Fever, Sepsis, Bacteremia Flashcards
Human body temperature is regulated by _____
With fever, temperature ____ shifts upwards
the hypothalamus
•Like the ”thermostat” of the brain
“set point” shifts upwards
Central temperature
Central(rectal) -about 0.5°C higher!
•Rectal temperature most closely estimates core temperature
Adults > 65 have ____ average body temperatures
Adults > 65 have lower average body temperatures (and less likely to mount fever in response to infection)
Fever induced by ____?___
pyrogenic cytokines leads to increased heat production (egshivering) or decreased heat loss (peripheral vasoconstriction)
How is hyperthermia different from fever?
Hyperthermia is NOT cytokine mediated, “set point” of hypothalamus remains unchanged
•Occurs when environmental heat load or body metabolic heat production exceeds normal heat loss capacity
- Ex. Heat stroke, thyrotoxicosis, neuroleptic malignant syndrome
- Can be rapidly fatal if untreated
Approach to fever –differential diagnosis
IMADE?
Infection –viral, bacterial, fungal
Malignancy –lymphoma
Autoimmune –SLE
Drugs –serotonin syndrome, neuroleptic malignant syndrome
Endocrinopathy –thyroid storm
Important to know
What is the temporal pattern of illness?
Acute
Subacute
Chronic
- Acute viral infection, bacterial infection
- Subacute atypical infections, malignancy, autoimmune
- Chronic atypical infections, malignancy, autoimmune
“Fever AND ______”
sore throat?
Viral URI, strep pharyngitis
“Fever AND ______”
cough?
Cough: viral URI, pneumonia, flu, COVID
“Fever AND _____”
rash
Cellulitis
“Fever AND _____”
Dysuria
Dysuria:UTI, pyelonephritis
Sepsis = can’t miss
What is it?
Definition: Life-threatening organ dysfunction caused by dysregulated host response to infection
Key findings
•Hypotension
•Altered mental status
•Acute Kidney Injury
•Coagulopathy
•Increased respiratory rate
May or may not present with fever!
Fever of Unknown Origin (FUO)
Definition?
Etiology?
Workup?
Definition: febrile illness (temperature of 101°F [38.3°C] or higher) for three weeks or longer without an etiology despite a one-week inpatient evaluation
•Notjust a new fever without an identified cause
- Etiology:•May be infection, autoimmune, malignancy (remember ”IMADE” mnemonic)
- Workup: •Complete history and physical•Extensive lab and imaging workup
Low WBC count is a classic finding with _______
SLE
Sepsis WBC? High/low?
Don’t be fooled –sepsiscan present with a high or low WBC count!
Very high WBC count (ie>30,000) concerning for _________
leukemia/lymphoma
Thrombocytopenia can be seen in sepsis, is due to _____
often due to disemminatedintravascular coagulation (DIC)
Lactic acidosis
What is it?
What does it indicate?
Lactic acidosis = serum lactate concentration above 4 mmol/L
•Can be a marker of impaired tissue oxygenation due to tissue hypoperfusion!
specificity helps with ruling (in/out) disease
In - SPIN
sensitivity helps with ruling (in/out) disease
Out - SNOUT
Blood culture - Presence of these organisms is always clinically significant (3):
- Staphylococcus aureus
- E. coli
- Pseudomonas aeruginosa
Chest x-ray – Bacterial Pneumonia vs. COVID19 Pneumonia?
Bacterial Pneumonia•Focal infiltrate: can be suggestive of bacterial pneumonia
Typical findings with COVID-19:•Bilateral infiltrates•Basal and peripheral predominance
Chest x-ray -SLE typical findings?
Pleural involvement and pleural inflammation in lupus is common (pleuritis)
•Can see pleural effusion on CXR
Suspected CNS infection is a ______, what do you do?
Symptoms?
medical emergency and important indication for lumbar puncture
•Symptoms include fever, headache, meningismus
•Bacterial meningitis has a 14% to 25% mortality rate!
Thus rapid diagnosis and treatment = critical
Antipyretics MOA?
Antipyretics work by reducing level of PGE2in the thermoregulatory center of hypothalamus
PGE2 production depends on enzyme cyclooxygenase (COX) acting on substrate of arachidonic acid
Antipyretics work by inhibiting COX thus preventing PGE2 from being produced
Acetaminophen
action on peripheral tissues vs. brain?
Why preferred compared to NSAIDS?
when to use caution?
Poor COX inhibitor in peripheral tissues no significant anti-inflammatory effect
- Effective COX inhibitor in brain because acetaminophen oxidized by p450 system, and oxidized form inhibits COX
- Effective at reducing fever
- Preferred antipyretic, less renal toxicity compared to NSAIDs + no harmful effect on GI mucosa
- Use cautiously and at low doses with hepatic dysfunction
NSAIDs - where are they effective?
AE?
Avoid in which patients?
- Inhibit COX peripherally and centrally
- Effective at reducing fever
- Adverse effect on platelets, GI mucosa; also has significant renal toxicity
- Avoid in patients with cirrhosis, CKD, CHF! Caution with CAD
Aspirin MOA?
Avoid in what patients?
works by inhibiting COX
- Unique mechanism of action –irreversibly inhibits both COX-1 and COX-2
- Effective antipyretic
- Avoid aspirin in infants due to risk of Reye’s syndrome!
When sepsis is suspected…
- Obtain basic labs including serum chemistries, blood count, cultures, imaging studies, lactic acid
- Fluid resuscitation EARLY in management with IV crystalloid
- Start antimicrobial therapy within 3 hours of presentation