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Dan Park

on 23 June 2014

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Transcript of Fever

BUT. There are a handful of less common serious causes
of pediatric fever that have the potential for morbidity
and mortality +/- LEGAL HEADACHES
Why do we care?
1. High Prevalence
2. Clinical exam can be unreliable
Herd Immunity
Infants between 1 and 28 days old with a fever should be presumed to have a serious bacterial infection.
<28 days
Everyone gets admitted.
Too high-risk to discharge
Viral URI sx do NOT count
as a fever source in this age
H&P are NOT reliable to r/o
SBI includes: UTIs (20%),
bacteremia (3%),
meningitis (1%)
Bugs: E.coli, GBS, HSV >> Listeria, Salmonella, Staph.aureus
1. CBC + diff
2. Blood culture
3. Cathed urine
4. CSF
5. Consider: CXR and
rapid viral testing
Timely abx: Amp+ Cefotax or
Amp+ Gent

+ Acyclovir for any of the following:
ill, vesicular lesions,
csf pleocytosis
seizure, focal neurologic signs,
abnormal neuroimaging, resp distress, apnea,
thrombocytopenia, elevated LFTs

Remember, disseminated HSV and HSV encephalitis
may not present with a rash
29-60 days
28 day old will pick up bacteria from the birth canal
Herd immunity doesn't really help against what mom
can give you

High prevalence of disease at <28 days

<2 weeks the
chance of an SBI is 1/10
Prevalence of SBI is
between 2-4 weeks

no shield between blood/brain/urine (membranes
wide open)
Fever without a source
H&P is NOT reliable to r/o SBI
Viral URI sx do NOT count as fever source
SBI includes UTIs (up to 15%), bacteremia (1%),
meningitis (0.2-0.4%) ;
SBI prevalence 1/100 to 1/1000
Bugs: E.coli, GBS, S.pneumo >> N. meningitides, H flu (type B), Staph aureus
Caution: Serum WBC does NOT predict meningitis (Bonsu. Annals EM. 2003)
All recommend minimum workup: CBC, cathed UA and urine culture
Blood Cx
Abx pre DC home
29-60 days
29-60 days
If abnl WBC
If resp sx
If resp sx
If abnl WBC
Low risk: Must have a reliable caregiver who can return in 24 hours
Option #1: No antibiotics and close follow up in 24 hours
Option #2: Ceftriaxone IV/IM after LP with close follow up in 24 hours
High risk: Admit
While RSV+ infants have decreased SBI risk, rate of
concurrent UTI=
Goal: Kill strep pneumo
Suggested w/u
1. CBC + diff
2. Blood cx
3. Cathed ua/cx
4. CSF </= 6 weeks
5. Consider: CXR/rvp,
stool culture
Named viral syndromes
count as a source: HSV gingivostomatis,
Coxsackie hand-foot-mouth, RSV bronchiolitis
Unnamed, nonspecific viral infections MAY count as a source
for vaccinated, well-appearing kids
Prevalence of SBI is getting lower
1/1000 to 1/10,000 +
Odds are in your favor: physiology+ vaccinations+ screening tools
After three months the likelihood of SBI is very low. You're falling below
the test threshold (think: PE work up; risks > benefits)
Clinical history/index of suspicion has to be high to test
Decision Density
Review the approach to the febrile neonate and why we do what we do
Discuss can't miss infectious emergencies that can burn you in court
Briefly discuss common cognitive biases that can lead to medical error
Anchoring errors
Availability errors
Premature Closure
> 60 days
Fever accounts for 1/3 of all presenting pediatric

Rarely represents a life-threatening pathology
Crocetti M et al. Pediatrics 2001
8 mo p/w fever + perioral rash
Admitted with UTI and discharged a few days later
Returned to ER 3 days later with daily fevers
Dx with "flu-like illness"
Subsequently diagnosed with Kawasaki disease
and suffered multiple coronary aneurysms and
required a heart transplant
Family sued the treating physicians claiming that they failed
to dx Kawasaki disease
A settlement was reached
Often difficult to diagnose

No definitive test
Criteria for Kawasaki include:
FEVER for 5 consecutive days
4 of the following
Vasculitis of small and medium blood vessels
Probably immune mediated
<5 yo; peak= 18-24 months (preschooler)
Younger kids present atypically
Prevalence= 1/10,000

Why do we care?
20% of untreated kids develop coronary aneurysms

Not elevated?
Albumin <3
Transaminitis (ALT)
WBC >12
Sterile pyuria
Treat+ Admit
Echo +/- treatment
A note on incomplete kids.
Easy to blow them off
BUT a population you don't want to miss
Higher rates of complications
If <6 months, it's gonna be bad
Fever >5 days in <6 mo just send all this stuff and talk to cards
Our job?
Admit them.
High dose aspirin 80mg/kg until fever goes away
then low dose until outpatient cards f/u
IVIG 2G/kg
Any kid returning to the ER with a fever after stopping IVIG for Kawasaki has Kawasaki until proven otherwise
If you're on the floor and you get one of these kids:
Remember, coronary aneurysms don't occur for a few weeks
But you can see
in the short term
Listen for murmurs
EKG, tele is a good idea
Low threshold to get an echo early on
Same goes with a CXR
Availability Bias
Recency effect
Common things are common
The Sound of Hoofbeats Means Horses
Out of sight out of mind
If you know you have a tendency to

things in recent memory
things that you haven't seen in a while

You might be able to avoid AVAILABILITY BIAS
21 month old p/w
, nasal congestion,
Temp >38 intermittently for 7 days with emesis
Trouble bearing weight on right leg and cried with ambulation
ROS otherwise negative

In ED: alert, nontoxic but fussy
Temp 38.1, HR 142, RR 24, 99% RA
No swelling or pain to palpation in extremities. Full range of motion.
Favoring right leg
with attempted weight bearing
WBC 21
CRP 17
Xrays negative

Admitted to floor for
presumed osteomyelitis
Blood cultures negative x 3
Continued fevers + non weight bearing
MRI negative
Started to bear some weight and discharged with dx of
transient synovitis
Returned 3 days later with worsening gait and fevers.
Decreased movements of right arm+ twitching of left leg
Hyperreflexic in lower extremities
Admitted to PICU
Left frontal craniotomy
Final culture grew multiple organisms
(Haemophilius, strep, anaerobes)
No source found
DC with 11 weeks of IV Flagyl and Ceftriaxone
Complete neurological recovery

4-7 yo
Hematogenous spread or direct extension from local infection
Septic intracranial emboli most commonly due to R L shunting from CHD
6% of kids with unrepaired cyanotic CHD develop intracranial abscesses
In some populations CHD is associated with as many as 26-50% of all pediatric intracranial abscesses
Tetralogy of Fallot is the most common CHD associated with intracranial abscesses
Yang et al. Surg Neurol. 1993
Togev R. Principles and Practice of Ped Inf Dis. 2009
Wong et al. Childs Nerv Syst. 1989
60-70% caused by Strep milleri group
Staph seen in abscesses after head trauma
Gram neg species found in neonates
Less common organisms (Toxo, Crypto, Nocardia) in
Classic presentation:
. 9-28%
Seizures seen in <50%
CT has good sensitivity and specificity (95%,99%)
MRI helpful in differentiating edema from necrosis and finding smaller lesions
Auvichayapat et al. J Med Assoc Thai. 2007
Manage signs of ICP (hyperosmolar fluids, seizure ppx, head elevation, sedation, hyperventilation)
In absence of septic shock,
defer abx
until specific bug is identified
If you start them, use broad spectrum approach to cover
Penicillin resistant strep pneumo, MRSA + common strep species, gram negatives, anaerobes
Steroids controversial
Vanc/Meropenem or Vanc/Flagyl
Mortality= 3-10%
Prognosis worse with: multiple abscesses, congenital heart disease, meningitis, poor neurologic status at presentation, young age
Fever+ Limp common
Often due to transient synovitis and sometimes infections of joints/bones/muscle

Intracranial abscesses are RARE but CONSIDER it in children with

Especially in kids with underlying heart disease, kids with hardware in their head, or chronic ear infections
We tend to focus on specific features in the presentation or triage
too early
in the work up
Might cause us to
jump to a diagnosis
on just a few pieces of info
May be a time saver if it's the right diagnosis
BUT dangerous if it's not
Being aware of this bias might be enough to avoid relying on a first impression too much and waiting on more objective info
6 mo p/w fever and lethargy
Focal seizures of right arm, self-limited
CSF c/w viral infection
Transferred to children's hospital
Focal seizures returned 32 hours later
MRI revealed lesion of tempoparietal area
Acyclovir started but patient eventually went on to have
permanent neuro deficits

Family sued claiming that ER docs who treated the baby were
negligent in failing to consider HSV

Hospital settled for 1 million
1/250,000 (you'll probably see it once)
1/3 of those affected are between 6 mo-20 yo
60-70% of affected infants have vesicular lesions
Three types: local, CNS, disseminated
Prognosis is bad for disseminated (60% mortality)

Classic CSF findings
95% of affected infants will have
increased WBCs
in CSF
(10-200; >>lymphocytes)

of affected infants will have
elevated protein
Diagnose with
(94% sensitivity)
CT can be normal in first week of infection
MRI is better
HSV causes 50% of all temporal lobe encephalitis
Treat with acyclovir 20mg/kg/dose q8 for 2-3 weeks
Decreases mortality from
70% to 20%
Neurologic sequelae in
of kids
Steroids are controversial (of course)
No consensus on starting empiric acyclovir in
febrile neonate workup
2/3 of affect infants are born to mothers without disease

Have a low threshold to start acyclovir
If you have CSF pleocytosis treat all infants with
acyclovir until PCR comes back (24 hours)
Kimberlin. Pediatr Infect Dis. 2005
Davis et al. PEC 2008
Cheap. Few side effects
(neutropenia, nephrotoxicity)
Premature Closure
Happens more at the
end of a shift
or when you're
Once we have an answer we tend to stop the workup
This is really common in radiology
Intubated 2 yo s/p cardiac surgery
Increased fio2 requirement today

Your colleague is leaving and you're
taking over.

He says that the increased
O2 requirement is probably due to a new LLL infiltrate
seen on today's film. Antibiotics started.
Yesterday's film
He was right. There is a new LLL infiltrate
Everything else seems like its in the same place as yesterday's film.
Hospital/ventilator acquired PNA or bad atelectasis prob causing increased O2 requirment
PTX likely secondary to positive pressure ventilation
Looking closer
This mental shortcut causes us to stop searching for further findings once one abnormality has been found. It is a universal human tendency
Premature Closure or Search Satisficing
Satisfy + Suffice = Satisfice
Classic Examples:
Coingestants in ODs

Removing foreign bodies from wounds

Fall from a height with heel pain--
calcaneal fracture is obvious but
what about spine/pelvis fractures?

Injuries to ring structures (pelvis, mandible, ankle)--
typically fracture in
more than one place
7 day old term neonate p/w fever, irritability, poor feeding,
and periumbilical erythema
Adequate prenatal care
Abdominal tenderness, purulent discharge
Periumbilical region indurated and erythematous
Omphalitis + abdominal wall cellulitis diagnosed
Blood cultures, broad spectrum abx started
Labs/cultures negative

Over next 15 hours periumbilical
violaceous coloration
and painful induration and edema of abdominal
wall increased
Antibiotics broadened
Abd xray and U/S showed soft tissue edema
Surgery following along
Clinically deteriorated
Violaceous coloration spread
Seizures, intubated, pressors
Fasciotomy showing extensive abdominal NF
DIC, renal failure, death
Clinical course of acute omphalitis is usually benign
Necrotizing fasciitis is uncommon but a medical emergency
60% mortality rate

Non-specific findings early in the course
Leukocytosis, left shift

Suspicious clinical features
Indurated/painful skin + fever+ toxic
Violaceous coloration
(can spread quick)
How do you die?
Septic shock, DIC, multiorgan failure
What do you do?
Keep a
high index of suspicion
Supportive care, early broad-spectrum antibiotics
Call surgery
to debride of necrotic tissue
If you have a case of omphalitis keep NF in mind as a close second diagnosis
To avoid premature closure
15% of medical errors are due to
diagnostic error
Cognitive error
The most
is the most
Relying too heavily on your
first impressions
or someone else's
>1.5 cm cervical lymphadenopathy
Intracranial Abscesses
Today's film
In developing countries contiguous spread is more common.
2/3 of all intracranial abscesses in China occur as a complication from otitis media

The combo of herd immunity + prevnar has almost eliminated occult bacteremia

Giving empiric antibiotics for febrile, well-appearing kids might be a thing of the past

Emphasis is shifting to ruling out occult UTIs

Don't forget: gastro, pyelo, osteo, septic joints, soft tissue, rheum stuff

Testing approach dictated by: well appearing/not well appearing, pre-test probability, and reliability of parents

Pediatric Fever and Pitfalls:
A Review

Before 2000
2-3% risk of occult bacteremia
Carstairs et al. Annals EM 2007
Occult bacteremia in post PCV era
Enough people are immunized, protecting most of the community
Full transcript