LABORATORY ABNORMALITIES IN SEPSIS
The usual hemodynamic parameters associated with sepsis include decreased peripheral
resistance (PR) with increased cardiac output (CO) accompanied by tachycardia/respiratory
alkalosis. Patients with fever are often diagnosed as septic. Although sepsis is associated with
hemodynamic abnormalities, i.e.,;PR/:CO, many disorders mimicking sepsis also have
similar findings, such as acute pancreatitis, GI bleed, etc. If hemodynamic abnormalities are
present, but not accompanied by GI, GU, or intravenous clinical disorders associated with
sepsis, then it should be assumed that the patient has a noninfectious mimic of sepsis.
As with hemodynamic parameters, laboratory data may mislead the unwary into
incorrectly ascribing laboratory abnormalities to an infectious rather than a noninfectious
process. An increase in white peripheral blood cell count with a shift to the left is a nonspecific
reaction to stress, and is not specific for infection. Leukocytosis does not differentiate bacterial
from viral infections. An increase in white count with a shift to the left is a measure of the
intensity of the systemic response to stress of infectious or noninfectious disorders. Similarly,
an increase in fibrin split products (FSPs), increase in lactic acid, decrease in serum albumin,
decrease ina-2 globulins, decrease in fibrinogen, or an increase in PT/PTT are compatible but
not characteristic of infection.
Laboratory parameters that are more indicative of infection include leukopenia or
thrombocytopenia. The only laboratory abnormalities that are specific for sepsis are organisms
in the blood, i.e., gram/acridine orange stains of buffy coat smears/high grade positivity in
blood cultures (excluding contaminants). Increased cytokine/endotoxin levels are also
suggestive. Highly elevated C-reactive protein (CRP) levels have also been described as a
marker for sepsis. Positive buffy coat smears are not present in all patients with bacteremia,
and when positive are diagnostic and rapid. The bacteria/fungi present in buffy coat smears
are helpful in determining the origin of the septic process by their association with particular
organ system involvement, i.e., poorly stained pleomorphic gram-negative bacilli (Bacteroides
fragilis) point to a GI, but not GU/IV source. The morphology/arrangement of the bacteria in
buffy coat smears is also useful in selecting appropriate empiric antibiotic coverage (26–30)
(Table 3).
EMPIRIC ANTIMICROBIAL THERAPY
The selection of appropriate antibiotic therapy for sepsis depends on accurate localization of
the infectious process to the abdomen/pelvis, GU tract, or IV line. Because each organ has its
normal resident flora that becomes the pathogenic flora when the organ function is disrupted,
empiric coverage is directed against the normal resident flora (Table 4). Factors in antibiotic
selection include hepatic/renal insufficiency, allergic status of the patient, tissue penetration of
the antibiotic, safety profile of the antibiotic, resistance potential of the antibiotic, and cost.
If the spectrum is appropriate for the source of sepsis, no regimen is superior to others in
terms of clinical outcome. However, clinicians should utilize the most clinically/cost-effective
regimens with a low resistance potential and begin therapy as soon as the diagnosis of sepsis is
made. The basis of empiric therapy for sepsis depends on eliminating the source of sepsis and
covering the patient with antibiotic therapy appropriate for the septic source (31–42). The use
of steroids and anti-cytokine therapies remain controversial and of unproven benefit (43–46).
Table 2 Clinical Mimics of Sepsis
.Acute gastrointestinal hemorrhage
.Acute pulmonary embolism
.Acute myocardial infarction
.Acute pancreatitis
.Diabetic ketoacidosis
.SLE flare
.Relative adrenal insufficiency
.Diuretic-induced hypovolemia
.Rectus sheath hematoma
Source: From Refs. 9 and 22.
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