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Systemic Inflammatory Response Syndrome (SIRS) - what is it?
a systemic inflammatory response to a wide variety of severe clinical insults, manifested by 2 or more of the following
temperature > or = to 38 C or < 36 C
heart rate > 90 bpm
respiratory rate > 20 breaths/min or PaCO2 <32
WBC > 12000 or < 4000 OR bands > 10% (“shift to the left”) (INCREASE IN IMMATURE NEUTROPHIL FORMATION)
Systemic Inflammatory Response Syndrome (SIRS) - can a patient have SIRS without sepsis?
YES!! → such as traumatic injuries, pancreatitis, or burns; SIRS is a poor predictor of sepsis according to studies
Sepsis - definition? suspected infections?
a life-threatening organ dysfunction that is caused by an abnormal host response to an infection; initially, the infection may be “suspected,” rather than “proven,” based on the clinical examination and the patient’s history (SEPSIS = infection + organ dysfunction)
a “suspected” infection is the presence of one or more of the following:
positive cultures from blood, sputum, urine, etc
receiving ABX, anti-fungals, or another anti-infective therapy
altered mental status in elderly
possible pneumonia (infiltrate on chest radiograph)
nursing home patient with indwelling urinary catheter
pressure ulcers
acute abdomen
infected wounds, especially with history of diabetes
immunosuppression
Sepsis - examples of organ dysfunction
HYPOTENSION!!
acute hypoxemia (LUNG dysfunction)
acute drop in UOP (<0.5 mL/kg [<30-40 mL/hr])
lactate of 2 or greater
abrupt mental status change
platelets below 100,000; coagulopathy
Sepsis - qSOFA (quick sepsis related organ failure assessment) score
a bedside evaluation (WITHOUT LABS) to identify patients with suspected organ dysfunction
evaluates 3 criteria (1 point for each)
systolic BP LESS than or equal to 100
respiratory rate greater than or equal to 22/min
glasgow coma scale <15 (altered mentation)
score of 2-3 indicates a high probability of organ dysfunction
Septic Shock - what is it?
clinically identified by an infection, PLUS
vasopressor requirement to maintain a MAP GREATER than or equal to 65, despite adequate fluid resuscitation
serum lactate > 2, despite fluid resuscitation
Infection vs. Sepsis vs. Septic Shock (identification based on vitals/interventions)
infection - BP 110/80, pH 7.34, lactate 1.5, temp 39C, WBC 15000, acute abdomen
sepsis - BP 78/36 BEFORE fluids, 102/58 after 500 mL fluid bolus, base excess -5 (BASE DEFICIT, ACIDOSIS), pH 7.30, lactate 3, acute abdomen
septic shock - BP 78/36 BEFORE fluids, UNCHANGED after 500 mL fluid bolus x4; base excess -5; pH 7.31, lactate 6
Sepsis/Septic Shock (PATHOPHYSIOLOGY)
INFECTING ORGANISM → uncontrolled inflammatory response response due to release of mediators
→vasodilation →DECREASED SVR
→INCREASED capillary permeability/significant leak →DECREASED vascular tone
→impaired O2 extraction/utilization; maldistribution of blood flow →ANAEROBIC METABOLISM
→accelerated coagulation and micro-emboli formation →DIC
→ myocardial dysfunction → DECREASED CO (late sign)
→pulmonary dysfunction → ARDS
*activation of coagulation, inflammatory cytokines, complement, and kinin CASCADES with the release of a variety of endogenous mediators*
Sepsis - RISK FACTORS
extremes of age
chronic health problems
invasive procedures/devices
surgical wounds
genitourinary infections
prolonged hospitalizations
translocation of GI bacteria (NPO)
acquired immunodeficiency syndrome (AIDS)
use of cytotoxic and immunosuppressive agents
alcoholism
malignant neoplasms; bone marrow suppression
transplantation procedures
history of splenectomy
Septic Shock (EARLY signs/symptoms)
tachycardia, bounding pulse
BP is low, RESPONSIVE to vasopressors
skin is warm, flushed
respirations are deep, somewhat fast
lactate >2
confusion → mental status change (ESPECIALLY in elderly people)
oliguria
fever (temp >38C)
Septic Shock (LATER/PROGRESSIVE signs and symptoms)
HYPOTENSION, may NOT be responsive to vasopressors
tachycardia, pulse is WEAK and THREADY
lactate 4
skin is cool, pale
respirations are rapid OR may be slow
lethargy, coma
anuria
hypothermia (temp <36C)
Real or Myth? - a patient with sepsis or septic shock always has a fever, an elevated WBC and positive blood cultures?
MYTH MYTH MYTH MYTH (ABSOLUTELY NOT REAL)
Septic Shock - Hemodynamics (EARLY vs. LATE)
EARLY
INCREASED CO/CI (body is COMPENSATING!!)
DECREASED CVP (PRELOAD), PAP, and PAOP
DECREASED SVR
INCREASED SvO2 (d/t impaired oxygen consumption)
INCREASED O2 DELIVERY
DECREASED O2 CONSUMPTION
LATE
DECREASED CO/CI
INCREASED CVP (PRELOAD), PAP, and PAOP
SVR (variable)
SvO2 (variable)
DECREASED O2 DELIVERY
DECREASED O2 CONSUMPTION
Septic Shock - DIAGNOSTIC TEST RESULTS (Early vs. Late)
EARLY
ABGs → respiratory alkalosis, mild decreased PaO2, or may have combined respiratory alkalosis and metabolic acidosis
PT/PTT INCREASED or NO CHANGE
Platelets DECREASED or NO CHANGE
WBC (variable)
Bands INCREASED
Glucose INCREASED
Lactate INCREASED
Troponin INCREASED
LATE
ABGs→ metabolic acidosis; SEVERELY LOW PaO2
PT/PTT SEVERELY INCREASED
Platelets SEVERELY LOW
WBC LOW
Bands SEVERLY INCREASED
Glucose DECREASED (liver dysfunction →reduced gluconeogenesis)
BUN, creatinine INCREASED
Liver enzymes INCREASED
Lactate INCREASED
Troponin INCREASED
Septic Shock - TREATMENTS (fluids, pressors)
INITIAL FLUID CHALLENGE (30mL/kg of crystalloid (2.1 L for 70 kg) ASAP to achieve these goals:
MAP greater than or equal to 65; UOP greater than or equal to 0.5 mL/kg/hr (30mL/hr), decrease in tachycardia
hypotension persists? →vasopressors (LEVO is first-line; epinephrine is recommended when a second vasopressor agent is needed)
no response? → may have catecholamine-refractory septic shock (alpha receptors in arterial bed are not responsive to pressors)
START VASO!! (0.03-0.04); enhances effectiveness of initial pressor
still not effective? → consider extreme metabolic acidosis or corticosteroid insufficiency related to critical illness; SODIUM BICARB or STEROIDS may be considered, although neither have demonstrated to improve mortality rates
Septic Shock - TREATMENTS (in addition to fluids/vasopressors)
obtain 2 blood cultures ASAP prior to ABX administration
begin broad-spectrum ABX ASAP; within 3 hours of recognition of septic shock
obtain serum lactate ASAP and remeasure within 2-4 hours if first lactate is 2 or greater
identify source of INFECTION!! → helps direct antibiotic therapy
MAP remains below 65 OR lactate is 4 or greater, REASSESS FLUID STATUS
measure CVP, assess fluid responsiveness with either a passive leg raise or fluid challenge; perform/assess a bedside ECHO; measure ScvO2/SvO2
INOTROPIC THERAPY (dobumatine!! for patients with cardiac dysfunction, as evidenced by high filling pressures and low cardiac output or clinical signs of hypoperfusion after successfully restoring BP with effective volume resuscitation)
OXYGENATION GOALS
maintain SpO2 95% or greater
ScvO2 greater than or equal to 70%; SvO2 greater than or equal to 65% (when CVP and MAP goals are met)
→ScvO2/SvO2 not met? →consider further fluids, dobutamine infusion (max 20 mcg/kg/min), consider transfusion of PRBCs if hgb 7 or less
Septic Shock - THERAPEUTIC ENDPOINTS (summary)
MAP greater than 65
decreased lactate/improved base deficit
normalization of heart rate
UOP greater than 0.5 mL/kg/hr (>30 mL/hr)
warm extremities
mental status return to baseline
source control
central venous oxygen saturation (ScvO2 > or = to 70%; SvO2 greater than or equal to 60%) → if CVP or PA line is availble
CVP 8-12
Anaphylaxis - what is it?
an allergic reaction rapid in onset/may cause death
occurs after previous exposure to the substance
hives/angioedema in 88% of cases; respiratory tract involvement in 50% of cases; shock occurs in 30%
Anaphylactic Shock - etiology/PATHOPHYSIOLOGY
IgE-mediated immediate hypersensitivity reaction to protein substances
Penicillin, contrast media, bee stings, foods, latex
PATHO
antigen-antibody reaction → histamine released
→INCREASED capillary permeability/massive dilation/DECREASED CO/bronchospasm, laryngeal edema, urticaria (hives)
→HYPOTENSION!!
Anaphylactic Shock - TREATMENT
remove from agent
O2
0.3-0.5 mg of 1:1000 epinephrine INTRAMUSCULAR (more rapid absorption than subq) to decrease dilation/bronchospasms
aggressive fluid resuscitation (1-4L) to treat relative hypovolemia
antihistamine (diphenhydramine (Benadryl) 25-50 mg IV to decrease allergic response)
inhaled beta-adrenergic agents to decrease bronchospasm
steroids IV (high-dose) → peaks in 4-6 hours, give ASAP to get “on board” to decrease inflammatory response
MODS (multiple organ dysfunction syndrome) - general definition
the progressive insufficiency of 2 or more organs in an acutely ill patient, such that homeostasis cannot be maintained without intervention
MODS (multiple organ dysfunction syndrome) - cardiovascular, pulmonary, neurological MARKERS
cardiovascular - hypotension/tachycardia, dysrhythmias, need for vasopressors, decreased SVR, abnormal CVP (low or high), positive troponin
pulmonary - tachypnea/dyspnea, hypoxemia
neurological - confusion/delirium/disorientation, lethargy, coma, seizure
MODS (multiple organ dysfunction syndrome) - renal, endocrine, hepatic MARKERS
renal - elevated Cr/BUN, decreased GFR, oliguria, life-threatening electrolyte imbalances
endocrine - hyperglycemia OR hypoglycemia, adrenal insufficiency
hepatic - elevated liver enzymes, hypoglycemia, decreased albumin, jaundice
MODS (multiple organ dysfunction syndrome) - hematological, metabolic MARKERS
hematological - thrombocytopenia, coagulopathy, increased D-dimer levels, decreased protein C levels (impaired ability to prevent coagulation system from being overactive)
metabolic - metabolic acidosis, elevated LACTATE
SOFA (Sequential Organ Failure Assessment) Scoring System - what is it?
unlike qSOFA, this scoring system DOES use lab results to determine extent of organ dysfunction; six organ systems assessed →
cardiovascular (HYPOTENSION)
neurological (GLASGOW COMA SCALE)
pulmonary (PaO2/FiO2)
renal (SERUM CREATININE or UOP)
hepatic (BILIRUBIN LEVEL)
hematologic (PLATELET COUNT)