Moving beyond simple irritable bowel syndrome to chronic abdominal pain

• Chronic abdominal pain syndrome is a more generalised, constant pain, which can develop in patients with a history of irritable bowel syndrome.
• Inappropriate prescribing can aggravate the situation; opioids cause constipation and can increase gut sensitivity.
• Antidepressant drugs are the cornerstone of treatment; they work, even if there is no identifiable depression.

Abdominal surgery of any type may cause visceral afferent sensitisation that may result in chronic pain

A 45-year-old woman attends for urgent review. She is obviously distressed with severe abdominal pain. She describes experiencing abdominal pain as a child, at which time, she was diagnosed with a “sensitive stomach”.

Symptoms became worse when she was in her 20s, perhaps after an episode of campylobacteriosis. Her bowel habit was variable; the pain was worse with loose motions.

Chronic pain started in her 30s, with more prominent constipation, and she was given antispasmodics and Coloxyl with Senna tablets to relieve this. Her nausea was treated with ondansetron. She had multiple visits to the accident and medical clinic, resulting in prescriptions for opiates, codeine and oxycodone.

She has seen a dietitian but has had no relief from a low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diet.

Change in pain pattern over time

Among the general population, 10–15 per cent have irritable bowel syndrome, based on community studies using a questionnaire-based diagnosis. Only 1 per cent of the population have severe IBS (frequent consultations, disabling symptoms) and 0.1–0.2 per cent could be considered to have chronic abdominal pain syndrome.

The background problem in the patient described above is gut sensitivity worsened by a gastroenteritis illness. The pattern of abdominal pain has changed. Cramping lower abdominal pain, becoming worse, with a change in bowel motions towards loose motions, is a typical symptom of IBS.

Over several years, she has had a gradual change to chronic abdominal pain – this is more generalised, constant pain, unrelated to bowel habit. There are often other somatic complaints in these patients, and major effects on family/social/ work activities. Multiple treatments may have been tried and have failed, with many adverse reactions.

It is important not to aggravate the situation with inappropriate prescribing. Even small doses of codeine and oxycodone may cause constipation with IBS. Ondansetron frequently causes constipation. Opioids also cause constipation and can actually cause increased gut sensitivity. A paradoxical increase in pain occurs with increasing opioid dose because of central sensitisation. Narcotic injections in response to acute presentations to accident and medical clinics or primary care are clearly counterproductive.

Dietary changes such as a low-FODMAP diet can only work if the primary mechanism of pain is distension from “trapped wind” in the setting of visceral hyperalgesia. Suggesting difficult, complex dietary changes in the setting of chronic abdominal pain may only add to the patient’s anxiety and frustration.

Any benefit from further diagnostic studies is unlikely. It is important not to retreat into a diagnosis-by-exclusion mentality. There is no end to the clinical studies that could conceivably be considered relevant. Typically, these patients have had several gastroscopies and colonoscopies as well as an abdominal CT scan. At some stage, the call needs to be made that nothing more will be achieved for the patient by further diagnostic testing and that the shift in focus is towards better management.

There is often a sense of helplessness and frustration. It is important the patient does not feel abandoned; another careful, sympathetic review often leads to a new plan.

Many patients will have the unrealistic expectation of a “quick fix” for their situation; this can lead to mutual frustration and treatment failure. It should be emphasised that treating IBS is a process, and the goal of treatment is to improve their quality of life.

First step – thorough explanation

An explanation and discussion of the brain–gut axis in the context of pain is useful and illustrates the complexity of chronic pain.

The brain–gut axis is a direct (hardwired) bidirectional pathway. No other organ in the body is as closely connected with identical neurotransmitters as the gut is to the brain.

The brain is able to modulate a spinal gate to pain; this should be closed to unpleasant stimuli. Central nervous system amplification of the visceral signals occurs with psychological distress, raising the afferent signals to conscious awareness. A defect in central pain inhibition has the potential to result in a maladaptive central pain response, especially when there are exaggerated, strong emotional responses. Afferent pain fibres are distributed in the brain to provide simple localisation of the painful stimulus, but there is also distribution to areas involved in the emotional and behavioural responses to pain.

Abnormal distribution of pain signals to the brain occurs with chronic pain. Uncoupling of afferent stimuli with pain sensation results in the development of a chronic pain experience that is no longer linked to the initial trigger.

IBS patients report up to twice the number of appendectomies and hysterectomies and up to three times the number of cholecystectomies, compared with patients without IBS. Abdominal surgery of any type may cause visceral afferent sensitisation that may result in chronic pain, even in the presence of normal gut function.

Focus on managing symptoms

The goal in managing chronic abdominal pain is to go beyond focusing on the diagnosis, to managing the symptoms and improving quality of life. The first task is to set realistic goals, with an aim to gradually reduce (not eliminate) abdominal pain by re-regulation of the brain’s control of pain.

Stress lowers pain thresholds. The chronic illness state is maintained by anxiety and depression, leading to poor coping strategies (including helplessness, vulnerability, low self-esteem, hypervigilance and pessimism).

Pharmacological options

Antidepressant drugs are the cornerstone of treatment in chronic abdominal pain. They work, even if there is no identifiable depression.

Tricyclic antidepressants have a role in IBS by decreasing visceral hypersensitivity, but they also have a role in chronic pain (of all types) with central modulation of pain perception. Selective serotonin reuptake inhibitors also have a definite role in chronic pain. The combination of an SSRI in the morning and a low-dose TCA at night is also possible.

Amitriptyline is useful if sleep is impaired. Nortriptyline is less sedating and less likely to cause dry mouth. Start at low doses (no more than 5mg) and gradually titrate up depending on tolerance. There is often sensitivity to side effects of TCAs; I rarely recommend more than 20mg nocte. Combined noradrenergic and serotonergic inhibition (such as with venlafaxine) has a theoretical advantage but significant side effects that can limit its use in IBS.

Adding pregabalin or gabapentin to other pain-directed central-acting agents is supported by basic and clinical data showing reduced visceral hypersensitivity. Both these drugs were originally intended as anticonvulsants, but most clinical use has been for the treatment of neuropathic pain and fibromyalgia. Data are limited on the use of pregabalin and gabapentin in IBS and chronic abdominal pain, but they are likely to be helpful.

Experience with the use of atypical antipsychotics (such as quetiapine) is limited. Quetiapine has a complex mechanism of action but has potential clinical benefits, including an analgesic effect, anxiety reduction and establishment of normal sleep patterns. The main potential use may be in low doses as an augmentation to antidepressants.

Clinicians face two main barriers when trying to treat IBS patients with antidepressants. The first is the general reluctance of these patients to take “mind-altering” agents. The second is an underestimation of the psychological component of their symptoms.

Before prescribing, an explanation of the mechanism of pain control (reducing visceral hypersensitivity by central mechanisms) is needed, as well as an understanding that an antidepressant (mood-elevating) effect is unlikely at the proposed low dose. It is important, again, to acknowledge the patient’s pain.

It is also important to emphasise that this approach of pain modulation is going to work better in the long term compared with continuing direct analgesia. The negative impact of long-term opiates should be stressed (potentially giving paradoxical increase in pain with central sensitisation).

The final point to encourage uptake is to suggest that remodelling of pain pathways is the goal, and it may be possible to stop medication after one year.

Non-pharmacological treatments

Cognitive behavioural therapy, hypnosis and mindfulness meditation have been evaluated for IBS. CBT can help patients recognise misperceptions and maladaptive thoughts regarding their symptoms and enhance their coping abilities.

Mindfulness meditation is a form of relaxation involving an active, non-judgemental awareness of a person’s body sensations and emotions.

Hypnosis is an effective, viable treatment option in IBS that improves IBS symptoms and quality of life, and reduces stress and anxiety. Beneficial effects have been shown to persist at long-term follow-up. An app called Nerva has proven to be a useful option.

The key to success with these patients is to realise the situation has changed: what was simple IBS is now a chronic pain problem. This can bring in a new range of treatment options for them.

However, it does require a lot of time with careful and often repeated explanations, and an acceptance from both patient and doctor that the journey towards meaningful improvement in quality of life will be slow.

Details of this case study have been changed to protect patient confidentiality

Alan Fraser is a gastroenterologist with Auckland Gastroenterology Associates and Endoscopy Auckland, and associate professor of medicine at the University of Auckland