STUDY - Technical - New Dacian's Medicine
Dysphagia
Translation Draft
I've started a new "chapter" of my study, the one related to gastrointestinal function disorders, where I'm going to start with dysphagia.
I've started a new "chapter" of my study, the one related to gastrointestinal function disorders, where I'm going to start with dysphagia.
Let's start with a series
of definitions first!
Dysphagia is defined as a feeling of "stinging" or obstruction of food passing through the mouth, pharynx or esophagus (a sensation that should be distinguished from other symptoms related to swallowing). Aphagy signifies complete esophageal obstruction, which is usually due to the immobilization of the bowl and is a medical emergency. Difficulties in initiating swallowing occur in disorders of the voluntary phase of swallowing. However, once initiated, swallowing is normally completed.
Odinofagia is painful swallowing, commonly occurring along with dysphagia. Globus farherus is the sensation of bolus located in the throat, however no difficulty is encountered when swallowing occurs. The wrong targeting of food leading to nasal regurgitation and laryngeal and pulmonary suction of food during swallowing is characteristic for oropharyngeal dysphagia. Phagophobia, i.e. fear of swallowing, and refusal to swallow can occur in hysteria, rabies, tetanus and pharyngeal paralysis due to aspiration phobia. Painful inflammatory lesions that cause odinophagia can also cause refusal to swallow. Some patients may feel the food as it descends through the esophagus. This esophageal sensitivity is not, however, associated with food stiffness or obstruction. Similarly, the feeling of epigastric fullness, which occurs after eating or after swallowing air, should not be confused with dysphagia.
Let me present some elements about the physiology of swallowing! The process of swallowing begins with a voluntary (oral) phase, during which the food bowl is pushed into the pharynx by the contraction of the tongue. The bowl then activates the orofaryngeal sensory receptors that initiate the involuntary phase (pharyngeal and esophageal) or the swallowing reflex. The swallowing reflex is a complex series of events that serves both to push food through the pharynx and esophagus and to prevent their entry into the air.
When the bowl is pushed back by the tongue, the larynx moves forward and the upper esophageal sphincter opens. As the bowl moves through the pharynx, the contraction of the upper pharyngeal constrictor against the contracted soft palate initiates a peristaltic contraction that rapidly progresses down to move the bowl through the pharynx and esophagus.
The lower esophageal sphincter opens as food enters the esophagus and remains open until peristaltic contraction has pushed the bowl into the stomach. Peristaltic contraction in response to swallowing involves inhibition followed by sequential contraction of muscles along the entire swallowing path, which is called primary peristaltic. The inhibition that precedes peristaltic contraction is called swallowing inhibition.
Local distance of the esophagus due to food activates intramural reflexes in the smooth muscles and produces secondary peristaltic, limited to the thoracic esophagus. Tertiary contractions are nonperistaltic as they occur simultaneously over a long esophageal segment. Tertiary contractions may occur in response to esophageal swallowing or distension or may occur spontaneously.
Now we're going to talk about the physiology of dysphagia... The normal transport of a bolus ingested through the swallowing path depends on the size of the ingested bowl, the luminal diameter of the swallowing path, the peristaltic contraction and the swallowing inhibition, including the normal relaxation of the upper and lower esophageal sphincters during swallowing. Dysphagia caused by a large bowl or light strait is called mechanical dysphagia, while dysphagia due to incoordination or weakening of peristaltic contractions or impaired swallowing inhibition is called motor dysphagia.
Mechanical dysphagia can be caused by a very large food bowl, intrinsic narrowing or extrinsic compression of the lumen. In adults, the esophageal lumen can relax up to a diameter of 4 cm due to the elasticity of the esophageal wall. When the esophagus cannot dilate more than 2.5 cm in diameter, dysphagia for normal solid foods may occur but it is always present when it cannot relax over 1.3 cm.
Circumferential lesions cause more dysphagia than lesions of interest only a portion of the circumference of the esophageal wall, because the unaffected segments retain their distensibility.
The causes of mechanical dysphagia are multiple (the most common being carcinomas, peptic strictures and other benign strictures and the lower esophageal ring) and are represented by: 1. luminal (A. large bolus and B. foreign body), 2. intrinsic narrowing (A. inflammatory conditions causing edema and custom swelling on a. stomatitis, b. pharyngitis, epiglotitis, c. esophagitis with viral i. forms with herpes simplex, varicella-zosterian, cytomegalovirus, ii. bacterial, iii. mycotic/ candidiasis, iv. mucocutaneous diseases and v. caustic lesions, B. membranes and rings with a. pharyngeal manifestations such as Plummer-Vinson syndrome, b. oesophageal such as congenital and inflammatory and c. the ring of the lower esophageal mucosa or the Schatzki ring, 3. benign strictures such as a. peptic, b. caustic and drug-induced, c. inflammatory such as a. peptic, b. caustic and drug-induced, c. inflammatory Crohn's disease, candidiasis, mucocutaneous lesions, ischemic d., postoperative e., postirradiation and congenital f., 4. malignant tumors represented by a. primary carcinomas with forms i. squamous cell carcinoma Ii. adenocarcinoma, iii. carcinosarcoma, iv. pseudosarcoma, v. lymphoma, vi. melanoma and live. Kaposi sarcoma and b. metastatic carcinomas, 5. benign tumors like a. leiomyoma, b. lipoma, c. angioma, d. inflammatory fibriloid polyp and e. epithelial papilloma), without forgetting extrinsic compression with the manifestations represented by cervical a. spondylitis, 2. vertebral osteophytes, 3. abscesses and retropharyngeal tumors, 4. enlarged thyroid gland, 5. Zenker Diverticul, 6. vascular compression (a. aberrant right subclavian artery, dextropositioned aorta, c. left atrium enlargement and d. aortic aneurysm), 7. posterior mediastinal masses, 8. pancreatic tumor, pancreatitis and 9. hematoma and postvagotomy fibrosis.
Motor dysphagia may be the result of difficulty in initiating peristaltic swallowing or abnormalities and swallowing inhibition due to diseases of the striated or smooth esophageal muscles. Stria's muscle disorders concern pharynx, upper esophageal sphincter and cervical esophagus. The striated musculature is innervated by a somatic branch of the vagus having the cellular bodies of the lower motor neurons located in the ambiguous nucleus. These neurons are cholinergic, have an excitatory role and are the exclusive determinants of muscle activity.
Peristalsis in the striated muscle segment is given by the sequential central activation of neurons that irritate the muscles at different levels along the esophagus. Motor dysphagia of the pharynx results from neuromuscular disorders that cause muscle paralysis, simultaneous nonperistaltic contraction or loss of the opening of the upper esophageal sphincter. The disappearance of the opening of the upper esophageal sphincter is caused by paralysis of the geniohioid muscle and other suprahyoid muscles or loss of swallowing inhibition of the cricopharyngeal muscle.
Because each part of the pharynx is irritated by ipsilateral nerves, a lesion of motor neurons affecting a single part leads to unilateral pharyngeal paralysis. Although lesions of the striated muscles also involve the cervical part of the esophagus, clinical manifestations of pharyngeal dysfunction usually overshadow the manifestations due to the interest of the esophagus. Smooth muscle segment disorders interest the thoracic part of the esophagus and the lower esophageal sphincter.
The smooth musculature is innervated by the parasympathetic component of the preganglionary vagal fibers and postganglionary neurons in the myenteric ganglia. The vagal pathway is made up of parallel excitatory and inhibitory pathways, which use acetylcholine and nitric oxide respectively as neurotransmitters. Activation of inhibitory nerves causes inhibition which is followed by the resumption of contraction.
These paths are involved in the resting tone of the lower esophageal sphincter, as well as the opening and inhibition of the deglutition-induced lower esophageal sphincter, followed by peristaltic contractions in the esophageal body. Dysphagia occurs when peristaltic contractions are weak or nonperistaltic or when the lower sphincter fails to open normally. The loss of contractile power occurs due to muscle weakness, as in scleroderma. Nonperistaltic contractions and impaired relaxation of the esophageal sphincter result from a defect in vagal inhibitory innervation and are responsible for dysphagia in achalasia.
The causes of motor (neuromuscular) dysphagia are represented by (the most common are pharyngeal paralysis, cricopharian achalasia, esophageal scleroderma, achalasia, diffuse esophageal spasm and associated motor disorders): I. difficulty in initiating the reflex of swallowing with A. tongue paralysis, B. oropharyngeal anesthesia, C. lack of saliva (e.g. in Sjogren's syndrome), D. lesions of the sensory nerve components of the glosopharyngeal and vague nerves , E. lesions of the swallowing center, II. pharyngeal and esophageal striated muscle disorders with A. muscle weakness due to 1. lower motor neuron lesions (bulbar paralysis) from a. stroke, b. motor neuron disease, c. poliomyelitis (postpolio syndrome), d. polyneuritis, e. amyotrophic lateral sclerosis and f. familial disautonomy, 2. neuromuscular (myasthenia gravis), 3. muscle disorders such as a. polymyositis, b. dermatomyositis and c. myopathy (myotonic dystrophy, oculopharyngeal myopathy), B. nonperistaltic contractions or alteration of impaired swallowing inhibition at level 1. pharynx and upper esophagus in a. rabies, b. tetanus, c. extrapyramidal tract disease and d. upper motor neuron lesions (pseudobulbar paralysis), 2. upper esophageal sphincter (SES) with a. paralysis of the suprahyoid muscles (causes being the same as in pharyngeal muscle paralysis) and b. cricopharyngeal achalasia, III. disorders of the esophageal smooth muscle represented by A. paralysis of the esophageal body causing weak contractions such as 1. scleroderma and related collagen diseases, 2. myopathy of cavitational viscera, 3. myotonic dystrophy, 4. metabolic neuromyopathy (amyloid, alcohol?, diabetes?) and 5. achalasia, B. nonperistaltic contractions or impaired swallowing inhibition such as 1. oesophageal body (a. diffuse esophageal spasm, b. vigorous achalasia, c. variants of diffuse esophageal spasm), 2. lower esophageal sphincter (a. achalasia i. primary, ii. secondary - Chagas disease, carcinoma, lymphoma, intestinal neuropathic syndrome of pseudoabsorption, toxins and drugs - and b. inferior esophageal muscle ring contractil).
Anamnesis can provide a presumptively correct diagnosis in over 80% of cases. The type of food that causes dysphagia provides useful information. Difficulty only for solid foods involves mechanical dysphagia with a lumen that is not severely narrowed. In advanced obstruction, dysphagia occurs in both liquids and solids.
By contrast, motor dysphagia due to achalasia and diffuse esophageal spasm is determined equally to solids and liquids right from the onset. Patients with scleroderma have dysphagia in solids, which is not related to the position of the body, and to fluids lying down, but not to the vertical. When peptic stricture occurs in patients with scleroderma, dysphagia becomes more persistent. The duration and evolution of dysphagia are useful for diagnosis.
Short-term transient dysphagia may be due to an inflammatory process. Progressive dysphagia lasting from a few weeks to a few months is suggestive for esophageal carcinoma. Episodic solid dysphagia lasting several years indicates a benign disease characteristic of the lower esophageal ring. The patient's localization of dysphagia is useful in determining the level of oesophageal obstruction, the lesion being at or below the site of the perception of dysphagia. The associated symptoms bring important diagnostic clues.
Nasal regurgitation and tracheobronsic aspiration in swallowing are hallmarks of pharyngeal paralysis or a tracheoesophageal fist. Tracheobronsic aspiration not related to swallowing may be secondary to achalasia, Zenker diverticulum or gastroesophageal reflux. Significant weight loss, which is disproportionate to the degree of dysphagia, is highly suggestive of carcinoma. When dysphonia precedes dysphagia, the primary lesion is usually in the larynx. Dysphonia following dysphagia may suggest damage to the recurrent laryngeal nerve by extending the esophageal carcinoma beyond the walls of the esophagus. Sometimes dysphonia may be due to a laryngitis secondary to gastroesophageal reflux. The association of laryngeal symptoms with dysphagia also occurs in various neuromuscular disorders.
The hiccup suggests a lesion in the distal portion of the esophagus. Unilateral wheezing associated with dysphagia indicates a mediastinal mass of interest to the esophagus and a large bronchi. Chest pain with dysphagia occurs in diffuse esophageal spasm and associated motor disorders. Chest pain similar to diffuse esophageal spasm may also occur in oesophageal obstruction due to a large bowl. A prolonged history of heartburn and reflux that precedes dysphagia indicates peptic stricture.
Similarly, a history of prolonged nasogastric intubation, ingestion of caustic agents, ingestion of pills without water, history of radiotherapy or associated mucocutaneous diseases may provide the cause of esophageal stricture. If odinophagia is present, candidiasis or herpetic esophagitis or drug-induced esophagitis should be suspected. In patients with AIDS or other immunodeficiency disorders, esophagitis due to opportunistic infections such as Candida, herpes simplex virus, cytomegalovirus and tumours such as Kaposi sarcoma and lymphomas should be suspected.
Physical examination is important in motor dysphagia due to disorders of the striated, neurological and oropharyngeal muscles. In addition to signs of generalized neuromuscular disease, signs of bulbar or pseudobulbar paralysis including dysartria, dysphonia, ptosis, lingual atrophy and hyperactive mandibular reflex should be carefully sought. The neck should be examined for thyroid hypertrophy or vertebral animal.
Careful inspection of the oral cavity and pharynx may reveal lesions that may interfere with the passage of food through the mouth or esophagus due to pain or obstruction. Skin and extremity changes may suggest the diagnosis of scleroderma and other vascular collagen diseases or mucocutaneous diseases, such as pemfigus or bullous epidermolysis, which may affect the esophagus. Metastatic diseases in the lymph nodes or liver may be obvious. Pulmonary complications of acute aspiration pneumonia or chronic aspiration may be present.
I'll finish with some diagnostic procedures. All patients with dysphagia should be carefully investigated, as treatment depends on the underlying cause. if oropharyngeal dysphagia is suspected, videofluoroscopy of oropharyngeal swallowing should be performed. if mechanical dysphagia is suspected from anamnesis, diagnostic elective procedures are baritat transit, esophagoscopy and endoscopic biopsy. Baritat transit and esophageal motility studies are diagnostic tests for motor dysphagia. Esophagogastroscopy may be necessary in patients with motor dysphagia to rule out an associated structural abnormality.
On June 12th we will continue with nausea, vomiting and indigestion.
Dysphagia is defined as a feeling of "stinging" or obstruction of food passing through the mouth, pharynx or esophagus (a sensation that should be distinguished from other symptoms related to swallowing). Aphagy signifies complete esophageal obstruction, which is usually due to the immobilization of the bowl and is a medical emergency. Difficulties in initiating swallowing occur in disorders of the voluntary phase of swallowing. However, once initiated, swallowing is normally completed.
Odinofagia is painful swallowing, commonly occurring along with dysphagia. Globus farherus is the sensation of bolus located in the throat, however no difficulty is encountered when swallowing occurs. The wrong targeting of food leading to nasal regurgitation and laryngeal and pulmonary suction of food during swallowing is characteristic for oropharyngeal dysphagia. Phagophobia, i.e. fear of swallowing, and refusal to swallow can occur in hysteria, rabies, tetanus and pharyngeal paralysis due to aspiration phobia. Painful inflammatory lesions that cause odinophagia can also cause refusal to swallow. Some patients may feel the food as it descends through the esophagus. This esophageal sensitivity is not, however, associated with food stiffness or obstruction. Similarly, the feeling of epigastric fullness, which occurs after eating or after swallowing air, should not be confused with dysphagia.
Let me present some elements about the physiology of swallowing! The process of swallowing begins with a voluntary (oral) phase, during which the food bowl is pushed into the pharynx by the contraction of the tongue. The bowl then activates the orofaryngeal sensory receptors that initiate the involuntary phase (pharyngeal and esophageal) or the swallowing reflex. The swallowing reflex is a complex series of events that serves both to push food through the pharynx and esophagus and to prevent their entry into the air.
When the bowl is pushed back by the tongue, the larynx moves forward and the upper esophageal sphincter opens. As the bowl moves through the pharynx, the contraction of the upper pharyngeal constrictor against the contracted soft palate initiates a peristaltic contraction that rapidly progresses down to move the bowl through the pharynx and esophagus.
The lower esophageal sphincter opens as food enters the esophagus and remains open until peristaltic contraction has pushed the bowl into the stomach. Peristaltic contraction in response to swallowing involves inhibition followed by sequential contraction of muscles along the entire swallowing path, which is called primary peristaltic. The inhibition that precedes peristaltic contraction is called swallowing inhibition.
Local distance of the esophagus due to food activates intramural reflexes in the smooth muscles and produces secondary peristaltic, limited to the thoracic esophagus. Tertiary contractions are nonperistaltic as they occur simultaneously over a long esophageal segment. Tertiary contractions may occur in response to esophageal swallowing or distension or may occur spontaneously.
Now we're going to talk about the physiology of dysphagia... The normal transport of a bolus ingested through the swallowing path depends on the size of the ingested bowl, the luminal diameter of the swallowing path, the peristaltic contraction and the swallowing inhibition, including the normal relaxation of the upper and lower esophageal sphincters during swallowing. Dysphagia caused by a large bowl or light strait is called mechanical dysphagia, while dysphagia due to incoordination or weakening of peristaltic contractions or impaired swallowing inhibition is called motor dysphagia.
Mechanical dysphagia can be caused by a very large food bowl, intrinsic narrowing or extrinsic compression of the lumen. In adults, the esophageal lumen can relax up to a diameter of 4 cm due to the elasticity of the esophageal wall. When the esophagus cannot dilate more than 2.5 cm in diameter, dysphagia for normal solid foods may occur but it is always present when it cannot relax over 1.3 cm.
Circumferential lesions cause more dysphagia than lesions of interest only a portion of the circumference of the esophageal wall, because the unaffected segments retain their distensibility.
The causes of mechanical dysphagia are multiple (the most common being carcinomas, peptic strictures and other benign strictures and the lower esophageal ring) and are represented by: 1. luminal (A. large bolus and B. foreign body), 2. intrinsic narrowing (A. inflammatory conditions causing edema and custom swelling on a. stomatitis, b. pharyngitis, epiglotitis, c. esophagitis with viral i. forms with herpes simplex, varicella-zosterian, cytomegalovirus, ii. bacterial, iii. mycotic/ candidiasis, iv. mucocutaneous diseases and v. caustic lesions, B. membranes and rings with a. pharyngeal manifestations such as Plummer-Vinson syndrome, b. oesophageal such as congenital and inflammatory and c. the ring of the lower esophageal mucosa or the Schatzki ring, 3. benign strictures such as a. peptic, b. caustic and drug-induced, c. inflammatory such as a. peptic, b. caustic and drug-induced, c. inflammatory Crohn's disease, candidiasis, mucocutaneous lesions, ischemic d., postoperative e., postirradiation and congenital f., 4. malignant tumors represented by a. primary carcinomas with forms i. squamous cell carcinoma Ii. adenocarcinoma, iii. carcinosarcoma, iv. pseudosarcoma, v. lymphoma, vi. melanoma and live. Kaposi sarcoma and b. metastatic carcinomas, 5. benign tumors like a. leiomyoma, b. lipoma, c. angioma, d. inflammatory fibriloid polyp and e. epithelial papilloma), without forgetting extrinsic compression with the manifestations represented by cervical a. spondylitis, 2. vertebral osteophytes, 3. abscesses and retropharyngeal tumors, 4. enlarged thyroid gland, 5. Zenker Diverticul, 6. vascular compression (a. aberrant right subclavian artery, dextropositioned aorta, c. left atrium enlargement and d. aortic aneurysm), 7. posterior mediastinal masses, 8. pancreatic tumor, pancreatitis and 9. hematoma and postvagotomy fibrosis.
Motor dysphagia may be the result of difficulty in initiating peristaltic swallowing or abnormalities and swallowing inhibition due to diseases of the striated or smooth esophageal muscles. Stria's muscle disorders concern pharynx, upper esophageal sphincter and cervical esophagus. The striated musculature is innervated by a somatic branch of the vagus having the cellular bodies of the lower motor neurons located in the ambiguous nucleus. These neurons are cholinergic, have an excitatory role and are the exclusive determinants of muscle activity.
Peristalsis in the striated muscle segment is given by the sequential central activation of neurons that irritate the muscles at different levels along the esophagus. Motor dysphagia of the pharynx results from neuromuscular disorders that cause muscle paralysis, simultaneous nonperistaltic contraction or loss of the opening of the upper esophageal sphincter. The disappearance of the opening of the upper esophageal sphincter is caused by paralysis of the geniohioid muscle and other suprahyoid muscles or loss of swallowing inhibition of the cricopharyngeal muscle.
Because each part of the pharynx is irritated by ipsilateral nerves, a lesion of motor neurons affecting a single part leads to unilateral pharyngeal paralysis. Although lesions of the striated muscles also involve the cervical part of the esophagus, clinical manifestations of pharyngeal dysfunction usually overshadow the manifestations due to the interest of the esophagus. Smooth muscle segment disorders interest the thoracic part of the esophagus and the lower esophageal sphincter.
The smooth musculature is innervated by the parasympathetic component of the preganglionary vagal fibers and postganglionary neurons in the myenteric ganglia. The vagal pathway is made up of parallel excitatory and inhibitory pathways, which use acetylcholine and nitric oxide respectively as neurotransmitters. Activation of inhibitory nerves causes inhibition which is followed by the resumption of contraction.
These paths are involved in the resting tone of the lower esophageal sphincter, as well as the opening and inhibition of the deglutition-induced lower esophageal sphincter, followed by peristaltic contractions in the esophageal body. Dysphagia occurs when peristaltic contractions are weak or nonperistaltic or when the lower sphincter fails to open normally. The loss of contractile power occurs due to muscle weakness, as in scleroderma. Nonperistaltic contractions and impaired relaxation of the esophageal sphincter result from a defect in vagal inhibitory innervation and are responsible for dysphagia in achalasia.
The causes of motor (neuromuscular) dysphagia are represented by (the most common are pharyngeal paralysis, cricopharian achalasia, esophageal scleroderma, achalasia, diffuse esophageal spasm and associated motor disorders): I. difficulty in initiating the reflex of swallowing with A. tongue paralysis, B. oropharyngeal anesthesia, C. lack of saliva (e.g. in Sjogren's syndrome), D. lesions of the sensory nerve components of the glosopharyngeal and vague nerves , E. lesions of the swallowing center, II. pharyngeal and esophageal striated muscle disorders with A. muscle weakness due to 1. lower motor neuron lesions (bulbar paralysis) from a. stroke, b. motor neuron disease, c. poliomyelitis (postpolio syndrome), d. polyneuritis, e. amyotrophic lateral sclerosis and f. familial disautonomy, 2. neuromuscular (myasthenia gravis), 3. muscle disorders such as a. polymyositis, b. dermatomyositis and c. myopathy (myotonic dystrophy, oculopharyngeal myopathy), B. nonperistaltic contractions or alteration of impaired swallowing inhibition at level 1. pharynx and upper esophagus in a. rabies, b. tetanus, c. extrapyramidal tract disease and d. upper motor neuron lesions (pseudobulbar paralysis), 2. upper esophageal sphincter (SES) with a. paralysis of the suprahyoid muscles (causes being the same as in pharyngeal muscle paralysis) and b. cricopharyngeal achalasia, III. disorders of the esophageal smooth muscle represented by A. paralysis of the esophageal body causing weak contractions such as 1. scleroderma and related collagen diseases, 2. myopathy of cavitational viscera, 3. myotonic dystrophy, 4. metabolic neuromyopathy (amyloid, alcohol?, diabetes?) and 5. achalasia, B. nonperistaltic contractions or impaired swallowing inhibition such as 1. oesophageal body (a. diffuse esophageal spasm, b. vigorous achalasia, c. variants of diffuse esophageal spasm), 2. lower esophageal sphincter (a. achalasia i. primary, ii. secondary - Chagas disease, carcinoma, lymphoma, intestinal neuropathic syndrome of pseudoabsorption, toxins and drugs - and b. inferior esophageal muscle ring contractil).
Anamnesis can provide a presumptively correct diagnosis in over 80% of cases. The type of food that causes dysphagia provides useful information. Difficulty only for solid foods involves mechanical dysphagia with a lumen that is not severely narrowed. In advanced obstruction, dysphagia occurs in both liquids and solids.
By contrast, motor dysphagia due to achalasia and diffuse esophageal spasm is determined equally to solids and liquids right from the onset. Patients with scleroderma have dysphagia in solids, which is not related to the position of the body, and to fluids lying down, but not to the vertical. When peptic stricture occurs in patients with scleroderma, dysphagia becomes more persistent. The duration and evolution of dysphagia are useful for diagnosis.
Short-term transient dysphagia may be due to an inflammatory process. Progressive dysphagia lasting from a few weeks to a few months is suggestive for esophageal carcinoma. Episodic solid dysphagia lasting several years indicates a benign disease characteristic of the lower esophageal ring. The patient's localization of dysphagia is useful in determining the level of oesophageal obstruction, the lesion being at or below the site of the perception of dysphagia. The associated symptoms bring important diagnostic clues.
Nasal regurgitation and tracheobronsic aspiration in swallowing are hallmarks of pharyngeal paralysis or a tracheoesophageal fist. Tracheobronsic aspiration not related to swallowing may be secondary to achalasia, Zenker diverticulum or gastroesophageal reflux. Significant weight loss, which is disproportionate to the degree of dysphagia, is highly suggestive of carcinoma. When dysphonia precedes dysphagia, the primary lesion is usually in the larynx. Dysphonia following dysphagia may suggest damage to the recurrent laryngeal nerve by extending the esophageal carcinoma beyond the walls of the esophagus. Sometimes dysphonia may be due to a laryngitis secondary to gastroesophageal reflux. The association of laryngeal symptoms with dysphagia also occurs in various neuromuscular disorders.
The hiccup suggests a lesion in the distal portion of the esophagus. Unilateral wheezing associated with dysphagia indicates a mediastinal mass of interest to the esophagus and a large bronchi. Chest pain with dysphagia occurs in diffuse esophageal spasm and associated motor disorders. Chest pain similar to diffuse esophageal spasm may also occur in oesophageal obstruction due to a large bowl. A prolonged history of heartburn and reflux that precedes dysphagia indicates peptic stricture.
Similarly, a history of prolonged nasogastric intubation, ingestion of caustic agents, ingestion of pills without water, history of radiotherapy or associated mucocutaneous diseases may provide the cause of esophageal stricture. If odinophagia is present, candidiasis or herpetic esophagitis or drug-induced esophagitis should be suspected. In patients with AIDS or other immunodeficiency disorders, esophagitis due to opportunistic infections such as Candida, herpes simplex virus, cytomegalovirus and tumours such as Kaposi sarcoma and lymphomas should be suspected.
Physical examination is important in motor dysphagia due to disorders of the striated, neurological and oropharyngeal muscles. In addition to signs of generalized neuromuscular disease, signs of bulbar or pseudobulbar paralysis including dysartria, dysphonia, ptosis, lingual atrophy and hyperactive mandibular reflex should be carefully sought. The neck should be examined for thyroid hypertrophy or vertebral animal.
Careful inspection of the oral cavity and pharynx may reveal lesions that may interfere with the passage of food through the mouth or esophagus due to pain or obstruction. Skin and extremity changes may suggest the diagnosis of scleroderma and other vascular collagen diseases or mucocutaneous diseases, such as pemfigus or bullous epidermolysis, which may affect the esophagus. Metastatic diseases in the lymph nodes or liver may be obvious. Pulmonary complications of acute aspiration pneumonia or chronic aspiration may be present.
I'll finish with some diagnostic procedures. All patients with dysphagia should be carefully investigated, as treatment depends on the underlying cause. if oropharyngeal dysphagia is suspected, videofluoroscopy of oropharyngeal swallowing should be performed. if mechanical dysphagia is suspected from anamnesis, diagnostic elective procedures are baritat transit, esophagoscopy and endoscopic biopsy. Baritat transit and esophageal motility studies are diagnostic tests for motor dysphagia. Esophagogastroscopy may be necessary in patients with motor dysphagia to rule out an associated structural abnormality.
On June 12th we will continue with nausea, vomiting and indigestion.
Let's hear it for good!
Dorin, Merticaru