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Written by

Dr Ganesan Baranidharan Dr Ganesan Baranidharan is a consultant in pain medicine, Leeds Teaching Hospitals NHS Trust, UK

Visceral pain: a complex phenomenon

Published 21 April 2017

Dr Ganesan Baranidharan discusses the complex presentation of abdominal visceral pain and highlights the challenges in managing this condition.

Key learning points

  • Abdominal visceral pain results from activation of nociceptive neurons from abdominal visceral structures.
  • The initial phase of the abdominal visceral pain presents as a diffuse and poorly defined sensation, yet is felt mostly in the midline of the body. This is followed by referred pain which is sharper, more localised and can be associated with neuropathic features.
  • Treatment involves both identifying and treating the primary pathology and managing the pain itself, based on the biopsychosocial model. Patient education and self-management should be introduced early.


This article will focus on defining visceral pain and will highlight the challenges in managing this complex pain entity. Pain is defined as an unpleasant sensory and emotional experience, associated with actual or potential tissue damage, or described in terms of such damage. Visceral organs were considered to be insensitive to pain in the past, but our understanding has since improved. The neuroanatomy of visceral organs is complex, with both sympathetic and parasympathetic outflow. The dorsal roots play a prime role in the mechanism of visceral pain.

What is abdominal visceral pain?

Abdominal visceral pain results from activation of nociceptive neurons from abdominal visceral structures, which are very sensitive to distension, ischaemia and inflammation, but relatively insensitive to other painful stimuli, such as cutting or burning. Abdominal viscera, apart from the pancreas, are innervated by both the parasympathetic and sympathetic nervous systems.

Clinical presentation

The initial phase of acute visceral pain is a ‘true visceral pain.’ The sensation is diffuse and poorly defined, yet felt mostly in the midline of the body. Low density sensory innervation and an extensive CNS divergence cause the diffuse nature of the pain. The pain is perceived in either the lower sternum or epigastric region, regardless of the abdominal organ it emanates from. Acute visceral pain is often associated with autonomic disturbances, such as sweating, pallor, nausea and vomiting.1 In visceral pain, the intensity does not always correlate with the severity of the organ damage. Chronic visceral pain emerges from the hyperresponsiveness of neuronal cells, and also from the interplay with glial cells and endocrine and immune signalling. These processes can lead to ongoing visceral hypersensitivity.2 

This initial phase is then followed by a referral pattern to a parietal somatic area, which correlates to the sensory dorsal root of the viscerosomatic projection. This complex phenomenon of afferent input correlating to the visceral and somatic neurons leads to referred pain. Referred pain is sharper, more localised and can be associated with neuropathic features, such as allodynia and hyperalgesia. These neuropathic skin changes can persist even after remission of the primary visceral problem.1

Visceral hyperalgesia is a neurophysiological and central sensitisation phenomenon that makes the visceral organ hypersensitive.1 Examples include gastric ulcer irritation, causing pain on ingestion of food, or mild bladder distention, causing significant pain in an inflamed bladder.

Augmentation of pain due to the sensory interaction between two different internal organs that share at least part of their afferent circuitry, is termed viscero-visceral hyperalgesia. A person with gall bladder calculosis (T5 spinal projection) and ischaemic heart disease (T5 spinal projection) will have increased acute attacks of both conditions. On treating one condition (for example, angioplasty for ischaemic heart disease), we may see a reduction in the second condition.3,4


Treatment of visceral pain can be challenging. The patients tend to have a background dull ache followed by acute exacerbations. Treatment involves both identifying and treating the primary pathology and managing the pain itself. Patients should have appropriate assessment and investigations before referral to a chronic pain team is made. Pain management will be based on the biopsychosocial model. A team approach is key in managing these patients. Education and self-management should be introduced early in the management plan.

Optimal management of the acute exacerbation is vital to avoid emergency admissions, and management of chronic background pain is essential. The acute exacerbations will need clinical assessment to rule out causes such as pancreatitis, cholecystitis, intestinal adhesions, obstruction and perforation. This will be followed by symptom management with strong analgesics.

Opioids are commonly used to control pain during acute exacerbations and should be used with caution within a multimodal treatment approach. When using opioids on a long-term basis, the risks and benefits of the treatment should be discussed with the patient, and the aim should be to control the pain with a small steady dose. The side effects can aggravate the underlying cause, such as reduced gut motility.

Patients with neuropathic symptoms can be managed with antineuropathics, such as antidepressants and anticonvulsants. Antispasmodics also have a role in some visceral pain conditions, such as renal colic.4

Patient education and self-management strategies are key, as these tend to be long-term pain patients with frequent acute exacerbations.4 A team approach, with involvement of all primary and secondary care personnel may be warranted in some difficult cases.

  • Consultant anaesthesia and pain medicine, Leeds Teaching Hospitals NHS Trust, honorary clinical associate professor, University of Leeds

Date of preparation: April 2017; MINT/PAEU-16049