Sei sulla pagina 1di 49

Tutorial Dysphagia

Dahlia Septiawati Darari genadita Zaras Yudisthira Saga Ziad Alaztha

Skenario

Seorang wanita 30 tahun tidak menikah mengeluh ada rasa tidak enak setiap kali sesudah makan di dada tengah. Keluhan ini berkembang secara lambat dan bertambah berat sesudah satu tahun ini. Bila makan agak padat lebih enak dari pada kalau makan makanan yang lebih cair. Pada pemeriksaan KU baik, tidak ditemukan kelainan yang berarti.

Pertanyaan 1. Apakah disfagia dan apa dispepsia? 2. Apa DD atau Diagnosis kerja pasien ini? 3. Bagaimana menegakkan

Dysphagia vs Dyspepsia
Dysphagia Dysphagia is a medical term for difficulty with swallowing. It may be a sensation that suggests difficulty in the passage of solids or liquids from the mouth to the stomach Dyspepsia Dyspepsia is upper abdominal pain or discomfort that is episodic or persistent and often associated with belching, bloating, heartburn, nausea or vomiting

Anatomy and Physiology of Deglutition

Deglutition is the act of swallowing in which a food or liquid bolus is transported from the mouth through the pharynx and esophagus into the stomach Normal deglutition involves a complex series of voluntary and involuntary neuromuscular contractions proceeding from the mouth to the stomach

commonly divided into oropharyngeal and esophageal stages

Oropharyngeal Stage

The tongue initially forms the food bolus (green) with compression against the hard palate.

Displacement of the food bolus into the pharynx by the tongue initiates deglutition

Relaxation of the cricopharyngeal muscle (the physiological upper esophageal sphincter) permits movement of the food bolus into the proximal esophagus

Esophageal Stage
As food is propelled from the pharynx into the esophagus, involuntary contractions of the skeletal muscles of the upper esophagus force the bolus through the mid and distal esophagus

The medulla controls this involuntary swallowing reflex, although voluntary swallowing may be initiated by the cerebral cortex

The lower esophageal sphincter relaxes at the initiation of the swallow, and this relaxation persists until the food bolus is propelled into the stomach

Oropharyngeal Dysphagia & Esophageal Dysphagia


In oropharyngeal dysphagia, symptoms arise from the dysfunctional transfer of a food bolus in the pharynx past the upper esophageal sphincter into the esophagus. Stroke is the leading cause of oropharyngeal dysphagia.

Esophageal dysphagia is caused by disordered peristaltic motility or conditions that obstruct the flow of a food bolus through the esophagus into the stomach. Achalasia and scleroderma are the leading motility disorders, while carcinomas, strictures and Schatzki's rings are the most common obstructive lesions.

Anamnesis tambahan

Batuk

Penurunan berat badan

Gejala yang progresive

Nyeri

Kelemahan

Halitosis

Associated Symptoms and Possible Etiologies of Dysphagia


Condition Progressive dysphagia Sudden dysphagia Diagnoses to consider Neuromuscular dysphagia Obstructive dysphagia, esophagitis

Difficulty initiating swallow


Food sticks after swallow Cough Early in swallow Late in swallow Weight loss In the elderly With regurgitation Progressive symptoms Heartburn Intermittent symptoms Pain with dysphagia

Oropharyngeal dysphagia
Esophageal dysphagia Neuromuscular dysphagia Obstructive dysphagia Carcinoma Achalasia Peptic stricture, scleroderma Rings and webs, diffuse esophageal spasm, nutcracker esophagus Esophagitis Postradiation Infectious: herpes simplex virus, monilia Pill-induced Obstructive dysphagia Neuromuscular dysphagias Cerebrovascular accidents, muscular dystrophies, myasthenia gravis, multiple sclerosis Zenker's diverticulum Achalasia Neuromuscular motility disorders

Pain made worse by: Solid food only Solids and liquids Weakness and dysphagia Halitosis Dysphagia relieved with repeated swallows Dysphagia made worse with cold foods

Pemeriksaan Fisik
Neurologic evaluation patient's mental status, motor and sensory functioning, deep tendon reflexes and cranial nerves, and a cerebellar examination cranial nerve motor components of cranial nerves V, VII, IX, X and XII, and sensory fibers from cranial nerves V, VII, IX and X Adequate saliva production A tongue blade and handheld mirror allow indirect inspection of the soft palate and vocal cord mobility nasopharyngoscopy

Thyroid masses and lymphadenopathy that cause obstructive dysphagia can be palpated on examination of the neck

Observing the patient swallowing a variety of liquids and solids

Bimanual palpation of the floor of the mouth, tongue and lips Examination of the teeth

A widened anteroposterior chest diameter and distant breath sounds are signs of chronic obstructive pulmonary disease

The patient's abdomen should be examined for masses and organomegaly

Differential Diagnoses of Dysphagia


Oropharyngeal dysphagia Neuromuscular disease Diseases of the central nervous system Cerebrovascular accident Parkinson's disease Brain stem tumors Degenerative diseases Amyotrophic lateral sclerosis Multiple sclerosis Huntington's disease Postinfectious Poliomyelitis Syphilis Peripheral nervous system Peripheral neuropathy Motor end-plate dysfunction Myasthenia gravis Skeletal muscle disease (myopathies) Polymyositis Dermatomyositis Muscular dystrophy (myotonic dystrophy, oculopharyngeal dystrophy) Cricopharyngeal (upper esophageal sphincter), achalasia Achalasia Esophageal dysphagia Neuromuscular disorders

Spastic motor disorders Diffuse esophageal spasm Hypertensive lower esophageal sphincter Nutcracker esophagus Scleroderma

Oropharyngeal dysphagia Obstructive lesions

Esophageal dysphagia Obstructive lesions Intrinsic structural lesions Tumors Strictures Peptic Radiation-induced Chemical-induced Medication-induced Lower esophageal rings (Schatzki's ring) Esophageal webs Foreign bodies Extrinsic structural lesions Vascular compression

Tumors

Inflammatory masses Trauma/surgical resection Zenker's diverticulum Esophageal webs

Extrinsic structural lesions


Anterior mediastinal masses Cervical spondylosis

Differential Diagnosa

1. Achalasia 2. Scleroderma 3. Diffuse and Segmental Esophageal Spasm 4. Nutcracker Esophagus

Pemeriksaan Penunjang
Laboratory Evaluation A complete blood count screens for infectious or inflammatory conditions Thyroid function studies

Barium swallow studies Suspected obstructive lesion (e.g., Schatzki's ring, tumor) Suspected esophageal motility disorder

Double-contrast upper gastrointestinal evaluation Suspected esophageal mucosal injury Evaluation of oropharyngeal anatomy and function (fluoroscopy) Suspected gastroesophageal reflux disease Gastroesophageal endoscopy Suspected acute obstructive lesion (impacted food bolus) Evaluation of the esophageal mucosa Confirmation of a positive barium study with biopsies or cytology

Barium Studies
Barium Swallow: evaluates the pharynx and esophagus including the swallowing mechanism. It identifies intrinsic and extrinsic structural lesions but lacks precision in identifying the nature of obstructive lesions Double-contrast studies provide better visualization of esophageal mucosa. Fluoroscopy can identify abnormalities in the mouth and oropharynx and, if observed closely, can provide some detail about function, detecting reflux and abnormal peristalsis.

Gastroesophageal Endoscopy

Gastroesophageal endoscopy provides the best assessment of the esophageal mucosa. Masses or other lesions identified by barium studies should initiate esophagogastroscopy with biopsy and cytology. In patients with acute onset of dysphagia while eating, gastroesophageal endoscopy can directly remove an impacted food bolus and dilate strictures. Endoscopy has the added benefit of detecting infection and erosions, and providing biopsy capability.

Pemeriksaan Penunjang
Manometry Abnormality not identified on barium study or by endoscopy

pH monitoring Suspected gastroesophageal reflux disease

Videoradiography Suspected risk of aspiration

Ph Monitoring

Despite several drawbacks, esophageal pH monitoring remains the gold standard for diagnosing patients with suspected reflux disease. A nasogastric probe is inserted into the patient's esophagus and records pH levels. These levels are compared with the patient's record of symptoms over a 24-hour period to determine if acid reflux contributes to the

An algorithmic approach to the diagnostic evaluation of dysphagia

Information from Castell DO. Approach to the patient with dysphagia. In: Yamada T, ed. Textbook of gastroenterology. 2d ed. Philadelphia: Lippincott Williams & Wilkins, 1995.

Tinjauan Pustaka

Definition

A Greek term that means "does not relax

Normally The act of swallowing (deglutition) normally initiates a peristaltic wave that propels ingested material down the esophagus. Deglutition also triggers relaxation of the lower esophageal sphincter (LES), a process that allows the swallowed material to enter the stomach.

Achalasia is a disease of unknown cause in which there is a loss of peristalsis in the distal esophagus (whose musculature is comprised predominantly of smooth muscle) and a failure of LES relaxation.

Epidemiology
Achalasia has an annual incidence of approximately 1 case per 100,000. Men and women are affected with equal frequency. The disease can occur at virtually any age, but onset before adolescence is decidedly unusual. Achalasia is usually diagnosed in patients who are between the ages of 25 and 60 years.

Etiology
The etiology of achalasia is not known Autoimmune disorder associated with HLA-DQw1 antibodies to enteric neurons Chronic infections with herpes zoster or measles viruses

Etiology

Malignancy: the most common cause of pseudoachalasia in most populations

Chagas' disease: Seen in Central and South America, esophageal infection with the protozoan parasite Trypanosoma cruzi can result in a loss of intramural ganglion cells leading to aperistalsis and incomplete LES relaxation

Other causes: A variety of other diseases have been associated with achalasia-like motor abnormalities. These include amyloidosis, sarcoidosis, neurofibromatosis, eosinophilic gastroenteritis, multiple endocrine neoplasia type 2B, juvenile Sjgren's syndrome, chronic idiopathic intestinal pseudo-obstruction, and Fabry disease.

Pathophysiology

Achalasia results from the degeneration of neurons in the esophageal wall. Histologic examination reveals decreased numbers of neurons (ganglion cells) in the myenteric plexuses, and the ganglion cells that remain often are surrounded by lymphocytes and, less prominently, by eosinophils. This inflammatory degeneration preferentially involves the nitric oxide-producing, inhibitory neurons that effect the relaxation of esophageal smooth muscle. However the cholinergic neurons that contribute to LES

Clinical Manifestations

Disphagia

Weight loss: usually in the range of 5 to 10 kg

Regurgitation of material retained in the flaccid esophagus may occur, especially during recumbency at night, and may result in aspiration

Chest pain is more common in younger patients

Difficulty belching

Dysphagia for solids (91 percent) and liquids (85 percent) is the primary clinical feature of achalasia. Although dysphagia for liquids can occur in patients with other esophageal motility disorders this symptom is most characteristic of achalasia and strongly suggests the diagnosis.

Diagnosis
Patients typically experience symptoms for years before seeking medical attention.
In one series of 87 patients with newly diagnosed achalasia, the mean duration of symptoms was 4.7 years.

Patients who have a clinical history suggestive of achalasia require radiographic, manometric, and endoscopic evaluation to confirm the diagnosis.

Radiographic Studies
A barium swallow is the primary screening test when achalasia is suspected on clinical grounds. The diagnostic accuracy of barium swallow for achalasia is approximately 95 percent. The barium swallow typically shows a dilated esophagus that terminates in a beak-like narrowing caused by the persistently contracted lower esophageal sphincter (LES). In some cases, the dilation is so profound that the esophagus assumes a sigmoid shape.

A barium swallow diagnostic accuracy is approximately 95% Absence of peristalsis In some patients, spastic contractions in the esophageal body ("vigorous" achalasia)

Manometry
Elevated resting LES pressure In the LES, the loss of inhibitory neurons typically causes LES pressures to rise to hypertensive levels. Incomplete LES relaxation Normally, there is complete relaxation of the LES after a swallow; in contrast, LES relaxation in response to a swallow may be incomplete or absent in achalasia.

Gastroesophageal Endoscopy

Endoscopic evaluation is generally recommended for most patients with achalasia primarily to exclude malignancies at the esophagogastric junction that can mimic primary achalasia clinically, radiographically, and manometrically. Thus recommended for people with symptoms Duration of symptoms less than six months Presentation after age 60 Excessive weight loss in relation to the duration of symptoms Difficult passage of the endoscope through the gastroesophageal junction

Exclude malignancies Dilated esophagus, residual material. Inflammation and ulceration Stasis - candida infection. The LES does not open spontaneously, traversed easily with gentle pressure

Treatment

Medical Therapy
No treatment reliably restores function in the body of the esophagus, although the return of peristaltic activity has been observed occasionally after the administration of therapies designed solely to decrease LES pressure. Used primarily for patients who are unwilling or unable to tolerate more effective invasive forms of therapy Nitrates and calcium channel blockers relax the smooth muscle of the LES both in normal individuals and in patients with achalasia, and these agents have been used to treat the disorder with limited success. The drugs usually are taken sublingually 10 to 30 minutes before meals.

Botulinum Toxin

BTX reduce the LES pressure by selectively blocking the release of acetylcholine from presynaptic cholinergic nerve terminals in the

BEFORE

AFTER

Balloon Dilatation
Weaken the LES by tearing the muscle fibers.

Short to medium-term results (<10 years) 899 patients - 65% success rate, mean follow-up of 6.5 years Single PD - effective in 85% of 144 patients, followed for an average of 6.5 years. A systematic review of the literature published in 1998: 2418 patients 2/3 of patients had good to excellent improvement after one or more dilations during a mean follow-up of 4.6 years

Long-term results (>10 years)

Few studies One study 50% developed recurrent symptoms after 10 years In a prospective follow-up of 54 patients (Single pneumatic dilation) 5 year remission rate of 40% 10 year remission rate of 36% Repeated dilations only mildly improved the clinical response.

Complications

Esophageal perforation 3% - 5% Intramural hematomas Esophageal mucosal tears Fever (resolves spontaneously) Severe postprocedural chest pain 15% Gastroesophageal reflux disease - incidence of 2%

Surgical Myotomy
Surgical myotomy via the modified Heller approach results in good to excellent relief of symptoms in 70 to 90 percent of patients with few serious complications. The surgeon weakens the LES by cutting its muscle fibers. The mortality rate (approximately 0.3 percent) is similar to that reported for pneumatic dilation.

Figure 1. In preparation for a myotomy the flap of gastric fundus is retracted into the chest through the previously made incision.

Figure 2. Illustration of the technique and extent of myotomy. The myotomy is done through all layers using a scissors and started on the esophageal body.

Figure 3. Reconstruction of the cardia after a myotomy illustrating the gastric flap covering the distal 4 cm of the myotomy.

Figure 4. Completed reconstruction of the cardia after a myotomy illustrating the subdiaphragmatic position of the gastric fundic flap. Note that the tails of the tied apical sutures of the flap have been passed through the diaphragm and tied at the margins of the myotomy 2 cm apart.

Results in good to excellent relief of symptoms 70-90% with few serious complications The mortality rate - approximately 0.3% Reflux esophagitis - 10% (fundoplication) The few long-term studies available suggest that surgical myotomy results in:
sustained remission rates of approximately 85% at 10 years, and 65% at 20 years.

Development Of Esophageal Cancer


Increased risk for developing esophageal cancer (squamous cell type) A population-based study in Sweden:
Risk increased 16-fold compared with controls. Cancer diagnosed an average of 14 years after diagnosis. A similar increase in risk has been noted in a report from the United States Some series note no increase in risk, particularly with early treatment of achalasia

No need for regular endoscopic surveillance.

Potrebbero piacerti anche