CAUSES — There are many possible underlying causes of acute pancreatitis, but 60 to 75 percent of all cases are caused by gallstones or alcohol abuse.

Gallstone pancreatitis — Because the gallbladder and pancreas share a drainage duct, gallstones (usually smaller than 1 cm) that lodge in this duct can prevent the normal flow of pancreatic enzymes and trigger acute pancreatitis. Gallstone pancreatitis is more common in women than in men. (See “Patient information: Gallstones”).

Alcoholic pancreatitis — Alcohol is also a common cause of acute pancreatitis. Alcoholic pancreatitis is more common in men and usually occurs in individuals with long-standing alcohol abuse.

Drug-induced pancreatitis — A large number of drugs used to treat medical conditions can trigger acute pancreatitis; for example, dideoxyinosine, DDI (used for treating AIDS), 6-mercaptopurine, 6- MP (an immunosuppressant drug), angiotensin-converting enzyme (ACE) inhibitors (used for treating high blood pressure), and others.

Post-ERCP — Endoscopic retrograde cholangiopancreatography (ERCP) is an endoscopic test that involves the injection of dye into the bile duct and pancreatic duct. Acute pancreatitis develops in about 3 to 5 percent of people who undergo ERCP. Certain patients, such as those who are female or younger, are more prone to develop this complication. Most cases of ERCP-induced pancreatitis are mild. (See “Patient information: ERCP (endoscopic retrograde cholangiopancreatography)”).

Hereditary conditions — Acute pancreatitis can be caused by hereditary conditions, for example, familial hypertriglyceridemia (high blood triglyceride levels) and hereditary pancreatitis. The genetic basis for hereditary pancreatitis is being studied, and genetic blood tests are now available. These conditions may cause acute pancreatitis, usually in children and young adults. Idiopathic — No underlying cause can be identified in about 20 percent of people with acute pancreatitis. This condition is called idiopathic pancreatitis. Only about 3 percent of people will experience additional attacks over time, a condition called idiopathic recurrent pancreatitis.

Other causes — In rare cases, acute pancreatitis is caused by infections, such as mumps or viral hepatitis, or by abdominal injury.

SYMPTOMS — Sudden, constant pain in the upper part of the abdomen is a hallmark of acute pancreatitis, although other medical conditions can also cause this pain pattern. In about half of all people who experience pain during acute pancreatitis, the pain wraps around the trunk and also involves the back in a band-like pattern. The pain typically lasts days and is often relieved by leaning forward. In mild cases of acute pancreatitis, the pain may be limited to slight abdominal tenderness. In about 5 to 10 percent of patients, there is no pain at all. In people with gallstone pancreatitis, gallbladder pain may occur before pancreatic pain. Gallbladder pain (referred to as biliary colic) is typically described as a moderately severe pain in the right upper region of the abdomen extending to the back and right shoulder. The pain gradually increases in intensity and may be accompanied by nausea and vomiting. Although the term “colic” implies that the pain is intermittent, it typically is steady. Gallbladder pain lasts six or eight hours at most and often follows a meal. In people with alcoholic pancreatitis, the symptoms of acute pancreatitis often occur one to three days after an alcohol binge or after stopping drinking. Pain is accompanied by nausea and vomiting in about 90 percent of people. In severe cases of acute pancreatitis, the initial symptom may be shock or coma.

DIAGNOSIS — Diagnosing acute pancreatitis can be difficult because the signs and symptoms of other medical conditions can mimic those of pancreatitis. The diagnosis is usually based upon careful consideration of a person’s medical history, the signs and symptoms noted during a physical examination, and the results of specific diagnostic tests. Once a diagnosis of acute pancreatitis is made, additional tests are used to determine the underlying cause. This step ensures that a person will receive the correct treatment to prevent pancreatitis from recurring. Additional tests also help predict the likely course of pancreatitis over time. This step is important because in a small percentage of people with acute pancreatitis, the condition will progress to a more serious condition called severe acute pancreatitis, often referred to as “necrotizing pancreatitis”. If tests suggest that necrotizing pancreatitis is likely, early intensive medical treatment may help improve the outcome.

Medical history — A medical history often provides clues about the underlying cause of acute pancreatitis. A healthcare provider will ask about previous symptoms of gallstones and alcohol intake; these two factors account for the majority of cases of acute pancreatitis. The provider will also ask about other medical conditions, medications, and if any family members have experienced similar symptoms.

Physical examination — The healthcare provider will perform a physical examination to check for the signs and symptoms of acute pancreatitis. These signs and symptoms vary with the severity of the attack, and their number and extent can help predict the course of pancreatitis. The provider will ask about abdominal pain, nausea, and vomiting, and will check for other signs and symptoms of acute pancreatitis, including fever, rapid heart rate, and shallow breathing or difficulty breathing. A patient will be checked for less common signs and symptoms, including bruise-like areas on the stomach or back, jaundice (yellowish discoloration of the skin), red nodules under the skin, inflammation of the leg veins, and pain and inflammation of the joints.

DIAGNOSTIC TESTS — Diagnostic tests help confirm the presence of acute pancreatitis and predict the course of the condition. The number and type of testing is tailored to the severity of acute pancreatitis and the most likely underlying causes.

Pancreatic enzymes — During acute pancreatitis, enzymes that normally flow from the pancreas into the digestive tract leak out of the pancreas and into the bloodstream. Tests can detect two of these enzymes (amylase and lipase) in the blood.

Serum amylase — A serum amylase test determines levels of amylase in a blood sample, and is the most commonly used test to aid the diagnosis of acute pancreatitis. A marked increase (more than three times the upper limit of normal) in the level strongly suggests acute pancreatitis. Levels of amylase in the blood rise within six to 12 hours after acute pancreatitis begins and remain elevated for three to five days in uncomplicated attacks.Tissues other than the pancreas also produce amylase, though the levels are not usually as high as with acute pancreatitis; this pattern helps differentiate most cases of acute pancreatitis from other conditions. Elevation of the serum lipase also helps to confirm the diagnosis and distinguish it from other conditions associated with elevated levels of amylase.

Serum lipase — The serum lipase test determines levels of lipase in a blood sample. Elevated serum lipase levels help to confirm the pancreatic origin of elevated serum amylase levels.

Markers of inflammation — Rising blood levels of some substances signal inflammation, although these markers are non-specific because they do not point to the source of inflammation. These markers include C-reactive protein (CRP), neutrophil elastase, procalcitonin, tumor necrosis factor, and interleukin-6 (IL-6). Studies are ongoing to determine if levels of inflammatory markers are helpful to predict the course of acute pancreatitis. At the present time, these markers are not routinely used.

Liver enzymes — Liver enzymes can sometimes be helpful for determining the cause of pancreatitis. For example, elevated levels of alanine aminotransferase (ALT) at the beginning of symptoms suggest that a person has gallstone pancreatitis. Although often referred to as liver function tests, these enzymes are not true indicators of the status of liver function.

Imaging tests — Imaging tests provide information about the structure of the pancreas, the ducts that drain the pancreas and gallbladder, and the tissues surrounding the pancreas.

Abdominal X-ray — In acute pancreatitis, an x-ray of the abdomen may reveal a normal appearance of the digestive tract or abnormalities that are characteristic of acute pancreatitis. These abnormalities include paralysis of regions of the small intestine and spasm of part of the colon. In severe cases, both the small intestine and colon may cease to function. An abdominal x-ray may also point to other conditions that mimic acute pancreatitis, such as blockage of the intestine and a tear in the intestinal wall.

Chest X-ray — About one-third of people with acute pancreatitis have abnormalities on a chest x-ray. These abnormalities may include elevation of the diaphragm (the large muscle that separates the abdomen and the chest), collection of fluid in the chest cavity, collapse of the base of the lungs, and inflammation of the lungs.

Abdominal ultrasound — An abdominal ultrasound test can also aid the diagnosis of acute pancreatitis. This test is particularly useful for identifying gallstones in the gallbladder or in the ducts that drain the gallbladder as the cause of acute pancreatitis. However, this test cannot identify the more serious abnormalities associated with moderate and severe pancreatitis.

Computed tomography scan — The computed tomography (CT) scan is the most useful radiology test for diagnosing acute pancreatitis. This test is often done if conditions other than pancreatitis are suspected, if conservative medical care fails to relieve the symptoms of acute pancreatitis, or if complications such as necrotizing pancreatitis are suspected. The CT scan is especially useful for determining the extent of pancreatitis. It can identify enlargement or abnormal contours of the pancreas, inflammation of the tissues surrounding the pancreas, collection of fluid around the pancreas, and collection of gas in the pancreas or in the tissues behind the pancreas. The type and number of these abnormalities have been found to correspond to the severity of pancreatitis.

Magnetic Resonance Imaging scan (MRI) — MRI may be used to diagnose acute pancreatitis, to assess the severity of disease, to identify complications of pancreatitis such as fluid collections and areas of necrosis or dead tissue. An MRCP (magnetic resonance cholangiopancreatography), which can be performed along with an MRI, can identify the bile duct and pancreatic duct as well as small gall stones within the bile duct. This information can help guide further treatment. However, MRI may not be available in all locations and sick patients sometimes find it difficult to undergo this procedure as it is time-consuming (>30 minutes).

Endoscopic retrograde cholangiopancreatography — As mentioned above, ERCP can cause acute pancreatitis. However, it may also provide helpful information in people who are suspected of having pancreatitis due to gallstones or other problems with the bile or pancreatic ducts, especially if attacks of acute pancreatitis are recurrent. In addition, ERCP permits treatment of some causes of  pancreatitis. An example is removal of a gallstone that has become impacted in the common bile duct. (See “Patient information: ERCP (endoscopic retrograde cholangiopancreatography)”). Fine needle aspiration — In this procedure, a thin needle is used to collect tissue and/or fluid in and around the pancreas, usually with CT guidance. This is recommended if the patient has a persistent fever or if areas of dying tissue in the pancreas (called necrotizing pancreatitis) fails to improve or worsens despite treatment. The small sample of pancreatic tissue/fluid that is removed is sent for laboratory analysis, including staining for bacteria and culture. This analysis can help determine if the damaged pancreatic tissue has become infected. If infection is present in dead pancreatic tissue, further treatment may involve removal of the dead tissue by surgery.

Serum triglyceride levels — A serum triglyceride blood test determines levels of the fat-like triglycerides. This test is useful for diagnosing familial hypertriglyceridemia or simple hypertriglyceridemia in adults. In patients with pancreatitis due to hypertriglyceridemia, the triglyceride levels are usually very high (>1000 mg/dL with normal being 150 mg/dL).

Genetic tests — Genetic tests are useful for diagnosing hereditary forms of pancreatitis. Examples include genetic tests for mutations of the hereditary pancreatitis gene.

TREATMENT — The goals of treatment of acute pancreatitis are to alleviate pancreatic inflammation and to correct the underlying cause. Treatment usually requires hospitalization for at least a few days. The specific treatment measures used depend upon whether a person has mild or moderate to severe pancreatitis.

Mild pancreatitis — Mild pancreatitis is typically self-limited, and the symptoms usually resolve with simple supportive care, which entails monitoring, drugs to control the pain, and intravenous fluids. Although doctors typically discourage eating during the first few days, most people with mild pancreatitis are able to gradually resume eating within three to seven days.

Moderate to severe pancreatitis — Moderate to severe pancreatitis requires more extensive monitoring and supportive care. In cases of necrotizing pancreatitis, treatment may also entail antibiotics and surgery.

Monitoring — Moderate to severe pancreatitis can lead to potentially life-threatening complications, including damage of the heart, lung, and kidneys. Patients who develop kidney failure may need dialysis until kidney function returns. Those who have severe lung injury may need to be on a ventilator (a machine that facilitates breathing). People with pancreatitis of this severity may be closely monitored in an intensive care unit where advanced supportive care is available if needed.

Intravenous fluids — Intravenous fluids can help prevent the dehydration that often results from moderate to severe pancreatitis.

Feeding and eating — Studies suggest that early enteral feeding (feeding through a tube advanced into the middle part of the small intestine) may actually help prevent infections, reduce the likelihood of complications, and lessen the severity of pancreatitis. Parenteral feeding (feeding through an intravenous line placed in the upper chest) is an alternative for people who cannot tolerate enteral feeding or who cannot get enough nutrients with enteral feeding.  People with moderate to severe pancreatitis can resume eating gradually once the pain resolves and bowel functions return to normal.

Antibiotics — About 30 percent of people with severe acute pancreatitis develop an infection of the damaged pancreatic tissue. Antibiotics can prevent this infection and control infections that are already present, especially in patients with necrosis (dead tissue) of the pancreas or major organ (eg, kidney, lung) failure. Studies have shown that antibiotics reduce the likelihood of infection and death in people with severe necrotizing pancreatitis. This treatment may entail intravenous antibiotics and oral antibiotics. Because these antibiotics increase the risk of fungal infection, treatment may also include antifungal drugs.

Necrosectomy — Acute pancreatitis is sometimes complicated by extensive damage and/or infection to the pancreatic tissue. In these cases, doctors usually recommend removal of the damaged and/or infected tissue, a procedure referred to as a “necrosectomy.” It can be performed by surgically opening the abdomen and removing the affected tissue, or with less invasive procedures (eg, endoscopic or radiologic placement of drainage tubes into the area). Whether the procedure is done surgically or by a non-surgical procedure depends upon the condition of the patient and the expertise available in the hospital.

Specific treatments of gallstone pancreatitis — In people who have gallstone pancreatitis, the treatment of pancreatitis is usually coupled with the treatment of gallstones.

Endoscopic papillotomy — Most gallstones that cause attacks of acute pancreatitis pass on their own, but some stones cause prolonged blockage that leads to complications. In people with gallstone pancreatitis who also have jaundice (yellowing of the skin) or a gallbladder infection, a procedure called endoscopic papillotomy can be used to quickly relieve the obstruction.This procedure is not necessary for people who have already passed their gallstones. Because many patients are very ill, doctors sometimes place a stent (a thin plastic tube) to drain the obstructed bile duct rather than attempting to remove the stone. Placement of a stent is usually faster and safer than endoscopic papillotomy.

Surgery — Gallstone pancreatitis recurs in 30 to 50 percent of people after an initial attack of pancreatitis. Doctors usually recommend cholecystectomy (surgical removal of the gallbladder) to prevent this recurrence. This surgery can now be performed through a tiny incision in the abdominal wall, a procedure called laparoscopic cholecystectomy. During surgery, the ducts joining the gallbladder, pancreas, and small intestine are examined for residual gallstones. If any stones remain after surgery, they can be detected and removed during endoscopic retrograde cholangiopancreatography (ERCP). This procedure can be performed while a patient is hospitalized with mild acute pancreatitis, or at a later time if the attack of acute pancreatitis is severe.

CAUSE — The specific cause of achalasia is unknown. However, patients with achalasia have two problems in the esophagus (the tube which carries food from the mouth to the stomach).

The first is that the lower two-thirds of the esophagus does not propel food toward the stomach properly.

The second problem is in the lower oesophageal sphincter (LES), a circular band of muscle that lies at the junction of the esophagus and the stomach. The LES normally helps prevent food from flowing backwards, from the stomach into the esophagus. The LES should relax in response to swallowing to allow food to enter the stomach. In patients with achalasia, the LES fails to relax, creating a barrier that prevents food and liquids from passing into the stomach. One theory about achalasia is that the nerve cells responsible for relaxation are destroyed by an unknown cause. Damage to the LES and esophagus causes large volumes of food and saliva to accumulate in the esophagus. Patients can initially compensate for this but eventually the barrier progresses to the point where food and saliva cannot reliably enter the stomach, and, as a result, build up in the esophagus.

SYMPTOMS — The symptoms have a slow onset and progress gradually; many people delay seeking medical attention until symptoms are advanced. The major symptom is difficulty swallowing (liquids or solids). Other symptoms include chest pain, regurgitation of swallowed food and liquid, heartburn, difficulty burping, a sensation of fullness or a lump in the throat, hiccups, and weight loss.

DIAGNOSIS — Achalasia is usually suspected based upon the presence of the symptoms described above, but tests are needed to confirm the diagnosis. In addition, it is important to rule out other conditions with similar symptoms, such as gastroesophageal reflux disease, pseudoachalasia (a rare condition in which certain tumours can mimic the features of achalasia), and an infection called Chagas’ disease, which is seen almost exclusively in Central and South America.

Chest x-rays — A simple chest x-ray may reveal distortion of the esophagus and absence of air in the stomach, two abnormalities that suggest achalasia.

Barium swallow test — The barium swallow test is the primary screening test for achalasia. The test involves swallowing a chalky-tasting, thick mixture of barium while x-rays are taken. The barium shows the outline of the esophagus and LES.

Barium swallows are usually performed under fluoroscopy, a continuous low-grade x-ray, which is helpful for studying the motion in the esophagus. In achalasia, barium swallows usually reveals an absence of contractions in the esophagus after swallowing. Sometimes this test reveals spastic contractions of the esophagus in response to swallowing; this variation of achalasia is known as vigorous achalasia.

After the barium swallow, patients should drink extra fluid. Stools may be light in colour for a few days after testing as a result of the barium.

Manometry — Manometry refers to the measurement of pressure within the esophagus and the LES. Pressures are measured by advancing a thin tube through the mouth or nose into the esophagus. The test is done after patients have had nothing to eat or drink for eight hours, while patients are awake. Patients will be asked to swallow while the tube is in place. Manometry is always used to confirm achalasia. The test typically reveals three abnormalities in people with achalasia: high pressure in the LES at rest, failure of the LES to relax after swallowing, and an absence of useful (peristaltic) contractions in the lower esophagus. The last two features are the most important and are required to make the diagnosis.

Endoscopy — Endoscopy allows for direct visualization of the inside of the esophagus, LES, and stomach using a thin, lighted, flexible tube. Endoscopy is done while a patient is sedated. This test is usually recommended for people with suspected achalasia and is especially useful for detecting other conditions that mimic achalasia. (See “Patient information: Upper endoscopy”).

In people with achalasia, endoscopy often reveals distortion of the esophagus and the presence of residual food; it may also reveal inflammation, small ulcers caused by residual food or pills, and candida (yeast) infection. The endoscope can be advanced through the LES and into the stomach to check for stomach cancer. Cancer in the upper part of the stomach can produce symptoms almost identical to those of achalasia, and is called pseudoachalasia (meaning “false” achalasia). Thus, biopsies (small samples of tissue) are often obtained in the lower portion of the esophagus. Having a biopsy while sedated is not painful and is very safe.

TREATMENT — Several options are available for the treatment of achalasia.

Unfortunately, none can halt or reverse the underlying problem. However, all of the treatments are effective for improving symptoms.

Two of these treatments (drug therapy and botulinum toxin injection) work by reducing the LES pressure while two other treatments (balloon dilatation and surgery (myotomy)) work by mechanically weakening the muscle fibres of the LES.

Drug therapy — Two classes of drugs, nitrates and calcium channel blockers have muscle-relaxing effects. These drugs can relax the LES and decrease symptoms in people with achalasia. They are usually taken by placing a pill under the tongue 10 to 30 minutes before meals.

Drug therapy is the least invasive option for treating achalasia. However, most people find that long-term drug therapy is inconvenient, ineffective, and sometimes associated with side effects such as headache and low blood pressure. Furthermore, these drugs tend to lose their effectiveness over time. For these reasons, medications are recommended for patients who are not interested in or not healthy enough for other treatments.

Balloon dilatation (pneumatic dilatation) — Balloon dilatation mechanically stretches the contracted LES. This procedure is effective for relieving symptoms of achalasia in two-thirds of patients, although chest pain persists in some people. Up to half of patients may require more than one treatment for adequate relief. Patients receive general anaesthesia and are generally able to go home at the end of the day.

Procedure — People undergoing balloon dilatation are typically placed on a liquid diet 12 hours to two days in advance (a longer period is recommended in patients with a great deal of food in the esophagus). Using fluoroscopy, a physician advances a guide wire down the esophagus and positions it inside the LES. A deflated balloon is then advanced along this guide wire, positioned inside the LES, and inflated for about 60 seconds. The balloon is then deflated and withdrawn, and the person is monitored in a recovery area for five to six hours to detect any complications of the procedure. If there are no complications, people can usually resume eating after six hours. If a person’s day-to-day symptoms do not improve, additional sessions can be performed.

Success rate — A single balloon dilatation session continues to relieve symptoms of achalasia in about 60 percent of people one year after the procedure and in about 25 percent of people five years after the procedure. Higher success rates have been reported in some studies. The success rate at later time points has not been well studied, but some people have remained symptom-free for as long as 25 years.

Complications — About 15 percent of people experience severe chest pain immediately after balloon dilatation, and some experience fever.

The most significant complication of balloon dilatation is creation of a hole (perforation) in the wall of the esophagus; this complication occurs in about 2 to 6 percent of people undergoing the procedure, and it is most likely to occur during the first dilatation session. Symptoms of persistent or worsening pain in the hours after the procedure may indicate a perforation. Some doctors routinely check x-ray and/or swallow tests immediately after the procedure to check for a perforation. Most perforations are small, and some heal on their own with antibiotics and intravenous feeding. However, many doctors recommend surgery to repair these tears, regardless of their size. There is no way to predict perforation; however, it is sensible to choose a doctor who has a great deal of experience performing balloon dilatation procedures.

Other possible complications of balloon dilatation include bruising of the oesophageal wall, damage to the oesophageal lining, the development of small pockets (diverticula) in the esophagus or upper stomach, and the development of gastroesophageal reflux disease (GERD). Because the LES is the principal barrier which prevents the reflux of stomach contents into the esophagus, its disruption can lead to acid reflux. GERD occurs in about 2 percent of people after balloon dilatation, but is usually easily controlled with acid-reducing medications.

Surgery (myotomy) — Myotomy can be used to directly cut the muscle fibres of the LES. The surgical technique used most often is called the Heller myotomy. In the past, surgery was performed through an open incision in the chest or abdomen, but it can now be performed through a tiny incision using a thin, lighted tube (a laparoscope or a thoracoscope). This new approach is less traumatic and shortens recovery time. Patients who undergo myotomy are given general anaesthesia, and generally stay in the hospital for one to two nights.

Success rate — Surgery relieves symptoms in 70 to 90 percent of people. Symptom relief is sustained in about 85 percent of people 10 years after surgery and in about 65 percent of people 20 years after the surgery. Thus, surgery is a more permanent solution for achalasia than balloon dilatation or botulinum toxin injection (see below). However, surgery can also be associated with complications, is more invasive than balloon dilatation (and more costly).

Complications — like balloon dilatation, there is a risk of reflux following myotomy, which, over time, can cause damage to the esophagus. Surgeons generally perform a fundoplication (wrapping a portion of the stomach around the esophagus to prevent regurgitation of stomach contents) at the time of surgery; however, this does not always prevent reflux. Patients should be regularly monitored for this complication, and may require acid suppressing medications. The procedure requires general anaesthesia, and patients are hospitalized for one to two days.

Some post-operative pain is expected, which can be controlled with pain medications.

Botulinum toxin injection — Botulinum toxin injection is the newest treatment for achalasia. The botulinum toxin temporarily paralyses the nerve cells that signal the LES to contract thereby helping to relieve the obstruction. Botulinum toxin injection may also be used as a diagnostic test in people with suspected achalasia who have inconclusive test results. Procedure — the injection procedure is performed during routine endoscopy, while patients are sedated. The botulinum toxin is injected directly into the LES. Success rate — A single botulinum toxin injection session relieves symptoms in 65 to 90 percent of people in the short term (three months to approximately one year). Additional injections can relieve symptoms in patients whose symptoms return. Botulinum toxin injection is more likely to be effective in people over the age of 50 years and in people who have the vigorous form of achalasia. When compared with balloon dilatation, botulinum toxin has a similar effectiveness for relieving symptoms in the first one to two years after the procedure; however, this prolonged effectiveness requires multiple botulinum toxin injections in 40 to 50 percent of people. The long-term safety and effectiveness of botulinum toxin injection is unknown.

Complications — about 25 percent of people have chest pain for a few hours after the procedure while about 5 percent develop heartburn. Damage of the oesophageal wall and lining are rare. The short-term safety of botulinum toxin injection appears to be greater than the short-term safety of both balloon dilatation and surgery; this greater short-term safety may make botulinum toxin injection a better choice for people with other medical conditions who must avoid more invasive procedures. Because the amounts of botulinum toxin used are very small, there is virtually no risk of botulism poisoning from this procedure.

LONG-TERM RISK OF ESOPHAGEAL CANCER — People with achalasia have an increased risk of oesophageal cancer, particularly if obstruction is not adequately relieved. As a result, doctors recommend regular endoscopic screening for early detection of this cancer.

REFERENCES
West, RL, Hirsch, DP, Bertelsmann, JF, et al. Long term results of pneumatic dilation in achalasia followed for more than 5 years. Am J Gastroenterol 2002; 97:1346.
Spiess, AE, Kahrilas, PJ. Treating achalasia: From whalebone to laparoscope. JAMA 1998; 280:638.
Eckardt, VF, Kanzler, G, Westermeier, T. Complications and their impact after pneumatic dilatation for achalasia: Prospective long-term follow-up study. Gastrointest Endosc 1997; 45:349.
Pasricha, PJ, Ravich, WJ, Hendrix, T, et al. Intrasphincteric botulinum toxin for the treatment of achalasia. N Engl J Med 1995; 332:774.