Sepsis resident survival guide: Difference between revisions
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Systemic inflammatory response syndrome (SIRS) represents the complex findings resulting from systemic activation of the innate immune response triggered by localized or generalized infection, trauma, thermal injury, or sterile inflammatory processes. However, criteria for SIRS are considered to be too nonspecific to be of utility in diagnosing a cause for the syndrome or in identifying a distinct pattern of host response. | Systemic inflammatory response syndrome (SIRS) represents the complex findings resulting from systemic activation of the innate immune response triggered by localized or generalized infection, trauma, thermal injury, or sterile inflammatory processes. However, criteria for SIRS are considered to be too nonspecific to be of utility in diagnosing a cause for the syndrome or in identifying a distinct pattern of host response. | ||
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| style="font-size: 85%; background: #545454; color: #F8F8FF; padding: 5px 10px; font-weight: bold;" | SIRS is considered to be present when patients have two or more of the following clinical findings: | | style="font-size: 85%; background: #545454; color: #F8F8FF; padding: 5px 10px; font-weight: bold;" | SIRS is considered to be present when patients have two or more of the following clinical findings: | ||
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Sepsis is defined as the presence (probable or documented) of infection together with systemic manifestations of infection. Diagnostic criteria for sepsis are as follows: | Sepsis is defined as the presence (probable or documented) of infection together with systemic manifestations of infection. Diagnostic criteria for sepsis are as follows: | ||
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| style="font-size: 85%; background: #545454; color: #F8F8FF; padding: 5px 10px; font-weight: bold;" | Sepsis = infection (documented or suspected) and some of the following: | | style="font-size: 85%; background: #545454; color: #F8F8FF; padding: 5px 10px; font-weight: bold;" | Sepsis = infection (documented or suspected) and some of the following: | ||
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Severe sepsis is defined as sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion. | Severe sepsis is defined as sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion. | ||
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| style="font-size: 85%; background: #545454; color: #F8F8FF; padding: 5px 10px; font-weight: bold;" | Severe sepsis = sepsis-induced tissue hypoperfusion or organ dysfunction (any of the following thought to be due to the infection) | | style="font-size: 85%; background: #545454; color: #F8F8FF; padding: 5px 10px; font-weight: bold;" | Severe sepsis = sepsis-induced tissue hypoperfusion or organ dysfunction (any of the following thought to be due to the infection) | ||
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Revision as of 15:01, 5 March 2015
Sepsis Resident Survival Guide |
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Overview |
Causes |
Diagnostic Criteria |
FIRE |
Diagnosis |
Treatment |
Do's |
Don'ts |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, M.D. [2]; Vidit Bhargava, M.B.B.S [3]
Overview
Diagnostic Criteria
Systemic Inflammatory Response Syndrome
Systemic inflammatory response syndrome (SIRS) represents the complex findings resulting from systemic activation of the innate immune response triggered by localized or generalized infection, trauma, thermal injury, or sterile inflammatory processes. However, criteria for SIRS are considered to be too nonspecific to be of utility in diagnosing a cause for the syndrome or in identifying a distinct pattern of host response.
SIRS is considered to be present when patients have two or more of the following clinical findings: |
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Sepsis
Sepsis is defined as the presence (probable or documented) of infection together with systemic manifestations of infection. Diagnostic criteria for sepsis are as follows:
Sepsis = infection (documented or suspected) and some of the following: |
General variables
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Inflammatory variables
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Hemodynamic variables
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Organ dysfunction variables
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Tissue perfusion variables
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Severe Sepsis
Severe sepsis is defined as sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion.
Severe sepsis = sepsis-induced tissue hypoperfusion or organ dysfunction (any of the following thought to be due to the infection) |
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Septic Shock
Septic shock is defined as sepsis-induced hypotension persisting despite adequate fluid resuscitation, in the absence of other causes for hypotension.
- Septic shock in adult patients refers to a state of acute circulatory failure characterized by persistent arterial hypotension unexplained by other causes.
- Septic shock in pediatric patients is defined as a tachycardia (may be absent in the hypothermic patient) with signs of decreased perfusion including decreased peripheral pulses compared with central pulses, altered alertness, flash capillary refill or capillary refill 2 seconds, mottled or cool extremities, or decreased urine output.
Causes
Life Threatening Causes
Common Causes
- Community acquired pneumonia: 48% develop severe sepsis.[6]
- Diabetes and renal disease may explain the higher rates of infection related septic shock.
- Immunosuppression
Management
The following guidelines are based on 'Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012'.[7]
Characterize the symptoms: ❑ Fever ❑Hypothermia ❑ Altered mental status ❑ Mottling ❑ Ileus ❑ Oliguria | |||||||||||||||||||||||||||||||||||||||||||
Examine the patient: ❑ Tachycardia ❑ Tachypnea ❑ Edema ❑ Hyperglycemia ❑ Hypotension after an initial 30 ml/Kg bolus ❑ Decreased capillary refill | |||||||||||||||||||||||||||||||||||||||||||
Order labs: ❑ Random blood sugar (RBS) ❑ Complete blood count (CBC) ❑ Plasma C reactive protein (CRP) ❑ Plasma procalcitonin ❑ Pulse oximetry ❑ Urinalysis/Renal function tests ❑ PT/INR ❑ Liver function tests ❑ Serum lactate ❑ Central venous pressure (CVP) | |||||||||||||||||||||||||||||||||||||||||||
Consider alternative diagnosis: ❑ Infections ❑ Acute pancreatitis ❑ Diabetic ketoacidosis Lower gastrointestinal bleeding Myocardial infarction | |||||||||||||||||||||||||||||||||||||||||||
Initial resuscitation: Goals to achieve in first 6 hours ❑ Central venous pressure (CVP) 8-12 mm Hg ❑ Mean arterial pressure (MAP) ≥ 65 mm Hg ❑ Urine output ≥ 0/5 mL/Kg/hr ❑ Central venous O2 sat. 70% ❑ If lactate levels elevated, target is normalization | |||||||||||||||||||||||||||||||||||||||||||
Diagnosis: ❑ Perform 2 sets of blood cultures (aerobic and anaerobic) atleast, before starting antibiotics
❑ Perform imaging studies as appropriate to locate a source | |||||||||||||||||||||||||||||||||||||||||||
Antimicrobial therapy: ❑ Initiate within 1st hour of diagnosis Reassess regimen daily ❑ Use low procalitonin levels for prognosis ❑ Usual duration of therapy 10 days ❑ Longer in neutropenics, slow responders, undrainable foci, immunologically compromised | |||||||||||||||||||||||||||||||||||||||||||
Choice of antibiotics | |||||||||||||||||||||||||||||||||||||||||||
Unknown organism ❑ Empiric therapy with broad spectrum antbiotic with good tissue penetrance | Neutropenic pt with severe sepsis (goal is to cover Acinetobacter & Pseudomonas spp) ❑ Use combination empirical therapy | Severe infections + resp failure + septic shock ❑ Extended spectrum beta lactam andaminoglycoside/fluoroquinolone | Streptococcus pneumoniae ❑ beta lactam + macrolide | Culture specific organism ❑ Shift to appropriate anti-bacterial, antiviral or antifungal | |||||||||||||||||||||||||||||||||||||||
Remove source/foci of infection: ❑ Use minimally invasive process ❑ Source removal best done in first 12 hours ❑ Remove intravascular access devices if they are a possible source ❑ Oral chlorhexidine gluconate to reduce oral contamination as a risk factor for ventilator associated pneumonia | |||||||||||||||||||||||||||||||||||||||||||
Hemodynamic support Fluid therapy: ❑ Administer crystalloids, use albumin when demand for fluids is too high ❑ Use dynamic variables (change in pulse pressure, stroke volume) and static variables (arterial pressure,heart rate) to assess status Vasopressors (to achieve target MAP ≥ 65 mm Hg): Inotropic therapy: ❑ Trial of dobutamine infusion 20 μg/Kg if cardiac output low with elevated cardiac filling pressure | |||||||||||||||||||||||||||||||||||||||||||
Corticosteroids: ❑ Use continuous flow IVhydrocortisone 200 mg/day if shock doesn’t improve with fluids & vasopressor ❑ Taper when vasopressors no longer required | |||||||||||||||||||||||||||||||||||||||||||
Blood products: ❑ Transfuse blood when hemoglobin < 7.0 g/dL ❑ Transfuse platelets if < 10,000/mm3 or < 20,000/mm3 in those with high risk | |||||||||||||||||||||||||||||||||||||||||||
Mechanical ventilation for sepsis induced ARDS': ❑ Target tidal volume of 6 mL/Kg ❑ Target plateau pressure ≤ 30 mm Hg ❑ Use PEEP (positive end expiratory pressure) to avoid alveolar collapse ❑ Raise patients bed to 30-45° ❑ Attempt weaning when all foll. criteria are met:
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Other supportive therapy Sedation & neuromuscular blockade: ❑ Use minimal sedation/neuromuscular blockade in mechanically ventilated patients Glucose control: Renal replaement therapy: DVT prophylaxis: Stress ulcer prophylaxis Feeding: Goals of care: ❑ Discuss goals or care, patient aspirations and future directives with family with 72 hours of admission | |||||||||||||||||||||||||||||||||||||||||||
Do's
- Patients who are suspected of being severely infected, should be routinely screened for sepsis.
- Administer antimicrobial therapy within 1 hour of diagnosis of sepsis.
- Delay intervention, if source/foci of infection is peri-pancreatic necrosis.
Dont's
- Do not use empiric combination therapy for more than 3-5 days.
- Do not use antimicrobial agents in severely inflamed patients, from a non-infectious cause.
- Do not use hydroxyethyl starch for fluid therapy resuscitation of severe sepsis and septic shock.
- Do not use low dose vasopressin/dopamine/phenylephrine as monotherapy.
- Do not use low dose dopamine for renal protection.
- Do not use corticosteroids in the absence of shock.
- Do not use erythropoietin as a specific treatment of anemia associated with sepsis.
- Do not use antithrombin.
- Do not use fresh frozen plasma to correct clotting abnormalities in the absence of bleeding or planned invasive procedure.
- Do not use following supportive therapies as their role is not clear:
- IV selenium
- Do not routinely use pulmonary artery catheters.
- Do not use bicarbonate therapy as prophylaxis of hypoperfusion induced lactic acidosis if pH > 7.15.
References
- ↑ Jones, GR.; Lowes, JA. (1996). "The systemic inflammatory response syndrome as a predictor of bacteraemia and outcome from sepsis". QJM. 89 (7): 515–22. PMID 8759492. Unknown parameter
|month=
ignored (help) - ↑ Brun-Buisson, C.; Doyon, F.; Carlet, J.; Dellamonica, P.; Gouin, F.; Lepoutre, A.; Mercier, JC.; Offenstadt, G.; Régnier, B. (1995). "Incidence, risk factors, and outcome of severe sepsis and septic shock in adults. A multicenter prospective study in intensive care units. French ICU Group for Severe Sepsis". JAMA. 274 (12): 968–74. PMID 7674528. Unknown parameter
|month=
ignored (help) - ↑ Sands, KE.; Bates, DW.; Lanken, PN.; Graman, PS.; Hibberd, PL.; Kahn, KL.; Parsonnet, J.; Panzer, R.; Orav, EJ. (1997). "Epidemiology of sepsis syndrome in 8 academic medical centers". JAMA. 278 (3): 234–40. PMID 9218672. Unknown parameter
|month=
ignored (help) - ↑ Kumar, A.; Roberts, D.; Wood, KE.; Light, B.; Parrillo, JE.; Sharma, S.; Suppes, R.; Feinstein, D.; Zanotti, S. (2006). "Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock". Crit Care Med. 34 (6): 1589–96. doi:10.1097/01.CCM.0000217961.75225.E9. PMID 16625125. Unknown parameter
|month=
ignored (help) - ↑ Bernard, GR.; Vincent, JL.; Laterre, PF.; LaRosa, SP.; Dhainaut, JF.; Lopez-Rodriguez, A.; Steingrub, JS.; Garber, GE.; Helterbrand, JD. (2001). "Efficacy and safety of recombinant human activated protein C for severe sepsis". N Engl J Med. 344 (10): 699–709. doi:10.1056/NEJM200103083441001. PMID 11236773. Unknown parameter
|month=
ignored (help) - ↑ Dremsizov, T.; Clermont, G.; Kellum, JA.; Kalassian, KG.; Fine, MJ.; Angus, DC. (2006). "Severe sepsis in community-acquired pneumonia: when does it happen, and do systemic inflammatory response syndrome criteria help predict course?". Chest. 129 (4): 968–78. doi:10.1378/chest.129.4.968. PMID 16608946. Unknown parameter
|month=
ignored (help) - ↑ Dellinger, RP.; Levy, MM.; Rhodes, A.; Annane, D.; Gerlach, H.; Opal, SM.; Sevransky, JE.; Sprung, CL.; Douglas, IS. (2013). "Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012". Crit Care Med. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. PMID 23353941. Unknown parameter
|month=
ignored (help)