The diagnosis of GERD is usually made when typical symptoms are present. Reflux can be present in people without symptoms and the diagnosis requires both symptoms or complications and reflux of stomach content.

Other investigations may include esophagogastroduodenoscopy (EGD). Barium swallow X-rays should not be used for diagnosis. Esophageal manometry is not recommended for use in diagnosis, being recommended only prior to surgery. Ambulatory esophageal pH monitoring may be useful in those who do not improve after PPIs and is not needed in those in whom Barrett's esophagus is seen. Investigation for H. pylori is not usually needed.

The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and allows monitoring GERD patients in their response to medical or surgical treatment. One practice for diagnosis of GERD is a short-term treatment with proton-pump inhibitors, with improvement in symptoms suggesting a positive diagnosis. Short-term treatment with proton-pump inhibitors may help predict abnormal 24-hr pH monitoring results among patients with symptoms suggestive of GERD.

Endoscopy, the looking down into the stomach with a fibre-optic scope, is not routinely needed if the case is typical and responds to treatment. It is recommended when people either do not respond well to treatment or have alarm symptoms, including dysphagia, anemia, blood in the stool (detected chemically), wheezing, weight loss, or voice changes. Some physicians advocate either once-in-a-lifetime or 5- to 10-yearly endoscopy for people with longstanding GERD, to evaluate the possible presence of dysplasia or Barrett's esophagus.

Biopsies performed during gastroscopy may show:

- Edema and basal hyperplasia (nonspecific inflammatory changes)

- Lymphocytic inflammation (nonspecific)

- Neutrophilic inflammation (usually due to reflux or "Helicobacter" gastritis)

- Eosinophilic inflammation (usually due to reflux): The presence of intraepithelial eosinophils may suggest a diagnosis of eosinophilic esophagitis (EE) if eosinophils are present in high enough numbers. Less than 20 eosinophils per high-power microscopic field in the distal esophagus, in the presence of other histologic features of GERD, is more consistent with GERD than EE.

- Goblet cell intestinal metaplasia or Barrett's esophagus

- Elongation of the papillae

- Thinning of the squamous cell layer

- Dysplasia

- Carcinoma

Reflux changes may not be erosive in nature, leading to "nonerosive reflux disease".

The diagnosis of nutcracker esophagus is typically made with an esophageal motility study, which shows characteristic features of the disorder. Esophageal motility studies involve pressure measurements of the esophagus after a patient takes a wet (fluid-containing) or dry (solid-containing) swallow. Measurements are usually taken at various points in the esophagus.

Nutcracker esophagus is characterized by a number of criteria described in the literature. The most commonly used criteria are the Castell criteria, named after American gastroenterologist D.O. Castell. The Castell criteria include one major criterion: a mean peristaltic amplitude in the distal esophagus of more than 180 mm Hg. The minor criterion is the presence of repetitive contractions (meaning two or more) that are greater than six seconds in duration. Castell also noted that the lower esophageal sphincter relaxes normally in nutcracker esophagus, but has an elevated pressure of greater than 40 mm Hg at baseline.

Three other criteria for definition of the nutcracker esophagus have been defined. The Gothenburg criterion consists of the presence of peristaltic contractions, with an amplitude of 180 mm Hg at any place in the esophagus. The Richter criterion involves the presence of peristaltic contractions with an amplitude of greater than 180 mmHg from an average of measurements taken 3 and 8 cm above the lower esophageal sphincter. It has been incorporated into a number of clinical guidelines for the evaluation of dysphagia. The Achem criteria are more stringent, and are an extension of the study of 93 patients used by Richter and Castell in the development of their criteria, and require amplitudes of greater than 199 mm Hg at 3 cm above the lower esophageal sphincter (LES), greater than 172 mm Hg at 8 cm above the LES, or greater than 102 mm Hg at 13 cm above the LES.

After the initial diagnosis of Barrett's esophagus is rendered, affected persons undergo annual surveillance to detect changes that indicate higher risk to progression to cancer: development of epithelial dysplasia (or "intraepithelial neoplasia").

Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in Barrett be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. For more accuracy and reproductibility, it is also recommended to follow international classification system as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000).

In patients who have dysphagia, testing may first be done to exclude an anatomical cause of dysphagia, such as distortion of the anatomy of the esophagus. This usually includes visualization of the esophagus with an endoscope, and can also include barium swallow X-rays of the esophagus. Endoscopy is typically normal in patients with nutcracker esophagus; however, abnormalities associated with gastroesophageal reflux disease, or GERD, which associates with nutcracker esophagus, may be seen. Barium swallow in nutcracker esophagus is also typically normal, but may provide a definitive diagnosis if contrast is given in tablet or granule form. Studies on endoscopic ultrasound show slight trends toward thickening of the muscularis propria of the esophagus in nutcracker esophagus, but this is not useful in making the diagnosis.

It can be diagnosed with an X-ray while the patient swallows barium (called a barium study of the esophagus), by a computerized tomography scan, a biopsy, or by an endoscopy.

Screening endoscopy is recommended among males over the age of 60 who have reflux symptoms that are of long duration and not controllable with treatment. Among those not expected to live more than 5 years screening is not recommended.

The differential diagnosis of gastric outlet obstruction may include: early gastric carcinoma hiatal hernia, gastroesophageal reflux, adrenal insufficiency, and inborn errors of metabolism.

The most confirmatory investigation is endoscopy of upper gastrointestinal tract.

Laboratory

- Individuals with gastric outlet obstruction are often hypochloremic, hypokalemic, and alkalotic due to loss of hydrogen chloride and potassium. High urea and creatinine levels may also be observed if the patient is dehydrated.

Abdominal X-ray

- A gastric fluid level may be seen which would support the diagnosis.

Barium meal and follow through

- May show an enlarged stomach and pyloroduodenal stenosis.

Gastroscopy

- May help with cause and can be used therapeutically.

A gastroenterologist is a medical professional that can diagnose esophagitis. To diagnose esophagitis, the doctor will interview the patient regarding their signs and symptoms. If the doctor suspects esophagitis, tests can be ordered. Esophagitis can be diagnosed by an upper endoscopy, biopsy, upper GI series (or barium swallow), and laboratory tests.

An upper endoscopy is a procedure to look at the esophagus by using an endoscope. While looking at the esophagus, the doctor is able to take a small biopsy. The biopsy can be used to confirm inflammation of the esophagus.

An upper GI series uses a barium contrast, fluoroscopy, and an X-ray. During a barium X-ray, a solution with barium or pill is taken before getting an X-ray. The barium makes the organs more visible and can detect if there is any narrowing, inflammation, or other abnormalities that can be causing the disease. The upper GI series can be used to find the cause of GI symptoms. An esophagram is if only the throat and esophagus are looked at.

Laboratory tests can be done on biopsies removed from the esophagus and can help determine the cause of the esophagitis. Laboratory tests can help diagnose a fungal, viral, or bacterial infection. Scanning for white blood cells can help diagnose eosinophil esophagitis.

Some lifestyle indicators for this disease include: stress, unhealthy eating, smoking, drinking, family history, allergies, and an immunodeficiency. It is important for the doctor to review the patient's medical history before diagnosing with esophagitis. Specific subtypes and other causes should be taken into account when making the final diagnosis.

The treatment for bile reflux is the same as the treatment for acidic reflux. In general, everything that can

reduce acidic reflux can reduce bile reflux. Examples include lifestyle modification, weight reduction, and the avoidance of eating immediately before sleep or being in the supine position immediately after meals. In addition, smoking has been found to be a factor in the development of acidic reflux. Thus, all of these factors should be applied to bile reflux as well.

Likewise, drugs that reduce the secretion of gastric acid (e.g., proton pump inhibitors)

or that reduce gastric contents or volume can be used to treat acidic bile reflux. Because prokinetic drugs increase the motility of the stomach and accelerate gastric emptying, they can also reduce bile reflux. Other drugs that reduce the relaxations of the lower esophageal sphincter, such as baclofen, have also proven to reduce bile reflux, particularly in patients who are refractory to (medically unresponsive to) proton pump inhibitor therapy.

Medications used in managing biliary reflux include bile acid sequestrants, particularly cholestyramine, which disrupt the circulation of bile in the digestive tract and sequester bile that would otherwise cause symptoms when refluxed; and prokinetic agents, to move material from the stomach to the small bowel more rapidly and prevent reflux.

Biliary reflux may also be treated surgically, if medications are ineffective or if precancerous tissue is present in the esophagus.

If it is caused by esophagitis, in turn caused by an underlying infection, it is commonly treated by treating the infection (typically with antibiotics). In order to open the stricture, a surgeon can insert a bougie – a weighted tube used to dilate the constricted areas in the esophagus. It can sometimes be treated with other medications. For example, an H2 antagonist (e.g. ranitidine) or a proton-pump inhibitor (e.g. omeprazole) can treat underlying acid reflux disease.

The patient swallows a barium solution, with continuous fluoroscopy (X-ray recording) to observe the flow of the fluid through the esophagus. Normal peristaltic movement of the esophagus is not seen. There is acute tapering at the lower esophageal sphincter and narrowing at the gastro-esophageal junction, producing a "bird's beak" or "rat's tail" appearance. The esophagus above the narrowing is often dilated (enlarged) to varying degrees as the esophagus is gradually stretched over time. An air-fluid margin is often seen over the barium column due to the lack of peristalsis. A five-minutes timed barium swallow can provide a useful benchmark to measure the effectiveness of treatment.

Because of its sensitivity, manometry (esophageal motility study) is considered the key test for establishing the diagnosis. A catheter (thin tube) is inserted through the nose, and the patient is instructed to swallow several times. The probe measures muscle contractions in different parts of the esophagus during the act of swallowing. Manometry reveals failure of the LES to relax with swallowing and lack of functional peristalsis in the smooth muscle esophagus.

Characteristic manometric findings are:

- Lower esophageal sphincter (LES) fails to relax upon wet swallow (<75% relaxation)

- Pressure of LES 100 is considered achalasia, > 200 is nutcracker achalasia.

- Aperistalsis in esophageal body

- Relative increase in intra-esophageal pressure as compared with intra-gastric pressure

The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, thus indicating that their primary diagnosis was accurate.

More specifically, peptic ulcers erode the muscularis mucosae, at minimum reaching to the level of the submucosa (contrast with erosions, which do not involve the muscularis mucosae).

Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrast x-rays. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment, or when they first appear in a person who is over age 45 or who has other symptoms such as weight loss, because stomach cancer can cause similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on people in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Additionally, a false negative result is possible with a blood test if the person has recently been taking certain drugs, such as antibiotics or proton-pump inhibitors.

The diagnosis of "Helicobacter pylori" can be made by:

- Urea breath test (noninvasive and does not require EGD);

- Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform "H. pylori" cultures;

- Direct detection of urease activity in a biopsy specimen by rapid urease test;

- Measurement of antibody levels in the blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;

- Stool antigen test;

- Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon to detect H. pylori. To perform this exam the person will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. After an hour, the person will be asked to blow into a bag that is sealed. If the person is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.

The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the "greater (large) curvature" of the stomach; most are also a consequence of chronic "H. pylori" infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the person stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.

Treatments for esophagitis include medications to block acid production, to manage pain, and to reduce inflammation. Other treatments include antibiotics and intravenous nutrition.

To treat reflux esophagitis, over the counter antacids, medications that reduce acid production (H-2 receptor blockers), and proton pump inhibitors are recommended to help block acid production and to let the esophagus heal. Some prescription medications to treat reflux esophagitis include higher dose H-2 receptor blockers, proton pump inhibitors, and prokinetics, which help with the emptying of the stomach.

To treat eosinophilic esophagitis, avoiding any allergens that may be stimulating the eosinophils is recommended. As for medications, proton pump inhibitors and steroids can be prescribed. Steroids that are used to treat asthma can be swallowed to treat eosinophil esophagitis due to nonfood allergens. The removal of food allergens from the diet is included to help treat eosinophilic esophagitis.

For infectious esophagitis, a medicine is prescribed based on what type of infection is causing the esophagitis. These medicines are prescribed to treat bacterial, fungal, viral, and/or parasitic infections.

An endoscopy can be used to remove ill fragments. Surgery can be done to remove the damaged part of the esophagus. For reflux esophagitis, a fundooplication can be done to help strengthen the lower esophageal sphincter from allowing backflow of the stomach into the esophagus. As for patients that have a narrowing esophagus, a gastroenterologist can perform a procedure to dilate the esophagus.

Some home remedies and lifestyle changes to help with esophagitis include losing weight, stop smoking, lowering stress, avoid sleeping/lying down after eating, raise your head while laying down, taking medicines correctly, avoiding certain medications, and avoiding foods that cause the reflux that might be causing the esophagitis.

If the disease remains untreated, it can cause scarring and discomfort in the esophagus. If the irritation is not allowed to heal, esophagitis can result in esophageal ulcers. Esophagitis can develop into Barrett's esophagus and can increase the risk of esophageal cancer.

The prognosis for a person with esophagitis depends on the underlying causes and conditions. If a patient has a more serious underlying cause such as a digestive system or immune system issue, it may be more difficult to treat. Normally, the prognosis would be good with no serious illnesses. If there are more causes than one, the prognosis could move to fair.

LPR presents with non-specific symptoms and signs that make differential diagnosis difficult to achieve. Furthermore, symptoms of the disorder overlap greatly with symptoms of other disorders. Therefore, LPR is under-diagnosed and under-treated. As there are multiple potential etiologies for the respiratory and laryngeal symptoms of LPR, diagnosing LPR based on symptoms alone is unreliable. Laryngoscopic findings such as erythema, edema, laryngeal granulomas, and interarytenoid hypertrophy have been used to establish the diagnosis; however, these findings are nonspecific and have been described in the majority of asymptomatic subjects undergoing laryngoscopy. Response to acid-suppression therapy has been suggested as a diagnostic tool for confirming diagnosis of LPR, but studies have shown that the response to empirical trials of such therapy (as with proton-pump inhibitors) in these patients is often disappointing. Several studies have emphasized the importance of measuring proximal esophageal, or ideally pharyngeal acid exposure, in patients with clinical symptoms of LPR to document reflux as the cause of the symptoms.

Additionally, several potential biomarkers of LPR have been investigated. These include inflammatory cytokines, carbonic anyhydrase, E-cadherin and mucins; however, their direct implications in LPR are still being established. The presence of pepsin, an enzyme produced in the stomach, in the hypopharynx has also become an increasingly researched biomarker for LPR. Research suggests that the stomach enzyme pepsin plays a crucial role in the complex mechanism behind LPR.

Before a diagnosis can be made, a physician will need to record the patient’s medical history and ask for details about the presenting symptoms. Questionnaires such as the Reflux Symptom Index (RSI), Quality-of-Life Index (QLI) for LPR, Glottal Closure/Function Index (GCI) and Voice Handicap Index (VHI) can be administered to gain information about the patient's medical history as well as their symptomatology. A physical examination will then need to be performed with particular concentration around the head and neck. A scope with a specialized camera lens made of fiber optic strands is gently fed down the throat and feeds back images to a monitor. This provides a clear view of the throat and larynx. Signs of LPR include redness, swelling, and obvious irritation. Other, more invasive tests, such as fibre-optic transnasal laryngoscopy, 24-hour ambulatory dual probe pHmetry, pharyngeal pHmetry, transnasal esophagoscopy (TNE) and biopsy may be used. A noninvasive test for diagnosis of LPR is the collection of refluxate where the refluxed material is collected and analyzed. Another noninvasive diagnostic test that can be used is an empirical trial of proton-pump inhibitor therapy; however, this test is mostly successful in diagnosing GERD.

There is no agreed-upon assessment technique to identify LPR in children. Of the debated diagnostic tools, multichannel intraluminal impedance with pH monitoring (MII-pH) is used as it recognizes both acid and non-acid reflux. A more common technique that is used is 24-hour dual probe pH monitoring. Both of these tools are expensive and are therefore not widely used.

Most damage to the pyloric valve occurs as a complication of gastric surgery. Other causes of biliary reflux may be:

- Peptic ulcer

- Gallbladder surgery (cholecystectomy)

A significant fraction of cases are idiopathic, with no identified specific etiology.

A diagnosis of gastric dilatation-volvulus is made by several factors. The breed and history will often give a significant suspicion of gastric dilatation-volvulus, and the physical exam will often reveal the telltale sign of a distended abdomen with abdominal tympany. Shock is diagnosed by the presence of pale mucous membranes with poor capillary refill, increased heart rate, and poor pulse quality. Radiographs (x-rays), usually taken after decompression of the stomach if the dog is unstable, will show a stomach distended with gas. The pylorus, which normally is ventral and to the right of the body of the stomach, will be cranial to the body of the stomach and left of the midline, often separated on the x-ray by soft tissue and giving the appearance of a separate gas filled pocket (double bubble sign).

Younger people with ulcer-like symptoms are often treated with antacids or H2 antagonists before endoscopy is undertaken.

People who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (misoprostol) in order to help prevent peptic ulcers.

On chest radiography, a retrocardiac, gas-filled viscus may be seen in cases of intrathoracic stomach, which confirms the diagnosis. Plain abdominal radiography reveals a massively distended viscus in the upper abdomen. In organoaxial volvulus, plain films may show a horizontally oriented stomach with a single air-fluid level and a paucity of distal gas. In mesenteroaxial volvulus, plain abdominal radiographic findings include a spherical stomach on supine images and 2 air-fluid levels on erect images, with the antrum positioned superior to the fundus.

- Upper GI contrast studies:

The diagnosis of gastric volvulus is usually based on barium studies; however, some authors recommend computed tomography (CT) scanning as the imaging modality of choice.

Upper gastrointestinal (GI) contrast radiographic studies (using barium or Gastrografin) are sensitive and specific if performed with the stomach in the "twisted" state and may show an upside-down stomach. Contrast studies have been reported to have a diagnostic yield in 81–84% of patients.

Often performed for an evaluation of acute abdominal pain, a computed tomography (CT) scan can offer immediate diagnosis by showing two bubbles with a transition line. Proponents of CT scanning in the diagnosis of gastric volvulus report several benefits, including:

1. the ability to rapidly diagnose the condition based on a few coronal reconstructed images,

2. the ability to detect the presence or absence of gastric pneumatosis and free air,

3. the detection of predisposing factors (i.e., diaphragmatic or hiatal hernias), and

4. the exclusion of other abdominal pathology.

- Endoscopy:

Upper gastrointestinal (GI) endoscopy may be helpful in the diagnosis of gastric volvulus. When this procedure reveals distortion of the gastric anatomy with difficulty intubating the stomach or pylorus, it can be highly suggestive of gastric volvulus. In the late stage of gastric volvulus, strangulation of the blood supply can result in progressive ischemic ulceration or mucosal fissuring.

The nonoperative mortality rate for gastric volvulus is reportedly as high as 80%. Historically, mortality rates of 30–50% have been reported for acute gastric volvulus, with the major cause of death being strangulation, which can lead to necrosis and perforation. With advances in diagnosis and management, the mortality rate from acute gastric volvulus is 15–20% and that for chronic gastric volvulus is 0–13%.

Immediate treatment is the most important factor in a favorable prognosis. A delay in treatment greater than six hours or the presence of peritonitis, sepsis, hypotension, or disseminated intravascular coagulation are negative prognostic indicators.

Historically, GDV has held a guarded prognosis. Although "early studies showed mortality rates between 33% and 68% for dogs with GDV," studies from 2007 to 2012 "reported mortality rates between 10% and 26.8%". Mortality rates approach 10% to 40% even with treatment. A study determined that with prompt treatment and good preoperative stabilization of the patient, mortality is significantly lessened to 10% overall (in a referral setting). Negative prognostic indicators following surgical intervention include postoperative cardiac arrhythmia, splenectomy, or splenectomy with partial gastric resection. Interestingly, a longer time from presentation to surgery was associated with a lower mortality, presumably because these dogs had received more complete preoperative fluid resuscitation and were thus better cardiovascularly stabilized prior to the procedure.

People under 55 years without alarm symptoms can be treated without investigation. People over 55 years with recent onset dyspepsia or those with alarm symptoms should be urgently investigated by upper gastrointestinal endoscopy. This will rule out peptic ulcer disease, medication-related ulceration, malignancy and other rarer causes.

People under the age of 55 years with no alarm features do not need endoscopy but are considered for investigation for peptic ulcer disease caused by "Helicobacter pylori" infection. Investigation for "H. pylori" infection is usually performed when there is a moderate to high prevalence of this infection in the local community or the person with dyspepsia has other risk factors for "H. pylori" infection, related for example to ethnicity or immigration from a high-prevalence area. If infection is confirmed, it can usually be eradicated by medication.

Medication-related dyspepsia is usually related to NSAIDs and can be complicated by bleeding or ulceration with perforation of stomach wall.

Management of symptoms for patients within this subgroup of the GERD spectrum is difficult. Once these patients are identified, behavioural and dietary changes are advised. Dietary modifications may include limiting the intake of chocolate, caffeine, acidic food and liquids, gaseous beverages and foods high in fat. Behavioral changes may include weight loss, cessation of smoking, limiting alcohol consumption and avoiding the ingestion of food shortly before bed. Lifestyle changes in children diagnosed with LPR include dietary modifications to avoid foods that will aggravate reflux (e.g., chocolate or acidic and spicy food), altering positioning (e.g., sleeping on your side), modifying the textures of foods (e.g., thickening feeds to heighten awareness of the passing bolus), and eliminating the intake of food before bed.

Proton pump inhibitors (PPIs) are the leading pharmaceutical intervention chosen for the relief and reduction of LPR and are typically recommended for ongoing use twice a day for a period of 3–6 months. PPIs have been shown to be ineffective in very young children and are of uncertain efficacy in older children, for whom their use has been discouraged. While PPIs may provide limited clinical benefits in some adults, there is insufficient evidence to support routine use. Many studies show that PPIs are not more effective than placebos in treating LPR.

When medical management fails, Nissen fundoplication can be offered. However, patients should be advised that surgery may not result in complete elimination of LPR symptoms and even with immediate success, recurrence of symptoms later on is still possible.

One way to assess treatment outcomes for LPR is through the use of voice quality measures. Both subjective and objective measures of voice quality can be used to assess treatment outcomes. Subjective measures include scales such as the Grade, Roughness, Breathiness, Asthenia, Strain Scale (GRBAS); the Reflux Symptom Index; the Voice Handicap Index (VHI); and a voice symptom scale. Objective measures often rely on acoustic parameters such as jitter, shimmer, signal-to-noise ratio, and fundamental frequency, among others. Aerodynamic measures such as vital capacity and maximum phonation time (MPT) have also been used as an objective measure. However, there is not yet a consensus on how best to use the measures or which measures are best to assess treatment outcomes for LPR.

Neonatal bowel obstruction is grouped into two general categories: high, or proximal, obstruction and low, or distal obstruction, both of which are suspected by failure to pass meconium at birth. High obstruction can be suspected based on the double bubble sign. Cases without distal gas are usually related to duodenal atresia, while high obstruction with distal gas need an upper gastrointestinal series because of the need to distinguish duodenal web, duodenal stenosis and annular pancreas from midgut volvulus, the latter being a surgical emergency. Confirmation is ultimately by surgical intervention.

A low obstruction is suspected on plain film, but needs follow up with a gastrografin enema, which itself can be therapeutic. The differential for low obstruction is ileal atresia, meconium ileus, meconium plug syndrome and Hirschsprung disease. In cases of meconium ileus or ileal atresia, the colon distal to the obstruction is hypoplastic, usually less than 1 cm in caliber, as development of normal colonic caliber "in utero" is due to the passage of meconium, which does not occur in either of these conditions. When diffusely small caliber is seen, it is referred to as microcolon. Radiographs in meconium ileus classically demonstrate a bubbly appearance in the right lower quadrant due to a combination of ingested air and meconium. If, on contrast enema, reflux into the dilated distal small bowel loops can be achieved, the study is both diagnostic and therapeutic, as the ionic contrast medium can dissolve the meconium to allow passage of enteric content into the unused colon.

If contrast cannot be refluxed into the distal small bowel, ileal atresia remains a diagnostic possibility. Jejunal and ileal atresia are caused by "in utero" vascular insults, leading to poor recanalization of distal small bowel segments, a condition in which surgical resection and reanastamosis are mandatory. Hirschsprung disease is due to an arrest in neural cell ganglia, leading to absent innervation of a segment distal bowel, and appears as a massively dilated segment of distal bowel on contrast enema. Surgical resection is necessary for this condition as well. Imperforate anus also requires surgical management, with the diagnosis made by inability to pass the rectal tube through the anal sphincter. Supportive intravenous hydration, gastric decompression, and ventilatory support may be needed due to poor neonatal nutrition resulting from dysfunctional bowel absorption.