P. 1
Presentation of Diptheria

Presentation of Diptheria

|Views: 225|Likes:
Published by R-o-N-n-e-l

More info:

Published by: R-o-N-n-e-l on Nov 27, 2009
Copyright:Attribution Non-commercial

Availability:

Read on Scribd mobile: iPhone, iPad and Android.
download as PPT, PDF, TXT or read online from Scribd
See more
See less

01/11/2013

pdf

text

original

Definition

• Is an infectious diseases cause by corynebacteruim diphtheria, characterized by the formation of pseudomembrane, commonly in the faucial area and tonsils, and the elotoration of powerful exotoxin affecting the important viscera of the heart and kidneys and the peripheral nervous system. Diphtheria causes the progressive deterioration of myelin sheaths in the central and peripheral nervous system leading to degenerating motor control and loss of sensation. Diphtheria is a contagious disease spread by direct physical contact or breathing the aerosolized secretions of infected individuals. Acute febrile infection of the tonsils, throat, nose, larynx or a wound marked by a patches of grayish membrane from which bacilli is readily cultured.

Etiology
• Corynebacteruim diphtheriae (Klebs• loeffler bacillus) Is typically a slender, curved and slightly tapered clubbed organism which gram + to variable, facultatively aerobic

Mode of transmission
• Contact with a patient, carrier, articles soiled with discharged of infected person • Source: discharged from nose pharynx, eyes or lesion on other parts of body of infected person.

Period of communicability
• Variable until virulent bacilli has disappeared from secretions and lesions: usually 2 weeks and seldom more than 4 weeks.

Sign and symptoms
• • • • • • • • Fatigue Dysphagia Nausea/vomiting Chills High fever Neck swelling Bull neck Toxaema (except in nasal type): apathy, malaise, weakness and pulse disproportionately rapid to temperature.

Pathogenesis
• The typical pseudomembrane is formed by leukocytes, fibrin, necrotic tissue and micro organism; which is adherent to the underlying tissues and leaves a raw bleeding area when detached. • The toxin elaborated by the organism initiates and contributes to the further growth of lesion and formation of more toxins which attacks the myocardium, kidneys, liver, cranial and peripheral nerves producing foci of necrosis and degeneration. • The site of membrane formation influence the clinical features, produced more toxins absorbed from the upper respiratory tract than lower respiratory.

Pathophysiology
• the damage to body is a results of liberation of soluble toxins in the local lesion. • Size of membrane reflects the amount of toxins being produce. • The larger the membrane the more toxins present in blood. • Toxin-tissue union in many body ports but special affinity appears to exist in certain parts, heart and peripheral nerves.

Diagnostic test
• • • • • Nose and throat swab Virulence test Shick test Moloney test Differential diagnosis

Nose and throat swab
• Culture of both nose and throat in all types ( swab are streak on fresh pais loeefler serum apgar, blood tellurite or tisdale media and examine 8- 24 hours of incubation. • Negative results do not rule out diphtheria.

Virulence test
• Direct smear property stained will appear typical gram (+) organism but although having an advantage of being simple delay is not entirely reliable.

Schick test
• Intradermal injection of dilute diphtheria toxins ( 0.1cc) • (+) to individual w/o immunity, hence susceptible to diphtheria • After 48-72 hours (+) reaction reveals itself as local circumscribed area of redness 13 cm in diameter, but occasionally larger.

Moloney test
• Test to determined hypersensitivity to diphtheria toxoid • Performed by injecting 1.0cc fluid toxoid intradermally. • If (+) an area erythema will developed in 24 hours.

Medication
• Serum therapy • antibiotic

Serum therapy ( diphtheria antitoxin)
• Early administration aim to neutralizing the toxins present in general circulation before it absorbed by the tissues. • Skin testing is required before administration of antitoxin for allergic reaction.

One must be guided with some several factor: a. The day of disease which patient is first observed b. Apparent severity of the lesion, namely the extent of membrane. c. Evidence of toxemia.

Dosage and route in administration of antitoxin
Type Dose Route Anterior nasal 10,000-20,000 Intramuscular units Faucial 15,000-25,000 IM/IV units Pharyngeal/lary 20,000-40,000 IV ngeal units Combined, late 40,000-80,000 IV cases units

Antibiotics
Effective for sensitive strain a. Penicillin G potassium, 100,000 mg/kg/day in 4 doses, IM or IV. b. Erythromycin, 40mg/kg in 4 doses, oral, for 7-10 days

Prophylaxis
• Active immunization • Passive immunization

Active immunization
• Based on principle that the small doses of toxins stimulates the production of antitoxin in the body. • Most desirable period is between 612 months of age, preferably 9 months.

Method of active immunization
a. toxin-antitoxin – is a preparation in w/c the active immunizing substance, the toxin has been buffered or attenuated, with suitable amount of antitoxins. -has been replace by toxoid w/c is prepared by addition of 1.4% formalin, thus attenuating the toxin. The dose is 0.5cc subQ for 3 doses interval of 3 months

Toxoid • As in routine of DPT immunization program of infancy and childhood and provide protection about 10 years. • Booster doses is given at suitable interval until adulthood. • Protection may not absolute, but disease become milder and minimum of complication. • Given subQ or IM by large gauge needle coz danger of blockage by particles of precipitate.

Passive immunization
• For susceptible person who has been directly exposed to an unquestioned case of the disease. • Advisable to protect them at once by injection of 10,000 units of antitoxins, IM and last about 3-4 weeks. • Antitoxin prevent development of the disease.

Nursing management
• Rest • Care of nose and throat • Ice collar • Diet

Rest
• Patient should be confined to bed at least 2 weeks, not permitted to feed himself, bathe, or to make exertion. • Patient is restless, especially when dyspneic of laryngeal diphtheria, therefore warm, fresh air must be ensured. • In severe cases even making bed is omitted to conserved energy.

• Vomiting is exhausting, therefore no procedure that might nauseate the patient should be used. • This means small, frequent feeding, rather than larger ones at longer intervals. • Another important point in rest is to prevent straining at defecation

Care of nose and throat
• Nose, throat, mouth should be kept clean. • Gentle swabbing must be done to prevent bleeding. • Liquid albolene is soothing to mucous membrane after cleansing and it prevent dryness and excoriation caused by the discharges from the lesions. • The whole room must be moist atmosphere, with humidity carefully regulated, in order to lessen irritability to nose and throat.

Ice collar
• Sometimes ice collar is more effective than warm application in relieving pain of the sore throat. • Kept aroud the neck as intended. • Rubber collar must be placed in cloth or gauge to protect patient skin and prevent wetting patient clothing.

Diet
• When throat is very sore, soft foods. • Small amounts given frequently. • Fruit juices help to maintain alkalinity of blood, citrus may comfort when in sore throat. • Creamed soups, purees, soft eggs, jellies, custards, broth and buttermilk should provide a balanced ration if a sufficient amount can be swallowed.

complication
• • • • • • Toxemia Neuritis Difficulty swallowing and breathing Pneumonia Kidney failure Death

Toxemia
• a. Due to toxemia Toxic myocarditis- Myocarditis is inflammation of the heart muscle that can cause an irregular heartbeat and lead to heart failure. It often is fatal. Due to action of toxins in the heart muscles. Usually during the first 10-14 days. Diminution in intensity of first heart sound. Arrhythmia E.C.G elevation of S-T segment prolongation of P-R interval evidence of heart block.

b. c. d. e. f.

Abdominal pain due to enlargement of the liver caused by cardiac failure, so called “ chronic passive congestion”.

Neuritis
• Caused by absorption of toxin in the nerves. • May appear early o late may affect the: a. Palate (paralysis of soft palate); nasal twang and regurgitation occurring the 3rd week na last 1-2 weeks. b. Extra ocular muscles (ocular palsy) bilateral paralysis of ocular muscles of accommodation causing blurring of vision during 5th week, strabismus.

c. Diaphragm (paralysis) occurs 6th-10th week; simulating guillain-barre d. Motor and skeletal muscle (motor and sensory paralysis)) respiratory difficulty limb or trunk weakness. e. Toxic nephritis with albuminuria, cast an edema may also occur

Difficulty swallowing and breathing
• Soft-palate paralysis prevents normal swallowing and can lead to choking or aspiration of food into the lungs, causing aspiration pneumonia. • Paralysis of the diaphragm can lead to difficulty breathing, pneumonia, and even respiratory failure and death. In addition, the membrane at the back of the throat or in the voice box can partially or completely block the airway, resulting in suffocation.

Pneumonia
• Pneumonia can result from the infection itself, or it can be secondary to the swallowing and breathing difficulties

Kidney failure
• The toxin produced by Corynebacteruim diphtheriae can cause kidney failure directly, or kidney failure can develop secondarily as a complication of heart failure.

Death
• The mortality rate is about 5 to 10 percent, although it can climb as high as 20 percent in children under the age of five years. In recent years, the mortality rate in diphtheria epidemics in the independent states of the former Soviet Union has ranged from 3 to 23 percent.

Types of diphtheria(2)
• Respiratory diphtheria • Non respiratory diphtheria

Respiratory diphtheria
Faucial and pharyngeal (tonsilar, uvular, palatar). • Low grade fever, malaise, H/A, sore throat. • w/in 24 hours, small yellowish spot appear in tonsils w/c coalesce to form the adherent pseudomembrane, w/c extends to the rest of fauces and nasopharynx. • Cervical nodes enlarged • Dysphagia and noisy breathing with nasal voice, regurgitation of fluids due to palatal weakness

• Very toxic infection, the bullneck appearance –due to massive enlargement of lymph glands. • Death may occur due to bronchopneumonia or toxic myocarditis.

Laryngotracheal diphtheria (tracheal, bronchial) • More commonly in infants • Hoarseness with barking cough and noisy breathing (croupy cough, braze-metallic cough) • Inspiratory stridor, aphonia, dyspnea with subclavicular and suprasternal retractions. • In severe cases with progressive obstruction leads to suffocation, cyanosis, cardiac failure and death.

Nasal (anterior, posterior) • Occurs mostly at 1st three years of life. • Persistent serous nasal discharged later become bloody and foul smelling. • Discharges: serous –serosanguinous – mucopurulent –(excoriating anterior nares and upper lips) – impetiginous appearance. (Lateral or bilateral.)

Non respiratory diphtheria
• Ocular (conjucntival) reddened • Ears (aural) purulent discharged • Wound and ulcer in the skin • Genito urinary tract – external genitalis, ulcerative lesions on vulva and vagina. • Umbilical of the newborn.

Epidemiology
• Incidence • December to February –higher prevalence occurring at cooler months. • Mainly disease of childhood, peak incidence between 2 to 5 years. • Rare below 6 months due to transplacental transmission of immunity acquired from mother who presumably developed active immunity from inapparent infection.

Prognosis
• The prognosis depends on the size and location of the membrane and on early treatment with antitoxin; the longer the delay, the higher the death rate. The most vulnerable patients are children under age 15 and those who develop pneumonia or myocarditis. Nasal and cutaneous diphtheria are rarely fatal.

You're Reading a Free Preview

Download
scribd
/*********** DO NOT ALTER ANYTHING BELOW THIS LINE ! ************/ var s_code=s.t();if(s_code)document.write(s_code)//-->