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Sepsis > Sepsis > Flashcards

Sepsis Flashcards

1
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

AKA Cytokine storm
Release of large quantities of cytokines in response to stimulus
Cytokines are chemical mediators of inflammation and immune response
Causes multiple organ dysfunction

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2
Q

SIRS Criteria

A 
At least 2 of 4:
1. Fever (>38 C, 100.4F) or hypothermia (<36 C, 96.8F)
2. Tachycardia (>90 bpm)
3. Tachypnea (>24 breaths/minute)
4. Leukocytosis (>12,000cells/mm3)
Leukopenia (<4000 cells/mm3) OR
Left shift (>10% immature band cells)
AKA elevated or lower WBC count

A diffuse fungal infection could make a patient hypothermic and leukopenic

Many things could cause a patient to have SIRS, so this definition is not used as much anymore

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3
Q

Sepsis

A

At least 2 of 4 SIRS criteria
PLUS
Suspected or proven infection

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4
Q

Severe sepsis

A

At least 2 of 4 SIRS criteria
PLUS
suspected or proven infection
PLUS
end-organ dysfunction in one or more organ systems
(CV, renal, resp, hema, metabolic acidosis)

Sig. decreased urine output
Changes in mental status
Decreased platelets
Difficulty breathing
Abnormal heart function
Abdominal pain
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5
Q

Septic shock

A

At least 2 of 4 SIRS criteria
PLUS
suspected or proven infection
PLUS
end-organ dysfunction in one or more organ systems
(CV, renal, resp, hema, metabolic acidosis)
PLUS
Hypotension (systolic bp <90mmHg or >40 mmHg decrease from baseline) despite adequate fluid resuscitation, requiring pressor therapy

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6
Q

Refractory septic shock

A

At least 2 of 4 SIRS criteria
PLUS
suspected or proven infection
PLUS
end-organ dysfunction in one or more organ systems
(CV, renal, resp, hema, metabolic acidosis)
PLUS
Hypotension (systolic bp <90mmHg or >40 mmHg decrease from baseline) despite adequate fluid resuscitation, requiring pressor therapy
AND THEN
It lasts for 1 hour despite fluid resuscitation and pressor therapy
May lead to death

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7
Q

New classification of Sepsis syndromes

A

Since 2016 Society of Critical Care Medicine

Early sepsis > Sepsis > Septic shock

Leads to multiple organ dysfunction syndrome (MODS) and death

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8
Q

Early Sepsis and qSOFA

A

Assuming they already have an infection

Quick Sequential (sepsis-related) Organ Failure Assessment score (qSOFA)

qSOFA score <2: 3% risk of mortality
qSOFA score >=2: 18-24% risk of mortality

Resp rate >=22
Altered mentation
Systolic blood pressure <=100mmHg

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9
Q

Sepsis

A

Life-threatening organ dysfunction caused by infection with dysregulated host response

When your body’s inflammatory response to infection gets out of hand

SOFA score:
Increase of 2+ points
Not diagnostic of sepsis or infection (need other things to tell us if patient is actually sick with infection)
Assess for end-organ dysfunction
Identify patients who are at risk of death

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10
Q

Septic Shock

A

Vasodilation or distribution problem due to sepsis causing circulatory, cellular, or metabolic derangements

Sepsis (assuming patient has an infection)

Requirement of vasopressors to maintain mean arterial pressure (MAP) of >65 mmHg
Keep BP up, profusion, organs get the blood they need

Lactate >2mmol/L

> 40% mortality vs >10% with sepsis alone

28 day mortality is 40-70%

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11
Q

Shock

A
  1. Diminished cardiac output or reduced effective circulating blood volume
  2. Impairs tissue perfusion and leads to cellular hypoxia
  3. Can lead to cell death and eventually organ failure and death if not corrected immediately

Can be reversible or fatal

Caused by many things (not just infection):

  1. Infection (inflammatory cytokines)
  2. Anaphylaxis (severe allergic reaction- vasodilator response, pass out, die)
  3. Cardiac abnormality (if your heart can’t pump regularly)
  4. Hypovolemia (bleeding out, losing blood for organs)
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12
Q

Multiple Organ Dysfunction Syndrome (MODS)

A

Progressive

Primary (result of defined insult) or secondary (result of indirect insult to due host response)

No universally accepted criteria (use SOFA score)

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13
Q

Sepsis stats

A

> 750,000 cases of severe sepsis or septic shock a year
As many as AMIs
Most common cause of death in ICU (non-cardiac)
3rd leading cause of death in US

Frequency increasing:

  1. More aggressive surgery
  2. More resistant organisms (infections have become resistant to antibiotics)
  3. More immune compromise from diseases and meds (cancer)
  4. Increased elderly living with chronic diseases (AIDS, because we can treat it)
  5. Widespread use of catheters/mechanical devices (foreign bodies in people, increasing risk of infection)
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14
Q

What constitutes poor prognosis with septic shock?

A 
Increased age
Comorbid medical conditions
High APACHE II score
Elevated lactate
Insufficient response to vasopressors
Delay in treatment
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15
Q

Infectious causes of sepsis

A
  1. Opportunistic infections (wouldn’t normally cause infections in immunocompetent hosts)
  2. Host factors (comorbid disease like COPD, diabetes, hypertension)
  3. Indwelling lines/catheters/foreign bodies (obstruction of normal drainage)
  4. Microbial factors (evading immune system and antibiotics we use to treat; toxins we cannot treat)
  5. Microbes (gram+,gram-, fungi, virus)
  6. Infections
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16
Q

Pneumonia

A

Lung infection

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17
Q

Peritonitis

A

Infection in abdominal cavity (with liver disease)

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18
Q

Pyelonephritis

A

Kidney infection

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19
Q

Abscess

A

Especially intra-abdominal

If you have surgery and they nick the bowel and the contents leak out into the belly, that could form an abscess

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20
Q

Cholangitis

A

Infection in gall bladder

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21
Q

Cellulitis and necrotizing fasciitis

A

Skin, fascia, muscle, bone; think all layers

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22
Q

Cardiogenic shock

A

Caused by:

  1. Myocardial infarction (patient is hypotensive because heart muscle can no longer pump)
  2. Ventricular rupture (from trauma)
  3. Arrhythmia (rhythm not compatible with life)
  4. Cardiac tamponade (Heart leaks out into space between heart muscle and pericardium, fluid presses on heart and prohibits it from pumping blood)
  5. Pulmonary embolism

Mechanism:
Failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic compression, or obstruction to outflow

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23
Q

Hypovolemic shock

A 
Caused by:
Fluid loss (hemorrhage, vomiting, diarrhea, burns, trauma)

Mechanism:
Inadequate blood or plasma volume

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24
Q

Systemic inflammation

A

Caused by:

  1. Overwhelming microbial infections (bacterial and fungi)
  2. Superantigens (toxic shock)
  3. Trauma, burns, pancreatitis

Mechanism:

  1. Cytokine cascade activation
  2. Vasodilation and pooling of blood and intravascular coagulation
  3. Endothelial activation/injury (immune system inflammatory response that is causing the shock)
  4. Leukocyte-induced damage
  5. DIC
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25
Q

Stages of shock

A

Non-progressive (reversible)
1. Compensatory mechanisms allow for survival

Progressive

  1. Failing compensatory mechanisms
  2. Increasing tissue hypoxia
  3. Beginning lactic acidosis due to anaerobic metabolism

Irreversible
1. Leads to death

26
Q

Shock circulatory pathophysiology

Sepsis progression

A
  1. Peripheral vasoconstriction due to autonomic nervous system stimulus and adrenal catecholamines (body trying to deal through stress hormones)
  2. Shunting (redistribution of blood to heart and brain; decrease renal and liver function)
  3. Decreased pH across capillary beds
  4. Hemodilution with hypovolemia (peripheral interstitial fluids move into vascular space to replace volume loss)

Followed by:

  1. Blood pressure and volume decreases
  2. Peripheral vasoconstriction reaches a maximum
  3. Lactic acidosis due to anaerobic metabolism
  4. Decreased capillary perfusion (endothelial hypoxia; could lose peripheral organs)
  5. Disseminated intravascular coagulation (pooling of blood, clotting, clotting factors then used up, leading to more bleeding)

Followed by:

  1. Arteriolar vasodilation
  2. Increased capillary hydrostatic pressure (volume then leaks out into tissue because it cannot be kept in, causing interstitial edema [anasarca- really puffy people], all of the fluid is out of circulation and in the tissue)
  3. Decreased function of vital organs (due to lack of perfusion)
  4. Severe metabolic lactic acidosis (and tissue necrosis)

Finally,
Irreversible phase and death

27
Q

Differential Diagnosis

A 
VINDICATE
Vascular (DVT)
Infectious (cellulitis, fasciitis, myositis, osteomyelitis)
Neoplasm
Drugs/toxins
Inflammatory (phlebitis)
Congenital/genetic
Autoimmune
Trauma (sheet rock wound)
Endocrine/metabolic
28
Q

CBC

A

Complete blood count
WBC count
Platelets
Hemoglobin

29
Q

CMP

A

Comprehensive metabolic panel
Electrolyte status
Renal function
Liver function

30
Q

Empiric Chemotherapy

A
  1. Apparent site of infection, patient history, and prevailing patterns of bugs and resistance must be considered
  2. Relatively broad coverage is indicated
  3. Changes in drug choice should be based on culture and susceptibility results, clinical response of the patient and adverse effects

Broad spectrum is often used for empiric therapy

31
Q

Indications for combination chemotherapy

A
  1. For enhanced therapeutic effect (synergism)
  2. To allow for lower doses of individual drugs to minimize toxicity
  3. To delay development of resistance
  4. For the treatment of “mixed” infections
  5. To initiate therapy in life-threatening situations when pathogen is not known

Combo chemo is often used for empiric therapy

32
Q

Air in subcutaneous tissue?

A

Indication of infection causing associated tissue destruction

Faculative aerobic organisms grow because polymorphonuclear neutrophils exhibit decreased function under hypoxia. Hydrogen, nitrogen, Hydrogen sulfide are produced and accumulate in tissues because of reduced water solubility

Seen on x ray

33
Q

Debridement

A

Clean out all dead tissue

34
Q

Elevated lactate

A
  1. Tissue hypoxia from hypoperfusion
  2. Metabolic activity switches from oxidative metabolism (mitochondrial ETC) to non-oxidative or anaerobic metabolism
  3. Lactate is produced by reduction of pyruvate by lactate dehydrogenase, which regenerates NAD+
  4. Sufficient NAD+ is needed for glycolysis and aerobic production of ATP
35
Q

Iatrogenic

A

Medical procedure leads to infection

Ex. Catheters

36
Q

Therapies for increasing blood pressure in sepsis

A
  1. Intravenous fluids to restore intravascular volume
  2. Vasopressors to improve blood pressure by causing vasoconstriction
  3. Inotropes to increase cardiac contractility (able to pump better)
  4. Some medications have both vasopressor and inotropic effects

To restore blood volume:
Replace RBCs, platelets, clotting factors

37
Q

Other therapies for sepsis

A
  1. Ventilatory support with oxygen due to tissue hypoxia
  2. Dialysis support for renal failure
  3. Corticosteroids for adrenal failure (if your stress hormones don’t work, we need to give more so that body can respond better)
  4. Nutritional support
38
Q

Mechanism of sepsis

A
  1. Host becomes infected
    Crosses epithelial barrier (cuts)
    Sometimes stays confined to subepithelial tissue through localized inflammation
  2. Bacteremia: bacteria in blood stream
    Low level- cleared via Kupffer cells in liver and splenic macrophages
  3. Endotoxins released by microbe
  4. Procession depends on host recognition
39
Q

Host response (3 steps)

A
  1. Host recognizes microbial molecules
  2. Production of cytokines, chemokines, leukotrienes, prostaglandins
  3. Rubor, Tumor, Calor, Dolor

Redness- increased circulation to area
Swelling- increased vascular permeability
Warmth- influx of inflammatory cells; also go to hypothalamus and cause fever

40
Q

Cytokines

A

Soluble proteins that interact with cells to produce changes in growth/activation of immune cells, inflammation and immune response

41
Q

Chemokines

A

Soluble molecules which guide immune cells into a particular area

42
Q

Systemic disease host response

A

Local defenses are enhanced by increasing circulation to the area, increasing circulating neutrophils, and elevated microbial recognition molecules

43
Q

TNFa

A

Cytokine

Causes leukocytes and vascular endothelial cells to:

  1. Produce and release other cytokines (including itself)
  2. Express cell-surface molecules to improve adhesion of neutrophils so they can come into tissue and fight infection
  3. Increase inflammatory production of prostaglandins and leukotrienes
44
Q

IL-8 and IL-17

A

Cytokines

Attract neutrophils

45
Q

IL-1B

A

Causes fever

Too much IL-1B can cause disease

46
Q

IL-6

A

Promotes clotting via tissue factor induction on monocytes and vascular endothelial cells

Acute phase response
Protein synthesis in the liver

47
Q

Tissue factor binds factor VIIa

A

And converts factor X and IX to active forms

48
Q

Disseminated Intravascular Coagulation

A

[Consumption coagulopathy or microangiopathic hemolytic anemia]

Abnormal clumps of thickened blood (clots) form inside blood vessels. These abnormal clots use up the blood’s clotting factors, which can lead to massive bleeding in other places

Serious sign of end stages of sepsis

Can occur with an amniotic fluid embolism

Process:

  1. Infection
  2. Tissue damage and endothelial disruption
  3. Release of TF in circulation
  4. Activation of coagulation via intrinsic pathway

Increased local inflammatory markers, activation of clotting pathways, depletion of anti-thrombin, increased plasminogen activator 1 causes fibrinolysis

Excess of thrombin»Thrombosis
Consumption of platelets and clotting factors»Haemorrhage

Both lead to organ failure

49
Q

Coagulation abnormalities

A
  1. Intravascular thrombosis
    Wall off microbes to prevent spread
    Intravascular fibrin deposition, thrombosis
    And bleeding (from DIC)
  2. Activation of extrinsic and intrinsic clotting pathways (fibrin and clotting)
  3. Impaired protein C/protein S inhibition and depletion of antithrombin (protein C and S lead to clotting), leading to unopposed clotting
  4. Increased plasminogen activator inhibitor 1 causes fibrinolysis
50
Q

D dimer

A

Check this when you have a patient in DIC

When fibrin undergoes fibrinolysis, it releases D dimers

Therefore showing if there was thrombosis or not

51
Q

Schistocytes

A

Fibrin causes mechanical damage to RBCs

Fragmented RBCs

Seen under microscope after a peripheral smear is attained

If RBCs are damaged, they’re no longer carrying O2 and the body will get rid of them, leading to anemia.

Give patient RBCs

52
Q

Waterhouse-Friderichsen Syndrome

A

Hemorrhage into adrenal glands so that they can’t function anymore.

Typical of neisseria meningitdis (college campuses)

If your body does not have these endogenous stress hormones, they must be given (adrenocorticoid therapy needed)

53
Q

Shock liver

A

Passive congestion

Everything pools
No distinction, just a pool of blood and fluid

54
Q

Nutmeg liver

A

Associated with passive vascular congestion

Found at autopsy

Typical after patient has died and you are unsure what happened

55
Q

Large Dermal Purpura

A

Bleeding in the skin; especially with neisseria meningitidis

From DIC

56
Q

What causes 76% of all orthopedic infections?

A

Staphylococcus.

  1. S. aureus
  2. S. epidermidis

Stnd treatment for biomaterial infection is removal and temporary insertion of antibiotic-impregnated spacer and replacement of implant

Biofilm cells are tolerant of antibiotics

57
Q

Staphylococci (and most medically sig species)

A

Gram+
Clusters
Pairs or single cells

Non-motile, non-spore forming
Catalase+, oxidase-
Facultative anaerobes

Major component of normal flora (skin and nares)

Medically significant:
S. aureus
S. epidrmidis
S. saprophyticus
ALL CONS
58
Q

Clinical Syndromes (of staphylococci)

A 
Toxic shock syndrome
Endocarditis 
Necrotizing pneumonia
Sepsis
Cellulitis
Necrotizing fasciitis
Pustolosis/Folliculitis
Brain abscess
Furuncle or carbuncle
Impetigo
Surgical wounds
Epidural abscess
Device associated infections: vascular devices, prosthetic joints, CNS catheters
59
Q

Virulence Factors (Staphylococcus)

A
  1. Cytolysins
  2. Multiple bi-component leukocidins
  3. Phenol-soluble modulins
  4. Enterotoxins (superantigens- GP bacteria)
  5. Adherence factors
    PRotein A binds the Fc region of antibodies (coats itself in your own antibodies so you can’t recognize it)
    Fibronectin-binding proteins
    Collagen-binding proteins
  6. Other secreted proteins
    Proteases
    Nucleases
    Hyaluronidase
    Coagulase
60
Q

Bacterial causes of sepsis

A 
1. Staph
CONS #1 (coagulase-)
S. aureus #2
2. E. coli
3. Strept

more common than viruses, fungi (candida albicans)

61
Q

Pathophysiology of septic shock (what you need to know)

A
  1. Innate immune system recognizes microbes
  2. Immune factors activate endothelial cells and additional leukocytes
  3. Immune system over-response including secondary mediators
  4. Systemic endothelia damage, vasodilation, capillary leakage
  5. Multiple organ failure
  6. Death

Sepsis (1 decks)

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