Indigestion (chronic epigastric pain or meal-related discomfort)

6 Indigestion (chronic epigastric pain or meal-related discomfort)




Case


A 39-year-old female psychologist consults because of problems with indigestion for the past year. She states that after eating a meal she feels very uncomfortable and full. The discomfort she experiences is not at the level of pain, but does interfere with her life. She also feels bloated and is unable to finish normal-sized meals now. She has these symptoms after most meals. She very occasionally will have heartburn (retrosternal burning discomfort in her chest travelling up towards the throat). She never has acid regurgitation and denies dysphagia. She is slightly nauseous at times, but denies vomiting. She has not noticed any change in her bowel habit. Her weight has fluctuated up and down, but overall has been stable. She remembers her mother suffered for years with indigestion problems. She is not taking non-steroidal anti-inflammatory drugs supplied ‘over the counter’.


She has already consulted a gastroenterologist who performed an upper endoscopy; she was told the test was normal (no peptic ulcer, no cancer and no reflux oesophagitis), but was given a trial of proton pump inhibitor for 2 months. It did not help her.


Physical examination is unremarkable. You order a Helicobacter pylori 13C urea breath test, which comes back negative. In view of the previously negative upper endoscopy and characteristic history, you diagnose functional or non-ulcer dyspepsia (postprandial distress syndrome based on the Rome III criteria). You provide the patient with dietary advice (low fat and small regular meals) and prescribe a prokinetic agent (domperidone, 10 mg before meals). The patient returns a month later and advises you that she has had a good response to this approach. You further reassure her about the benign nature of the condition although you do warn her that while the symptoms can fluctuate they usually persist long term.




Mechanisms Underlying Epigastric Pain


A diverse range of physiological or pathological mechanisms can result in chronic or recurrent epigastric pain. These include (1) inflammation, not only acute, but also chronic; (2) abnormal motor activity producing distension or excessive contraction of hollow organs; (3) hypersensitivity of hollow viscera in the upper gastrointestinal tract; (4) stretching of the capsules of solid viscera, for example the liver; (5) malignant invasion of nerves; and (6) organ-specific responses, such as acid and pepsin acting on nerve fibres in the base of a peptic ulcer. Based on the afferent relays or pathways for pain impulses, activated by these processes, three different types of pain can be appreciated clinically. These types can occur in isolation or together in the one individual. Visceral pain arises from nociceptors situated in the walls of the abdominal viscera, somatic pain from nociceptors situated in the parietal peritoneum and supporting tissues, and referred pain by activation of strong visceral impulses spilling over to the somatic afferent neurones in the same spinal cord segment (Ch 4). Visceral pain tends to be dull, perceived in the midline and poorly localised; it may be described in terms other than ‘pain’, and may be accompanied by symptoms of autonomic disturbance. Somatic pain, like referred pain, tends to be sharp or aching, sustained, lateralised and yet relatively poorly localised; it may be worse on movement. Referred pain tends to be sharp or aching in character, lateral or bilateral and roughly localised to the somatic dermatome. When patients describe pain as superficial, it may arise from lesions in the abdominal wall or hernial sac, but may occasionally also represent referred pain, from disease in intraabdominal or thoracic viscera.



Clinical Assessment


Epigastric pain, which is considered to represent a sense of tissue damage, should be distinguished from discomfort; the latter refers to a subjective, negative feeling that does not reach the qualification or intensity level of pain. Discomfort can include a number of other symptoms including early satiation (inability to finish a normal-sized meal), postprandial fullness and nausea (Ch 9). It is useful to determine the major complaint: whether the symptoms are related to meal ingestion or not, and whether they are intermittent (recurrent or cyclical) or continuous. As with any symptom, the other specific features need to be ascertained, including the site, mode of onset, intensity, character, and precipitating and relieving factors (see Ch 7). For the purposes of this discussion, a duration of 3 months or longer is taken as indicating chronicity, which distinguishes dyspepsia from the acute symptoms present in disorders such as perforated peptic ulcer, acute cholecystitis and acute pancreatitis (Ch 4).





Differential diagnosis of dyspepsia


The differential diagnosis of dyspepsia is extremely wide, including diseases not only of the gastroduodenum, but also all of the other organs situated in the upper abdomen. Therefore, it is crucial to identify the precise symptoms. Leading questions are often required to elicit the complaints that trouble the patient most. Even when a detailed history has been obtained, the exact clinical diagnosis is often difficult—symptoms such as nocturnal waking, or relief or aggravation by eating often fail to discriminate between the different diagnoses. Patients with dyspepsia can, however, be subdivided into two main categories, based on the known or proposed underlying pathophysiology (Table 6.1). Thus dyspeptic symptoms may be ascribed to:




Table 6.1 Differential diagnosis of epigastric pain or meal-related epigastric discomfort









Organic Functional dyspepsia


















Chronic Peptic Ulcer


Patients with an uncomplicated peptic ulcer classically describe intermittent symptoms of ‘burning’ or ‘gnawing’ epigastric pain, which they may locate by finger point; the pain tends to be worse before meals and is relieved by taking food or antacids. Epigastric pain may waken the patient at night, commonly at about 2.00 a.m., when it is again relieved by food or antacids. The diagnosis is further strengthened if the history is clearly episodic with symptoms present for a few months at a time, followed by periods of remission (periodicity). The intensity and duration of pain vary from recurrence to recurrence, and the symptom-free intervals vary unpredictably. A history of prompt and good symptomatic relief by a course of H2-receptor antagonists or proton pump inhibitors suggests an acid-related disorder (either peptic ulcer or reflux). There may be associated symptoms of heartburn and occasional vomiting. It is usually not possible to differentiate between gastric and duodenal ulceration by symptoms alone; in gastric ulcer, however, pain relief associated with food may be short-lived and anorexia, nausea and weight loss are more prominent. Unfortunately, classical ulcer-type symptoms also do not discriminate peptic ulcer disease from functional dyspepsia.


Chronic peptic ulcer, in most cases, is caused by H. pylori infection (Ch 5) or NSAIDs; an acid hypersecretory state (e.g. the Zollinger-Ellison syndrome due to a gastrin-producing tumour) is a rare but important cause to be aware of in practice.



Gastric cancer


A short history of new onset dyspepsia occurring in a patient over the age of 55 years should raise the suspicion of gastric cancer (Ch 17). Symptoms of pain or discomfort on a daily basis, together with early satiety, increase the probability. Weight loss, anorexia and vomiting are common symptoms, especially when the malignancy is advanced (hence not curable)—these are the alarm features or red flag symptoms. Dysphagia can occur with tumours arising from the cardia or distal oesophagus.




Cholelithiasis


‘Biliary colic’ is associated with the sudden onset of severe or very severe epigastric pain that may pass through or around to the back (Ch 4). Typically there are episodes of pain that occur unpredictably, usually with associated nausea and vomiting. With inflammation of the gall bladder, the pain may shift to the right upper quadrant and become ‘peritoneal’ in type. With biliary colic, movement does not aggravate the pain. The pain is usually not ‘colicky’ but sustained, albeit varying in intensity. Symptoms may be induced by a fatty meal. In the absence of typical biliary pain there appears to be no association between the presence of gallstones in the gall bladder and dyspepsia. If a gallstone enters the common bile duct (choledocholithiasis), there may be associated features of intermittent jaundice, dark urine, pale stools, or with sepsis episodic fever and rigors (see Ch 23).




May 30, 2016 | Posted by in GASTROENTEROLOGY | Comments Off on Indigestion (chronic epigastric pain or meal-related discomfort)

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