis, laryngeal clefts, tracheo-esophageal fistula, foregut malformations, or vascular rings of the aorta or pulmonary arteries that compress the esophagus or trachea may all contribute to feeding problems and dysphagia. Tumors of the aerodigestive tract which can certainly cause dysphagia include hemangiomas, lymphangiomas, papillomas, leiomyomas, and neurofibromas.
Swallowing is a complex process. Some 50 pairs of muscles and many nerves work to move food from the mouth to the stomach. This happens in three stages. First, the tongue moves the food around in the mouth for chewing. Chewing makes the food the right size to swallow and helps mix the food with saliva. Saliva softens and moistens the food to make swallowing easier. During this first stage, the tongue collects the prepared food or liquid, making it ready for swallowing.
The second stage begins when the tongue pushes the food or liquid to the back of the mouth, which triggers a swallowing reflex that passes the food through the pharynx (the canal that connects the mouth with the esophagus). During this stage, the larynx (voice box) closes tightly and breathing stops to prevent food or liquid from entering the lungs.
The third stage begins when food or liquid enters the esophagus, the canal that carries food and liquid to the stomach. This passage through the esophagus usually occurs in about 3 seconds, depending on the texture or consistency of the food
Evaluation of Dysphagia
History:
In taking the history it is important to note the duration of the dysphagia. Also important is whether the problem is difficulty swallowing or pain on swallowing (odynophagia). Odynophagia suggests inflammatory or malignant neoplastic processes. The level of sensation of the difficulty in swallowing (“the catch”) should be sought. Suprasternal pain suggests a hypopharyngeal location of disease. A substernal or subxyphoid location of symptoms suggests an esophageal source. These locators can be misleading, though, as distal esophageal problems can occasionally present with suprasternal discomfort. Dysphagia to solids suggest esophageal or other structural obstruction. Dysphagia to liquids suggests pharyngeal disorders, including neuromuscular disease. Weight loss in a patient with dysphagia is an indicator of the significance and duration of the disease. Dietary changes in response to the dysphagia give insight into the nature and severity of disease. History of voice changes, hemoptysis, regurgitation of food, nasal leakage of liquids, and otalgia are all important to elicit. Previous surgery or trauma of the pharynx, chest, or abdomen should be sought. Patients should be probed about ingestion of caustic substances.
Review of Systems:
Review of systems often reveals systemic diseases that cause dysphagia. These include spinal osteoarthritis, tuberculosis, and thyroid enlargement. Systemic neuromuscular or autoimmune disorders may cause problems with esophageal motility. Otalgia may indicate upper digestive tract malignancy. Use of alcohol or tobacco raises suspicion of malignancy. A family history of digestive disease should be sought, such as history of oculopharyngeal dysphagia and muscular dystrophy. Use of certain medications such as antihistamines, anticholinergics, antidepressants, and antihypertensives can affect salivary gland function or the neurology of swallowing.
Physical Examination:
General factors such as body habitus, drooling, and mental status should be noted. Voice quality (e.g. a wet sounding voice suggesting pooling of secretions), Wheezing or labored breathing, and any cranial nerve weakness should be noted. Gurgling noise in the neck or crepitus in the neck may indicate the presence of Zenker’s diverticulum. Inspection or palpation of the tongue and tongue strength may unmask fibrillation or fasciculation of one or both sides. The oropharynx should be inspected for palatal elevation and posterior pharyngeal motion on phonation. Lateral movement of the mucosa of the posterior pharynx indicates weakness on the opposite side. Nasopharyngoscopy and hypopharyngoscopy can check for symmetry of the pharyngeal constrictors. Laryngeal examination is important but can be made difficult by the presence of pooled secretions. However, the nature of secretions gives clues to the nature of the disorder. Thick mucoid secretions are from standing accumulation such as paralysis or adynamic motor dysfunction. Foamy secretions in the piriform sinus or laryngeal vestibule indicate turbulence secondary to anatomic obstruction such as a nonrelaxing cricopharyngeal muscle or stricture. Vocal fold movement during variable pitch phonation, whispering, loud voicing, and during inspiration should be observed. Arytenoids should be inspected for immobility. The interarytenoid mucosa is erythematous and edematous in gastroesophageal reflux disease.
Imaging Studies for Evaluation of Dysphagia
Imaging studies for dysphagia should be chosen based on the history associated with the dysphagia.
Plain Films:
Plain films are indicated in diagnosing specific causes of dysphagia, such as inflammatory (epiglottitis, retropharyngeal abscess) or radio-opaque foreign bodies. The advantages of this modality are that it is cheap and quick. The disadvantages are its inability to detect mechanics of the swallow and inability to resolve mucosal surfaces.
Barium Esophagram
The barium esophagram involves the use of a cup of liquid barium that is swallowed, then followed fluoroscopically to the stomach. Because the study is documented only on plain film, it is not considered a dynamic swallow study. The air contrast esophagram uses effervescent granules followed by administration of barium to provide better anatomic detail. The advantages of the study are that it is widely available, and with air contrast it provides better anatomic detail. The disadvantages are that the study involves radiation exposure, the logistics are difficult in bedridden patients, and the study is not a dynamic one so it cannot adequately detect dynamic dysfunction. The study is indicated in patients in whom structural disorders are suspected (e.g. dysphagia to solid foods and not to liquids) because of its relatively good level of anatomic detail.
Manometry:
Manometry uses a catheter that measures pressures at various intervals along the length of the esophagus. With each swallow, data on strength, timing, and sequencing of pressure events are obtained. The advantage of the study is that it is an actual test of pressure wave physiology. The disadvantages of the study are that it is not widely available, cannot diagnose visible lesions, is unpleasant, and is a technically demanding study to perform. For these reasons this study is rarely used except in cases where elevated intraluminal pressures must be followed (e.g. achalasia). The study may be indicated for patients who need recurrent intraluminal pressure assessment for achalasia or diffuse esophageal spasm.
Bolus Scintigraphy:
Bolus Scintigraphy is a study in which a short-lived radioactive isotope is mixed with a single swallowed bolus. A gamma camera images the radiation field and counts the number of radiation particles present. The advantages of this study are that it uses less radiation than standard radiography and it allows quantitative measurement of the fraction of the bolus aspirated. Disadvantages are that the study provides no anatomic detail. It uses only a single bolus-different consistencies of boluses are not tested. Also, the test is not widely available. Scintigraphy may be indicated to follow improvement in a patient with a history of aspiration or to follow esophageal emptying in achalasia.
Ultrasound:
Ultrasound can image the upper digestive tract, assess mobility and bolus transit, and identify vallecular stasis. The advantages of the study are that it uses no radiation, is portable, and normal food can be used. The disadvantages are that it is not widely available and the study is segmental in nature so that anatomic detail is poor.
Flexible Endoscopic Evaluation of Swallowing (FEES):
The flexible endoscopic evaluation of swallowing utilizes commonly available and portable equipment to evaluate swallowing. In this study, the flexible nasopharyngoscope is passed thought the nose to the nasopharynx in order to view the upper aerodigestive tract. Anatomy and function of the upper aerodigestive tract are assessed (palate, pharynx, larynx function, salivary pooling, and sensation). Then swallowing is assessed with boluses of varying consistencies. A description of the study follows: First, the flexible scope is passed through he anesthetized nasal fossa with the tip in the posterior part of the nasal fossa. The palate is checked from the nasopharyngeal surface. Subtle palate weakness can be detected. Oral sounds, e.g. “k,k,k,” “ss,” and spontaneous speech are observed as part of palate function testing. Even mild unilateral weakness can be detected with this test. After checking the palate, the tip of the scope is moved beyond the edge of the palate and is turned downward. This allows a panoramic assessment of the laryngopharynx and observation of pooling of secretions in the piriform sinuses, vallecula, and laryngeal vestibule. Next, the tip of the fiberscope is positioned parallel to the posterior pharyngeal wall opposite to the epiglottis to obtain a larynx view. Vocal cord mobility and closure are assessed in this view. Sensory testing can be performed at this point by touching the tip of the fiberscope to various points on the hypopharynx and larynx to assess symmetry of reaction.
A more quantitative sensory testing modality involves the use of controlled pulses of air in set pressures to determine sensory threshold of laryngeal closure. After this structural assessment the tip of the endoscope is pulled back to the level of the soft palate and food of various consistencies is administered. This is often followed by administration of methylene blue dye. This allows visualization of leakage during the oral phase, visualization of overflow aspiration from the hypopharynx and visualization of tell-tale signs of aspiration with blue dye staining the laryngeal vestibule. Overall, the advantages of the FEES are that the equipment is simple, widely available, portable, does not expose the patient to radiation, can be used to train the patient in speech therapy via biofeedback. It allows a better assessment of neurologic status (including sensation) and gives a more detailed rendering of the anatomy than is available from other methodologies. The disadvantages of the FEES include the "blind spot" that occurs during the swallow, which prevents direct visualization of aspiration and penetration, and the fact that the cricopharyngeus and esophagus cannot be assessed. FEES is indicated in evaluation of oral and pharyngeal sources of dysphagia.
Causes of Dysphagia
Foreign Bodies:
In the pharynx, fish and chicken bones are the usual foreign body culprits. Foreign bodies of the pharynx usually lodge themselves in the pharyngeal or lingual tonsils or in the piriform sinuses. The patient has a globus sensation or sharp pain when attempting to swallow. Patients usually present within a few hours, but foreign bodies are actually identified on endoscopy in only 25% of patients who complain of their presence. Most of the time the foreign body passes, and mucosal trauma from the passage of the body produces symptoms for several days. In most cases, radiography is not necessary. Simple examination with a head mirror and/or a nasopharyngoscope should be performed. Usually, the pharyngeal foreign body can be identified and removed all at the same time. In rare cases, general anesthesia may be required. If complete examination reveals no foreign body but suspicion is high, then repeat exam should be performed in 24 hours. If symptoms persist, radiographs or endoscopy may be considered. Serious complications can result from persistent foreign bodies. The include retropharyngeal abscess (the most common cause of which is a fish bone in the retropharyngeal space), perforation, and cellulitis. In the face of these complications, the patient will present with the foreign body complaint in addition to fever, dysphagia, and odynophagia.
The most common esophageal foreign bodies in adults are meat impactions and bones. Coins and button batteries are not uncommon in children. Most adults have other esophageal pathology contributing to the impaction of the foreign body. Denture use is a common predisposing factor as dentures decrease sensation on the palate leading to misjudging of the size of the bolus. Impaction usually occurs at areas of physiologic narrowing. These include the cricopharyngeus, the point where the esophagus is compressed by the aortic arch, the left main-stem bronchus, and the lower esophageal sphincter. They may also lodge at areas of pathologic narrowing such as a peptic stricture or a Schatzki's ring. Symptoms vary from none to complete obstruction with drooling. Other symptoms include dysphagia, odynophagia, foreign body sensation, excessive salivation, vomiting, chest pain and rarely wheezing (secondary to tracheal displacement). Physical exam is usually normal. Evidence of emphysema in the neck or chest may be a sign of perforation. Fever may be evidence of mediastinitis. All patients with esophageal foreign bodies should undergo radiography, usually a PA and lateral chest and neck film. Failure to detect a foreign body does not rule it out-esophagoscopy should be performed in such cases.
In management of esophageal foreign bodies, airway protection is critical as esophageal foreign bodies may become airway foreign bodies. Asymptomatic coins in the distal esophagus should be given 12 hours to pass, whereas coins in the mid to upper esophagus should be removed as soon as possible to avoid regurgitation of the coin into the airway. Rigid and flexible endoscopy are equally efficacious for most foreign bodies. Flexible endoscopy does not require general anesthesia, but it also does not protect the trachea. Sharp or pointed objects may cause significant trauma and should be removed via rigid endoscopy. After removal of a foreign body, a chest X-ray should be obtained and the patient should be observed for 24 hours for signs and symptoms of mediastinitis. Button batteries are particularly dangerous and should be removed immediately because their ability to cause direct corrosion, low voltage burns, and direct pressure necrosis, leading to complications such as perforation, and tracheal and aortic fistulas. They can be distinguished from coins because button batteries have a halo on PA films because of their bilaminar structure. Careful endoscopy should be performed at the time of removal, minding the fact that the battery may have corroded the esophageal wall. Barium esophagrams should be performed 24 hours after removal of a button battery and again 14 days later to check for fistulization. Alternative methods to address foreign bodies includes the use of Balloon catheters to remove foreign bodies, but they do not provide for control of the foreign body. Glucagon has been shown to relax the lower esophageal sphincter, but it is not successful in foreign body treatment when other pathology is present.
Cricopharyngeal Achalasia:
A prominent cricopharyngeus can cause dysphagia by failure of adequate opening of the pharyngoesophageal segment. This failure to open occurs secondary to failure of pharyngeal and laryngeal elevation during swallowing, abnormal cricopharyngeal contraction, or inflammatory (e.g. gastroesophageal reflux disease, GERD) or neoplastic process. Symptoms range from a "globus" sensation to significant dysphagia with pooling of secretions and aspiration. Medical therapy includes treatment of GERD and Botox injection into the cricopharyngeus for temporary relief. If Botox works to correct dysphagia, cricopharyngeal myotomy may provide more permanent relief. In this somewhat controversial procedure, a careful releasing scalpel incision is made in the cricopharyngeal muscle avoiding mucosal damage. In properly chosen patients, this procedure has a high success rate. Patients with clear signs of cricopharyngeal spasm/hypertrophy on radiology and manometry are most likely to benefit.
Zenker's Diverticulum:
The Zenker's diverticulum is an acquired mucosal herniation through a posterior portion of the cricopharyngeus in an area of congenital weakness in the muscle known as Killian's dehiscence. Symptoms caused by the diverticulum include coughing up undigested food, aspiration, and chronic mucus production. Small diverticula can be treated by cricopharyngeal myotomy alone. Larger diverticula require dissection off of the rest of the esophagus and transection with the defect sutured in layers. Diverticulopexy, or suspension of the diverticulum vertically in pre-vertebral fascia is used to shorten the procedure and reduce risk in high risk elderly patients. Endoscopic techniques use a variation of the Van Overbeek's diverticuloscope and the CO2 laser to perform the diverticulotomy. The GIA stapler can also be used to divide and secure the pouch endoscopically.
Lateral Pharyngeal Pouches and Diverticula:
Lateral pharyngeal pouches are transient or persistent protrusions of the upper lateral pharyngeal wall in an area of weakness of the unsupported thyrohyoid membrane. They usually do not require surgical treatment, but can be treated in a similar fashion to Zenker's diverticula.
Cervical Spine Disease:
Large osteoarthritic spurs may develop on the cervical spines of patients with long-standing osteoarthritis. These spurs are a common finding in patients with diffuse idiopathic hyperostosis. The spurs are usually asymptomatic, but they may affect swallowing. Surgical resection of the spurs has been shown to help in some patients.
Anterior surgical approaches to the spine that require dissection and retraction of the larynx and pharynx can cause temporary or prolonged dysphagia secondary to interruption of the motor or sensory innervation.
Tracheostomy:
Tracheostomy affects swallowing in several ways. First, by tethering the trachea to the anterior neck skin (especially with use of the Bjork flap), the tracheostomy prevents proper laryngeal elevation during the pharyngeal phase of swallowing. Direct pressure from the trachea with or without the cuff increases extrinsic esophageal pressure and leads to regurgitation and even aspiration. Tracheostomy may decrease sensitivity of the glottic closure reflex, resulting in increased risk of aspiration. To minimize these complications the smallest sized tracheostomy possible should be used and the airway should be closely monitored and frequently suctioned.
Strictures/Caustic Ingestion:
Strictures most often result from reflux of gastric acid into the esophagus, but also can result from ingestion of caustic substances. Rarely, strictures are caused by medications such as doxycycline, oral potassium chloride, and quinidine. Alkali ingestion occurs most frequently in children and causes rapid liquefaction necrosis and penetrates deeper than acid. Acid causes coagulation necrosis and creates an eschar that prevents deep burns. The acute reaction in the ingestion of caustic substances includes odynophagia, dysphagia, and inflammatory edema. Supraglottic edema can cause stridor and airway distress. Deep burns, especially with alkali, can cause perforation. Initial endoscopic evaluation is necessary within 24-48 hours of ingestion. If the injury is deep enough, stricture formation is noted 3-6 weeks later. Radiographic studies should be performed after three weeks to assess for the formation of strictures. The treatment for strictures, should they occur is dilatation or even excision.
Achalasia:
Achalasia is characterized by distal esophageal flaccidity associated with failure of the distal esophageal sphincter to relax. Patients present with dysphagia for solids greater than liquids. Radiology reveals a bird's beak deformity. Manometric studies confirm increased intraluminal pressure. Therapies include nitrates and calcium channel blockers, injection of botulinum toxin into the lower esophagus, endoscopic balloon dilation or, usually as a last resort, myotomy.
Diffuse Esophageal Spasm:
Patients with diffuse esophageal spasm suffer substernal cramp-like pain that may mimic myocardial infarction. Contrast and manometric studies demonstrate diffuse spastic activity. Treatment includes medical and surgical options similar to achalasia with referral to GI medicine.
Gastro-esophageal Reflux Disease (GERD):
GERD is recognized in about 10-15% of the population. The disease does not typically cause dysphagia, so other causes should be explored. The cause of GERD is related to incompetence of the lower esophageal sphincter. Regurgitation of stomach contents may cause sensation of subxyphoid pressure. Severe disease may lead to stricture formation, Barrett's esophagus, and increased risk of esophageal cancer. Radiography shows evidence of lower esophageal sphincter incompetence or sliding hiatal hernia in 1/3 of patients. Indirect laryngoscopy may show interarytenoid erythema or edema. Manometry shows decreased lower esophageal sphincter tone. The gold standard for diagnosis is the 24 hour pH probe. Treatment is with anti-reflux medications such as H2 blockers and proton pump inhibitors along with life-style modifications.
Cancer of the Larynx or Pharynx:
Cancer of the upper aerodigestive tract is often associated with odynophagia. Patients usually have a history of heavy smoking and/or drinking and unilateral throat pain on swallowing radiating to the ipsilateral ear or to the angle of the mandible. Careful physical exam usually identifies the lesion.
Cancer of the Esophagus:
Cancer of the esophagus carries a very vague symptom complex and is usually diagnosed late in its course, accounting for the poor survival rate. A chief symptom is dysphagia to solids more than liquids.
Stroke:
Swallowing difficulty after stroke may occur in up to 47% of cases. Most patients recover within one week. However, there is a high rate of aspiration pneumonia in these patients. Causes for dysphagia after stroke include delayed triggering of the swallow reflex, cricopharyngeal dysfunction, reduced lingual and pharyngeal control, and weak cough. With brain stem strokes, direct cranial nerve deficits can lead to further impairment of glottis closure and coordination of phases of swallowing. Treatment consists of rehabilitative speech therapy and placement of a nasoduodenal feeding tube or gastric feeding tube to avoid aspiration. Also frequent pulmonary toilet is required. If laryngeal impairment is permanent, vocal cord medialization procedures, narrow field laryngectomy, or other procedures may be useful.
Laryngeal Nerve Injury:
Isolated recurrent laryngeal nerve injuries result in dysphagia and aspiration secondary to decreased glottic closure pressures and neurogenic dysfunction of the inferior constrictor and cricopharyngeus muscles. Treatment is often by true vocal fold gelfoam injection for temporary medialization of the paralyzed vocal fold, followed later by medialization thyroplasty.
Parkinson's Disease:
Affecting 1% of people over age 50, Parkinson's disease is a progressive disorder of the CNS marked by the classic triad of resting tremor, bradykinesia and rigidity. Dysphagia in Parkinson's disease is addressed by dietary modification and gastric feeding tube placement for end-stage disease.
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Muscular Dystrophy:
Muscular dystrophy can result in spasm of the SCM, masticator, or cricopharyngeus muscles. An oculopharyngeal form of muscular dystrophy also exists.
Myasthenia Gravis:
Dysphagia may be the presenting symptom in this disorder of acetylcholine receptors and aspiration pneumonia may be the terminal event. Dysphagia and fatigue are typically worse later in the day.
Autoimmune Disorders:
Autoimmune disorders that carry a high incidence of dysphagia include systemic sclerosis, system lupus erythematosis, dermatomyositis, mixed connective tissue disease, mucosal pemphigoid, epidermolysis bullosa, Sjogren's syndrome (xerostomia) and Rheumatoid arthritis (cricoarytenoid joint fixation).
Aging:
Dysphagia affects 2% of the population over the age of 65. Oral preparatory phase problems result from poor dentition, and oral phase problems result from loss of tongue connective tissue. Pharyngeal phase changes include increased pharyngeal transit time and prolonged upper esophageal sphincter relaxation time. With these physiologic changes, any superimposed pathology is easily noticed in the otherwise healthy elderly individual.
Children:
In children and infants, nasal obstruction may present with feeding difficulties. Nasal masses, choanal atresia, and choanal stenosis fall in this category. Oral lesions such as cleft lip or palate, mucoceles, ranulas, and Warthin's duct stenosis may cause dysphagia. Upper aerodigestive tract anomalies such as laryngomalacia, vocal cord paralysis, laryngeal clefts, tracheo-esophageal fistula, foregut malformations, or vascular rings of the aorta or pulmonary arteries that compress the esophagus or trachea may all contribute to feeding problems and dysphagia. Tumors of the aerodigestive tract which can certainly cause dysphagia include hemangiomas, lymphangiomas, papillomas, leiomyomas, and neurofibromas.
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