Fever with rash Flashcards

1
Q

A 3-year-old boy presents for his second visit to see you. Two days
ago he was seen with a 4-day history of intermittent fever spiking
to 40°C and irritability. His examination at that time was
remarkable only for dry oral mucosa and cracked lips. You advised
the mother to give 4 oz of an electrolyte solution in the clinic and
was sent home with instructions for symptomatic care.
Since then the fever has not subsided and mother noted her child
to cry when walking and avoids placing weight on his soles. The
mother denies any sick contacts. The patient does not have a
cough, nausea, vomiting ,or diarrhea. He has been eating and
drinking, and the mother states that he is still producing urine.
Physical Examination
Vital Signs: BP 90/56, HR 136, RR 24, Rectal Temp 38.8, Oxygen
Sat. 99% on Room air; weight 18 kg
General: The patient is sitting on his mother’s lap; awake and
alert, good eye contact; cries if he is made to stand on his feet
HEENT: Atraumatic/normocephalic; PERRL, bilat conjunctival
injection, no discharge. The perioral area is swollen and
erythematous and the lips are cracked. There is pharyngeal
erythema with no exudate, vesicles, or lesions seen. MMM. No
LAD upon palpation. Neck is supple; there is no nuchal rigidity.
Resp: Lung sounds clear to auscultation. No
wheezing/rales/rhonchi.
Chest: Sandpaper rash on chest and upper abdomen which is
resolving per mother. No vesicles or lesions.
CV: RRR, no murmurs, rubs, or gallops; pulses 2+ and equal in all
ext.
ABD: Soft, nontender/nondistended. Positive bowel sounds, no
flank tenderness.
EXT: palms and soles are swollen, erythematous, tender to
palpation. No vesicles or lesions present. Cap refill less than 2 sec.
GU: There is an erythematous rash and peeling skin on the groin
and penis. Testes descended.
Neurological: Awake, alert; able to ambulate but cries when
weight is placed on soles.

CBC
Hgb 11, Hct 0.33, WBC 11.0, Neuts 0.65, Lym 0.22, Plt 560
MCV 75, MCH 20, MCHC 25, RDW 15
Urinalysis
Light yellow, clear, sp gr 1.010, pH 6.0, wbc 8-10, rbc 0-1, few
epithelial cells, few hyaline casts, Leukocyte esterase positive,
nitrite negative
2D echo
Echocardiogram showed a normal ventricular size and function
and no effusion. The coronary arteries were well visualized and
were of normal size.
15 L ECG
100 bpm, no axis deviation, no PR prolongation, no QRS widening,
no atrial or ventricular hypertrophy, no ST changes, no T wave
inversions, no accessory waves or ectopic beats; no previous EKG
available for comparison
CXRay
Mild hyperinflation, no focal opacity

A
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2
Q

What is the other name for Kawasaki disease?

A

mucocutaneous lymph node syndrome

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3
Q

What are the criteria for kawasaki disease?

A

Incomplete

Criteria
1 Conjunctival injection, usually non-exudative
2 Cervical lymphadenopathy of at least 1.5 cm diameter
3 Lip and oral cavity involvement such as swollen or dry
lips, erythematous tongue, or pharyngeal erythema
4 Trunk or genital area erythema
5 Hand or foot erythema, swelling, or desquamation

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4
Q

Give differentials for fever with rash

A

Measles, EBV,
adenovirus

Toxin mediated
illness (GAS like
scarlet fever and
TSST)

Drug reactions
(SJS/TEN and EM)

Systemic onset JIA

Mercury
hypersensitivity
_____________________________________________________
1. Measles, EV, Adenovirus
Has mucocutaneous lesions with rashes (has both
enanthems and exanthem)

Lacks changes in extremities found in KD
Clinical features are different (cough, colds,
coryza of measles, HSM of EBV, etc.)

  1. Toxin mediated illness (GAS like scarlet fever and
    TSST)
    Enanthem and exanthem

Generally lacks ocular and articular involvement, has preceding GAS infection

  1. Drug reactions (SJS/TEN and EM)
    -Desquamating lesion
    -Precedent drug intake
  2. Systemic onset JIA
    -Has same skin lesion with fever
    -More indolent course
  3. Mercury hypersensitivity
    -Same desquamating lesion and rashes
    -Prior intake of mercury
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5
Q

What are the diagnostics for Kawasaki disease?

A

Diagnostics
Echo
12L ECG
CBC
Other examinations: urinalysis, AST, albumin

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6
Q

What are the lab findings suggestive of Kawasaki disease?

A

Additional findings suggestive of Kawasaki
● Albumin<3
● Anemia
● WBC>12,000
● Elevated ALT
● Platelets>450,000 after 7 days of fever
● Pyuria

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7
Q

How is Kawasaki disease managed?

A

Admit the patient for treatment and arrange for an
echocardiogram
Start ASA high dose, or start IVIG
Monitor acute phase reactants (ESR, CRP)
Continue supportive treatment as an outpatient and have the
patient follow up in one week for an echocardiogram
Advise the patient’s mother to continue with aspirin and
follow up in 2 days

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8
Q

What are the complications of Kawasaki disease?

A

Complications
Coronary artery aneurysm, myocardial infarction, thrombocytosis,
sterile pyuria, and gall bladder hydrops.

Continuing care
2D echo at 4-6 weeks after discharge, then yearly thereafter
Anthropometrics monitoring
Nutritional counselling
Injury prevention

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9
Q

What are the other differentials for fever with rash?

A

VIRAL EXANTHEMS
1. Measles (p.54)
2. Rubella (p.55)
3. Roseola infantum (p.56)
4. Chickenpox (p.57)
5. Erythema infectiosum (p.56)
6. Hand-foot-mouth disease (p.64)

Meningococcemia

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10
Q

What is the cause of meningococcemia?

A

Neisseria meningitides
§ Commensal of nasopharynx

IP: 3-4 d (2-10d)
Transmission:
- Close contact through aerosol droplets or contact with
respiratory secretions
- Humans are the only natural reservoir
Epidemiology
- Serogroups A,B,C,W,Y
- Highest rate of disease in infants < 1 yo
- Carriage of bacteria during adolescence and young adulthood

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11
Q

What are the risk factors of meningococcemia?

A

Risk factors:
1. Respiratory viral infections (flu)
2. Male
3. Smoking, marijuana, binge drinking
4. Crowded living (dormitories)
5. Underlying chronic ds
6. Low SE status

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12
Q

What is the pathophysiology of meningo?

A

Patho
- NM colonizes nasopharynx –> NM secrete protease degrading
IgA on mucosa –> bacterial resistance to phagocytosis –>
inflammatory cascade sec to LPS
- severe ds secondary to capillary leak syndrome, DIC, prolonged
myocardial dysfunction –> MOF –> death
- Procoagulant state
- highest level of Ab protective at birth and adults
- lowest Ab level at 6mos-2yo: highest ds incidence

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13
Q

What are the clinical manifestations of meningo?

A

Suspect case definition
An illness with sudden onset of fever (>38.5C rectal or >38C axillary) and one or more of the ff:
*neck stiffness
bulging fontanel
non-blanching rash (petechiae, purpura)

Probable Case definition
A suspect case plus one or more of the ff:
Clinical diagnosis of meningococcal disease by the attending physician
*clinical diagnosis of meningococcal disease by the attending physician
*gram(-) diplococci in the CSF
*turbid CSF
*increased cell count in CSF

Confirmed case definition
A suspect or probable case with one or more of the ff:
*isolation of N. meningitidis from a sterile site (CSF or blood)
*identification of N. meningitidis DNA from a sterile site (CSF or blood)
*positive latex agglutination test for N. meningitidis (CSF)

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14
Q

Most death occur w/in 48hrs
Case fatality rate 5-10%
Most cases asymptomatic carriage in nasopharynx
Consider even in a <2d fever with a very toxic looking child
1. Meningococcal meningitis (30-50%) – most common presentation of invasive ds
- Fever, headache, photophobia, nuchal rigidity, bulging fontanel, lethargy, vomiting

  1. Acute meningococcal septicemia – nonspecific s/sx: fever, irritability, lethargy, respiratory sx, vomiting, sore throat, diarrhea. Followed by cold hands and feet, abN skin color, prolonged CRT, non-blanching petechial rash
  2. Fulminant meningococcal septicemia – rapid
    progression from non-specific sx to septic shock
    - Prominent petechiae and purpura fulminans w/in
    hours
    - Diffuse vasculitis (skin, heart, adrenals, mucus mem)
    - N sensorium to confusion
    - DIC
    - Rash: fine MP –> non-blanching petechial –>
    prominent petechiae and purpura
  3. Waterhouse-Friderichsen syndrome – fulminant cases. Diffuse adrenal hemorrhage leading to adrenal failure
  4. Occult meningococcal bacteremia – fever only, rare
  5. Chronic meningococcemia – rare. Fever, arthralgia, headache, splenomegaly, MP or petechial rash x 6-8wks. Non-toxic appearance
A
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15
Q

What are the prognostic factors of meningo?

A

Prognostic factors

A. Poor
a. Hypo or hyperpyrexia
b. Hypotension or shock, sz
c. Purpura fulminans
d. Leukopenia, thrombocytopenia, acidosis
e. High endotoxin and TNF-a

B. Poorer
a. Petechiae <12h before admission
b. No meningitis
c. Low or N ESR

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16
Q

Diagnostics of meningo?

A

Dx
1. CSF analysis, GS/CS – gram (-) diplococci. Gold standard
2. PCR
3. Latex agglutination test -
4. CBC – high/low WBC, elev neu, band forms, low RBC,
dec plt
5. UA – inc ptn, RBC
6. Elev ESR, CRP
7. ABG, e’, BUN, Crea, PT/PTT
8. CXR – r/o PN, ARDS
9. Echo – r/o myocardial dysfunction, pericarditis
10. MRI – ID deep muscle and bone involvement

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17
Q

what is the management for meningo?

A

Mgt
1. Empiric abx: 3rd gen ceph
2. DOC: x5-7d
a. Penicillin G 300,000 U/kg/d in 4-6 div doses
(inc resistance to penicillin)
b. Ceftriaxone 100mkd 1-2x/d
c. Cefotaxime 200-300 mkd q6-8h
3. Supportive – ET and MV, IVF, correction of e’ abN, ICP
4. CS – for severe septic shock due to adrenal
insufficiency

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18
Q

Complications of meningo?

A

Complication
1. Adrenal hemorrhage
2. Endophthalmitis
3. Arthritis
4. Endocarditis, pericarditis, myocarditis
5. PN, lung abscess, pneumonitis
6. Renal infarcts
7. Focal skin infarct – most common: amputation,
scarring, skin grafting
8. Deafness: most freq neuro sequelae
9. Brain abscess, sz, neuro impairment

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19
Q

How is meningo prevented?

A

Prevention
1. Household, school, or day care contacts during the 7d
before onset of illness should receive prophylaxis
2. Prophylaxis for medical personnel intimately exposed
(intubation, suctioning)
a. Rifampicin 10mkdose q12h x 4doses;
5mkdose for <1mo
b. Ceftriaxone 125mg IM SD for <15 yo, 250mg
SD for >15yo
c. Ciprofloxacin 500mg po SD for >18yo
3. Meningococcal vaccination for high risk population
a. Quadri vax Men ACWY-D 2 doses 12 weeks
apart @9-23mos

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20
Q

What is the common vasculitis of childhood?

A

CH 515: HENOCH-SCHONLEIN PURPURA
- Small vessel vasculitis

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21
Q

What is the epidemiology of HSP?

A

Epid
- Common in whites and Asians
- M>F
- 3-10 yo
- Usually follows URTI

Patho
- Leukocytoclastic vasculitis and IgA deposition in the small vessels of skin, joints, GIT, kidneys

22
Q

What are the clinical manifestations of HSP?

A

CM
1. Rash – palpable purpura: hallmark
- Starts as small lesions, pink macules (wheals
developing into petechiae, raised
purpura/ecchymoses, some bullae, erosions) on LE and butt (dependent areas), symmetric that coalesce
- Lesions last 3-10d
- Recurs upto 4 mos after

  1. Arthritis, arthralgia – oligoarticular with predilection to
    LE, self-limited
  2. Edema of hands and feet
  3. GI (80%) – vomiting, diarrhea, abdominal pain,
    paralytic ileus, melena
    - WOF intussusception
  4. GU (50%) – microscopic hematuria, proteinuria,
    hypertension, frank nephritis, NS, RF
  5. ICH, sz, headache, beh changes
23
Q

What are the diagnostics of HSP?

A

Dx
- Clinical
1. CBC – leukocytosis, thrombocytosis, anemia
2. Elev ESR, CRP
3. Abd UTZ – r/o intussusception

24
Q

How is HSP managed?

A

Mgt
1. Supportive – mild and self-limited course
2. CS – for significant GI involvement or life-threatening
manifestations
- Prednisone 1mkd for 1-2weeks then taper

25
Q

Complications and prognosis

A

Complications
1. Renal ds – major long term complication (1-2%) 6mos
after dx
- UA and BP monitoring for several mos after dx
Prognosis
- Self-limited
- 15-60% recur within 4-6 mos

26
Q

CH 181: TOXIC SHOCK SYNDROME

A

Etiology
- Due to TSST-1 producing strains of S.aureus

27
Q

what is the pathophysiology of TSS?

A

Patho
- TSST-1 act as superantigens w/c trigger cytokine
release leading to massive fluid loss and end-organ
cellular injury

Epid:
- Highest rates in menstruating women 15-25 yo
(tampon use)
- Non-menstrual TSS associated with infected nasal
packing and wounds, sinusitis, PN, tracheitis,
empyema, burns, abscess, osteomyelitis

28
Q

What are the clinical manifestations of TSS?

A

CM
1. Acute onset HG fever (>38.8C), diarrhea, vomiting,
headache, myalgia
2. Diffuse red macular rash appears within 24 hrs (sunburn
like/scarlatiniform)
3. Recovery occurs within 7-10d with desquamation esp
of palms and soles
4. Sore throat, mucosal hyperemia, Strawberry tongue
5. Hypotension
6. Involvement of >3 of the ff organ systems:
a. GIT: vomiting, diarrhea at onset of illness
b. Msk: severe myalgia or CPK >2x the UL of N
c. Mucosa: vagina, oropharyngeal,
conjunctival hyperemia
d. Renal: BUN, crea >2x UL, or >5 wbc/hpf w/o
UTI
e. Liver: TB, AST, ALT >2x N
f. Hema: plt <100K
g. CNS: disorientation or alteration in
consciousness w/o focal neuro signs when
fever and hypotension are absent

29
Q

How is TSS diagnosed?

A

CLINICAL

Major criteria:
Acute fever; temp >38.8C (101.8F)
Hypotension (orthostatic, shock, BP below age-appropriate norms)
Rash (erythroderma with convalescent desquamation)

Minor criteria (Any 3 or more)
mucous membrane inflammation (vaginal, oropharyngeal or conjunctival hyperemia, strawberry tongue)
vomiting, diarrhea
liver abnormalities (bilirubin or transaminase greater than twice upper limit of normal)
renal abnormalities (urea nitrogen or creatinine greater than twice upper limit of normal or greater than 5 wbc per HPF
muscle abnormalities (myalgia or creatinine greater than twice upper limit of normal
CNS abnormalities (alteration in consciousness without focal neurologic signs)
Thrombocytopenia (100,000/mm3 or less)

Exclusionary criteria
Absence of another explanation
Negative blood cultures (except occasionally for Staph aureus)

30
Q

How is Staph toxic shock syndrome diagnosed through laboratory tests?

A

B. Laboratory
1. Cx – usually (-) for blood, throat, CSF
2. CBC – leukocytosis with PMN shift ton the left
3. PBS – mild leukocytosis w/ significant immature
neutrophils
4. Elev ALT, CKMM, BUN, Crea, PT, aPTT, hypogly
5. UA – myoglobinuria, hemoglobinuria, sterile pyuria

31
Q

Management of TSS?

A

Mgt
1. Abx: to decrease toxin production
Oxacillin 150-200 mkd IV q4/6 x 10-14d
Cefazolin 75-100 mkd q8
nafcillin 100-200 mkd q4-6h IV
+ clindamycin 30-40 mkd q6/8 IV/ IVIG 150-400 mkd x5 d

  1. MRSA: vancomycin 40-60 mkd IV q6/8

Prevention
- Change tampon q8hWhat

32
Q

What is Kawasaki disease?

A

“mucocutaneous LN syndrome/ infantile polyarteritis nodosa”
Acute nonspecific systemic vasculitis (medium-sized arteries)

§ Most common: coronary artery
- Leading cause of acquired heart disease in children of
developed countries

33
Q

Epidemiology of Kawasaki disease?

A

Epid
- Asians, occurs worldwide
- M>F 1.5:1
- <5yo (80%)
- Unknown cause. Possible infectious/genetic due to:
§ Young age group affected
§ Epidemics with wave-like
geographic spread
§ Self-limited acute febrile illness
§ CM: fever, rash, exanthem,
cervical LNE
§ Asian predilection
- Highest risk for CAA:
§ <6mos
§ >5yo
- Predictors of poor outcome:
§ Young age
§ Male
§ Persistent Fever
§ Poor response to IVIG
§ Low WBC, plt, Na, alb
§ Elev CRP, transaminitis
- risk factor: Asian, pacific islander

34
Q

What is the pathophysiology of Kawasaki disease?

A

Patho
- Vessels lose its structural integrity and weakens,
resulting in dilatation and saccular or fusiform
aneurysm formation
- Arteritis in coronary and iliac arteries
- Interstitial myocarditis, pericarditis, inflamm of SA
node and AV conduction system, endocarditis, and
valvulitis

3 phases:
1. Neutrophilic necrotizing arteritis – from endothelium
to coronary saccular aneurysm. 1st 2 wks.
2. Subacute/chronic vasculitis via lym, plasma cells, eo.
Form fusiform aneurysm
3. Progressive sclerosis thrombi: formation in lumen causing occlusion

35
Q

What are the clinical manifestations of KD?

A

CM
3 Phases:
1. Acute febrile phase – 1-2wks
- Fever

  1. Subacute phase – wk 3-5. when fever has abated
    - Desquamation, thrombocytosis, coronary aneurysms
    (highest risk of sudden death if with aneurysm)
    - Lasts until 4th week
  2. Convalescent phase – wk 6-8. begins when all clinical signs have disappeared
    - Until ESR and CRP are normal at 6-8wks after onset

Other manifestations:
1. Perineal desquamation (acute phase), periungual
desquamation
2. GI: nausea, vomiting, abdominal pain, GB hydrops
3. Cough, colds
4. Significant irritability
5. Arthralgia, arthritis
6. CV: CAA, CHF, myocarditis
- CAA develop in 25% untreated at wk 2-3
- Giant CAA: >8mm. pose greatest risk for rupture, MI, stenosis
7. NV: aseptic meningitis, SNHL
8. Urethritis/meatis
9. KD shock syndrome: cardiogenic shock

36
Q

What are the diagnostics for KD

A

Dx
A. Clinical
Fever (HG up to 40C persisting for >5 days, remittent,
unresponsive to abx) + >4 of the ff:
1. Bilateral bulbar conjunctival injection w/o exudates
2. Erythema of the oral and pharyngeal mucosa with strawberry tongue, and dry, cracked lips w/o
ulceration
3. Nonsuppurative cervical LNE (>1.5cm), usually
unilateral
4. Edema and erythema of the hands and feet
5. Polymorphous exanthema: MP, diffuse erythroderma, erythema multiforme-like (nonvesicular and nonpetechial) with accentuation in groin area
Fever + <4 criteria or with coronary lesions (echo or angio) still diagnostic,
If with >4 fx (esp #4), can be fever of 4 days

Incomplete/Atypical Kawasaki Disease
- Any infant/child with prolonged unexplained fever with
<4 fx AND compatible lab or echo findings
B. Lab
1. CBC – anemia, leukocytosis, plt N in 1st week then
rapidly inc by 3rd-4th week
2. Elev ESR, CRP
3. 2D Echo – should be done at dx, repeated within wks
2-3, then wks 6-8
4. Dec alb, Na
5. Sterile pyuria
6. Elev transaminase, GGT
7. CSF pleocytosis

37
Q

What is the management for Kawasaki disease?

A

Mgt
1. Acute phase
- IVIG 2g/kg single IV within 10d of illness onset but
ASAP after dx
§ After 10d: give if
i. with persistent fever w/o
other explanations
ii. CA abN with elev ESR, CRP
§ ASA moderate dose (30-50 mkd)
to high dose (80-100mkd) q6h
until afebrile for 48h

  1. Convalescent phase
    - After high dose ASA d/c, low dose ASA (3-5mkd) until no evidence of CA changes 6-8wks after ds onset
  2. Long term tx for CA abN
  • ASA 3-5 mkd OD indefinitely
  • Clopidogrel 1mkd (max 75mg/d)
  1. Cardio referral
38
Q

What are the complications of Kawasaki disease?

A

Complications

  1. Aneurysms
    CAA 20-25% ASA alone within 10d
    <5% IVIG+ASA

Prognosis
- recurs in 1-3%
- 50% small CAA return to N by 1-2 yrs

39
Q

What is acute rheumatic fever (ARF)?

A

Etiopatho
- Group A streptococcus (GAS)
- Inflammatory lesion found in the heart, brain, joints
and skin
- Valvular damage: involves MV> AV> TV, PV
- Aschoff bodies in atrium: inflammatory lesions with
swelling, fragmentation of collagen fibers, altered
staining characteristics of connective tissue
- Low risk: <2 per 100,000 school aged children or <1 per
1,000 population
- Occurs in 3% of untreated ATP
- Worldwide, remains most common form of acquired
HD in all age groups
- Most important prevention is abx vs GAS pharyngitis
- Peak 5-15 yo
- Developed countries (<5/100K), developing (100/100K)
- Risk factors: FHx, overcrowded, poor sanitation

40
Q

What is the pathophysiology of ARF?

A

Patho
1. Cytotoxicity theory – GAS produces Streptolysin O
toxin w/c is toxic to cells

  1. Immune-mediated pathogenesis/ hypothesis of
    molecular mimicry – immunologic cross-reactivity
    between GAS and cardiac cells
  2. Pathogenic hypothesis – binding of GAS protein to type
    IV collagen resulting to heart CM
41
Q

What are the clinical manifestations of ARF?

A

CM
1. History of streptococcal pharyngitis 1-4 weeks (until 12
wks) before onset of sx
2. Pallor, malaise, easy fatiguability, abdominal pain

2015 Modified Jones Criteria
- Detect initial RF only

Major manifestation: “CASES”
1. Arthritis (70%) – most common, earliest fx.
- often asymmetric, affecting large joints (ankles, wrists,
knees, elbows)
- low risk: polymigratory polyarthritis
- Mod/high risk: monoarthritis, polyarthritis,
polyarthralgia
- Highly responsive to salicylates, NSAIDs
- Self-limited x 2-4 weeks
- Inverse relationship with severity of heart involvement

  1. Carditis (50%) – most serious manifestation. Only
    permanent sequelae. Single most important prognostic
    factor
    - Clinical (with murmur) or subclinical (no murmur, only
    echo)
    - Pancarditis: pericardium, myo, endo
    § pericarditis: audible friction rub,
    pericardial effusion
    § myocarditis: unexplained HF
    (gallop, soft heart sounds),
    cardiomegaly (Poor fxn)
    § endocarditis/valvulitis: apical
    holosystolic murmur of MR or
    basal early diastolic murmur.
    Universal finding. (valvular
    problem)
    - hallmark: valvular damage
    - characteristic fx: MR
    - apical systolic murmur (AR/MR), resting tachycardia,
    gallop rhythm, distant/muffled heart sounds,
    pericardial friction rub, CHF
    - major conseq = chronic, progressive valvular ds
    requiring valve replacement
  2. Erythema marginatum (<10%) – evanescent, pink rash
    with pale centers and rounded serpiginous margins
    - Trunk, inner proximal extremities
    - Does not occur on the face
    - Disappear on exposure to cold and reappear after hot
    shower
  3. Subcutaneous nodules (2-10%) – “severity”
    - Round, hard, painless nonpruritic, freely movable
    swellings
    - Symmetrical, singly or in clusters on extensor surfaces
    of large and small joints, scalp, or spine (legs,
    olecranon, occiput, interscapular area, elbow)
    - Lasts for weeks
  4. Sydenham chorea (15%) – “chronicity”. “St.Vitus
    dance/chorea minor”
    - Purposeless, involuntary, nonstereotypical movt of
    trunk or ext
    - after 1-4 wks and lasts 4-18 mos
    - With muscle weakness and emotional lability
    - Relapsing grip/Milkmaid’s grip: irregular contraction
    and relaxation of fingers while squeezing the
    examiner’s hand
    - Exacerbated by stress, disappear with sleep
    - May be standalone criteria
42
Q

What is RF with carditis?

A

Acute history
PE: muffled heart sounds
ECG: no signs of changer enlargement
2D echo: valves not thickened, coapting

43
Q

What is RHD?

A

Chronic history
PE: muffled, distinct murmur
ECG: with chamber enlargement
2D echo: permanent valvular damage

44
Q

what are the minor manifestation?

A

Minor manifestation: “FARE”
1. Arthralgia (joint pains)
a. Low risk: polyarthralgia
b. Mod/high risk: monoarthralgia
2. Fever
a. Low risk: >38.5C
b. Mod/high risk: >38C
3. Elev Acute Phase Reactants
a. Low risk: ESR >60 mm/h or CRP >3 mg/dL
b. Mod/high: ESR >30 mm/h or CRP >3 mg/dl
4. ECG: Prolonged PR interval
PLUS Evidence of antecedent GAS within the last 45d:
- Hx of sore throat/scarlet fever unsubstantiated by lab
data is inadequate evidence of recent infection
- Any 1 of the ff as sign of preceding infection:
1. Elevated or rising ASO or other strep Ab (streptozyme)
– most reliable evidence
2. (+) throat culture
3. Rapid antigen test for GAS
4. Recent scarlet fever

45
Q

What are the diagnostics for ARF?

A

Dx:
1. CBC: anemia, leukocytosis
2. Elev ESR, CRP
3. Elev ASO >330
4. Throat CS
5. Streptozyme - measures 5 Ab including anti-DNAseB
Ab, antistreptolysin O (ASO) elev
6. 2d echo – valve abN, functional disturbance
7. ECG – sinus tachy, prolonged PR (heart block), low
voltage ST changes
8. CXR – N, cardiomegaly, Pulmo congestion

46
Q

What is the revised Jones criteria for the dx of RF and RHD?

A

The revised Jones criteria for the dx of RF and RHD
1. Initial RF
- Evidence of preceding GAS +
§ 2 major criteria
§ 1 major + 2 minor
§ PLUS evidence of recent strep
infection (ASO >330, (+) throat
C/S, streptozyme)
2. Recurrent RF
- With a reliable past hx of ARF or established RHD, with
documented GAS infection
§ 2 major criteria
§ 1 major + 2 minor
§ 3 minor
3 circumstances wherein RF diagnosed without satisfying Jones:
1. When chorea is the only major manifestation
2. When indolent carditis is the only manifestation on
first checkup, months after the apparent onset of ARF
3. Apparent ARF in a limited number of patients with
recurrences of ARF in high risk populations

47
Q

What is the management?

A

Mgt
1. Antibiotics
a. Primary prevention (prophylaxis)
- To treat strep pharyngitis and eradicate Strep
- To prevent first episode of RF
- Pen VK 200-500mg qid x 10d
- Benzathine penicillin G 0.6-1.2 M U IM SD
- Erythromycin 250mg tid x 10d,
- Cephalexin 25-100 mkd po q6
- Azithromycin 12 mkd po od x 5d
b. Secondary prevention
- To prevent recurrences of RF
- Prevent colonization and or infection in patients wo
have had a previous attack of RF
- Penicillin VK 250mg BID q21d
- Benzathine penicillin 0.6-1.2 M U q21d IM q21d
Duration of prophylaxis
1) RF w/o carditis – 5 yrs after last attack or until 21 yo
(whichever is longer)
2) RF w/ carditis, but no valvular ds – 10 yrs after last
attack or until 21 yo (whichever is longer)
103
3) RF w/ carditis and persistent valvular ds – 10 yrs after
last attack or until 40 yo (whichever is longer,
sometimes lifetime)
4) Occupation at risk for GAS – until on job

48
Q

What is Scarlet fever?

A

Etiopatho
- Group A beta hemolytic streptococcus (GAS/GABHS) /
streptococcus pyogenes pyrogenic producing exotoxin
A,B,C
§ Most common cause of bacterial
pharyngitis à RF, GN
- Age: 5-15 yo
- Produce exotoxin A, B, or C. M protein is an important
GAS virulence factor that facilitates resistance to
phagocytosis
Transmission
- Close contact

49
Q

What are the clinical manifestations of Scarlet Fever?

A

CM
1. URTI
2. Rash: appear w/in 1-2 d, diffusely blanching, finely
papular erythematous producing bright red
discoloration which blanches with pressure
- starts in the neck, trunk à extremities, exacerbated in
creases of elbows, axilla, groin (spares face).
- Fades in 3-4d with desquamation downwards
- Skin goose-pimple and rough
- Red cheeks with pallor around mouth
- Scarlatiniform rash – fine, red, papular, “sandpaper”
rash of scarlet fever. It begins from the face then
becomes generalized. Cheeks are red and area around
the mouth is more pale (circumoral pallor-like). Rash
blanches with pressure. More intense in the skin
creases, esp antecubital fossae, axillae, inguinal
creases (Pastia’s lines/Pastia’s sign)
3. (+)tourniquet test/ Rumpel-Leeds phenomenon –
capillary fragility can cause petechiae distal to a
tourniquet or constriction from clothing
4. Strawberry tongue (white à red)
5. Hyperemic throat
6. Rapid onset significant sore throat
7. Fever >38C
8. Headache
9. Nausea/vomiting, abdominal pain
10. No URTI sx
11. red, enlarged tonsils with exudate, strawberry tongue,
palatal petechiae
12. Cervical LNE – swollen, tender, anterior cervical LN

50
Q

how do we diagnose Scarlet fever?Labs?

A

Dx
1. CBC – leukocytosis, WBC 12-16K, 95% PMN. During the
2nd week, 20% with eosinophilia
2. Throat CS
3. PCR, ASO, streptozyme

51
Q

Management of Scarlet Fever

A

Mgt
1. Penicillin V 250-500 mg q8/12 po x 10d
2. Amoxicillin 25-50 mkd po q8/12
3. Allergy:
Ceph x 10d: Cefuroxime 20-30 mkd po q12
Clindamycin 10-30 mkd q6/8 po
erythro/clarith/azith