Anesthesiology Clin N Am

22 (2004) 379 – 404

HIV and anesthesia

Samuel C. Hughes, MDa,b,*
a
Department of Anesthesia and Perioperative Care, University of California – San Francisco,
San Francisco, CA, USA
b
Department of Anesthesia, San Francisco General Hospital, Room 3C-38, 1001 Potrero Avenue,
San Francisco, CA 94110, USA

HIV is a newly recognized microbe that was not discovered until the 1980s
[1]. This compares, for example, with centuries of concern for smallpox. HIV
infection is responsible for AIDS, a disease that crept quietly and unnoticed into
our nation’s health sometime in the late 1970s [2]. The first reported description,
in 1981 [3], went virtually unnoticed by most physicians but was, in fact, the
herald for the greatest health crisis of the late twentieth and early twenty-first
century. On a global basis, 40 million people (34 –46 million) were living with
HIV/AIDS by the end of 2003 with 5 million new cases that year (Fig. 1) [4,5].
Although 4.2 million (3.6 – 4.8 million) of the newly infected persons were
adults, as many as 810,000 were children under the age of 15. In sub-Saharan
Africa, the AIDS epidemic appears to rival the Bubonic plague, or ‘‘pestilence,’’
as it was referred to in England circa 1348 – 1349. This was later referred to as
the ‘‘Black Death’’ and it has been called the greatest biomedical disaster in
European history [2,6]. It is estimated that the pestilence caused the deaths of
20 million people, or 30% to 50% of the total population in many parts of
Europe. In some regions of Africa, the AIDS epidemic may be approaching the
magnitude of this historic catastrophe (Table 1). In the United States and Western
Europe, the epidemic, while tragically real, does not approach the sub-Saharan
experience. However, most anesthesiologists will care for HIV-positive patients
at some time, regardless of where they practice. They will need to learn about a
disease that ‘‘didn’t exist’’ when many of them were trained. Certainly, the last
6 to 10 years have seen great advancement in the understanding and successful
treatment and therapy of this disease. This has meant that patients are living much
longer and will need advanced medical and surgical care. It has been estimated
that 20% to 25% of HIV-positive patients will require surgery during their illness

* Department of Anesthesia, San Francisco General Hospital, Room 3C-38, 1001 Potrero Avenue,
San Francisco, CA 94110.
E-mail address: hughess@anesthesia.ucsf.edu

0889-8537/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.atc.2004.06.001
380 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

Eastern Europe
Western Europe & Central Asia
North America
600 000 1.5 million
995 000 East Asia & Pacific
North Africa
Caribbean & Middle East South 1 million
470 000 & South-East Asia
600 000
6.4 million
Sub-Saharan
Latin America Africa Australia
1.6 million & New
26.6 Zealand
million 15 000

Total: 40 million
New Infections, Adults & Children, 2003: 5 million

Fig. 1. Regional incidence of adults and children estimated to be living with HIV/AIDS as of the end
of 2003. The data are from the Joint United Nations Program on HIV/AIDS (UNAIDS) and the World
Health Organization. Updated information can be obtained from http://www.unaids.org. (Reprinted
from Joint United Nation Program on HIV/AIDS (UNAIDS): AIDS Epidemic Update. Geneva
(Switzerland): World Health Organization; 2003; with permission.)

[7]. Many patients are unaware of their HIV infection, and because the disease is
increasingly being spread through heterosexual contact, it is the rare operating
suite that will not care for HIV-positive patients over time (Fig. 2) [8].
In the United States, there have been 886,575 cases of AIDS reported to the
Centers for Disease Control and Prevention (CDC) as of December 2002, with
501,669 deaths [9]. Although the true number of new HIV infections each year
is unknown, it was estimated that there were 42,136 new cases in 2002. The
estimates of persons living with HIV in the United States range anywhere
from 850,000 to 950,000 [4] to well over 1 million cases, with as many as
200,000 people or more being unaware of their infection.
Deaths from AIDS are now declining in the United States [10] with a clear
link to antiretroviral therapy (Fig. 3) [11]. However, between 1982 and 1994 HIV
infections went from not being mentioned to being the leading cause of death
among persons 25 to 44 years of age. Although HIV infection is no longer the
leading cause of death in this age group, the CDC has estimated that half of the
new infections occur in people under 25 years of age, with 70% of AIDS cases
being diagnosed in persons aged 25 to 44 years of age. The infection among
heterosexual men and women has obvious implications for labor and delivery
suites as well as operating rooms throughout the United States.

Populations at risk
The transmission of HIV varies greatly in different populations. In the
developing world and in the United States, treatment of sexually transmitted
Table 1
Regional HIV/AIDS statistics and features, end of 2003
Percentage of Main modes of
Adults and children Adult HIV-positive transmission for Adult and child
Start of Adults and children newly infected prevalence adults who are persons living deaths due to
epidemic living with HIV/AIDS with HIV ratea women with HIV/AIDS AIDS

S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

Sub-Saharan Africa Late 1970s to 25.0 – 28.2 million 3.0 – 3.4 million 7.5 – 8.5 58% Hetero 2.2 – 2.4 million
early 1980s
North Africa and Middle East Late 1980s 470,000 – 730,000 43,000 – 67,000 0.2 – 0.4 55% Hetero, IDU 35,000 – 50,000
South and Southeast Asia Late 1980s 4.6 – 8.2 million 610,000 – 1.1 million 0.4 – 0.8 36% Hetero, IDU 330,000 – 590,000
Eastern Asia and Pacific Late 1980s 700,000 – 1.3 million 150,000 – 270,000 0.1 – 0.1 24% IDU, Hetero, 32,000 – 58,000
MSM
Latin America Late 1970s to 1.3 – 1.9 million 120,000 – 180,000 0.5 – 0.7 30% MSM, IDU, 49,000 – 70,000
early 1980s Hetero
Caribbean Late 1970s to 350,000 – 590,000 45,000 – 80,000 1.9 – 3.1 50% Hetero, MSM 30,000 – 50,000
early 1980s
Eastern Europe and Early 1990s 1.2 – 1.8 million 180,000 – 280,000 0.5 – 0.9 27% IDU 23,000 – 37,000
Central Asia
Western Europe Late 1970s to 520,000 – 680,000 30,000 – 40,000 0.3 – 0.3 25% MSM, IDU 2600 – 3400
early 1980s
North America Late 1970s to 790,000 – 1.2 million 36,000 – 54,000 0.5 – 0.7 20% MSM, IDU, 12,000 – 18,000
early 1980s Hetero
Australia and New Zealand Late 1970s to 12,000 – 18,000 700 – 1,000 0.1 – 0.1 7% MSM <100
early 1980s
Total 40 million 700 – 1,000 1.1% 1.2 3 million
[34 – 46 million] [0.9 – 1.3] [2.5 – 3.5 million]
Abbreviations: Hetero, heterosexual contact; IDU, intravenous drug use; MSM, men who have sex with men.
a
The proportion of adults (15 – 49 years of age) living with HIV/AIDS in 2003, using 2003 population numbers. The ranges around the estimates in this table define
the boundaries within which the actual numbers lie, based on the best available information. These ranges are more precise than those of previous years, and work is under
way to increase even further the precision of the estimates that will be published mid-2004. (Data from Joint United Nation Program on HIV/AIDS (UNAIDS): AIDS

381
epidemic update. Geneva (Switzerland): World Health Organization; 2003.)
382 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

Fig. 2. Estimated rates for adults and adolescents living with HIV infection or AIDS (per 100,000
population) in the United States in 2002. Rates have been adjusted for reporting delays. Rates of HIV
infection include only persons living with HIV infection that has not progressed to AIDS. Rates are
calculated for the following areas that have laws or regulations requiring confidential name-based
HIV infection reporting since 1998: Alabama, Arizona, Arkansas, Colorado, Florida, Idaho, Indiana,
Iowa, Louisiana, Michigan, Minnesota, Mississippi, Missouri, Nebraska, Nevada, New Jersey, New
Mexico, North Carolina, North Dakota, Ohio, Oklahoma, South Carolina, South Dakota, Tennessee,
Utah, Virginia, West Virginia, Wisconsin, Wyoming, and the US Virgin Islands. (Reprinted from
Centers for Disease Control and Prevention. Cases of HIV infections and AIDS in the United States,
2002. HIV AIDS Surveill Rep 2002;14:1 – 40.)

diseases in women has been shown to significantly decrease HIV transmission

[12]. In Northern Europe and the United Kingdom, HIV infection remains
predominately a disease of homosexual men [13]. In Spain and Italy and parts
of Eastern Europe, HIV infection is closely linked with intravenous drug abuse,
not unlike many urban centers in the United States [14,15]. However, in an
analysis in 2004 from the 29 states that have mandatory HIV infection reporting,
heterosexually acquired HIV infection disease represented 35% of all new HIV
cases. Nearly two thirds (64%) of these cases were women [16]. For women in
the United States in 2002, injection-drug use accounted for approximately 30% of
the AIDS incidence, while heterosexual contact accounted for 68% of the cases
[9]. In Central Africa, where more than 30% of women delivering in some urban
centers are HIV positive, HIV is predominately a heterosexual disease (Fig. 4)
[17]. Although sub-Saharan Africa currently has the greatest number of persons
with the disease, the growth of the epidemic in developing countries, particularly
Southeast Asia and the Indian subcontinent, is extremely rapid. In Thailand, the
spread of HIV is linked to both drug abuse and heterosexual spread. In 1987, very
little HIV was detected, but by 1995, one out of every 80 people in the popula-
 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404 383

90,000 Newly diagnosed AIDS cases 1993 Definition

Deaths Implementation
80,000 Persons living with AIDS

No. of persons living with AIDS

No. of cases and no. of deaths

70,000

60,000

50,000

40,000

30,000

20,000

10,000

0
1986 1988 1990 1992 1994 1996 1998 2000 2002
Year

Fig. 3. AIDS cases and deaths and persons living with AIDS in the United States by year (1985 –
2002). This figure demonstrates the significant decline in newly diagnosed cases of AIDS in the United
States, as well as the dramatic decline in deaths from HIV/AIDS. This has lead to a greatly increased
number of people living with AIDS. Data have been adjusted for reporting delays. (Reprinted from
Centers for Disease Control and Prevention. Cases of HIV infections and AIDS in the United States,
2002. HIV AIDS Surveill Rep 2002;14:1 – 40.)

tion were infected. This rate is three to five times higher than the rate in the
United States and it occurred in only a very few years. Thailand’s 100% condom
use program has reined in the epidemic recently with the prevalence of infection
hovering around 2% in 2002. Among 21-year-old military conscripts, the
prevalence has dropped from a high of 4% to less than 1% in 2002. India and
China, however, have significant problems that are only now unfolding, and the
extent of the spread of HIV infection remains to be seen. Some estimates suggest
that there are 10 million infections in India presently, and if left unchecked, they
could have 25 million cases of HIV infection by 2010. It is believed that 80% of
the infections are transmitted through heterosexual contact. Sadly, despite the
distribution of free drugs in some areas, relatively few patients will be treated
(Kaiser Family Foundation, Sabin Russell, April 2004).
Anesthesiologists are now faced with a complex disease that only appeared in
the literature in 1981 and couldn’t be definitively diagnosed until 1985 [3].
Although the death rates are declining because of a better understanding of the
disease and because of aggressive drug therapy, the clinician needs to understand
the disease, numerous new drug therapies and drug interactions, opportunistic
and associated infections, and infection control techniques. With this knowledge,
the anesthesiologist can plan for anesthetic intervention for surgery, as well as
labor and delivery and other areas of our practice. The ever-increasing therapeutic
pharmacologic interventions must be taken into particular consideration. Oppor-
384 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

40

35

30
HIV prevalence (%)

25

20

15

10

0
1986 1988 1990 1992 1994 1996 1998 2000 2002

Source: National AIDS Programmes (partly compiled by the US Census Bureau)

Fig. 4. Stable HIV prevalence among pregnant women in selected urban areas in Africa (1985 – 2002).
The high infection rate in some urban African centers is shown. Not shown is KwaZula-Natal, South
Africa, where the HIV prevalence among antenatal clinic attendees is 37%. This contrasts with success
in Uganda, where the rate is now 8% versus the 30% figure in two urban clinics a decade ago.
(Reprinted from Joint United Nation Program on HIV/AIDS (UNAIDS): AIDS epidemic update.
Geneva (Switzerland): World Health Organization; 2003; with permission.)

tunistic infection remains a problem with tuberculosis a particular concern [18].

This article focuses on these issues and related concerns in the operating room, as
well as the obstetric suite, which are now a common interface with the HIV-
positive patient.

HIV infection
HIV-1 is a retrovirus and a single-strand RNA virus. After entering the cell,
the virus is copied by a reverse transcriptase; this enables the virus to produce
double-strand DNA, which then integrates into the host’s cells. HIV-2 is a similar
virus that produces AIDS as well. This virus is common in western Africa but is
rarely seen in the United States (in this article, HIV refers to HIV-1). The most
common mode of infection is sexual transmission through the genital mucosa
[19]. Within 2 days the virus can be detected in the internal iliac lymph nodes,
and within 5 days (4 –11 days) the virus can be cultured from the plasma. There is
a rapid rise in plasma viremia at this point that spreads to lymphoid organs and
the brain [20]. The CD4+ T lymphocytes (CD4+ cells) are infected early in the
course of the disease, and the remaining cell count per cubic millimeter helps
define the disease progression. The decline of the CD4+ cell count marks HIV
progression from the initial infection. Plasma viral load (which can be quanti-
tated) is initially extremely high, then declines in the clinical latency period. As
 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404 385

constitutional symptoms and opportunistic infections occur (usually 6– 12 years

after infection), viral load again increases in the terminal patient. Because of the
high viral load, patients who have an acute infection are extremely infectious, as
are those in the late stages of the disease.
Acute infection is a transient, symptomatic illness with symptoms including
fever, fatigue, rash, headache, lymphadenopathy, pharyngitis, myalgia or arthral-
gia and nausea, vomiting, and diarrhea. In two studies, 87% of a group of newly
infected patients had acute symptoms and 95% sought medical evaluation
[20,21]. The viral half-life is approximately 6 hours and the turnover may be
as high as l billion per day. It has been said that HIV is ‘‘the fastest genome
evolution ever described’’ [22]. Although the virus may remain seemingly
innocuous for 10 years or more in some individuals, ultimately a rising viral
count, extreme compromise of the immune system, and a CD4+ cell count of
fewer than 200 cells/mL heralds the final stages, and the clinical diagnosis of
AIDS is made with the occurrence of one of the index conditions (Box 1). A
CD4+ cell count of fewer than 200 cells/uL puts the patient at significant risk for
opportunistic infections and likely greater risk during surgery. A study in 1992
suggested a mortality rate of 6 months postoperatively of 13.3% if the CD4+ cell
count was fewer than 50 cells/mL versus a 0.8% mortality rate if the count was
fewer than 200 cells/mL [23]. Although a lower cell count clearly relates to the
gravity of the disease and should alert the anesthesiologist to be vigilant, it is
doubtful that the numbers quoted are relevant today with aggressive antiviral
therapy and good medical care.

HIV Disease: general considerations

HIV disease is a complex medical disorder that has wide systemic expression
and results in multiorgan disease (Box 2). These problems are well described and
the management of the HIV-seropositive patient has, in effect, become a medical
subspecialty [24]. The neurologic, pulmonary, cardiovascular, and hematologic
changes and abnormalities are of particular concern to anesthesiologists.

Neurologic involvement
Neurologic involvement begins within days of the initial infection [20] and
when HIV has been isolated from the cerebrospinal fluid (CSF) during primary
infection [25]. There are indications of the cellular immune system activation in
the central nervous system (CNS), even in the absence of obvious neurologic
symptoms or signs. Acute encephalitis has been reported with primary infection
but seems uncommon. However, conditions reported with acute infection include:
myelopathy, peripheral neuropathy, brachial neuritis, cauda equina syndrome,
and Guillain-Barré syndrome [26]. It is not known what determines the extent of
neurologic involvement. However, it is speculated that particular strains of the
virus are neurotropic or monocytotropic and thus more likely to cause unique
neurologic involvement. The latent phase of the disease appears marked by an
386 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

Box 1. Index conditions for the diagnosis of AIDS in HIV-positive

patients
 Bacterial infection, multiple or recurrent
 Candida of the bronchi, trachea, lungs, or esophagus
 CD4+ T-lymphocyte count <200 cells/ML
 Cervical cancer, invasive
 Coccidioidomycosis, disseminated or extrapulmonary
 Cryptococcosis, extrapulmonary
 Cryptosporidiosis, chronic intestinal (>1 month)
 Cytomegalovirus other than liver, spleen, lymph nodes
 Cytomegalovirus retinitis or CMV (with loss of vision)
 Herpes simplex virus with chronic ulcers (>1 month),
bronchitis, pneumonitis, esophagitis
 HIV-related encephalopathy
 Histoplasmosis, diseminated or extrapulmonary
 Isophoriasis, chronic intestinal (>1 month)
 Kaposi’s sarcoma
 Burkitt’s lymphoma
 Immunoblastic lymphoma
 Lymphoma of the brain, primary
 Mycobacterium avium complex or kansasii, disseminated
or extrapulmonary
 Mycobacterium tuberculosis, any site
 Mycobacterium, any other species, pulmonary
or extrapulmonary
 Pneumocystis carinii pneumonia
 Pneumonia, recurrent
 Progressive multifocal leukoencephalopathy
 Recurrent Salmonella septicemia
 Toxoplasmosis of the brain
 Wasting syndrome due to HIV

CDC 1993 revised classification system for HIV infection (defi-

nition became effective in January 1993). MMWR 1992;41:RR-17.
Index clinical conditions remain as listed in December 1999.

autoimmune process triggered by HIV. Demyelinating neuropathies that resemble

subacute Guillain-Barré syndrome or chronic inflammatory demyelinating poly-
neuropathy may be seen. They may respond to corticosteroids, plasmapheresis, or
intravenous immunoglobulin [27].
The later stages of the disease lead to severe immunologic compromise and a
wide variety of infectious or opportunistic infections. Meningitis is frequent with
cryptococcal infection, a common source, but tuberculosis and syphilitic menin-
 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404 387

Box 2. Complications of HIV multiorgan disease

Respiratory
 Pneumocystis carinii
 Bacterial pneumonia
 Tuberculosis
 Aspergillosis
 Cytomegalovirus
 Oral/pharyngeal candidiasis, herpetic infections

Hematologic
 Leukopenia, lymphopenia
 Thrombocytopenia
 Anemia
 Drug toxicity, bone marrow suppression

Cardiac
 Pericarditis effusion
 Pericarditis
 Myocarditis (late stages of infection)
 Dilated cardiomyopathy
 Endocarditis (intravenous drug abuse)
 Pulmonary hypertension
 Drug-related cardiotoxicity
 Thromboembolitic events
 Myocardial infarction

Gastrointestinal
 Infectious diarrhea, proctitis
 Gastrointestinal bleeding
 Acalculous cholecystitis
 Vomiting, loss of appetite, cachexia
 Dysphagia (Candida albicans, cytomegalovirus), esophagitis
 Liver disease, hepatitis B and C, other infections

Neurologic problems in AIDS patients

 Distal, symmetrical sensory neuropathy: numbness, tingling,
painful dysesthesias and paresthesias
 Chronic, inflammatory demyelinating polyneuropathy
388 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

 AIDS encephalopathy or AIDS dementia complex: cognitive,

motor, and behavioral changes
 Vacuolar myelopathy: sensory disturbance, spasticity and hy-
perreflexia (acute or chronic progression)
 Segmental (focal) myelopathy, acute or subacute
(less common)
 Opportunistic infections or malignancies, including: toxoplas-
mosis, cryptococcal meningitis, progressive multifocal leuko-
encephalopathy, cytomegalovirus, herpes symplex virus, brain
lymphomas, or tuberculous lesions

gitis are possible. The infectious nature of CSF in the HIV-infected patient must
always be considered. Early in the epidemic, brain biopsies were frequently
performed to diagnosis possible tuberculosis lesions versus toxoplasmosis or
CNS lymphomas. Currently, these are most often diagnosed without surgery but
demonstrate the extent of potential neurologic involvement of the CNS, particu-
larly in the late stages of the disease.

Pulmonary complications
Pulmonary complications are largely related to infectious agents. The epi-
demic began with an obscure report of four homosexual men who had Pneumo-
cystis carinii, which seemed like only a medical curiosity at the time [3]. In 1992,
P carinii pneumonia was the cause of death in 14% of patients, while another
18% died of an unspecified pneumonia [28]. However, deaths from P carinii
have declined from the 33% reported in 1987 and continue to decrease with drug
prophylaxis to prevent infection and with advances in the management of HIV.
However, tuberculosis, aspergillosis, and numerous bacterial organisms are
frequently causes of pulmonary complications. Outbreaks of tuberculosis have
occurred in the United States that were related to HIV disease [29], and HIV
disease and tuberculosis will remain significantly linked epidemics well into the
future, particularly in the developing world [18,30]. This is also a significant
problem in the homeless population in the United States.

Cardiovascular system
Patients who have HIV infections are living longer, and the extent of
involvement of the cardiovascular system is increasingly apparent [31 – 33]. This
involvement is multifactorial in origin and includes chronic viral infection,
coinfection, drug therapy, and immunosuppression, all of which affect the heart.
AIDS is an increasingly recognized cause of—or is strongly associated with—
cardiomyopathy, pulmonary hypertension, right ventricular dysfunction, myocar-
ditis, pericardial effusion, and many coronary artery diseases [34,35]. In clinical-
 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404 389

pathologic studies in the pre-HAART (highly active antiretroviral therapy) time

period, dilated cardiomyopathy was described in 30% to 40% of AIDS patients
with an estimated annual rate of 15.9/1000 [36,37]. In pooled autopsy data in
Italy, of 440 patients who died of complications from HIV infection, documented
dilated cardiomyopathy was found in 2.7% of patients, while 14.6% of patients
were found to have had cardiovascular disease [38]. Pulmonary hypertension
(PH) is a rare but serious complication, with 10 cases reported in one series [35].
The incidence has been estimated at approximately 1/200, which is dramatically
higher than the incidence of 1/200,000 found in the general population [39,40].
Mehta and colleagues [41] reviewed a series of 131 cases of HIV-related PH
recently. The causes may be similar to that of the sporadic form of PH or the
familial form that is remodeling in the media and adventitia of the pulmonary
arterial tree, the extracellular matrix, and the plexiform lesions [35]. The
prognosis of patients who have HIV-related PH is very poor and quite similar
to other patients who have PH. The hemodynamic burden is the major de-
terminant of prognosis of the patient who has HIV-related PH. It is unclear if
better management of HIV disease will alter development of PH or the outcome.
Familial PH is related to a mutation of the BMPR2 gene [42]; a genetic marker
that increases the risk for PH in the HIV-infected patient may be found, which
would allow for screening and perhaps better management.
Myocarditis has been commonly associated with HIV infection and was found
in 40% to 52% of patients who died of HIV in a large pathologic study [38].
Unfortunately, no specific organism was found in more than 80% of patients, but
in others, Toxoplasma gondii, Cryptococcal neoformans, Myobacterium tuber-
culosis, and other organisms were found. Pericardial effusions were estimated to
have occurred in 11% of asymptomatic AIDS patients before the introduction of
HAART, but this therapy has significantly reduced the incidence.
Finally, although treatment may decrease some cardiac manifestations of HIV
disease, coronary artery disease is increasing with the present management.
Antiretroviral therapy commonly causes dyslipidemia in HIV-infected patients.
This response is quite common and often severe and has an atherogenic profile. It
is likely affected by the underlying host genetic predisposition to dyslipidemia.
The end result of antiretroviral therapy is an increase in low-density lipoprotein
cholesterol and a decrease in high-density lipoprotein cholesterol with an increase
of triglycerides. The latter may be dramatically increased. The protease inhibitors
seem to be most closely associated with dyslipidemias. Thus, it is not surprising
that HAART has been significantly associated with myocardial infarction, and
patients on this therapy are at a unique risk for major cardiovascular disease
despite their often relatively young age.
Hematologic abnormalities occur with acute HIV infection and are indeed a
hallmark of the disease. A lymphocytosis composed of CD8+ T lymphocytes may
appear within 2 weeks of infection. Mild thrombocytopenia is common but not
clinically important [43]. However, Kaslow and colleagues noted that thrombo-
cytopenia occurred in 2.8% of patients with a CD4+ T cell count of more than
700 cells/mL, but this rate increased to 10.8% when cell counts decreased below
390 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

250 [44]. Thrombocytopenia may develop as the disease progresses because of a

variety of causes, such as HIV-related immune thrombocytopenia, retroviral
infection of megakaryocytes, or drug-induced thrombocytopenia [45]. The
antiretroviral drug, zidovudine (AZT) for example, can cause bone marrow sup-
pression. This is usually reversible if administration of the drug is stopped.

Vertical transmission: HIV infection from mother to infant

In the United States, HIV infection in newborns has undergone a dramatic
decline of more than 60% [46]. On a worldwide basis, however, as many as
600,000 infants may be infected with HIV each year during the perinatal period
[17,47]. Maternal – infant or vertical transmission is the primary means through
which children become infected with HIV. If untreated, 15% to 40% of infants
born to HIV-seropositive mothers will become infected in utero during labor or
delivery or while breastfeeding [48]. The risk of intrauterine infection is 4.4% and
may not be affected by maternal AZT therapy [49]. The intrapartum period
accounts for 60% of the risk of perinatal HIV transmission; the remainder is
through breastfeeding [50,51].
It has now been demonstrated that the maternal plasma HIV-1 RNA level is
the best predictor of the risk of perinatal HIV-1 transmission and that reducing
this level below 500 viral copies per mL will minimize this risk [52,53]. Breaks in
placental barrier, prolonged rupture of membranes (>4 hours), high cervicovagi-
nal viral load (may not correlate with systemic viral load), lack of AZT treatment,
and vaginal delivery lead to increased rates of vertical transmission [50 –55]. The
AIDS Clinical Trial Group Study 076 demonstrated a reduction in vertical
transmission of HIV from 25.5% to 8.3% with maternal AZT therapy [48,56].
The US Public Health Service Task Force issued recommendations to include the
use of zidovudine chemoprophylaxis to prevent perinatal transmission and to
offer the parturient antiretroviral therapy during pregnancy to treat the primary
infection [54]. Combination antiretroviral therapy (eg, zidovudine, lamivudine,
nelfinavir or indinavir, and other drugs as indicated) during pregnancy has
been successfully used and leads to a decreased viral load, increased CD4+
T lymphocyte cell count and lack of HIV vertical transmission [55]. Management
of HIV infection in the parturient has recently been thoroughly reviewed [57].
Shorter courses of zidovudine and nevirapine have been successfully tried and
may prove effective and more affordable in the developing world [58,59]
although development of viral resistance has occurred after brief therapy with
nevirapine and may put the mother at greater risk.

Drug therapy: side effects and drug interaction

The routine use of new, increasingly intensive antiretroviral therapies has led
to significant declines in morbidity and mortality in HIV disease (Fig. 3)
 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404 391

[9,11,60]. Data now suggests intensive combination drug therapy, including a

protease inhibitor, should be routine for patients with advanced disease. This is
commonly called HAART, highly active antiretroviral therapy [61,62]. However,
the potential for significant drug interactions is now quite clear.
There is an ever-increasing list of antiretroviral drugs available for the
management of HIV disease, each with unique side effects. The drugs fall into
four categories: nucleoside analog reverse transcriptase inhibitors, nonnucleoside
analog reverse transcriptase inhibitors, protease inhibitors, and the new category
of fusion inhibitors (Table 2).
Protease inhibitors have proven highly effective but also have wide-ranging
side effects. Hyperlipidemia, glucose intolerance, abnormal fat distribution and
high serum amniotransferase concentrations have been reported [63], but rarely
hepatitis. For example, the manufacturers’ drug inserts for the protease inhibitors
report hemorrhage in patients with hemophilia and drug therapy, but there is little
documented in the literature. While there are numerous other side effects, the
most important concern may be the inhibition of cytochrome P-450 (CYP) 3A4,
which is important for the metabolism of many drugs. It has been demonstrated
that ritonavir, a potent inhibitor of P-450 3A (CYP3A) and CYP2D6, signifi-
cantly inhibits the metabolism of fentanyl among volunteers receiving a brief
course of ritonavir (Fig. 5) [64]. Ritonavir reduced the clearance of fentanyl by
67%, from 15.6 ± 8.2 to 5.2 ± 2 mL
min 1
kg 1 ( P < .01). The results suggest a
strong interaction between ritonavir and fentanyl and indicate the need to modify
fentanyl, and likely other anesthetic dosing in these patients, at least when
ritonavir is initially used. The risk of respiratory depression over a longer period
after administration than would otherwise be expected after fentanyl administra-
tion seems likely, particularly with higher fentanyl doses. When even smaller
bolus doses of fentanyl are used, it is advisable to maintain respiratory monitoring
for a longer period than usual. Caution is urged when administering benzodia-
zepines and opioids to patients receiving protease inhibitors, but there is a paucity
of clinical data upon which to base firm recommendations. My experience,
however, suggests that with careful titration, routine drugs such as midazolam,
fentanyl, and morphine can be administered safely. Conversely, the US Food
and Drug Administration approval of the protease inhibitors was very rapid and
based on very little clinical experience, so clinicians must be alert to possible
unreported side effects, direct drug interactions, and other drug toxicities.
Ritonavir is now used in many HIV drug regimens (eg, ‘‘ritonavir-boosted’’)
precisely because of the potent inhibitory effect it has on the cytochrome
P-450 system. It has been shown to boost the effectiveness of other protease
inhibitors. However, as seen in Table 2, the potential drug interactions are
significant. This is likely, to some extent, with all the protease inhibitors, which
are mainstays of HAART.
Patients who are HIV-seropositive may be taking numerous other drugs for
prophylaxis or treatment of P carinii, tuberculosis, toxoplasmosis, mycobacterium
avium, fungal infection, or herpes simplex [65]. These drugs, as well as the use of
antiviral therapy, have led to a decrease in deaths from opportunistic infections.

Table 2
Antiretroviral drugs for management of HIV infection
Drug
Nucleoside/Nucleotide analogues
Abacavir (Ziagen)
Adefovir (Hepsera)
Didanosine (DDI, Videx)
Emtricitabine (Emtriva, FTC)
Lamivudine (3TC, Epivir)b
Stavudine (d4T, Zerit)
Tenofovir (Viread, PMPA)
Zalcitabine (ddC, HIVID)
Zidovudine (ZDV, AZT, Retrovir)b
Protease inhibitors
Amprenavir (Agenerase)
Atazanavir (Reyataz)
Fosamprenavir (Lexiva, GW433908)
Indinavir sulfate (Crixivan)
392
Dosea Side effects
S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404
300 mg bid Mild nausea, headache; hypersensitivity; skin rash; myalgia
120 mg/d Gastrointestinal disturbances, increased liver enzymes, renal toxicity
200 mg bid Pancreatitis (fatalities reported), peripheral neuropathy, diarrhea
200 mg qd Headache, diarrhea, nausea, rash (1% discontinue participation);
active against hepatitis B but not approved
150 – 300 mg, b.i.d., 150 – 300 mg Generally benign, often second drug of choice for triple therapy;
QD - commonly used with ZDV, may have diarrhea, headache, nausea, but is well tolerated;
several dosing patterns few drug interactions.
40 mg bid Peripheral neuropathy (may be severe), pancreatitis
300 mg qd Acute renal failure and Fanconi syndrome reported. Active against
hepatitis B.
0.75 mg tid Peripheral neuropathy (correlation with severity of disease),
pancreatitis, stomatitis
200 – 300 mg bid, numerous Marrow suppression, anemia, hepatic steatosis, myopathy, lactic
dosing patterns, comes in acidosis, headache, gastrointestinal disturbances; inhibits cytochrome
IV formula P-450; few drug interactions, however
1200 mg bid Rash, limited data; inhibits cytochrome P-450 (see Fosamprenavir)
400 mg qd or 300 mg qd + ritonavir Jaundice in 10%, nausea, diarrhea, elevation of liver enzymes
100 mg qd (boosted dosing)
1400 mg bid or 700 mg bid + ritonavir Complex interactions with some HIV medications. Some combinations
100 mg qd contraindicated. Amprenavir is a metabolite. Rash, nausea, diarrhea.
May increase transaminase levels.
800 mg tid Nephrolithiasis (increased H2O intake recommended), abdominal
discomfort, hyperbilirubinemia; may increase levels of midazolam,
triazolam; appears to inhibit cytochrome P-450.
 Lopinavir + Ritonavir (Kaletra)
Nelfinavir mesylate (Viracept)
Ritonavir (Norvir)
400/100 mg bid (also liquid form;
approved for children >6 mo)
750 mg tid
600 mg bid, often used now in lower
dose (100 – 200 mg) to boost other
Interacts with other HIV medications; ritonavir is potent inhibitor of
cytochrome P450 (CYP2D6) (see entry for ritonavir)
Diarrhea; well tolerated; causes cytochrome P-450 enzyme induction
and may decrease serum levels of some drugs (fentanyl, midazolam)
Nausea, vomiting, diarrhea, anorexia; elevated triglycerides,
creatine kinase, transaminases; inhibits cytochrome P-450 (potent);

S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

HIV medications clinically significant alterations in serum levels of antiretrovirals,
cholesterol lowering agents, anti arrhythmics, sedative hypnotics,
methadone, sildenofil, and recreational drugs
Saquinavir mesylate 600 mg tid Nausea, diarrhea, abdominal discomfort (Invirase or Fortoase)
(improved with Fortoase); inhibits cytochrome P-450
Nonnucleoside reverse transcriptase inhibitors
Delavirdine (Rescriptor) 400 mg tid May increase concentrations of some antiarrhythmic drugs, plasma
level of sedative hypnotics, calcium-channel blockers, and warfarin;
rash, headache, nausea; inhibits cytochrome P-450
Efavirenz (Sustiva) 600 mg/d in PM Dizziness, light-headedness; may be teratogenic, not recommended
in pregnancy.
Nevirapine (Viramune) 200 mg qd Skin rash, severe in some cases requiring increasing to twice daily
hospitalization; induces cytochrome P-450 98%.
Fusion inhibitors
Enfuvirtide (Fuzeon, T-20) binds to 90 mg sq bid Injection site reactions occur in 98% at least once, but rarely lead to
HIV envelop and prevents viral fusion discontinuation of therapy. Insomnia, headache, dizziness, nausea.
with target cell membranes Eosinophilia bacterial pneumonia greater in Phase III trial.
This is a list of drugs commonly used or disused as of March 2004. The rapid approval by the US Food and Drug Administration of many of the drugs in this table means
that there is often minimal clinical experience. This is particularly true with regards to the parturient. The clinician should be alert to unusual or unexpected side effects or
drug interactions. Updated information can be obtained from http://HIVinsite.ucsf.edu. This UCSF website by Dr. S. Deeks and P. Volberding (AIDS Knowledge Base-4)
is updated regularly with detailed information on each drug.
a
Drug doses and combinations continue to change with experience, viral sensitivity, and individual responses.
b
Zidovudine (300 mg) and lamivudine (150 mg) are now combined into one tablet and marketed as Combivir and administered twice daily. Many other combinations
are available or being considered. Note that drug doses change depending on how they are combined with other drugs and experience over time.

393
394 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

Fig. 5. Plasma concentrations of fentanyl after an intravenous dose of 5 mg/kg fentanyl following
pretreatment with oral placebo (left) or ritonavir (right) in 11 healthy volunteers. (Reprinted from
Olkkola KT, Palkama VJ, Neuvonen PJ. Ritonavir’s role in reducing fentanyl clearance and
prolonging its half-life. Anesthesiology 1999;91:681 – 5; with permission.)

All of the drugs listed may have considerable side effects and the potential of
unique drug interactions. A careful review of the drugs currently in use by the
patient, updated laboratory analysis (Hct, liver enzymes, CD4+ cell count), direct
questioning of the patient for drug side effects, and consultation with the primary
care physician or HIV specialist will be extremely useful, when possible, given
the lack of experience with these drugs.

Anesthetic considerations
When planning an anesthetic for a patient who has HIV/AIDS, as in any patient
with a major illness, a careful review of the disease process and the current status
of the patient’s disease and management is vital. HIV infection is a multiorgan
disease (see Box 2), and therapies continue to evolve. Complex drug interactions,
as noted by the examples of ritonavir (Norvir), are only now emerging as more
experience is gained. Patients with more advanced disease progression (CD4
T lymphocyte count of fewer than 200 cells/mg) need particularly close evaluation,
because opportunistic infections and malignancies are increasingly likely in this
group. Pulmonary complications may put them at greater risk for postoperative
complications. As patients survive longer, more disease processes of aging (heart
disease, hypertension, chronic obstructive pulmonary disease, and so forth) may
complicate care. In the 1980s, HIV/AIDS was a disease of the young, but the
increasing life expectancy with the infection, as well as new HIV infections
occurring in older patients, is challenging this distinction.
Preoperative assessment must begin with a careful history. Reviewing the
medications and basic laboratory evaluations to include a CD4 count will be
highly informative. Patients who have high CD4 counts (>500 –700 mm3 CD4+)
are likely not to present unusual or unique concerns. Many patients in this stage
of the disease are not treated with antiretrovirals, so the issue of potential drug
interactions will not be a concern. However, at the opposite end of the spectrum
 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404 395

are patients who have a very low CD4 count (<200 mm3) on multiple HIV
medications with numerous other drugs to manage or prevent opportunistic
infections. In this patient group, more extensive laboratory evaluations may be
useful to include blood count, clotting functions, and liver and renal function tests.
A viral load will demonstrate the effectiveness of HIV therapy. An electrocardio-
gram and chest radiography may also be advised, even in a younger patient. If
there is any history of cardiac or pulmonary dysfunction, a more extensive pre-
operative evaluation is needed. Electrocardiogram, chest radiography, and possi-
bly echocardiography pulmonary function tests and arterial blood gas evaluations
may prove necessary in some patients. HIV medications may cause hyperglyce-
mia, hyperlipidemia, lipodystrophy, and accelerated coronary arteriosclerosis. As
HIV-infected patients continue to live longer, this can be expected to increase.
Therefore, cardiac considerations are increasingly important [31 – 42].
General anesthesia has not been linked to adverse outcomes despite theoretical
concerns [34 –42,66 – 70]. Although transient immunologic changes have been
demonstrated, this does not appear to be a clinical issue. An earlier report cau-
tioned against inhalation anesthetics [70], this seems overly speculative. Since
that time, extensive clinical experience has not uncovered problems with
inhalation agents. The presence or absence of underlying pulmonary disease is
likely far more important. For example, in a patient who has advanced disease
and a history of repeated infection of P carinii resulting in pulmonary damage,
avoiding endotracheal intubation may be reasonable, in which case a regional
anesthetic might be beneficial. However, this general consideration is not unique
to patients who have HIV/AIDS.
Regional anesthesia has been more controversial in HIV-infected patients [71].
Although there is now extensive experience with most regional techniques in this
patient population without unique, adverse sequelae being reported, the early
concerns focused on the safety of spinal and epidural anesthesia. It was feared
that an HIV infection would be extended to the CNS. However, it has long been
quite clear that there is infection of the CNS in the earliest phases of the disease
progression. In fact, failure to culture HIV from the CSF is likely the result of
sampling error, not the lack of viral presence [72]. The safety of regional
anesthesia has been addressed in the parturient by several authors [73 –76].
The safety of regional anesthesia in HIV-infected patients was first addressed
in a prospective study of the immunologic function and clinical course of 30 HIV-
infected parturients at San Francisco General Hospital. We demonstrated that
regional anesthesia could be performed without adverse sequelae [73]. The
patients had extensive laboratory and medical evaluations before delivery and
were followed for at least 4 to 6 months postpartum. There were no neurologic or
infectious problems related to the regional anesthetics administered (n = 18) or
the obstetric course. The immune function of the parturients remained stable in
the peripartum period (CD4+ T lymphocytes, CD8+ T lymphocytes, and serum
p24 antigen). Another review of 96 HIV-positive parturients confirmed these
findings, as did a more recent review [74,76]. Thus, the routine use of epidural
analgesia for HIV-infected parturients is widely practiced. Regional anesthesia for

Table 3
Possible drug interactions with ritonavir (Norvir)
Coadministered drug
Amiodarone (Cordarone)
Astemizole (Hismanal)
Diazepam (Valium)
Digoxin (Lanoxin, others)
Fentanyl (Duragesic, various)
Meperidine (Demerol)
Potential clinical effects
Increased amiodarone effects
(eg, cardiac arrhythmias)
Increased astemizole effects
(eg, cardiac arrhythmias)
Increased diazepam effects (eg,
increased sedation, confusion,
respiratory depression)
Increased digoxin effects
Increased fentanyl effects (eg,
increased sedation, confusion,
respiratory depression)
Increased normeperidine effects
Mechanism of interaction
Inhibition of CYP450 3A4
by ritonavir
Inhibition of CYP450 3A4
by ritonavir
Inhibition of CYP450 3A
by ritonavir
Possible inhibition of P-gp
by ritonavir
Inhibition of CYP450 3A4
by ritonavir
Induction of CYP450 1A2
by ritonavir; inhibition of
p-glycoprotein reducing
first-pass metabolism
of meperidine
396
S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404
Management Suggested alternative agents
Do not coadminister —
Do not coadminister Cetirizine Fexofenadine
Loratadine
Do not coadminister Lorazepam Oxazepam
Temazepam (see entry
for midazolam)
Monitor digoxin —
concentrations closely
Monitor closely when —
using together; start
with low dose and
titrate to pain response
as indicated
Avoid combination Morphine
Methadone (Dolophine)
Midazolam (Versed)
Quinidine (Quindex, others)
Saquinavir (Invirase, Fortovase)
Warfarin (Coumadin)
Data from HIV InSite (http://hivinsite.ucsf.edu), March 2004.
Decreased methadone effects
(eg, methadone withdrawal)
Increased midazolam effects (eg,
increased sedation, confusion,
respiratory depression)
Increased quinidine effects
(eg, cardiac arrhythmias)
Increased saquinavir effects
Decreased warfarin effects (e.g.,
decreased INR, increased risk
of clotting)
Possible induction of Monitor and adjust —
CYP450 2C9, 3A4 and methadone as indicated
2D6 by ritonavir
Inhibition of CYP450 3A4 Single dose intravenous Lorazepam (author suggests
by ritonavir midazolam may be used; careful titration of midazolam
chronic midazolam in small doses is acceptable)
S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404
administration (oral or
intravenous) should
be avoided
Inhibition of CYP450 3A4 Do not coadminister —
by ritonavir
Inhibition of CYP450 3A4 Consider ritonavir-boosted —
by ritonavir saquinavir (commonly used
for this purpose)
Possible inhibition of Monitor INR and adjust —
CYP450 3A4, 2C9 and warfarin as indicated
1A2 by ritonavir
397
398 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

cesarean section and other surgical procedures may be particularly beneficial, in

that limited parenteral opioids are usually required and thus the possible side
effects that may occur with delayed metabolism caused by protease inhibitors can
be avoided (Table 3) [63,64]. At San Francisco General Hospital, we have had
extensive clinical experience with various regional anesthetic techniques—
primarily with male patients in the general operating room—since the beginning
of the AIDS epidemic over 20 years ago. Spinal and epidural anesthesia, as well
as other regional techniques, have been used extensively with no obvious adverse
sequelae noted. Thus, when regional anesthesia is indicated in the HIV-positive
patient and there are no clear, routine contraindications (eg, coagulopathy, infec-
tion at the site of block placement), it can be used in a routine manner.
The use of the combined spinal epidural (CSE) technique is increasingly
popular, and although there are scattered reports of meningitis in non– HIV-
infected patients associated with this technique, it is not clear that there are any
unique risks in the HIV-infected patient. Indeed, although the use of the CSE
technique—particularly during labor—is debated in the general, non – HIV-
infected obstetric patient, with the focus being on breaching the dura [77], there
are case series with thousands of parturients using the CSE technique without
unique infections. most recently, it seems prudent to be particularly fastidious
with technique and infection control in HIV-infected patients [78].
The use of an epidural blood patch (EBP) is appropriate when indicated to
treat a postdural puncture headache (PDPH). Despite the theoretic risks, there are
no serious complications related to this technique in the HIV-seropositive patient
[79 –83]. The report by Tom and colleagues [80] in men was quite careful in the
acute and long-term follow-up of HIV-positive patients who received an EBP.
Thus, although conservative management of a PDPH may be considered initially,
there is no evidence to suggest that there are any unique risks of an EBP in the
HIV-seropositive patient. Conversely, there is a long list of possible neurologic
sequelae from not treating a PDPH appropriately and promptly [84].

Management of elective cesarean delivery

Management of HIV-seropositive women includes attempts to minimize the
infant’s exposure to maternal blood and genital secretions to decrease perinatal
HIV transmission. This involves avoiding the following: percutaneous umbilical
cord sampling, fetal scalp clips (when possible), fetal scalp sampling, delivery
techniques that could produce abrasions in the infant’s skin (ie, vacuum or
forceps), and immediate removal of maternal blood and fluids from the infant.
However, numerous studies began to suggest a relationship between the mode of
delivery and the vertical transmission rate [85 – 88]. Two large studies have dem-
onstrated a significant decrease in the risk of vertical transmission with elective
cesarean delivery (Table 4) [89,90]. It must be kept in mind that a parturient with
a viral load below the limits of detection or one of several combination drug
therapies may also have an extremely low HIV vertical transmission rate with a
 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404 399

Table 4
Elective cesarean delivery to reduce the transmission of HIV: rates of vertical transmission
Elective cesarean delivery Other mode of delivery
No antiretroviral therapy 10.4% 19.0%
Antiretroviral therapy 2.0% 7.3%
These data demonstrate the strong correlation between elective cesarean delivery and a lower risk of
vertical HIV transmission (odds ratio: 0.73).
Data from the International Perinatal HIV Group. The mode 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.

vaginal delivery, thus avoiding surgery. Cesarean sections are associated with
higher maternal mortality rates, increases in postoperative morbidity, and in-
creased uterine rupture in subsequent pregnancies; these risks may be further
magnified in the developing world [66,91 – 93]. However, the American College
of Obstetricians and Gynecologists has stated that HIV-infected women should be
offered a scheduled cesarean delivery to further reduce the risk of vertical
transmission beyond that achievable with drug prophylaxis alone [94]. Thus,
anesthesiologists will likely see more of these patients for operative delivery.
The available data indicate no reduction in the transmission rate if the cesarean
delivery is performed after the onset of labor or rupture of membranes [94].
Delivery at 38 completed weeks’ gestation is recommended to reduce the
likelihood of the onset of labor or rupture of membranes before delivery. Pregnant
patients should also receive antiretroviral therapy according to currently accepted
guidelines for nonpregnant adults [57,95]. It is further noted that no combination
of therapies can absolutely guarantee the lack of newborn transmission. The
patient’s autonomy in making this decision must be respected. The risk factors for
perinatal HIV transmission continue to be evaluated [96]. Discussion and
controversy will continue around the issue of testing for HIV and management
of the disease [97,98]. However, more aggressive medical and surgical manage-
ment of the HIV-seropositive parturient will have benefits for both the mother and
the newborn.

Summary
The duration of the HIV/AIDS epidemic will soon reach the quarter century
mark if we accept the report in 1981 of P carinii in several young men as its
beginning. The virus clearly had earlier roots, however, and likely crossed from
an African monkey to man well before that date. The initial shock and fear has
faded somewhat as we better understand the disease, how to protect ourselves
from infection, and how to treat it more successfully if infected. However, tens of
millions of human lives will be lost before the epidemic is brought under control
on a worldwide basis. Just as the Black Death changed politics and culture of
fourteenth-century Europe, parts of the developing world in particular will likely
undergo great social and economic stress and change because of HIV. In the
400 S.C. Hughes / Anesthesiology Clin N Am 22 (2004) 379–404

Western world, the luxuries of modern medical care and pharmaceutical inter-
vention will save the lives of many. Thus, anesthesiologists will no doubt care for
HIV-infected patients at all stages of life in the future, from infants to the elderly.
A thorough knowledge of the disease and its complications, its treatment, and
possible drug interactions will be necessary. It is likely that we will continue to
see innovative therapies, and it will be necessary to be well informed of the bene-
fits and risks of these as we provide anesthesia care.

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