Wednesday, March 28, 2012

Diarrhea Disease


              General introduction

Concept    common disease in childhood

 

                  frequency and characters of stool

 

Ages          6m~2y      50% 1y

 

Seasons     viral origins—late autumn and spring beginning
           bacterial origins—summer

                   noninfectious diarrhea— every season

 

  Predisposing factor-1

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   Rotavirus

Ø   Astrovirus

Ø   Calicivirus: Norwalk virus,  sapovirus

Ø   Enterovirus: Coxsackie virus, echovirus,  enteric adenovirus

Ø   Coronavirus: torovirus

 

o    Bacillus coli 

   enteropathogenic E. coli ………………………EPEC
    enterotoxigenic E. coli …………………………ETEC
    enteroinvasive E. coli …………………………..EIEC
    enterhemorrhagic E. coli ………………………EHEC
    enteroadherent aggregative E. coli ……………EAEC

 

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

 

                                                     o   Dietary factors

*  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   Dehydration

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    Vomiting and diarrhea :Alkalinity intestinal juice lost

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: 3.55.5 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/moderateisotonic/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.