Unit 1: Sepsis/Septic Shock Flashcards
Sepsis
life-threatening organ dysfunction caused by a deregulated host response to infection
- start of the infection and can lead to septic shock w/ tissue damage, organ failure, and death
- this occurs when the inflammatory response is no longer localized and there is an uncontrolled physiologic response
- organ dysfunction and hypoperfusion in the presence of an infection
Septic Shock
sepsis w/ underlying circulatory and cellular/metabolic abnormalities profound enough to substantially increase mortality
- occurs when circulatory and metabolic abnormalities are profound; increased mortality
- circulatory system is unable to supply adequate amounts of oxygen to the tissues
- decreased cardiac output
- decreased oxygen delivery
- decreased oxygen consumption
Cardiac Output
amount of blood ejected by the heart each minute
- affected by contractility which is the force of the mechanical contraction
- poor contractility decreased stroke volume thus decreasing cardiac output
Oxygen Delivery (DO2)
amount of oxygen delivered to the tissues
Oxygen Consumption (VO2)
reflects the amount of oxygen extracted from the blood at the tissue level
-can be measured through evaluation of a blood sample, a mixed venous oxygen saturation (SvO2)
Type of Shock: Distributive Shock
is the result of disease states such as sepsis, anaphylaxis, or neurogenic or spinal shock that cause poor vascular tone and vasodilation resulting in increased vascular capacity and venous pooling
-in this form of shock, blood volume is adequate, but a state of hypovolemia exists b/c of venous pooling and decreased venous return to the right heart
Pathophysiology
- invasion of a pathogen initiates a series of complex responses by the hosts immune system
- the initial, immediate response is the activation of the innate immune response; nonspecific to any antigen
> Innate Immune response Involves:
- mobilization of macrophages and neutrophils to the area
- activation of pro-inflammatory cytokines or signaling molecules
- activation of complement proteins, proteins that immobilize and breakdown pathogens
- activation of coagulation system; activated coagulation produces a fibrin mesh to help localize the invading organism and activates bradykinin which dilates vessels and increases capillary permeability
- local blood vessels dilate, increasing circulation to the involved area, allows influx of immune cells; local redness, warmth and edema; done in effort to kill invading organism and keep response localized
- sepsis occurs when the inflammatory response is no longer localized
- response becomes amplified and uncontrolled
- the normal deactivation process, which decreases the production of pro-inflammatory cytokines and produces anti-inflammatory cytokines, is impaired
- the excessive release of proinflammatory cytokines = damage to the endothelial cells lining the blood vessels producing vasodilation, decreased vasomotor tone, and increasing capillary permeability
How Sepsis and Septic Shock become a Result
result when pro-inflammatory cytokines overpower anti-inflammatory cytokines
- results in excessive systemic inflammation, massive peripheral vasodilation, and increased capillary permeability
- endotoxins released by gram-negative bacteria and exotoxins produced by gram-positive bacteria add to the pro-inflammatory effect
- excessive inflammation = enhanced coagulation = widespread fibrin deposits and excessive clotting throughout vascular system; also results in decreased fibrinolysis (breakdown of clots)
Decreased Fibrinolysis
breakdown of clots becomes decreased
-occurs d/t decreased levels of activated protein C and antithrombin III seen in septic patients
>Protein C: modulates production of thrombin and promote fibrinolysis
>Thrombin: modulate the conversion of fibrinogen to fibrin clots
>Antithrombin III: deactivates thrombin
-decreased levels of both protein C and antithrombin III = enhanced thrombin formation = clot formation and impaired fibrinolysis = impaired blood flow d/t microvascular clots and organ dysfunction
Clinical Manifestations of Septic Shock
reflect the poor vascular tone and vasodilation that results in increased vascular capacity and blood pooling in the venous system
- adequate blood volume, but relative hypovolemia exists b/c of decreased venous return to the right heart
- invasion of a pathogen initiates a series of complex immune system responses
Risk Factors for Septic Shock
- 10-52% of ICU patients w/ sepsis die from septic shock
- age
- comorbidities
- invasive lines/monitoring devices
- chemotherapy
- immunosuppressive drugs
- antibiotic resistance
Early Stages of Septic Shock/Sepsis
“hyperdynamic or warm” sepsis
>reflect the initial inflammatory response
-tachycardic
-bounding pulses
-warm, flushed skin
-febrile
-BP normal as a result of compensatory responses
-initial signs of decreased organ perfusion may be present; confusion, decreased urine output
-increased cardiac output as long as there is adequate fluid resuscitation
-filling pressures low (CVP and PAOP) b/c of increased cardiac output
-systemic vascular resistance (SVR) low b/c of systemic vasodilation
-venous oxygen levels temporarily increase d/t increase in cardiac output
Late Stages of Sepsis/Septic Shock
“hypodynamic or cold” shock
- cool, pale skin; cyanotic and mottled
- weak and thready pulses
- hypothermia
- tachycardia persists (trying to compensate)
- BP remains low
- signs of end-organ hypoperfusion; lethargy, or coma, and anuria
- decreased cardiac output w/ variable filling pressures depending on fluid resuscitation
- systemic vascular resistance (SVR) remains low
- venous oxygen levels decrease
- decreased/absent urine output/bowel sounds (organs shutting down)
Diagnosing Sepsis
> Identification of infection through evaluation of indicators of infection
- fever
- increased WBC
- changes in BP, HR, and RR
> Signs of specific infection
- lung consolidation
- frequent or painful urination
- peritonitis
> Laboratory Tests
- CBC
- Metabolic Profiles
- Urine testing
- cultures
> Imaging
- General radiographs
- CT scans
- MRI
Sequential Organ Failure Assessment (SOFA)
guides assessment of sepsis
- higher the score = higher mortality (0-4)
- evaluation begins w/ a quick SOFA (qSOFA); evaluates for increased respiratory rate, decreased BP, and altered mentation
- if indicated, continue w/ SOFA (ICU)
- SOFA used in critical care to describe organ dysfunction or failure and describes the severity of the organ failure
Nursing Assessment: qSOFA score
the presence of 2 of any of these criteria prompts further evaluation of organ dysfunction:
>Any change in mental status
>Systolic BP <100 mmHg
>Respiratory rate >22 breaths/min
- pts assigned one point for each abnormal parameter
- non-ICU patients w/ a total score of 2 or 3 are considered at elevated risk for an extended ICU stay or death and should be assessed for evidence of organ dysfunction using the SOFA
The qSOFA score
developed to be easily and quickly implemented in clinical settings outside the ICU w/ technology or lab tests
- qSOFA is a predictor of mortality risk and not a defining characteristic of sepsis; used to identify patients who require further assessment for organ failure
- consists of patients Glasgow Coma Scale (GCS), systolic BP, and respiratory rate
- patients w/ a suspected infection and qSOFA score of 2 or greater have a greater risk for morbidity d/t sepsis
Systemic Inflammatory Response Syndrome (SIRS) Criteria
- Temp: <96.8 or >100
- HR >90 (except A. fib)
- RR >20
- WBC <4, >12, or 10% BANDS (immature neutrophils signaling infection)
Abnormal SOFA Parameters
> Respiratory:
-PaO2:FiO2 <300 mmHg / respiratory failure requiring need for mechanical support
> Coagulation
-Platelets <100,000, INR >1.5, or PTT >60 seconds
> Hepatic:
-Bilirubin >2 mg/dL
> Cardiovascular:
-hypotension requiring vasopressor support/ SBP <90
> Neurologic:
-GCS <12
> Renal: Creatinine >2 mg/dL, or urine output <5 ml/kg/hr. x 2 hrs.
Medical Management
First line therapy: PREVENTION
- handwashing
- meticulous aseptic technique for invasive procedures
- elimination of invasive therapies when possible
- aggressive mouthcare (brushing teeth w/ chlorhexidine products) may prevent ventilator-associated pneumonia
Bundle of Care Campaign
developed to help standardize the complex treatment need in pts w/ severe sepsis
-includes activities that need to be completed within 1 hour after identifying sepsis; should begin immediately
Bundle of Care Criteria
(Within 3 hours of suspected sepsis)
- Measure Lactate (lactic acid) level; repeat if >2
- Obtain blood cultures (prior to antibiotics)
- Administer broad spectrum antibiotics within 1 hr.
- Fluid resuscitation: 30 ml/kg of crystalloid (normal saline or lactated ringers) for hypotension or lactate level 4 or greater, or if there are 2 SBP <90
(Within 6 hours)
-Vasopressors if BP is unresponsive during or after fluid resuscitation; maintain mean arterial pressure (MAP) at 65 mmHg or above
Lactate Levels
- used as a marker of tissue hypoxia d/t inadequate oxygen delivery in sepsis
- cannot be used in isolation as a “test” for sepsis; adjunctive assessment tool
- elevated levels can be attributed to lactic acidosis from tissue hypoxia or from a nontissue hypoxic state
- high = not enough oxygen to tissues
Complications of Sepsis
- Disseminated Intravascular Coagulopathy (DIC)
- Multiple Organ Dysfunction Syndrome (MODS)
Complications: DIC and what it does
- hematological disorder; enhanced coagulation
- occurs b/c of enhanced coagulation from the release of procoagulant factors as part of the inflammatory response associated w/ sepsis
- clotting/thrombic phase and a bleeding phase
> Initial Thrombotic Stage:
- last hours or several days
- large amounts of thrombin are produced in response to decreased levels of protein C and antithrombin III = excessive production of fibrin clots and consumption of clotting factors
- excessive coagulation leads to clots lodging in the microvasculature = ischemia and necrosis
- cyanosis and ischemia in the fingers and toes and tip of nose
- organ ischemia may be present
- risk for thrombophlebitis, PE, and stroke
> Bleeding stage:
- initiation of fibrinolysis
- although impaired in sepsis, occurs in attempt to break down and remove the clot
- the breakdown causes increased circulating fibrin degradation products, which are powerful anticoagulants; they impair the activity of thrombin resulting in a decreased ability to form a fibrin clot
- combo of lack of available clotting factors and the anticoagulant properties of the fibrin degradation products = excessive bleeding d/t inability to form clots
Diagnosis of DIC
based on clinical picture w/ lab results
- decreased fibrinogen
- increased fibrin degradation products
- increased D-Dimer (indication of clot breakdown)
- decreased platelets
- prolonged PT and PTT
- decreased antithrombin III levels
Management of DIC
-vigorous tx of underlying disorders
-treating the disorders caused by the excessive clotting and bleeding:
>hypotension
>hypoxemia
>respiratory distress
>metabolic acidosis associated w/ poor tissue perfusion
>volume replacement w/ crystalloids
>blood replacement
>replacement of clotting factors w/ fresh frozen plasma and platelets
Complications: Multiple Organ Dysfunction Syndrome (MODS)
- result of the excessive inflammation
- decreased O2 to the organ systems = impaired tissue perfusion
- organs fail d/t poor oxygen utilization, microvascular dysfunction, maldistribution of blood flow, and metabolic acidosis
- often lungs fail first (ARDS) followed by the renal system, hepatic system, and GI system
- focus = support all body systems
Nursing Management: Assessment and Analysis
> Clinical manifestations r/t initial increase in cardiac output that occurs d/t the tachycardia and decreased systemic vascular resistance
-presents as warm and flushed w/ bounding pulses
Later manifestations reflect the prolonged poor tissue perfusion
-hypotension, tachycardia, hyperventilation, decreased LOC, weak pulses, cold cyanotic mottled skin
-urine output and bowel sounds decreased or absent
-w/o successful intervention = manifestations of enhanced coagulation (necrotic tissues in extremities)
-later stages, excessive bleeding from any puncture wounds, IV sites, or wounds begin
Nursing Diagnoses
altered tissue perfusion r/t inadequate cardiac output
Nursing Assessments for Sepsis/Septic Shock
- Neurological Status
- Vital Signs
- Hemodynamic Parameter
- Urine Output
- Skin color and temperature
- Bleeding
- Laboratory Tests
- Lactate/ Base Deficit
- Clotting studies
Assessments: Neurological Status
-decreased LOC occurs as a result of decreased cardiac output and hyperventilation which = a decrease in cerebral blood flow
Assessment: Vital Signs
- Hypotension b/c of vasodilation; producing relative hypovolemia and decreased venous return
- Tachycardia (compensatory mechanism)
- Initially febrile, later hypothermia; bodys inability to continue adaptive response
Assessment: Hemodynamic Readings
- initially cardiac output is increased
- as sepsis progresses, cardiac output decreases as a result of continued decreases in filling pressures (CVP and PAOP)
- initially systemic vascular resistance (SVR) is low as a result of widespread vasodilation; can increase d/t compensation and vasopressor therapy
Assessment: Urine Output
decreased urine output as a result of decreased cardiac output and initiation of compensatory mechanisms
Assessment: Skin color and temperature
- initially skin flushed and warm b/c of increased cardiac output
- later, cold skin and clammy = progression of shock
- tissue necrosis in extremities may = the enhanced coagulation of DIH
Assessment: Bleeding
excessive bleeding from wounds and puncture sites b/c of consumption of clotting factors in DIC
Assessments: Laboratory Tests
> ABGs: initial may reflect a respiratory alkalosis d/t hyperventilation (excreting CO2 excessively)
- hypercapnia (increased CO2) and hypoxia as respiratory failure worsens
- later reveals metabolic acidosis d/t anaerobic metabolism
> Venous Oxygen Saturation:
- decreased SvO2 and ScvO2 = inadequate oxygen delivery
- later may be increased d/t maldistribution of blood flow; not indicative of recovery
> Metabolic Profile:
-renal failure and liver failure e/b increased BUN and creatinine and liver function test results as a result of decreased organ perfusion
Assessment: Lactate/ Base deficit
-increased lactate and negative base deficit = poor perfusion at cellular level
Assessment: Clotting studies
indicative of progression to DIC
- decreased levels of fibrinogen
- increased fibrin degradation products
- increased D-Dimer levels (indicator of clot breakdown)
- decreased platelets
- prolonged PT and aPTT
- decreased antithrombin III levels
Nursing Actions for Sepsis/Septic Shock
- Meticulous hand washing + aseptic technique w/ all procedures
- Administer Oxygen as ordered
- Anticipate and Prepare for Intubation
- Obtain Lactate level
- Obtain 2 blood cultures from two different sites, obtain urine, sputum, and wound cultures
- Administer antibiotics as ordered after cultures obtained
- Administer fluid replacement as ordered
- Administer vasoactive drips (norepinephrine) as ordered
- Provide mouth care q 4 hours and PRN
- Supportive care: nutrition, turning, DVT prophylaxis, ROM exercises, mobilize as tolerated
Nursing Actions: Administer oxygen as ordered
-maximizing oxygenation
Nursing Actions: Anticipate and Prepare for Intubation
to improve oxygenation or if respiratory failure ensues
Nursing Actions: Obtain Lactate level
- indicator of adequacy of perfusion
- increased levels signal presence of anaerobic (w/ O2) metabolism (>2)
Nursing Actions: Obtain 2 blood cultures from two different sites, obtain urine, sputum, and wound cultures
identify offending organism
Nursing Actions: Administer antibiotics as ordered after cultures obtained
antibiotics are first-line in attempt to control infection
Nursing Actions: Administer fluid replacement as ordered
aggressive fluid replacement is initial treatment to restore filling volumes (CVP and POAP/ preload) and blood pressure
Nursing Actions: Administer vasoactive drips as ordered
ex: norepinephrine, epinephrine, phenylephrine
- restore vascular tone if fluid replacement therapy is not effective at increasing blood pressure and cardiac output
Nursing Teachings
- cause of sepsis and importance of hand washing
- allow family member visitation during hospitalization
Evaluating Care Outcomes
- Interventions w/ antibiotics and fluids is essential in maintaining cardiac output
- Vasoactive support if fluid replacement is not effective at maintaining BP
- Hemodynamic monitoring and laboratory assessments help monitor effectiveness of treatment
- Supportive care (mouth care, frequent turning, nutrition, DVT prophylaxis)
- Successful treatment results in satisfactory blood pressure (BP) level and cardiac output, and adequate tissue perfusion
