Sepsis in Trauma
Ayan Sen
Derek C. Angus
I. Introduction
Sepsis is a common, expensive, and frequently fatal condition, likely to increase in frequency as the US population ages.
It is a frequent complication in patients who survive initial trauma resuscitation and is largely responsible for the third peak of death based on Trunkey’s trimodal death distribution in civilian trauma.
II. Definition of Sepsis
Sepsis is a broad term including severe sepsis (infection complicated by acute organ dysfunction) and septic shock (infection leading to shock). When a patient develops an infection, the process that leads to sepsis is widely regarded as a broad innate immune response, consisting of rapid release of multiple cytokines and other inflammatory molecules and activation of immune cells. The clinical manifestation of this response is described as the Systemic Inflammatory Response Syndrome (SIRS). Under the consensus definitions, the different components of sepsis are as follows:
Infection is a pathologic process caused by the invasion of normally sterile tissue or fluid or body cavity by pathogenic or potentially pathogenic microorganisms. Caveats include infection by cytopathic toxin producing organisms which do not necessarily invade the host tissue. SIRS results from a systemic activation of the innate immune response, regardless of cause. SIRS occurs when patients present one or more of the following findings: Body temperature >38°C or <36°C; heart rate >90/min; respiratory rate >20/min, or PaCO2 <32 mm Hg; and white blood cell count of >12,000 cells/mcL or <4,000 cells/mcL.
Bone et al. defined sepsis as SIRS plus infection, “severe sepsis” as sepsis associated with organ dysfunction, hypoperfusion, or hypotension, and “septic shock” as sepsis with arterial hypotension, despite adequate fluid resuscitation. The 2003 definition was widened to suggest that SIRS was only one of a long list of potential signs of infection and that severe sepsis is simply infection complicated by acute organ dysfunction.
Typical acute organ dysfunction includes acute respiratory distress syndrome (ARDS), hypotension or hyperlactemia, acute kidney injury, gastrointestinal ileus and raised transaminases, altered mental status, and thrombocytopenia.
None of the findings of the SIRS response is specific for diagnosis. In trauma, the systemic inflammatory response may be due to the injury and not a secondary infection.
III. Risk Factors
Patient factors can predispose toward severe sepsis and septic shock.
Risk factors for sepsis in trauma patients—see Table 13-1.
IV. Diagnosis of Sepsis in Trauma
The diagnosis and prognosis of sepsis is complicated by the variable and non-specific nature of the signs and symptoms of sepsis in trauma. Early recognition and directed treatment can lower mortality and morbidity.
Table 13-1 Risk Factors for Sepsis in Trauma Patients | ||||||||
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Early post-injury inflammatory signs and markers likely reflect tissue damage rather than sepsis.
The physical examination is the underpinning to detect the source of infection.
Many signs exist to help identify that an infected patient “is septic.”
Frequently, sources of infection in trauma patients involve the lungs (pneumonia), invasive lines, abdominal sepsis (due to injury or surgery), urinary tract, sinuses, gallbladder and decubitus ulcers (Table 13-2).
Biomarkers such as white cell count and C-reactive protein (CRP) have low specificity.
Procalcitonin (PCT) may aid as a diagnostic (bacterial infection) or prognostic marker. Current evidence suggests that serum PCT can be used as “an adjunctive diagnostic tool for discriminating infection as the cause for fever or sepsis presentations” in their guidelines for the evaluation of new fever in critically ill adults.
Positive blood cultures (BC), if not from a contaminant, are diagnostic of Bacteremia but do not define SIRS. Culture results are not typically available until after treatment with antibiotics, and source control must be initiated prior to these data. Obtain appropriate cultures before starting antibiotics provided this does not delay antimicrobial administration; obtain two or more BCs; one or more BCs should be percutaneous; one BC from each vascular access device in place >48 hours.
Other sites should be cultured as clinically indicated.
Imaging studies can confirm a source and aid sampling.
A specific anatomic site of infection should be established as rapidly as possible and within first 6 hours of diagnosis of sepsis.
Formal evaluation for a focus of infection amenable to source control measures (e.g., abscess drainage, tissue debridement) should be done.
Implementation of source control measures should be done as soon as possible following successful initial resuscitation. (Exception: Infected pancreatic necrosis, where surgical intervention is best delayed.)
Remove intravascular access devices if infected.
Microbiology of sepsis in trauma:
In trauma patients, sepsis is caused by gram-positive and gram-negative bacteria in roughly equal proportions. Empiric coverage for both groups may be necessary.
The most prevalent organisms are Escherichia coli and Staphylococcus (aureus or coagulase negative). Meningococcemia and Streptococcemia are comparatively fewer in numbers.
E.coli and Klebsiella are common but Pseudomonas is also a common ICU pathogen. Sixty percent of hospital-acquired isolates of S. aureus are methicillin-resistant. Staph resistance to vancomycin is rare. S. epidermidis has 85% methicillin resistance. Initial antibiotic therapy should take resistance patterns and local antibiograms into account.
Enterococcus causes SSTI, CR-BSI, and UTI. Thirty percent of them are resistant to vancomycin.
Table 13-2 Diagnostic Criteria for Sepsis
Infection,a documented or suspected, and some of the following:b
General variables
Fever (core temperature >38.3°C)
Hypothermia (core temperature <36°C)
Heart rate >90 min−1 or >2 SD above the normal value for age
Tachypnea
Altered mental status
Significant edema or positive fluid balance (>20 mL/kg over 24 h)
Hyperglycemia (plasma glucose >120 mg/dL or 7.7 mmol/L) in the absence of diabetes
Inflammatory variables
Leukocytosis (WBC count >12,000 uL−1)
Leukopenia (WBC count <4,000 uL−1)
Normal WBC count with >10% immature forms
Plasma C-reactive protein >2 SD above the normal value
Plasma procalcitonin >2 SD above the normal value
Hemodynamic variables
Arterial hypotensionb (SBP <90 mm Hg, MAP <70, or an SBP decrease >40 mm Hg in adults or <2 SD below normal for age)
SvO270%b
Cardiac index >3.5 L-min−1 M−23
Organ dysfunction variables
Arterial hypoxemia (PaO2/FiO2, <300)
Acute oliguria (urine output <0.5 mL kg−1 h−1 or 45 mmol/L for at least 2 h)
Creatinine increase >0.5 mg/dL
Coagulation abnormalities (INR > 1.5 or aPTT >60 s)
Ileus (absent bowel sounds)
Thrombocytopenia (platelet count <100,000/μL−1)
Hyperbilirubinemia (plasma total bilirubin >4 mg/dL or 70 mmol/L)
Tissue perfusion variables
Hyperlactatemia (>1 mmol/L)
Decreased capillary refill or mottling
WBC, white blood cell; SBP, systolic blood pressure; MAP, mean arterial blood pressure; SvO2, mixed venous oxygen saturation; INR, international normalized ratio; aPTT, activated partial thromboplastin time.
aInfection defined as a pathologic process induced by a microorganism.
bSvO2 sat >70% is normal in children (normally, 75–80%), and CI 3.5–5.5 is normal in children; therefore, NEITHER should be used as signs of sepsis in newborns or children.
cdiagnostic criteria for sepsis in the pediatric population are signs and symptoms of inflammation plus infection with hyper- or hypothermia (rectal temperature >38.5 or <35°C), tachycardia (may be absent in hypothermic patients), and at least one of the following indications of altered organ function: Altered mental status, hypoxemia, increased serum lactate level, or bounding pulses.
Updates on Sepsis Definition based on the 2001 ACCP/SCCM criteria
From Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med 2003;31:1250–1256.Full access? Get Clinical Tree