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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