22
Infections Related to Steroids in
Immunosuppressive/Immunomodulating
Agents in Critical Care
Lesley Ann Saketkoo and Luis R. Espinoza
Section of Rheumatology, Department of Medicine, Louisiana State University Health Sciences Center,
New Orleans, Louisiana, U.S.A.
INTRODUCTION
This chapter will discuss considerations necessary in the management of the critical care
patient taking exogenous glucocorticoids and/or biologic agents for chronic autoimmune or
inflammatory disease. Discussion will focus on complications of therapy in relation mainly to
serious infections—defined as infection that is fatal, life threatening, or causing prolonged
hospitalization. The use of biologic agents as they are newer therapies will be highlighted in
the discussion.
GLUCOCORTICOIDS
Glucocorticoid therapy is the central therapeutic agent for the immediate control of active
inflammatory and autoimmune disease due to its blanket and immediate effects on the
immune system. However, its use is fraught with a catalogue of damaging and disabling
complications that will not be listed here. For this reason, it has been used as a bridge therapy
during the time it takes for other less harmful therapeutics to take effect. The hospital-based
physician needs to be aware of two potentially devastating complications in the management
of the in-patient receiving exogenous corticosteroids: (i) hypothalamic suppression leading to
adrenal insufficiency and (ii) risk of serious infection.
Consensus in defining levels of immune suppression with glucocorticoid use is difficult
to reach due to immunologic complexities inherent in underlying diseases being treated with
corticosteroids as well as variances in patient sensitivity based on genetic make-up. But it is
generally accepted that the degree of immune suppression increases with level of dosing and
observation of physical changes such as cushingoid features, striae, and vascular friability.
Level of dosing effecting immune response has been suggested through vaccine response
studies and studies ascertaining infections as follows:
l Daily prednisone of 10 mg (or its equivalent) or a greater or cumulative dose of 700 mg
carried an increased relative risk of 1.6 versus placebo (1)
l Daily prednisone of 10 mg (or its equivalent) or greater carried 1.5 increased risk of
infection (2)
l Daily prednisone greater than 40 mg or greater carried an eightfold increased risk of
infection (2)
From the above and other studies we glean a tentative definition of prednisone in
relation to immunologic suppression as:
l Low dose: less than 10 mg daily
l Moderate dose: 10 to 40 mg daily
l High dose: greater than 40 mg daily