Part 17-1. Infectious Diseases
PART 17. Infectious Disease
Section 1. General Consideration
Chapter165. Fever
#
Category of fever in children
1) short duration fever with
localizing sign
;
Dx. by Hx. & P/Ex. with or without laboratory tests
2) fever without localizing
signs
;
Hx.³ª P/Ex.¿¡ ÀÇÇØ¼´Â Áø´ÜÇÏÁö ¾Ê°í,
laboratory test¿¡ ÀÇÇØ Dx.
3) FUO
#
Thermoregulation
1) hypothalamic
thermoregulatory center controls BT
;
peripheral cold & warm neuronal receptorÀÇ balancing signal¿¡ ÀÇÇØ
control µÊ.
2) another regulatory factor
;
temperature of blood circulating in the hypothalamus
3) normal core temperature
;
37¡É (¡¾1~1.5¡É)·Î
set point µÇ¾î ÀÖÀ½.
;
axillary temperature - core temperature º¸´Ù 1¡É Á¤µµ ³·´Ù.
(by cutaneous vasoconstriction)
;
*circardian rhythm - low at early
morning, highest at 4:00~6:00 P.M.
#
Heat generation & heat conservation
; balanced against heat loss
1) heat generation
;
cell metabolism¡è, cell activity¡è,
involuntary shivering¡è
2) heat conservation
;
vasoconstriction, heat preference behavior
3) heat loss
;
obligate heat loss. (evaporation-radiation-convection-conducton)
;
vasodilation, sweating, cold preferance behavior
#
Cause of fever
1) infection
2) vaccines
3) biologic agents :
granulocyte-macrophage colony-stimulating factor, interferon, interleukins
4) tissue injury :
infarction, pul. embolism, trauma, intramuscular inj., burns
5) malignancy : leukemia, lymphoma,
hepatoma, metastatic disease
6) drugs : drug fever,
cocaine, amphotericin B
7) immunologic-rheumatologic
disorders : SLE, rheumatoid arthritis
8) granulomatous diseases :
sarcoidosis
9) endocrine disorders :
thyrotoxicosis, pheochromocytoma
10)
metabolic disorders : gout, uremia, Fabry disease, type 1 hyperlipidemia
11)
unknown or poorly understood entities : familial Mediterranean fever
12)
Factitious (self-induced) fever
#
¡ÚEtiology¿¡ °ü°è¾øÀÌ feverÀÇ final pathway
; production of endogenous
pyrogens(PGE2)
; À̰ÍÀÌ
hypothalamic temperature set-point¸¦ Á÷Á¢ º¯È½ÃÅ´.
¡æ heat generation and heat
conservation ( Fig 165-1 )
#
Heat Production
; O2 consumption¡è,
CO2 production¡è, cardiac output¡è
; *exacerbate cardiac insufficiency in patients with
¨ç
heart disease
¨è chronic anemia (sickle
cell disease)
¨é
pulmonary insufficiency with chronic lung disease
¨ê
metabolic instabilaty in children with DM or inborn errors of metabolism
#
6 Mo ~ 5 yrs
; nonspecific febrile illnessÀÇ ÇÑ
part·Î seizure frequency¡è¡è
Fever Patterns
; remittent fever : daily
elevated Temp. returning to the baseline but above normal
; intermittent fever : daily
fever returning to the normal
; hectic fever : intermittent
or remittent with Temp. excursion of£¾ *1.4¡É
; sustained or continuous
fever : fluctuation of elevated Temp. of £¼ *0.3¡É
#
fever patternÀÌ not diagnostic in most infectious
processes
#
¡Úfever patternÀÌ Æ¯Â¡ÀûÀÎ disease
; malaria, Hodgkins ds.
(Pel-Ebstein fever), cyclic neutropenia
Treatment
#
¡ÚAntipyretics Tx Benefit
; chr. cardiopul ds.
; metabolic ds.
; neurologic ds.
; risk for febrile seizure
2)
antipyretic Tx.
: common
infection ds.ÀÇ course¸¦ º¯È½ÃŰÁö´Â
¸øÇÔ.
effect controversal
#
¡ÚHyperpyrexia (> 41¡É)
; severe infection
; hypothalamic disorder
;
CNS hemorrhage
4)
pregnancy µ¿¾ÈÀÇ high fever
: teratogenic
effect
5)
antipyreticsÀÇ ±âÀü
: hypothalamic cyclooxygenase inhibitor·Î ÀÛ¿ë
PG E2 synthesis inhibition
Hyperthermia
;
high BT not caused by hypothalamic thermoregulaton mechanism, due to
a.
endogenous heat production Áõ°¡ (malig. hyperthermia. vigorous
exercise, neuroleptic. malig. synd., hyperthyroidism )
b.
heat loss °¨¼Ò (atropine intoxication)
c.
prolonged exposure to high environmental temperature (heat stroke)
malignant
hyperthermia |
neuroleptic
malig. synd. |
AD
disorder ¿øÀÎ : a. Hx. of
drug exposure b.
previously affected family members c.
exposure to high environmental temp. d.
absence of the hypothalamic regulated circadian rhythm e.
myopathic disorder |
a.
exposure to phenothiazine-like agent ¡Ø
malignant hyperthermia¿Í ±¸ºÐ ¾ÈµÊ ¡Ø
Tx. : dantrolene supportive
care |
Drug Fever
; ´Ù¸¥
fever ³ª´Â ¿øÀξøÀÌ drug administrationÀ¸·Î
fever À¯¹ßµÇ°í drug discontinutionÀ¸·Î
fever°¡ »ç¶óÁüÀ¸·Î¼ Áø´ÜµÇ°í, Ư¡ÀûÀÎ
fever patternÀ̳ª eosinophilia, rash, pruritus,
drug allergy µî°ú Áö¼ÓÀûÀÎ °ü°è ¾øÀ½.
; at any time after therapy
initiation (*median - 8 day, average
- 21 days)
;
average temp. range : 38 ¡ 43¡É
Etiology
a. antibiotics : penicilline,
cephalosporine
b. anticonvulsants : phenytoin,
carbamazepine
c. antineoplastic : bleomycin,
daunorubicin, cytarabine, L-asparaginase
d. cardiovascular : hydralazine,
methyldopa(aldomet), quinidine
Treatment
; withdrawal of drug (°è¼Ó Ä¡·á½Ã ´Ù¸¥ ¾àÀ¸·Î ´ëÄ¡)
; *72½Ã°£³» fever
resolve
#
subsequent exposure to the drug °æ¿ì
; dose not necessarily
reproduce a drug fever.
Rash With Fever
¡ÚEtiology
; direct inoculation (
anthrax or tularemia )
;
hematogenous dissemination
( septisemia due to meningococci, Rickettsiae, other bacteria )
;
contiguous spread from adjacent foci of infection ( impetigo, herpetic lesion )
;
effect of toxin ( scarlet fever )
;
Ag-Ab reaction ( rheumatic fever )
;
delayed hypersensitivity ( erythema nodosum )
Chapter 166. Clinical use of the microbiology laboratory
Laboratory Finding
Diagnosis Of Bacterial Infection
Gram stain
:
useful in giving rapid result interpretating the subsequent cultural data
:
esp. in resp. specimen
Special Cultures
:
in blood agar. chocolate agar, eosin methylene blue, MacConkey agar
:
capped syringe, special swab supplied in oxygen-free tube »ç¿ë
for collection of anaerobes c/s
Blood Cultures
;
50~100§¢ bottle - 5~6§¢
blood äÃë
#
¢¾Why Repeated Culture ?
; infectionÀÇ Ä¡·á°¡ ¾î·Á¿î
high risk patient°¡ AB Tx. ¹Þ°í ÀÖ´Â °æ¿ì Ä¡·áÀÇ ¼º°ø¿©ºÎ¸¦
º¸±â À§ÇØ
;
repeated organismÀÌ nonpathogenic isolateÀ϶§
contaminationÀÇ ¿©ºÎ¸¦ º¸±â À§ÇØ
CSF examination
1)
CSF stain : viral & bacterialÀÇ ±¸ºÐ¿¡´Â À¯ÀÍ, specific organismÀ» ã¾Æ³»Áö´Â
¸øÇÔ.
2)
acute & rapid method for Dx
: counterimmunoelectophoresis
& agglutination of Ab-coated latex beads
3)
specific Ag detect À§ÇØ antisera »ç¿ëµÇ´Â °æ¿ì
¨ç
S. pneumoniae
¨è H. influenzae type b
¨é
N. meningitidis
¨ê
Streptococci (group B)
¨ë
E. coli Kl
Urine Cultures
;
collection by ¨ç
clean catched mid-stream
¨è
catheterization
¨é
suprapubic puncture
;
catheter collection - £¾ 103/ml(reflect
infection)
;
clean catch urine
- £¾105/ml
: considered abnormal
- 104~105/ml
: possibly abnormal
- *gram(-)¿¡ ±¹ÇÑ
- gram(+), yeast, pt with
diuresis or chronic PN , pt on AB ¿¡´Â ´Ù¸¥ ±âÁØ
Stool Cultures
1)
rectal swab or stool specimens c/s
a. identify common bact.
pathogen : Salmonella, Shigella
b. to determine the
predominant flora of intestine
2)
added pathogen
a. Helicobacter pylori
b. Y. enterocolitica
c. C. difficle
d. Aeromonas
e. Plesiomonas
f. Vibrio
g. E. coli
Exudate and Transudate
¨ç
c/s ¨è
stain ¨é
glucose ¨ê cell counts
Nasopharyngeal, Throat & Skin Swab
#
Most Efficient Method
; *dry rayon, dacron, calcium alginate swab
; dry µÇ±â Àü ½Å¼ÓÇϰÔ
transport medium
¡ØÁÖ Pathogenic Organism
; Corynebacterium diphtheria
; Bordetella pertussis
; N. gonorrhea
¡Ø94°´
Pathognomic Or Nonpathognomic
; Strep. pyogenes
; N. meningitidis
; H. influenzae
;
staphylococcus
Antibody-Based Techniques
#
¡Úclinical use of FA (fluorescent antibody)
; B. pertussis
; Legionella pneumophilia
; N. gonorrhea
--> conjugated Ab
#
M. Tuberculosis
; *no antibody used
; *acid-fast fluorescent stainingÀÌ
Ziehl-Neelson or Kinyoun acid-fast staining¿¡ ºñÇØ more sensitive, but less specific
Antibiotic Sensitivity Tests
#
most prevalent technique
; *agar disc diffusion method
-
inoculation 18~24hr ÈÄ¿¡ zone of inhibition of bacterial
growth ÃøÁ¤
#
MIC (minimal inhibitory concentration)
; organism¿¡ ´ëÇÑ Æ¯Á¤ÇÑ
antibioticsÀÇ bacteriostatic concentration
#
MBC (minimal bactericidal concentration)
;
bacteriaÀÇ 99.9%¸¦ Á×ÀÏ ¼ö ÀÖ´Â
antibioticsÀÇ lowest concentration Áï
bactericidal end point
#
it is important to measured conc. of drug needed to kill bacteria
¢ÀDNA probes
; Mycoplasma pneumonia, M.
tuberculosis, M. aviumintracellulare, enteric organism
Laboratory Dx. Of Viruses
Rapid Viral Detection
1)
smears of mucosal cell stained by immunologic reagents
-
identity the Ag of resp. virus ( RS virus, influenza )
2)
ELISA
; specific antiserum ÀÌ¿ë
; *rota virus infection (infantile gastroenteritis), Hepatitis B
surface Ag detect
Isolation
1)
urine culture
; ¡Ø89°´
most useful for isolation of CMV
; *good source of isolation of mumps. adenovirus
2)
specimen should be transported at 4¡É
3)
best throat specimen
taken by vigorous throat swabbing,
removing some superficial cells
4)
¡Ø°´ vesicular fluidÀÇ
culture°¡ ÇÊ¿äÇÑ °æ¿ì
; vaccinia, varicella, herpes
simplex, enterovirus
Viral Genome And Virion Detection
1)
PCR : complementary nucleotides ÀÌ¿ë
¡æ
detect viral gene sequences
2)
electron microscopy ( EM )
:
direct visualization of virions within infected cells
Serologic Test
#
Speciemen
; *Àû¾îµµ 2°³ÀÇ blood specimen ÇÊ¿ä
-
early acute phase (acute serum) & later 14-21 days (convalescent serum)
; *2nd specimenÀÌ earlier than 14 daysÀ̸é 3rd blood specimen 4~6wks later
#
Etiologic Dx titer
; acute phase serum¿¡¼ º¸´Ù
convalescent serum¿¡¼ 4¹è ÀÌ»ó ¡èÇØ¾ß ÇÑ´Ù.
#
¢ÞSingle specimenÀÌ
Dx.À» supportÇÏ´Â
°æ¿ì
1) E-B Ab
2) Young infant¿¡¼ÀÇ
Ab°¡ mother¿¡ ¾ø´Â °æ¿ì
3) infant°¡ Ä¿°¨¿¡ µû¶ó¼
infant¿Í mother¿¡¼
Ab levelÀÌ µ¿ÀϽÃ
4)
Mumps ÀǽÉãÁ presence of Ab to the soluble (s)
fraction of the mumps virus in the acute serum, when Ab to viral [V] Ag may be
absent or very low
; Acute infection½Ã
IgM viral specific Ab
; general population°ú ºñ±³ÇÏ¿©
high Ab level
#
methods for Ig M Ab detection
; diffcult to standardize
¡æ F (+) result°¡
common
Ig G Ab assay : viral pathogen ¡æ
induce humoral immunity (primary inf.ÈÄ ¼ö³â Áö¼Ó)
¡æ useful for established immune
status
Method for Detecting Ab
#
*CF Ab : useful in recent inf. but
less useful in past inf.
#
Neutralizing Ab
; remain for life, early Ds.¿¡
serum ¾ò°Ô µÇ¸é Ab rise difficult
- Neutralization test : c/s¿¡¼º¸´Ù
disadvantage
#
HI Ab
; correlate fairly well with
neutralizing ab.
; erythrocyte agglutination
(+) viurs
-
*myxovirus, rubella, some enterovirus
; ¡Úuseful
test for Parainfluenzae virus Ab
#
fluorescent Ab detected by indirect fluorescent technique
#
¡ÚELISA & latex agglutination test
; *now most used
;
viral Ag ÀÌ plastic well or to latex beads¿¡
attachµÇ¾î °Ë»çµÊ.
Section 2. Clinical Syndromes Caused by a Variety of Infectious Agents
Chapter 167. Fever without a Focus
Fever As A Manifestation Of Serious Bacterial Disease
Table 167-1
Fever Without A Focus
1)
36°³¿ùÀÌÇÏ¿¡¼ ƯÈ÷ Áø´Ü¿¡ dilemmaÃÊ·¡
2)
3°³¿ùÀ̳»ÀÇ febrile infantÀÇ
40-60%°¡ viral pathogen
3)
¢ÀExclusion finding of Bacterial infection
; infants appear generally
well
; previously healthy
;
no evidence of skin, soft tissue, bone, joint, or ear infection
; total white blood cell count of >
5,000 or < 15,000 cells/¥ìL
; absolute band count of <
1,500 cells/¥ìL
;
normal urinalysis
--> negative predictive
value´Â 98%ÀÌ»óÀ̸ç, bacetremia¿¡ ´ëÇØ¼´Â
99%ÀÌ»óÀÌ´Ù.
4)
3°³¿ùÀÌÇÏÀÇ ill-appearing (toxic) febrile
infant¿¡¼ÀÇ ´ëÃ¥
1. prompt hospitalization
2. culture (blood, urine, CSF)
3. immediate parenteral antimicrobial
therapy
: ceftriaxone or cefotamixe + ampicillin
(for L. monocytogenes)
¡æ
focal signs¾ø´Â ill-appearing patientsÀÇ
initial therapy
¢ÀPC resistant Strept.
pneumoniae¿¡ ÀÇÇÑ meningitis¿¡¼´Â vancomycinÃß°¡.
Occult Bacteremia
1.
bacteremia without an obvious focus of infection
2.
occult bacteremia°¡Áø childrenÀÇ
85%¿¡¼ culture»ó
S. pneumoniae (+)
³ª¸ÓÁö positive culture¿¡¼´Â
H. influenzae type b, N. meningitidis, Salmonella species
3.
¢ÀIncreased Risk For Occult Bacteremia
¨ç temperature: 39.4¡ÉÀÌ»ó
¨è total WBC count: <
5,000 or > 15,000
¨é elevated absolute
neutrophil count, band count, ESR, or C-reactive protein
4.
3-36°³¿ù infant¿¡¼
temp. 39¡ÉÀÌ»ó, WBC > 15,000À϶§
--> bacteremia incidence
13%
--> *3-36°³¿ù»çÀÌ¿¡¼ bacteremia incidence°¡
Áõ°¡ÇÏ´Â ÀÌÀ¯
;
maturational immune deficiency
;
decrease in opsonic IgG Ab against polysaccharide Ag. of bacteria
5.
bacteremia Ä¡·á ¾Ê´Â °æ¿ì
¨ç resolve without
sequelae
¨è persist
¨é produced localized
inf. (meningitis, pn., cellulitis, septic arthritis)
6.
H. influenzae¿¡ ÀÇÇÑ bacteremia°¡
S. pneumoniae¿¡ ÀÇÇÑ bacteremiaº¸´Ù ´õ ½ÉÇÑ
bacterial infectionÀ» ÀÏÀ¸Å²´Ù.
; H. influenzae type b
bacteremia´Â meningitis, epiglottitis,
cellulitis, osteoarticular infection°°Àº focal infectionÀ» ¾ß±â.
5%¿¡¼ occult bacteremiaº¸ÀδÙ.
7.
pneumococcal bacteremia¿¡¼ spontaneous resolutionµÇ´Â
transient bacteremia incidence
;
30-40%
8.
3-36°³¿ùÀÇ toxic-appearing febrile child¿¡¼
infectionÀÇ focal signÀÌ ¾ø¾îµµ
severe bacterial diseaseÀÇ high risk°¡ ÀÖÀ¸¸é
immediate antibiotic Tx.ÇÊ¿ä
#
¢ÀPractice guideline (published in Pediatrics & Annals of
Emergency medicine in 1933)
1)
3-36mo nontoxic infant with temp. < 39¡É
;
obseved outpatients without diagnostic test or antibiotics medication
2)
non-toxic with rectal temp.¡Ã 39¡É
;
two option
-
blood culture & empirical antimicrobial therapy
-
complete blood cell count
-->
if WBC ¡Ã 15,000 cells/¥ìL,
blood culture & empirical antimicrobial therapy
3)
others infants
;
after blood culture, observed without antimicrobial therapy
10.
ill appeared child¿¡¼ fever°¡ °è¼ÓµÇ°í
focus ¹ß°ßµÇÁö ¾Ê°Å³ª H. influenzae³ª
N. meningitidis°¡ 1st blood culture»ó
(+)ÀÎ °æ¿ì
;
meningitis¿©ºÎ ±Ô¸í, repeat blood culture³»¸®°í ÀÔ¿øÇؼ ÀûÀýÇÑ
antibiotic Tx.¸¦ ÇÑ´Ù.
Fever With Petechiae
;
*Age¿Í
°ü°è¾øÀÌ high risk for
life-threatening bacterial infection
;
8-20%¿¡¼ serious bacterial infection
;
7-10%¿¡¼ meningococcal sepsis or
meningitis
;
H. influenzae type b´Â meningococcusº¸´Ù
less common, serious bacterial illness¾ß±â
Fever In Patients With Sickle Cell Anemia
1)
sickle cell anemia¿¡¼ M/C cause of death : infection
2)
2¼¼ÀÌÇÏ¿¡¼ infection incidence°¡Àå ³ô´Ù.
3)
infectionÀÇ riskÁõ°¡ ¿øÀÎ
1. functional asplenia
2. defect in properdin pathway
(alternate complement)
4)
common pathogens
1. pnuemococus (sepsis or meningitis)
2. H. influenzae (meningitis)
3. Salmonella (osteomyelitis)
4. E. coli (pyelonephritis)
5)
Tx.
½Å1.
seriously ill, temp 40¡É¡è, WBC count < 5,000/¥ìL,
or >30,000/¥ìL, pulm. infiltrates,
sickle cell ds.ÀÇ
Cx., severe pain
: hospitalization
2. other febrile infant : ceftriaxone IM
& cultureÈÄ outpatient·Î
manage
6)
prevention of pneumococcal sepsis
: long term Pc.(¸ÅÀÏ
oral·Î ¶Ç´Â 3-4ÁÖ¸¶´Ù IM)À¸·Î
adolescence±îÁö Tx.
H. influenzae¿¡ ´ëÇØ¼´Â
daily oral amoxacillin
Hyperpyrexia
½Å
*Temp. >41¡É
;
uncommon
;
temp 39.1-40.0¡É or 40.1-41.0¡Éº¸´Ù
serious bacterial infectionÀÇ high rate°ü·Ã¼º ¾øÀ½.
FUO
#
¢ÀDefinition
1) history of fever of more than 1wk
duration (2-3wks if adolescent)
2) ducumentation of fever by health care
provider
3) no apparent diagnosis 1wk after
investigation was begun in either an inpatient or outpatient setting
#
*Principal Causes Of FUO
;
infection, connective tissue (autoimmune) disease
; other causes
- neoplasms, drug fever
#
FUO¿Í AIDS
; HIV-1 infection½Ãµµ
fever(+), AIDSÇϳª·Î´Â FUO¿¡ ºÎÇÕÇÏÁö ¾Ê´Â´Ù.
; FUO¿Í
AIDSÀִ ȯÀÚ¿¡¼´Â common, unusual
pathogenÀÇ opportunistic infectionÀ» ¶ÇÇÑ °¡Áü
#
*6°³¿ùÀÌ»ó Áö¼ÓµÇ´Â FUOÀÇ ¿øÀÎ (children¿¡¼´Â uncommon)
; granuolmatous or autoimmune
diseaseÀǹÌ
¢¾Table
167-3
; ¢Þviral
cause of FUO
-
cytomegalovirus, hepatitis, infectious mononucleosis, HIV
; *¡ãcommon autoimmune
hypersensitivity disease
-
juvenile rheumatoid arthritis
Diagnostic Clues In The Child With Fever Of Unknown
Origin
History
1. 6¼¼ÀÌÇÏ
: resp. or G-U tract infection
localized infection
(abscess, osteomyelitis)
junvenile rheumatoid
arthritis
leukemia
2. adolescent
: Tbc
inflammatory bowel disease
autoimmune disease
lymphoma
*
Pica
: Toxocara or infection of Toxoplasma
gondii
*
medication
: over-the-count preparation &
topical agent (atropine induced fever)
Physical Examination
#
¢Þsweat (-) in the presence of
elevated or changing body temperature
; dehydration from vomiting,
diarrhea, central or nephrogenic DI
; anhidrotic ectodermal
dysplasia
; familial dysautonomia
; exposal to atropine
#
Eye lesion
¨ç red, weeping eye
:
connective tissue disease ƯÈ÷ polyarteritis nodosa
¨è palpebral conjuctivitis
:
measle, coxsackie viral infection, Tbc, IM, lymphogranuloma venereum,
cat-scratch or New-castle disease viral infection
¨é bulbar conjunctivitis
:
Kawasakie disease, leptospirosis
¨ê petechial conjunctival hemorrhage
:
endocarditis
¨ë uveitis
:
sarcoidosis, juvenile rheumatoid arthritis, SLE, Kawasaki disease, Behcet
syndrome, vasculitis
¨ì chorioretinitis
: CMV, toxoplasmosis,
syphilis
¨í proptosis
:
orbital tumor, thyrotoxicosis, metastasis of neuroblastoma, orbital infection,
Wegener granulomatosis, pseudotumor
#
¢ÀOphthalmoscopic examination of nailfold capillary abnormalities
; *dermatomyositis & systemic
scleroderma°°Àº connective tissue
disease
-
markedly dilated capillary pattern
- Figure 167-1 A & B
#
hypothalamic dysfunction¿¡ ÀÇÇÑ FUOÀÇ ¿øÀÎ
; failure of pupillary
constriction due to abscence of the sphincter constrictor muscle
#
¡Ø°´ Fever Blister
; pneumococcal,
streptococcal, malarial, rickettsial infection
; meningococcal meningitis
; rarely seen in
meningococcemia, salmonella, staphylococcal infection
#
repetitive chill & temp. spikes
; common in septicemia (ƯÈ÷,
renal, liver or biliary, endocarditis, malaria, brucellosis, rat-bite fever,
loculated pus)
Laboratory studies
1)
*WBC & UA
¨ç *absolute neutrophil count < 5,000/mm3
; against fulminant bacterial
infection other than typhoid fever
¨è *PMNL > 10,000/mm3 or nonsegmented
PMNL > 500/mm3
; high chance of severe
bacterial infection
2)
Giemsa or Wright stain with blood smear
: malaria, trypanosomiasis, babesiosis,
relapsing fever
3)
ESR
; *ESR(>30mm/hr, Westergen method)
-
inflammationÀ» ÀǹÌ
-
infectious, autoimmune, & malignant¿¡ ´ëÇÑ evaluation
;
low ESR
-
juvenile rheumatoid arthritis, infectionÀÇ °¡´É¼ºÀ» ¹èÁ¦ÇÏÁö ¸øÇÔ
; ¡Ø94
ESR > 100
-
Tbc, Kawasaki disease, malignancy,
autoimmue disease
4.
Radioactive scan
¨ç galium citrate(67Ga)
: tumor, abscessÀÇ
inflammatory tissue (leukocyte)¿¡ localized
¨è 99mTc phosphate
: X-ray¿¡¼
bone lesionÁõ¸í ÇϱâÀü¿¡ osteomyelitis detect
¨é *Indium-III granulocyte or iodinated IgG
: useful detecting localized
pyogenic process
Treatment
¢Þ FUO¿¡¼
¹«ºÐº°ÇÑ antibiotic treatment°¡
À§ÇèÇÑ ÀÌÀ¯
; endocarditis, meningitis,
parameningeal infection, osteomyelitisÀÇ Áø´ÜÀ» ¸ðÈ£ÇÏ°Ô ÇÑ´Ù.
; ±×·¯³ª,
anti Tbc treatment´Â ¿¹¿Ü
Prognosis
; adultº¸´Ù
better prognosis
; unclear etiology : 25%
Chapter 168 Sepsis & Shock
Bacteremia & Septicemia
#
bacteremia
;
disease¿¡ °ü°è¾øÀÌ ÀϽÃÀûÀ¸·Î blood culture¿¡¼
bacteria°¡ recoveryµÇ´Â °æ¿ì
#
septicemia
;
acute disease¿Í °ü·ÃµÈ bacteremiaÀÇ
severe formÀ¸·Î¼ septic shockÀ¸·Î
progressÇÒ ¼ö ÀÖ´Â °æ¿ì
#
*BacteremiaÀÇ
Á¤µµ
; transient or low grade
(< 100 CFU/ml blood) bacteremia
: follow instrumentation of
resp., G-I, G-U tract
; *high grade (> 100-1000 CFU/ml blood) bacteremia
: in sepsis condition may
progress to septic shock
Epidemiology
1.
Immunocompetent nonhospitalized patient
¨ç community acquired
bacteremia-sepsis from local tissue infection
¨è colonization &
local mucosal invasion by particulary virulent pathogen
; *S. pneumoniae, H. influenzae b, N. meningitidis
2.
Hospitalized patient
¨ç catheter sepsis or
surgical wound
;
S. aureus, S. epidermidis
¨è immunocompromized
neutropenic patient
; *E. coli, pseudomonas, Acinetobacter, Klebsiella-Enterobacter,
Serratia
¨é polymicorbial sepsis
; in high risk patient with
central venous catheterization, gastrointestinal disease, neutropenia,
malignancy
3.
Pseudobacteremia-associated with contaminated solution such as
; microbial disinfectant,
heparinized flush solutions, intravenous infusions, albumin, cryoprecipitate,
contaminated equipment
Pathogenesis Of Sepsis & The Systemic
Inflammatory Response Syndrome (SIRS)
¢ÀFigure
168-1 & Figure 168-2
;
bacterial products¿¡ ´ëÇÑ host response
- gram-negative bacteria ¡æ
endotoxin
-
gram-positive bacteria ¡æ lipoteichoic aicd-peptidoglycan
complex
;
blood stream³»·Î bacterial cell wall components°¡
releaseµÉ¶§, cytokines´Â Ȱ¼ºÈµÈ´Ù.
- *TNF, IL-1, -6 & -8, platelet-activating factor (PAF),
interferon-¥ã
#
¢ÀPhysiologic response by cytokines
¨ç activation of
complement system
¨è activation of Hageman
factor (factor XII)
¨é adrenocorticotrophic
hormone & beta-endorphin release
¨ê stimulation of
polymorphonuclear neutrophils
¨ë stimulation of the
kallikrein-kinin system
½Å4.
TNF & other inflammatory mediators
¨ç vascular permeability ¡è,
diffuse capillary leakage
¨è vascular tone ¡é
¨é imbalance between
perfusion & the increased metabolic requirements of tissue
½Å5.
shock
¨ç def.
: a systolic blood pr.
below the 5th percentile for age or by cool extremities
¨è delayed capillary
refill (> 2 sec.)
: no considered a
reliable indicator of decreased peripheral perfusion
6. early (warm) septic shock :
peripheral vascular resistance ¡é
7. tissue oxygen consumption˼
septic shock¿¡¼
oxygen deliveryÃʰú
¨ç early peripheral
vasodilation
¨è late vasoconstriction
¨é myocardial depression
¨ê hypotension
¨ë ventilatory insufficiency
¨ì anemia
8. cardiac indexÁõ°¡:
sepsis¿¡¼
9. pulmonary function: often severely
impaired
Clinical Manifestation
1. septic shockÀÇ
primary sign & Sx.
: fever, shaking chills, hypertension,
tachycardia, hypothermia, cutaneous lesion (petechiae,
ecchymoses, ecthyma gangrenosum,
diffuse erythema, cellulitis), ÀǽÄÀå¾Ö (confusion,
agitation, anxiety,
excitation, lethargy, obtundation, coma)
2. secondary Mx.
: hypotension, cyanosis, systemic
peripheral gangrene (purpura fulminans), oliguria or
anuria, jaundice
(direct-reacting hyperbilirubinemia), sign of heart failure
3. cold shock
¨ç Ư¡
: cold, clammy, cyanotic &
pale extremities, unresponsive to verbal or painful stimuli
¨è evidence of a focus of
infection such as
: meningitis, pneumonia,
arthritis, cellulitis, pyelonephritis, immunocompromised status
(malignancy, T & B
lymphocyte defect, prior splenectomy)
Laboratory Manifestation
1.
postive blood culture
; gram, Wright, Methylene
blue, acridine orange stain of the buffy coat or petechial lesion
2.
metabolic acidosis
3.
thrombocytopenia
4.
anemia
5.
PT ¡è, PTT ¡è
6.
serum fibrinogen level ¡é
7.
Pa O2 ¡è& Pa CO2 ¡é
8.
¡Ø90 neutrophilÀÇ
morphology º¯È
¨ç neutrophilÀÇ
vacuolization
¨è toxic granulation
¨é Dohle body
¨ê elevated neutrophil
& band
¨ë neutropenia
¨ç-¨é
: bacterial sepsis
¨ê : bacterial infection
¨ë : ominous sign of fulminant
septic shock
Treatment
¨ç community acquired ds. (H.
influenzae, N. meningitidis, S. pneumoniae)
; ceftriaxone
¨è nosocomial sepsis
; cephalosporin (3rd) or
extended gram (-) sepectrum PC + aminoglycoside
¨é S. pneumoniae°¡
PC resistant
; vancomycin Ãß°¡
#
shock
¨ç fluid restriction
(N/S, albumin, hetastarch, dextran sol.)
¨è IV sympathomimetic
agent
; 1st - dopamine, dobutamine
; 2nd - epinephrine, NE,
sodium nitropruside
#
hypoxia
;
PEEP (5-20 cm H2O)
#
DIC
¨ç replace consumed
coagulation factors
: fresh frozen plasma, cryoprcipitate,
platelets
¨è heparin
: thromobosis, peripheral gangrene¿¡ ´ëÇØ
#
overexuberant host response¸¦ ¸ñÀûÀ¸·Î
;
IV Immunoglobulin, monoclonal IgM to endotoxin, granulocyte transfusion
#
corticosteroid effect
; adult ¿¡¼´Â
not beneficial
; adrenal hemorrhage
(Waterhouse-Fridrichsen syndrome)
; *meningitis caused by H. influenzae type b
Prognosis
;
gram (-) enteric sepsis: 40-60%
#
¡ÚPoor Prognostic Sign In Meningococcal Sepsis
;
hypotension
;
coma
;
leukopenia (< 5,000)
;
thrombocytopenia (< 100,000)
; *low fibrinogen level (<150mg/dl)
;
absence of meningismus
;
absence of CSF pleocytosis with bacteria noted on gram stain of CSF
; *rapid appearance of petechia (in 1hr)
;
hypothermia
#
±×¿Ü TNF, bacterial No./ml blood,
endotoxin level
: prognosis¿Í ¿¬°ü
Prevention
1.
2°³¿ù-4¼¼ÀÇ all children
: immunization against H. influenzae
type b
2.
high risk pt
: 2¼¼¿¡ *23-valent pneumococcal vaccine, quadrivalent
meningococcal vaccine (group A, C, Y, W-135)
3.
pneumococcal infection¿¡ ´ëÇÑ PC prophylaxis
: splenic dysfunction (sickle cell
anemia pt) & splenectomy
4.
H. influenzae³ª meningococcal ds.¿¡
exposureµÈ pt.¿¡ close contactÇÑ °æ¿ì
: Rifampin
Chapter 169. Infections Of The Central Nervous System
#
CNS˂ acute infection˼
children¿¡¼ CNS ds ÀÇ
Sx, SgÀ» µ¿¹ÝÇÑ feverÀÇ
mc causeÀÌ´Ù.
#
ÀϹÝÀûÀ¸·Î CNS infectionÀº
viralÀÌ bacterialº¸´Ù
more common
#
etiology¿¡ °ü°è¾øÀÌ acute CNS infectionÀ» °¡Áø ȯÀÚ´Â
similar syndromeÀ» °¡Áø´Ù. ;
( infortunately, most of these Sx are
quite non-specific )
#
common sx : headache, nausea, vomiting, anorexia, restlessness, irritability
common sg : fever, photophobia, neck
pain, rigidity, obtundation, stupor, coma, seizure, focal neurologic deficity
#
signÀÇ severity¿Í
constellationÀº specific pathogen, host, infectionÀÇ anatomic distribution¿¡ ÀÇÇØ Á¤ÇØÁü
#
diffuse CNS infection
+- Menigitis : meninges
+- encephalitis : brain parenchymal
involvement
; ¸¹Àº ȯÀÚ¿¡¼ anatomic barrier°¡
not distinctÇϱ⠶§¹®¿¡ meningeal, parenchymal
involvement¼Ò°ßÀ» º¸À̸é meningoencephalitis¸¦ ²À »ý°¢ÇØ ÁÖ¾î¾ß ÇÑ´Ù.
#
Brain absess : best examples
of a focal infection of the CNS
: neurological expression´Â absessÀÇ
site¿Í extent¿¡ ÀÇÇØ °áÁ¤
#
diffuse CNS infection Dx : careful examination of CSF obtained by lumbar
punture
Table 169-1
¢Þ169.1 Acute Bacterial Meningitis
The Neonatal Period
Etiology
#
within 2mo
; *group B streptococci, gram(-) enteric bacilii, L. monocytogen
; *H. influenza(both nontypable and type b strains)
#
2mo-12yrs
; *H. influenza type B, S. pneumoniae, N. meningitidis
; H. influenza type bÀÇ
vaciination »ç¿ëÀü¿¡´Â H. influenza°¡
far common
#
H. influenza vaccinated children & older unvaccinated children, adults
; *N. meningitidis or S. pneumoniae
#
alteration of host defense
; P. aeruginosa, S. aureus,
salmonella, S. epidermis, L. monocytogenes
#
H. influenza type B
; 2¼¼ÀÌÇÏ¿¡ ÈçÇÏÁö¸¸ ¸ðµç ¿¬·É¿¡ ¿Ã ¼ö ÀÖ´Ù.
Epidemiology
#
¡ÚRisk factors for menigitis
; attenuated immunologic
response to specific pathogen with young age
-
major risk factor
- 1mo-12mo ¿¡¼ greatest risk
-
1mo-5yr »çÀÌ¿¡¼ menigitis°¡ ÀüüÀÇ
95% Â÷Áö
; recent colonization with
pathogenic bacteria
; invasive disease¸¦ °¡Áø »ç¶÷°ú
close contact
; crowding
; poverty
; black race
; male sex
; possiblly absence of breast
feeding for infant 2¡5 mo of age
#
Occult bacteremia¸¦ °¡Áø ȯÀÚ¿¡¼ menigitisÀÇ
risk°¡ Áõ°¡Çϴµ¥ À̶§ÀÇ etiology»ó
odds ratio
pneumococcus ( 85 ¹è
)
H. influenza type B ( 12 ¹è
)
meningococcus ( 1 )
#
Epidemiology»ó À¯ÀÇÁ¡µé
; specipic host defence
defect, d/t altered immunolglobulin in response to encapsulated pathogen
¡æ
bacterial menigitis¡è
; defect of the complement
system ( C5 - C6 )
-
associated with reccurent meningococcal infection
;
defect of properdin system
-
associated with significant risk of lethal meningococcal infection
;
splenic dysfunction or asplenia
-
assiciated with increased risk of pneumoccocal,
-
H. influenza type B and rarely meningococcal menigitis and sepsis
;
T-lymphocyte defect
-
assiciated with increased risk of L. monocytogens
;
cong, or acquired CSF communication across the mucocut. barrier
-
associated with increased risk of pneumococcal
;
lumbosacral dermal sinus and meningomyelocele
-
associated with staphylococcal and enteric bacterial menigitis
;
penetrating cranial trauma and CSF shunt infection
-
assiciated with increased risk of staphylococcal and other cutaneous bacteria
H. Influenzae Type b
;
80% normal children in throat or nasopharynx
- H. influenza
- 2-5% carry H. influenza
type b
;
H. influenzae type bÀÇ carriage´Â
1mo¡4yrs ¶§
predominent
;
invasive H. influenzae type B bacteremia and meningitis
- unvaccinated children
- ¡ã
in infant 2 mo-2yr age
- peak incidence 6-9mo. (caseÀÇ
50%°¡ 1¼¼ÀÌÇÏ)
;
risk markedly increased among family or day care center contact pts
;
other risk factor
a.
otitis media due to H. influenzae
b. HIV infection
c. CSF leakage
d. occult bacteremia
Streptococcus Pneumoniae
; from family contact after
birth
-
transient in 2-4mo
-
*if recent (£¼1mo) is risk factor for serious infection
; incidence : 1-3 / 100,000
; peak season - midwinter
month
; risk factors
a.
black > white ( 5 ¡ 36 ¹è )
( black and
sickle cell anemia ½Ã 300 ¹è ÀÌ»ó
)
b. sickle cell anemiaÀÇ
4%°¡ 5¼¼ÀÌÇÏ¿¡¼ pneumococcal menigitis,
if no vaccination.
c.
otitis med
d.
sinusitis
e.
pneumonia
f.
CSF otorrhea or rhinorrhea
g.
chronic GVHD following BM transplantation
h.
splenetomy
N. meningitidis
¨ç
sporadic (group B.) epidemic (A and C)
¨è
peak season ; winter and spring
¨é
nasopharyngeal carriage ; 1-15% of adult
¨ê
risk factors
a. recent colonization places the
nonimmune young children
b. contact in a day care facility
colonized family member
ill patient with meningococcal infection
Pathology
#
vascular and parenchymal cerebral change°¡ PMNÀÇ
small arteriole, veinÀÇ subintimal regionÀ¸·ÎÀÇ
infiltration¿¡ ÀÇÇØ ³ªÅ¸³ª°í vasospasm, vasculitis,
thrombosis of small cortical necrosis, occlusion of major venous sinuses,
necrotizing arteritis producing subarachnoid hemorrhage, rarely cerebral
cortical necrosis°¡ autopy¿¡¼ identifiable thrombosis¾øÀÌ ³ªÅ¸³´Ù.
#
cerebral infarctionÀÌ vascular occlusionÀÇ
sequelae·Î ³ªÅ¸³´Ù.
#
spinal n. root infiltration ¡æ meningitis sign
#
cranial n. infiltraion ¡æ optic, oculomotor, facial,
auditory n.¿¡ cranial neuropathy
#
cranial N.ÀÇ Àå¾Ö by IICP
¨ç oculomotor N. palsy ; tentorial
herniation µ¿¾È temporal lobe compression¿¡ ±âÀÎ
¨è abducence N. palsy ; nonlocalized
sign of IICP
¨é ¥²-¥µ N. palsy ; by septic
carvernous sinus thrombosis
#
IICP mechanism
; cell death (cytotoxic cbr.
edema)
; cytokine-induced increased
capillary vascular permeability (vasogenic cbr. edema)
; increased hydrostatic
pressure (interstitial cbr. edema)
; following obstructed
reabsorption of CSF in the arachnoid villus or obstruction of the flow of fluid
within or exiting from the ventricle.
; SIADH (excessive water
retention ¡æ IICP¡è)
; brain extracellular spaceÀÇ
hypotonicity
-->
cell swelling and lysis
-->
cytotoxic edema
#
ICP°¡ Á¾Á¾ 300cmH20±îÁö ¿À¸£´Â °æ¿ìµµ ÀÖ°í,
reduced cerebral blood flow --> cbr. perfusion pr. (mean
arterial-intracranial pr.)°¡£¼50cmH20À̸é
cbr. perfusionÀÌ futher compromised.
#
herniationµµ meningitis ȯ¾ÆÀÇ ¾à
5%
; suggest
a.
marked IICP
b.
cerebral absess
c.
subdural empyema
#
neonatal period Áö³ ÈÄ¿¡´Â hydrocephalus´Â
meningitisÀÇ uncommon acute complicationÀÌ´Ù.
#
tentorial, falx, cerebellar herniation : rare
#
¶§¶§·Î brain base¿¡¼
cisternÁÖÀ§ÀÇ arachnoid villiÀÇ
adhersive thickening¿¡ ÀÇÇØ communicating
hydrocephalus°¡ ÀϾ ¼ö ÀÖ´Ù. ---> CSF normal
resorptionÀ» interfere.
#
less often, foramina magendie, Luschka, aqueduct of SylviasÀÇ
fibrosis and gliosis¿¡ ÀÇÇØ obstructive
hydrocephalus°¡ developedµÈ´Ù.
#
raised CSF proteinÀÇ ¿øÀÎ
¨ç
BBBÀÇ vascular permeability Áõ°¡
¨è
capillary or vein¿¡¼ subdural space·Î
albumin rich fluidÀÇ loss.
;
subdural effusionÀÌ ±Ã±ØÀûÀ¸·Î ¿Ã ¼ö ÀÖ´Ù.( late phase¿¡ ¿Â´Ù
)
#
¢ÀHypoglycorrhachiaÀÇ ¿øÀÎ (Reduced CSF Glucose Level)
; decreased glucose transport
by cerebral tissue
;
latter may produce a local lactic acidosis
#
¢¾Mechanism of Cbr cortex damage
; focal or diffuse effect of
vascular occlusion(infarction, necrosis)
; hypoxia
; bacterial invasion
(cerebritis)
; toxic encephalopathy
(lactic acidosis)
; IICP
; ventriculitis
; transudation (subdural
effusion)
-->
impaired consciousness, seizure, hydrocephalus, cranial n. deficits, motor and
sensory deficits, and later psychomotor retardation
Pathogenesis
;
hematogeneous dissemination from distant site of infection
- *¡ãcommon
- usually precedes or
concomitant bacteremia
- nasopharynxÀÇ
bacterial colonizationÀÌ usual sourse.
;
H. influenza type b¿Í meningocci
- epihterial cell¿¡
attach ¡æ circulaton
;
N. meningitis
- phagocytic vacule ¡æ
epitherial cell ¿¡ ingestion
;
entry to CSF
- lateral ventricleÀÇ
choroid plexus¸¦ ÅëÇØ
-->
extracerebral CSF¿Ísubarachnoid space
-->
rapidly multiply ( ¡ñ complement¿Í
AbÀÇ CSF concentrationÀÌ
bacterial proliferationÀ» ¾ïÁ¦Çϱ⿡´Â inadequate )
;
gram(-) bact. cell wall lipopolysaccharide (endotoxin) & pneumococcal cell
wall component (teicholic acid, peptidoglycan)ÀÌ marked inflamm.
response¸¦ stimulation by production of
¨ç
TNF
¨è
interleukin I
¨é
PGE2
¨ê
cytokine inflammatory mediators
;
subsequent inflammatory response
¡æ
neutrophilic infiltration, increased vascular permeability, alteration of the
BBB, vascular thrombosis
;
excessive cytokine-induced inflammationÀº CSF°¡
sterilizedµÈ ÈÄ¿¡µµ °è¼ÓµÇ°í À̵éÀº pyogenic meningitisÀÇ
chronic inflammatory sequelae¿¡ ºÎºÐÀûÀ¸·Î ¹Ý¿µ.
;
infectionÀÇ contiguous focus·ÎºÎÅÍ
bacterial invasion¿¡ ÀÇÇÑ menigitis´Â
rare
-
paranasal sinusitis, OM, mastoiditis, orbital cellulitis ...
;
occur during endocarditis, pneuminia, thrombophlebitis
;
associated with severe burns, indwelling cathers or contaminated equipment
Clinical Manifestation
#
sudden onset
¨ç
shock, purpura, DIC, reduced level of consciousness°¡
rapidly progressive( esp, meningococcal spp.)
¨è
24hr³»¿¡ death
¨é H. influenzae type b
and pneumococcal menigitis´Ârare
#
¼öÀϰ£ÀÇ URI or G-I Sx. ¼±Çà
#
nonspecific findings
; fever (90-95%), anorexia,
poor feeding, URI Sx., myalgia, arthralgia, tarchycardia, hypotension, various
cutaneous sign : petechea, purpura, erythmatous macular rash
#
Specific Signs
1) meningeal irritation sign
¨ç
nuchal rigidity
¨è
back pain
¨é
Kernig sign : hipÀ» 90¡Æflexion½ÃŲ »óÅ¿¡¼
leg extension½Ã subsequent pain(+)
¨ê
Brudzinski sign : supine¿¡¼ neck flexion½Ã
knee & hipÀÇ ºÒ¼öÀÇÀû flexion
;
12 ¡ 18 mo Àü¿¡´Â
not evident
2) papilledema
;
IICP ¶§
;
uncomplicated meningitis½Ã´Â Àß ¾È³ªÅ¸³².
;
¢¾³ªÅ¸³´Ù¸é
a.
intracranial abscess
b.
subdural empyema
c.
occlusion of dural venous sinus µîÀÇ *chronic process suggest
3) focal neurologic sign
;
due to vascular occclusion or focal inflammation
;
10¡20%¿¡¼ focal neurologic sign
(+)
;
*pneumococcal menigitis¿¡¼ 30%À̻󿡼 ³ªÅ¸³´Ù
-
due to vigorous inflammatory response.
4) seizure in meningitis
;
*due to cerebritis, infarction,
electrolyte imbalance
;
20-30% of meningitis
;
*more common in H. influenzae &
pneumococcus than meningococcus
;
*seizure persist after the 4th day of
illness
-
*poor prognosis
5) IICP
;
headache, emesis, bulging fontanel, diastasis of the sutures, oculomotor or
abducens nerve paralysis, hypertension withbradycardia, apnea,
hyperventilation, decorticate or decerebrate posturing, stupor, coma,
herniation sign.
6) Alteration of mental
status
;
*due to IICP, cerebritis, hypotension
;
irritability, stupor, obtundation, coma
;
comatose patient in meningitis
-
poor px. sign.
-
more often with pneumococcal or meningococcal than H. influenza
Complication
1)
Neurologic Cx.
; seizure, IICP, cranial N.
palsy, stroke, cbr. or cbll herniation transverse myelitis, ataxia, dural
venous sinus thrombosis, subdural effusion
2)
Subdural effusion
; *10-30%
-
85-90% asymptomatic
; more common in young infant
; ¡Ø91
Symptomatic Subdural Effusion
-
bulging fontanel, diastasis of suture, emesis, seizure, fever, increased head
circumference, abnormal results of cranial transillumination
-
aspiration
-
fever no indication of aspiration
; CT - confirm
3)
Subdural empyema
; 1% of subdural effusion
4)
SIADH
; occurs in majority of
meningitis
; hyponatremic and reduced
s-osmorality (30-50%)
¡æ
exacerbate cerebral edema or independently hyponatremia seizure
; TxÀÇ
late course¿¡ central diabetes inspidus°¡
hypothalamus or pituitary dysfunctionÀÇ °á°ú·Î ¿Â´Ù.
5)
Fever
; more easily resolve in
meningococcal and pneumococcal (90%) than H. influenza (70%)
-
by the 6th day of therapy
; prolonged fever (£¾10
days)
-
15% of H. influenzae, 9% of pnumococcal, 6% of meningococcal
-
*cause
/
intercurrent viral infection, nosocomial or 2¡Æbacterial infection,
thrombophlebitis pericarditis drug reaction, arthritis
; *secondary fever
-
afebrile ÇØÁø ÈÄ¿¡ ´Ù½Ã fever ³ªÅ¸³ª´Â °æ¿ì
-
nosocomial infection
6)
infectious pericarditis, arthritis
; due to bacterial dissemination or
immune complex desposition
; occur earlier in the course
of Tx than dose immune-mediated ds
7)
¡ÚThrombocytosis, Eosinophilia, Anemia
; *anemia
-
*¡ãcommon
in H. influenzae
-
causes
/ hemolysis
/ BM suppression
8)
DIC
; *¡ãoften associated with
rapidly progressive pattern of presentation
; ¡ãcommonly
in patient with *shock and prupura
(purpura fulminans)
9)
¢¾Repeated episode of meningitis (3 pattern) :rare
; recrudescence
-
reappearence during therapy with appropriate AB
-
CSF
/
*growth of bacteria & resistance
of antibiotics
; relapse
-
occurs between 3days and 3wk after therapy
-
*persistent CNS infection (subdural
empyema, ventriculitis, cerebral abscess) or other site infection (mastoid,
cranial osteomyelitis, orbital infection)
-
*often asso. with inadequate choice,
dose, duration of AB therapy
; recurrence
-
new episode of meningitis due to reinfection
-
same bacterial species or andther pyogenic pathogen
-
¡ÚSuggest
/
acquired or congenital anatomic communication between CSF & mucocutaneous
site
/
defect in immune host defense
Differential Diagnosis
1)
other organism meningitis
; Tb, Norcardia, Syphilis,
lyme disease
;
Fungus ( coccidioides, Histoplasma , Blastomyces )
; compromised host - candida
, Cryptociccus, Aspergillus
; Parasite : Toxoplasma
gondii, Cysticercus
; Virus( most frequently )
; noninfectious illness :
malignancy, collagen vascular syndrome, toxin
2)
focal infection of the CNS
; brain abscess, parenchymal
infection ( ex. subdural empyema )
3)
acute viral meningoencephalitis
; *most likely infection to be confused with bacterial meningitis.
; bacterial meningitisº¸´Ù
less illÇÏ¿© DdxÇÏÁö¸¸, ±×·¸Áö ¾ÊÀº °æ¿ì°¡ ÀÖ¾î Èûµé´Ù.
4)
¡ÚPartially Treated Bacterial Meningitis
; 25-50% of bacterial
meningitis children
; CSF¸¦
obtainÇϱâÀü¿¡ oral antibioticsÀÇ »ç¿ëÇÑ °æ¿ì
; effects
-
gram stain to less than 60%
-
reduce of incidence of growth of bacteria in CSF culture
; ¡Úno
effects
-
*CSF glucose, protein, neutrophil
profile, detection of bacterial antigen in CSF
Diagnosis
;
confirm by CSF analysis
¨ç microorganism(+), gram s., c/s
¨è neutrophilic pleocytosis
¨é protein¡è
¨ê glucose¡é
#
Lumbar puncture (LP)
; flexed lateral decubitus
position
; L3-L4, L4-L5 intervertebral
space
; ¡Ø95ÁÖ
Cotnraindication
-
evidence of IICP
/
bulging fontanel
/
cranial nerve(III,VI) palsy with depressed level of consciousness
/
hypertension & bradycardia with resp. abnormalities
-
severe cardiopulmonary compromised state requiring resuscitation for shock or
in patients whom positioning for LP comprimise cardiopulmonary function
-
infection of skin overlying the site of the LP
; relative CIx
-
thrombocytopenia
-
*DIC or petechiae´Â CIxÀÌ µÇÁö
¾Ê°í, immunosuppressed
patients with chronic thrombocytopeniaÀ» °¡Áø
ȯÀÚÀÇ °æ¿ì transfusionÈÄ °¡´É
; ¡ÚLP¸¦
À§¿Í°°Àº °æ¿ì·Î
ÀÎÇØ ¿¬±âÇÏ´õ¶óµµ empiric AB Tx.´Â Áï°¢ÀûÀ¸·Î
½ÃÀÛÇØ¾ß ÇÑ´Ù
; CT scan »ó
IICP, brain abscessÀÇ evidence°¡ ÀÖ´õ¶óµµ Ä¡·á°¡
delay µÇ¾î¼´Â ¾ÈµÈ´Ù.
; *LP´Â IICP°¡ Tx. µÇ°í brain abscess°¡ excludedµÈ ÈÄ¿¡
½Ç½ÃÇÑ´Ù.
#
concurrent immunoelectrophoresis (CIE)
; *to identify Ag of ¨ç H. influenzae
¨è
S. pneumoniae
¨é
N. meningitidis type A, C, Y, W135
#
¡ÚLatex Particle Agglutination
; *¡ãpopular, widely used
;
CSF¿¡¼ most consistently detect
; antigenuriaµµ
common
;
serumÀº false positive°¡ ¸¹¾Æ good specimenÀÌ ¾Æ´Ï´Ù.
;
Antibiotics Tx.¸¦ ÇÏ¿´´õ¶óµµ therapy½ÃÇà ¼öÀϳ»¿¡
AgÀ» detectÇÒ ¼ö ÀÖ´Ù.
; H. influenzae type B
vaccinationÀ» ÃÖ±Ù¿¡ ¹ÞÀº ȯ¾Æ¿¡¼´Â urine & serum¿¡¼
Ag detection method¿¡¼ false(+)
-
CSF¿¡¼´Â ±×·± ÀÏÀÌ ¾ø´Ù.
#
blood C/S
; *80¡90% (+) in childhood
meningitis
; menigitis°¡ ÀǽɵǴ ¸ðµç ȯ¾Æ¿¡¼ ½ÃÇàÇØ¾ßÇÑ´Ù
; ƯÈ÷ °æÇèÀû Ç×»ýÁ¦¸¦
LPÀü¿¡ »ç¿ëÇÑ °æ¿ì
#
CSF leukocyte counts
; usually 1000¡è
-
neutrophilic predominance (75-95%)
; turbid £½
leukocyte counts £¾ 200¡400
; Á¤»ó
-
*neonate : 30°³ÀÌÇÏ, older chikdren : 5¡6°³ÀÌÇÏ
-
lymphocyte, monocyte°¡ ´ëºÎºÐ
; ¡Úlower
CSF leukocyte (£¼250)
-
acute bact. meningitis ptÀÇ 20%
; ¡Úabsent
pleocytosis
-
*overwhelming sepsis & severe
meningitis
-
*poor prognostic sign
; pleocytosis with lymphocyte
predominance
-
during early stage of acute bact, meningitis
; neutrophilic pleocytosis
-
during early stage of acute viral meningitis
; viral menigitis¿¡¼ÀÇ
shift to lymphocyte-monocyte predominance´Âinitial LPÈÄ
12¡ 24hr ³»¿¡ ÀϾÙ
#
Gram stain
; 70~90% (+)
#
Traumatic LP
¨ç
traumatic LP½Ã ´Ù¸¥ site¿¡ ´Ù½Ã ½ÃÇà½Ã óÀ½º¸´Ù ´ú
hemorrhagic, CSF³» RBC´Â Æ÷ÇÔµÊ.
¨è
gram stain, c/s, glucose level¿¡ ¿µÇâÀ» ÁÖÁö ¸øÇÔ.
-
±×·¯³ª CSF leukocytosis and protein
concentrationÀº ¿µÇâ (+)
Treatment
Initial AB Therapy
;
illnessÀÇ innitial manifestationÀÇ
nature¿¡ ÀÇÁ¸ÇÑ´Ù.
;
LPÈÄ Áï°¢ÀûÀ¸·Î AB Tx
- 24½Ã°£ À̳»¿¡
rapid progression without IICP
;
*LP½ÃÇàÇÏÁö¾Ê°í, brain CTÀü¿¡ AB Tx, µ¿½Ã¿¡ IICP Tx
- *IICP or focal neurologic finding (+)
;
more protacted subacute course³ª 1-7 day periodÀÌ»ó
ill
- IICP, focal neurologic
deficits¿¡´ëÇÑ evaluationÇØ¾ßÇÑ´Ù.
;
initial (empiric) choice of Tx
- H. influenza type B, S.
pneumoniae, N. meningitidisÀÇantibioitic susceptibility
- 3rd geneation cephalosporin
/
*ceftriaxone or cefotaxime
a.
ceftriaxone : 100mg/kg/d qd or 50mg/kg/d q 12hrs
b.
cefotaxime : 200mg/kg/d q 6hrs
/
¢ÀÃÖ±Ù¿¡´Â PC resistant S. pneumoniae¶§¹®¿¡
vancomycin or rifampin¸¦ ÇÔ²²
»ç¿ë.
- ½ÇÁúÀûÀ¸·Î
24hrÀ̳»¿¡ CSF´Â sterilizationµÈ´Ù.
- ¥â-lactam
antibiotis¿¡ allergic pts
/
CM : 100 mg/kg/24hr div 6hrs
/
¸¹Àº bacteria¿¡
bacteristatic agentÀÌÁö¸¸ H. influensae type b,
S. pneumoniae, N.
/
¢¾Adverse Effect
:
aplastic anemia, shock-like gray infant syndrome,
:
dose depent BM suppression ¡Å
drug moniteringÀÌ ÇÊ¿ä.
- 1-2 MoÀÇ
infant³ª T lymphocyte def. ó·³
L. moncytogenes°¡ ¿øÀαÕÀ¸·Î »ý°¢µÉ ¶§
/
Ampicillin + Ceftriaxone or Cefotaxime
/
Trimethoprime + Sulfamethoxazole IVµµ alternate Tx.
- ¡Úlmmunocompromised
& G(-) bact. meningitis
/
*ceftazidine£«aminoglycoside
Duration Of Antibiotic Theraphy.
#
uncomplicate H. influenzae type B meningitis
; 7 -10 days
; ampicillin¿¡ Àß µè°í,
¥â-lactamase µîÀ»
production ÇÏÁö ¾ÊÀ¸¸é initial AB¸¦
ampicillinÀ¸·Î change
#
penicillin¿¡ relative resistantÇÑ
S. pneumoniae (5¡25%) menigitis
; CM
; ¸¸¾à
C-M¿¡ resistanceÇϸé
vancomycin
# uncomplicated penicillin senstive pneumococcal
meningitis
; penicillin 30ؿU/kg/24hr
#4 for 10-14 days
#
choice for uncomplicated N. meningitidis meningitis
; penicillin 30ؿU/kg/24hr
#4 for *5-7days
#
¡Ø90 causative organismÀ»
¹ß°ßÇÏÁö ¸øÇϰí
CSF»ó bacterial infectionÀÇ
evidence°¡ ÀÖ´Â °æ¿ì
; ceftriaxone, cefotaxime
7-10 days
#
¡Ø82 CT scan Ix
a. focal sign (+)
b. dose not respond to Tx.
c. parameningeal focus may be
present
d. increased head
circumference
e. IICP sign
#
routine repeated LP is not indicated
; ¡ÚLx. Of
Repeat Exam. Of CSF
a.
some neonates
b.
patients with gram (-) bacillary meningitis
c.
not respond to conventional AB Tx. within 48-72hr
#
Improvement of CSF profile (Ä¡·á¿¡ È¿°ú°¡ ÀÖ´Ù°í º¸¿©Áö´Â °æ¿ì)
; *Gram stainÀÌ (+) but sterile
; increased CSF glucose level
; appearance of
lymphocyte-monocyte cells
#
¢ÀG(-) Bacillary Meningitis
; 3ÁÖ µ¿¾È or CSF sterilization 2ÁÖ ÈıîÁö »ç¿ë
; E. coli
-
cefotaxime, ceftriaxone¿¡ ´ëºÎºÐ sensitive
; P. aeruginosa
-
ceftazidine¿¡ ´ëºÎºÐ sensitive
#
Side effect of AB Tx. for meningitis
; phlebitis, drug fever,
rash, emesis, oral candidiasis, diarrhea, reversible gall bladder
pseudolithiasis (ceftriaxone)
Supportive Care
#
Repeated medical and neurological assessment are essential
; identify early sign of
cardiovascular CNS, metabolic complication
#
Neurologic assessment
; frequently *during first 72hr due to
greatest risk of neurologic Cx.
-
ÀÌ ÈÄ¿¡´Â ÇÏ·ç¿¡ Çѹø¾¿ assesment ½ÃÇà
a. pupillary reflex
b.
level of consciousness
c.
motor strength
d.
cranial n.sign
e.
evaluation for seizure
#
Important laboratory studies
a.
BUN
b.
s- Na, Cl, K, HCO3
c.
urine output, SG
d.
complete blood & plt counts
e.
coagulation factor for petechiae, purpura, abn, bleeding
¡Ø96 NPO with ¥³
fluid administration (restricted)
; *1/2¡1/3 of maintenance or
800-1000ml/m2/day
; IICP³ª
SIADH °¡ ¾ø´Ù°í evaluationµÉ ¶§ ±îÁö
-
1,500-1,700 m1/m2/D
; systemic hypotension½Ã
fluid restriction˼ not appropriate
-
¿Ö³ÄÇϸé reduced BP·Î
cerebral perfusion pressure°¡ 50cm H2OÀÌÇÏÀ̸é
subsequient
CNS ischemia°¡ ³ªÅ¸³²
#
Septic shock µ¿¹Ý½Ã
; fluid resuscitation£«vasoactive
agent
(Na-Nitroprusside, dopamine,
epinephrine)
; goal : blood flow³ª
vital signÀ¸·ÎÀÇ O2 delivery¿¡ ¿µÇâÀ» ÁÖÁö ¾Ê°í
IICP ¹æÁö
#
IICP Tx.
; endotracheal intubation
& hyperventilation (PCO2£½25mmHg)
; ¥³
furosemide, Laxis(1mg/kg)
-
intracranial blood valumeÀÇ Áõ°¡ ¾øÀÌ venodilation, diuresis¸¦ ÅëÇØ
brain swelling °¨¼Ò
; mannitol (0.5-1 g/kg)
osmotherapy
-
brain°ú plasma »çÀÌÀÇ
osmolar gradient¿¡ µû¶ó fluid°¡
CNS¿¡¼ plasma·Î À̵¿½ÃÄÑ osmotic diuresis ·Î ¹èÃâ½ÃÅ´.
¡Ø96 Seizures
; diazepam
(0.1-0.2mg/kg/dose) or lorazepam (0.05mg/kg/dose) for immediate control of
seizure
-
diazepamÀÌ respiratory supressionÀÌ
lorazepam º¸´Ù ´õ ³ô´Ù.
; seizure ÀÇ
immediate management ÈÄ phenytoin (15¡
20mg/kg, loading dose, 5mg/kg, maintenance dose)
; to reduce the likelihood of
recurrence
#
¡ÚDexamethasone Tx (0.15mg/kg/dose q 6hrs ¡¿ 4 days)
; AB medication --> rapid
killing of bacteria --> cell lysis·Î toxic producrs»ý¼º
--> cytokine-mediated inflammatory response
; effects
-
less fever
-
lower CSF protein & lactate level reduction
-
reduction in permanent auditory n. damage (sensorineural hearing loss)
; ´ëºÎºÐ
H. influenzae type b¿¡¼´Â °á°ú°¡ ÀÖ¾úÁö¸¸ ´Ù¸¥ organism¿¡¼µµ È¿°ú°¡ ÀÖÀ» °ÍÀ¸·Î »ý°¢µÊ
; »ç¿ë½Ã±â
-
*antibiotics Åõ¿©
Á÷Àü¿¡ Åõ¿©ÇÏ´Â
°ÍÀÌ maximum benefit
; Cx : G-I bleeding,
hypertension, hyperglycemia, leukocytosis, rebound fever after last dose
Prevention
H. Influenzae Type B
#
¡ÚRifampin prophylaxis
; household contacts
-
*close family members less than 4yr
no immunized fully°¡ ÀÖ´Â
°æ¿ì
-
*people who lives in residence of
index case or spent a minimum of 4hr for at least 5 of 7days proceding
hospitalization
-
diagnosis°¡ confirmµÇ¸é Áï°¢ ½Ç½Ã
/
2nd index case°¡ 1st case ÀÔ¿ø ÀÏÁÖÀÏ À̳»¿¡ ³ªÅ¸³¯ È®·üÀÇ
50% ÀÌ»óÀ̱⠶§¹®
; day-care center contacts
-
less risk than houshold contacts
-
*2 or more index case and not fully
immunized children under 2yrÀÌ ÀÖ´Â
°æ¿ì
-
*>25hr/wk of close contact
; Dose
-
*20mg/kg/24hr once each day for 4
days (max. 600mg)
; Rifampin is contraindicated
to pregnancy
;
S/E - discolors the urine, swear red orange, stains contact lenses, reduce the
serum concentrations of some drug
N. meningitidis
; ¡Ø83ÁÖ
age³ª immunization ¿©ºÎ¿¡
°ü°è¾øÀÌ ¸ðµç
meningococcal meningitis¿Í Á¢ÃËÇÑ »ç¶÷¿¡
prophylaxis ÇØ¾ß ÇÔ
; *rifampin 20mg/kg/dose #2 for 2 days (max. 600mg)
; vaccine
-
meningococcal quadrivalent vaccine for serogroups A, C, Y and W135
- Indication
/
*2¼¼ÀÌ»óÀÇ high
risk children
:
*asplenia, functional splenic
dysfunction, terminal complement protein deficiency
Streptococcus pneumonia
; normal host´Â
chemoprophylaxis¿Í vaccination°¡ ÇÊ¿ä¾ø´Ù
;
high risk patiens´Â 23-valent pneumoccal vaccineÇÊ¿ä
;
sickle cell anemia pt´Â chemoprophylaxisÇÊ¿ä
( PC, Amx, Bactrim )
Prognosis
#
mortality rate in neonatal period
; 1-8%
; highest mortality rate in pneumococcal
meningitis
#
severe neurodevelopmental sequele ; 10-20%
#
albeit subtle, neurobehavioral morbidity ; 50%
#
¡Ø89 Poor Prognostic Sign
; < 6 mo
; >106 CFU /ml
in CSF
; seizures more than 4days
into therapy
; coma or focal neurologic
sign on presentation
#
*Áø´Ü ÀüÀÇ SxÀÇ duration°ú outcome°ú´Â ¹«°ü
4)
neurologic sequele
; hearing loss (sensorineural
hearing loss), mental retardation, seizure, delay in acquisition of language,
behavioral problem, visual impairment
; sensorineural hearing loss
-
¡ã of bacterial meningitis
- cause
/
labyrinthitis following cochlear infection
/
direct inflammation of auditory N
-
ºóµµ
/
peumococcal menigitis : 30 %
/
menigococcal menigitis : 10 %
/ H.
influenza type b menigitis : 5 ¡ 20 %
-
Dexamethasone »ç¿ëÀÌ severe hearing loss incidence¸¦ °¨¼Ò½ÃŲ´Ù
- dischargeÀü¿¡ ²À audiologic assesment
169.2 Viral Meningoencephalitis
;
menigitis¿Í brain tissue¿¡
acute inflammatory process
;
CSF : pleocytosis
;
absence of microorganisms on Gram stain and Routine culture
;
self limited ÀÌÁö¸¸ some case¿¡¼
substantial morbidity¿Í mortality°¡ °üÂû
Etiology
;
seasonal pattern (+)
;
*enterovirus ( 80 % ÀÌ»ó)
;
arbovirus, herpes virus ( common )
;
Mumps ( vaccineÀÌ »ç¿ëµÇÁö¾Ê´Â Áö¿ª¿¡¼ common )
Epidemiology
;
´ëºÎºÐÀÌ enterovirus¿¡ ÀÇÇØ ¾ß±âµÇ¹Ç·Î
basic epidermiologic patternÀº prevalence¸¦ ¹Ý¿µÇÑ´Ù
;
person to person spread
;
IP : 4 ¡ 6 days
;
most case in temperate climates occur in the summer and fall.
Common Pathogen
1)
arbovirus
; infected accidentally by an
arthropod vector mosquito or tic (varemia)
; insect vector
2)
enterovirus
; small RNA containing virus
; aseptic meningitis - severe
encephaltis, death
;
epidermics - newborns in nurseries
3)
herpesvirus
a. hespes simplex type 1
& 2
;
HSV-1
-
severe, sporadic encephalites in children, adult
-
brain involvement : focal
-
antiviral Tx(-) ; 70 % ¿¡¼ coma, death
;
HSV-2
-
neonate ; diffuse brain involvement¸¦ °¡Áø severe encephalitis
-
delivery½Ã mother·Î ºÎÅÍ
virus
b. varicella zoster virus
(VZV)
;
chicken pox¿Í ÀϽÃÀûÀ¸·Î, ¹ÐÁ¢ÇÏ°Ô °ü·ÃµÈ
acute encephalitis ÀÏÀ¸Å´
; *most common
manifestation - cerebellar ataxia, acute encephalitis
;
spinal & cranial nerve root¿Í ganglia Â÷´Ü
-
³ªÁß¿¡ hespes zosterÀÇ ÇüÅ·Π³ªÅ¸³²
c. cytomegalovirus (CMV)
;
congeital infection or compromised hosts¿¡¼ disseminated
disease
; normal infant , children : not
d. Ebstein-Barr virus (EBV)
;
myriad of CNS syndromes¿Í °ü°è ( see chapter 215 )
e. respiratory virus,
Rubella, Rubeolar¿¡ ÀÇÇØ¼µµ meningoencephalitis¾ß±â
f. Mumps meningoencephalitis
: mildÇÏÁö¸¸ µå¹°°Ô 8¹ø
CN¿¡ damage¸¦ ÁÖ¾î
deafness ¾ß±â
Pathogenesis And Pathology
1)
ingestion of enterovirus ¡æ lymphatics(multiplication) ¡æ mosquito or insect bite
¡æ to blood stream(seeding) :
hematogenous spread
¡æ several organ infection(further
viral multiplication)
¡æ secondary propagation of large
amounts of virus
¡æ CNS invasion
¡æ neurologic disease evidence (+)
2)
neurologic damage is caused
a. direct invasion and
destruction of neural tissue
by actively multiplying virus. : direct neural destruction
b. viral Ag¿¡ ´ëÇÑ
host reaction
: demyelinization, vascular and perivascular destruction
¡ç host's vigorous tissue response°¡
induced
: ´ëºÎºÐÀÇ neural destructionÀº ¾Æ¸¶
direct viral invasion¿¡ ÀÇÇØ ¾ß±â
3) brain tissue secretion
<-- meningeal
congestion and mononuclear infilteration, perivascular cuffs of lymphocytes and
plasma cell myelobreakdown À» °¡Áø perivascular tissue necrosis
various
stage¿¡¼ neuronal disruption --->
neuronophagia, endothelial proliperation, necrosis.
4)
marked demyelinization £« preservation of nurons &
their axon
"postinfections" or
"allergic" encephalitis
5)
cbr cortex
a. Temporal lobe : severely
affected by Herpes
virus (intranuclear inclusion bodies)
b. entire brain : Arbovirus
c. basal structure : Rabies
(Negri bodies)
d. spiral cord, nerve roots, peripheala
nerve : vaiable
Clinical Manifestation
#
¢¾Specific Form Or Complicating Manifestations Of Encephalitis
; Guillain-Barre Syn.
; Acute transverse myelitis
; Acute hemiplegia
; Acute cerebellar ataxia
#
progression, severityÀÇ Á¤µµ´Â meningeal and parenchymal
invovementÀÇ Á¤µµ¿Í agent¿¡ ÀÇÇØ °áÁ¤
#
illness˂ onset˼
acuteÇϰí CNS Sx°ú
signÀº ¸îÀϵ¿¾ÈÀÇ nonspecipic acute
febrile illness µÚ¿¡ ¿Â´Ù
#
headache, hyperesthesia : common sx, focal or generalized
#
aldolesence : retrobulbar pain, fever, nausea, vomiting, neck pain, back pain,
leg pain, photophobia, exanthemÀÌ CNS sign°ú µ¿¹ÝµÇ¾î ³ªÅ¸³ª±âµµ
ÇÑ´Ù
( ƯÈ÷ echovirus,
coxachivirus, VZA, mealses, rubella )
Laboratory Abnormality And Diagnosis
1) CSF. : in viral encephalitis
¨ç
color : clear
¨è
leukocyte : 0 - several thousand
¨é
cell type : PMNL (initial) ¡æ Monocyte ( 8 ¡
12 hr ÈÄ )
¨ê
protein : N to slight¡è ¡æ brain destructionÀÌ
extensiveÇϸé high : HSV encephalitisÀÇ
late stage ¿¡.
¨ë glucose : N
( Mumps µî ÀϺο¡¼´Â substantial depression
of CSF glucose concentration )
2)
serum specimen´Â illnessÀÇ
early¿¡ ¾ò¾îÁ®¾ß Çϰí viral culture°¡
not diagnoticÇÏ´Ù¸é
2-3wksÈÄ¿¡ ´Ù½Ã serologic study¸¦ ÇØ¾ßÇÑ´Ù
<½Å>3)
serologic method´Â too many potential serotypes¸¦ °¡Áø
enterovirusÀÇ idenfication¿¡´Â
not practicalÇÏÁö¸¸
known
circulating viral type¿¡ ÀÇÇØ ¾ß±âµÈ caseÀÇ
confirm¿¡ È¿°úÀûÀÌ´Ù . ( nonenteroviral CNS
infection )
<½Å>4)
PCR: new technique
not yet clinically available
<½Å>5)
electroencehalogram
neuroimaging studies
Diagnosis And Differential Diagnosis
bacterial
infection ; mc ( H. influenza type b, S. peumoniae, N, meningitis )
other : Tuberculosis,
T. pallidum ( syphilis )
Borralia burgdorferi ( Lyme disease )
bacillus associated with cat-scratch ds
parameningeal
bacterial infection : similar to viral CNS infection
: brain absess, subdural or epidural empyema
nonbacterial
infectious agents : rickettsia, mycoplasma, protoza, fungus
CNS
inflammation : malignancy, collagen-vascular disease, intracranial hemorrhage,
drug, toxin
Prevention
polio,
meales, mumps, rubella ÀÇ attenuated viral vaccineÀÌ
effective
Rabies¿¡ ´ëÇÑ
domestic animal vaccine programÀÌ rabies encephalitisÀÇ
frequency¸¦ ³·Ãá´Ù
Arbovirus¿¡ ´ëÇÑ
vaccine˼ less successful
<½Å> insect vectorÀÇ
conrolÀÌ À̵é incidenc¸¦
reduce
Treatment
;
bacterial cause°¡ excludeµÇ±â Àü¿¡
parenteral antibiotics therapy°¡ administeredµÇ¾î¾ß ÇÑ´Ù
;
Herpes simplex encephalitis¿¡
acyclovir»ç¿ëÀ» Á¦¿ÜÇϰí´Â viral
meningoencephalitisÀÇ tx´Â nonspecificÇÏ´Ù
3)
mild infection ; symptomatic relief
severe infection ; maintaining life and
supporting organ system
4) +- headache, hyperesthesia ; rest
|
non-aspirin containing analgesics
|
room
light ¡é
|
noise, visitor ¡é
| fever : acetaminophen
+- pain, vomiting ; codein, morpine,
phenothiazine derivatives
¡æ °¡´ÉÇÏ´Ù¸é
children¿¡¼ sign, sxÀÇ
misleadingÀ» ³ªÅ¸³¿À¸·Î À̵éÀÇ
»ç¿ëÀ» ÃÖ¼ÒÈÇÏ¿©¾ß
ÇÑ´Ù
5)
all patient with severe encephalitis sould be monitored carefully
6)
intracranial pressuree monitoring Ix
IICP
evidence (+)
epidural
spaceÀÇ pressure transduderÀÇ
placement (+)
7)
all fluid, electrolyte medication˼ parenterally
8)
glucose, Mg, Ca : must be maintained : seizure ¡é
9)
supportive and rehabilitative effort : very important after recovery
* motor incordination, convulsive
disorder, squint, total or partial deafness, behavioral disturbance°¡ °ð ³ªÅ¸³´Ù.
10)
visual disturbance ; d/t chorioretinopathy and perceptual amblyopia
; delayed appearance
11)
viral meningoencephalities¿¡¼ recoveryÈÄ
grossly normal ÀÏÁö¶óµµ neurodevelopmental
and
audiologic evaluationÀº ¹Ýµå½Ã routine follow up ÇØ¶ó
Prognosis
most
children completely recover
px
: º´ÀÇ severity, speicfic etiology, age¿¡ ÀÇÁ¸
severeÇÑ case¿¡¼
substantial parenchymal involvementÀÇ evidence°¡ ÀÖ´Ù¸é
px´Â poor Çϰí
intellectual, motor, psychiatric, epileptic, visual. auditory deficiiy°¡ ¿Ã ¼ö ÀÖ´Ù.
severe sequelae : HSV ¿¡¼ ¿¹°ß
infant¿¡¼
older childrenº¸´Ù poor long-term outcome
; ÃÖ±ÙÀÇ data´Â ¾î·±
observationÀ» ³í¹ÚÇÑ´Ù
±×·¯³ª enteroviral CNS
infectionÀ» °¡Áø 2¼¼ÀÌÇÏÀÇ patientsÀÇ ¾à
10 %¿¡¼ seizure, IICP, coma µî
long term neurologic outcomes¸¦ °¡Áø´Ù.
Chapter 170. Pneumonia
#
non-infectious cause
¨ç
aspiration of food and/or gastric acid
¨è
foreign bodies
¨é
hydrocarbons
¨ê
lipoid substance
¨ë
hypersensitive reaction
¨ì
drug or radiation induced peumonitis
#
the common microbiologic cause
1. resp. viruses
:
TMC cause of pneumonia during first several years of life
2. mycoplasma pneumonia
:
predominant role in the school age & old child
3. selected bacteria
- ¼ýÀûÀ¸·Î´Â
Áß¿äÇÏÁö ¾ÊÀ½
-
more severe inf.
-
most common bacteria
¨ç Streptococcus pneumoniae
¨è S. pyogens
¨é Staphylococcus aureus
¨ê Haemophylus influenza type b
-
use of effective vaccines
--> less common with the widespread
#
less common cause
¨ç
non-respiratory viruses
¨è
enteric Gram negative bacteria
¨é
Mycobacteria
¨ê
Chlamydia spp.
¨ë
Rickettsia spp.
¨ì
Coxillea
¨í
Pneumocyst carinii
¨î
fungus
#
anatomic classification
¨ç
lobar
¨è
lobular
¨é
alveolar
¨ê
interstitial
Pneumonias Of Viral Origin
Etiology
#
¡ÚCommon Viruses
;
Respiratory syncytial virus (RSV)
;
parainfluenza viruses 1, 2, 3
;
influenza viruses
;
adenoviruses 3, 4, 7
#
type & severity of illness
: age,
sex, season, crowding ¿¡ ÀÇÇØ ¿µÇâ
¨ç
peak age
bronchiolitis --> 1¼¼ ÀÌÇÏ
viral pneumonia --> 2-3¼¼
¨è
boy¡è
¨é
winter¡è
Clinical Manifestation
1. rhinitis, cough
temp.¡é than bacterial pneumonia
tachypnea with intercostal, subcostal, supracostal retraction
nasal flaring
severe inf.-->cyanosis & respiratory fatigue
2. P/Ex.
: rale &
wheezing
Diagnosis
1. X-ray (Fig 170-1)
¨ç
diffuse infiltrate in perihilum
¨è
transient lobar infiltrate
¨é
hyperinflation
2. WBC
:
sl. elevated (< 20.000), lymphocyte predominant
3. ESR, CRP
:
normal or sl. elevated
4. Definite Dx.
:
isolation of virus --> tissue culture (5-10 days)
5. Serologic test
- antibody to specific viral antigen ¡è
- ¿ªÇÐÀû µµ±¸·Î »ç¿ë
Treatment
1.
supportive Tx.
2.
some patients --> hospitalization
: IV fluid, oxygen, assisted
ventilation
3.¡Ø96
oral amantadine ( or rimantadine)
¨ç influenza A -->
prevention & Tx
¨è inf. ÀÇ
onset 48hr³» »ç¿ëÇØ¾ß È¿°ú
4.
aerosolized ribavirin
¨ç RSV
¨è expensive
Prognosis
1. most children -->
recovery with no sequelae
2. Cx.
¨ç
bronchiolitis obliterans
¨è
unilat. hyperlucent lung
¨é
fatal acute fulminant pneumonia
-
adenovirus 1, 3, 4, 7, 21ÀÌ °¡Àå À§Çè
Bacterial Pneumonia
General consideration
;
*not a common infection
;
¡Ø89 TMC event disturbing the
defense mechanism of lung
-
viral inf.
¨ç normal secretionÀÇ ¼º»ó º¯È
¨è phagocytosisÀúÇØ
¨é modifies bacterial flora
¨êresp.
passageÀÇ normal epithelial layer¸¦
disrupt
- ¼öÀϳ» Á¾Á¾
bacterial pn.·Î ÁøÇà
;
*Recurrent pneumonia
¨ç
abnormalities of Ab production (e.g. agammaglobulinemia)
¨è
cystic fibrosis
¨é
cleft palate
¨ê
cong. bronchiectasis
¨ë
ciliary dyskinesia
¨ì
TEF
¨í
abnormalities of PMNL
¨î
neutropenia
¨ï
pul. blood flow ¡è
¨ð
deficient gag reflex
¨ñ
iatrogenic factor --> trauma, anesthesia, aspiration
Pneumococcal Pneumonia
# S. pneumoniae ==> TMC
cause of bacterial inf. of the lung
1)
Pathology & Pathogenesis
1. upper airway or
nasopharynx --> periphery of the lung
2. reactive edema
¨ç
support proliferation of the organism
¨è
aid inspread into adjacent portion
3.
one or more lobe, part of lobes --> involve
cf)
bronchopulmonary system --> uninvolved
# infant
¨ç lobar pn. --> µå¹³
¨è bronchial distributionÀ» µû¶ó¼
patchy or diffuse ds.
¨é small airways ÁÖÀ§·Î
limited area consolidation
2)
Cl/m
: shaking chill, high
fever, cough, chest pain in older children
1. Infants
a. mild URI Sx.
for several day (stuffy nose, fretfulness, appetite ¡é)
--> abrupt high fevr 39¡É ¡è, restlessness,
apprehension
--> respiratory distress
:
grunting, flaing of alae nasi,
retraction of supraclavicular, intercostal, subcostal area,
tachypnea, tachycardia
--> air hunger & cyanosis
b. P/E
¨ç dullness, B/S¡é,
fine & crackling rale <-- affected side
¨è abd. distension : reflecting
gastric dilatation or ileus
liver enlargement : Rt. diaphragm downward displacement
superimposed cong. heart failure
menigismus : esp. RUL pn.½Ã
¨é physical findingÀº
illnessÀÇ clinical courseµ¿¾È Àß º¯ÇÏÁö ¾Ê´Â´Ù.
2. Children & Adolescents
a. brief mild
URI
¨ç shaking chill, 40.5¡É
fever
¨è drowsiness with intermittent
restlessness
tachypnea,
dry, hacking unproductive cough
anxiety, delirium
circum-oral cyanosis
splinting on the affected side
knee drawn up to the chest
lie on affected side
b. P/Ex. :
change during the course of illness
¨ç classic Sg. of consolidation
(2-3day)
- dullness, fremitus¡è, tubular B/S, disappearance of
rales
¨è resolution
- moist rales, productive cough with blood tinged mucus
¨é pleural effusion or empyema
+-¥¡) visible lag in respiration on
affected side
|
with excursion¡è on opposite site
| ¥¢) dullness over area of effusion
| ¥£) fremitus & B/S ¡è
+-¥¤) tubular breathing above fluid
level & unaffected side
3)
Lab/F
a. ¨ç
WBC : 15.000-40.000 (PMNL¿ì¼¼)
cf) WBC 5.000ÀÌÇÏ --> poor Px.
¨è Hb. : normal or sl. decreased
¨é ABGA : hypoxemia without
hypercapnea
b. isolation of
pneumococci
¨ç
nasopharyngeal secretion
cf) 10-15% of population --> uninfected carrers of S. pneumoniae
¨è
pleural fluid from thoracentesis --> diagnostic
¨é
bactetemia : 30% in pneumococcal pn.
4)
X-ray finding (fig 170-1, 170-2)
¨ç
lobar consolidation : infant or young children¿¡¼´Â rare
¨è
pleural reaction with fluid
¨é
X-ray»ó complete resolution
: 3-4wks after disappearance of all Sx.
5)
DDx.
1. other bacteria and viral
pn.
2. pneumona¿Í È¥µ¿ÇÒ ¼ö ÀÖ´Â
condition
¨ç bronchioliotis
¨è CHF
¨é bronchiectasisÀÇ ¾ÇÈ ¨ê FB aspiration
¨ë sequestered lobe ¨ì
atelectasis
¨í pulmonary abscess ¨î
allergic bronchitis
3. RLL pn.¸¦ °¡Áø
old children
--> diaphragmatic irritaton
--> reffered pain to the RLQ
--> acute appendicitis¿Í È¥µ¿
4. severe meningismus
--> meningitis¿Í È¥µ¿
6)
Cx.
1. concomitant pneumococcal
inf. & metastatic inf
--> infrequent
2. empyema --> infant
7)
Px.
1. preantibiotic era
¨ç mortality rate
- infant & small children : 20-50%
- older children : 3-5%
¨è high incidence chronic empyema
2. ÀûÀýÇÑ
antibiotics Tx.
- mortality rate : 1% ÀÌÇÏ
8)
Tx.
1. drug of choice
: Penicillin 10¸¸unit/kg/24hr
2. decision of
hospitalization
¨ç severity of illness
---+ ¿¡ ÀÇÁ¸
¨è ability of family to supply good
nursing care --+
¨é young infant
: hospitalization
¥¡) for IV fluid & antibiotics
¥¢) cilnical course --> more
variable
¨ê pleural effusion or empyema
3. oxygen with resp.
distress
¨ç sedatives & analgesicsÀÇ ÇÊ¿ä °¨¼Ò
¨è cyanotic change°¡ ¿À±âÀü¿¡ °ø±Þ
Strptococcal Pneumonia
;
Gr. A streptococci
;
uncommon but predisposing state Á¸Àç
- epidemic influenza,
exanthemµî
;
*3-5¼¼ more frequent
;
*rare in infant
Pathology
1.
lower respiratory infection : tracheitis, bronchitis, interstitial pneumonia
2.
lobar pn.´Â µå¹³
3.
*pleurisy ; ºñ±³Àû
ÈçÇÔ
--> serous, thinly
purulent, fibrin¡é
4.
lesion
¨ç
necrosis of tracheobronchial mucosa
¨è
formation of ragged ulcer
¨é
large exudate
¨ê
edema
¨ë
localized hemorrage
Clinical Manifestation
;
pneumococcal pn.¿Í À¯»ç
;
sudden
;
*high fever, chills, sg of
respiratory distress
;
at times, extreme prostration
Laboratory Finding
1.
leukocytosis
2.
ASLO Áõ°¡
3.
*organism culture from pleural
fluid/blood/lung aspirate --> definite Dx.
4.
bacteremia : 10%
5.
chest X-ray
¨ç
diffuse bronchopneumonia
¨è
often large pleural effusion
6.
*complete resolution : 10ÁÖ
ÀÌ»ó
Differential Diagnosis
¨ç
staphylococcal pn.
¨è
mycolasma pn.
Complication
¨ç *empyema : 20%
¨è
septic foci on bone, joint
Treatment
; *Penicillin 10¸¸unit/kg/24hr iv for
2-3wk
--> oral after clinical improvement
;
empyema --> thoracentesis
Staphylococcal Pneumonia
;
*rapid progressive inf. with
prolonged morbidity & high mortality
;
*more common in infant
Epidemiology
;
viral URI ¼±Çà
;
*30%°¡ 3°³¿ù ÀÌÇÏ, 70%°¡ 1¼¼
ÀÌÇÏ
;
male ¡è
Pathogenesity & Pathology
¨ç confluent bronchopneumonia
¨è unilat. or prominent on one side
¨é extensive area of hemorrhagic
necrosis & irregular cavitation
¨ê multiple abscess
; rupture of small subpleural
abscess
-->
pyopneumothorax
--> *bronchopleural
fistula
Clinical Manifestation
1)
Sx.
¨ç 1¼¼ ÀÌÇÏ
: staphylococcal skin lesion ¶Ç´Â resp tr. infÀÇ
Sx & Sg
¨è abrupt high fever,
cough, resp. distress
;
if undisturbed, lethergic, irritable, toxic --> severe dyspnea, shocklike
state
¨é GI disturbance with
vomiting, anorexia, diarrhea, abd. distention
==> *rapid progressionÀÌ Æ¯Â¡
2)
P/Ex.
; early : diminished B/S,
scattered rale, rhonchi
-->
affected lung
;
effusion, empyema, pyopneumothorax, dullness on percussion
; marked diminished B/S &
vocal fremitus
; lag in resp. excursion on
affected side
; * young infant¿¡´Â tachypneaÁ¤µµ¿Í
¸ÂÁö ¾Ê´Â
ºó¾àÇÑ ¼Ò°ß¶§¹®¿¡ misleading °¡´É
Laboratory Finding
1.
WBC Áõ°¡
; *2¸¸ÀÌ»ó -- older infant &
children
; *normal WBC in young infant
;
5.000 ÀÌÇϽà --> poor Px.
2.
culture by tracheal aspiration, pleural tap, blood --> diagnostic
3.
mild to moderate anemia
4.
pleural fluid
¨ç
exudate with PMNL 300- 100,000/mm3
¨è
protein : 2.5g/dl ÀÌ»ó
¨é
low glucose (blood¿¡ ºñÇØ)
Roentgenographic manifestation
1.
Ãʱâ
; nonspecific
bronchopneumonia
-->
*soon, patch infiltrate and limited
extent or dense, homogeneous and involve entire lobe or hemithorax
; *Rt. lung : 65%
; bilat. - 20%ÀÌÇÏ
2.
pleural effusion or empyema
3.
pyopneumothorax
4.
pneumatocele
; *clinical improvement procede X-ray finding
; *persist for months
#
¢Þover a few hrs, progression from
bronchopn. to effusion or pyopneumothorax with/without pneumatocele
--> suggestive staphylococcal pneumonia
Differential Diagnosis
1.
early stage pneumonia´Â DDx.Çϱâ Èûµë
2.
¡ÚPossibility Of Dx.
;
abrupt onset & rapid progression of Sx.
;
Hx. of frunculosis
;
recent hospital admission
;
maternal breast abscess
3.
¢¾Empyema or pneumatocele À» ÃÊ·¡ÇÏ´Â bacterial pneumonia
¨ç
staphylococcus
¨è
streptococcus
¨é
klebsiella.
¨ê
H. influenza
¨ë
pneumococcal pneumonia.
¨ì
1¡ÆTb pneumonia with cavitation
¨í
aspiration of nonopaque FB --> pumonary abscess
¡Ø93ÁÖComplication.
;
empyema, pyopneumothorax, pneumatocele
-
natural course·Î »ý°¢Çϱ⵵ ÇÑ´Ù.
; *sta. pericarditis, meningitis, osteomyelitis, multiple metastatic
abscess
; ÇÑ±ÛÆÇ
(p503)
-
Æó³ó¾ç, ³óÈä, ±â°üÁö È®ÀåÁõ,
ÁßÀÌ¿°, ºÎºñµ¿¿°, ½É¸·¿°,
ÆÐÇ÷Áõ, ³ú¸·¿°, °ñ¿°,
º¹¸·¿°, »êÁõ, ³úÁõ
Prognosis
1.
mortality 10-30%
; ¡Ø91
varies with
¨ç
length of illness prior to hospitalization
¨è
age of pt.
¨é
adequacy of Tx.
¨ê
other illness or Cx.
2.
course : 6-10ÁÖ°£ ÀÔ¿ø
Treatment
-
antibiotcs & drainage
-
oxygen, semireclining position
-
acute phase : IV hydration & nutrition
-
blood transfusion, assist ventilation
1.
¢¾semisynthetic penicillinase-resistant PC (naficillin
200mg/kg/24hr)
; IV immediately after
culture (reportÀü±îÁö)
2.
¡Ø94 chest tube drainage
; *even if small effusion or empyema
;
BPF °¨¼Ò, repeated pleural tapÀÇ Çʿ伺 °¨¼Ò
; largest caliber »ç¿ë
; *pyopneumothorax½Ã Áï°¢
; removal
-
*improvement & lung expansionµÇ±â
½ÃÀÛÇϸé Á¦°Å(ºñ·Ï ¼Ò·®ÀÇ pus°¡ drainµÇ´õ¶óµµ)
- *5-7ÀÏÀÌ»óÀº
ÇÏÁö ¾ÊÀ½
Haemophilus influenza Pneumonia
;
nasopharyngeal infÈÄ
--> epiglottitis, pneumonia,
meningitis
;
pneumonia : second in frequency
;
*winter - spring
Clinical Manifestation
;
*usually lobar pneumonia
;
*Ư¡ÀûÀÎ X-ray
finding¾øÀ½
¥¡) segmental infiltrate
¥¢) single or multiple
lobe involvement
¥£) pleural effusion,
pneumatocele
¥¤) disseminated pul. ds.
& bronchopn.
;
male ¡è
;
*more insidious in onset
;
*course is usually prolonged over
several weeks
;
febrile, tachypnea with nasal flaring & retraction
;
P/Ex
¥¡)
rale & tubular B/S
¥¢)
localized dullness on pucussion
;
pathology
¨ç PMNL or lymphocytic
infl.
¨è extensive dustruction
of epithelium of small airway
¨é interstitial infl.
¨ê marked or hemorrhagic
edema
Differential Diagnosis
;
Dx. --> isolation of organism from blood, pleural fluid & lung aspirate
;
mod. leukocytosis with relative lymphopnea
;
*latex agglutination test of urine
-
absence of positive cultureÀ϶§ À¯¿ë
;
if atelectasis --> bronchoscopy·Î FB rule out
Complication
;
frequent in young infant
¨ç
bacteremia
¨è
pericarditis
¨é
cellulitis
¨ê
empyema
¨ë
meningitis ( # CSF exam.ÀÌ H. influenza pn.Áø´Ü½Ã ²À °í·ÁµÊ
)
¨ì
pyoarthrosis
Treatment
;
ampicillin (100mg/kg/24hr), CM (100mg/kg/24hr) or ceftriaxone (100mg/kg/24hr)
--> initial
;
sensitive°¡ ³ª¿À¸é ampicillin´Üµ¶ °¡´É
;
¥¡) needle aspiration or closed
chest drainage
--> *initial AB¿¡
¹ÝÀÀÀÌ ÁÁÀ¸¸é oral Tx. for 10- 14days
¥¢) open drainage -->
infrequently need
;
X-ray »ó complete resolution : 2-4ÁÖ
Carpter 171. Gastroenteritis (Àüü chapter°¡ »õ·Î »ý±è)
#
Clinical manifestation
; organism°ú
host¿¡ ÀÇÁ¸
#
Presumptive Etiologic Diagnosis
¨ç epidemiologic clue
¨è clinical menifestation
¨é physical exam.
¨ê knowledge of the
pathophysiologic mechanism of enteropathogen
#
¡ÚTwo Basic Type Of Acute Infectios Diarrhea
1) inflammatory diarrhea by bacteria
¨ç
invade the intestine directly
¨è
produce cytotoxin
2) noninflammatory diarrhea
¨ç
enterotoxine production by some bacteria
¨è *destruction of villus
cell by virus
¨é
adherence and/or translocation by bacteria
#
¡ÚƯ¡
¨ç most self limited
--> lab/study°¡ ºÒÇÊ¿äÇÑ °æ¿ì°¡ ¸¹´Ù.
¨è all patients require
fluid & electrolyte treatment
¨é a few patients -->
antimicrobial Tx.
Epidemiology
#
Major Mechanism Of Transmission For Diarrheal Pathogen
;
fecal-oral ( vehicles : food, water )
#
¡ÚSmall InoculationÀ¸·Î Inf.µÇ´Â Enterpathogen
--> person-to-person contact
¨ç shigella
¨è enteric viruses
¨é G. lambria
¨ê cryptosporidium
¨ë E-coli 0157:H7
#
Factors Rhat Increase Susceptibility To Infection
; young age, immune
deficiency, measles, malnutrition, travel to the endemic area, lack of breast
feeding, exposure to unsanitary codition, ingestion of contaminated food or
water, level of maternal education, day care center attendance
Causative agents
Table 171-1
#
chronic or persistent diarrhea
; lasting 14days or longer
; due to
¨ç
infectious agent
-
G. lambria, Cryptosporidium, enteroaggregative or enteropathogenic E coli
¨è
any enteropathogenic inf. of immunocompromised host
¨é
residual symptom due to damaged intestine
Table 171-2 Noninfectious Causes Of Diarrhea
Bacterial Enteropathogen
1. inflammatory diarrhea
¨ç Aeromonas spp.
¨è Campylobacter jejuni
¨é Closstridium difficile ¨ê
enteroinvasive E coli
¨ë enterohemorrhagic E coli ¨ì Plesimonas
shigelloides
¨í salmonella spp
¨î shigella spp.
¨ï Vibrio parahemolyticus. ¨ð
Yersinia enterocolitica
2. noninflammatory
diarrhea
¨ç enteropathogenic E coli
¨è enterotoxigenc E coli
¨é V cholerae
# Antimicrobial TxÀÇ ¸ñÀû
¨ç shorten the clinical course
¨è causative agent ÀÇ secretion °¨¼Ò
¨é complication °¨¼Ò
Table
171-3
Parasitic Enteropathogen
1. Á¾·ù
¨ç G. lambria --> TMC in U.S.A
¨è Cryptosporidium
¨é Entameba hystolytica
¨ê Strongyloides stercoralis
¨ë Isospora belli-----------------+
AIDS¿¡¼ ¹ß°ß
¨ì Enterocytozoon bieneusi ------+
2. Stool¿¡¼
parasite, ova exam.ÀÇ Ix.
¨ç Hx. of recent travel to endemic
area
¨è other enteropathogen¿¡ ´ëÇÑ
stool culture --> negative
¨é 1 wk. ÀÌ»ó Áö¼ÓµÇ´Â
diarrhea
¨ê immunocompromised Pt.
3. Tx. --> Table
171-4
Viral enteropathogen
¨ç rota V
¨è enteric adenoV
¨é astrovirus
¨ê calicivirus
General approach to childhood
A) Sx & Sg
1. GI tract involvement
: diarrhea, cramps & emesis
2. systemic manifestation
: fever, malaise, seizure
3. extraintestinal inf.
a)
local spread
: vulvovaginitis, UTI, keratoconjunctivitis
b)
remote spread
: endocarditis, osteomyelitis, meningitis, pneumonia, hepatitis,
peritonitis,
chorioamnionitis, soft tissue inf. & septic thrombophlebitis
4. immune-mediated
extraintestinal manifestation
--> Table 171-5
: º¸Åë diarrhea ÇØ¼ÒÈÄ ÀϾÙ
B)
Main objectives in the approach to a child with acute diarrhea
¨ç
degree of dehydration --> fluid & electrolyte Tx.
¨è
prevent spread of enteropathogen
¨é
determine the etiologic agent & provide specific therpy
# Table 171-6
Exam. of stool
1. exam for mucus, blood,
leukocyte
--> colitis
# fecal leukocyte
¨ç colonic mucosa¸¦
diffuseÇÏ°Ô invasion
¨è invasive or cytotoxine producing
organism
2. stool culture
a) °¡´ÉÇÑ
diseaseÃʱ⿡ ½ÃÇà
#
Hemolytic uremic syndrome
¨ç blood diarrhea
¨è fecal leukocytes
¨é immunocompromised Pt.
3. modified Lab. procedure°¡ ÇÊ¿äÇÑ °æ¿ì
¨ç Y. enterocolitica ¨è
V parahemolyticus
¨é V cholera ¨ê
Aeromonas
¨ë C. difficle
¨ì Comphylobacter
4. serologic & toxin assay
--> E coli subtype
5. C difficile toxin -->
diagnosis of antimicrobial- associated colitis
6. Proctosigmoidoscopy
¨ç
colitisÀÇ Sx. ÀÌ ½ÉÇÒ ¶§
¨è inflammatory enteritis
synd.
Management Of Fluid, Electrolyte & Refeeding
#
children
; more suseptible than adult
to dehydration
¨ç
assess the degree of dehydration
¨è ongoing loss
¨é daily requirement
Oral Hydration
; Tx. of choice
1. Home remedies
:
decarbonated soda beverage, juices, tea µî --> not suitable
¨ç ºÎÀûÀýÇÑ high osmolality -->
diarrhea ¾ÇÈ
¨è low sodium conc. -->
hyponatremia
¨é inappropriate carbohydrate to
sodium ratio
2. maintenance sol.
--> Table 171-7
3.
rehydrationÈÄ --> refeeding ½Ãµµ
breast
feeding Àº °¡´ÉÇÑ »¡¸® ½ÃÇà
Antidiarrheal Compound
#
classification by their mechanism
¨ç alteration of
intestinal motility
¨è adsorption of fluid or
toxin
¨é alteration of
intestial micreflora
¨ê alteration of fluid
& electrolyte solution
Prevention
¨ç
handwashing, gown -> soiling, glove
¨è
education to patient & their family
¨é
seperation
Acute Foodborne & Water-Borne Diseases
# major cause of
morbidity & mortality in all developed country
1. diagnosis
¨ç °øÅëÀÇ À½½ÄÀ̳ª ¹°À» ¸ÔÀº »ç¶÷µé¿¡¼ À¯»çÇÑ acute illness
¨è nausea, emesis, diarrhes,
neurologic Sx.
2. pathogenesis &
severity of bacterial diseaseÀÇ ÀÇÁ¸ÀÎÀÚ
¨ç toxinÀ» »ý¼ºÇÏ´Â
organism (S. aureus, B. cereus)
¨è »ý¼ºµÈ
toxin
¨é invasive ¿©ºÎ
¨ê À½½Ä³» replication
3. severity of disease
due to viral, parasitic, chemical cause
--> food, water¸¦ ÅëÇØ inoculation µÇ´Â ¾ç¿¡ ÀÇÁ¸
4.
¨ç
epidemiology·Î specific agent ÀǽÉ
¨è
incubation period & clinical synd. --> DX
¨é
specific Lab. testing --> confirm
5. grouped by
incubation period (Table 171-8)
a) 1hr À̳» IP
¨ç chemical poisioning
¨è toxins form fish or shellfish
¨é proformed toxin of S. aureus, or
B. cereus
b) long IP
¨ç enterotoxin-producing bacteria
¨è invasive bacteria
¨é Norwalk V.
¨ê some form of mushroom poisioning
Clinical Syndrome
(Table 171-8)
7.
Tx. --> supportive
¿¹¿Ü) fetal
¨ç botulism
¨è paralytic shellfish poisioning
¨é long acting Mushroom poisioning
Chap.172 Osteomyelitis & Septic Arthritis
Osteomyelitis
# hematogenous O.M : M.C in ¡Â
10 year children
Pathology & Pathogenesis
1. virulent organism ->
focal inf. in bone
-> suppuration & ischemic necrosis
-> fibrosis & bony repair
2. entire bone involved :
marrow, cortex, periosteum
3. acute hematogenous O.M :
localization of bloodborne bacteria
* sta. aureus : adhesion to connective tissue elements in bone
* local trauma -> thrombosis
-> inf.ÀÇ localized
* source of bacteremia
a. focal suppurative inf.
b. inapparent, unidentified colonization or inf.
4. inf. : begin in the
metaphyseal region of long bone
a. contain stagnant network of end arterioles & capillary
b. lacks effective phagocytic cells
: production of inflam.
exudate
-> septic thrombosis of vessels & compromised vascular supply
-> ischemic bony infarction with local pain
-> sufficient pus : intact periosteumÀ» elevation½Ã۱â À§ÇØ
subperiosteal space¿¡ collectionµÊ
-> disruption of the periosteal component of blood supply
& infarction of cortical bone
*
sequestrum
: formation of necrotic bone area
-> later stageµ¿¾È free foreign bodyÀ» Çü¼ºÇϱâ À§ÇØ
underlying viable bone°ú
seperationµÇ°Å³ª or gradual resorptionµÊ
*
involucrum
: during the reparative phase of acute O.M
elevated periosteumÀÇ osteogenic precursor cell
-> new bone formation in the subperiosteal region
-> infected focusÀ» enveloped
5. in infants
a.
transphysial vessels -> traverse the cartilagenous growth plate
-> inf.ÀÌ marrow cavity, epiphysis·Î
extend
->
pyarthrosis or septic arthritis
b.
ischemic necrosis of growth plate
-> growth disturbance
6. Brodie abscess
: rim of
sclerotic tissue·Î µÑ·¯½ÎÀÎ subacute or chronic
localized abscess
: ÁÖ·Î
distal tibia
: dull
pain & local tenderness
:
spontaneous sterilization or chronic nidus of inf.
-> surgical or long-term medical Tx.
Etiology
1. sta. aureus : TMC
2. H.influenza : 3yr ÀÌÇÏ
3. group B strep & coliform : in
neonate
4. pseudomonas : puncture wound ,
intravenous drug users
5. salmonella & Brucella : vertebral
bone
esp. salmonella - in hemoglobinopathies pt.
6. anaerobes : trauma, human bites,
decubitus ulcer
7. strep. pneumoniae, strep. pyogenes
8. G(-)bacilli : salmonella, brucella,
kingella, pseudomonas, serratia
9. N.gonorrhea
10. actinomycetes : spine, jaw
11. mycobacteria , fungus
Clinical Manifestation
1. in neonates
a. iatrogenic procedureÈÄ
(heel puncture, fetal scalp monitoring)
b. pseudoparalysis : in infants
c. common eti. : sta. ,
group B strep., coliforms
d. multifocal disease(50%¡è)
e. involved boneÀÇ ÀÎÁ¢
joint Àß Ä§¹ü
2. in sickle cell disease
a. vaso-occlusive crises
b. multiple bone involve
c. sta., salmonella
3. vertebral O.M
a. ÁÖ·Î
8¼¼ ÀÌ»óÀÇ children¿¡¼
hematogenous inf.
b. Sx. & Sg. : poorly
localized
fever, back pain, abd. pain, referred pain in the thigh, gait
disturbance
c. percussion of the spinous
process : point tenderness
paraspinous m.
spasm with limitation of movement
->more diagnostic
d. eti. : sta. aureus,
G(-)bacilli
e. destruction of vert. body
& paraspinous abscess
-> spinal
cord compressionµÇ¾î emergency op.
4. pelvic O.M
a. poorly localized
b. pain : buttock, hip, knee
gait disturbance
c. afebrile
d. sta. aureus, salmonella,
mycobacteria
Diagnosis
1. microbiologic studies
a. blood culture : 50-60%
bone aspiration
or biopsyÀÇ material culture : increased
positive
b. if culture method
impossible
S.
pneumoniae, H. influenza -> positive urine bacterial Ag test
c. chronic draining O.M
: boneÀÇ
needle biopsy
d. Tbc suspect
:
tuberculin skin test & chest X-ray
: mycobacterial
culture
2. imaging studies
1) X-ray
a. negative in
the 1st week
b. deep
soft-tissue swelling with obscuring of fat line
c. vertebral OM
: erosion and collapse of vert. body
d. 10-14days :
periosteal reaction(periosteal elevation, subperiosteal new bone formation)
: bony destruction (rarefaction, lysis)
2) three-phase bone
scan(99mTc-MDP)
a. cellulitis
without OM : initial phase - focal increased uptake
later phase (esp.bone phases) - decline
b. OM : in all
three phase (esp. bone phase) - localized uptake
c. advantage
: Á¶±â¿¡ involvedµÈ
multiple siteÀ» detect
d. gallium-67
citrate scan & labelled WBC scan
: pelvic bone OM
3) CT
4) MRI
3. marker of acute inflammation
1) WBC Áõ°¡
2) ESR Áõ°¡
3) CRP Áõ°¡
Differential Diagnosis
1. pyomyositis, cellulitis, bursitis,
abscess, septic arthritis, diskitis
2. trauma
3. primary or secondary bony malig.
: neuroblastoma,
osteogenic & Ewing sarcoma
4. leukemia, lymphoma
5. bony infarction
6. DDx. of pelvic OM
1) arthritis(toxic &
septic)
2) retroperitoneal abscess
3) avascular necrosis of
femoral head
# chronic recurrent multifocal OM (CROM)
1. noninfectious, inflammatory
condition
2. multiple site involve,
remission & exacerbations
3. lack of isolation of etiologic
agent
" response
to empiric antimicrobial therapy
4. female > male (2¹è)
5. involve site
a. metaphyses of
tubular bone (prox. & distal tibia)
b. sternal end
of clavicle
c. femur,
fibula, radius, ulna, vertebra
6. associated condition
a. palmoplantar
pustulosis
b. Sweet synd.
c. vertebral
sclerosis
d. psoriasis
7. bony biopsy
: acute inflammation,
granulation tissue, noncaseating granuloma
: pathogen culture(-)
8. DDx
a. multifocal
acute or subacute pyogenic OM
b. leukemia
c. neuroblastoma
d. histiocytosis
X
9. Px : excellent
* exacerbationµ¿¾È
NSAID & physiotherapy¿¡ response ÁÁÀ½
* severe case :
steroid
# Diskitis
1. involve site : intervertebral
disk esp. L4-L5 & L3-L4 interspace
2. 5¼¼ÀÌÇÏ Àß ¹ßº´ : disk-vertebral
interface»óÀÇ catilaginous end plateÀÇ
vasculature
-> involution with age
3. etiology : sta. aureus(TMC)
4. clinical manifestation :
irritability, gradual onset of limb, refusal to sit, stand or walk
& low grade fever
5. physical exam
.normal or
localized or diffuse spinal tenderness
.muscles spasm
with limitation of movement
6. ESRÁõ°¡
, WBC normal
7. X-ray finding
+- disk space
narrowing
+- irregular
erosion of adjacent vert. surface
-> Sx onsetÈÄ 1-2ÁÖ¿¡ (-)
8. Technetium & gallium scan
Treatment
¢ÞTable 172-1 & Table 172-2
#
¡ÚInitial Response To Tx
;
resolution of systemic & local sg.
;
decline in WBC, ESR, CRP
;
resolution or at least lack of progression of radiologic changes
#
duration
; *3-6wks recommand in uncomplicated case
; ESRÀÌ Á¤»óÀÌ µÉ¶§±îÁö Åõ¿©ÇÑ´Ù.
-
Á¤»óÀÌ µÇÁö ¾ÊÀº °æ¿ì¿¡´Â oral AB·Î ¹Ù²Ù¾î °è¼Ó Åõ¿©ÇÑ´Ù.
/
dichloxacillin, oxacillin
/
minor inf.½Ã Tx¿ë·®º¸´Ù 2-3¹è
/
IV Ab, 1-2Mo --> oral Ab, 2-4Mo
#
SBT(seurm bactericidal titer)
;
acute OM 1 : 2 (peak 1 : 8)
;
chronic OM 1 : 4 (peak
1 : 16)
#
¡ÚOp Indication
;
removal of sequestra & sinus tract
;
curretage of Brodie abscess
;
irrigation with debridement of OM associated with foreign body, decubitus ulcer
or open fx
Prognosis & Complication
1. Px for uncomplicated OM : good
2. Cx & sequale
a. septic arthritis
b. involvement of bone
& cartilagenous growth plate
-> bony deformity & altered growth
Septic Arthritis
Pathology & Pathogenesis
1. hematogenous dissemination of
bacteria
2. contiguous spread of OM
3. direct inoculation
¢ÞTable 172-3
Etiology
#
H. influenza type b
; *¡ãcommon
at 2mo-5yr
; 20-50%
; complicated by concurrent
other disease
-
meningitis (10-30%)
-
cellulitis (10-30%)
- otitis media (10%)
- OM (5-10%)
- pneumonia(5%)
#
sta. aureus
; *¡ãcommon
in neonates & at more than 5yr
; *2nd ¡ãcommon at 2mo-5yr
#
neonatal septic arthritis
. group B strep.
. E. coli
. candida albicans
. S. pneumonia, neisseria
spp., G(-) bacilli
#
sexually active adolescent
: N. gonorrhea
#
streptobacillus moniliformis, spirillum minus, Borrelia burgdoferi, C.
diphtheria
#
chronic septic arthritis
. Brucella
. mycobacteria
. fungi
Clinical Manifestation
1. main feature
: joint region¿¡
localizedµÈ acute inflammation
-> pain,
tenderness, swelling, erythema, decreased range of motion
2. in neonate
. irritability, poor
feeding(few systemic sg.)
. pseudoparalysis
. diaper change -> pain
. in infants : multiple jt.
involve & contiguous OM
3. older pts
. pain : localized to the
involved site
but referred pain, hip ->
knee
pelvis -> back, hip, & ant. thigh
4. antalgic position
: intra-articular pr. &
pain °¨¼Ò
+- hip - flexion, abduction & external rotation
| knee & ankle - partial
flexion
| shoulder - adduction &
internal rotation
+- elbow - midflexion
5. antalgic gait
pain -> gait
disturbance(limp)
6. pyogenic sacroilitis
. fever
. pain : hip, thigh,
back, buttock
-> movement½Ã aggrevated
. diagnostic sg.
- localized tenderness over the region of sacroiliac jt.
- compression of the iliac wing -> pain Áõ°¡
7. gonococcal septic arthritis
. disseminated
bacteremic inf.
. monoarticular inf.
:
knee, shoulder, wrist, ankle, interphalangeal jt.
. disseminated
gonococcal inf.
-
female(4¹è)
-
during menstruation or 2nd or 3rd trimester of preg.
8. Tb arthritis
. chronic, simple jt.
involve
. knee, wrist, hip,
interphalangeal, metacarpal jt., spine, ankle jt., synovial sheath
Diagnosis
1. initial lab
: ESR, CRP, WBC,
neutrophil Áõ°¡
2. blood culture : 30-40%(+)
3. diagnostic arthrocentesis : suspect µÇ´Â
all pt.
* synovial fluid
.
grossly purulent fluid with WBC count > 10¸¸/¥ìL
: not obtained
.
culture : 70-80%(+)
. G.
stain : 50%(+)
4. serum or synovial Ag detective test
: septic arthritis ·Î º¸±â¿¡´Â ºÒÃæºÐÇÑ
nonspecific, nonlocalizing SxÀ¸·Î oral Abc.·Î
partially treatµÈ
ȯ¾Æ¿¡ »ç¿ë
5. N. gonorrhea
: recovery of synovial
fluid -> difficult
¡Å
blood, cervix, urethra, rectum, nasopharynx culture
Table
172-4
6. X-ray
. swelling with widening of
the joint space
. superficial & deep
periarticular soft tissue swelling
. displacement or loss of
fat plane & edema of fat pads
. hip joint : effusion
-> lat. displacement of the femoral head or subluxation
. septic arthritis °¡
10-14ÀÏ ÀÌ»ó Áö¼Ó½Ã
:
osteoporosis or subluxation
. OMµ¿¹Ý½Ã
: periosteal elevation with or without lytic lesion
7. U/S , CT & scan
8. synovial biopsy, special stain &
culture
: chronic arthritis by
M.tuberculosis or fungi -+
sarcoidosis, rheumatologic reaction -+- DDx °¡´É
Differential Diagnosis
1. suppurative arthritis
. OM, deep cellulitis,
pyomyositis, psoas or retroperitoneal abscess, synovitis,
septic bursitis,
reactive arthritis
. SLE, serum sickness, H-S
purpura, Kawasaki disease, metabolic jt. disease
. viral arthritis
:
interphalangeal-metacarpal jt.(TMC), knee, wrist, ankle, elbow jt.
2. toxic synovitis
. 5¼¼ ÀÌÇÏ,
ÁÖ·Î hip
. viral URIÈÄ
. mild fever, limp,
irritability
extremity :
mininal limitation of motion
. ESR & WBC : normal
3. migratory or recurrent polyarthritis
. rheumatic fever
. JRA
. Lyme disease
. serum sickness
. DGI & Reiter synd.
: DDx(Abc
TxÈÄ)
+- DGI : rapidly resolve
+- Reiter : continuous jt Sx & development of new jt. effusion
Treatment
#
¢¾Principle
; AB therapy
; irrigation & drainage
of the joint
;
immobilization of the joint in a functional position
#
¡ÚDuration Of AB Tx
; *S. aureus - 4-6wks
; *strep. pneumoniae, H. influenza type b,
group A streptococci - 14-21days
; gonococcus - 7-10 days
; neonate &
immunocompromised host - longer duration
#
fever : 3-5ÀÏ Áö¼Ó
but more persist : Cx(abscess, loculation, OM) suspect
jt. inflammation
: 5-7Àϳ» resolve but jt. swelling : 10-14ÀÏ Áö¼Ó
4. IV Abc Tx -> high dose oral
Tx·Î changeÇÏ´Â ±âÁØ
. remission of
fever
. reduction in
inflammatory marker
. synovial
swelling °¨¼Ò
5. S. aureus suspect
: antistaphylococcal
PC(methicillin, oxacillin, or nafcillin)
-> iv route (not intra-articular)
6. H. influenza type B
:
cephalosporin(ceftriaxone or cefuroxime)
or CM +
antista. PC
7. G(-) enteric bacilli
: antipseudomonal PC +
aminoglycoside
8. Kingella Kingae
: PC
9. N. gonorrhea
. parenteral 3rd
generation cephalosporin
(ceftriaxone or cefoxitin)
. susceptability
test»ó PC¿¡ sensitiveÇÑ °æ¿ì
: oral amoxicillin 3-5ÀÏ initiate
. sexually
active adolescent
: doxycycline(for treat concurrent chlamydia trachomatis genital inf.)
10. fungal arthritis
: IV or
intra-articular amphotericin B or 5-fluorocytosine
11. open surgical drainage Ix
. every case of
septic arthritis of hip
. most inf.
involving the shoulder
. recurrent
purulent or culture (+) effusion or 7ÀÏ ÀÌ»ó Áö¼Ó½Ã
12. emergent open drainage of hip ÀÇ
Ix
. reduce the
intra-articular pr.
. avoiding
septic necrosis of the femoral head & the chance of permanent jt. damage
. removal of
necrotic bone & inflammatory mediators
13. supportive Tx
. Ä¡·á ù72½Ã°£
or synovial inflammation ¼Ò°ß improve µÉ ¶§ ±îÁö
functional positionÀ¸·Î joint
immobilization (splint)
-> ÀÌÈÄ passive range of motion exercise
a. maintain physiologic circulation of synovial fluid
b. reduce the risk of contracture
. for the upper
limb
shoulder - adduction & internal rotation
elbow - midflexion
. for the
lower limb
hip & ankle - extension
ankle - neutral position
Prognosis
- poor prognostic feature
.
young age(<6Mo)
.
delayed therapy(Sx ³ªÅ¸³Áö 5ÀÏ °æ°ú)
.
sta. aureus, G(-), fungal pathogens
.
hip or shoulder jt. involve
.
associated OM with epiphyseal damage
Chapter 173. Infections In The Compromised Host
½Å* pts with a specific
T-lymphocyte defect caused by HIV
. neutropenia caused by antiviral
drug
. indwelling central lines, IV
drug abuse
-> breech of the
integrity of the skin & mucous memb.
. secondary malignancy
. malnutrition
. exposure to inf.(Tbc., sexually
transmitted disease, hepatitis)
Compromised Host With Immunodeficiency
¡ÚTable
173-1
¡ÚTable
173-2
Clinical Manifestation
* immunocompromised host ÀÇ
inf.½Ã general clinical features
a. any organism
:
immunocompromised host¿¡¼ potentioal pathogen
b. fever : sensitive
& specific sg.
c. fever¿Ü ´Ù¸¥
Sx & Sg¾øÀ» ¼öµµ ÀÖ´Ù
d. skin & mucous
memb.ÀÇ low microbial virulence &
components of normal flora
: life-threatening inf.
e. extreme
granulocytopenia with absolute neutrophil count of 0.5 X 109cell/L
or less
: predictive of impending inf.
f. 5¼¼ÀÌ»ó
children¿¡¼ CD4+ T lymhyocyte count
200/mm3ÀÌÇÏ (20%ÀÌÇÏ)
: HIV infected pt.¿¡¼ P. carinii pneumoniaÀÇ
riskÁõ°¡
g. mutiple inf. :
common
h. known &
suspected bact. inf.
: maximal tolerated dose·Î Áï½Ã Abc Ä¡·á
i. inf. Tx·Î ÀÌ¿ëµÇ´Â
drug : side effect °¡Áü
Infection In Pts With Immunodeficiency
Ab deficiency
(1) X-linked
agammaglobulinemia
: S.
aureus, H. influenza, strep. pneumoniaeµî¿¡ susceptible
: viral
& protozoal inf.
: ÁÖ·Î
upper & lower resp. tracts
-> chronic & recurrent pul. inf.
->
bronchiectasis
:
arthritis & pneumonitis -> mycoplasma
:
enteritis -> salmonella & campylobacter
(2) selective Ig A defi.
: viral
inf.¿¡ ´ëÇÑ susceptability´Â
no increase
(3) hyper-IgM synd.
: Ig G, Ig
A & Ig E °¨¼Ò & neutropenia
:
agammagolbulinemiaÀÇ Æ¯Â¡ÀûÀÎ inf.¿Ü¿¡µµ
P. carinii pneumonitisÀÇ riskÁõ°¡
(4) IgG subclass defi.
: sinopul.
disease, menigitis, bacteremia, OM, pyoderma
# IgG
subclass 2 defi.
: polysaccharide-encapsulated bact.(H. influenza, pneumococcus) &
immunization with
polysaccharide bacterial vaccine¿¡ ´ëÇØ poor Ab response º¸ÀÓ
Defect in cell-mediated immunity
a. cong. T-lymphocyte defi.
+- T-lym. function °¨¼Ò
+- protective by passive transfer of maternal IgG
-> inf. after birth
* early
infections Cx
: chronic mucocutaneous candidiasis, chronic rhinitis, otitis media,
recurrent pn., & diarrhea
b. acquired T-lymphocyte
defect
: AIDS (most common)
Combined B & T-lymphocyte defects
. severe combined immunodefi.
synd.(SCID)
Wiskott-Aldrich synd.
ataxia-telangiectasia
. life-threatening inf.
: surface systemic
candidiasis, CMV inf., bact. inf., P-carinii pneumonitis
. live-attenuated polio &
measles vaccin
: serious inf. ÃÊ·¡
Lymphocyte-phagocyte defects
* leukocyte adhesion
deficiency
. delayed seperation of the umbilical cord
. cellulitis
. gingivitis
. necrotic skin lesion
Complement deficiency
. familial rheumatologic
disorder
. pneumococcemia,
menigococcemia, gonococcemia
Phagocyte-Neutrophil Defects
. S. aureus, G(-) bacilli,
C. albicans
. systemic bacterial inf. :
sepsis, pneumonia, meningitis
. pyogenic lymphadenitis,
hepatic abscess, gingivitis, pn. & OM
. risk of inf. Áõ°¡
: neutrophil count < 1,000
* neutropenia
a. cong. : cyclic neutropenia
severe infantile agranulocytosis
benign familial neutropenia
b. acquired : antineutrophil Ab(autoimmune conditions, AIDS)
: drug reaction
(phenothiazine, sulfonamide, PC, CM, cancer chemotherapy)
: febrile viral illness
:
BM deficiency
½Å* CGD - normal neutrophil count
- deficient mechanism of bact. killing
½Å* hyper-IgE synd.
: variable leukocyte function
. clinical manifestation
: severe
neutropenia( < 500 neutrophil )
- high risk of fulminant bact. sepsis
. Tx
a.
depend on
- microorganism responsible for the inf.
- duration & severity of the neutropenia
- possibility of BM recovery
- associated impairment of host defense
b.
Abc
c.
corticosteroid : CGD pt¿¡¼ granuloma resolve
d.
granulocyte transfusion
- bact. or fungus : IV bactericidal Abc¿¡ unresponsiveÇÒ¶§
- ´ÜÁ¡ : .expensive
.CM virus inf. riskÁõ°¡
.allosensitization to HLA Ag.
.GVH dis. in immunosuppressed pts
.amphotericin B °ú combine½Ã
pul. infiltrate & hypoxia
.transfusion reaction
. prevention
½ÅCGP pt. : broad spectrum Abc combination
trimethoprim-sulfamethoxazole
-> improve phagocytic killing
: recombinent human interferon-¥ã
(50 ¥ìg/M2 subcutaneous 3ȸ/wk)
+ oral
trimethoprim-sulfamethoxazole
-> inf. rate °¨¼Ò
Defective Opsonization
. splenectomy, cong.
asplenia, splenic dysfunction from sickle cell dis.
:
bact. inf.Áõ°¡
- strep. pneumoniae, H. influenza, salmonella
. PC prophylaxis
:
sickle cell dis. & age 6MoÀÌ»ó
. routine immunization
¿Ü¿¡µµ 2¼¼¶§ pneumococcal
vacination
Infection With Organ & Tissue Transplantation
BM transplantation
Autologus BMT
: 5-10%, ÁÖ·Î
lung
Allogenic BMT
a. inf. & GVH dis.
: serious Cx.
b. ÁÖ·Î
G(-) bacilli & G(+) cocci
½Åc. table 173-3
# transplantation ÈÄ 1Mo
. granulocytopenia : profound
. mucous memb. damage -> mucositis
. indwelling catheter -> G(+) cocci, G(-) bacilli, fungus
. RS virus pneumonitis
: serious consequence
# BMTÈÄ
30-100ÀÏ
. granulocytopeniaº¸´Ù´Â immune systemÀÇ
derangement¿¡ ÀÇÇØ
. CM virus : no prophylaxis ½Ã 50-60% infected
. interstitial pneumonia
- common in leukemia pt.
- BMTÈÄ 60Àϰ濡 occur
- CM virus , P. carinii, RSV, idiopathic(30%)
# BMT 100ÀÏ ÈÄÀÇ
inf.
. chronic G-V-H associated Ab deficiency
-> pneumococcal sepsis or meningitis, sinopul. inf.
. varicella-zoster virus reactivation
. hemorrhagic cystitis
: due to reactivation of papovavirus BK
. rotaviral enteritis
. pseudomembranous colitis(C. difficile)
. human herpesvirus virus-6 inf.
d. Tx of inf. after BMT
1. depend
on
. transplantationÈÄ °æ°úÇÑ ½Ã°£
. neutropenia
. acute or chronic G-V-H dis.
2.
approach : febrile neutropenia patient with malignancy ¿Í °°À½
-
prompt institution of empiric bactericidal broad-spectrum antibiotics
- neutrophil count °¡ 500ÀÌ»ó µÉ ¶§±îÁö °è¼Ó
3.
acyclovir : herpes simplex, varicella-zoster viral inf.
4.
ganciclovir and CMV hyperimmune globulin
: serious primary CMV pneumonia
e. prevention
1) IV
gamma globulin
fluorinated quinolones
preventing acute graft-versus-host ds.
2)
prevention of CMV virus
. avoiding administration of CMV-positive blood products and marrow
. reducing the incidence of graft-versus-host ds. by acyclovir
. allogenic BMTÈÄ 120ÀÏ µ¿¾È weekly blood, urine,
throat culture
Liver transplant
½Å1) 1st Mo posttransplantation
. highest
risk of inf.
. average
2.5 episode of inf.
2) 2nd & 3rd Moµ¿¾È
: inf.
rate°¨¼Ò (0.35, 0.17 episodes)
3) surgical procedure
: biliary
& liver·Î G-I tract microbial flora inf.Áõ°¡
4) early inf.
. G(-)
enteric bacterial pneumonia
. soft tissue and wound infections
.
intra-abdominal abscesses : enterococci, anaerobic, G(-) enteric-bacteria
.
peritonitis
.
disseminated candidiasis
.
cholangitis : "charcot triad" (fever, abd. pain, jaundice)
: liver
rejection°ú ±¸ºÐ ÇÊ¿ä
by liver biopsy, Gram stain, culture
. hepatic
abscess : biliary or vascular obst.¶§¹®
(cf. cholangitis : biliary stricture or the use of ERCP¶§¹®)
. ischemic
injury to the bile ducts
a. hepatic a. occlusion or bile duct anastomotic breakdown
b. produce bile leakage and G(-) or candidial peritonitis
c. detect by culture of the abd. drain
. CM virus
inf.
a. 30-60% of children
b. found in 1st 3Mo post-transplantation
c. CMV hepatitis
: up to 15% of transplanted children
d. pneumonitis, gastroenteritis
. EBVÀÇ
reactivation
a. mononucleosis-like synd.ÀÏÀ¸Å´
b. late-onset
lymphoproliferative synd.À¸·Î ÁøÇà
c. immunosuppresive therapyÀÇ dosageÁÙÀÓÀ¸·Î
improve
5) Evaluation(of the febrile liver
transplant recipient)
. culture(blood, abd. drains)
. chest roentgenography
. abd. ultrasound and CT imaging
. doppler assessment of hepatic artery blood flow
. percutaneous liver biopsy : cholangitis ¿Í rejection±¸ºÐ
6) Tx
: broad-spectrum
antibiotics and aspiration or drainage of abscesses
7) prevention
. prophylactic
antibacterial agents
.
acyclovir, and trimethoprim-sulfamethoxazole (P. carinii)
.
avoiding neutropenia (due to azathioprine)
.
maintaining good surgical technique
Renal transplants
1) inf. : major cause of death
½Å a. UTI - TMC inf.
- highest incidence (10%) during 1st Mo post-transplant
- À̽ñ⿡ p. aeruginosa : MC cause
- 1st Mo ÀÌÈÄ : E. coli MC
½Å b. CM virus inf.
a) reduced by . prophylactic
antiviral drug
. CMV-Ab(-) blood products
. selection of seronegative organ donors
b) MC clinical pattern
. 1-4Mo after transplantation
. fever, malaise, myalgia, arthralgia, leukopenia
c) hepatitis, pneumonitis
c. other
herpes virus(H. simplex, varicella zoster, E-B virus)
P. carinii, aspergillus spp., candidia, viral hepatitis
2) Tx of inf.
a.
directed at the specific manifestation and the responsible microbiologic agent
b. culture
(urine, blood, sputum)´Â antibiotics ¾²±â Àü
c. biopsy
: rejection °ú inf.±¸ºÐ
3) prevention
a.
Trimethoprime-sulfamethoxazole
: pyelonephritis & P. carinii pneumonitisÀÇ
incidenceÁÙÀÓ
b. careful
evalution of the urinary tract for abnormalities
(urethral, ureteral, and vesicoureteral stricture, ureteral reflux,
lymphocele, neurogenic bladder)
: recurrent urinary tract
inf.ÀÇ ¿øÀÎ identify
Heart transplant
# mediastinitis
.
infected surgical wound
-> S. aureus, S. epidermidis, G(-) bacilli
.
fever, sternal tenderness, erythema, & purulent drainage with bone
destruction
Infection In Patients With Cancer
# inf. risk
a. damage to the skin & mucous
memb.
b. indwelling catheters
c. malnutrition
d. prolonged Abc usage
e. hospitalization
# anticancer Tx
:
one aspect of immue system ÀÌ»óÀ» involve
a. corticosteroid & radiation
: destruction of both T & B lymphocytes
b. MTx & other antifols
: inhibit DNA synthesis
c. alkylating agent (cyclophosphamide)
: block DNA replication
d. 6-mercaptopurine
:
interfere with purine synthesis
Inf. In The Nongranulocytic Patients
a. viral inf., P. carinii,
toxoplasma gondii, fungus
b. pneumococcal pn., otitis
media, strep. pharyngitis, UTI
Inf. In The Gronulocytopenic Cancer Patients
1) granulocyte count 500 cells/mm3
ÀÌÇÏ
: high
risk of serious inf.
2) fever : only manifestation of
inf.
(due to granulcytopenia and poor inflammatory response)
Etiology
; G(+) cocci(most frequent),
G(-) bacilli
; ¡ÚCoagulase(-) Staphylococci, S. Aureus, ¥á-Hemolytic Strep.
-
*¡ãfrequent
in bood culture
b.
alpha-hemolytic streptococcal bacteremiaÁß¿¡¼
: acute septic shock synd. occur
- adult resp. distress synd.°ú À¯»ç
- cytarabine Åõ¿©½Ã MC manifestation
c. P.
aeruginosa, E. coli, Klebsiella pneumoniae
: most common G(-) bacilli
d. prolonged Abc
Tx
-> apportunistic fungal inf. (candida & aspergillus)
Clinical Manifestation
a. G(-) sepsis
: S. epidermidis, E. coli, pseudomonas inf.¿¡ ÀÇÇÑ
septic shock (30-50% of episode) º¸´Ù severe
b. oropharyngeal
inf.
. ulcerating stomatitis, gingivitis, periodontal lesion
. mucositis : anaerobics, candida, herpes simplex
c. esophagitis
d. cutaneous sg.
of disseminated inf.
. ecthyma gangrenosum
. nodule
. gangrenous cellulitis
. thrombotic arterial occlusion with dist. ischemia
e. pneumonia in
granulocytopenic cancer pts
. stable
. local rales, tachypnea,
chest pain, ARDS
. pul. infiltrate
: abscent or faint
: neutrophil count 500ÀÌ»ó µÉ¶§ obvious
: noninfectious disorder ¿¡ ÀÇÇØ¼µµ ³ªÅ¸³²
( hemorrhage, malig., emboli, edema, reaction to granulocyte
transfusion,
radiation or CTx-induced pneumonitis )
. G(-) enteric bacteria or fungus¿¡ ÀÇÇØ
# aspergillus : wedge-shaped infiltrates
: typical of arterial invasion & subsequent thrombotic
pul. infarction
# pul. cavitation
: aspergillosis
: mucormycosis
: G(-) enteric bact.(rare)
f.
sinusitis, hepatic & splenic candidiasis, severe diarrhea(C. difficile)
Diagnosis
a. blood
culture : peripheral vein & lumen of central venous catheter
b. culture
or biopsy : local cutaneous lesion
c. chest
X-ray : infiltrate, infarction, cavitation
d. nasal secretion & sputum culture :
aspergillus
e. sinus
X-ray & CT : aSx sinusitis
f.
esophageal endoscopy : odynophagia
- esophageal lesion»ó pseudohyphae(+) : disseminated
candidiasis
g. serum
CRP ¡Ã 40mg/h : bact. inf.
h. lumbar
puncture : meningitis
i.
fibrotic bronchoscopy, BAL, transbronchial biopsy, open lung biopsy
: identify the microorganism responsible for pneumonia
Treatment
(
of infants in febrile neutropenia cancer patient)
(1) Prompt initiation
of empiric broad-spectrum, bactericidal antibiotics
a.
monotherapy
. ceftazidine, cefoperazone, or imipenem/cilastatin
. ±×ÈÄ S. epidermidis ³ªÅ¸³¯ °æ¿ì
: vancomycin ÷°¡
. monotherapy´Â mild neutropenia(500-1,000
neutrophil)°æ¿ìÀÌ¸é¼ S. epidermidis°¡
pathogenÀ̶ó
»ý°¢ µÇÁö ¾ÊÀ»¶§ »ç¿ë
b. double
beta-lactam therapy
1. extended G(-) spectrum carboxy- or ureido-penicillin
(ticarcillin with or without clavulanic acid, mezlocillin, piperacillin)
and a cephalosporin
(ceftazidine, cefoperazone, cefotaxime, ceftriaxone)
- disadvantage
. selection of resistant bacteria
. possible antibiotic antagonism
. poor antistaphylococcal coverage
2. anti-pseudomonas beta-lactam penicillin or cephalosporin
+ aminoglycoside
- avoid the risk of the emergence of resistent organism
- synergistic
- anaerobic coverage
- disadvantage
. nephrotoxicity
. hypokalemia
. ototoxicity
. poor coverage of staphylococci
c.
triple drug regimen
: extended G(-) spectrum penicillin or a cephalosporin
+ vancomycin
+ aminoglycoside(gentamicin, tobramycin, amikacin)
- most beneficial in a risk of serious staphylococcal, enterococcal
or bacterial multiple-resistant inf.
(2) Duration and
modification of antimicrobial therapy
1)
antibiotic Tx 72½Ã°£ ÈÄ afebrile ÇØÁö°í,
bacterial source °¡ identifyµÇ´Â °æ¿ì
- Tx. should be modified based on the antibiotic sensitivity
- ±×·¯³ª spectrumÀÌ ³Ê¹« Á¼¾ÆÁö¸é
bacteremia°¡ ³ªÅ¸³¯ risk°¡ ³ô±â ¶§¹®¿¡
broad spectrum
antibiotic ¸¦ °è¼Ó »ç¿ëÇØ¾ß ÇÑ´Ù.
2)
antibiotic Tx´Â response°¡ ÁÁÀº
(afebrile, negative repeat culture,
free of signs and symptoms of inf.) pt.¿¡¼ Àû¾îµµ 7Àϰ£ »ç¿ë
3)
antibiotics°¡ stopµÈÈÄ
neutrophil count´Â 500À» ³Ñ¾î¾ß ÇÑ´Ù.
4)
high risk pt.
- profound neutropenia, mucositis
- signs of persistent inf.
- central line tract inf.
- bleeding
- impending invasive procedure or chemotherapy
°æ¿ì neutrophil count°¡
500ÀÌ»ó µÉ ¶§ ±îÁö antibiotics¸¦ °è¼Ó »ç¿ëÇÏ´Â °ÍÀÌ
benefitÇÏ´Ù.
5) ¾î¶²
clinicians˼ defervescence or clinical
well-being¿¡ »ó°ü¾øÀÌ fever¿Í
neutropenia°¡ ÀÖ´Â ¸ðµç ȯÀÚ´Â neutrophil count°¡
500ÀÌ»ó µÉ¶§±îÁö
antibiotics¸¦ °è¼Ó »ç¿ëÇÏ¿©¾ß ÇÑ´Ù°í ±Ç°íÇÑ´Ù.
6)
febrile despite broad-spectrum antibiotic Tx and no pathogen is identified
- reassess the patient's condition
# etiology of persistent fever
a. nonbacterial pathogen
: candida, aspergillus, toxoplasma, herpes simplex,
cytomegalovirus,
Epstein-Barr virus, enterovirus
b. emergence of a second resistant species of bacteria
c. inadequate serum or tissue antibiotics levels
d. drug fever
e. deep
tissue (abscess) or catheter inf.
f. fever resulting from the underlying malig.
7)
if no identified cause of fever is evident, the fever and neutropenia remains
after 5-7days
of antibiotics therapy,
there
is no progression or deterioration in the patient's condition and the patient
appears
clinically well.
- the original antibiotics may be continued
8)
illÇÏ¿© º¸À̰ųª inf.ÀÇ
manifestationÀÌ progressÇÒ °æ¿ì
- vancomycin or 3rd generation cephalosporinÀ» ÷°¡
(initial empiric regimen¿¡ µé¾îÀÖÁö ¾ÊÀº °æ¿ì)
9)
antibiotics¸¦ modificationÇÏ¿´´Âµ¥µµ
ºÒ±¸Çϰí neutropenicÇϸé¼
7ÀÏ °£ febrileÇѰæ¿ì
1. intravenous amphotericin B¸¦ startÇÔ
(33%¿¡¼ invasive fungal ds. °¡Áü)
2. amphotericin B¸¦ initiation Çϱâ Àü
invasive candidiasis, aspergillosis, or mucormycosisÀÇ
source¸¦ °áÁ¤Çϱâ À§ÇØ ÇàÇÏ¿©¾ß ÇÒ evaluation
- biopsy of lesion
- several bl. and urine culture
-
chest and sinus roentgenograms repeated
- abd. CT : to identify hepatic or splenic microabscess
- opthalmologic examination
: to identify candidal ophthalmitis
3. daily for 2wks (fungal inf.ÀÌ identify ¾ÈµÈ °æ¿ì)
- ±× ÈÄ stopÇÏ¿© ȯÀÚ
condition À» re-evaluate
4. documented fungal inf. °æ¿ì
- prolonged amphotericin B and aspiration or incision and drainage of
cutaneous lesion
or deep abscess
5. side effect : nephrotoxicity
- ÁÙÀ̱â À§ÇØ nephrotoxic drugÀÇ »ç¿ëÀ» ÁÙÀÓ
(aminoglycoside -> 3rd generation cephalosporin ´ëü,
chemotherapeutic agent(cisplatin) »ç¿ë ÁÙÀÓ)
6. new fungal agent (fluconazole)
- effective
- amphotericin ÀÌ not tolerate Çϰųª
severe nephrotoxicity°¡ ÀÖ´Â °æ¿ì
10) central
venous catheter, implanted device¿¡ ÀÇÇÑ documented bacteremia
( catheter-related sepsis )
- bacteremia¹ß»ý½Ã antibiotics¸¦
lineÀÇ sterilizationÀ» À§ÇØ
lumen³»·Î ÁÖÀÔ
- respond to systemic antibiotics
- no need to remove the catheter
- difficult to sterilize line inf.
. tract inf.
. sepsis due to Bacillus sp., fungi
. G(-) enteric bacteria
. multiple organism
11)
Empiric antiviral therapy for the febrile neutropenic patientÀÇ
indication
: typical mucocutaneous lesions suggestive of herpes simplex
or
varicella zoster
-> intravenous acyclovir is the choice
7) Prevention
-
difficult
(1) method
: reverse isolation, total protective environment
(2)
prophylactic antibiotics
1) oral nonabsorbable
- colistin, nystatin, and polymyxin
2) oral absorbable
- trimethoprim-sulfamethoxazole
: for P. carinii, G(-) enteric bacteria
# side effect
. delay bone marrow recovery
. drug rash
- new fluorinated quinolones
&nb