Transitory exacerbations of severe pain over a baseline of moderate pain or less may be described as “breakthrough pain” (Haugen et al 2010). Breakthrough pain is common in both acute and chronic pain states. These exacerbations may be precipitated by volitional actions of the patient (so-called incident pain), such as movement, micturition, coughing, or defecation, or by non-volitional events, such as bowel distention. Spontaneous fluctuations in pain intensity can also occur without an identifiable precipitant.
Breakthrough pain must be distinguished from exacerbations of pain associated with failure of analgesia. “End-of-dose failure (of analgesia)” is commonly observed as therapeutic levels of analgesic fall. This phenomenon occurs most frequently when the interval between scheduled doses exceeds the known duration of action of analgesics with a short half-life. Since there are substantial interindividual differences in drug metabolism and excretion, some analgesics, which may typically have a 4-hour duration of action, may be effective for only 2–3 hours in certain individuals. Similarly, variability in the duration of analgesic effect is observed with long-acting formulations such as oral morphine or transdermal fentanyl. End-of-dose failure is addressed through either dose or schedule modification.
In a survey by Portenoy and Hagen (1990a) of 63 cancer patients with pain requiring opioid analgesics, 41 (65%) reported breakthrough pain. Patients had a median of four episodes per day, the duration of which ranged from seconds to hours (median, 30 minutes; range, 1–240 minutes). Pain characteristics were extremely varied. Twenty-two (43%) of the 51 different pains described were paroxysmal in onset, the remainder were more gradual, and 21 (41%) were both paroxysmal and brief (lancinating pain). Fifteen (29%) of the pains were related to end-of-dose failure from a fixed dose of opioid on a regular schedule. Twenty-eight (55%) of the pains were precipitated; of these, 22 were caused by an action of the patient (incident pain), and 6 were associated with a non-volitional precipitant, such as flatulence. The pathophysiology of the pain was believed to be somatic in 17 (33%), visceral in 10 (20%), neuropathic in 14 (27%), and mixed in 10 (20%). Pain was related to the tumor in 42 (82%), the effects of therapy in 7 (14%), and neither in 2 (4%). Diverse interventions were used to manage these pains, with variable efficacy. In a study of 194 cancer patients with pain, Jacobsen and co-authors (1994) stated that 61% reported one or more episodes of breakthrough pain. These episodes were typically paroxysmal (56%), predictable (63%), and precipitated by patient action (67%). They had a mean duration of 20 minutes (range, 5 seconds to 1.5 hours) and occurred an average of 10 times per day (range, 1–80). In a survey of 22 hospice patients by Fine and Busch (1998), 86% reported breakthrough pain, with an average of 2.9 episodes per 24-hour period and a mean pain intensity of 7 on a 10-point scale. These episodes lasted an average of 52 minutes (range, 1–240). The range of time to relief of breakthrough pain was 5–60 minutes with a mean of 30 minutes.
Pain exacerbations represent a heterogeneous phenomenon. The clinical approach to these problems is influenced by the specific underlying mechanism. It is therefore useful to define the specific breakthrough pain syndrome:
Tumors that secrete human chorionic gonadotropin (hCG), including malignant and benign tumors of the testis (Daniels and Layer 2003, Duparc et al 2003, Foppiani et al 2005) and rarely cancers from other sites (Wurzel et al 1987, Forst et al 1995, Liu et al 1999), may be associated with chronic breast tenderness or gynecomastia. Approximately 10% of patients with testis cancer are found to have gynecomastia or breast tenderness at initial evaluation, and the likelihood of gynecomastia is greater with increasing hCG levels (Tseng et al 1985). Breast pain can be the first manifestation of an occult tumor (Haas et al 1989, Mellor and McCutchan 1989, Cantwell et al 1991).
Paraneoplastic pemphigus is a rare mucocutaneous disorder associated with non-Hodgkin’s lymphoma and chronic lymphocytic leukemia. The condition is characterized by widespread shallow ulcers with hemorrhagic crusting of the lips, conjunctival bullae, and uncommonly, pulmonary lesions. Characteristically, histopathological evaluation reveals intraepithelial and subepithelial clefting, and immunoprecipitation studies reveal autoantibodies directed against desmoplakins and desmogleins (Camisa et al 1992, Allen and Camisa 2000).
Paraneoplastic Raynaud’s syndrome is a rare manifestation of solid tumors. It has been reported with lung cancer, ovarian cancer, testicular cancer, and melanoma (Wilmalaratna and Sachdev 1987, Borenstein et al 1990, DeCross and Sahasrabudhe 1992).
Most treatment-related pain is caused by tissue-damaging procedures. Such pain is acute, predictable, and self-limited. Chronic treatment-related pain syndromes are associated with either a persistent nociceptive complication of an invasive treatment (such as a post-surgical abscess) or, more commonly, neural injury. In some cases these syndromes occur long after the therapy is completed, thus resulting in a difficult differential diagnosis between recurrent disease and a complication of therapy.
Chemotherapy-induced peripheral neuropathy is a common problem that is typically manifested as painful paresthesias in the hands and/or feet and signs consistent with an axonopathy, including “stocking–glove” sensory loss, weakness, hyporeflexia, and autonomic dysfunction (Ocean and Vahdat 2004). The pain is usually characterized by continuous burning or lancinating pain, either of which may be increased by contact. Drugs most commonly associated with peripheral neuropathy are the vinca alkaloids (especially vincristine), cisplatin, oxaliplatin, and paclitaxel. Procarbazine, carboplatin, misonidazole, and hexamethylmelamine are less common causes. Data from several studies indicate that the risk for neuropathy associated with cisplatin and oxaliplatin can be diminished by amifostine (Spencer and Goa 1995, Penz et al 2001), glutathione (Cascinu et al 1995, 2002), and calcium and magnesium infusion at the time of treatment (Gamelin et al 2004). Recent data indicate that prophylactic vitamin E may reduce paclitaxel neuropathy (Argyriou et al 2006a).
Avascular necrosis of the femoral or humeral head may occur either spontaneously or as a complication of intermittent or continuous corticosteroid therapy (Cook et al 2001, Virik et al 2001) or high-dose chemotherapy with bone marrow transplantation (Fink et al 1998). Osteonecrosis may be unilateral or bilateral. Involvement of the femoral head is most common and typically causes pain in the hip, thigh, or knee. Involvement of the humeral head is usually manifested as pain in the shoulder, upper part of the arm, or elbow. Pain is exacerbated by movement and relieved by rest. There may be local tenderness over the joint, but this is not universal. Pain usually precedes radiological changes by weeks to months; bone scintigraphy and MRI are sensitive and complementary diagnostic procedures for detection of radiographically occult avascular necrosis. Even though radionuclide bone scanning and MRI are both sensitive methods, MRI is preferred because it has greater sensitivity and greater specificity than bone scanning does (DeSmet et al 2000). Early treatment consists of analgesics, a decrease in or discontinuation of steroids, and sometimes surgery. With progressive bone destruction, joint replacement may be necessary.
Lumbosacral or brachial plexopathy may follow cisplatin infusion into the iliac artery (Castellanos et al 1987) or axillary artery (Kahn et al 1989), respectively. Pain, weakness, and paresthesias develop in affected patients within 48 hours of the infusion. The mechanism for this syndrome is thought to be due to small-vessel damage and infarction of the plexus or nerve. The prognosis for neurological recovery is not known.
In patients with germ cell tumors treated with PVB, persistent Raynaud’s phenomenon is observed in 20–30% (Berger et al 1995a). This effect has also been observed in patients with carcinoma of the head and neck treated with combination PVB therapy (Kukla et al 1982). Pathophysiological studies have demonstrated that hyper-reactivity in the central sympathetic nervous system results in reduced function of smooth muscle cells in the terminal arterioles (Hansen et al 1990).
Chronic gynecomastia and breast tenderness are common complications of anti-androgen therapies for prostate cancer (McLeod and Iversen 2000). The incidence of this syndrome varies among drugs; it is frequently associated with diethylstilbestrol and bicalutamide, is less common with flutamide and cyproterone, and is uncommon in patients receiving luteinizing hormone–releasing hormone agonist therapy. Gynecomastia in the elderly must be distinguished from primary breast cancer or a secondary cancer in the breast (Olsson et al 1984, Ramamurthy and Cooper 1991).
Aromatase inhibitor therapy for the treatment of hormone-responsive breast cancer is often accompanied by musculoskeletal pain and stiffness. Common manifestations include hand osteoarthritis, tendonitis, trigger finger, and carpal tunnel syndrome. In one series of 51 patients, arthralgia and/or bone pain was reported in 61%. Pain was severe in 30%, continuous in 41%, central in 50%, and peripheral in 79% and resulted in discontinuation of the drug in 20% of patients (Presant et al 2007). The mechanism is not known. Additionally, other pain syndromes, including Raynaud’s syndrome and carpal tunnel syndrome, have been observed (Nishihori et al 2008).
Osteonecrosis of the jaw is described as an intraoral complication after the intravenous administration of nitrogen-containing bisphosphonates. It is an uncommon complication whose incidence rate has climbed in recent years (Migliorati et al 2010). It is defined as an unexpected development of necrotic bone in the oral cavity and is commonly associated with administration of the bisphosphonates pamidronate and zoledronate. Clinical features include local pain, soft tissue swelling, and/or loose teeth. Symptoms can mimic routine dental problems such as decay or periodontal disease (Migliorati et al 2006). Osteonecrosis of the jaw is also often correlated with previous dental procedures during bisphosphonate therapy, such as tooth extractions. To reduce this risk, clinical dental examination and a panoramic jaw radiograph should be performed before patients begin bisphosphonate therapy; dental treatment and other oral procedures should be completed before initiating bisphosphonate therapy, and patients should be informed and instructed about the importance of maintaining good oral hygiene and having regular dental assessment (Cavanna et al 2007).
In June 2008 the Food and Drug Administration issued a special warning regarding the possibility of severe and sometimes incapacitating bone, joint, and/or muscle (musculoskeletal) pain in patients taking bisphosphonates. The severe musculoskeletal pain may occur within days, months, or years after starting bisphosphonate treatment. Some patients have reported complete relief of symptoms after discontinuing the bisphosphonate, whereas others have reported slow or incomplete resolution. The risk factors for and incidence of severe musculoskeletal pain associated with bisphosphonates are unknown (Lenzer 2008).
Surgical incision at virtually any location may result in chronic pain. Although persistent pain is occasionally encountered after nephrectomy, sternotomy, craniotomy, inguinal dissection, and other procedures, these pain syndromes are not well described in the cancer population. In contrast, several syndromes are now clearly recognized as sequelae of specific surgical procedures. The predominant underlying pain mechanism in these syndromes is neuropathic as a result of injury to peripheral nerves or plexus.
Chronic pain of variable severity is a common sequela of surgery for breast cancer. Although chronic pain has been reported to occur after almost any surgical procedure on the breast (from lumpectomy to radical mastectomy), it is most frequent after procedures involving axillary dissection (Vecht et al 1989, Vecht 1990, Hladiuk et al 1992, Maunsell et al 1993). This pain syndrome is common after axillary lymph node dissection and occurs in 30–70% of patients (Keramopoulos et al 1993; Maunsell et al 1993; Tasmuth et al 1995, 1996; Carpenter et al 1998; Warmuth et al 1998; Kakuda et al 1999; Smith et al 1999; Kuehn et al 2000; Taylor 2004).
The risk for and severity of pain are correlated positively with the number of lymph nodes removed (Hack et al 1999, Johansson et al 2000) and are inversely correlated with age (Warmuth et al 1998, Hack et al 1999, Smith et al 1999). Data are conflicting on whether preservation of the intercostobrachial nerve during axillary lymph node dissection can reduce the incidence of this phenomenon (Temple and Ketcham 1985, Salmon et al 1998, Freeman et al 2003, Torresan et al 2003, Taylor 2004, Ivanovic et al 2007).
The incidence is reduced, but not zero when axillary dissection is avoided either by sentinel node excision without full dissection (Schulze et al 2006, Baron et al 2007, Langer et al 2007, Lucci et al 2007) or when nodes are irradiated without dissection (Albrecht et al 2002).
The pain is usually characterized as a constricting and burning discomfort that is localized to the medial part of the arm, axilla, and anterior chest wall (Wood 1978, Granek et al 1983, Vecht et al 1989, Paredes et al 1990, van Dam et al 1993). Pain may begin immediately or as late as many months following surgery. The natural history of this condition appears to be variable, and both subacute and chronic courses are possible (International Association for the Study of Pain: Subcommittee on Taxonomy 1986, Ernst et al 2002). An onset of pain later than 18 months following surgery is unusual, and careful evaluation to exclude recurrent chest wall disease is recommended in this setting. On examination an area of numbness is often found within the region of the pain (van Dam et al 1993, Schell 2006, Baron et al 2007, Ivanovic et al 2007). Chronicity of pain is related to the intensity of the immediate postoperative pain (Stevens et al 1995, Tasmuth et al 1996), postoperative complications, and subsequent treatment with chemotherapy and radiotherapy (Tasmuth et al 1995).
It is most commonly associated with neurapraxia of the intercostobrachial nerve during the process of axillary lymph node dissection (Vecht et al 1989, Bratschi and Haller 1990, van Dam et al 1993). There is marked anatomical variation in the size and distribution of the intercostobrachial nerve, which may account for some of the variability in the distribution of pain observed in patients with this condition (Assa 1974).
This syndrome must be differentiated from post-mastectomy frozen shoulder (Johansen et al 2000, Deutsch and Flickinger 2001), axillary web syndrome (Moskovitz et al 2001), and breast cellulitis (Hughes et al 1997). In some patients with pain after breast surgery a trigger point can be palpated in the axilla or chest wall.
Chronic neck and shoulder pain after radical neck dissection is common (Dijkstra et al 2001). Shoulder pain is most often caused by damage to the spinal accessory nerve (cranial nerve XI) (van Wilgen et al 2003). In other cases it can result from musculoskeletal imbalance in the shoulder girdle following surgical removal of neck muscles (Talmi et al 2000). Similar to droopy shoulder syndrome (Swift and Nichols 1984), this syndrome can be complicated by the development of thoracic outlet syndrome or suprascapular nerve entrapment, with selective weakness and wasting of the supraspinatus and infraspinatus muscles (Brown et al 1988).
Escalating pain in patients who have undergone radical neck dissection may signify recurrent tumor or soft tissue infection. These lesions may be difficult to diagnose in tissues damaged by radiation and surgery. Repeated CT or MRI may be needed to exclude tumor recurrence. Empirical treatment with antibiotics should be considered (Bruera and MacDonald 1986, Coyle and Portenoy 1991).
Two major studies of post-thoracotomy pain have been conducted (Kanner et al 1982, Keller et al 1994). In the first (Kanner et al 1982), three groups were identified; the largest (63%) had prolonged postoperative pain that abated within 2 months after surgery. Recurrent pain following resolution of the postoperative pain was usually due to neoplasm. A second group (16%) experienced pain that persisted following thoracotomy and then increased in intensity during the follow-up period. Local recurrence of disease and infection were the most common causes of the increasing pain. A final group had a prolonged period of stable or decreasing pain that gradually resolved over a maximum 8-month period. This pain was not associated with tumor recurrence. Overall, the development of late or increasing post-thoracotomy pain was due to recurrent or persistent tumor in more than 95% of patients. This finding was corroborated in the more recent study, which evaluated the records of 238 consecutive patients who underwent thoracotomy; recurrent pain was identified in 20 patients, all of whom were found to have tumor regrowth (Keller et al 1994).
Patients with recurrent or increasing post-thoracotomy pain should be evaluated carefully, preferably with chest CT or MRI. Chest radiographs are insufficient to evaluate recurrent chest disease. In some patients, post-thoracotomy pain appears to be caused by a taut muscular band within the scapular region. In such cases the pain may be amenable to trigger point injection of local anesthetic (Hamada et al 2000).
Patients with post-thoracotomy or post-mastectomy pain are at risk for the development of frozen shoulder (Maunsell et al 1993). This lesion may become an independent focus of pain, particularly if complicated by reflex sympathetic dystrophy. Adequate postoperative analgesia and active mobilization of the joint soon after surgery are necessary to prevent these problems.
Phantom limb pain is perceived to arise from an amputated limb, as though the limb were still contiguous with the body. Phantom pain is experienced by 60–80% of patients following limb amputation but is severe in only about 5–10% of cases (Ehde et al 2000, Nikolajsen and Jensen 2000, Flor 2002). The incidence of phantom pain is significantly higher in patients with a long duration of pre-amputation pain and in those with pain on the day before amputation (Weinstein 1994, Nikolajsen et al 1997b). Patients who had pain before the amputation may experience phantom pain that replicates the earlier one (Katz and Melzack 1990).
Phantom pain is more prevalent after tumor-related than after traumatic amputations, and postoperative chemotherapy is an additional risk factor (Smith and Thompson 1995, Flor 2002). The pain may be continuous or paroxysmal and is frequently associated with bothersome paresthesias. The phantom limb may assume painful and unusual postures and may gradually telescope and approach the stump. Phantom pain may initially magnify and then slowly fade over time. There is growing evidence that preoperative or postoperative neural blockade reduces the incidence of phantom limb pain during the first year after amputation (Pavy and Doyle 1996, Enneking and Morey 1997, Katz 1997, Nikolajsen et al 1997a).
Some patients experience spontaneous partial remission of the pain. Recurrence of pain after such a remission or late onset of pain in a previously painless phantom limb suggests the appearance of a more proximal lesion, including recurrent neoplasm (Chang et al 1997).
Phantom pain syndromes have also been described after other surgical procedures. Phantom breast pain after mastectomy, which occurs in 15–30% of patients (Kroner et al 1989, Kwekkeboom 1996, Tasmuth et al 1996, Rothemund et al 2004, Dijkstra et al 2007), also appears to be related to the presence of preoperative pain (Kroner et al 1989). The pain tends to start in the region of the nipple and then spreads to the entire breast. The character of the pain is variable and may be lancinating, continuous, or intermittent (Kroner et al 1989, Rothemund et al 2004).
A phantom rectum pain syndrome occurs in approximately 15% of patients who undergo abdominoperineal resection of the rectum (Ovesen et al 1991, Boas et al 1993). Phantom rectal pain may develop either in the early postoperative period or after a latency of months to years. Late-onset pain is almost always associated with tumor recurrence (Ovesen et al 1991, Boas et al 1993). Rare cases of phantom bladder pain after cystectomy and phantom eye pain after enucleation have also been reported.
Stump pain occurs at the site of the surgical scar several months to years following amputation (Davis 1993). It is usually the result of neuroma development at a site of nerve transection. This pain is characterized by burning or lancinating dysesthesias, which are often exacerbated by movement or pressure and blocked by injection of a local anesthetic.
Surgical trauma to the pelvic floor can cause a residual pelvic floor myalgia, which like the neoplastic syndrome described previously, mimics so-called tension myalgia (Sinaki et al 1977). The risk for disease recurrence associated with this condition is not known, and its natural history has not been defined. In patients who have undergone anorectal resection, this condition must be differentiated from the phantom anus syndrome (see above).
Chronic pain complicating radiation therapy tends to occur late in the course of a patient’s illness. These syndromes must always be differentiated from recurrent tumor.
Radiation-induced brachial and lumbosacral plexopathies were described previously (see above).
Chronic radiation myelopathy is a late complication of spinal cord irradiation. Its latency is highly variable but is most commonly 12–14 months. The most common manifestation is a partial transverse myelopathy at the cervicothoracic level, sometimes in a Brown-Sequard pattern (Schultheiss and Stephens 1992). Sensory symptoms, including pain, typically precede the development of progressive motor and autonomic dysfunction (Schultheiss and Stephens 1992). The pain is characterized as a burning dysesthesia localized to the area of spinal cord damage or below. Imaging studies, particularly MRI, are important to exclude epidural metastases and demonstrate the nature and extent of intrinsic cord pathology, which may include atrophy, swelling, or syrinx. On MRI the signs of radiation myelitis include high-intensity signals on T2-weighted images or gadolinium enhancement of T1-weighted images (Koehler et al 1996, Alfonso et al 1997). The course of chronic radiation myelopathy is characterized by steady progression over a period of months, followed by a subsequent phase of slow progression or stabilization.
Chronic enteritis and proctocolitis occur as a delayed complication in 2–10% of patients who undergo abdominal or pelvic radiation therapy (Yeoh and Horowitz 1987, Nussbaum et al 1993). The rectum and rectosigmoid are more commonly involved than the small bowel, a pattern that may relate to the retroperitoneal fixation of the former structures. The latency is variable (3 months–30 years) (Yeoh and Horowitz 1987, Nussbaum et al 1993, Tagkalidis and Tjandra 2001). Chronic radiation injury to the rectum can be manifested as proctitis (with bloody diarrhea, tenesmus, and cramping pain), obstruction as a result of stricture formation, or fistulas to the bladder or vagina. Small bowel radiation damage typically causes colicky abdominal pain, which can be associated with chronic nausea or malabsorption. Barium studies may demonstrate a narrow tubular bowel segment resembling Crohn’s disease or ischemic colitis. Endoscopy and biopsy may be necessary to distinguish suspicious lesions from recurrent cancer (Chi et al 2005).
Radiation therapy for tumors of the pelvic organs (prostate, bladder, colon/rectum, uterus, ovary, and vagina/vulva) may produce a chronic radiation cystitis (Pillay et al 1984, Joly et al 1998, Perez et al 1999). The late sequelae of radiation injury to the bladder can range from minor temporary irritative voiding symptoms and asymptomatic hematuria to more severe complications such as gross hematuria, contracted non-functional bladder, persistent incontinence, and fistula formation. Clinical findings can include frequency, urgency, dysuria, hematuria, incontinence, hydronephrosis, pneumaturia, and fecaluria.
One-third of patients with lymphedema as a complication of breast cancer or its treatment experience pain and tightness in the arm (Newman et al 1996), and pain is a major part of the morbidity in affected patients (McWayne and Heiney 2005). In some patients, pain is due to secondary rotator cuff tendonitis caused by internal derangement of tendon fibers as a result of impingement, functional overload, and intrinsic tendinopathy. Conservative treatment with NSAIDs and physical therapy is safe and effective (Herrera and Stubblefield 2004). Nerve entrapment syndromes of the carpal tunnel or brachial plexus develop in some patients (Ganel et al 1979, Vecht 1990). Severe or increasing pain in a lymphedematous arm is strongly suggestive of tumor invasion of the brachial plexus (Kori et al 1981, Kori 1995).
Persistent perineal discomfort is an uncommon delayed complication of pelvic radiotherapy. After a latency of 6–18 months, burning pain can develop in the perianal region; the pain may extend anteriorly to involve the vagina or scrotum (Minsky and Cohen 1988, Mannaerts et al 2002). In patients who have undergone abdominoperineal resection, phantom anus pain and recurrent tumor are major differential diagnoses.
Brachytherapy in patients with prostate cancer may produce a chronic radiation-related pelvic pain syndrome that is exacerbated by urination or perineal pressure. Data suggest that it may be partly related to higher central prostatic radiation doses (Wallner et al 2004).
Osteoradionecrosis is another late complication of radiotherapy. Bone necrosis, which occurs as a result of endarteritis obliterans, may produce focal pain. Overlying tissue breakdown can occur spontaneously or as a result of trauma, such as dental extraction or denture trauma (Epstein et al 1987, 1997). Delayed development of a painful ulcer must be differentiated from tumor recurrence.
Adequate assessment is a necessary precondition for effective pain management. In the cancer population, assessment must recognize the dynamic relationship between the symptom, the illness, and larger concerns related to quality of life. Syndrome identification and inferences about pain pathophysiology are useful elements that may simplify this complex undertaking.
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