Cancer Pain: Introduction and Medical Management

Overview and Medical Management of Cancer Pain YuryKhelemsky, M.D. Anesthesiology and Pain Medicine

In addition, the possibility that pain is unrelated to either the malignancy or its treatment needs to be considered.,[object Object]

1300 outpatients with metastatic cancer approximately 2/3 had cancer-associated pain

Prevalence of moderate or severe pain increases during the late phases of malignancy. In a survey of 200 terminal patients, approximately 80 percent had significant pain associated with their disease ,[object Object]

540 hospitalized cancer patients found that 85 percent of those with bone involvement had pain which required analgesic medication compared to only 5 percent of those with leukemia

200 patients referred to a specialized cancer pain clinic, pain was caused by tumor growth in about 80 percent of cases.

667 patients, pain was more frequent in those with metastatic disease (59 versus 36 percent in those with nonmetastatic cancer). ,[object Object],[object Object]

Additionally pharmacologic, interventional, psychiatric, physical modalities should be utilized for symptomatic relief,[object Object]

#1, mild pain, utilizes nonopioid and adjuvant drugs.

#2, an opioid is added for increasing pain.

#3, most severe pain, more potent opioids are used. This approach is designed to be simple to understand and usable around the world.

Field testing has found the WHO guidelines effective for 70 to 100 percent of patients with cancer,[object Object]

Interventional procedures (intrathecal pumps, neuro-ablative techniques, sympathetic blocks, etc.) should be considered if pain is poorly controlled or patient has intolerable side effects with medications,[object Object]

Realize that anxiety and depression may exacerbate, rather than exaggerate, the pain.

The emotional response to pain and dying is often called suffering, and may not be easily separated from the rest of the pain experience. ,[object Object]

Faces Pain Scale, originally designed for use in children, may be useful in cognitively-impaired patients

McGill Pain Questionnaire (MPQ): best, but not self administered and takes up to 20 min

Memorial Pain Assessment Card: rapid assessment

Non-specific: autonomic changes, agitation/confusion, apathy inactivity, irritability, refusal to eat,[object Object]

Pathophysiology:noxious mechanical, thermal, or chemical stimuli which trigger nociceptors. Ischemia, inflammation, and perhaps substances produced by a nearby tumor may sensitize nociceptors to ordinarily nonnoxious stimuli.

Pathway:myelinated A-delta fibers (mechanical/thermal) and C fibers (mechanical/thermal/chemical)  dorsal horn  contralateral spinothalamic and spinoreticular tracts thalamus and reticular formation,[object Object]

Often associated with nausea and diaphoresis

Examples of primary and referred visceral pain in patients with cancer include the pain associated with pancreatic cancer, small bowel obstruction, and pleuritis

Mechanisms not well characterized, but visceral autonomic afferents may be involved

Referred Pain: poorly understood, but may be due to convergent somatic and visceral nociceptive input in dorsal horn (diaphragmatic irritation felt in shoulder,[object Object]

Usually constant but may be interrupted by paroxysms of dramatically increased pain. There may be no area of tenderness, or areas of exquisite sensitivity to normally innocuous stimuli (allodynia).

Symptoms and signs of autonomic instability (eg, tachycardia, sweating)

Relative resistance to opioids, makes it the most challenging to treat,[object Object]

Demyelinated axons may become sites of ectopic activity and aberrant (ephaptic) conduction of C or A-delta fiber impulses

NMDA receptors may be involved in perception and maintenance of neuropathic pain is suggested by the response to treatment with ketamine (also methadone).

Primary central pain processaffect the spinothalamic system and thalamocortical projections(radiation myelopathy, and spinal cord and thalamic tumors.),[object Object]

Evidence to support improved efficacy of combination drugs (i.e. percocet, etc.) is limited in cancer pain

NSAIDs (ketorolac) may also be useful in the treatment of neuropathic pain

Little literature substantiating better efficacy for one NSAID versus another, but may switch between drugs if side-effects,[object Object]

Dyspepsia and Gastric Ulceration: relative protection with coxibs. Take with food, misoprostol, H2 Blockers, PPI.

Nephrotoxicity: prescribe with caution in CRI

Hepatotoxicity: even at recommended doses, esp. with EtOH use or starvation. LFT elevations usually mild and reversible after d/c Rx.

COX-2 Inhibitors: Cardiovascular Risk ,[object Object]

In addition, selective COX-2 inhibition, as well as nonselective inhibition of COX, elevates blood pressure. These are two of several proposed links between these agents and ischemic cardiovascular events.,[object Object]

Not clear if low-dose co-administration of ASA mitigates risk

Bottom line: use lowest effective dose and avoid use in patients with CHF, CRI, CV risks. Non-selective NSAIDS appear to be safer in smaller doses. ,[object Object]

Predictably induce tolerance to and physical dependence on their effects. Despite the development of tolerance to opioid analgesia, disease progression is usually responsible for increasing analgesic requirements

When considering the initiation of opioid analgesia for cancer pain, it is important to realize that their benefits usually far outweigh their side effects and potential addictiveness ,[object Object]

Initial agents: start with short half-life drugs (morphine, oxycodone, fentanyl, etc.). Once pain becomes constant transition to longer acting agents.

Methadone and Levorphanol are of special note, as they may provide more continuous action with intermittent (PRN) dosing. ,[object Object]

Cancer Pain: Introduction and Medical Management

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Cancer Pain: Introduction and Medical Management

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