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Visceral pain is defined as pain that results from the activation of nociceptors of the thoracic, pelvic, or abdominal viscera (organs) in the human body. Visceral structures are highly sensitive to distension (stretch), ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain such as cutting or burning.
Visceral pain is diffuse, difficult to localize, and often referred to a distant, usually superficial, structure. (1986). 9780444807571 ISBN 9780444807571 It may be accompanied by symptoms such as nausea, vomiting, changes in vital signs as well as emotional manifestations. The pain may be described as sickening, throbbing, pulsating, deep, squeezing, and/or dull.Urch CE & Suzuki R. Pathophysiology of somatic, visceral, and neuropathic cancer pain. In: Sykes N, Bennett MI & Yuan C-S. Clinical pain management: Cancer pain. 2 ed. London: Hodder Arnold; . p. 3–12
When both visceral and parietal nociceptors are activated, both pain modalities will be perceived simultaneously (for example, appendicitis may be associated with dull visceral pain at the level of the umbilicus (T10-T11) as well as sharp parietal pain at the lower right quadrant of the abomen).
The liver parenchyma and lung alveoli are virtually free of nociceptive innervation; nevertheless, bile ducts and the connective tissue covering of the liver are sensitive to pain, as are the bronchi and parietal pleura.
Visceral pain is typically associated with autonomic symptoms (e.g. pallor, sweating, nausea, vomit, changes in vital signs including blood pressure, heart rate and/or temperature). Strong emotional reactions are also common presenting signs and may include anxiety, anguish and a sense of impending doom.
Importantly, perceived intensity of pain may often be unrelated to the actual clinical severity of the underlying pathology causing the painCervero F" Gut 2000; 47:56–57Carr, D.B. (2005). "Visceral Pain" International Association for the Study of Pain. VXIII, No.6 (e.g. silent heart attack). More rarely, intense visceral pain may be associated with a more innocuous aetiology (e.g. severe flatulence).
The dermatomes experiencing referred pain may become affected by secondary hyperalgesia - especially when the causative visceral pain has been recurrent or chronic. Secondary hyperalgesia may persist after the underlying condition has been resolved.
Treatment of the pain in many circumstances should be deferred, until the origin of the symptoms has been identified. Masking pain may confound the diagnostic process and delay the recognition of life-threatening conditions. Once a treatable condition has been identified there is no reason to withhold symptomatic treatment. Also, if cause for the pain is not found in reasonable time then symptomatic treatment of the pain could be of benefit to the patient in order to prevent long-term sensitization and provide immediate relief. (2025). 9780931092312, IASP Press. ISBN 9780931092312Song SO, Carr DB. Pain: Clin Updates 1999; VII:1.
Symptomatic treatment of visceral pain relies primarily upon pharmacotherapy. Since visceral pain can result secondary to a wide variety of causes, with or without associated pathology, a wide variety of pharmacological classes of drugs are used including a variety of analgesics (ex. opiates, NSAIDs, cannabinoids), antispasmodics (ex. loperamide, benzodiazepines), antidepressants (ex. TCA, SSRI, SNRI) as well as others (ex. ketamine, clonidine, gabapentin). In addition, pharmacotherapy that targets the underlying cause of the pain can help alleviate symptoms due to lessening visceral nociceptive inputs. (2025). 9780683304626, Lippincott Williams & Wilkins. ISBN 9780683304626 For example, the use of nitrates can reduce Angina pectoris by dilating the coronary arteries and thus reducing the ischemia causing the pain. The use of spasmolytics (antispasmodics) can help alleviate pain from a gastrointestinal obstruction by inhibiting the contraction of the gut. (1986). 9780444807571, Elsevier. ISBN 9780444807571 There are issues associated with pharmacotherapy that include (ex. constipation associated with opiate use), chemical dependence or addiction, and inadequate pain relief.
Invasive therapies are in general reserved for patients in whom pharmacological and other non-invasive therapies are ineffective. A wide variety of interventions are available and shown to be effective, a few will be discussed here. Approximately 50–80% of pelvic cancer pain patients benefit from .Patt RB. Cancer pain. Philadelphia: JB Lippincott; 1993 Nerve blocks offer temporary relief and typically involve injection of a nerve bundle with either a local anesthetic, a steroid, or both. Permanent nerve block can be produced by destruction of nerve tissue. Strong evidence from multiple randomized controlled trials support the use of neurolytic celiac plexus block to alleviate pain and reduce opioid consumption in patients with malignant pain originating from abdominal viscera such as the pancreas.Eisenberg E, et al. Pain: Clin Updates 2005; XIII:5. Neurostimulation, from a device such as a spinal cord stimulator (SCS), for refractory angina has been shown to be effective in several randomized controlled trials. A SCS may also be used for other chronic pain conditions such as chronic pancreatitis and familial Mediterranean fever. Other devices that have shown benefit in reducing pain include transcutaneous electrical nerve stimulators (TENS), targeted field stimulation, both used for somatic hyperalgesic states, external neuromodulation, pulsed radiofrequency ablation and neuraxial drug delivery systems.
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