Fever Flashcards
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
EXAMINER’S GUIDE: TYPHOID FEVER
1. Listed down salient features of case
- 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
- Systematic approach to diagnosis, discussed differentials
Infection
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
- Order diagnostic tests
[ ] CBC
[ ] Stool exam
[ ] Stool culture
[ ] Blood culture
[ ] Screening tests for differentials (dengue titers)
- Interpret lab results
- Management
- Management
[ ] Emergency measures
[ ] Antibiotics (IV Ceftriaxone 75 mkd, oral Cefixime 15mkd for
7-10 days)
[ ] Preventive measures (handwashing, food preparation, etc)
- Preventive Pediatrics
- 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
what is Otitis media? Give 2 main categories and etiology
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
Give pathophysiology of otitis media
Patho:
Release of proinflammatory cytokines à increase inflammation –> eustachian tube dysfunction
Mobility – most sensitive and specific in detecting MEE
What are the clinical manifestations of otitis media
CM (AAP AOM dx)
- Acute onset of sx
- (+)MEE
- Signs of acute middle ear inflammation
- Moderate to severe bulging of the TM/new-onset
otorrhea not caused by otitis externa - Mild bulging of the TM and recent <48h onset of ear
pain/intense TM erythema - HiB: simultaneous purulent and erythematous
conjunctivitis + OM ipsilaterally
What are the diagnostics for otitis media?
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
What is the management of otitis media?
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
What are the complications of otitis media?
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
What is UTI? give causes and pathophysiology
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
What are the clinical manifestations of UTI?
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)
- 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 - 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 - Presumptive UTI – presence of clinical sx and UA
findings referable to UTI not supported by UCS - 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
What are the diagnostics for UTI?
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
- 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% - 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
- 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
- CBC and BCS – elev WBC, neu
- Elev CRP, ESR – nonspecific but may help the dx.
- 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 - 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 - Voiding cystourethrogram (VCUG) – Assess reflux
- Procalcitonin (>1ng/ml)– stronger predictor in the dx of
acute pyelonephritis
What is VUR? grading?
- 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
What is the management of UTI?
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
recommended antimicrobials for UTI
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
- Complicated UTI
- Refer to IDS, nephrologist, and urologist
- Po Ciprofloxacin, Levofloxacin, Co-amoxiclav
- IV Amikacin, Gentamicin, Piperacillin-Tazobactam,
Ertapenem, Meropenem x 7-14d - 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 - Abx switch may be done if UCS has a different sn &/or
if poor response after 48-72h
How do we prevent UTI?
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
What is the etiology of Dengue fever?
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
What is the pathophysiology of dengue?
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
What are the phases of dengue and clinical manifestations?
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`
Differentiate dengue hemorrhagic from dengue shock syndrome?
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)
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
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
Study fluids and algorithm for management of compensated shock
Guidelines for blood transfusion
- No preventive BT (like plt transfusion)
- Should be given only when there are definite and
established indications and in practically all cases
component therapy should be utilized. - 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 - PRBC or FWB, plasma if with:
a. Significant bleeding (melena,
hematemesis)
b. Decreasing hct inspite of IVF - plt concentrate
a. if plt <50K with bleeding - cryoprecipitate 1bag/5kg or FFP 10-20ml/kg, plt
concentrate
a. for DIC
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
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
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)
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)
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
