Transcript Management of fever on the wardx

Management of fever on the
ward/ PUO
M Armstrong
THE CASE
Mr. H, 67 year old
Day 6 post R TKJR
PMH:
DM2
HTN
OA- Previous L THJR
You are the ward call and the treating team have
gone home.
Mr. H, spikes a fever to 38.7
You are called by the nurse.
What will you do?
What would you do?
ABCD
On review:
RR 28, sats 93% on 2L NP (pre-op 96%ra), T38.2,
HR 105, BP 102/60 (pre-op noted to be 140/82)
• What could be causing his fever? What are the
main causes of fever in hospitalized patients
post surgery, i.e. in this patient?
• How would you like to investigate him and
manage him?
Fever
• A common symptom
• In top 10 general practice presentations
• 5% of ED presentations
• Many reasons to have fever while in hospital
- Infection is the most common cause of fever of
short duration
Definition
“an elevation in core body temperature above the daily range for an
individual” UTD
Normal temperature varies over the course of the day (low ~6am, high
~4-6pm with variation ~0.5), control is via the thermoregulatory center
in the anterior hypothalamus
No clear consensus of what actually constitutes a fever but UTD
defines morning reading over 37.2 and evening over 37.7 as greater
then 99th percentile for healthy subjects (based on ‘92 study of 700
oral temperature readings *tympanic likely to be higher)
Older patients likely have a lower set point and may have lower fevers
with more severe fevers (immunosuppression is less well defined, but
likely that febrile response is blunted)
Pathophysiology
Increased “set-point” from hypothalamus in
response to infection/ inflammation.
Elevated prostaglandin E2 mediated (hence how
an antipyretics work)
-activates neurons in vasomotor centre>
vasoconstriction, increased peripheral heat
production and liver/ fat thermogenesis
“chills and rigours”
PYROGENS
“any substance that causes fevers”
Exogenous
-microbes and their toxins (e.g. LPS, TSST-1)
Endogenous (pyrogenic cytokines)
-specific cytokines produced on activation of TLR
-cytokines are proteins that regulate immune, inflammatory and
hematopoietic processes
-IL-1, IL-6, TNF, IFN-alpha
All end up increasing production of PGE2
Assessment
• Usually follows a fairly uniform course with some
modifications according to the severity of patient
status, epidemiologic factors, and the patients
background
• Fever without with-out an initial obvious source
is not PUO but “fever without localizing signs”
UTD “most febrile illnesses either resolve before a
diagnosis can be made or develop distinguishing
characteristics that lead to a diagnosis”
Assessment- history/ exam
• Important as 85% of adults with several days
fever will have localizing symptoms/ signs
• Of patients with no localizing signs, more then
a 3rd still have bacterial infection (think LRTI/
UTI)
History/ exam
• Just like the usual…
-But
Methodical approach
Review vitals and trend
Look for signs associated with localized symptoms
Beware of hidden areas/ traps (remove covers, think
teeth, temporal arteries, sinuses , thyroid, axillae, joint
flexures, natal clefts, perineum, prostrate, genitalia
Reassessment over time and 2nd opinions can be
important
Warning signs
• Beware of potentially severe infection
-A short time frame of fever to presentation
(<12 hours)
-Incapacitated (“bedbound” “never been this
sick”)
-Pallor, mottled skin, cold peripherals
-Severe muscle and joint pain (in in absence of
significant fever)
Concerning vitals
• Tachypnoea [>30]
-often overlooked but a strong predictor or severity
of disease (and an early sign)
• Tachycardia [>120]
-over 120 is unusual and portends septic shock
• Hypotension [<100]
-regard as septic shock until proven otherwise, do
not assume only 2nd dehydration, be aware of
patients baseline blood pressure
Concerning vitals
• Temperature [>39]
-Don’t forget “cold sepsis” and trends
-Over 39 in adults likely to be from a significant
infection
Features that can suggest bacterial
infection
• Rigors (can be confusing in history taking)
-if true rigor suspect bacterial infection until proved
otherwise (admit, investigate)
• Altered LOC/ behaviour change
-CNS infection or systemic, can be subtle (ask
family)
• Repeated vomiting in absence of diarrhoea
-can be a sign of bacteraemia, intra-abdominal
pathology or CNS pathology.
Investigations
• Be guided by localizing features and clinical
circumstances
-FBC
-Blood cultures
-CXR
-Urine microscopy and culture
-LP
-CRP/ESR
-Nose/Throat swabs for PCR tests
Initial Management
• Infections requiring urgent treatment or
concerning vitals/ signs
-Broad-spectrum empiric antibiotics
SIRS criteria and sepsis
http://nrsged.wikispaces.com/6.+SIRS+vs+Sepsis
Back to the case…
radiopaedia.org
PUO
• Classic definition (Petersdoft and Beeson
1961)
-an illness of at least 3 weeks’ duration
-a fever above 38.3 on several occasions
-no diagnosis reached after one week of
intelligent and intensive investigation
Further separated into 4 categories
1.
2.
3.
4.
“Classical” PUO
PUO in hospitalized patients (nosocomial)
PUO in HIV-infected patients
PUO in neutropenic patients
Establishing that a patient has PUO
The following evaluation should be unrevealing:
1. History
2. Physical examination
3. Complete blood count, including differential and platelet count
4. Blood cultures (before antibiotics, 3 sets drawn from different
sites with an interval at least several hours between sets)
5. Routine blood chemistry including LFT’s and bilirubin
6. HAV, HBV, HCV if LFT’s abnormal
7. Urine analysis and culture
8. CXR
If any symptoms or signs suggest specific organ involvement then
further targeted investigation has been unrevealing
Changing epidemiology
Since 1950’s fraction of PUO’s undiagnosed has been
increasing
Early PUO series included few connective tissue disease,
which are now better characterized
Extra-pulmonary TB, solid tumors, intra-abdominal
abscesses are now easier to diagnose
Infective endocarditis is now easier to diagnosis and there
are less cases of “culture negative” endocarditis due to
better culture techniques (although in the current era
more PUO are culture negative IE or IE due to difficult to
isolate organisms)
Causes of PUO
* (Table from Infectious Diseases: A clinical approach, Yung et al)
Infection (15-25%)
Neoplasm (<20%)
Inflammatory
disorders (15-25%)
Miscellaneous
Systemic:
Bacterial- TB*, salmonellosis,
brucellosis, psittacosis, meliodosis
Viral- CMV, EBV, HIV
Other: Q fever, malaria, amoebiasis,
toxoplasmosis
Localised:
With abscess formation*
-in/around kidney
-in/around liver
-around colon
-in pelvis
-in/ around spleen
-dental
Without abscess formation
-endocarditis
-osteomyelitis
-cholangitis
-pericarditis
Lymphomas and lleukaemia
Solid tumours: kidney, lung, liver,
gastric, atrial myxoma,
disseminated carcinoma
Giant cell arteritis
PMR
Adutl onset Still’s disease
SLE
Granulomatous disease (Crohn’s,
sarcoidosis, granulomatous
hapatitis)
PAN
Other vasculitides
Drug fever (rash in only 25%)
VTE
Haematoma
Endocrine disorders (subacute
thyroiditis, Addison’s disease,
hyperthyroidism,
pheochromocytoma)
EtOH hepatitis and cirrhosis
Chronic aortic dissection
Factitious fever
Others
*The most common infective causes
in many studies
*9-51% remain
undiagnosed
PUO in sub-populations
Age- older age groups more likely to get auto-immune
multisystem disease
HIV/AIDS- need to take into account immunosuppression
(CD4 count and viral load)
-need to think of mycobacteria (MAC) and lymphomas
Neutropenia- most often linked to bacteraemia. Fungal
infections replace bacteria infections in prominence after
the acute period (7 days). Fever is often confounded by
sick patients with multiple possible causes of fever
including the underlying diagnosis
POSTOPERATIVE FEVER
-fever above 38 common in first few days secondary
surgical trauma
Need to think of timing and type of surgery:
Immediate- onset in theatre or within hours of surgery
Acute- onset within first week of surgery
Subacute- onset from one to four weeks post surgery
Delayed- onset more then one month after surgery
Immediate:
-drugs or blood products in the peri-operative
period
-trauma (prior or as part of surgery)
-infections present prior to surgery
-malignant hyperthermia
*fever due to trauma of surgery usually resolves in
2-3 days
Acute:
-nosocomial infections (SSI, catheter related
infection)
-pneumonia (including VAP, aspiration)
-UTI (including CAUTI)
Non infectious causes- MI, VTE, Pancreatitis,
EtOH withdraw, acute gout
Subacute:
-SSI (more common then in the acute period)
-catheter related in infection
-C. dif
-drug fevers
-thrombophlebitis
-VTE
Delayed:
most delayed fevers are due to infection
-SSI due to more indolent organisms (eg,
Coagulase negative staph in PJI)
-cellulitis (disrupted venous/ lymphatics)
-infective endocarditis (perioperative
bacteraemia)
-viral/ parasitic infections from blood products
What about atelectasis?
Concurrence probably coincidental rather causal
UTD- “there was no association between fever
and the presence of, or the degree of,
atelectasis”
“Wind, Water, Wound, What did we do?”
Drug fever:
-Antimicrobials (sulfonamides, penicillins,
vancomycin, nitrofurantoin, antimalarials)
-H1 and H2 antagonists
-Anti-epileptics
-NSAIDs
-Anti-HTN (hydralazine, methyldopa)
-Antiarrhymic drugs (quinidine, procainamide)
-Antithyroid drugs
-Digoxin and aminoglycosides (rare)
“Fever of unknown origin is more often caused
by an atypical presentation of a common entity
than by a rare disorder”
Clinical approach- HX
-A thorough history often repeated
1. Verify presence of fever, continuous/ intermittent
2. Establish onset/ duration
3. Seek localising symptoms
4. Establish severity
5. Obtain co-lateral information (family, GP)
6. Consider past history for clues
7. Ask about medications, including OTC, SCAM,
immunosuppression, antimicrobials, allergies
8. Ask about country of birth, travel, occupation, animal
contacts
9. Sexual history/ IVDU
Clinical approach- Ex
Think head to toe “check list”
-eyes (scleritis, uveitis, conjunctival haemorrhage)
-Optic fundi
-temporal arteries
-sinuses
-? Change in behaviour/ cognition
-oral cavity (teeth and gums)
-thyroid
-hands
-heart- new murmurs/ rub (listen carefully to the heart for rubs/ new murmurs)
-lymph nodes
-sternum ? Bone tenderness
-abdominal organs- ? organomegaly
-blood vessels/ rash- ? vasculitis
-rectal/ pelvic exam
-genitalia
-lower limbs- ? DVT
Clinical approach- IX
• Initial approach as for any fever
- Other early tests may include ANA, RF, HIV,
EBV serology, CMV serology, CRP/ESR, LDH, CK
- If no leads from above consider stool
specimen for MCS, Q fever, brucellosis,
leptospirosis, syphilis, psittacosis,
toxoplasmosis, TB screening, anti-ENA, ANCA,
dsDNA, SPEP, cryoglobulins,
Ix- imaging
•
•
•
•
•
•
CT CAP or more specific CT scans
US of abdomen/ pelvis
MRI
ECHO
Doppler US legs (VTE)
Nuclear med scans (gallium labelled leukocyte
scan)
• PET scans
Ix- invasive tests
• Lumbar puncture
• Tissue biopsies- lymph nodes, skin, renal,
muscle, bone biopsies, temporal artery biopsy,
bone marrow, liver
-remember to send for culture (including
mycobacterial and fungal) and not just
histology!
“Most adults who remain undiagnosed after an
extensive evaluation have a good prognosis”