JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Evron, S.
Right arrow Articles by Ezri, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Evron, S.
Right arrow Articles by Ezri, T.
Related Collections
Right arrow Obstetrics
Right arrow Pain

Anesth Analg 2004;98:503-511
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000097193.91244.50


OBSTETRIC ANESTHESIA

Human Immunodeficiency Virus: Anesthetic and Obstetric Considerations

Shmuel Evron, MD*, Marek Glezerman, MD{dagger}, Ethan Harow, DO{ddagger}, Oscar Sadan, MD§, and Tiberiu Ezri, MD||

*Obstetric Anesthesia Unit, the {dagger}Department of Obstetrics and Gynecology, the {ddagger}Ambulatory Surgical Unit, §Delivery Ward, ||Department of Anesthesia, The Edith Wolfson Medical Center, Holon (Israel), Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel

Address correspondence and reprint requests to M. Glezerman MD, Professor and Chairman, Department of Obstetrics and Gynecology, The Edith Wolfson Medical Center, Holon, Israel. Address email to glezerman{at}Wolfson.health.gov.il


    Abstract
 Top
 Abstract
 Introduction
 Conclusions
 References
 
The pandemic of acquired immune deficiency syndrome (AIDS) is on the threshold of its third decade of existence. The World Health Organization-United Nations statistics show that human immunodeficiency virus (HIV)/AIDS pandemia is set to get much worse. Women of reproductive age are the fastest growing population with HIV. Common signs and symptoms have become more moderate or subclinical, and new clinical presentations have emerged. It is quite apparent that HIV-disease affects multiple organ systems. Advances have been made in elucidating the pathogenesis of HIV. In addition, the molecular technique of viral load determination and the CD + 4 T-lymphocyte count enable evaluation of the disease, its prognosis, and its response to therapy. There is limited specific information concerning the overall risk of anesthesia and surgery of HIV/AIDS patients. However, as far as can be determined, surgical interventions do not increase the postoperative risk for complications or death and should therefore not be withheld. There is also little evidence to suggest that HIV or antiretroviral drugs increase the rate of pregnancy complications or that pregnancy may alter the course of HIV infection. General anesthesia is considered safe, but drug interactions and their impact on various organ systems should be considered preoperatively. Regional anesthesia is often the technique of choice. Yet, one must take into consideration the presence of neuropathies, local infection, or blood clotting abnormalities. It should be emphasized that all practicing anesthesiologists should be familiar with the disease and should use prenatal anesthesia consultations and a team approach to assure optimal treatment for HIV patients.


    Introduction
 Top
 Abstract
 Introduction
 Conclusions
 References
 
Acquired immune deficiency syndrome (AIDS) was first recognized more than 20 years ago, and since then it has reached pandemic proportions. Within 2 decades, more than 50 million people have been infected with the human immunodeficiency virus (HIV) and 20 million have died. Worldwide, two-thirds of the 36 million known carriers of HIV are living in sub-Saharan Africa (1). In the United States (US), 950,000 people have HIV/AIDS. In the year 2001, 15,000 of those people died from the disease (1). New infections occur at approximately 40,000 per year (2). Young women are the fastest growing population with HIV in the US. Almost 30% of new HIV infections in the year 2000 were among women. Eighty-two percent of the new infections occurred in ethnic/racial minorities, predominantly among African Americans. The parturient transmits the HIV perinatally; thus the epidemic in children parallels the epidemic among women (2,3). The transmission of the disease in nonbreast-fed infants occurs 30% of the time in utero and 70% during labor and delivery (4).

The overall risk of anesthesia and surgery in HIV positive patient needs further study. Twenty to 25 percent of HIV-positive patients will require surgery during their illness (5). Anesthesiologists need to be aware of the disease when deciding on the course of anesthesia. This multiorgan disease may be complicated either by opportunistic infections, tumors, substance abuse, or antiretroviral therapeutic drugs, which all can have an impact on anesthesia.

HIV is a member of the lentivirus family, a subtype of human retroviruses. It is characterized by a cytopathic action, a long latency period, and persistent viremia. As a result of impaired cell-mediated immunity, the infected person is more susceptible to viral, bacterial, mycobacterial, and malignant disease (6). Of the untreated patients, 10% will develop symptomatic AIDS in the first 2–3 yr of infection. The remainder will develop the disease over a 10-yr time period (7).

Diagnosis of HIV Infection
As the viral envelope is composed of different glycoproteins, antibodies to these proteins or to the p24 antigenic core can be detected. The diagnostic techniques include serologic tests, viral culture, genomic detection, and amplification of viral ribonucleic acid (RNA) or proviral deoxyribonucleic acid (DNA).

Specific HIV antibodies can be detected serologically 2–8 wk (usually within 3 wk) after infection. The first antibodies to appear are immunoglobulin (Ig) M to the viral envelope glycoprotein. After a few days the IgG to p24 core antigen and gycoprotein-gp120 appear. Antibody detection tests are the enzyme-linked immunosorbent assay (ELISA) and the more specific Western blot test (8).

HIV diagnosis can be made by direct detection of HIV using the ELISA test for p24 core antigen or by amplification and detection of proviral DNA or HIV RNA using polymerase chain reaction. This can be important for the monitoring of HIV treatment for detection of HIV in neonates of infected mothers (9). Viral load determination is used for diagnostic quantification and monitoring of HIV treatment (10). These viral load levels usually correlate with CD4+ T cell lymphocyte count. A successful anti-HIV therapy means viral load suppression to an undetectable blood level.

Clinical Manifestations of HIV Infection
Over time, antiretroviral therapy has changed the epidemiologic, demographic and clinical characteristics of AIDS. The signs and symptoms can be caused by the HIV infection, opportunistic infections, neoplasm, or by the antiretroviral drugs. As the highly active antiretroviral therapy (HAART) became more effective, life expectancy and the clinical appearance has become moderated or subclinical.

Central and Peripheral Nervous System.
Some 30% of adults and 50% of children suffering from AIDS will develop neurological disorders (11). In the early stage of infection, headaches, photophobia, meningoencephalitis, depression, irritability, Guillain-Barre-like syndromes, or cranial and peripheral neuropathy can be observed. The latent phase of the disease is associated with demyelinating neuropathy and cerebrospinal fluid pathology. The late period of HIV infection is associated with meningitis, focal or diffused encephalopathy, myelopathy, myopathy, and peripheral neuropathy.

As the central nervous system (CNS) is the first crucial organ to be affected by anesthetic drugs, early diagnosis of HIV deserves careful evaluation of cognitive and neurologic dysfunction. Patients with AIDS are more sensitive to opioids and benzodiazepines, which also reflects the extent of neurological involvement. The probable mechanism is based on increased interleukin-1 levels causing an increased {gamma} aminobutyric acid-mediator production (12). HIV infection, intracranial masses, or opportunistic infections may cause cerebral edema, cerebral hemodynamic disturbances, and increased intracranial pressure (ICP). These deserve anesthetic consideration and measures for reducing ICP and generally preclude the use of neuraxial anesthesia in patients with increased ICP. Peripheral neuropathy is the most frequent neurological complication in HIV patients (13). It affects approximately 35% of patients with AIDS and manifests clinically as a polyneuropathy and myopathy.

An autonomic dysfunction in the HIV-infected person may appear with or without CNS abnormalities. AIDS patients may present with uncommon autonomic disturbances, such as orthostatic syncope, hypotension, and diarrhea (14).

Pulmonary Abnormalities.
The pulmonary manifestations of patients infected with HIV are caused mainly by opportunistic infections. The most common of these, Pneumocystis carinii infection, has become rarer with the use of HAART and prophylactic drug therapy (15). An immunocompromised person with a CD4+ lymphocyte count of <200 cells/mm3 is at increased risk for developing P. carinii pneumonia. The disease may present as adult respiratory distress syndrome and may be complicated by pneumatoceles, pneumothorax, or respiratory failure (16). Computed tomography of the chest in the early stages of the disease may reveal bilateral haziness of both lungs, whereas chest radiograph appears normal (17).

Tuberculosis (TB) is another concern in AIDS patients. The incidence of HIV-associated TB has been increasing, especially among women of childbearing age (18). Patients with both infections may present with atypical manifestations of TB that causes difficulty in making a diagnosis. Other pathologies that may affect the lungs are Kaposi’s sarcoma, lymphomas, and cavitary lung disease caused either by fungal pathogens or Nocardia.

Cardiac Manifestations.
Advances in the treatment of HIV infection have improved longevity of HIV patients, thereby they develop more cardiac involvement (Table 1) (19). In the advanced stage of the disease, myocarditis is more common and is caused by opportunistic infections or neoplasm-like lymphomas and Kaposi’s sarcoma (20).


View this table:
[in this window]
[in a new window]
 
Table 1. Manifestations of Human Immunodeficiency Virus Infection
 
There are reports of various abnormalities associated with a hypercoagulable state (21). These include pulmonary hypertension, accelerated coronary arteriosclerosis, a decrease in left ventricular contractility and myocardial infarction in young HIV patients. Preoperative cardiac evaluation is therefore mandatory and appropriate perioperative cardiovascular monitoring of these patients is of crucial importance (22).

Gastrointestinal Abnormalities.
Gastrointestinal abnormalities are commonly encountered in patients with AIDS (Table 1). Signs and symptoms may originate from the oropharynx, esophagus, stomach, and hepatobiliary system (23). The main cause of dysphagia is Candida albicans esophagitis. Other common pathogens are cytomegalovirus (CMV), herpes virus, Kaposi’s sarcoma, histoplasmosis, and squamous cell carcinoma. In advanced AIDS, esophageal reflux is common, which may increase the risk for pulmonary aspiration on induction of general anesthesia (24). Abnormal liver function tests are also common in advanced AIDS and reflect the decreased metabolic and secretory ability of the liver in addition to coagulation abnormalities. Finally, electrolyte abnormalities are caused by diarrhea and decreased oral intake resulting from dysphagia or nausea.

Hematological Abnormalities.
A wide spectrum of hematologic abnormalities in HIV patients is very common and may appear at any stage of the disease (Table 1). Bone marrow involvement and coagulation abnormalities may result from HIV infection, anti-HIV drugs, nutritional factors, and bone marrow infiltration by opportunistic infection or neoplastic diseases (25).

The literature contains reports of thrombotic episodes and various predisposing abnormalities related to a hypercoagulable state that correlate with the severity of HIV disease (26). The coexistence of HIV-related illness, such as malignancies and autoimmune disease, as well as antiretroviral drug therapy itself, may also predispose these patients to thromboembolic events (26).

Another coagulation abnormality seen in the HIV patients is idiopathic thrombocytopenic purpura that is caused by platelet serum immunoglobulin, or direct adverse effects of HIV infection on the megakaryocytes (25). Some of the antiretroviral (zidovudine) or antiopportunistic drugs (ganciclovir) may contribute to these hematologic abnormalities as a result of bone marrow suppression (25).

Renal Abnormalities.
HIV patients are at risk for developing various renal diseases caused by HIV infection, viral hepatitis, drug abuse, antiretroviral drugs, and dehydration (27). The HIV-associated nephropathy is a distinct clinico-pathological syndrome presenting as a nephrotic syndrome. The use of angiotensin-converting enzyme inhibitors, steroids, and antiretroviral treatment may slow down its progression to end-stage renal failure (28). The use of an antiretroviral drug, such as adefovir, may cause acute toxic tubular necrosis (29). Indinavir, which is also commonly used, is associated with a 3% incidence of nephrolithiasis (30).

Endocrinologic and Metabolic Abnormalities.
The course of HIV infection or AIDS can be complicated by a variety of endocrine and metabolic abnormalities. This may be a direct effect of HIV on the respective glands, by opportunistic infections, neoplasm, or antiretroviral drugs. Primary or secondary adrenal insufficiency is still the most serious endocrine complication in HIV patients (31). Thyroid function tests in AIDS patients may be abnormal, although clinical hypothyroidism is rare.

Hypoglycemia is another metabolic abnormality that may be caused by islet cell damage resulting from pentamidine treatment. Hyperinsulinemic hypoglycemia may be associated with hypopituitarism in an AIDS patient or as a complication of protease inhibitor treatment (22).

HIV and Pregnancy
One-third of new HIV positive patients in 2000 were women (1). In the US, the nationwide seroprevalence of HIV during pregnancy has been reported as 1.7 per 1000 pregnancies (32). The majority of pediatric HIV infections resulted from vertical transmission of the virus from mother to infant. This occurred 4.4% of the time during pregnancy, 60% of the time during delivery, and 35.6% of the time during breastfeeding (33).

A meta-analysis of the International Perinatal HIV group included 15 prospective European and North American studies of 8500 parturients. A reduction of vertical transmission by more than 50% was observed when elective cesarean delivery was performed (34). More recently, elective cesarean delivery combined with antiretroviral therapy has reduced vertical transmission to <5% (35). The American College of Obstetricians and Gynecologists (ACOG) committee opinion of May 2000 stated that when viral loads are more than 1000 copies per milliliter, the benefit from elective cesarean delivery is beyond that achieved by antiretroviral therapy alone (36). It has been further noted that the mode of delivery should be individually assessed and that the viral load testing has to be followed every 3 mo. Many practitioners do not recommend elective cesarean delivery for HIV-infected women who are compliant with antiretroviral therapy and have undetectable HIV viral loads (37). The revised ACOG Committee Opinion also considers routine delivery by cesarean section to be problematic and potentially dangerous, especially in rural hospitals in Africa where maternal mortality approximates 230 per 100,000 (36). The incidence of complications is significantly increased when the CD4+ count is <200 mm-3 (38,39). Routine HIV testing should be offered to every pregnant person at risk of HIV infection.

The percentage of women diagnosed before delivery in the US has improved from 51% in 1993 to 80% in 1996 (40). The European Collaborative study has shown that 14% of HIV-infected pregnant women are immunocompromised, and there is no evidence to suggest that pregnancy alters the course of HIV infection (41).

Intrauterine growth retardation and premature delivery were reported among infants of HIV-infected women regardless of their infectious condition (41).

HIV Therapy Interaction with Anesthesia and Obstetrics
Combined HAART has dramatically improved survival of HIV-diseased patients, has delayed the progress of the disease, and has caused a decline in AIDS incidence and death. More than 14 drugs have been used. Most of them produce side effects that interact with anesthetic drugs. Some of these adverse effects may mimic signs and symptoms of the HIV disease itself. Side effects may also result from drugs used for prevention or treatment of opportunistic infections.

Pregnancy may affect timing and choice of therapy, but it is not considered a contraindication or a reason to postpone treatment, although dosing must take into consideration blood volume and volume of distribution changes during pregnancy. In addition, there are potential toxic drug effects on the fetus and the newborn (42,43). New guidelines suggest that pregnant women should continue or start with combined HAART therapy at a maximally suppressive regimen, although little data on animal and human toxicity support these recommendations (43). Additional information is available at http://www.aidsinfo.nih.gov.

Antiretroviral Drugs
Three classes of antiretroviral drugs have gained Food and Drug Administration approval and are currently used in the management of HIV disease (44) (Tables 2–4).


View this table:
[in this window]
[in a new window]
 
Table 2. Antiretroviral Drugs [Nucleoside Analogue Reverse Transcriptase Inhibitors (NRTIs)] and Side Effects
 

View this table:
[in this window]
[in a new window]
 
Table 3. Antiretroviral Drugs (Non-Nucleoside Reverse Transcriptase Inhibitors) and Side Effects
 

View this table:
[in this window]
[in a new window]
 
Table 4. Antiretroviral Drugs (Protease Inhibitors) and Side Effects
 
Nucleosides analog reverse transcriptase inhibitors. These drugs inhibit the completion of reverse transcription by binding to the viral DNA. Side effects commonly reported with zidovudine treatment include headache, insomnia, nausea, and vomiting. Prolonged therapy can lead to neuropathy, malaise, myalgia and myopathy with increased creatinine-phosphokinase, and pancytopenia. Peripheral neuropathy is the most common side effect of zalcitabine. It correlates with the severity of HIV infection and may affect 30% of patients treated (45). Lamivudine is the least neurotoxic of the currently used nucleoside analogues. It may exacerbate preexisting neuropathy (46). However, combined antiretroviral therapy was shown to improve HIV-related peripheral neuropathy (47). Peripheral neuropathy is generally reversible on cessation of therapy.
Non-nucleotide reverse transcriptase inhibitors (NNRTIs). These drugs inhibit the enzyme reverse transcriptase by direct binding. Because they bind only to the HIV-1, resistance to them develops rapidly when given as a single drug. The recommendations are to use NNRTIs in combination with three or more drugs to enhance their effectiveness (48). The NNRTIs most commonly used are nevirapine, delavirdine, and efavirenz (Table 3). Their major side effect is skin rash, including Stevens-Johnson’s syndrome. Nevirapine causes cytochrome P450 enzyme induction (CYP3 A3/4) and may decrease serum levels of some anesthetic or sedative drugs (i.e., midazolam, fentanyl) (49).
Protease inhibitors (PIs) (Table 4). These drugs inhibit the HIV protease by binding to the active cleavage site. The most commonly used PIs are saquinavir, ritonavir, indinavir, and nelfinavir. Side effects are gastrointestinal symptoms, hyperglycemia, peripheral neuropathy, obstructive uropathy (30), increased liver enzymes, and hypertriglyceridemia (50). Efavirenz is a potent teratogenic drug that should be avoided during the first trimester of pregnancy (45). Indinavir may be associated with mild hyperbilirubinemia, hematuria, and renal failure resulting from obstructive uropathy (30). The PIs are metabolized by the cytochrome P450 isoenzyme cytochromeP3A4 (CYP3A4). They competitively inhibit the enzyme and may increase the effects of drugs metabolized by cytochrome P450. Therefore, these anesthetic drugs should be titrated carefully (49). Ritonavir is the most potent inhibitor of CYP3A4 and CYP2D6 and is a less potent inhibitor of CYP2C9/10 (51). Fentanyl, a synthetic opioid analgesic, is metabolized mainly by CYP3A4 (51) and to a lesser extent by other CYPs (52).

Anesthetic Management
Assessment of risk and coexisting diseases during preoperative evaluation should focus on the patient’s status, type of surgery, and anesthesia, which, combined with the Centers for Disease Control stage of HIV infection, the immunologic status (CD4+ cell count), and the coexistence of opportunistic infections and malignancies, should allow a good prediction for the perioperative risk of the HIV-patient to be construed. Advanced HIV infection, when accompanied with opportunistic infections or malignancies, may complicate the perioperative course and management. The CD4+ count/mortality relationship is useful in risk assessment. Regardless of surgical procedure, there is a 13.3% mortality rate 6 mo postoperatively when the CD4+ count is <50 mm-3 and a 0.8% mortality rate when the CD4+ count is more than 200 mm-3 (53).

Preoperative assessment consists of the history, physical examination, and laboratory studies. The history should include evaluation of opportunistic infections and malignancy and concurrent treatments with antiretroviral or antiopportunistic drugs. The laboratory work-up should include complete blood count, clotting functions, and glucose, liver, and renal function tests. Verification of the immunological status, i.e., the CD4+ lymphocyte cell count and viral load during the previous 3 mo, is important. Chest radiograph and electrocardiogram should be performed in all patients. Patients with a history or signs of cardiac or pulmonary dysfunction should undergo a more thorough evaluation (blood gases, pulmonary function tests, echocardiography, cardiac effort test, and radioactive cardiac scanning or even cardiac catheterization). One must remember that these patients have often been subjected to cardiotoxic antiretroviral drugs, may be in a hypercoagulable state, may have accelerated coronary arteriosclerosis, and often have decreased left ventricular contractility (19–22). They will require appropriate preoperative work-up and therapy before any anesthetic or surgical procedure.

Anesthetic Techniques
Factors that need to be considered when administering general anesthesia include the possible effects of anesthesia and opioids on the immune system, the pulmonary and neurologic status of the HIV patient, and possible interactions with anti-HIV medications. Laboratory data suggest a detrimental effect of opioids on immune function (54). However, the clinical significance of short-term opioid administration during general anesthesia is unclear and there are not enough clinical data available to justify its avoidance. The presence of neurologic manifestations, such as overt dementia, may impair the ability of the patient to provide preoperative consent (55) and may increase brain sensitivity to sedative or psychoactive drugs (opioids, benzodiazepines, and neuroleptics). Opportunistic infections may be associated with increased ICP, predominantly with toxoplasmosis. Because these infections respond rapidly to medical therapy, surgery should be postponed whenever possible when they are present. Increased ICP and CNS infections (meningitis, encephalopathy, or myelopathy) are contraindications to neuraxial anesthesia (56).

The diagnostic approach to patients with HIV infection and neuropathy, myopathy, or other neurological deficit consists of taking a comprehensive neurological history and physical examination. Blood studies are needed to exclude diabetes mellitus, vitamin deficiencies, alcoholism, hereditary diseases, and infectious diseases such as CMV or Lyme disease. Cerebrospinal fluid analysis and nerve or muscle biopsy may be required. Radiological studies of the spinal cord should be performed as part of the neurological evaluation to exclude compressive lesions in symptomatic patients. This is particularly important in a patient scheduled for a surgical procedure under regional anesthesia (57).

The complications associated with the use of succinylcholine, such as hyperkalemia or hyperpyrexia, are only a potential risk to be considered in the HIV patient with progressive neuropathy, myopathy, and muscle wasting. No such complication in HIV patients has been reported in the literature; hence, the use of succinylcholine is not absolutely contraindicated (58).

Pulmonary complications can occur as a consequence of opportunistic infections. This may lead to respiratory distress and hypoxemia, aggravated by a decrease in functional residual capacity seen during pregnancy. Regional anesthesia may be a preferable technique in these patients. However, a high motor block with intercostal muscle paralysis may not be tolerated. Regional anesthesia was shown to be associated with reduced morbidity and mortality in a wide range of patients, including treated HIV parturients having cesarean delivery under spinal anesthesia (59).

Toxic Side Effects and Drug Interaction with Anesthesia
Before administration of any anesthetics, the anesthesiologist should be aware of the possible toxic side effects or to the possible interaction of antiretroviral drugs with the anesthetics. For example, neuropathy or myopathy may dictate change of anesthetic techniques. Anemia and thrombocytopenia are major toxic side effects of zidovudine. PIs can affect glucose metabolism. Foscarnet and PIs can cause renal toxicity. Foscarnet can also alter calcium and magnesium balance. Other side effects include increased liver enzymes (trimethoprim-sulfamethoxazole), bronchospasm (aerosolized pentamidine), and ventricular arrhythmias (IV pentamidine).

Pis, such as ritonavir, are inhibitors of CYP450, which impair the metabolism of multiple anesthetics and analgesics, such as midazolam and fentanyl, and cardiac drugs, such as amiodarone and quinidine (51). Nevirapine is an inducer of CYP450 and therefore increasing doses of anesthetic drugs may be required in patients receiving the drug (60). Etomidate, atracurium, remifentanil and desflurane are not dependent on CYP450 hepatic metabolism, and therefore, are preferable drugs.

When considering the type of anesthesia, regional anesthesia has the advantage of not interfering with the immune system or with antiretroviral drugs. Contraindications to regional anesthesia in these patients are sepsis and platelet abnormalities. The presence of neuropathy may reduce the appeal of regional anesthesia but there are no data to contradict its use. In a review of 96 HIV positive parturients, of whom 36 delivered under regional anesthesia, the advantages of regional anesthesia were confirmed (61). In a recent article (59), the effect of spinal anesthesia was studied in 45 HIV-treated parturients who underwent cesarean delivery. There were no perioperative complications or changes in immune function or viral load. The American Medical Association addressed the issue of providing care for patients with HIV and stated that physicians have an ethical duty to provide any treatment needed to HIV patients and avoid discrimination against such patients (62).

Postdural puncture headache may occur after regional anesthesia and may necessitate epidural blood patch. Tom et al. (63) found no increase in neurologic abnormalities in 6 HIV patients receiving an epidural blood patch during a follow-up period of 2 yr. There is no evidence to contraindicate the use of blood patch in HIV-positive patients. However, the small numbers reported may justify a conservative management as a first choice (64).

Magnetic resonance imaging (MRI) studies of the spinal cord in 55 symptomatic HIV patients showed neurologic involvement of the spinal cord in 49 patients, mostly of infectious origin (57). Currently, MRI is not often done in the preoperative HIV patient presenting with neurologic involvement, but is considered in a comprehensive neurological work-up or for neurosurgical indications to verify soft tissue pathology. There are increasing numbers of compromised HIV patients who are drug abusers, diabetics, postorgan transplantation recipients, and on long-term steroid treatment developing spinal infections. They are often diagnosed too late, mostly presenting with back pain or other neurologic signs or symptoms (65). Prolonged epidural catheterization in such severely compromised patients may be contraindicated (66). However, a series of 350 cancer patients who had prolonged epidural catheterization and were monitored closely for possible infection and promptly treated had no adverse sequelae (67).


    Conclusions
 Top
 Abstract
 Introduction
 Conclusions
 References
 
The pandemic of AIDS is on the threshold of its third decade of existence. The World Health Organization and United Nations statistics indicate that HIV/AIDS pandemia will get much worse. Women of reproductive age are the fastest growing population with HIV. Common signs and symptoms have become more moderate or subclinical, and new clinical presentations have emerged. It is quite apparent that HIV disease affects multiple organ systems. Advances have been made in elucidating the pathogenesis of HIV. In addition, the molecular technique of viral load determination and the CD+4 T-lymphocyte count enable the evaluation of the disease, its prognosis, and its response to therapy. There is limited specific information concerning the overall risk of anesthesia and surgery on HIV/AIDS patients. However, as far as can be determined, surgical interventions do not increase the postoperative risk for complications or death and should therefore not be withheld. There is also little evidence to suggest that HIV or antiretroviral drugs increase the rate of pregnancy complications or that pregnancy may alter the course of HIV infection. General anesthesia is considered safe, but drug interactions and their impact on various organ systems should be considered preoperatively. Regional anesthesia is often the technique of choice. Yet, one must consider the presence of neuropathies, local infection or blood clotting abnormalities.

Anesthesiologists must be familiar with this disease, and prenatal anesthesia consultations and a team approach will optimize treatment for the pregnant woman with HIV.


    References
 Top
 Abstract
 Introduction
 Conclusions
 References
 

  1. UNAIDS. Report on global HIV/AIDS epidemic. Geneva: UNAIDS, 2002.
  2. DeCock KM, Janssen RS. An unequal epidemic in an unequal world. JAMA 2002; 288: 236–8.[Free Full Text]
  3. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines. MMWR Morb Mortal Wkly Rep 2002;51:RR-6. Available online at http://www.cdc.gov/std/treatment/TOC2002TG.htm.
  4. DeCock KM, Fowler MG, Mercier G, et al. Prevention of mother-to-child transmission in resource-poor countries. JAMA 2000; 283: 1175–82.[Abstract/Free Full Text]
  5. Eichler A, Eiden U, Kessler P. AIDS and anesthesia. Anaesthetist 2000; 49: 1006–17.[ISI][Medline]
  6. Feinberg MB, Greene WC. Molecular insights into human immunodeficiency virus type 1 pathogenesis. Curr Opin Immunol 1992;4:466–74. Review. In: Sande MA, Volbording PA, editors. The medical management of AIDS. 5th ed. Philadelphia: WB Saunders, 1997: 17–28.
  7. Ho DD. Viral counts in HIV infection. Science 1996; 272: 1124–5.[ISI][Medline]
  8. Demeter LA, Reicman RC. Detection of human immunodeficiency virus infection. In: Mandell GL, Bennett JE, Dolin R, eds. Mandel, Douglas and Bennett’s principals and practice of infectious disease. 5th ed. Philadelphia: Churchill Livingstone, 2000: 1369–74.
  9. Zijenah LS, Humprey J, Nathoo K. Evaluation of prototype Roche DNA amplification kit incorporation the new SSK 145 and SKCC1B primers in detection of human immunodeficiency virus type 1 DNA in Zimbabwe. J Clin Microbiol 1999; 37: 3569–71.[Abstract/Free Full Text]
  10. Saag MS. Quantitation of HIV viral load: a tool for clinical practices. In: Sande MA, Volberding PA, eds. The medical management of AIDS. 5th ed. Philadelphia: WB Saunders, 1997: 57–74.
  11. Price RW. Understanding the AIDS dementia complex (ADC). The challenge of HIV and its effects on the central nervous system. Res Pub Assoc Res Nerv Ment Dis 1994; 72: 1–45.
  12. Miller LG, Galpern WR, Dunlap K, et al. Interleukin-1 augments gamma-aminobutyric acid-A4 receptor function in brain. Mol Pharmacol 1991; 39: 105–8.[Abstract]
  13. Wulff EA, Wang AK, Simpson DM. HIV-associated peripheral neuropathy, epidemiology, pathophysiology and treatment. Drugs 2000; 59: 1251–60.[ISI][Medline]
  14. Villa A, Foresti V, Confa lonieri F. Autonomic nervous system dysfunction associated with HIV infection in intravenous heroin users. AIDS 1992; 6: 85–9.[ISI][Medline]
  15. Stansell JD, Huang L. Pneumocystis carinii pneumonia. In: Sande MA, Volberding PA, eds. The medical management of AIDS. 5th ed. Philadelphia: WB Saunders, 1997: 275–300.
  16. Wachter RM, Russi MB, Block DA, et al. Pneumocystis carinii pneumonia and respiratory failure in AIDS: improved outcome and increased use of intensive care units. Am Rev Respir Dis 1991; 143: 251–6.[ISI][Medline]
  17. Opravil M, Marincek B, Fuchs WA, et al. Shortcomings of chest radiography in detecting Pneumocystis carinii pneumonia. J Acquir Immune Defic Syndr 1994; 7: 39–45.
  18. Thillagavathie P. Current issues in maternal and perinatal tuberculosis: impact of the HIV-1 epidemic. Semin Neonatol 2000; 5: 189–96.[Medline]
  19. Rerkpattanapipat P, Wongprapanut N, Jacobs LE, et al. Cardiac manifestations of acquired immunodeficiency syndrome. Arch Intern Med 2000; 160: 602–8.[Abstract/Free Full Text]
  20. Lipshultz SE. Dilated cardiomyopathy in HIV infected patients. New Engl J Med 1998; 339: 1153–5.[Free Full Text]
  21. Mesa RA, Edell ES, Dunn WF, et al. Human immunodeficiency virus infection and pulmonary hypertension. Mayo Clinic Proc 1998; 73: 37–45.[ISI][Medline]
  22. Yanovsk JA, Miller KD, Kino T, et al. Endocrine and metabolic evaluation of human immunodeficiency virus infected patients with evidence of protease inhibitor-associated lipodystrophy. J Clin Endocrinol Metabol 1999; 84: 1925–31.[Abstract/Free Full Text]
  23. Ammatuna P, Campisi G, Giovannelli L, et al. Presence of Epstein-Barr virus, cytomegalovirus and human papillomavirus in normal oral mucosa of HIV infected and renal transplant patients. Oral Dis 2001; 7: 34–40.[ISI][Medline]
  24. Cello JP. Gastrointestinal tract manifestations of AIDS. In: Sande MA, Volberding PA, eds. The medical management of AIDS. 5th ed. Philadelphia: WB Saunders, 1997; 181–95.
  25. Hambleton J. Hematologic manifestations of HIV infection. In: Sande MA, Volberding PA, eds. The medical management of AIDS. 5th ed. Philadelphia, WB Saunders, 1997; 239–46.
  26. Saif MW, Greenberg B. HIV and thrombosis: a review. AIDS Patient Care STDS 2001; 15: 15–24.[ISI][Medline]
  27. Kimmel PL. The nephropathies of the infection: pathogenesis and treatment. Curr Opin Nephrol Hypertension 2000; 9: 112–22.
  28. Betjes MG, Weening J, Krediet RT. Diagnosis and treatment of the HIV-associated nephropathy. Neth J Med 2001; 59: 111–7.[ISI][Medline]
  29. Tanji N, Tanji K, Kabhan N, et al. Adefovir nephrotoxicity: possible role of mitochondrial DNA depletion. Human Pathol 2001; 32: 734–40.[ISI][Medline]
  30. Saltel E, Angel JB, Futter NG, et al. Increased prevalence and analysis of risk factors for indinavir nephrolithiasis. J Urol 2000; 164: 1895–7.[ISI][Medline]
  31. Eledrisi MS, Verghese AC. Adrenal insufficiency in HIV infection: a review and recommendations. Am J Med Sci 2001; 321: 137–44.[ISI][Medline]
  32. HIV and AIDS—United States, 1981–2001. MMWR Morb Mortal Wkly Rep 2001; 50: 430–4.[Medline]
  33. Mofenson LM. A critical review of studies evaluating the relationship of role of delivery to prenatal transmission of human immunodeficiency virus. Pediatr Infect Dis J 1995; 14: 169–77.[ISI][Medline]
  34. International Prenatal HIV Group. The mode of delivery and the risk of delivery and the risk of vertical transmission of human immunodeficiency virus type 1. A meta-analysis of 15 prospective cohort studies. N Engl J Med 1999; 340: 977–87.[Abstract/Free Full Text]
  35. Mandelbrot L, Le Chanadee J, Berrebi A, et al. Prenatal HIV-1 transmission and interaction between zidovudine prophylaxis and mode of delivery in the French Prenatal Cohort. JAMA 1998; 280: 55–60.[Abstract/Free Full Text]
  36. American College of Obstetricians and Gynecologists. ACOG committee opinion 234: scheduled cesarean delivery and the prevention of vertically transmitted HIV infection. Washington, DC: American College of Obstetricians and Gynecologists, 2000.
  37. Rowland BL, Vermillion ST, Soper DE. Scheduled cesarean delivery and the prevention of human immunodeficiency virus transmission: a survey of practicing obstetricians. Am J Obstet Gyncol 2001; 185: 327–31.[ISI][Medline]
  38. Montesinos VM, Sanchez JC, et al. Post-cesarean section morbidity in HIV-positive women. Acta Obstet Gynecol Scand 1999; 78: 789–92.[ISI][Medline]
  39. Semprini AE, Catagre C, Rarizza M, et al. The incidence of complications after caesarean section in HIV-positive women. AIDS 1995; 9: 913–7.[ISI][Medline]
  40. CDC Report regarding selected public health topics affecting women’s health. Successful implementation of prenatal HIV prevention guidelines: a multistate surveillance evaluation. MMWR Morb Mortal Wkly Rep 2001; 50: RR-6.
  41. Newell ML, Thorne C. Pregnancy and HIV infection in Europe. Acta Paediat Suppl 1997; 421: 10–4.
  42. Taylor GP, Low-Beer N. Anti retroviral therapy in pregnancy: a focus on safety. Drug Saf 2001; 24: 683–702.[ISI][Medline]
  43. Guidelines for the use of antiretroviral agents among HIV-infected adults and adolescents. MMWR Morb Mortal Wkly Rep 2002; 51: RR-07.
  44. Hughes SC, Daily PA. Human immunodeficiency virus in the delivery suite. In: Hughes SC, Levinson G, Rosen MA, Shnider SM, eds. Shnider and Levinson’s anesthesia for obstetrics. 4th ed. Philadelphia: Lippincott, Williams & Wilkins, 2002: 583–95.
  45. Blum AS, Dal Pan GJ, Feinberg J, et al. Low dose zalcitabine-related toxic neuropathy: frequency, natural history and risk factors. Neurology 1966; 46: 999–1003.
  46. Cupler EJ, Dalakas MC. Exacerbation of peripheral neuropathy by lamivudine. Lancet 1995; 345: 460–1.
  47. Markus R, Brew BJ. HIV-1 peripheral neuropathy and combination antiretroviral therapy. Lancet 1998; 352: 1906–7.[ISI][Medline]
  48. Report of the NIH panel to define principles of therapy of the infection and guidelines for the use of antiretroviral agents in HIV-infected adults and adolescents. MMWR Morb Mortal Wkly Rep 1998; 47(No RR-5): 1–38.[Medline]
  49. Viramune (Nevirapine) in Physician’s Desk Reference. 52nd ed. Montvale, NJ: Medical Economics, 1998: 2559–62.
  50. Deeks SG. Practical issues regarding the use of antiretroviral therapy for HIV infection. West J Med 1988; 168: 133–9.
  51. Olkkola KT, Palkama VJ, Neuvonen PJ. Ritonavir’s role in reducing fentanyl clearance and prolonging its half-life. Anesthesiology 1999; 91: 681–5.[ISI][Medline]
  52. Guitton J, Buronfosse T, Desage M, et al. Possible involvement of multiple cytochrome P450S in fentanyl and sufentanil metabolism as opposed to alfentanil. Biochem Pharmacol 1997; 53: 1613–9.[ISI][Medline]
  53. Farizo KM, Buehler JW, Chamberland ME, et al. Spectrum of disease in persons with human immunodeficiency virus in United States. JAMA 1992; 267: 1798–805.[Abstract]
  54. Bryant H, Bernton E, Haladay J. Immunosuppressive effects of chronic morphine treatment in mice. Life Sci 1992; 41: 1731–8.
  55. Birnbach DJ, Bourlier RA, Choi R, Thys DM. Anesthetic management of caesarean section in patient with active recurrent genital herpes and AIDS-related dementia. Br J Anaesth 1995; 75: 639–41.[Abstract/Free Full Text]
  56. Singh U, Rocke DA. Acquired immunodeficiency syndrome and obstetric anesthesia. In: Birnbach DS, Gatt SP, Datta S, eds. Textbook of obstetric anesthesia. Philadelphia: Churchill Livingstone, 2000: 668–82.
  57. Thurnher MM, Post MJ, Jinkins JR. MRI of infections and neoplasm of the spine and spinal cord in 55 patients with AIDS. Neuroradiology 2000; 42: 551–63.[ISI][Medline]
  58. Baraka AS, Jalbout MI. Anesthesia and myopathy. Curr Opin Anesth 2002; 15: 371–6.
  59. Avidan MS, Groves P, Blott N, et al. Low complication rate associated with cesarean section under spinal anesthesia for HIV-1 infected women on antiretroviral therapy. Anesthesiology 2002; 97: 320–4.[ISI][Medline]
  60. Sahai J. Risks and synergies from drug interaction. AIDS 1996; 10 (Suppl 1): S21–5.
  61. Gershon RY, Manning-Williams D. Anesthesia and the HIV-infected parturients: a retrospective study. Int J Obstet Anesth 1997; 6: 76–81.
  62. Kern JMcD, Gray BB. AIDS litigation for the primary care physician. In: Sade MA, Volberding PA, eds. The medical management of AIDS. 3rd ed. Philadelphia: WB Saunders, 1992: 477–83.
  63. Tom DJ, Gulevich SJ, Shapiro HM, et al. Epidural blood patch in the HIV positive patient: review of clinical experience. Anesthesiology 1992; 76: 943–7.[ISI][Medline]
  64. Wlody DJ. Human immunodeficiency virus. In: Chestnut DH (ed). Obstetric anesthesia principles and practice. 2nd ed. St Louis: Mosby, 1999: 860–74.
  65. Broner FA, Garland DE, Zigler JE. Spinal infections in the immunocompromised host. Orthop Clin North Am 1996; 27: 37–46.[ISI][Medline]
  66. Savioz D, Chilcott M, Ludwig C, et al. Preoperative counts of CD4 T-lymphocytes and early post-operative infective complications in HIV-positive patients. Eur J Surg 1998; 161: 483–7.
  67. Du Pen SL, Peterson DG, Williams A, Bogosian AJ. Infection during chronic epidural catheterization: diagnosis and treatment. Anesthesiology 1990; 73: 905–9.[ISI][Medline]
Accepted for publication September 8, 2003.





This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Evron, S.
Right arrow Articles by Ezri, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Evron, S.
Right arrow Articles by Ezri, T.
Related Collections
Right arrow Obstetrics
Right arrow Pain


Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press