Fever Flashcards

1
Q

Case
7 year-old female from Cavite, consulted for fever
HISTORY
1 week PTC, while at school, patient complained of a vague
headache. At the clinic, she was noted to have low-grade fever.
She was sent home on Paracetamol with only temporary relief of
fever.
1 day PTA, patient had fever of 39.8C with associated pink spots
on her abdomen and crampy abdominal pain. Fever persisted
despite giving two doses of Paracetamol.
Persistent fever and three episodes of diarrhea (greenish, watery,
no blood) prompted consult.
PAST MEDICAL HISTORY
Had chicken pox last year, no known allergies, no asthma
FAMILY MEDICAL HISTORY
Unremarkable
BIRTH AND MATERNAL HISTORY
Born full term to a 25-year-old G2P1 mother with unremarkable
birth and maternal history.
IMMUNIZATIONS
Completed EPI, given 1 dose of MMR; Hep B, DTap and Hib
boosters as a toddler, given influenza vaccine 3 months ago
NUTRITION
Mix-fed, given age-appropriate milk formula
Started complementary feeding at 5 mos
Eats 3 meals a day (has school lunch), eats 2 snacks consisting of
junkfood and fishballs from a nearby vendor
DEVELOPMENTAL
At par with age, no problems at school
PHYSICAL EXAM
Awake, ambulatory but weak, not in distress
BP 105/70, HR 55, RR 20, T 40C
Wt 22 kg (z 0), Ht 130 cm (z +1)
Pink conjunctivae, anicteric sclerae, no tonsillopharyngeal
congestion, no cervical lymphadenopathy
Equal chest expansion, clear breath sounds, no retractions
Adynamic precordium, loud S1 S2, PMI not displaced, regular
rhythm, no murmurs
(+) Pink, non-pruritic macular rash on chest, abdomen and back,
flat abdomen, soft, hyperactive bowel sounds, liver edge 2 cm
below right costal margin, slightly tender
Pink nail beds, full pulses, no edema, good CRT
LABORATORY EXAMS
CBC: Hgb 130, Hct 0.38, WBC 8.5, N 55%, L 41%, M 3%, E 1%, Plt
280
Urinalysis: Yellow, clear, pH 7, SG 1.01, WBC 1/hpf, RBC 0/hpf,
glucose none, nitrite negative, protein none, casts none
EKG
Stool exam: Greenish brown, mucoid, PMN 5-10, no ova/parasite
seen
FOBT: negative
Dengue IgG non-reactive, IgM non-reactive
Stool culture: negative
Blood culture: Growth of Salmonella typhi

A
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2
Q

EXAMINER’S GUIDE: TYPHOID FEVER
1. Listed down salient features of case

A
  1. Listed down salient features of case
    [ ] Persistent 1 week fever low > high grade
    [ ] Rose spots, abdominal pain and diarrhea
    [ ] Bradycardia, rose spots, borborygmi, tender hepatomegaly
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3
Q
  1. Systematic approach to diagnosis, discussed differentials
    Infection
A

Bacterial (AGE, Typhoid, Shigellosis)
Viral exanthems (measles, rubella)
Other viral illnesses (dengue, coxsackie, viral hepatitis)
Parasitic (amebiasis, schistosomiasis)
Immunologic causes
Kawasaki disease
Scarlet fever
Toxic shock syndrome

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4
Q
  1. Order diagnostic tests
A

[ ] CBC
[ ] Stool exam
[ ] Stool culture
[ ] Blood culture
[ ] Screening tests for differentials (dengue titers)

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5
Q
  1. Interpret lab results
A
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6
Q
  1. Management
A
  1. Management
    [ ] Emergency measures
    [ ] Antibiotics (IV Ceftriaxone 75 mkd, oral Cefixime 15mkd for
    7-10 days)
    [ ] Preventive measures (handwashing, food preparation, etc)
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7
Q
  1. Preventive Pediatrics
A
  1. Preventive Pediatrics
    [ ] Developmental surveillance
    [ ] Atopy screen
    [ ] Monitor weight, height
    [ ] Blood pressure
    [ ] Eye exam
    [ ] Immunizations
    [ ] Deworming (albendazole 400 mg q6mos, mebendazole 500
    mg q6mos)
    [ ] Dental care
    [ ] Nutrition counseling
    [ ] Physical activity
    [ ] Injury and poisoning prevention
    [ ] Child maltreatment prevention
    [ ] Counseling on lead and toxicant exposure
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8
Q

what is Otitis media? Give 2 main categories and etiology

A

2 Main Categories:
1. Acute otitis media/suppurative (AOM)
2. Inflammation with middle ear effusion/suppurative/
secretory OM/ otitis media with effusion (OME)

2 most important identifiable risk factors for OM:
1. Family socioeconomic status
2. Extent of exposure to other children

Etiology:
1. S.pneumoniae
2. HiB
3. Moraxella catarrhalis
4. Viral: RSV, influenza, adenovirus, enterovirus

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9
Q

Give pathophysiology of otitis media

A

Patho:
Release of proinflammatory cytokines à increase inflammation –> eustachian tube dysfunction
Mobility – most sensitive and specific in detecting MEE

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10
Q

What are the clinical manifestations of otitis media

A

CM (AAP AOM dx)

  1. Acute onset of sx
  2. (+)MEE
  3. Signs of acute middle ear inflammation
  4. Moderate to severe bulging of the TM/new-onset
    otorrhea not caused by otitis externa
  5. Mild bulging of the TM and recent <48h onset of ear
    pain/intense TM erythema
  6. HiB: simultaneous purulent and erythematous
    conjunctivitis + OM ipsilaterally
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11
Q

What are the diagnostics for otitis media?

A

Dx:
1. Otoscopy: Bulging of TM – most specific finding of
AOM (97%)
- N TM: pearly gray
- AOM TM: TM diffusely red/erythematous or abnormal whiteness (scarring), effusion = amber, pale-yellow, or bluish; may have perforation, no cone of light; clear bubbles/ fluid layer indicates OME
2. Tympanometry
- The degree of TM mobility in response to (+) and (-)
otoscopy pressures to assess middle ear fluid: hallmark of AOM and OME
- Impaired mobility in chronic OM, MEE, or Eustachian
tube dysfunction

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12
Q

What is the management of otitis media?

A

Mgt:
1. Abx: indicated for:
a. <6mo: even presumed
b. 6-24mos: even suspected if T>39C,
significant otalgia, toxic appearance
c. >2yo: if confirmed, severe OM
- High suspicion of Bacterial resistance:
a. <2yo
b. Regular contact with large groups of
children (daycare)
c. Recent abx tx
- DOC/1st line: amoxicillin
d. <2yo: 40-45mkd x 10d
e. >2yo: 80-90mkd q12 po
- 2nd line: should be effective vs HiB, M.catarrhalis,
S.pneumonia:
Clarithromycin 15mkd po q12
Cefuroxime 30 mkd q12 po
Ceftriaxone 50 mkd q12/24 IV x 3d
Alt: Co-amoxiclav 20-40 mkd q8-12 po
Cefdinir 14 mkd q12/24 po
- Assess response after 72h.
f. Cure – resolution of s/sx (exclusive of
effusion) w/in 72h
g. Failure – persist after 72h
h. Relapse – reappearance of s/sx after initial
response within 4d of tx conclusion
2. Myringotomy: indications:
- AOM with severe, refractory pain
- Hyperpyrexia
- (+) complications: facial paralysis, mastoiditis,
labyrinthitis, CNS infection
- Immunocompromise from any source
3rd line of tx if 2 abx failed
3. Acetaminophen or ibuprofen - pain

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13
Q

What are the complications of otitis media?

A

Complications:
1. Intratemporal
a. Infectious dermatitis
b. Tympanic membrane perforation
c. Chronic suppurative OM: P.aeruginosa,
S.aureus
d. Acute mastoiditis + petrositis: WOF EOM
involvement, pinna displacement
Gradenigo syndrome: triad of suppurative
OM, paralysis of external rectus muscle,
ipsilateral orbital pain
e. Facial paralysis: emergent!
f. Cholesteatoma: can extend intracranially,
life threatening. Chronically draining ear.
g. labyrinthitis
2. intracranial
a. meningitis
b. epidural abscess
c. focal encephalitis
d. brain abscess
e. sigmoid/lateral sinus thrombosis
f. otitic hydrocephalus

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14
Q

What is UTI? give causes and pathophysiology

A

CH 538: URINARY TRACT INFECTION (UTI)
- considered an important risk factor for renal
insufficiency or ESRD
- in children, serves as indicator for anatomic and
functional abN of the GUT
Epidemiology
- <1yo: M>F (2.8-5.4:1)
- >1-2 yo: M<F (1:10)
Pathogenesis
- Most UTIs are ascending infections
a. Bacteria arise from fecal flora and colonize
the perineum and then enters the bladder
via the urethra
- Risk factors: voiding dysfunction, female,
uncircumcised male, toilet training, wiping from back
to front (F), tight underwear, bubble bath,
constipation, anatomic abN, obstructive uropathy,
neuropathic bladder, sex, pregnancy
- Protective: breastfeeding, circumcision
- Risk factors for recurrent UTI: age (<6mos), VUR grade
3-5, bowel bladder dysfunction (BBD)
- Most common DDx: VUR

Etiology:
- Caused by colonic bacteria
- F: E.coli (75-90%), Klebsiella, Proteus
- M&F: Staphylococcus saprophyticus, enterococcus

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15
Q

What are the clinical manifestations of UTI?

A

CM
1. Acute pyelonephritis – “Upper UTI”. UTI involving the kidney and renal pelvis with clinical symptomatology and UA finding referable to UTI and a (+) UCS
- abdominal, flank, or back pain, fever, malaise,
nausea/vomiting, lethargy, irritability (infant),
frequency, dysuria (older)

  1. Cystitis – “Lower UTI”. UTI involving the bladder and
    urethra manifesting with clinical sx and UA referable to UTI and a (+) UCS
    - Gross hematuria, dysuria
    - Urgency, frequency, malodorous urine, incontinence,
    suprapubic pain
    - Usually resolves within 1 week
    - Does not cause fever or renal injury
  2. Asymptomatic bacteriuria – UTI with (+) UCS w/o any s/sx
    - Most common in girls. Incidence declines with
    decreasing age
    - Benign. Does not cause renal injury except in pregnant women
  3. Presumptive UTI – presence of clinical sx and UA
    findings referable to UTI not supported by UCS
  4. Recurrent UTI - >2 episodes of acute
    pyelonephritis/presumptive UTIs or >3 episodes of
    cystitis or 1 episode of acute pyelonephritis and 1/2
    episodes of cystitis.
    It may be difficult to recognize UTI in children. Non-specific s/sx
    (fever may be the only sx).
    The presence of UTI should be considered in infants and children
    <2yo with unexplained fever.
    UTI is the most common serious bacterial infection in infants and
    younger than 2yo who have fever without an obvious focus.
    Always rule out inguinal/genital anatomic abN – phimosis, uncircumcised, etc
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16
Q

What are the diagnostics for UTI?

A

Always ask about the method of urine collection
Methods of Urine collection:
a. For <2yo: clean-catch urine (CCU) is
recommended. Sn 100%, Sp 95%
b. For >2yo: mid-stream urine (MSU). ~100%
Sn and Sp
c. Wee bag: only useful if UCS (-). Otherwise,
repeat UA using clean-catch or midstream
urine. Sn 85% Sp 59%
d. SPA or urethral catheterization – if above
methods fail/cannot be done. Sp 100%
- Consider the state of dehydration and general well
being of the child on the most appropriate urine
collection method
- Delay of >30 min in the transport of UA sample, failure
of the lab to preserve the urine for >4h and presence
of antimicrobial agent in the urine may decrease the
chances of isolating the true etiologic agent

  1. UCS – for confirmation and appropriate tx. Gold
    standard
    - (+) UCS if:
    *Suprapubic aspiration: any growth (>99%)
    *Catheterization: >10^5 –> 95%
    10^4-10^5 – > infection likely
    *Clean catch, midstream urine:
    >10^4 (boy) infection likely
    >10^5 (girl)(3 specimens) –> 95%
    10^5 (girl)(2 specimens) – > 90%
    >10^5 (girl)(1 specimen) –> 85%
  2. UA– screening tool
    - pyuria (WBC in urine) suggests infection
    a. Sterile pyuria: (+)WBC, (-)UCS. Occurs in
    partially treated UTIs, viral infection, renal
    TB, renal abscess, urinary obstruction,
    urethritis due to STIs, interstitial nephritis
    b. (+)nitrites, leukocyte esterase
    - It is necessary to have UA after 24h of unexplained
    fever.
    - (+) for nitrites, LE, pyuria or bacteriuria may suggest
    UTI

Bacteriuria (+), Pyuria (+): send for urine CS; treat as UTI, start antibiotics
Bacteriuria (+), Pyuria (-): send for urine CS; treat as UTI, start antibiotics
Bacteriuria (-), Pyuria (+): send for urine CS; start antibiotics if with symptoms
Bacteriuria (-), Pyuria (-): NOT UTI

  1. Dipstick test – screening tool (nitrite test, leukocyte
    esterase)
    Nitrite (+), leukocyte (+): send for urine CS; treat as UTI, start antibiotics
    Nitrite (+), leukocyte (-): send for urine CS, treat as UTI, start antibiotics
    Nitrite (-), leukocyte (+): send for urine CS, start antibiotics if with symptoms
    Nitrite (-), leukocyte (-) : NOT UTI

Nitrite – byproduct of bacteria
Leukocyte esterase – enzyme in WBC in the urine

  1. CBC and BCS – elev WBC, neu
  2. Elev CRP, ESR – nonspecific but may help the dx.
  3. KUB UTZ – to assess kidney size, hydronephrosis,
    ureteral dilation
    - Evaluate bladder anatomy
    - Indications
    a. First UTI <6mos old
    b. No response to abx within 24-48h
    c. Recurrent UTI
    d. Toilet-trained cases of UTI (Grade C)
    - If abN, do DMSA or VCUG (bottom up approach)
    - Should be performed promptly in patients who do not
    demonstrate good response within 2d of tx.
    - If with good response to tx, do VCUG or DMSA at
    earliest convenience
    - For >6mos, do UTZ only if with recurrent infection
  4. Dimercaptosuccinic acid (DMSA) scan – assess renal
    scarring and areas of acute pyelonephritic involvement
    - Top down approach: DMSA first, if with tracer uptake
    in photopenic areas suggesting active or recurrent UTI,
    do UTZ
  5. Voiding cystourethrogram (VCUG) – Assess reflux
  6. Procalcitonin (>1ng/ml)– stronger predictor in the dx of
    acute pyelonephritis
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17
Q

What is VUR? grading?

A
  • Retrograde propulsion of urine into the upper urinary
    tract during voiding
  • At least 1/3 of children with first UTI have VUR
  • Autosomal dominant
  • Can lead to cortical scarring due to intrarenal reflux
  • Can cause kidney failure and ESRD due to reflux
    nephropathy
    VUR >3 (out of 5) – minimal stage for ureteral dilation
  • Need for abx + surgery, for sx’c
    Long term consequences of reflux nephropathy:
    1. Hypertension
    2. Pregnancy complications
    3. Renal failure
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18
Q

What is the management of UTI?

A

Mgt
1. Presumptive UTI – empiric abx may be started
immediately after collecting UCS specimen
2. Acute uncomplicated UTI: Acute cystitis and
pyelonephritis (NAGCOM)
a. <2mos: Cefotaxime + Amikacin x 10-14d
b. >2mos-18yo: Coamoxiclav, cefuroxime,
ampicillin-Sulbactam x 7-14d, amoxicillin,
TMP-SMX, cefixime, cephalexin
c. Adolescents w/ acute cystitis: Cefuroxime,
nitrofurantoin, IV ampi-sul x 7-14d
- Oral tx = IV tx
- IV tx preferred if seriously ill, cannot tolerate po
- Switch to PO once afebrile x 24h and able to tolerate
po

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19
Q

recommended antimicrobials for UTI

A

Acute cystitis
most strains of E.coli: TMP-SMX or timethoprim (5-8 mg/kg/day in two divided doses)

Klebsiella and Enterobacter: Nitrofurantoin 5-7mg/kg/24hr in 3-4 divided doses
Note: Use of amoxicillin 5-mg/kg/24hr is also effective as initial treatment but has high rate of bacterial resistance

Acute pyelonephritis:
Ceftriaxone: 50-75mg/kg/25hr, not to exceed 2g)
Cefotaxime: 100mg/kg/24hr
Ampicillin 100mg/kg/24hr with an aminoglycoside such as gentamicin (3-5mg/kg/24hr) in 1-3 divided doses

Note: oral 3rd gen cephalosporins such as cifixime are as effective as parenteral ceftriaxone against a variety of gram negative organisms other than Pseudomonas

Pseudomonas: Aminoglycosides effective
Note: Aminoglycosides with risks for ototoxicity abd nephrotoxicity therefore, serum creatinine and trough gentamincin levels if available must be obtained before initiating treatment and monitored daily thereafter

Oral fluoroquinolone ciprofloxacin- alternative agent for resistant microorganisms

  1. Complicated UTI
    - Refer to IDS, nephrologist, and urologist
    - Po Ciprofloxacin, Levofloxacin, Co-amoxiclav
    - IV Amikacin, Gentamicin, Piperacillin-Tazobactam,
    Ertapenem, Meropenem x 7-14d
  2. Prophylaxis – indications:
    a. > Grade I/ dilating VUR and/or asx’c
    antenatal hydronephrosis with ureteral
    dilatation
    b. High-grade VUR or UVJO at risk for
    recurrent UTIs and renal scarring
    c. DOC:
    < 2mos: cephalexin, amoxicillin
    >2mos: TMP-SMX, nitrofurantoin
  3. Abx switch may be done if UCS has a different sn &/or
    if poor response after 48-72h
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20
Q

How do we prevent UTI?

A

Primary prevention
1. Urinate frequently, and avoid retaining your urine for a
long time after you feel the urge to void.
2. Wipe from front to back after a bowel movement to
prevent bacteria in the anal region from spreading to
the vagina and urethra.
3. Take showers rather than bubble baths.
4. Wash the skin around the vagina and anus daily.
5. Avoid using deodorant sprays or feminine products
such as douches in the genital area that could irritate
the urethra.
6. Wear cotton underwear.
7. If you are sexually active, make sure you wash your
genital area and urinate after intercourse. This will help
to remove any bacteria that could travel up the
urethra. Empty your bladder as soon as possible after
intercourse, and drink a full glass of water to help flush
bacteria.
Anticipatory guidance
1. Routine UA should be performed annually from 6mos old.
2. >13 yo, dipstick UA should be performed to screen for LE in female and male adolescents

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21
Q

What is the etiology of Dengue fever?

A

Etiology:
- Dengue virus 1,2,3,4
- Vector: Aedes aegypti mosquito breeding in clean,
stagnant water
- Infection with DENV type produces life-long immunity
against that type and a very short period of protection
against the other three serotypes – thereafter,
infection with a different strain may predispose to
more severe ds.

Epid
- WHO: 50-100M new cases annually
- Leading cause of hospitalization and mortality in
children
- Most significant vector-borne viral disease of public
health importance in tropical countries

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22
Q

What is the pathophysiology of dengue?

A

Patho
- Risk factor for DHF:
a. (+) infection-enhancing Ab
b. (-) cross-reactive neutralizing Ab
- Viremia level proportional to disease severity
- Elev complement levels à inc vascular permeability à
activate blood clotting and fibrinolytic system
- Capillary damage allows fluids, electrolytes, protein,
RBC to leak into extravascular space
IP: 3-14d
Communicability:
in mosquito, replication in 8-12d, then
infectious for life

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23
Q

What are the phases of dengue and clinical manifestations?

A

3 Phases of Dengue:
1. Febrile phase (d2-7) – sudden HG fever (39.4-
41C)x1-5d biphasic fever pattern, generalized
body ache, muscle and joint pains (back-break
fever or breakbone fever), headache, retroorbital
pain, facial flushing, sore throat,
hyperemic pharynx, macular or maculopapular
rash, petechiae, mild mucosal membrane
bleeding,
- cough, colds, cutaneous hyperesthesia/ hyperalgesia,
flu-like sx, anorexia, taste aberration
- (+) tourniquet test: Inflate BP cuff to midway between
SBP and DBP for 2 minutes. Count petechiae at
antecubital fossa. (+)= >10 petechiae per 1 square inch
- progressive decrease in total WBC count
2. Late febrile phase: warning signs of severe
dengue
a. Persistent vomiting
b. Severe abdominal pain
c. Mucosal bleeding
d. DOB
e. Early signs of shock
- Progressive leukopenia followed by rapid decrease in
plt count usually precedes plasma leakage
- Rash: transient, macular, generalized, blanches under P
during 1st 24-48h
3. Critical phase (d3-7) – 24-28h after fever
defervescence
- Increase in capillary permeability parallel with inc hct
levels
- Period of clinically significant plasma leakage x 24-48h
(hemoconcentration): progressive leukopenia followed
by thrombocytopenia & inc hct
- Warning signs mark the onset of this phase due to
plasma leakage
- Those with non-severe dengue improve
- Severe dengue develop Pleural effusion, ascites,
hypovolemic shock, severe hemorrhage, organ
impairment
- Shock à organ hypoperfusion à multiple organ
impairment (hepatitis, encephalitis, myocarditis),
metabolic acidosis, DIC, severe bleeding
4. Recovery/convalescent phase – gradual
improvement and stabilization of hemodynamic
status
Rash 1-2 days after defervescence: generalized
morbilliform MP rash at extremities, sparing palms and
soles. Disappears in 1-5 days à desquamation
(Hermann rash) on D5-7: isles of white in a sea of red,
gen. pruritus
- May have bradycardia, stable hct, hemodilution
- Diuresis ensues`

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24
Q

Differentiate dengue hemorrhagic from dengue shock syndrome?

A

Dengue Hemorrhagic Fever (DHF) – 1997 Classification
A. 1st phase
1. Fever
2. Malaise
3. anorexia
B. 2nd phase
Rapid clinical deterioration
1. Cold, clammy extremities, flushed face,
diaphoresis, restlessness, and irritability,
midepigastric pain, dec UO
2. Rash: scattered petechiae on forehead and
extremities, spontaneous ecchymoses, MP rash
3. Easy bruising and bleeding
4. Circumoral and peripheral cyanosis
Dengue Shock syndrome
1. Weak pulse, thready, rapid
2. Faint heart sounds
3. Hepatomegaly
4. Narrow pulse pressure (<20mmHg)

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25
How is dengue diagnosed?
Dx: A. Clinical DOH 2011 Revised Dengue Classification 1. Probable Dengue Fever: Live/travel to dengue endemic area (SE Asia (70%), Africa, America, Eastern Mediterranean, western Pacific) with fever x 2-7d with >2 of the ff a. Headache b. Body malaise c. Arthralgia d. Retro-orbital pain e. Nausea, vomiting f. Anorexia g. Diarrhea h. Flushed skin i. Rash (petechial/Herman’s rash) j. Tourniquet test (+) AND a. CBC – leukopenia w/ or w/o thrombocytopenia b. And/or DNS1 (+) or Dengue IgM (+) 2. Confirmed Dengue fever a. Viral culture isolation b. PCR 3. Dengue w/ warning signs: Live/travel to dengue endemic area with fever x 2-7d with any of the ff: a. Abdominal pain/tenderness b. Mucosal bleeding c. Clinical sign of fluid accumulation d. Persistent vomiting e. Lethargy, restlessness f. Hepatomegaly g. Dec UO, or no UOx6h h. Lab: elev Hct, and/or dec plt 4. Severe Dengue: Live/travel to dengue endemic area with fever x 2-7d and any of the above CM for dengue w/ or w/o warning signs + any of the ff: a. Severe plasma leakage - Leading to: a. Shock (DSS) b. Fluid accumulation with respiratory distress b. Severe bleeding c. Severe organ impairment i. Liver ALT or AST >1000 ii. CNS: sz, impaired consciousness iii. Heart: myocarditis iv. Kidney: renal failure B. Laboratories Preferably D1-6 of fever: 1. CBC – leukopenia (WBC <5K), then thrombocytopenia (plt <100k), hemoconcentration (20% rise from baseline) during critical phase 2. Dengue Viral culture 3. RT-PCR 4. Dengue NS1 Ag test – useful D1-3 5. Dengue IgM, IgG – D7 onwards - Method of choice at the end of the acute phase of infection - Should not be collected earlier than d5 or 6 wks after onset - Primary infection IgG in low titers at end of 1st week the inc slowly after several mos - Secondary infection: IgG detected in acute phase and persists for 10mos 6. PT/PTT – not routinely indicated. Prolonged bleeding time. Moderately decreased PT 7. Elev AST, metabolic acidosis with hyponatremia, hypochloremia, elev BUN, hypoalbuminemia (<3.5g/dL) 8. CXR – right lateral decubitus; r/o pleural effusion 9. UTZ – edematous gall bladder wall, ascites, pleural effusion
26
Give management of Dengue
Mgt Pxs with dengue w/o warning signs but w/signs of dehydration 1. Send home on ORS: pxs with all of the ff: a. Able to tolerate adequate volumes of oral fluids b. Pass urine at least once q6h c. Do not have any of the warning signs (esp when fever subsides) d. N hct (<40%) and N plt ct (>150K) e. Should have daily CBC, monitor defervescence, warning signs until out of critical period f. Advise to return immediately once with warning signs - Home care plan: a. ORS – reduced osmolarity ORS with Na 50- 70 mmol/L § No sports drinks or fluids containing high sugar/glucose § Plain water will cause electrolyte imbalance b. Paracetamol § Do not give ASA, Ibu, other NSAIDs § Tepid sponging § No Abx c. Dengue Home care card and advice on when to return to the hospital § Bed rest § Fluids § Fever management § Warning signs: bleeding, freq. vomiting, abdominal pain, drowsiness, mental confusion, seizures, pale, cold, or clammy hands and feet, DOB, decreased or no UO w/in 6h 2. Admit for oral rehydration fluids a. Px with any warning sign b. No warning sign but with any: complicated comorbidities: pregnancy, infancy, old age, obesity, DM, renal failure, chronic hemolytic ds; social circumstance: living alone, living far from HCC w/o reliable transport - In-hospital Oral ORS a. ORS b. IVF if ORS not tolerated: 0.9% saline or LR at M rate ORS after a few hrs of IVF 3. Admit to wards for IVF tx Admission criteria: strongly associated with severe dengue a. Shortness of breath b. Irritability or drowsiness c. Pleural effusion d. Abdominal pain e. Melena f. Elevated hematocrit (>20%) g. Decreased or decreasing platelet count (<100K) Vomiting not assoc with severe dengue, but may mean inability to tolerate ORS, thus consider admission IVF for pxs w/o warning signs/shock: 1. Judicious fluid therapy = fluid restriction, avoid fluid overloading 2. Calculated for IBW or ABW, whichever is less (max 50kg). 3. M+5% for critical phase (max = 50kg = 4600ml /48h) 4. IVF = isotonic solution: D5LRS, D5 acetated ringers, D5 NSS/D5 0.9 NaCl 5. For <6mos old: D5 0.45 NaCl = mix equal volumes D50.9 NaCL + D5W a. Do not use hypotonic fluids D5 0.3 NaCl 6. Hypotonic IVF is associated with hyponatremia 7. Compute M IVF 8. For mild dehydration, add replacement tx + maintenance tx to determine total fluid requirement (TFR) over 24h 9. Replacement Tx: a. <12mos: 50ml/kg b. >1 yo: 30ml/kg 10. Fluid rate should be adjusted according to the clinical condition, VS, UO, Hct levels (~3cc/kg/h) 11. Monitor: T pattern, volume of fluid intake and losses, UO (vol and freq), warning signs, CBC (hct, wbc, plt), CBG 4. Admit to ICU for IVF
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Study fluids and algorithm for management of compensated shock
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Guidelines for blood transfusion
1. No preventive BT (like plt transfusion) 2. Should be given only when there are definite and established indications and in practically all cases component therapy should be utilized. 3. Abnormal hemostasis: consumptive coagulopathy is not the major cause of bleeding but rather the profound shock and intractable acidosis. a. Fibrinogen is the most severely affected clotting factor 4. PRBC or FWB, plasma if with: a. Significant bleeding (melena, hematemesis) b. Decreasing hct inspite of IVF 5. plt concentrate a. if plt <50K with bleeding 6. cryoprecipitate 1bag/5kg or FFP 10-20ml/kg, plt concentrate a. for DIC
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Criteria for discharge
Criteria for discharge 1. afebrile x 24-48h 2. good well being 3. stable hct ivf and inc plt trend 4. at least 2-3d from last episode of shock
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What are the complications and prognosis of dengue?
Complications 1. Fluid and electrolyte loss 2. Febrile sz COVID-19 + Dengue – leukopenia, vomiting, fever, rash. Prognosis: DF: good DHF: death in 40-50%, WOF overhydration
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How do we prevent dengue?
Prevention DOH 4S vs Dengue 1. Search and destroy mosquito-breeding sites 2. Secure self-protection measures: long pants, long sleeves, mosquito repellant - DEET, citronella (use EPA-approved products) 3. Seek early consultation 4. Support fogging/spraying in hotspot area Dengue vaccine – currently suspended by DOH due to Dengvaxia controversy. Currently out of market - CYD-TDV (2015) - For 9-45yo. Licensed in 20 other countries - Live recombinant tetravalent 3 dose series (0/6/12 mo sched) - Efficacy 78.2% to seropositive to prevent dengue infection vs 38.1% to seronegative pxs - Inc risk of hospitalization and severe dengue in seronegative pxs for 30mos after 1st dose - Recommendation: pre-vaccination screening strategy in w/c only seropositive pxs are vaccinated (Dengue IgG ELISA)
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What is typhoid fever?
CH 198: TYPHOID FEVER Etiology - Salmonella enterica serovar Typhi - Salmonella paratyphi A, B, C Transmission - Most common: ingestion of food/water contaminated from human feces - Shellfish and vegetable grown in sewage contaminated water Communicability: as long as the infected person excretes S.typhi (after 1 week of illness to convalescence)
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What is the pathophysiology of typhoid?
Patho - Risk factors: enable viable org to reach SI § Achlorydia § Buffering medications § Rapid gastric emptying after gastrectomy § Large inoculum § Prior abx tx, antimotility agents - Toxin production à proinflammatory cytokines à Enterocolitis with diffuse mucosal inflammation and edema, with erosions and microabscesses à bacteremia à localized infection and organ suppuration IP: 7-14d, range 3-30d
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What are the clinical manifestations of typhoid fever?
CM: 1. HG fever, malaise, myalgia, abdominal pain, anorexia, hepatosplenomegaly, diarrhea, constipation, chills, diaphoresis, cough, sore throat, dizziness 2. T pattern: classic stepladder rise. rises in small increments then reaches 40C by the end of the 1st week 3. Diarrhea – (30%) small volume, greenish pea soup - Follows fever on the 2nd week 4. Constipation (50%) 5. Rose spots – MP rashes visible on d7-10 on lower chest or abdomen and lasts 2-3d 6. Relative bradycardia, neurologic manifestation, GI bleeding 7. Abdominal pain, abdominal distention, tenderness 8. Hepatosplenomegaly 9. Typhoid psychosis/encephalitis
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What are the complications of typhoid fever?
Complic 1. Hepatitis, cholecystitis, jaundice, intestinal hemorrhage and perforation, myocarditis, CNS
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standard case definition of typhoid?
WHO standard case definition 1. Probable – persistent fever (38C) lasting >3d with (+) serodx or Ag detection test, but no S.typhi isolation - A clinically compatible case epidemiologically linked to a confirmed case or outbreak 2. Confirmed case – with laboratory confirmed S.typhi (blood, BM, bowel fluid) 3. Chronic carrier – excretion of St.typhi in the urine or stool for >1yr after onset of typhoid fever (2-5%)
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What are the diagnostics for typhoid?
1.CBC with PC -leukopenia 4000-6000 cells/mm6 leukocytosis may be as high as 20,000-25,000 in the presence of pyogenic complications or intestinal perforation thrombocytopenia- marker for sever illness, WOF DIO normocytic anemia hypochromia with blood loss 2. Culture of appropriate specimen ***Blood CS-gold standard test for typhoid fever; highest during 1st week; taken at diff sites stool or urine culture--> 2nd-4th wk of illness bone marrow culture: not done routinely but indicated in highly suspicious cases with negative blood or stool culture Other: UA- transient albuminuria LFT- mild elevation of enzymes Renal function test stool for occult blood Serology: Salmonella IgG/IgM or typhidot=local studies revealed varying results. No local recommendation for its use at the moment Widal test- not recommended PCR and DNA probe of S. typhi=have not yet been developed for clinical use
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Management of typhoid
Fully susceptible Uncomplicated: Amoxicillin 75-100 mkd x 14d Chloramphenicol 50- 75 mkd x 14-21d Alt: ciprofloxacin 15mkd x 5-7d Complicated/Severe: Ciprofloxacin 15mkd x 10-14d Alt: chloramphenicol 100 mkd x 14-21d MDR: Uncomplicated: MDR Ciprofloxacin 15mkd x 5-7d Cefixime 15-20mkd x 7-14d Alt: Azithromycin 8-10 mkd x 7d Complicated/Severe: Ciprofloxacin 15mkd x 10-14d Alt: ceftriaxone 60mkd x 10-14d Cefoxamine 60mkd x 10-14d QR Uncomplicated: Azithromycin 8-10 mkd x 7d Ceftriaxone 75 mkd x 10-14d Complicated/Severe: Ceftriaxone 60mkd x 10-14d Cefotaxime 80kd x 10- 14d Alt: ciprofloxacin 20mkd x 7-14d Azithromycin 10- 20mkd x 7d Non-typhoid salmonella enteritis: Cefotaxime 100-200 mkd q6-8 x 5-14d Ceftriaxone 75mkd q24 x7d Ampicillin 100mkd q6-8 x7d Cefixime 15mkd x 7-10d Multi-drug resistant (DRTF) - Indications: § Severe typhoid fever (shock, abN sensorium) § Potentially life-threatening complications (intestinal hemorrhage, perforation, DIC, myocarditis) § Clinical deterioration or devt of complication during tx § No improvement within 5-7d § Household contact of documented DRTF - Increasing rates of ciprofloxacin resistance – judicious use as Salmonella GE is usually a self-limited disease
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How to prevent typhoid?
Prevention 1. Central chlorination and domestic water purification 2. Avoid street food 3. Typhoid vaccine for high risk populations
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What is leptospirosis? Give transmission and epidemiology
Leptospira Epid - Infect rats, mice, cattle, goats, sheep, horses, pigs, domestic dogs - Infected animals excrete spirochetes in urine for prolonged periods (in warm, moist environment --> flood) Transmission and Patho - Leptospira enter humans through mucus membrane (eyes, nose, mouth), wound, or ingestion of contaminated water --> circulation in blood stream to all organs --> endothelial lining damage of small BV with secondary ischemic damage to end organs
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What are the clinical manifestations of leptospirosis?
1) Anicteric leptospirosis – biphasic course A. Initial/septicemic phase – 2-3d. leptospires at blood, CSF a. Fever b. Flu-like sx: chills, lethargy, severe headache, malaise, nausea, vomiting c. Severe debilitating myalgia of LE>LS spine d. Abdominal pain e. Dec HR, hypotension f. Conjunctival suffusion with photophobia, orbital pain, (-)exudates/chemosis g. Gen. LNE h. Hepatomegaly i. Rash: transient (<24h) erythematous, MP, urticarial, petechial, purpuric, desquamating B. 2nd/Immune phase: tissue localization a) Fever b) Septic meningitis: elev CSF pressure, pleocytosis with PMN, N/elev protein, N glc x 1 wk c) uveitis 2) Icteric leptospirosis (Weil syndrome) 1. Severe (<10%) in adults >30 yo 2. Same initial phase 3. Immune phase: a. Jaundice, RUQ pain, hepatomegaly b. Renal failure (16-40%): #1 cause of death c. Dec plt, hemorrhage, CV collapse
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How is leptospirosis diagnosed?
Dx 1. Microscopic agglutination test (MAT): gold standard - >4x inc in titer at D12-3rd week, >1:200 or serial titers >1:100 2. ELISA, Latex agglutination, immunochrom. - D1-10: CSF - 2nd week: urine 3. UA: hematuria, ptn, casts (+) 4. BCS – definitive dx. Isolated 5d after sx onset (7-14d after exposure). 5. CBC – peripheral leukocytosis with a left shift, thrombocytopenia 6. Elev ESR 7. Mildly elev LFTs, bilirubin, ALP 8. CXR – blateral diffuse airspace disease, cardiomegaly, pulmonary edema, multiple patchy infiltrates (alveolar hemorrhage)
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How is leptospirosis managed?
mild 1st line: <8yo: Amoxicillin 50mkd q8 x 7d >8yo: doxycycline 2-4 mkd BID x 7d 2nd line: Azithromycin 1g LD then 10mkd OD x 2d mod-severe 1st line: Pen G 250,000-400,000 U q4-6 x 7d (NAGCOM) Pen G 6-8M U/m2/d q4 x7 d (Nelsons) 2nd line: Ampicillin 100mkd q6 x 7d Cefotaxime 100- 150mkd q6-8 x7d Ceftriaxone 80-100mkd q21 x 7d
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How to prevent leptospirosis?
Prevention 1. Rodent control 2. Avoid contaminated water, soil 3. Vax livestock, dogs 4. Protective clothing 5. PrEP: not routine, unless to travelers, soldiers, those engaged in occupational and recreational activities in highly endemic areas 6. PEP: depends on risk type - Preferred: Doxycycline 4mkdose SD po per week (max 200mg regardless of age); can be 100mg BID x 1d - Alt: Amoxicillin 50mkd q8 x 3-5d, Azithromycin 10mkd SD - If exposed >7d, repeat dose after 1 week
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Bacteremia in a child with non-toxic fever w/o obvious source of infection - Usually <3yo
Occult bacteremia
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What is the most common cause of occult bacteremia?
S. pneumoniae Other cause: HiB, N. meningitidis
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How do we diagnose occult bacteremia?
Dx 1. BCS, CBC 2. UCS, UA 3. Fecalysis, CSF analysis
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Management for occult bacteremia?
Paracetamol Antibiotics: Amoxicillin
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What is meningitis?
a. Acute bacterial: Gram (+) or (-) b. Acute aseptic meningitis: virus c. Chronic: TB or fungal 2. Viral encephalitis a. Acute: HSV, Jap Enceph, enterovirus b. Chronic: SSPE (measles) 3. Congenital infection – TORCH
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What are the different types of meningitis and findings
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What is tuberculous meningitis?
Etiopatho - From metastatic caseous lesions in the cerebral cortex or meninges that develop during lymphohematogenous dissemination of primary infection - Gelatinous exudates infiltrate the corticomeningeal blood vessels à inflammation, obstruction à infarction of cerebral cortex - Brainstem: site of greatest involvement § CN III, VI, VII - Communicating hydrocephalus: exudates block CSF flow - Most common in 6mos-4yo - Accompanies miliary TB (50%)
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What are the clinical manifestations of Tuberculous meningitis?
CM - More rapid progression in infants and young children - Acute onset hydrocephalus, sz, cerebral edema - Obtain HC and check fontanels
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Give the stages of Tuberculous meningitis
3 stages: 1. 1st stage – lasts 1-2wks. - Non-specific s/sx (fever, headache, irritability, drowsiness, malaise) - Infants: loss of developmental milestones 2. 2nd stage - Focal neuro signs (nuchal rigidity, sz, (+) Kernig sign and Brudzinski signs, hypertonia, CN palsy - Hydrocephalus, inc ICP, vasculitis - Encephalitis (disorientation, movt disorder, speech impairment) 3. 3rd stage - Coma, hemiparaplegia, hypertension, deteriorating VS and death
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How is meningitis diagnosed?
Dx 1. CSF analysis: AFB almost never seen on smear. Ground glass appearance of fluid w/c forms pellicle when spun. 2. PCR, ELISA, latex agglutination 95 3. CT/MRI: radiologic triad: basilar enhancement, communicating hydrocephalus, cerebral infarction, cerebral edema 4. Refer to pulmonology for dx of TB 5. CBC, BCS – PMN leucocytosis with a left shift 6. Serum e’s, glu – determine dehydration and SIADH
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Management of meningitis
Mgt 1. Anti-TB: 2HRZE + 10HR 2. Corticosteroids – improves survival but does not prevent severe disability x 2-4wks
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What is the etiopathogenesis of Viral meningitis?
Etiopatho - Echovirus - Coxsackie virus, adenovirus, CMV, HSV - Virus affects CNS parenchyma, causing encephalitis/ encephalomyelitis
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What are the clinical manifestations of viral meningitis?
CM 1. Fever, headache, altered sensorium, focal neuro signs, sz, meningeal signs, vomiting, poor feeding 2. Classical triad (older children): fever, headache, nuchal rigidity 3. Enterovirus – mild, self-limited ds with primary meningeal involvement to severe encephalitis - Most common cause of viral meningoencephalitis 4. Parechovirus – similar to enterovirus - more severe MRI lesions of cerebral cortex than enterovirus - important cause of septic meningitis/encephalitis in infants 5. HSV – focal brain involvement (frontal and temporal) - Temporal lobe encephalitis (HSV1) - Mild and transient meningoencephalitis (HSV2) - HSV1: severe sporadic encephalitis 6. VZV – most common manifestation is cerebellar ataxia - Severe encephalitis - Temporal presentation with chicken pox 7. Mumps – mild meningoencephalitis - Deafness from CN8 damage
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How is viral meningitis diagnosed?
Dx 1. CSF analysis – as above 2. EEG – slow wave activity without focal changes 3. CT/MRI – swelling of brain parenchyma 4. PCR, Ab titers for HSV, VZV, etc
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What is the management of viral meningitis?
Mgt 1. Supportive 2. Acyclovir 10-20 mkdose q8 x10-14d: HSV
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What is the cause of bacterial meningitis?
Etiopatho - 1st 2 mos: GBS, gram (-) enteric bacilli, L.monocytogenes, E.coli, Pseudomonas, Klebsiella, Salmonella - 2mos-12 yo: S.pneumoniae, HiB, N.meningitidis - Overall: viral infections are common - Entry of bacteria into the CSF and bacterial growth in this compartment leading to inflammation within the CSF and adjacent brain tissue Transmission: hematogenous
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What are the clinical manifestations of bacterial meningitis?
CM 1. Headache, nausea, vomiting, anorexia, restlessness, irritability, fever, neck pain & rigidity, obtundation, coma, focal neurologic deficits (vascular occlusion) 2. Nuchal rigidity secondary to inflammation of spinal nerves and roots to produce meningeal signs of irritation (Brudzinski, Kernig sign) 3. 12-18mos: may not have Brudzinski/Kernig 4. Sz due to cerebritis, infarction, electrolyte losses
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What are the diagnostics for bacterial meningitis?
Dx 1. Lumbar puncture and CSF GS/CS – pleocytosis >100/mm3, high CSF protein >1g/L, neu predominance, low sugar <40% - Contraindications: focal neuro signs, shock, extensive spreading purpura, unstable sz, coag abN, plt <50L, anticoag tx, local infection, RD, inc ICP (from any SOL) 2. BCS – reveals etiology in 80-90% 3. High CRP, ESR, procalcitonin – differentiates bacterial from viral causes 4. CBC - PMN leucocytosis with a left shift
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What are the management for bacterial meningitis?
Mgt 1. Empiric Abx: ceftriaxone 100mkd q12 IV or Cefotaxime 200 mkd IV q6 - Chloramphenicol 75-100 mkd IV q6 for >1mo old and allergic to penicillin - Vancomycin 45-60 mkd IV q6/8 + rifampin 20 mkd po q12 x 2 d - NAGCOM: Ampicillin/Cefotaxime + Amikacin/ Gentamicin 2. N.meningitidis: penicillin G x 5-7d - Alternative for pen allergy: meropenem 120 mkd IV q8 or vancomycin 3. S.pneumoniae: vancomycin + 3rd gen ceph or pen x 10- 14d 4. Penicillin-resistant: vancomycin 5. L.monocytogenes: ampicillin 200-400 mkd IV q4/6 - Alternative: TMP-SMX 20 mkd IV/po q6/8 6. HiB: ampicillin/ceftriaxone 100 mkd IV q12 7. E.coli: cefotaxime or ceftriaxone x 3 wks or at least 2 weeks after CSF sterilization 8. P.aeruginosa: ceftazidime 150 mkd q8 IV x3wks or at least after 2 weeks after CSF sterilization 9. Partially treated: Ceftriaxone or cefotaxime x 7-10d 10. GBS: Cefotaxime 11. Neonate: Ampicillin/cefotaxime/ceftriaxone + aminoglycoside (Gentamicin 7.5mkd IV q8) 12. 2mos-5yo: Ceftriaxone 100mkd q12-24/ chloramphenicol 100mkd IV q8 13. >5yo: Ceftriaxone/ Chloramphenicol 14. Dexamethasone 0.15mkdose q6h x 2d: for HiB, 2hrs before abx - Less fever, lower CSF protein, reduced CN8 damage
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What are the complications of bacterial meningitis?
Complications 1. Communicating hydrocephalus 2. Subdural effusion 3. SIADH: may exacerbate cerebral edema à hyponatremic seizures
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What is brain abscess?
- Most common between 4-8yo - Embolization due to CHD with R to L shunts, meningitis, chronic OM, mastoiditis (streptococci, HiB, pseudomonas), face & scalp infections, orbital cellulitis, dental infections (streptococci, fusobacterium, gram (-) bacilli), penetrating head injury (S.aureus, aerobic strep, G(-) bacilli, VP shunt infection - Affects cerebrum (80%), occipital lobe, cerebellum, brain stem (20%) - Majority single abscess - S.aureus, streptococci, anaerobes, gram (-) aerobic bacilli (Proteus, pseudomonas, haemophilus, Citrobacter) - May be contiguous infection (OM, mastoiditis, sinusitis, dental infection, face/scalp infection); hematogenous spread (lung, osteomyelitis, cardiac); or cranial trauma
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give triad of brain abscess
Triad: fever, headache, focal deficit
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Give the clinical manifestations of brain abscess
CM 1. Triad: fever, headache, focal deficit 2. Early: LG fever, headache, lethargy 3. Late: vomiting, severe headache, sz, focal neuro signs (hemiparesis), papilledema, coma
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What are the diagnostics for brain abscess?
Dx 1. BCS – (+) in 10% 2. Cranial CT/MRI – most reliable method - Hypodense center with outer uniform ring enhancement surrounded by variable hypodense region of brain edema Do not do CSF analysis/lumbar puncture to avoid herniation
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How is brain abscess managed?
Mgt 1. Empiric abx - Duration: 4-6 wks - Unknown cause: 3rd gen ceph + metronidazole 30 mkd IV q6; oxacillin 100-200 mkd IV q4/6 + ceftriaxone 100 mkd IV q12/ cefotaxime 200 mkd IV q6 - Head trauma/neurosx: nafcillin/oxacillin or vancomycin 45-60 mkd IV q6/8with 3rd gen ceph (ceftriaxone/cefotaxime)+ metronidazole - CHD: penicillin + metronidazole; ceftriaxone/cefotaxime + aminoglycoside (S.viridans, HiB) NAGCOM: Ceftriaxone 100mkd q12 + Metronidazole 7.5mkd q6 or 15mkd q12 - VP shunt: vancomycin + ceftazidime 150 mkd IV q8 - Immunocompromised: broad spectrum + amphotericin B 0.5-1 mkd OD IV - Spinal abscess: oxacillin (S.aureus, strep) - Cavernous sinus thrombosis: oxacillin + ceftriaxone/cefotaxime (S.aureus, s.pneumo, HiB) 2. Surgery - Aspiration for encapsulated abscess - Indications: gas in abscess, multiloculated, posterior fossa location, fungal cause, assoc with mastoiditis, periorbital cellulitis, sinusitis
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Give prognosis of brain abscess
Prognosis - High mortality: multiple abscess, coma - Long term sequelae: behavior and learning problems, hydrocephalus, sz, hemiparesis
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Most common fungal causing meningitis:
Cryptococcus neoformans Other cause:- Histoplasma capsulatum, candida, coccidiodes immitis - Immunocompromised pxs
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Give pathophysiology
Pathophysio - Pulmonary exposure to fungi by inhalation of airborne fungal spores --> inhalation --> primary pulmonary and LN focus --> impaired immune system disseminate infection to CNS
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Clinical manifestations of fungal meningitis
CM 1. Fever, headache, neck stiffness/pain, deterioration of mental status, CN deficits, sz
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Diagnostics of fungal meningitis
Dx 1. CSF analysis – as above 2. India ink – ID cryptococcus showing prominent capsule 3. CALAS – cryptococcal latex agglutination test – ID cryptococcal Ag causing agglutination of CSF 4. Fungal Cx
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What is the management of fungal meningitis?
Mgt: 1. Candida: Amphotericin B 0.1-1 mkd IV OD 2. Cryptococcal: Amphotericin B 0.7-1 mkd OD x 6 wks then Fluconazole LD 12 mkdose then MD 6-12 mkd OD po/IV x 10-12 wks
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- Most common recurrent fever syndrome in children
CH 163: PERIODIC FEVER, APHTHOUS STOMATITIS, PHARYNGITIS, ADENITIS (PFAPA) SYNDROME - Most common recurrent fever syndrome
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What are the clinical manifestations?
CM: 1. Recurring fever, malaise, exudative appearing tonsillitis with (-) throat culture, cervical LNE, oral aphthae 2. Headache, abdominal pain, arthralgia 3. Episodes last 4-6d, often with clock-like regularity (q3- 6wks) 4. Mild hepatosplenomegaly 5. Frequency and intensity of episodes decrease with increasing age
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What are the diagnostics?
Dx: 1. CBC – mild leukocytosis 2. Elev CRP, ESR
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Management?
Mgt: 1. Prednisone 0.6-2mg/kg SD 2. Cimetidine 20-40mkd – prevent recurrence
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What is FUO?
Fever >38C documented by health professional w/o identifiable cause for >3wks (OPD)/ >1wk (in-px) A. Neonates - GBS, E.coli, Listeria, HSV - ALL should be hospitalized - Tx: ampicillin + cefotaxime or ampicillin+gentamicin + acyclovir B. 1-3 mos old - Mostly viral - E.coli most common bacterial. - GBS, L.monocytogenes, Salmonella, N.menigitidis, S.pneumonia, HiB, S.aureus - UTI is most serious bacterial infection (E.coli) - Rochester criteria (low risk): well child +: 97 § WBC 5-15K: ANC <1500 § Urine <10 WBC (-) RBC, LE § Stool <5 (-)RBC - Tx: ampicillin + ceftriaxone or cefotaxime - Add vancomycin if with meningitis C. 3-36 mos old - Mostly viral - S.pneumonia, N.meningitidis, Samonella - Risk factors for bacteremia: T>39C, WBC >1500, elev ANC, band, ESR, CRP - Dx: UA, UCS – if uncircumcised or F<2yo D. Drug fever - Fever lyses after 72h off drug
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Fever of Unknown Origin chart
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Give differentials of FUO
DDx: URTI (p. 26) Bacterial sinusitis (p.45) Bronchiolitis (p.28) Pneumonia (p.29) Viral syndromes (p.54-69)
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