Flashcards in Hunter: Sepsis and Septic Shock Deck (89):
(blank) is rare, but can be serious
Fungemia (fungus in the blood)
How are bacteria and fungi normally cleared from the blood?
via the mononuclear phagocyte system (splenic macrophages and liver Kupffer cells)
Bacteremia or fungemia results when the numbers of microorganisms exceeds (blank)
the MPS clearance capacity
These two things are poorly cleared from the circulation by fixed macrophages of the MPS especially in the absence of opsonizing antibody
encapsulated bacteria and yeast
This type of bacteremia/fungemia occurs, lasting minutes to a few hours, and resolves; usually due to tissue trauma during medical procedures, can be due to manipulation of infected tissue, surgery in contaminated areas, or in early acute infections
This type of bacteremia/fungemia occurs, clears, then recurs with the same organism, and develops with undrained closed-space abscesses (intra-abdominal, pelvic, perinephric, hepatic)
Intermittent bacteremia can be seen in (blank) that fail to resolve, reflecting irregulat cycles of release into and clearance from the circulation of organisms infecting tissue
This form of bacteremia or fungemia is a cardinal feature of endocarditis and other types of endovascular infections (suppurative thrombophlebitis, infected aneurysms), reflecting constant shedding of organisms from endovascular foci into the circulation
What is the main example in which you would see continuous bacteremia or fungemia?
**continuous shedding of organisms from endovascular foci into the circulation
Continuous bacteremia also occurs early in these two cases
Compare transient, intermittent, and continuous bacteremia on a scale
transient: bacteria level spikes and then it falls
intermittent: cycles of spikes and falls
continuous: always present or ever increasing
T/F: Bloodstream infections are usually caused by a massive amount of organisms in a given volume of blood
false; Bloodstream infections are frequently caused by relatively few organisms in a given volume of blood (<1- 10 colony forming units/mL of blood)
How should you draw blood if you expect a bloodstream infection?
draw 20-30mL of blood twice from two different sites and culture them in both aerobic and anaerobic conditions
**do not take blood from an indwelling IV or intra-arterial catheter unless you suspect a catheter-related infection
Bacteremia or Fungemia Can Occur Secondary to Spread from an (blank)
ex: biofilms on catheters or cannulas
**treat by removing the device, antibiotics won't work
Most cases of clinically significant bacteremia or fungemia are the result of overflow from (blank)
an extravascular infection via hematogenous spread
In extravascular infection leading to bacteremia, microorganisms from a focus of infection often reach the capillary and venous circulation through (blank)
The process is dependent on the timing and interaction of multiple events and is thus much less predictable than intravascular infection
The probability of bacteremia or fungemia is dependent on what two factors?
1. source of infection
2. the microorganism
Most common sources of bacteremia?
UTI (E. Coli)
resp tract infections
infections of skin and soft tissues (ex: wound infection or cellulitis)
Any organism producing (blank) is likely to produce bacteremia at the same time
The frequency with which any organism causes bacteremia is related to both (blank) and how often it produces infections
its likelihood to invade the bloodstream
T/F: Some bacteria and fungi are very difficult to isolate from blood cultures, so although the bacteria may be invading the bloodstream, it may be hard to find the bacteria in the blood
an inflammation of a vein wall frequently associated with thrombosis and bacteremia
suppurative (septic) thrombophlebitis
Why has the rate of superficial thrombophlebitis increased?
increasing use of IV catheters
What happens in septic thrombophlebitis?
there is formation of a thrombus resulting from trauma to the vessel, stasis of blood flow, or hypercoagulable state
the thrombus is then seeded with organisms and an infection is established
the infection can then spread to adjacent structures, leading to septic embolization
What is the difference between organisms that cause infection in superficial thrombophlebitis and deep thrombophlebitis?
superficial: usu nosocomial bacteria (S. aureus, S. epidermidis, gram-negative anaerobes)
deep infections: caused by organisms that reside on adjacent mucous membranes or commonly infected sites (Bacteroides, E. Coli, H. influenzae, S. pneumo)
This is suspected in pts with risk factors like surgery and indwelling venous cannulas; bacteremia is usually present; surgical exploration might be required; removal of IV catheter is necessary
suppurative (septic) thrombophlebitis
used to describe pathogens in the blood that are causing sepsis
Some systemic responses to infection can be protective. But for non-protective responses, there is a progression of illness from (blank) to (blank)
systemic inflammatory response syndrome; multi-organ dysfunction syndrome
List the order of severity from systemic inflammatory response syndrome to multiple organ dysfunction syndrome
1. systemic inflammatory response syndrome
3. severe sepsis
4. septic shock
5. multiple organ dysfunction syndrome
What are the SIRS criteria (systemic inflammatory response syndrome)
Pt must have at least 2 of the following:
1. temp > 38C or 36C
2. HR > 90bpm
3. resp rate >20
4. white blood cells > 12,000 or <4,000
Sepsis in conjunction with at least one sign of organ failure or hypoperfusion, such as lactic acidosis (lactate >4 mmol/L), oliguria (urine output ≤ 0.5 mL/kg for 1 hour), abrupt change in mental status, mottled skin or delayed capillary refill, thrombocytopenia (platelets ≤ 100,000 cells/mL) or disseminated intravascular coagulation, or acute lung injury/acute respiratory distress syndrome
Severe sepsis with hypotension (or requirement of vasoactive agents, (e.g., norepinephrine) despite adequate fluid resuscitation in the form of a 20-40-ml/kg bolus
Dysfunction of two or more organ systems such that homeostasis cannot be maintained without intervention
multiorgan dysfunction syndrome
Approximately two-thirds of the cases of severe sepsis occur in patients with significant underlying illness. Sepsis-related incidence and mortality rates increase with (blank) and preexisting (blank)
Why is the incidence of cases of severe sepsis on the rise?
increasing longevity of patients w chronic diseases
high frequency in AIDS pts
widespread use of immunosuppressive drugs, indwelling catheters and mechanical devices
What is the most common microorganism that causes sepsis and septic shock?
gram-negative and gram-positive bacteria (45% of cases)
Do you always yield bacteria and fungi on a blood culture in cases of severe sepsis and septic shock?
no! negative findings are not unusual; in 20-40% of cases of severe sepsis, no bacteria shows up on the culture!
Sepsis in neonates is usually caused by (blank) and less often by (blank)
How do neonates infected w Strep. agalactiae or E. coli usually present?
What are the organisms most likely to cause sepsis in older children?
What is the most likely way an infant would be infected with Strep agalactiae?
oral contamination during passage through the birth canal
Sepsis is a complex interaction between what two components?
the direct toxic effects of the infecting organism
the derangement of the normal inflammatory response to infection
In response to local infection there is concurrent activation of the immune system and of (blank) mechanisms to control the reaction
The devastating effects of sepsis syndrome are caused by a combination of what 3 factors
1. expansion of the immune response to other sites besides site of infection
2. derangement of the balance b/w proinflammatory and anti-inflammatory cell regulators
3. dissemination (spreading) of the infecting organism
What is the difference between a localized and systemic infection?
a localized infection does produce inflammatory mediators that induce protective innate responses and eliminate the pathogen; systemic infections produce these same mediators but in large quantities that cause significant pathophysiologic changes and can lead to death
During an immune response to infection, microbial antigens trigger local cells to release (blank)
These molecules attract leukocytes, trigger dilation of vessels, slow blood flow through venules and capillaries, and increase (blank) of vessel walls allowing leukocytes and fluid to move into the infected extravascular space
The cytokines also induce the release and production of (blank), which are antimicrobial but are also serve as procoagulants
proinflammatory cytokines; leakiness; acute phase reactants
When vasodilation and coagulation spread beyond the site of infection, sepsis can result in...
resultant organ failure
Vascular endothelial injury is a major mechanism for multiorgan dysfunction
Stimuli such as (blank) induce vascular endothelial cells to produce and release a variety of cytokines, procoagulant molecules, platelet-activating factor, nitric oxide, and other mediators
Upregulated cell-adhesion molecules promote the adherence of (blank) to endothelial cells; toxic mediators released
Leukocyte-derived mediators and (blank) may contribute to vascular injury
Endothelial cell activation can also promote increased (blank), coagulopathy, microvascular thrombosis, and hypotension
leukocytes; platelet-leukocyte-fibrin thrombi; vascular permeability
In sepsis-induced DIC the (blank) is diffusely activated as part of the inflammatory response
At the same time, the (blank), which normally acts to keep the clotting cascade in check, is activated
coag cascade; fibrinolytic system
In DIC, describe the feedback spiral that is occurring.
both the coag system and fibrinolysis are activated, so new clots are always being formed, then broken down
In DIC, clotting factors and platelets are consumed in forming clots, and patients are at risk for complications from what two things
thrombosis (from the clots)
hemorrhage (from low platelets)
What can be given to patients with DIC?
This is a bad prognostic indicator in sepsis
What are the initial symptoms of sepsis?
signs of a systemic inflammatory response (fever, tachycardia, tachypnea, leukocytosis)
Sepsis can then progress to (blank)
**this would be considered septic shock
Two signs of organ dysfunction in sepsis
altered mental status
decreased urine output
T/F: A patient not initially meeting sepsis criteria can rapidly progress to full blown septic shock
In infants and the elderly, how can sepsis present differently?
may present w hypothermia instead of hyperthermia
leukopenia instead of leukocytosis
These are two lung pathologies that are present in most cases of severe sepsis
acute lung injury
acute respiratory distress syndrome
**end result of respiratory distress and hypoxia
One of the early complications of septic shock is (blank)
**thought to be caused by direct toxicity caused by inflammatory molecules
How is preload monitored in sepsis?
hydration; vasopressors; dobutamine
Sepsis places an unprecedented workload on the heart, which can precipitate these two conditions, especially in the elderly
acute coronary syndrome
This is an indicator of liver failure in sepsis
**also increased bilirubin, aminotransferases, and alkaline phosphatase
Is liver synthetic function usually affected by sepsis?
no, acute phase proteins are still produced unless the pt has been hemodynamically unstable for a really long time
Renal failure in sepsis is due to (blank), and is manifested by oliguria, azotemia, and inflammatory cells on urinalysis
Hydration and vasopressors are used to support perfusion
If renal failure is severe or the kidneys cannot be adequately perfused, then (blank) is indicated
T/F: There is no specific diagnostic test for sepsis, and the septic response can be quite variable among patients
Definitive etiologic diagnosis of sepsis requires (blank) of the microorganism from blood or a local site of infection. At least (blank) blood samples should be obtained (from two different venipuncture sites) for culture
In many cases, blood cultures are (blank); this result can reflect prior antibiotic administration, the presence of slow-growing or fastidious organisms, or the absence of microbial invasion of the bloodstream
In these cases, (blank) and culture of material from the primary site of infection or from infected cutaneous lesions may help establish the microbial etiology
isolation; two; negative; gram staining
Thrombocytopenia should prompt evaluation for (blank), with evaluation of fibrinogen and fibrin split products as well as partial thromboplastin (PT) and partial thromboplastin time (PTT)
Elevated blood urea nitrogen (BUN) and creatinine may result from renal (blank), and elevated liver function tests (LFTs) may result from hepatic (blank).
If this is elevated, it indicates poor overall tissue perfusion
How to initially treat a patient with sepsis?
give IV fluid bolus
give broad-spectrum IV antibiotics w/i 1 hour (whether or not blood cultures have been drawn)
Things that should be ordered in the work up of sepsis
chest X-ray (to look for source of infection)
ECG (to look for ischemia secondary to hypoperfusion)
What are the 4 treatment goals for patients with sepsis?
1. resuscitate the patient from septic shock by using measures to correct hypoxia, hypotension, and impaired tissue O2
2. start antibiotics as early as possible
3. identify the source of infection
4. maintain adequate organ system function
When to give antibiotics in cases of sepsis?
within the first hour after sepsis is recognized
T/F: Antibiotics should be initiated rapidly, even if the source of the infection is unknown. When you figure it out, you can switch the antibiotic.
Which bacteria, gram-positive or gram-negative causes most cases of sepsis?
gram positives are now just about as common as gram negatives
Sepsis due to (blank) organisms is rare, although the mortality rate is high
Only therapy proven to treat septic shock
early IV antibiotic therapy
What combination of antibiotics should be used in adults w sepsis?
+ clindamycin or metronidazole for anaerobes
fluoroquinolone + clindamycin
Restores intravascular volume, which is depleted in patients with severe sepsis. Improves cardiac output, organ perfusion, and mortality in severe sepsis
crystalloid (fluid bolus)
Improves blood pressure and cardiac output. More effective than dopamine in refractory septic shock
Improves cardiac output. May be used in combination with a vasopressor to increase cardiac output
Improves blood pressure in patients with septic shock
A method of continual assessment and reassessment of clinical and laboratory markers, with interventions aimed at normalizing those markers
The overarching goal is to eliminate mismatch between oxygen demand and oxygen supply (the hallmark of sepsis) by increasing supply and—where possible—by decreasing demand
early goal-directed therapy
This is one major part of treatment for sepsis
remove the source of infection!!
**surgical removal or drainage of infection site
remove indwelling IV or arterial catheters
replace foley and drainage catheters
T/F: Approximately 20-35% of patients with severe sepsis and 40-60% of patients with septic shock die within 30 days
Case-fatality rates are similar for culture-positive and culture-negative severe sepsis
T/F: Acute Physiology and Chronic Health Evaluation III (APACHE III) indicate that factoring in the patient's age, underlying condition, and various physiologic variables can yield estimates of the risk of dying of severe sepsis
In patients with no known preexisting morbidity, the case-fatality rate remains below 10% until the fourth decade of life; it gradually increases to exceed 35% in the very elderly