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1242 PART 11: Special Problems in Critical Care

antibody. In a patient with a creatinine level above 4.0 mg/dL who has
• Acute organic brain syndrome without focal neurologic deficits or been adequately hydrated, has been divorced from nephrotoxic drugs,
evidence of systemic vasculitis is unlikely to be due to vasculitis. and shows evidence of active glomerulonephritis, the question arises:
• Fever in patients with systemic autoimmune diseases should be Is more aggressive immunosuppression desirable? The answer to this
presumed to be infectious if accompanied by chills, leukocytosis question depends on the degree of potential disease reversibility. A renal
with a left shift, or hypotension. biopsy may help clarify this issue. The presence of significant chronic
• Patients who have been treated with significant doses of corti- disease should dampen enthusiasm for aggressive therapy. Review of
old records can be enlightening if long-standing loss of renal function
costeroids within the past year may require empiric replacement is documented. Clinicians have become increasingly aware that immu-
therapy during critical illness or surgical procedures until adrenal nosuppression in the lupus patient with advanced renal disease may
insufficiency can be excluded. be more hazardous than progression to complete renal failure. Patients
with lupus tolerate dialysis in a fashion comparable to other patients,
and results of renal transplantation are favorable. Paradoxically, patients
Approximately 10% to 25% of all rheumatic disease patients visiting with lupus who develop chronic renal failure often enjoy an ameliora-
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the emergency department require hospitalization and up to one-third tion of extrarenal symptoms. A few patients have recovered sufficient
of these patients will require intensive care. Patients with rheumatic renal function to allow withdrawal from dialysis. For all these reasons,
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diseases admitted to the medical ICU most often have problems not the overzealous administration of immunosuppression in patients with
directly related to their primary illness. Sepsis, massive gastrointestinal lupus and advanced renal disease should be approached with caution.
bleeding, and myocardial infarcts may arise secondary to treatment. ■
The major direction of care in these circumstances often comes from RESPIRATORY FAILURE AND LUNG INFILTRATES:
the intensivist. Circumstances do arise that require the unique insight IS IT LUPUS PNEUMONITIS?
of the experienced clinical rheumatologist, who at times must direct the Respiratory failure in the patient with SLE is an ominous development:
management of a disease-specific complication. Just as often the rheu- a paradigm of a compromised host who is on high-dose corticosteroid
matologist is asked to address a diagnostic dilemma spawned by puzzling therapy. The usual opportunistic pulmonary infections need to be
clinical and laboratory data. This chapter addresses the more common urgently excluded by bronchoalveolar lavage, bronchoscopic trans-
issues that prompt the rheumatologist and the intensivist to collaborate.
bronchial biopsy, or open lung biopsy. If no superimposed infections or
embolic etiology can be found and treated, lupus-related respiratory fail-
SYSTEMIC LUPUS ERYTHEMATOSUS ure remains a diagnosis of exclusion and can be caused by either lupus
■ FEVER: IS IT THE LUPUS? pneumonitis or diffuse pulmonary hemorrhage. Acute lupus pneumoni-
tis may occur as an initial manifestation of SLE and is characterized by
Fever in the patient with lupus presses the clinician for an urgent answer fever, tachypnea and hypoxemia which may be accompanied by cough,
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to the question: Is this caused by lupus activity or infection? Fever is a pleuritic chest pain, and hemoptysis. Radiologic findings are highly
common finding in active systemic lupus erythematosus (SLE) occurring variable but usually bilateral and at least bibasilar. This diagnosis is not
in up to approximately 50%. It may respond to the usual antipyretics or only one of exclusion; it unfortunately still rests solely on clinical suspi-
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require corticosteroids. Single-daily-morning dose prednisone may not cion. The other SLE-related cause of respiratory failure is diffuse alveolar
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control late afternoon or evening fevers and may require the use of split- pulmonary hemorrhage. Although invasive Aspergillus or tuberculosis
dosing. Leukocytosis and increased bands on peripheral smear are strong can erode a pulmonary vessel and cause hemorrhage, gross hemoptysis,
presumptive evidence for infection, as is the presence of shaking chills. when present, usually indicates alveolar hemorrhage. Hemoptysis is not
Complement proteins or components, including C3 and C4, are acute- usually seen in lupus pneumonitis; unfortunately, this finding is present
phase reactants and usually rise with infection. Low levels of complement in <50% of patients with alveolar hemorrhage. Blood or hemosiderin-
occur in some but not all patients with active lupus. Using discriminant laden macrophages found during bronchoscopy in a patient without
analysis, Inoue and colleagues showed that 95% of 74 febrile episodes heart failure can be helpful findings but are nonspecific. The presence of
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could be correctly classified as to the cause of fever when a combina- thrombocytopenia is not helpful, but bleeding sufficient to cause acute
tion of white blood count (low in SLE, normal to high with infection) respiratory failure most invariably causes an acute drop in hematocrit.
and gamma-globulin levels (high with SLE, normal with infection) are In fact, treatment should not be delayed in order to distinguish between
used as variables. In the ICU setting, the febrile patient with SLE is lupus pneumonitis and lupus-associated hemorrhage, because mortal-
probably best considered infected and treated with broad-spectrum anti- ity is extremely high in either syndrome and treatment strategies are
biotics pending results of cultures. Infection is most likely to be caused similar. Pulmonary hypertension, sometimes severe, is frequently pres-
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by nonopportunistic organisms, and coverage for gram-positive and ent. Cardiac filling pressures, in contrast to B-type natriuretic peptide
gram-negative aerobes represents adequate empirical therapy when no determinations, can occasionally be helpful discriminators to exclude
obvious source has been recognized. Systemic infections with Salmonella, acute cardiogenic pulmonary edema. Pulmonary artery thrombosis
endocarditis involving lupus-related valvular lesions, and pneumococcal masquerading as massive pulmonary emboli can occur in patients with
sepsis in the splenectomized (surgical or autosplenectomy) are among pulmonary hypertension or thrombotically active anticardiolipin (ACL)
the infections that have special significance for lupus patients. 4 antibodies. The mortality of lupus pneumonitis is high, and treatment
■ RENAL FAILURE: IS IT TREATABLE? should be aggressive. Individual preferences will dictate modes of ther-
apy, since no consensus exists on either the etiology of the syndrome or
In patients with SLE in the ICU, renal insufficiency may be caused effective treatment. Pulse methyl prednisolone, usually 500 to 1000 mg
by a variety of factors, including drugs, especially nonsteroidal anti- intravenously given for 3 to 5 days, or bolus cyclophosphamide at 0.5 to
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inflammatory drugs (NSAIDs), hypovolemia, sepsis, or previous renal 1.0 g/m has been used. The use of plasmapheresis and plasma-exchange
disease. In some cases, active lupus nephritis is a contributing factor. in severe, refractory SLE remains controversial. The use of rituximab in
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A careful examination of the urinary sediment is the most critical diag- severe, refractory, SLE has been reported as well.
glomerulonephritis. Lupus patients with active nephritis are often ■ BRAIN DYSFUNCTION: IS IT LUPUS?
nostic tool. Proteinuria, casts, and dysmorphic red blood cells indicate
hypertensive. Significant renal lupus (other than membranous disease) is A patient with acute, severe neurologic deficits and a history of SLE
often associated with low complement levels and elevation of anti-DNA or a clinical syndrome and laboratory evidence suggestive of systemic

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