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Clinical Approach to Sepsis and
Its Mimics in Critical Care
Burke A. Cunha
Infectious Disease Division, Winthrop-University Hospital, Mineola, New York,
and State University of New York School of Medicine, Stony Brook, New York, U.S.A.INTRODUCTION
Sepsis refers to bacteremia or fungemia with hypotension and organ dysfunction. The main
clinical problem with the “septic” patient is to determine whether the patient is septic or has a dis-
order noninfectious mimic of sepsis by hemodynamic or laboratory parameters. In the intensive
care setting, it is of critical importance to differentiate between sepsis and its mimics (1–6).
Diagnostic Approach
Many patients with fever and hypotension are not septic. Several clinical disorders resemble
sepsis. Patients do not become septic without a major breach in host defenses. The most
important clinical consideration in determining whether a patient is septic is to identify the
source of infection. Sepsis is a complication with only relatively few infections. Infections
limited to specific infections in a few organ systems are the only ones with septic potential.
Most sepsis derives from perforated obstructions or abscesses of the gastrointestinal (GI) tract/
pelvis, hepatobiliary tract, genitourinary (GU) tract, or may be related to central intravenous
(IV) lines. Even though the GI tract is the most frequent focus of infection leading to sepsis, not
all gastrointestinal disorders including infections have a septic potential. Lower gastrointes-
tinal tract perforations, intra-abdominal/pelvic abscesses, pylephlebitis, commonly result
clinically in sepsis. In contrast, gastritis and nonperforating gastric ulcer are rarely associated
with sepsis. Cholangitis in the hepatobiliary tract results in sepsis, but rarely, if ever,
complicates acute/chronic cholecystitis (6–13). IV line sepsis represents the ultimate breach in
host defenses since the pathogenic organisms from central catheters are introduced directly
into the bloodstream in high concentrations (14,15).
The primary task is to search for GI, GU, or an intravenous source of sepsis. It is almost
always possible to identify the septic source by physical exam, laboratory, or radiology tests.
Without local signs of entry site infection, IV-line sepsis should not be entertained if the central
IV line has been in place less than seven days.
If intra-abdominal and GU sources have been eliminated as diagnostic possibilities,
central IV lines, either temporary or long term, should be considered as a cause of sepsis. The
longer a central IV line is in place, the more likely the central IV line may be the cause of fever/
hypotension. Signs of infection at entry sites of central IV lines indicate likely IV-line sepsis,
but no superficial erythema/swelling does not rule out IV-line sepsis (14–16).
Disorders that mimic sepsis should be recognized to treat the condition and not to avoid
inappropriate treatment with antibiotics. Disorders that mimic sepsis (pseudosepsis) include
gastrointestinal hemorrhage, pulmonary embolism, myocardial infarction, acute pancreatitis,
diabetic ketoacidosis, systemic lupus erythematosus (SLE) flare, relative adrenal insufficiency,
inadequate steroid therapy, rectus sheath hematoma, and diuretic-induced hypovolemia
(6,17–21) Table 1.
CLINICAL SIGNS OF SEPSIS
Excluding the elderly, compromised hosts, and uremic patients, fever is a cardinal sign of
inflammation or infection. Fever should not be equated with infection since the chemical
mediators of inflammation and infection, i.e., cytokines, induce a febrile response mediated via
the preoptic nucleus of the anterior hypothalamus. All that is febrile is not infectious, and most,
but not all diseases causing sepsis are accompanied by temperatures 1028 F. With the
exceptions of drug fever and adrenal insufficiency, the disorders that mimic sepsis and