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Cancer Pain

Pathophysiology

Primary afferent sensory neurons are the major gateway in which sensory information from the peripheral tissues is transmitted to the spinal cord and the brain (1). These neurons innervate the skin and almost every internal organ of the body (1).

Nociceptor Stimulation by Tumours

Tumors are made up of many cells other than cancer cells (1,2). These can include immune system cells such as macrophages, neutrophils, and T cells (1,2). These cells will secrete various factors (prostaglandins, tumour necrosis factor alpha, endothelins, interleukin-1 and 6, epidermal growth factor, transforming growth factor-b and platelet derived growth factor) that sensitize or directly excite the primary afferent neurons (2).

Tumour Induced Acidosis

The intracellular and the extracellular pH of solid tumours are lower than that of the normal surrounding tissues (2). Local acidosis, which is associated by accumulation of acid metabolites, is the hallmark of tissue injury (2). Studies have that sensory neurons can be directly excited by protons or acid and further studies have shown that subsets of sensory neurons have different acid sensing ion channels (2). Both of these channels are sensitized and excited by a decrease in the pH (2). There are several mechanisms in which a tumour can result in a decrease in pH (2). When the inflammatory cells invade the neoplastic tissue, the protons that are released result in local acidosis (2). The large amount of the apoptosis that occurs in the tumour environment also will contribute to acidosis since these cells release intracellular ions which will create an acidic environment (2). This mechanism of action is important in the generation of bone cancer pain because osteolytic and osteoblastic cancers are associated with osteoclast proliferation and hypertrophy (2). Osteoclasts reabsorb bone by maintaining an extracellular microenvironment of low pH and since sensory neurons that innervate bone express VRI or ASICs (acid sensing ion channels), the sensory neurons will become depolarized and transmit pain signals to the spinal cord when exposure to the osteoclasts’ acidic extracellular microenvironment is achieved (2).

Tumour induced distention of sensory fibres

Rapid tumor growth will frequently entrap and injure nerves, causing mechanical injury, compression ischemia or direct proteolysis (2). Proteolytic enzymes that are made by the tumour cells also cause injury to sensory and sympathetic fibres, causing neuropathic pain (2). In general, nociceptive pain is mainly sustained by ongoing tissue injury (1,2). It is further divided into somatic and visceral nociceptive pain (2). Somatic nociceptive pain involves injury to somatic structures, like joints, muscles and or bone (2). It is described as aching, stabbing, throbbing or pressure-like in quality (2). Visceral nociceptive pain involves injury to the viscera (2). It is characterized by gnawing or crampy, when arising from the obstructure of a hollow viscus (like the bowel lumen) and aching or stabbing when arising from other visceral structures, such as organ capsules, myocardium or pleura (2).

Etiology

The presence of chronic cancer pain is due to the disease itself (3). Pathophysiological processes that contribute to the pain include tumor invasion, and organ obstruction (3). The various treatment modalities that are used to arrest the cancer, such as surgery, chemotherapy, and radiotherapy may also contribute to the pain (2,3). Musculoskeletal pain from inactivity, and cancer related infections can result in neuropathic pain (3). Secondary effects of cancer can include injury to the nervous system, distention of organ capsules or infiltration of adjacent soft tissues (3). These further contribute to the development of pain (3).

Risk Factors

The major risk factor for developing cancer pain is the presence of cancer itself (1,3). The severity of the pain increases with advancing stages of cancer (1,3). Chemotherapy treatments, radiation may also contribute to cancer pain through the direct damage of the tissues and their side effect profiles (1,3). Common chemotherapy agents that contribute to pain include cisplatin, doxorubicin, and fluorouracil (1,3). Some side effects of chemotherapy agents that result in pain include mouth sores and neuropathy (1,3). Surgery and radiation may leave scars or burning sensations that persist during the recovery process and this may contribute to the pain experienced by the patient (1,3).

Prognosis

In many patients, pain is the first sign of cancer (4). 30-50% of all cancer patients will experience pain that is moderate and severe in nature (4). Cancer can result in pain at any time during the disease, however, the frequency and the intensity of pain tends to increase during the advanced stages (4). 75-95% of patients with metastatic or advanced stage cancer will have significant amounts of cancer induced pain (4). The cancer pain may progress to neuropathic pain as the growth of the tumour may compress and destroy the sensory neurons that innervate the bone marrow through metastasis (4). Thus, it is important to note that because of the differences in the level of nociceptor activation and the involvement of other areas that contribute to the pain transmission (spinal cord, and forebrain) different therapies with different mechanisms of action may be more effective at various stages of cancer (4).

Clinical Presentation

Cancer pain may be acute in nature and is associated with generalized sympathetic hyperactivity (4). Thus, symptoms of diaphoresis, hypertension and tachycardia are often present (4). As the pain becomes chronic, tolerance to sympathetic hyperactivity develops quickly (4). Overt pain behaviours such as grimacing, moaning, and splinting and sympathetic hyperactivity are not present with chronic pain (4). Chronic pain can be described as a sharp, dull, shock-like, radiating, tingling, shooting pain that fluctuates in intensity and various in locations (4). Patients that have cancer pain experience a persistent discomfort known as background pain (4). Sometimes, patients that have controlled background pain may experience short lasting episodes of more severe discomfort known as breakthrough pain (4). Breakthrough pain could be due to activities such as movement (4). The features of this pain vary from person to person and it occurs in 40-80% of patients with cancer pain (4). It is a frequent occurrence and patients experience on average 3-4 episodes per day (4). Most episodes last for about 30 minutes, but the duration can be shorter or longer (4). The pain is described to be as moderate or severe (4).

Diagnosis

The diagnosis of cancer pain is based on patient description and a history of their underlying medical conditions and medications (1).

Monitoring

It is helpful to use a pain scale to monitor the extent of the pain that the patient is experiencing (4). This is to help guide and monitoring the effectiveness of the treatment that is being used (4).

Goals of Therapy

The main goal of therapy of chronic terminal cancer pain is to provide symptom relief to limit the amount of physical and emotional suffering that a patient may experience (1). It is of high importance to support the patient’s ability to enjoy the remaining life and avoid inappropriate prolongation of death (1).

References

  1. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 7th ed. Toronto: McGraw-Hill; 2007. P. 989-1003.
  2. Mantyh PW, Clohisy DR, Koltzenburg M, Hunt SP. Molecular Mechanisms of Cancer Pain. Nature Reviews Cancer 2002; 2:201-209.
  3. Goudas LC, Block R, Gialeli-Goudas M, et al. The epidermiology of cancer pain. Cancer Invest. 2005;23:182-5.
  4. Foley KM. Acute and chronic cancer pain syndromes. 3rd ed. New York: Oxford University Press; 2004. p.298-315.

Disclaimer

This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers


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