Showing posts with label Pediatrics. Show all posts
Showing posts with label Pediatrics. Show all posts
Wednesday, March 28, 2012
Diarrhea Disease
Concept common disease in childhood
frequency and characters of
stool
Ages 6m~2y 50% <1y
Seasons viral origins—late autumn and spring
beginning
noninfectious diarrhea—
every season
Ø Gastric
acid secretion , secretion and activity
of enzyme , quality and quantity of diet
change quickly.
Ø Water
metabolism ,tolerance of
hydropenia ,easy to body fluid
disorder.
Ø Nerves,
endocrine, circulation, liver and renal function: not mature, easy to digestive
tract function disorder.
Grow and
develop , demand for nutrients , burden of the stomach and intestines , easy to indigestion.
Artifical feeding:
enteritis morbility 10 times higher
than breast
feeding.
milk: nutritional
ingredient destroyed
milk tool:
disinfection.
Ø
Astrovirus
Ø
Calicivirus: Norwalk virus, sapovirus
Ø
Enterovirus: Coxsackie virus, echovirus, enteric adenovirus
Ø
Coronavirus: torovirus
enteropathogenic
E. coli ………………………EPEC
o
Campylobacter jejuni, Yersinia enterocolitica,
others
o
Fungi :blastomyces
albicans
o
Protozoa (parasite) :giardia
lamblia, amebic protozoa
Ø
Disorder intestinal function
Ø
Infect intestinal tract directly
Ø
Irritation of rectum (eg. bladder infection)
alteration of intestinal flora
Ø
Much antibiotics used transport of carbohydrate
lactase
* quality
and quantity of food (feeding starch and fat too early)
* Allergic
diarrhea: milk or bean
* Primary
and secondary disaccharidase deficiency
Ø
Osmotic diarrhea: much poorly absorbed and
hyperosmotic solute
Ø
Secretory diarrhea: electrolytes hypersecretion
Ø
Exudative diarrhea: inflammatory states causing
liquor exudation
Ø
Motility disturbance: dynamic abnormality of
intestine
Ø
Noninfectious diarrhea: feeding factors
o Metabolic
acidosis
o Electrolytes
disorder
Mild and
severe diarrhea
Ø
Mild: the times of stool and character change
—— stool :frequency ,loose, liquid,
color: yellow or greenyellow,
smell: sour flavor, shape: egg
soup
—— vomiting: seldom
—— general
poisoning symptom: without
—— dehydration, electrolytes abnormality
and general toxicity symptoms': none
Mild and
severe diarrhea
Ø
Severe: accompany dehydration, electrolytes
abnormality and general toxicity symptoms
—
digestive tract symptom : diarrhea serious ,mucus blood sample stool, anorexia, nausea,
abdominal
pain
and abdominal distention
—
general poisoning symptom : lethargy, dysphoria,
unconsciousness and coma
—
dehydration, electrolytes abnormality ,
acid base imbalance
Severity clinical signs of dehydration
Ø
Eat :calorie
, malabsorption®lipoclasis ®keto-bodies
Ø
Hypovolemia®pachemia®blood flow slowly®
hypoxia® anaerobic glycolysis ®
lactic acid
Ø
dehydration® blood flow ®excluding
acid ®
acid metabolic product
Ø
Dispirited, dysphoria, drowsiness, coma
Ø
Hypernea
(Kussmauls breathing),exhalation
cool
Ø
Expiratory gas smells ketone
Ø
Cherry lips
Ø
Nausea, vomit
K+ (potassium)<3.5mmol/L (normal: 3.5~5.5
mmol/L)
causes:
Ø
Excessive losses: vomit, diarrhea.
Ø
Inadequate intake.
Ø
Renal function of keeping kalium ,it continues excluding kalium when with
hypokalemia.
Ø
depressed
Ø
Tension of skeletal muscle ,tendon
reflex,
even respiratory
muscle weakness
Ø
Tension of smooth muscle , abdominal distention
intestinal sound or disappear
Ø
Myocardium excitability , arrhythmia, ECG: T-wave
is low or inversion, U-wave occurs,
prolonged P-R
interval and Q-T interval, ST section
descending.
Ø
Baseosis
Ø
Ca2+﹤1.75mmol/L
(7mg/dl) ;
Mg2+﹤0.6mmol/L
(1.5mg/dl).
Ø
Symptoms usually occur after dehydration and
acidosis resolved, or fluid replacement.
Ø
Clinical manifestation: thrill, tetany, convulsion.
Ø
If convulsion hasn’t relieved after supplement
calcium,
pay attention to hypomagnesemia.
Ø
Season: cool months (autumn and winter)
Ø
Age: 6m~2y
Ø
Symptom: fever, vomit, mild general toxicity
symptoms.
Ø
Stool: frequency, amount, water; yellow-water or
egg soup-like; a small amount of mucus.
Ø
Dehydration: mild/moderate,isotonic/hypertonic
Ø
Complication: convulsion, myocardium damaged.
Ø
Prognosis: self-limited, course: 3~8d.
Ø
Viral antigen detection: from stool.
Ø
Season: summer
Ø
Symptom: vomit and diarrhea, no obvious general
toxicity symptoms.
Ø
Stool: water-like or egg soup-like, without mucus,
blood or pus, no WBC (test under microscope).
Ø
Dehydration: dehydration, electrolyte and acid-base
disorder usually occur.
Ø
Prognosis: self-limited, course: 3~7d.
Ø
Similar with bacillary dysentery.
Ø
Symptom: diarrhea with fever, nausea, vomit,
abdominal pain, tenesmus. Severe general toxicity symptoms, e.g. ardent fever,
consciousness change, even septic shock.
Ø
Stool: with mucus, blood and pus, smell of fish,
with WBC (test under microscope).
Ø
Stool culture: pathogenic bacterium.
Ø
Pathogen: usually Blastomyces albicans.
Ø
Age: ﹤2y.
Ø
Complication by other infection, or after using
antibiotics for long time.
Ø
Persistent course, usually thrush companion.
Ø
Stool: yellow thin stool, more foam with mucus,
sometimes tofukasu-like.
Ø
test under microscope: fungal spore and hypha.
Ø
Gastric mucosa analosis ®
bacterium and yeast fungus
Ø
Intestinal mucosa thinner®indigestion
and malabsorption
Ø
Bacterium in upper small intestine ®enterocyte
damaged
Ø
Dynamic abnormality of intestine.
Ø
Using antibiotics for long time.
Ø
Immune function defect ®
liability to agents
vicious cycle
o
Not difficult
o
According to clinical manifestation, laboratory
tests and character of stool.
Ø
Usually ﹤6m,
bloating, breast-feeding.
Ø
Usually with eczema.
Ø
Normal appetite, growth and developed.
Ø
After cofood addition, stool turns to normal.
Ø
A special type of lactose intolerance
Ø
Epidemiology character
Ø
Stool culture: a dysentery bacillus discovered
Ø
Symptom: ardent fever, severe toxicity symptoms,
abdominal pain and distension, vomit frequently.
Ø
Stool: first, yellow thin or egg soup-like;
then, red pasty or adsuki bean
soup-like.
Ø
X-ray of abdomen: local aerate and expansion
in
small intestine, intestinal wall
pneumatosis.
*
Adjust and continue feeding, not abrosia or
restricting water, prevent malnutrition.
*
Prevent and cure dehydration.
*
Rational administration: proper antibiotics,
microecosystem preparation, assist-digestive drugs, mucosa protectant,
antivomit drugs. Usually disusing antidiarrheal.
*
Strengthen nursing, symptomatic treatment, prevent
complications.
*
Fluid therapy (next week lesson)
Measles
Measles is…
* an acute viral infection characterized by a maculopapular
rash erupting successively over the neck, face, body, and extremitis and
accompanied by a high fever.
ETIOLOGY
Measles virus
*An
RNA virus of the genus Morbillivirus in the family of Paramyxoviridae
*One
serotype, human’s only host
*Stable antigenicity
*Rapidly
inactivated by heat and light
*Survival
in low temperature.
EPIDEMIOLOGY
*Infection
sources
n Patients
of acute stage and viral carriers of
atypical measles
*Transmission
n Highly
contagious, approximately 90% of susceptible contacts acquire the disease.
n Respiratory
secretions: maximal
dissemination of virus occurs by droplet spray during the prodromal period
(catarrhal stage).
n Contagious
from 5 days before symptoms, 5 days after onset of rash
n Seasons:
in the spring, peak in Feb-May
PATHOGENESIS AND PATHOLOGY
*Portal
of entry
n Respiratory
tract and regional lymph nodes
n Enters
bloodstream (primary viraemia) è monocyte – phagocyte system è
target organs (secondary viraemia)
*Target
organs
n The
skin; the mucous membranes of the nasopharynx,
bronchi, and intestinal tract; and in
the conjunctivae, ect
Resulting
In-----
1)
Koplik spots and skin rash: serous exudation and proliferation
of endothelial cells around the capillaries
2)
Conjunctivis
PATHOGENESIS AND PATHOLOGY
3) Laryngitis, croup,
bronchitis :general inflammatory reaction
4)
Hyperplasia of lymphoid tissue: multinucleated
giant cells (Warthin-Finkeldey giant
cells) may be found
5)
Interstitial pneumonitis: Hecht
giant cell pneumonia.
6)
Bronchopneumonia: due to secondary bacterial infections
7)
Encephalomyelitis: perivascular
demyelinization occurs in areas of the brain and spinal cord.
8)
Subacute sclerosing panencephalitis(SSPE):
degeneration of
the cortex and white matter with intranuclear and intracytoplasmic inclusion
bodies
CLINICAL MANIFESTATION
Typical
Manifestation:
patients havn’t
had measles immunization, or vaccine failure with normal immunity or those
havn’t used immune globulin
1.
Incubation period (infection to symptoms) :
6-18days (average 10 days)
2.
Prodromal period:
n 3-4
days
n Non-specific
symptoms: fever, malaise, anorexia, headache
n Classical
triad: cough, coryza, conjunctivitis (with
photophobia, lacrimation)
CLINICAL MANIFESTATION
Enanthem (Koplik spots):
n Pathognomonic
for measles
n 24-48
hr before rash appears
n 1mm, grayish white dots with
slight, reddish areolae
n Buccal mucosa, opposite the
lower 2nd molars
n increase
within 1day and spread
n fade
soon after rash onset
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
3. Rash period
3-4days
Exanthem:
Erythematous, non-pruritic,
maculopapular
n Upper lateral of the neck, behind ears,
hairline,
face è
trunk arms and legs feet
n The severity of the disease is directly
related to
the extent and confluence of the rash
,
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
Temperature:
n Rises abruptly as the rash appears
n Reaches 40℃ or higher
n Settles after 4-5 days – if persists,
suspect secondary
infection
Coryza, fever, and
cough:
n Increasingly severe up to the time the rash
has covered the
body
Lymphadenopathy
(posterior cervical region, mesenteric) splenomegaly, diarrhoea, vomiting
Chest X ray:
n May be abnormal,
even in uncomplicated cases
CLINICAL MANIFESTATION
4. Recovery period
3-4days
Exanthem:
n Fades in order of appearance
n Branny desquamation and brownish
discoloration
Entire illness – 10 days
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
Atypical Manifestation:
1. Mild measles
n In
patients: administered immune globulin products during the incubation period
and immunized against measles; in infants <8mo
n Long
incubation period and short prodromal
phase
n Mild
symptom
n No
Koplik spot
n The
rash tends to be faint, less macular, pinpoint
n No
branny desquamation and brownish discoloration
occur as the rash fades
n No
complications and short course
CLINICAL MANIFESTATION
2.
Severe measles:
n In cases with
malnutrition, hypoimmunity and secondary
infection
n Persistent
hyperpyrexia, sometimes with convulsions and even
coma
Exanthem:
n Completely covered the skin
n Confluent, petechiae, ecchymoses
n The hemorrhagic type of measles (black
measles), bleeding
may occur from the mouth, nose, or
bowel. disseminated
intravascular coagulation (DIC)
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
3.
Atypical measles syndroma:
n Recipients
of killed measles virus vaccine, who later come in
contact with wild-type measles virus.
n Distinguished by high fever, severe headache,
severe abdominal
pain, often with vomiting, myalgias,
respiratory symptoms,
pneumonia with pleural effusion
Exanthem:
n First appears on the palms, wrists, soles,
and ankles, and
progresses in a centripetal direction.
n Maculopapular è
vesicular è purpuric or hemorrhagic.
n Koplik spots
rarely appear
CLINICAL MANIFESTATION
CLINICAL MANIFESTATION
4.
Measles absent of rush
n Immunodepressed, or passive immunized
recently cases and
occasionally in infants <9mo who have
appreciable levels
of maternal antibody
n Non-specificity
n Difficult to diagnosis
COMPLICATIONS
1.
Respiratory Tract
* Laryngitis,
tracheitis, bronchitis – due to measles itself
* Laryngotrachobronchitis
(croup) –cause airway obstruction to require tracheostomy
* Secondary
pneumonia – immunocompromised, malnourished patients. pneumococcus, group A
Streptococcus, Staphylococcus aureus and
Haemophilus influenzae type B.
* Exacerbation
of TB
COMPLICATIONS
2. Myocarditis
3. Malnutrition and Vitamin A deficiency
COMPLICATIONS
4.
CNS
*The
incidence of encephalomyelitis is 1-2/l,000 cases of measles
*Onset
occurs 2-5 days after the appearance of the rash
*No
correlation between the severity of the rash illness and
that of the neurologic involvement
n Earlier - direct viral effect in CNS
n Later – immune response causing demyelination
n Significant morbidity, permanent sequelae –
mental
retardation and paralysis
*Subacute
sclerosing panencephalitis (SSPE): extremely rare, 6-10 years after infection.
Progressive dementia, fatal. Interaction of host with defective form of virus
LABORATORY
EXAMINATION
*Isolation
of measles virus from a clinical specimen (e.g., nasopharynx, urine)
*Significant
rise in measles IgG by any standard serologic assay
*Positive
serologic test for measles IgM antibody
*Immunofluorescence
detects Measles antigens
*Multinucleated
giant cells in smears of nasal mucosa
*Low
white blood cell count and a relative lymphocytosis in PB
*Measles
encephalitis – raised protein, lymphocytes in CSF
DIAGNOSIS
characteristic
clinical picture:
Measles contact
Koplik spot
Features of the skin rash
The relation between the eruption and fever
Laboratory confirmation is rarely needed
DIFFERENTIAL DIAGNOSIS
*The rash of measles must be differentiated from
that of
*rubella;
*roseola
intantum;
*enteroviral infections;
*scarlet
fever;
*and
drug rashes.
DIFFERENTIAL DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
TREATMENT
*Supportive, symptom-directed
Antipyretics for fever
Bed rest
Adequate fluid intake
Be protected from exposure to strong
light
*Antibiotics for otitis media, pneumonia
*High doses Vitamin A in severe/ potentially severe
measles/ patients less than 2 years
100,000IU—200,000IU
PREVENTION
*1. Quarantine period
5 days after rash
appears, longer for complicated measles
*2. Vaccine
The initial
measles immunization is recommended at 8mo of
age
A second immunization is recommended
routinely at 7yr of
age
*3. Postexposure Prophylaxis
Passive
immunization with immune globulin (0.25mL/kg)
is effective for
prevention and attenuation of measles within
5 days of exposure.
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