Sepsis and Septic Shock- Hunter Flashcards
How can you describe intravascular infections?
bacteremia, viremia, fungemia, parasitemia
With the exception of a few specific infections, the detection of (blank) does not play a role in the diagnosis or managment of most viral infections.
viremia
Fungemia is (common/rare) but canbe serious
rare
What is failing if you have a bacteremia or fungemia?
a failure of host defenses to localize an infection at its primary tissue site
Bacteremia and fungemia can reflect the failure of a physician to do what?
remove, drain or sterilize sites of infection
Bacteria and fungi are normally cleared from blood by the (Blank
MPS (mononuclear phagocyte system i.e splenic macrophages and liver kupffer cells)
What 2 things comprise the MPS that clear bacteria and fungi?
splenic macrophages and liver kupffer cells
Whats up with encapsulate bacteria and yeast and their ability to be cleared?
poorly cleared from circulation by fixed macrophages of the MPS especially in the absence of opsonizing antibody
What is the most common bacteremia or fungemia?
Transient bacteremia or fungemia that lasts minutes to a few hours
Why do you get transient bacteremia and fugemia?
due to release of organisms into circ secondary to tissue trauma resulting from medical procedures
What are some ways you can get transient bacteremia and fugemia?
manipulation of infected tissue (abscesses, furuncles, cellulitis), instrumentation of colonized mucosal surfaces (dental procedures, cytoscopy, sigmoidoscopy)
What can surgery in contaminated areas (prostate, resection, debridement of infected burns, vaginal hysterectomy) cause?
transient bacteremia, or transietn fungemia
Transient bacteremia or fungemia also occurs early in (Blank) including pneumonia, meningitis, septic arthritis
acute infections
Transient bactermias usually have no immediate clinical signif but they are important in the pathogenesis of (blank)
infective endocarditis
(blank) occurs, clears, recurs with the same organism, and develops with undrained closed-space abscesses (intra-abdominal, pelvic, perinephric, hepatic)
Intermittent bacteremia or fungemia
What can be seen in focal infections that fail to resolve (pneumonia, osteomyelitis), reflecting irregular cycles of release into and clearance from the circulation of organisms infecting tissue
intermittent bacteremia or fungemia
What is a cardinal feature of endocarditis and other types of endovascular infections (suppurative thrombophlebitis, infected aneurysms)?
Continuous bacteremia or fungemia
What does continuous bacteremia or fungemia reflect?
continous shedding of organisms from endovascular foci into the circulation
Continuous bacteremia also occurs early (initial few weeks) in (Blank) and (Blank)
typhoid fever
brucellosis
If you see a bacteremic spike (recur and quickly disappear) what kind of bacteremia is this and what causes this?
Transient:
Dental extraction
If you see a bacteremia in small bell curve what kind of bacteremia is this and what causes it?
intermittent
-pneumococcal
If you see a bacteremia that ebs and flows and lasts for a long time what kind of bactermia is this and what causes it?
intermittent-gram negative sepsis
If you see a bacteremia that recurs and disappears continuosly what kind of bacteremia is this and what causes it?
intermittent
intra-abdominal abscess
If you see a bacteremia that stays the same and does not change what kind of bacteremia is this and what causes it?
continuous
infective endocarditis
If you see a bacteremia that gradually increases steadily what kind of bacteremia is this and what causes it?
continuous
catheter bacteremia
Bloodstream infections are frequently caused by relatively few organisms in a given volume of blood.
T or F
T
How many culture sets should you take when you are checking fo rbacteremia?
two culture sets
- aerobic
- anaerobic
Should you take two culture sets at the same time?
no at different times and at different sites
How much blood do you need per culture set?
20-30mL of blood per culture set
Blood should NOT be obtained from an (blank) or (blank) unless catheter-related infection is suspected
indwelling IV
intra arterial catheter
For the eval of catheter-associated bloodstream infection what should you do?
concomitantly draw venipuncture specimen with a catheter specimen
Bacteremia or fungemia can occur secondary to spread from an (blank)
IV device
Bacteremia or fungemia may also result from microbial growth on the inner or outter sufaces of IV devices such as..?
Biofilms on catheters or cannulas, shunts
Antibiotic treatment is often (successful/unsuccessful) as an approach to a contaminates IV device.
unsuccessful
Contaminated IV devices need to be (blank)
removed
Most cases of clinically signif bacteremia or fungemia are the result of overflow from an (blank) infection
extravascular infection
Microorganisms from a focus of infection often reach the capillary and venous circ through (blank)
lymphatic vessels
Most cases of clinically signif bacteremia or fungemia are the result of overflow from an extravascular infection ,,,, called (blank) spread
hematogenous
Bacteremia and fungemia from extravascular infections is dependent on the timing and interaction of multiple events and is thus much (blank) predictable than intravascular infection
less
If the extravascular infection is extensive and uncontrolled, as with an overwhelming staph pneuomnia, there may be (blank) of organisms per milliliter of blood (a poor prognositc sign)
hundred to thousands
An (blank) abscess may give off only a few organisms intermittently until it is discovered and drained
intra-abdominal abscess
The (blank) of infection affects bacteremia and fungemia
source
The most common sources of bacteremia are…?
UTI
RTI
infections of skin and soft tissue (wound infection or cellulitis)
Any organism producing meningitis is likely to produce (blank) at the same time
bacteremia
The frequency with which any organism causes bacteremia is related to what?
propensity to invade the bloodstream and how often it produces infections
Cases of E. Coli bacteremia are (rare/common). Why?
comon, cuz E. coli is the most common cause of UTI
T or F
some bacteria and fungi are very difficult to isolate from blood cultures
T
(blank) is an inflammation of a vein wall frequently associated with thrombosis and bacteremia
suppurative (or septic) thrombophlebitis
What is the pathogenesis of suppurative thrombophlebitis?
thrombus formation, which may result from trauma -> thrombosed site is then seeded with organisms and a focus of infection is established
What are some complications of suppurative thrombophlebitis?
complication include extension of suppurative infection into adjacent structures, further propagation of thrombi, bacteremia, and septic embolization
Staph aureus, S. epidermis, gram-negative bacilli, and candida albicans will result in suppurative thrombophlebitis in the (blank)
superficial veins (e.g saphenous, femoral, antecubital)
Bacteroides spp, peptostreptococcus, E. coli, group A or B strep will result in suppurative thrombophlebitis in the (blank)
pelvic veins, portal veins
H. influenza, strep pneumoniae, group A strep, peptostreptococcus, S. aureus will result in suppurative thrombophlebitis in (lank)
intracranial venous sinuses (cavernous, sagittal, lateral)
In superficial thrombophlebitis, which often follows IV therapy, organism that are common (Blank) offenders predoinate
nosocomial (found in hospital)
In superficial thrombophlebitis, which often follows IV therapy, organisms that are common nosocomial offenders predominate. What are these organisms?
Staph aureus, S. epidermis, gram-negative aerobes, candida albicans
Deeper infections of suppurative thrombophlebitis are more frequently causd by organisms that reside on (Blank) or (blank)
- adjacent mucous membranes
- commonly infected adjacent sites
Deeper infections are more frequently caused by organisms that reside on adjacent mucous membranes, what are these organisms?
bacteroides species in intestinal and vaginal sites
H influenza and strep pneumonia in acute otitis media and sinusitis
(blank) is suspected in patients with risk factors like surgery and presence of indwelling venous cannulas
suppurative thrombophlebitis
How can you find out what is causing your suppurative thrombophlebitis?
direct cultures of the infects site (bacteremia is usually present)
In some cases, (blank) is required, both for definitive treatment and to obtain specimens for cultures in suppurative thrombophlebitis
surgical exploration
How should you treat suppurative thrombophlebitis?
IV cather should be removed, vigorous antibiotic treatment of adjacent infections, and sometimes surgical excision and drainage
Humans mount both (blank) and (blnk) responses to microbes that transverse their epithelial barriers and enter underlying tissues
local and systemic
Some systemic responses are protective (blank), but others can be life threatening (Blank)
acute phase response
sepsis and septic shock
For the non-protective responses, there is a progression of illness from systemic inflammatory response syndrome (SIRS) to (blank) that is defined by a combo of clinical and lab findings
multi-organ dysfunction syndrome (MODS)
In clinical parlance, any patient with sepsis, severe sepsis, septic shock, or MODS is said to be (blank)
septic
(blank) is used to describe pathogens in the blood that are causing sepsis
Septicemia
How do you go from systemic inflammatory response syndrome to multiple organ dysfunction syndrome?
systemic inflammatory response syndrome-> sepsis-> severe sepsis-> septic shock-> multiple organ dysfunction syndrome
What can cause SIRS?
trauma, burns, pancreatitis
What is the definition of SIRS?
having at least 2 of the following:
- Temperature >38°C or 90 beats per minute
- Tachypnea or hyperventilation (respiratory rate >20 breaths per minute or PaCO2 12,000 cells/mL or 10% bands
What is sepsis?
SIRS with a suspected or proven infectious source (not all SIRS has an infectious etiology)
what is severe sepsis?
Sepsis in conjunction with at least one sign of organ failure or hypoperfusion
What are these:
- lactic acidosis
- mental status change
- mottled skin
- delayed cap refill
- thrombocytopenia
- DIC
- acute lung injury
- acute respiratory distress syndrome
Signs of organ failure
What is septic shock?
severe sepsis with hypotension (or requirement of vasoactive agents e.g norepinephrine) despite adequate fluid resusctation in the form of 20-40ml/kg bolus
What is Multiorgan dysfunction syndrome (MODS)?
MODS is at the far end of the spectrum that begins with SIRS. It is defined as dysfunction of 2 or more organ systems such that homeostasis cannot be maintained w/out intervention
What is cystitis?
inflammation of the urinary bladder
A 34-year-old female patient presents with pelvic pain and burning on urination. A clean catch urine sample reveals >105 Escherichia coli per milliliter, confirming the diagnosis of acute cystitis. She now has tachypnea, a temperature of 39° C, and a heart rate of 100 bpm. Her serum lactate is normal, but her white blood cell count is 14,500/ml. How would you classify this septic patient?
sepsis
(blank) is a contributing factor in >200,000 US deaths per year
severe sepsis
The incidence of severe sepsis and septic shock has increased over the past 30 years and the annual number of cases is now (blank)
greater than 700,000
Who does 2/3rds of sepsis cases occur in?
patients with signif underlying illness
Sepsis related incidence and mortality rates increase with (blank) and (Blank)
age and preexisting comorbidity
The rising incidence of severe sepsis in the US is attributatble to the (blank) of the pop and the relatively high freq with which sepsis develops in patients with (blank)
aging
AIDS
The widespread use of (blank), (blank), and (blank) play a role in sepsis development
immunosuppressive drugs, indwelling catheters, mechanical devices
Sepsis and septic shock can be a response to any class of microorganism, but (blank) are the most common
bacteria
(blank) accounts for 45% of sepsis cases
(blank) accounts for 45% of sepsis cases
(blank) accounts for 10% of sepsis cases
Gram-neg
Gram-pos
fungi, mix of microorganisms
T or F
microbes that do not invade the bloodstream can elicit distant organ dysfunction and hypotension
T
Blood cultures yield bacteria or fungi in only (blank) of cases of severe sepsis and (blank) cases of septic shock
20-40%
40-70%
If you get a pnt with neg blood cultures how do you find the etiologic agent?
via culture or microscopic exam of infected material from local site
Is it weird to find neg microbiologic findings?
no :)
The sources for sepsis are infections elswehere in the body. T or F
T
What organisms are associated with lung infections?
strep pneumoniae, H influenzae, Legionella species, Chlamydia pneumonia, aerobic gram-neg rods
What organisms are associated with wound, soft-tissue infections?
strep pyogenes, staph aureus, clostridium species, pseudomonas aeruginosa, anaerobes, caogulase-neg stpah, aerobic gram-neg rods
What organisms are associated with UTI?
E coli, Klebsiella, Enterobact, Proteus species, Enterococcus, Aerobic gram-neg rods
What organisms are associated with CNS?
Strep pneumoniae, N meningitidis, Listeria monocytogenes, E coli, H. influenza, Pseudomas aeruginosa, Klebsiella, staph
What organisms are associated with abdomen?
E coli, bacteroides fragilis, aerobic gram-neg rods, candida species
Sepsis in neonates (less than 1 month old) is usually caused by (blan) and less often by (Blank)
strep agalactiae
E. coli
App 2 of 1000 live-born infants are infected by S. agalactiae with a case fatalitiy rate of (blank)
5-10%
During labor and delivery the neonate can be infected with (blanK)
microorganisms
The most common cause of sepsis in older children inclued (Blank X 3)
strep pneumoniae, N meningitidis, Staph aureus
Children may initially present with (blank, blank, blank and blnk)
meningitis, skin infections, bacterial rhinosinusitis, otitis media
A 2-week-old baby girl hospitalized with fever and nuchal rigidity is now showing signs of neonatal sepsis. Blood cultures reveal a Streptococcus agalactiae bacteremia. What is the most likely way this infant was infected with the Group B streptococcus?
oral contamination during passage through the birth canal
Sepsis is a complex interaction between what 2 things?
1) direct toxic effects of infecting organism
2) derangement of the normal inflammatory host response to infection
In response to local infection there is concurrent activation of the immune system and of (blank) to control the reaction
down-regulatory mechanisms
What are the devastating effects of sepsis syndrome caused by?
combo of
1) expansion of the immune response to sites remote from that of infection
2) derangement of the balance b/w proinflammatory and anti-inflammatory cellular regulators
3) dissemination of infecting organism
Localized infections produce inflammatory mediators that induce (blank) responses and eliminate the pathogen or engage adaptive immunity
protective innate
(blank) produce the same mediators as localized infections but in larger quantities that cause signfic pathophysiologic changes and can lead to death.
Systemic infections
In (blank) infection, macophages activated to secrete TNF-alpha in the tissues-> increased release of plasma (blank) into tissue, increased phagocyte and lymphocyte migration into tissue, increased platelet adhesion to blood vessel wall-> phagocytosis of bacteria, local vessels occlusion. Containment of infection. Antigens drain or are carried to local lympho node-> survival and stimulation of adaptive immune response
local
proteins
In systemic infection-> macrophages activated in liver and spleen secrete TNF alpha into bloodstream-> (blank) causes decreased blood volume, hypoproteinemia, and neutropenia, followed by neutrophilia. Decreased blood volume causes (blank). DIC leads to wasting and multiple organ failure: septic shock-> death
systemic edema
collapse of vessels
During an immune response to infection, microbial antigens trigger local cells to release (blank)
proinflammatory cytokines
Proinflammatory cytokines attract (blank), trigger (blank) and slow (blank) through venules and capillaries, and increase (blank) of vessel walls allowing leukocytes and fluid to move into the infected extravasculr space.
leukocytes dilation of vessels blood flow "leakiness" (point is they make the vessels big and leaky and slow blood flow so stuff can get out)
The cytokines also induce the release and increase production of (blank), which are antimicrobial but also serve as procoagulants.
acute-phase reactants
When the 2 main effects of the inflammatory cascade (vasodilation and coagulation) spread beyond the site of loca infection, the syndrome of sepsis may result in (blank, blank, and blank)
hypoperfusion
coagulopathy
and resultant organ failure
If you have hemodynamic collapse, what will result?
hypoxic respiratory failure
shock
acute renal failure
With massive cytokine release, impaired (blank) can result due to impaired metabolite use
cardiac contractility
(blank) is a major mechanism for multiorgan dysfunction
Vascular endothelial injury
Stimuli such as TNF-alpha induce vascular endothelial cells to produce and release a variety of cytokines, (Blank), (blank) and (Blank)
procoagulant molecules, platelet-activating factor, nitric oxide
What promotes the adherence of neutrophils to endothelial cells?
upregulated cell-adhesion molecules
With sepsis and endothelial injury, (blank) mediators are released
toxic
(blank) mediators and (blank) thrombi may contribute to vascuar injury
Leukocyte-derived
platelet leukocyte fibrin
Endothelial cell activation can also promote increased (blank), (Blank), (blank) and (blank)
- vascular permability
- coagulopathy
- microvascular thrombosis
- hypotension
In sepsis-induced DIC the (blank) is diffusely activated as part of the inflammatory reponse, at the same time the (blank) system is activated
coaguation cascade
fibrinolytic system
SOOOO why does DIC happen?
cuz both the clotting system and the fibrinolytic system are being activated and deavtivated simultaneously, thus forming clots and breaking them down
Why is DIC so dangerous?
clotting factors and platelets are consumed in such clots, and patients are at risk for complications from both thrombosis and hemorrhage
How should you treat DIC?
platelets and fresh-frozen plasma
(blank) in sepsis is a bad prognostic facto
coagulopathy
A down-regulatory system has evolved to protect against the systemic effects of proinflammatory cytokines induced by (blank)
endotoxin (endotoxin tolerance)
On first exposure to endotoxin, macrophages produce a large amount of proinflammatory mediators; within a few hours, reexposure to even larger doses of endotoxin fails to induce a (blank) response
proinflammatory
An animal or human remains tolerant to endotoxin for (blank) days
2-3
Exploiting the phenomenon of (blank) may lead to a treatment for endotoxic shock
endotoxin tolerance
Sepsis begins with signs of a systemic inflammatory response. What are these signs?
fever, tachycardia, tachypnea, leukocytosis
What are the second signs of sepsis?
progression to hypotension and evidence of hypoperfusion
Altered (blank) is often the first sign of organ dysfunction, also decreased (blank) is another sign and both may be apparent prior to getting labs
mental status urine output (less than .5 ml/kg/h)
In infants and the elderly, initial presentation may lack some of the more salient features, that is, they may present with (blank) rather than hyperthermia, leukopenia rather than leukocytosis.
hypothermia
In patients at the extremes of age, any nonspecific systemic complaint-vomiting, fatigue, behavioral changes should prompt concern for (blank)
sepsis
T or F
a patient not intially meeting sepsis criteria can rapidly progress to full-blown septic shock
T
Inflammation induced in sepsis is especially damaging to the (blank), why?
lungs
-buildup of inflammatory fluid in the alveoli impairs gas exchange, favors lung collapse, and decreases compliance, with the end result of respiratory distress and hypoxemia
A septic patient who did not initially require mechanical ventilation may later require it if they develop (blank) after fluid resuscitation
ALI/ARDS
One of the early complication of septic shock is (blank)
myocardial depression
What is the mechanism behind cardiac failure induced by sepsis?
Direct toxicity caused by inflammatory molecues (not due to decreased profusion)
How do you keep the heart functioning in sepsis?
preload (hydration with close monitoring of CVP), afterload (vasopressors) and contractility (supported with dobutamine)
So how do you keep preload normal?
hydration
How do you keep afterload normal?
vasopressors
How do you keep contractility normal?
dobutamine
Sepsis places an unprecedented workload on a heart, which can precipitate (blank) or a (blank) especially in the elderly
acute coronary syndrome
myocardial infarction
Inotropic agents and vasopressors can induce (blank) so you must be careful with them.
tachycardia
(blank) is indicative of liver failure, with increases in bilirubin, aminotransferases, and alkaline phosphatase
Cholestatic jaundice
In sepsis, Liver synthetic function is usually not affected (acute phase proteins are still produced), unless patients are hemodynamically (blank) for long periods.
unstable
Rena failure in sepsis is due to (blank).
hypoperfusion
How is renal failure in sepsis manifested?
oliguria, azotemia and inflammatory cells on urinalaysis
How do you support the hypoperfusion found in renal failure caused by sepsis?
hydration and vasopressors
If renal failure is severe or the kidneys cannot be adequatley perfused then (blank) is indicated
hemodialysis
Is there a specific diagnostic test for sepsis?
NO and the response can be quite variable among patients
What is suggestive of a diagnosis of sepsis?
a patient w/ susupected or proven infection, fever, hypothermia, tachypnea, tachycardia, leukocytosis, leukopenia, acutely altered mental status, thrombocytopenia, elevated lactate level, or hypotension
Definitive etiologic diagnosis requires (blank) from blood or a local site of infection. At least 2 blood samples should be obtained (from 2 different venipuncture sites) for culture.
isolation of microorganism
In many cases, blood cultures are neg in sepsis, this result can reflect prior (blank), the presence of (blank) or the absence of (blank) of the bloodstream. If this happens what should you do?
- antibiotic use
- slow growing or fastidious organisms
- microbial invasion
gram staining
Cultures of (blank X 3) if indicated should be collected from all patients with severe sepsis
blood, urine, sputum
What will a CBC show with sepsis?
may show increased, or decreased WBC with evidence of left shift
(blank) should prompt eval for DIC, w/ evaluation of fibrinogen and fibrin split products as well as partial thromboplastin (PT) and partial thromboplastin time (PTT)
Thrombocytopenia
Elevated blood urea nitrogen (BUN) and creatine may result from (blank).
renal hypoperfusion
Elevated liver function tests (LFTs) may result from (blank)
hepatic hypoperfusion
Elevated lactate (greater than 4 mmol/L) indicates (blank)
poor overall tissue perfusion
(blank) may be increased or decreased in sepsis, and (blank) abnormalities are common.
Blood glucose
electrolyte
How should you treat sepsis?
if severe, put them in ICU
check oxygen and IV fluids w. crystalloid admin
-Broad-spectrum IV antibiotics, started w/in an hour (whether o not blood cultures have been drawn)
- MAKE SURE YOU COVER ALL CASES WITH ANTIBIOTICS
With sepsis, you need to find the source of infection, how do you do this?
UA, Chest X-ray, ECG
Why do you give a UA and chest-xray to find infection?
cuz majority of sepsis in the US is pneumonia, GI or UTI
Why do you give an ECG in sepsis?
to evaluate for cardiac ischemia secondary to hypoperfusion
Treatment of patients with septic shock has what goals?
- corrext hypoxia, hypotension and impaired tissue oxygenation (hypoperfusion)
- start antibiotis as early as poss
- identify source. kill it
- monitor CV. maintain organ function
In accordance with current guidelines, appropriate antibiotics should be given within the (blank) hour after sepsis is recognized
first
For antibiotic therapy, Blood, urine, and fluid cultures should be taken prior to (blank); but do not delay treatment for such purposes
initiation of therapy
When do you give empiric therapy in sepsis?
rapidly, if the source of infection is unknown swtich to correct antibotic when source is identified
T or F
gram-positive organisms are now as common a source for sepsis as gram-negative organisms
T
Sepsis due to (blank), althoguh carrying a high mortality rate, is rare. What should you do about this
fungal organisms
Only give antifungals if clinical picture dictates
How do you treat sepsis?
use broad spectrum or multiple antibiotics
In immunocompetent adults, an (blank) or a (Blank) is used as monotherapy
antispeudomonal penicillin (ticarcillin-clavulanate) or a carbapenem (impenem)
What is the combination therapy for sepsis?
third generation cephalosporin (e.g cefepime) plus anaerobic coverage (e.g clindamycin or metronidazole) or a fluoroquinolone plus clindamycin
How should you give antibiotics for sepsis?
IV
What are some other drugs used to treat sepsis?
crystalloid
norepinephrine
dobutamine
vasopressin
What is this:
Restores intravascular volume, which is depleted in patients with severe sepsis. Improves cardiac output, organ perfusion, and mortality in severe sepsis
Crystalloid
What is this:
Improves blood pressure and cardiac output. More effective than dopamine in refractory septic shock
Norepinephrine
What is this:
Improves cardiac output. May be used in combination with a vasopressor to increase cardiac output
Dobutamine
What is this:
Improves blood pressure in patients with septic shock
vasopressin
If your patient is still hypotensive or greater than 4 mmol/L after the first fluid bolus than initiate (blank)
EGDT (early goal-directed therapy)
What is EGDT?
method of clinical assessment and reassessment of clinical and laboratory markers, with interventions aimed at normalizing those markers.
The overarching goal of EGDT is what?
eliminating mismatch between oxygen supply and oxygen demand
What are the 3 goals of EGDT?
1: Cental venous pressure (CVP) 8-12 mm Hg:
2: Mean arterial pressure (MAP) greater than 5 mm Hg
3: central venous oxygen saturation (greater than 70%)
How do get your CVP normal?
continous infusion of crystalloid
How do you get your MAP normal?
add vasopressors (norepinephrine or dopamine)
How do you get your central venous oxygen saturation normal?
RBC transfusion, dobutamine -> to boost cardiac output
OR intubation and oxygenation
A 32-year-old woman is admitted to the hospital for acute pyelonephritis. The patient is treated with oral ciprofloxacin. After 4 days of therapy, she returns to the ED with persistent fever to 38.9°C (102°F), blood pressure of 90/55, and flank tenderness. The urine culture reveals Proteus mirabilis with greater than 100,000 colony-forming units per mL. When you arrive to examine her, you note that she is tachypnic, tachycardiac, and appears lethargic. Which of the following is the next step?
Obtain IV access and admin a fluid bolus
A 66-year-old female is noted to have acute pneumococcal pneumonia and is being treated with antibiotics, and with norepinephrine and dobutamine to maintain her blood pressure and urine output. Which of the following is a bad prognostic sign?
C. Lactic acid level of 6 mmol/L
This is craziness because its above 4!
(blank) or drainage of a focal souce of infection is essential
surgical removal
(blank) should be removed and the tip rolled over a blood agar plate for quantitative culture; after antibiotic therapy has been initiated, a new catheter should be inserted at a different site
Indwelling IV or arterial catheters
What type of catheters should be replaced?
foley and drainage catheters
App (blank) percent of patients with severe sepsis and (blank) percent of patients with septic shock die within 30 days
20-35%
40-60%
T or F
case-fatality rates are similiar for culture-positive and culture-negative severe sepsis
T
(blank) 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.
Acute phyisiology and Chronic Health Eval (APACHE III)
In patients with no known preexisting morbidity, the case-fatality rate remains below 10% until the (blank) decade of life; it gradually increased to exceed (blank) percent in the elderly
fourth decade of life
35%
Death is signif more likely in severely septic patients with (Blank), especially during the third to fifth decades
preexisting illness
(blank) offers the best opportunity to reduce morbidity and mortality from severe sepsis
prevention
In developed countries, most episodes of severe sepsis and septic shock are complications of (blank)
nosocomial infections
How can you prevent nosocomial infections?
- reducing number of invasive procedures
- limiting the use and duration of indwelling vascular and bladder catheters
- reducing incidence and duration of profound neutropenia
- aggressive treatment of localized nosocomial infections
What drugs should you not use so that you can prevent sepsis?
-indiscriminate use of antimicrobial agents
-glucocorticoids
-
