31 Pain in Acquired Immunodeficiency Syndrome

31 Pain in Acquired Immunodeficiency Syndrome
The Massachusetts General Hospital Handbook of Pain Management

Pain in Acquired Immunodeficiency Syndrome

Steven P. Cohen

Oh, write of me, not “Died in bitter pain,”
But “Emigrated to another star!”
—Helen Hunt Jackson (1830–1885)

I. Etiology of pain in patients with AIDS
II. Pain syndromes in patients with AIDS

1. Gastrointestinal pain

2. Thoracic pain

3. Rheumatologic manifestations of AIDS

4. Neurologic pain manifestation of AIDS

5. Herpes zoster
III. Treatment options

1. Opioid management for the HIV-positive patient

2. Nonopioid pain adjuvants

3. Nerve blocks and regional anesthesia

4. Nonpharmacologic interventions
Selected Readings

Pain is a common reason for the hospitalization of patients with acquired immunodeficiency syndrome (AIDS). The prevalence of pain in patients with AIDS has been reported to be between 40% and 60% in hospitalized patients, somewhat higher (around 70%) in ambulatory patients, and 97% in terminally ill patients. The incubation period of the human immunodeficiency virus (HIV) ranges from a few years to more than 10 years since the advent of new antiviral therapy and prophylactic treatment for opportunistic infections (OIs). As the life expectancy of these patients continues to increase, issues related to quality of life, including adequate pain control, take on increasing importance. It is therefore incumbent on physicians responsible for treating patients with AIDS to be familiar with the myriad of pain syndromes with which they present, and to provide adequate treatment.
This chapter reviews the etiology of pain manifestations in HIV-positive patients in different organ systems and discusses appropriate treatment strategies. Pain treatment is based on the underlying cause, when possible. Symptomatic measures, however, should not be delayed while the workup for the underlying cause is in progress or if the underlying cause cannot be treated effectively. Specific problems of pharmacologic and nonpharmacologic symptomatic pain relief in HIV-positive patients are also discussed. Figure 1 outlines a possible approach to the treatment of pain in these patients.

Figure 1. An approach to the treatment of pain in patients with AIDS.

Pain in patients with AIDS may be caused by the direct effects of the human immunodeficiency virus on the nervous system, by OIs, by tumors related to immunosuppression, or by the various therapies for HIV and its associated disorders. Several studies have examined the incidence of various types of pain syndromes in HIV-positive patients. Although the exact prevalence varies according to patient population, study methodology, and the extent of disease progression, the most common pain diagnoses are headaches, abdominal pain, peripheral neuropathies, and rheumatologic manifestations such as myalgias and arthralgias. When pain was classified by mechanism, Hewitt et al. found that 45% of pain syndromes were somatic, 15% were visceral, 19% were neuropathic, and 4% were unknown. Seventeen percent of pain complaints were headaches and could not be classified into these categories. Figure 2 represents a breakdown by location of the different pain syndromes in patients with HIV infection.

Figure 2. Pain symptoms, according to location, in AIDS patients.

1. Gastrointestinal pain
Pain in HIV disease can arise anywhere in the gastrointestinal (GI) tract, including the oral cavity, esophagus, anus and rectum, hepatobiliary system, and pancreas.
(i) Oral cavity
Between 20% and 50% of HIV-infected patients develop oral lesions during the course of their illness. These lesions often provide the first clue to infection with the virus and may herald disease progression and immunologic decline. Oropharyngeal candidiasis occurs in up to one third of HIV-positive individuals and over 90% of patients with AIDS. Because of its high incidence, Candida infections are the most common cause of pain in the oral cavity, even though most patients are asymptomatic. At least four different types of presentations have been described: hyperplastic, erythematous, angular cheilitis, and pseudomembranous or “thrush,” the most common kind.
Treatment is important, as pain and dysphagia may impair oral intake and contribute to wasting and overall deterioration. For mild cases, therapy includes topical antifungal agents, with systemic agents being reserved for more extensive disease.
Oral ulcers are common in individuals infected with HIV and may result from a variety of organisms, including viruses, fungi, and the bacteria implicated in necrotizing ulcerating infections (gingivitis, periodontitis, and stomatitis). Some of the antivirals used in the treatment of HIV infection such as zalcitabine (ddC) can also precipitate stomatitis. When oral ulcers are unresponsive to conventional therapy, the use of steroids and thalidomide may prove beneficial. In many cases, topical anesthetics and systemic analgesics are necessary for pain management.
(ii) Esophagitis
Approximately one third of patients with AIDS develop dysphagia and odynophagia. Candidal esophagitis is the most common cause of esophageal pathology, with the treatment of choice being systemic antifungal agents. The absence of oral involvement does not exclude a diagnosis of esophageal candidiasis.
Ulcerating and nonulcerating lesions of the esophagus can be caused by a wide variety of different pathogens including fungi, bacteria, and viruses. Cytomegalovirus (CMV) is the most commonly implicated, being present in 10% to 40% of all biopsies of esophageal ulcers. This pathogen can manifest as a single ulcer, as multiple ulcers, or as a diffuse esophagitis. Medications used to treat HIV, such as zidovudine (AZT) and zalcitabine, have also been implicated as being a cause of esophageal lesions.
(iii) Abdominal pain
Abdominal pain is a frequent complaint in patients with HIV, with an incidence of greater than 25% in some studies. The wide array of possible causes can pose a diagnostic dilemma for the clinician. Some are specific to the immunocompromised state of patients with AIDS, such as infections, neoplasms, and the side effects of drug treatments. Others are more common, such as peptic ulcer disease and gastroenteritis.
(iv) Hepatobiliary disease
Among the pathogens that affect the hepatobiliary tree in HIV infection, the most common is the Mycobacterium aviumintracellulare complex (MAC), found in the liver of 20% to 50% of patients at autopsy. Other organisms affecting the liver include M. tuberculosis and sexually transmitted organisms. AIDS cholangiopathy is a syndrome characterized by sclerosing cholangitis with or without papillary stenosis. Patients typically present with abdominal pain, fever, nausea, and vomiting. When a pathogen can be isolated, the most commonly found are CMV and Cryptosporidium. Sphincterotomies performed endoscopically have produced excellent results in the relief of pain.
Cholecystitis may occur coincidentally in AIDS patients with gallstones. More common, though, is acalculous cholecystitis resulting from OIs. The most common causes of AIDS cholangiopathy are CMV and Cryptosporidium, with MAC and Kaposi’s sarcoma (KS) being less frequently implicated.
(v) Pancreatitis
In HIV-infected patients, pancreatitis is most commonly associated with medications. OI agents such as CMV, Toxoplasma, and mycobacteria; neoplasms; and perhaps even the HIV virus itself can also cause pancreatitis.
(vi) Neoplasms
Kaposi’s sarcoma and non-Hodgkin’s lymphoma (NHL) are the two neoplasms that most commonly affect patients with AIDS. These tumors can occur anywhere in the GI tract, from the oral cavity to the liver, pancreas, and bowel. Among patients with skin or nodal KS, 40% also have GI involvement, giving rise to a wide range of GI symptoms including appendicitis, obstruction, perforation, and bleeding. In addition, the radiation used to treat KS can cause painful, ulcerating sores.
In the oral cavity, pain from NHL is usually from aggressively growing masses that can result in the destruction of bone and soft tissue. In the lower GI tract, lymphoma can cause abdominal pain, bowel obstruction, perforation, and bleeding. Treatment is with radiation therapy and systemic cancer chemotherapy.
(viii) Anorectal pain
In one study of 340 homosexual and bisexual men with AIDS, 34% were found to have anorectal disease. These patients can present with painful perirectal abscesses, fissures, fistulas, and hemorrhoids. Infectious causes of proctitis include herpes simplex virus (HSV), CMV, and other sexually transmitted organisms. A slight increase in anorectal carcinoma has also been noted in HIV-positive homosexual men. Therapy is directed at the underlying cause and includes surgery, antibiotics and stool softeners.
2. Thoracic pain
(i) Pulmonary
Because of its prevalence, pneumonia is the most common cause of chest pain in patients with AIDS. Although Pneumocystis carinii (PCP) is the most frequent pathogen found, patients with AIDS are susceptible to infection by a wide range of other organisms as well. Lung malignancy can also cause chest pain, with the two most important ones being KS and NHL. The presentation of pulmonary KS can be similar to that of OIs and includes cough, fever, pleuritic chest pain, dyspnea, and infiltrates on chest radiograph. Further adding to the difficulty in diagnosing malignancy is the fact that up to 50% of patients with pulmonary malignancy have superimposed infection.
Nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful in treating the pain associated with pulmonary disease. Opioids should be used with caution as they may further compromise an already tenuous respiratory status.
(ii) Cardiac
Pericarditis, myocarditis, and, in the intravenous (IV) drug–abusing population, endocarditis all occur with increased frequency in HIV-infected patients. Chest pain is a more salient feature in pericarditis than in myocarditis and endocarditis, although it may be conspicuously absent in chronic disease. Its prevalence in HIV positive patients ranges from as low as 3% to as high as 26.9%. Patients with heart disease may be sensitive to the hemodynamic effects of opioids and poor candidates for treatment with tricyclic antidepressants. In the absence of renal disease or coagulation defects, NSAIDs can be a useful adjuvant.
3. Rheumatologic manifestations of AIDS
It has been widely documented that musculoskeletal complaints occur with increased frequency in patients with HIV infection. In one series involving 101 patients in various stages of HIV disease, musculoskeletal involvement was noted in 72% of cases. Reiter’s syndrome was the first rheumatic disease reported in patients with HIV infection, and it is frequently claimed to be the most prevalent. The most common presentation of Reiter’s syndrome is oligoarthritis, preferentially affecting the large, weight-bearing joints in the lower extremities.
Septic arthritis and psoriatic arthritis arthropathy may also occur with greater frequency in patients with AIDS and should be treated the same way as in the non-HIV-infected population. An HIV-associated arthritis has also been described. The onset of this oligoarthritis tends to be gradual, ranging from 1 to 6 weeks, with the duration averaging about a month. The joints of the lower extremities are most frequently affected, although any joint in the body can be involved.
Therapy for rheumatologic arthropathies generally begins with the traditional NSAIDs, although in severe cases they alone may be insufficient. Second-line agents that have proven useful include gold, sulfasalazine, phenylbutazone, and certain antimalarial drugs. In refractory cases, the use of steroids, either systemically or via intra-articular injection, may be necessary.
An association between HIV infection and inflammatory muscle disease (myalgias and myopathies) was first recognized in 1983, with the most common disorder being polymyositis. Patients with polymyositis generally present with progressive muscle weakness, the lower extremities being more frequently affected than the arms. Myalgias and muscle cramps are also prominent complaints. Drugs used to treat HIV disease, particularly AZT, have been known to cause a toxic myopathy indistinguishable from that of polymyositis. This scenario classically develops after 6 to 12 months of treatment with doses exceeding 500 mg/day, and there is usually improvement after the drug is discontinued. Most patients with myalgias respond well to NSAIDs, although an aggressive physical therapy program may be needed if weakness exists. In severe cases, moderate doses of steroids for 4 to 6 weeks may be indicated.
4. Neurologic pain manifestation
Neurologic complications are common in HIV-infected patients: at least 10% present with neurologic symptoms. Perhaps because of its affinity for the central nervous system (CNS) and the ease with which the virus is able to cross the blood–brain barrier, involvement of the nervous system has been found in 30% to 63% of patients over the course of the illness.
(i) Headache
Patients with HIV infection frequently report headache, with an incidence varying from 17% to over 50% in patients with documented neurologic involvement. Because the cause varies according to the stage of disease and the medications being taken, knowledge of these factors can provide important clues to diagnosis. In otherwise healthy HIV carriers with normal CD4 counts, no prior opportunistic infections, and an absence of other neurologic manifestations, headaches are unlikely to be the result of serious neurologic disease. Common causes of headaches in healthy HIV carriers include tension headaches, migraines, and sinusitis.
Headaches in HIV-infected patients can also result from medication therapy. Antiretroviral therapies as well as drugs used to treat OIs have both been documented to cause headaches. Although it is often difficult to ascertain the precise incidence of drug-induced headaches, results from one study revealed a 16% prevalence of AZT-induced headaches.
(ii) Nonfocal brain disorders
HIV encephalopathy, also known as AIDS dementia complex (ADC), refers to a constellation of cognitive, behavioral, and motor symptoms that is thought to be caused by HIV-1. Headaches are not unusual in ADC and are usually attributed to aseptic meningitis. Another fairly common nonfocal CNS infection is CMV encephalitis, with early autopsy studies showing evidence of CMV infection in about 25% of brains. Although many of these patients are asymptomatic, some suffer a fulminant course with significant morbidity and mortality. In addition to headaches, symptoms of CMV CNS infection include confusion, delirium, seizures, and ataxia.
The most likely cause of meningitis in HIV patients is infection with the fungus Cryptococcus, estimated to affect between 5% and 15% percent of patients. The clinical symptoms of this entity vary widely, from none at all to the more classic picture of headache, nausea, vomiting, malaise, confusion, and signs of meningeal irritation such as neck stiffness and photophobia.
Probably the second most common cause of meningitis in the HIV-infected population is aseptic meningitis, believed to be caused by the virus itself. Both acute and chronic forms have been reported. Aseptic meningitis commonly occurs during the transition from asymptomatic to symptomatic disease, as the CD4 count is falling. Whether HIV meningoencephalitis is a distinct entity is still being debated. Nevertheless, symptoms of this controversial illness are usually self-limited and include headache, photophobia, and occasionally nausea. Pain treatment is symptomatic and includes NSAIDs, tricyclic antidepressants (TCAs), and calcium channel blockers.
(iii) Focal brain disorders
Cerebral toxoplasmosis is the most common focal brain lesion in AIDS, occurring in 5% to 10% of HIV-positive patients. Another frequent cause of focal CNS disease is progressive multifocal leukoencephalopathy (PML), with an incidence of 4% to 5%. Although there is no specific and reliable treatment for PML, there are numerous reports of spontaneous remission after the institution of highly active antiretroviral therapy. Primary CNS lymphoma is the third major focal brain disorder encountered in patients with AIDS, accounting for between 2% and 7% of CNS complications in HIV disease. Other malignancies such as Kaposi’s and other sarcomas also occur with increased frequency in patients with AIDS.
Symptoms of focal brain lesions generally relate to mass effect and include headaches, cognitive changes, seizures, and focal neurologic deficits. Cranial involvement and impingement on painsensitive neurovascular structures can cause constant headaches. Therapies include specific treatment directed at the organism responsible, radiation, and chemotherapy. Steroid therapy may be beneficial, reducing cerebral edema and mass effects. Adequate pain therapy can often be achieved using mild analgesics such as NSAIDs and tramadol, although stronger opioid therapy may occasionally be required for severe pain.
(iv) Central pain
The International Association for the Study of Pain (IASP) defines central pain as pain that is caused by a lesion or dysfunction in the CNS. Central pain may occur almost immediately following injury, or it may take years to develop. When delayed, the onset frequently coincides with changes in subjective sensory abnormalities. Characteristics of this phenomenon include continuous, spontaneous pain that is sometimes described as burning, shooting, or aching. It is often accompanied by allodynia, hyperesthesia, and hyperalgesia, and it may be exacerbated by cold temperatures. Some common causes of central pain in patients with AIDS include HIV myelopathy, infarcts, cerebral abscesses, neurosyphilis, and malignancies.
Unfortunately, there is no truly effective means of eradicating central pain. However, combination therapy with TCAs, antiseizure and antiarrhythmic agents, opioids, N-methyl-D-aspartate (NMDA) antagonists such as dextromethorphan, and alpha-2 agonists can often provide substantial relief.
(v) Peripheral neuropathies
Peripheral neuropathies have been reported to affect up to 35% of patients with AIDS, with the incidence increasing in advanced stages of the disease. The clinical spectrum of HIV-associated neuropathies is broad, with sensory neuropathies being most commonly encountered. Because of their insidious onset and the progressive nature of HIV disease, peripheral neuropathies often go unreported in this population.
Distal symmetrical polyneuropathy is the most common neuropathy complicating HIV disease, with symptoms usually starting in the toes (and later the fingers), and extending proximally. The most common type of distal polyneuropathy is that caused by the retrovirus itself; it is often referred to as HIV-related distal sensory polyneuropathy (HIVR-DSPN). The goal of treatment for this disorder is symptomatic relief with medications for neuropathic pain such as TCAs and anticonvulsants. For allodynia, the local application of lidocaine cream can be helpful. Although isolated reports exist touting its benefits, traditional treatment with antiretroviral therapy has not been shown to be effective.
Perhaps the second most common neuropathy is caused by medications used to treat HIV-infected patients. Although some patients with neurotoxic distal sensory polyneuropathy complain of a deep or aching pain in their distal extremities as opposed to the typical burning or shooting pain of HIVR-DSPN, in most cases the two are clinically indistinguishable. Affected patients typically present with complaints of burning, tingling, or numbness beginning in the distal parts of the extremities. Occasionally, superimposed shooting pains and allodynia are noted. If a neurotoxic neuropathy is suspected, the offending agent should be stopped immediately. In most cases, the effects are reversible, although improvement may take weeks or even months.
Deficiencies of vitamin B12 may produce DSPN characterized by pain, numbness, and paresthesias. In one study, 16% of HIVinfected patients were noted to have either low serum levels of B12 or impaired absorption, although other studies have failed to duplicate these results. The treatment of B12 neuropathy is replenishment of the vitamin.
Progressive polyradiculopathy (sacral ascending polyradiculopathy) typically occurs late in the course of HIV disease, when CD4 counts are low and OIs are present. This progressive neuropathy is one of the most devastating and dramatic neurologic complications of AIDS. Yet its response to early therapy is good, and this, as well as its fulminant course if left untreated, demand prompt recognition and timely treatment. Progressive polyradiculopathy classically strikes abruptly, with the initial abnormalities being present in the lumbosacral nerve roots. This typically manifests as pain and paresthesias in the buttocks and legs, with back pain being another symptom that is often encountered early. Over the next several weeks, this may be followed by rapid progression to paraparesis, ascending sensory loss, bowel and bladder dysfunction, and areflexia. If left untreated, these abnormalities can extend to the trunk and arms. The large majority of cases of progressive polyradiculopathy appear to be caused by CMV infection, which can sometimes be detected in the cerebrospinal fluid. However, because of the rapidly progressive course, treatment should be started immediately on the basis of clinical evidence. The mainstay of therapy is with antiviral agents.
Patients with focal mononeuropathies present with asymmetrical multifocal motor and sensory symptoms in the distribution of cutaneous nerves, mixed nerves, and nerve roots. In many patients, coexisting cranial neuropathies are present. In HIV-positive patients who are otherwise healthy, the disorder tends to be selflimited, with symptoms being restricted to one or two peripheral nerves. Some patients who develop symptoms early in their illness may even experience spontaneous remission. In patients with more widespread disease, the neuropathy may involve three or more nerves. In these individuals, CMV can often be isolated from nerve biopsies. Though the mainstay of treatment for CMV focal neuropathy is specific antiviral therapy, symptomatic treatment with neuropathic medications may also prove beneficial. In some patients, therapy with IV immunoglobulins, plasmapheresis, and in some cases corticosteroids may be indicated.
5. Herpes Zoster
Several studies have shown the incidence of acute herpes zoster (AHZ) to be higher in the HIV-positive population (from 5% to 10%) than in the general population. Outbreaks of the disease generally correlate with a declining state of immunity and are unusual in healthy persons under 50 years. Therefore, young patients with AHZ should be evaluated for causes of immunodeficiency.
Patients with herpes zoster normally present with pain and/or dysesthesias that typically precede a rash by 3 to 4 days. Infrequently, pain occurs without the development of visible lesions. Unlike non-HIV-infected patients with shingles, HIV-infected patients with shingles exhibit a high prevalence of atypical lesions and frequent recurrences.
In immunocompromised patients, varicella zoster virus (VZV) infections can be life-threatening, and prompt treatment is essential. As in the non-HIV-infected patient, the treatment of choice is anti-herpes-virus agents. Administration of the live attenuated viral vaccine is contraindicated in HIV-infected individuals.
Since the severity of pain during the acute phase of herpes zoster infection is predictive of the development of chronic pain, adequate pain management early in the disease is of paramount importance. Symptomatic pain therapy in acute attacks of AHZ includes treatment with NSAIDs, anticonvulsants such as gabapentin and topiramate (Topamax), and antidepressants. In addition to relieving pain, TCAs have been shown in randomized controlled studies to be effective in reducing the incidence of postherpetic neuralgia (PHN).
Nerve blocks that have been reported to be effective in shingles include intercostal nerve blocks for thoracic involvement, epidural analgesia, and subcutaneous infiltration with and without steroids. Although blocking sympathetic ganglia early in the course of the disease has been reported by some authors to be an effective treatment, a recent critical review of the literature found scant evidence for this view. In those patients refractory to conventional therapy, the use of narcotics may be indicated.
PHN is defined as pain in the affected dermatomes that persists longer than 3 months after crusting of the herpes lesions. Perhaps because of the association with a decline in immune status, AIDS patients with AHZ may be at a slightly higher risk for development of PHN, with an incidence between 10% and 15%. Two other factors that appear to influence the development of PHN include the severity of pain and the duration of lesions. The pain of PHN is often described as burning, aching, or tearing, with superimposed shooting sensations. The scars themselves and the areas around them are often hypoesthetic, but paradoxically, patients may present with allodynia, hyperesthesia, or hyperpathia. As with chicken pox, a severe form of pruritus may ensue.
The only pharmacologic therapies shown to be effective in randomized clinical trials in patients with PHN are TCAs, gabapentin, topical agents, and opioids. Empirical therapies with other anticonvulsants have yielded mixed results. Recently, topical local anesthetics such as the lidocaine patch, with or without capsaicin, have been demonstrated to be of benefit in the treatment of PHN associated allodynia. Good results have also been obtained with opioids. In spite of isolated reports to the contrary, in most cases local anesthetic blocks have limited value in the treatment of PHN. Transcutaneous electrical nerve stimulation (TENS) is associated with almost no adverse side effects and may be beneficial in some situations. Finally, in patients who continue to have refractory pain, surgical therapies such as spinal cord stimulation and neuroablative procedures may be considered.
These pain treatments are more fully described in Chapter 8, Chapter 9, Chapter 10 and Chapter 11.
1. Opioid management of the HIV-positive patient
In the United States, approximately 25% of HIV-infected patients have a history of IV drug abuse. Yet for many of these patients, the diseases they have and the pain they are faced with necessitates treatment with opioids. When treating these patients, the fundamental principle of pain management is the same as that for other patients: pain complaints should be taken seriously and treated aggressively. In one study, IV drug addicts were not found to complain more of pain or require larger doses of opioid analgesics than non–drug abusers.
For patients with chronic pain, long-acting opioids provide a steady state of analgesia and are associated with less euphoria than short-acting narcotics. Consequently, they also tend to have a lower abuse potential when used therapeutically. The fentanyl patch has perhaps the lowest potential for abuse, although innovative addicts have found methods to abuse even this.
When patients in methadone maintenance programs or those taking long-acting opioids for chronic conditions present with acute nociceptive pain, long-acting medications can be continued and patient-controlled analgesia can be added to provide additional analgesia for the acute phase and as a means of measuring opioid requirements. Mixed agonist–antagonists should be avoided in these patients as they may trigger withdrawal. In patients with inadequately treated pain, pseudoaddiction can be misinterpreted as drug-seeking behavior (see Chapter 30). Finally, only when the patient’s pain is under control should an attempt be made to treat addiction in motivated patients wishing to change their lifestyle.
2. Nonopioid pain adjuvants
The NSAIDs and acetaminophen provide safe and effective analgesia in many cases of mild to moderate pain. Advantages of these medications are their relative safety, their availability, and their low potential for abuse. Even in conditions that require stronger therapy, the opioid-sparing properties of these medications make them a good addition to any multimodal pain regimen. However, in view of the multiple organ system dysfunction patients with AIDS may suffer, clinicians must be aware of the toxic effects of these drugs. Acetaminophen carries a dose-dependent risk of hepatotoxicity and less commonly causes renal tubular necrosis. It may also decrease the clearance of AZT. In some situations, the newer specific cyclooxygenase-2 (COX-2) inhibitors, which have a more favorable side effect profile than traditional NSAIDs, may be preferable.
In light of the high prevalence of neuropathic pain and depression in HIV-infected patients, it is not surprising that TCAs often play a prominent role in pain therapy. In addition to their use in the treatment of neurogenic pain and some causes of headache, the side effects of decreased peristalsis and sedation may be helpful in patients with refractory diarrhea and insomnia.
The anticonvulsants carbamazepine and phenytoin have long been successful in neuropathic pain conditions, but both can interact with other drugs commonly used by patients with AIDS, such as isoniazid and TCAs. Newer agents, such as gabapentin and lamotrigine, and the antiarrhythmic mexiletine may be preferred in some patients.
Topical creams such as capsaicin for arthralgias, and lidocaine for PHN are not absorbed systemically and are thus associated with minimal side effects. However, both are expensive and it may not be feasible to apply them to large areas of skin several times each day.
3. Nerve blocks and regional anesthesia
Nerve blocks and regional anesthesia often prove to be useful adjuncts in AIDS patients in whom analgesics have failed to alleviate pain or who cannot tolerate them because of side effects. However, there are some special considerations that need to be addressed before proceeding with nerve blocks. Patients with HIV have a greater incidence of potentially progressive neurologic problems than the general population. Although it is not an absolute contraindication, for many pain specialists the existence of progressive neurologic disease mitigates against the use of spinal and epidural agents in patients who might otherwise be suitable candidates for neuraxial blockade.
Another concern is infection. One study found a higher infection rate in patients with AIDS who had had epidural catheters inserted for chronic pain than in the general population. But two other studies failed to reproduce the findings of an increased complication rate during epidural treatment in HIV-infected patients for labor analgesia and postdural puncture headaches (epidural blood patches). Certainly, the risks and benefits of steroid injections must be carefully balanced in these patients, especially those in the later stages of disease who are already markedly immunosuppressed.
Finally, patients with AIDS often present with thrombocytopenia and other coagulopathies, because of both their disease and their treatments. Coagulopathy is a contraindication to regional anesthesia. Other contraindications are systemic or local infection at the site of needle puncture, and leukopenia.
4. Nonpharmacologic interventions
Because of the nature of the immunodeficiency virus and its modes of transmission, a large percentage of HIV-positive patients are faced with the daunting paradox of being young and having an incurable disease. Consequently, many are emotionally unprepared for dealing with a fatal illness. Both psychological and social factors play a major role in the pain experience, necessitating a multidisciplinary approach to the AIDS patient with pain.
Unlike the plethora of medications these patients are often compelled to take, most noninterventional pain treatments are devoid of side effects. These treatments include self-hypnosis, biofeedback and other relaxation techniques, acupuncture, and group therapy. Physical therapy and other functional restoration programs can help reduce musculoskeletal pain and maintain strength and mobility. Finally, a good therapist who focuses on the cognitive and behavioral aspects of pain and illness can be indispensable in this population.

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Holloway RG, Kieburtz KD. Headache and the human immunodeficiency virus type 1 infection. Headache 1995;35:245–255.

Merigan TC Jr, Bartlett JG, Bolognesi D, eds. Textbook of AIDS medicine, 2nd ed. Baltimore: Williams & Wilkins, 1999.

Patton LL, van der Horst C. Oral infections and other manifestations of HIV disease. Infect Dis Clin North Am 1999;13:879–900.

Simpson DM, Olney RK. Peripheral neuropathies associated with human immunodeficiency virus infection. Neurol Clin 1992;10:685–711.

Wormser GP, ed. AIDS and other manifestations of HIV infection, 3rd ed. Philadelphia: Lippincott-Raven, 1998.

Hewitt DJ, McDonald M, Portenoy R, et al. Pain syndromes and etiologies in ambulatory AIDS patients. PAIN 1997;70:117–123.


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