Fig. 10.1
Visual analog scale
Fig. 10.2
Wong-baker scale
Fig. 10.3
PAINAD scale
Fig. 10.4
Memory pain assessment card
In keeping with the concept of “total pain,” one must explore the psychosocial and spiritual impact of the patient’s pain. How has the person coped with significant stressors in his past? Are anxiety or depression contributing to the pain? Has this individual relied on alcohol or other substances to cope? Has there been a history of opioid misuse or abuse? What kind of social support surrounds the patient? Finally, what is the meaning of pain for that individual? The answers to these questions can often provide insight into how to craft an effective management plan.
Perform a Complete Physical and Neurological Examination
If one has taken a truly comprehensive pain history, the physical and neurological examination should serve to confirm or further narrow the differential diagnosis for the patient’s pain. Additional testing should serve the purpose of both clarifying the diagnosis and assisting with the development of a management plan. Clearly, one must avoid burdensome studies or procedures that will not ultimately serve to lessen the patient’s pain.
Develop a Comprehensive Pain Management Plan
After a comprehensive history, physical examination, and appropriate studies, one can develop a comprehensive approach to the patient’s pain. Ideally, this should address not only the physical, but also the psychological and spiritual concerns of the patient. As part of the plan, regular follow-up is essential. The healthcare provider and patient should approach the plan as partners, both empowered to work toward relief.
Cancer Pain Syndromes of the Genitourinary Region
Patients with known or suspected prostate cancer may require transrectal prostate biopsy. In a prospective study, 16 % of patients undergoing transrectal prostatic biopsy without anesthesia reported at least moderate ≥5 intensity pain, and 19 % reported that they would not agree to undergo the procedure again without anesthesia [9]. Clinician experience as well as patient factors and preferences determine anesthetic technique for this. Published studies support infiltrative and noninfiltrative techniques. Significant pain reduction is reported with pudendal nerve block [10], periprostatic lidocaine infiltration [11], periprostatic tramadol [12], intrarectal 2 % lidocaine cream [13], and intrarectal ice applied 5 min prior to the procedure [14].
For women with intraepithelial neoplasia, cervical cryosurgery is associated with pain and cramping. Paracervical block with 1 % lidocaine and 1:100,000 epinephrine significantly reduces these symptoms [15]. Intramucosal block is an effective alternative [16]. Pretreatment with NSAIDs is not shown to reduce pain and cramping during cervical cryosurgery [17].
Perineal pain is commonly associated with cancers originating in the distal genitourinary system. A syndrome similar to tension myalgia of the pelvic floor can occur when tumor invades the musculature of the deep pelvis, causing an aching or heavy sensation that worsens with upright posture [18]. In patients who have undergone pelvic tumor resection, the onset of severe perineal pain may indicate recurrence of disease [19, 20].
In burning perineum syndrome, pelvic radiation therapy results in persistent perineal pain. The pain is typically described as burning in quality and it can radiate to the vagina or scrotum. The latency period of burning perineum syndrome is 6–18 months. Recurrent tumor should be excluded [21, 22].
When cancer metastasizes to the sacrum, it can produce severe pain that radiates to the buttocks, perineum, or posterior thighs, is worse with sitting or lying down, and improves when standing or walking [23, 24]. Tumor invasion of the muscles that rotate the hip can produce a malignant “pyriformis syndrome” with buttock (or posterior thigh) pain that worsens with internal rotation.
Pharmacologic Management of Cancer-Related Pain
Most cancer pain practitioners take a multifaceted, multidisciplinary approach to the comprehensive pain management of the patient with cancer. This type of pain management involves the use of pharmacologic treatments as well as nonpharmacologic treatments and interventions.
Cancer pain can be categorized as neuropathic or nociceptive. Nociceptive pain is further subdivided into somatic and visceral pain. It is important to understand the etiology of the pain as this will help the practitioner to select appropriate therapies.
World Health Organization (WHO) Analgesic Ladder
The World Health Organization provides a framework for analgesic administration in the setting of cancer-related pain. This framework is represented in Figs. 10.5 and 10.6.
Fig. 10.5
World Health Organization (WHO) analgesic ladder (reprinted from WHO.org)
Fig. 10.6
Pathologic supracondylar fracture of the left femur. (Source: Rommens and Hessmann [54])
Step 1: Mild Pain in the Urogenital Region in the Cancer Patient
Nonopioid analgesia represents the first step in the treatment of cancer-related pain. Pharmacologic treatment options in this category include acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs). Table 10.1 provides a list of NSAIDs commonly used in practice.
Nonselective COX inhibitors | Partially selective COX-2 inhibitors | COX-2 inhibitors |
|---|---|---|
Diclofenac sodium (50 mg twice daily) | Etodolac (200 mg every 6 h) | Celecoxib (200 mg daily) |
Diclofenac potassium (50 mg twice daily) | Meloxicam (7.5 mg daily) | – |
Fenoprofen (600 mg three times per day) | Nabumetone (500 mg twice daily) | – |
Ibuprofen (400 mg three times per day) | – | – |
Ketoprofen (50 mg four times per day) | – | – |
Naproxen (500 mg twice per day) | – | – |
Naproxen sodium (550 mg twice per day) | – | – |
Oxaprozin (1200 mg daily) | – | – |
Sulindac (150 mg twice per day) | – | – |
Piroxicam (20 mg daily) | – | – |
Acetaminophen (paracetamol) is a well-tolerated, antipyretic, and analgesic drug that is recommended in many circumstances as a first step in the pharmacologic management of mild cancer pain. The mechanism of action of acetaminophen is only partially understood. It is thought that acetaminophen is a weak inhibitor of prostaglandin synthesis and most likely works in the central nervous system (CNS) via the activation of serotonergic pathways [25]. Acetaminophen can cause severe liver toxicity and failure, especially in the setting of existing liver disease. Typically, the maximum dose of acetaminophen for adults is 4000 mg per day or 2000 mg per day in the setting of liver disease. In the setting of advanced liver disease or liver failure, an alternative therapeutic is recommended. Practitioners should recognize that acetaminophen is contained in many over-the-counter combination cold remedies
Nonsteroidal anti-inflammatory drugs represent a well-tolerated, heterogeneous group of compounds that produce analgesia through the inhibition of prostaglandin and other inflammatory mediator synthesis. NSAIDs include aspirin and other pharmaceuticals that inhibit the cyclooxygenase (COX). This enzyme is necessary for the conversion of arachidonic acid to prostaglandins, and leukotrienes that activate the nociceptive pathway. NSAIDs are also known to cause platelet inhibition. Aspirin-induced platelet inhibition is irreversible, while platelet inhibition by other NSAIDs is reversible.
NSAIDs are classified as either COX-2 selective, partially selective, or nonselective. Nonselective inhibitors are more inclined to cause gastrointestinal distress, bleeding, and ulcer formation, though any NSAID should be avoided in patients with a bleeding diathesis. Selective COX-2 inhibitors are associated with less risk of gastrointestinal bleeding but still are not for use in patients with a bleeding diathesis. Caution also needs to be taken with the NSAID class and renal or cardiac dysfunction as these drugs are known to decrease glomerular filtration rate and cause fluid retention and hypertension.
NSAIDs should be used with caution in patients with cancer. While these medications are considered a mainstay of analgesic therapy in the benign setting, the clinician must weigh the risks and benefits of the drug in patients with cancer. Patients with a bleeding diathesis should not receive NSAIDs due to risk of severe or even fatal bleeding. Patients who are on chemotherapy or who have severe bone marrow replacement are known to have thrombocytopenia which should be considered a contraindication for NSAID therapy.
Tramadol is also considered in this step. Tramadol is a racemic cyclohexyl analgesic that acts centrally acting analgesic that has agonist activity at the mu receptor similar to an opioid as well as norepinephrine/serotonin reuptake inhibition giving it nonopioid analgesic properties. Similar to tramadol is tapentadol which has stronger mu receptor agonist activity. Tapentadol functions more like a strong opioid in this sense and may be considered in the third step of the WHO analgesic ladder. Both tramadol and tapentadol should be used with caution in patients with a seizure disorder or who are concurrently treated with selective serotonin reuptake inhibitors or tricyclic antidepressants [27].
Step 3: Severe Pain in the Urogenital Region in the Patient with Cancer
For patients who cannot achieve satisfactory analgesia with step two of the WHO analgesic ladder, the next step is to begin a strong opioid in addition to adjunctive, nonopioid, analgesics. Opioids in this class include medications such as morphine, oxycodone, hydromorphone, fentanyl, and methadone.
Opioids and Pain Management in the Patient with Cancer
Opioids are considered the mainstay of treatment of cancer-related pain. Opioids are a class of drugs that are structurally similar to endogenous peptides known as endorphins, dynorphins, and enkephalins in that they act by binding to the opioid receptor on the presynaptic neuron in the CNS. Activation of the opioid receptor stabilizes the presynaptic membrane leading to a decrease in the exocytosis of substance P and glutamate in the pain pathway. Decreased exocytosis of substance P and glutamate leads to lesser activation of the postsynaptic neuron.
There are several types of opioid receptors in the CNS, including the mu, kappa, delta, and sigma receptors. Of note, only the mu opioid receptor (MOR), kappa opioid receptor (KOR), and delta opioid receptor (DOR) are of clinical importance when considering analgesia based on current knowledge and there are numerous subtypes of these receptors as well. The opioid receptor type and subtype predominance provides a fingerprint which determines susceptibility to particular opioids based on receptor affinity.
Opioids that are in use currently all exert at least some agonistic activity at the MOR with varying activity at other opioid receptors. Activity at the MOR is responsible for much of the analgesic properties as well as the side-effects of opioids.
Side effects of opioid receptor activity can commonly include euphoria or dysphoria, constipation, urinary retention, sedation, and nausea. Opioids are known to diminish airway reflexes and must be used in caution in patients with hypercarbic respiratory failure or sleep disordered breathing. Opioids also may cause histamine release and result in pruritus or a decrease in peripheral vascular resistance. These compounds are also well known for their abuse and diversion potential and should be used in caution in patients who would be considered high risk. There are numerous other side effects of opioids that limit their use in many clinical settings [28].
Morphine is often considered a prototype drug for the opioid class. It can be used orally as an immediate-release or sustained-release preparation. It is available in liquid or tablet form. In addition to oral use, morphine can be administered intravenously, subcutaneously, intramuscularly, intrathecally, or rectally. Typically, the drug is absorbed rapidly through the gastrointestinal tract and peak blood levels occur in 30 min. Bioavailability of the drug is limited by approximately two-third first pass metabolism in the liver, leaving approximately one-third of the orally administered drug available for serum concentrations.
In the liver, morphine is metabolized to morphine-3-glucuronide (M3G), which is pharmacologically inactive, as well as morphine-6-glucuronide (M6G), an active metabolite. These metabolites are excreted in the urine. Patients with renal failure may exhibit potential neurotoxic side effects of the morphine glucuronides including myoclonus and even seizures [29].
If a patient with cancer has ongoing pain in the urogenital system and the underlying pathology is unlikely to improve quickly, it may be advisable to utilize a regimen with a sustained-release opioid. Typically, a sustained-release opioid is given on a continual basis and an immediate release preparation is administered as needed to assist with breakthrough pain that is not fully alleviated by the sustained-release medication. Opioid side effects, such as constipation and nausea, must be addressed in this type of regimen. Often, nausea will abate over time, but constipation is a side effect that does not improve with ongoing opioid administration.
Treatment of Neuropathic Urogenital Pain in the Patient with Cancer
Neuropathic pain results from damage or impingement upon the somatosensory neural pathway. It is often treated differently than nociceptive pain as noted earlier. Neuropathic pain in the patient with cancer can occur as a result of the following:
tumor burden resulting in direct compressive forces
loss of structural integrity of the spine resulting in nerve compromise
nerve damage as a result of cancer treatments such as chemotherapy or radiation
The primary treatment of neuropathic pain in the patient with cancer should involve the removal of the offending agent where feasible. If tumor compression can be alleviated by radiation, surgery, or radiosurgical options, that should be considered the preferred method of treatment. No drug treatments are US FDA approved for the treatment of cancer-associated neuropathic pain, chemotherapy-induced peripheral neuropathy (CIPN), or radiation neuritis. Treatment recommendations are evidence-based as well as based on clinical experience. Current guidelines are derived from an expert panel and published by the American Society of Clinical Oncology (ASCO) in 2014 [30]. Patients should be informed that there are no approved treatments for neuropathy and there is little evidence for the efficacy of specific therapies.
The ASCO guidelines assert that duloxetine may be offered as first-line treatment for the alleviation of neuropathic pain in the patient with cancer. Duloxetine, a serotonin and norepinephrine reuptake inhibitor is known to augment one’s innate ability to modulate the pain signal through the descending pathway. Pain practitioners and oncologists often prescribe gabapentin and pregabalin for the treatment of neuropathic pain. The current ASCO guidelines state that there is not enough supporting evidence to recommend for or against these medications for neuropathic pain. The ASCO guidelines also make no recommendation on acetyl-L-carnitine or tricyclic antidepressants, which are also often prescribed as therapy for neuropathic pain. The guidelines further assert that there are no established agents for the prevention of CIPN based on scarce and inconsistent data.
Some opioids have been used in the treatment of neuropathic pain though it should be noted that these are not the preferred agents. Oxycodone is thought to be more effective for neuropathic pain based on the activity at the KOR. Also, methadone is used in some refractory cases. In addition to working as a classic opioid, methadone is known to work on the modulation of the pain signal as well.
Other Pharmacologic Management of Urogenital Pain in the Patient with Cancer
Steroids are often employed in the treatment of cancer-related pain. Oral or intravenous steroids are often used for refractory urogenital pain related to cancer especially in the setting of associated inflammation. Steroids are a hallmark of therapy in patients with spinal cord injuries as well as intestinal obstruction related to malignancy. Steroids are also used for the treatment of bone pain related to metastasis and to alleviate neuropathic pain in the setting of tumor compression. Steroids are accompanied by many long-term side effects including bone loss and osteoporosis, glaucoma, central obesity, hyperglycemia, and elevated blood pressure.
Antispasmodics are often used in the treatment of muscle spasm that may be associated with bone, nerve, or muscle involvement. This can be especially important in the setting of spinal cord damage that may lead to chronic muscle spasticity and chronic pain. Baclofen is commonly recommended in the setting of painful muscle spasm in the patient with cancer. Other pharmacologic agents include cyclobenzaprine, tizanidine, and benzodiazepines such as diazepam. Problematic side effects, such as sedation, are often dose limiting in the setting of muscle spasm associated with cancer pain.
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