1. NEKEMTE HEALTH SCIENCE COLLEGE
DEPARTMENT OF NURSING
FOR POST BASIC BSC STUDENTS
Title: Nursing managements of patient with
Leprosy (Hansen’s disease)
Nov. 2023
1/1/2024
BY ABDI WAKJIRA
1
2. COURSE OUTLINE
1/1/2024
By Abdi Wakjira( Bsc, Msc)
2
At the end of this chapter students will able to:-
Assess & provide nsg care for pt with Leprosy
Assess & provide nsg care for pt with Measles
Assess & provide nsg care for pt with Diphteria
Assess & provide nsg care for pt with Pertussis
Assess & provide nsg care for pt with Chicken pox
Assess & provide nsg care for pt with Influenza
3. LEPROSY (HANSON’S DISEASE)
Definition
A chronic bacterial disease of the skin,
peripheral nerves and, in lepromatous patients,
the upper airway
Infectious agent
Mycobacterium leprae
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4. Epidemiology
Occurrence- Although common in rural
tropics and subtropics, socio-economic
conditions may be more important than climate
itself. Endemic in south and southeast Asia,
tropical Africa and Latin America.
Reservoir- Humans
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5. Mode of transmission-
Not clearly established. Household
and prolonged close contact appear to be important.
Millionsof bacilli are liberated daily in the nasal
discharges of untreated lepromatous patients.
Cutaneous ulcers in lepromatous patients may shed
large number of bacilli.
Organisms probably gain access (entrance) through
the URT and possibly through broken skin.
In children less than one year of age, transmission is
presumed to be transplacental.
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6. Leprosy Cont…d
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Incubation period- 9 months to 20 years;
2-5 years on average.
Period of communicability- Infectiousness is lost
in most instances within 3months of continuous and
regular treatment with dapsone or clofazamin or
within 3 days of rifampicin treatment.
Susceptibility and resistance-
The presence and form of leprosy depend on the
ability to develop effective cell mediated
immunity.
7. Classification
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WHO classification: clinical diagnosis
o Paucibacillary (PB): 1-5 lesions, only 1 nerve involved
o Multibacillary (MB): >5 lesions, 2 or more nerves
involved
Laboratory confirmation by skin smears (often not feasible
in practice as laboratory infrastructure is needed):
o Negative: PB
o Positive: MB
Skin biopsy for negative skin smear (PB) and/or to rule
out other differential diagnosis
8. Clinical Manifestation
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BY ABDI WAKJIRA
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Clinical manifestations vary between two polar
forms:
lepromatous and tuberculoid leprosy.
1. Lepromatous (Multibacillary form)
Nodules, papules, macules and diffused infiltration
are bilaterally symmetrical and usually numerous
and extensive.
Involvement of the nasal mucosa may lead to
crusting, obstructed breathing and epistaxis.
Occular involvement leads to iritis and keratitis.
9. Clinical Manifestation cont…d
2. Tuberculoid (Paucibacillary form)
Skin lesions are single or few, sharply demarcated,
anesthetic or hyperesthetic and bilaterally
symmetrical. Peripheral nerve involvement tends to
be severe.
Borderline
Has features of both polar forms and is more liable to
shift toward the lepromatous form in untreated
patients and toward the tuberculoid form in treated
patients.
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BY ABDI WAKJIRA
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10. Mode of Transmission
Droplet infection: Leprosy is believed to
transmit through nasal discharge.
Contact infection: Studies indicate that
leprosy is transmitted through direct skin
contact.
Vector- born infection
Through placenta & milk
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12. Sign & symptoms
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Numbness & loss of touch, pain,
temperature sensation.
Granulomas of the nerves, respiratory
tract, skin & eye.
Pain less ulcer
Skin lesions
Loss of digits
Facial disfigurement
13. pathophysiology
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BY ABDI WAKJIRA
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M. laprae enters the body(skin, nose etc)
Peripheral nerves
Binds to Schwann cells of axon
Loss of axonal conductance
Deformity(loss of pain, temperature, touch, sensation)
14. Diagnosis
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BY ABDI WAKJIRA
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Complete skin examination (hyperesthesia,
anesthesia, paralysis, muscle wasting or
trophic ulcer which are signs of peripheral
nerve involvement),
with bilateral palpation of peripheral nerves
(ulnar nerve at the elbow, peroneal nerve at
head of fibula and the great auricular nerve)
for enlargement and tenderness.
15. Diagnosis Cont …d
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BY ABDI WAKJIRA
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Skin lesion are tested for sensation (light
touch, pink
prick, temperature discrimination).
Demonstration of AFB in skin smears made by
scraped incision method.
Skin biopsy confined to the affected area
should be sent to the experienced pathologists
in leprosy diagnosis.
16. Treatment
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BY ABDI WAKJIRA
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1. Dapsone three drugs for 12 months and then
2. Refampicin dapsone alone for the next12months.
3. Clfazamin
4. Aspirin for mild reactions and inflammation
5. Severe reaction can be treated with
corticosteroids
6. Surgical Managements
17. Nursing Care
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BY ABDI WAKJIRA
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Detect the disease in the initial stage
Keep watch over other susceptible
patients
Take care of localized wound
Rehabilitation of cured persons.
Provide health education.
Provide psychosocial support
Provide follow-up service.
20. Measles (Rubella)
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BY ABDI WAKJIRA
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Definition:
An acute highly communicable viral disease
Infectious agent
Measles virus, single - stranded, enveloped RNA
virus with 1 serotype; classified as a member of the
genus Morbillivirus in the paramyxoviridae family.
Epidemiology
Occurrence- Prior to widespread immunization,
measles was common in childhood so that more
than 90% of people had been infected by age
20;
few went through life without any attack.
Reservoir- Humans
21. Mode of transmission
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Airborne by droplet spread, direct contact with
nasal or throat secretions of infected persons, and
Less commonly by articles freshly solid with nose
and throat secretion.
Greater than 94% herd immunity may be needed to
interrupt community transmission.
Incubation period : 7-18 days from exposure to
onset of fever
22. Period of communicability
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BY ABDI WAKJIRA
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4 before to 4 days after the onset of rash.
Susceptibility and resistance:
All those who are non vaccinated or have not
had the disease are susceptible.
Permanent immunity is acquired after natural
infection or immunization.
23. Clinical Manifestation
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BY ABDI WAKJIRA
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ƒ
Prodromal fever, conjunctivitis, coryza, cough
and Koplik spots on the buccal mucosa
Rash: 2- 4days after prodrome, 14days after
exposure.
Maculopapular becomes confluent
Begins on face & head
Persists 5- 6 days
Fade in order of appearance.
Leucopoenia is common.
24. Measles clinical Case Definition
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Generalized rash lasting >3 days, and
Temperature >38.3 C (101 F), and
Cough, coryza, or conjunctivitis
26. Measles Diagnosis
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BY ABDI WAKJIRA
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Based on clinical and epidemiological grounds
Laboratory Diagnosis:
Isolation of measles virus from a clinical
specimen (e.g., nasopharynx, urine)
Significant rise in measles IgG by any
standard serologic assay (e.g., Enzyme linked
immunosorbentassay EIA, Hemagglutination
inhibition assay,HA)
Positive serologic test for measles IgM
antibody
28. Measles Vaccine
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Composition Live virus
Efficacy 95% (range, 90%-98%)
Duration of
Immunity Lifelong
Schedule 2 doses
Should be administered with mumps and
rubella as MMR
29. Nursing care
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1.Advise patient to have bed rest.
2. Relief of fever.
3. Provision of non-irritant small frequent diet.
4. Shorten the fingernails.
Prevention and control
1. Educate the public about measles immunization.
2. Immunization of all children (less than 5 years of
age)
who had contact with infected children.
3. Provision of measles vaccine at nine months of age.
4. Initiate measles vaccination at 6 months of age
during epidemic and repeat at 9 months of age.
31. FOR POST BASIC NURSING STUDENTS
TITLE: NURSING MANAGEMENT OF PATIENTS WITHDIPHTERIA
1/1/2024 BY ABDI WAKJIRA9BSc, MSc) 31
32. DIPHTERIA
Definition:
An acute bacterial disease involving primarily
tonsils, pharynx, nose, occasionally other
mucus membranes or skin and sometimes
the conjunctiva or genitalia.
Infectious agent:
Corynebacterium diphtheriae
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34. DIPHTERIA Cont …d
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BY ABDI WAKJIRA9BSc, MSc)
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Epidemiology
Occurrence- Disease of colder months in
temperate zones, involving primarily non-
immunized children under 15 years of age.
It is often found among adult population
groups whose immunization was neglected.
Unapparent, cutaneous and wound diphtheria
cases are much more common in the tropics.
Reservoir- Humans
35. DIPHTERIA Cont …d
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BY ABDI WAKJIRA9BSc, MSc)
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Mode of transmission: contact with a patient of
carrier. i.e. with oral or nasal secretions or infected
skin.
Asymptomatic respiratory tract carriage is
important in transmission. Where diphtheria is
endemic, 3-5% of healthy individuals can carry
toxigenic organisms
Skin infection and skin carriage are silent reservoirs
and organisms can remain viable in dust or on
fomites for up to 6 months
Transmission through contaminated milk and an
infected food handler has been documented
36. DIPHTERIA Cont …d
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BY ABDI WAKJIRA9BSc, MSc)
36
Incubation period: usually 2-5 days
Period of communicability: variable,
until virulent bacilli have disappeared from
discharges and lesion; usually 2
weeks or less.
37. DIPHTERIA Cont …d
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BY ABDI WAKJIRA9BSc, MSc)
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Susceptibility and resistance:
Susceptibility is universal.
Infants borne to immune mothers are relatively
immune, but protection is passive and usually lost
before 6 months.
Recovery from clinical disease is not always
followed by lasting immunity.
Immunity is often acquired through unapparent
infection.
Prolonged active immunity can be induced by
diphtheria toxoid
38. EPIDEMIOLOGY
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BY ABDI WAKJIRA9BSc, MSc)
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Children aged 1-5yrs are commonly infected
A herd immunity of 70% is required to prevent
epidemics
Contaminated objects like thermometers, cups,
spoons, toys and pencils can spread the disease
Overcrowding, poor sanitation and hygiene,
illiteracy, urban migration and close contacts
can lead to outbreak
39. PATHOGENESIS
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BY ABDI WAKJIRA9BSc, MSc)
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Within the first few days of respiratory tract infection , a dense necrotic coagulum
of organisms, epithelial cells, fibrin, leukocytes and erythrocytes forms, advances,
and becomes a gray-brown, leather-like adherent pseudomembrane . Removal is
difficult and reveals a bleeding edematous submucosa
The major virulence of the organism lies in its ability to produce the potent 62-
kd polypeptide exotoxin, which inhibits protein synthesis and causes local
tissue necrosis
Entry into nose or mouth
The organism remains in the superficial layers of skin lesions or respiratory tract
mucosa, inducing local inflammatory reaction
40. Cont…d
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BY ABDI WAKJIRA9BSc, MSc)
40
Local effect of diphtheritic toxin:
Paralysis of the palate and hypopharynx
Pneumonia
Systemic effects (Toxin absorption ):
kidney tubule necrosis
hypoglycemia
myocarditis and/or demyelination of nerves
Myocarditis:10-14 days
Demyelination of nerves: 3-7 weeks
41. Clinical Manifestation
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BY ABDI WAKJIRA9BSc, MSc)
41
Characteristic lesion marked by a patch or patches of an
adherent grayish membrane with a surrounding
inflammation (pseudo membrane).
Throat is moderately sore in pharyngo tonsillar
diphtheria, with cervical lymph nodes somewhat enlarged
and tender;
in severe cases, there is marked swelling and edema of
neck.
Late effects of absorption of toxin appearing after 2-6
weeks, including cranial and peripheral, motor and
sensory nerve palsies and myocarditis (which may occur
early) and are often severe.
42. Clinical Manifestation Cont …d
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Influenced by the anatomic site of infection,
the immune status of the host and the
production and systemic distribution of toxin.
Classification (location):
nasal
pharyngeal
tonsillar
laryngeal or laryngotracheal
skin, eye or genitalia
43. Clinical Manifestation Cont …d
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Nasal diphtheria: Infection of the anterior
nares- more common among infants,
causes serosanguineous, purulent, erosive
rhinitis with membrane formation
Shallow ulceration of the external nares and
upper lip is characteristic
Unilateral nasal discharge is quite
pathognomic of nasal diphtheria
Accurate diagnosis of nasal diphtheria
delayed-paucity of systemic signs and
symptoms
44. Clinical Manifestation Cont …d
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Tonsillar and pharyngeal diphtheria:
sore throat is the universal early symptom
Only half of patients have fever and fewer have
dysphagia, hoarseness, malaise, or headache
Mild pharyngeal injection unilateral or bilateral
tonsillar membrane formation extend to involve the
uvula, soft palate, posterior oropharynx,
hypopharynx, or glottic areas
Underlying soft tissue edema and enlarged lymph
nodes: bull-neck appearance
45.
46. Clinical Manifestation Cont …d
Laryngeal diphtheria: At significant risk for suffocation
because of local soft tissue edema and airway obstruction by
the diphtheritic membrane
Classic cutaneous diphtheria is an indolent, nonprogressive
infection characterized by a superficial, ecthymic, nonhealing
ulcer with a gray-brown membrane
47. Clinical Manifestation Cont …d
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Infection at Other Sites:
Ear (otitis externa), the eye (purulent and ulcerative
conjunctivitis), the genital tract (purulent and
ulcerative vulvovaginitis) and sporadic cases of
pyogenic arthritis
Diagnosis
Clinical features
Culture: from the nose and throat and any other
mucocutaneous lesion. A portion of membrane should be
removed and submitted for culture along with underlying
exudate
Elek test: rapid diagnosis (16-24 hrs)
48. Diagnosis Cont …d
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Enzyme immunossay
PCR for A or B portion of the toxic gene “tox”
Hypoglycemia, glycosuria, BUN, or abnormal ECG for liver,
kidney and heart involvement
Differential diagnosis:
1. Common cold
2. Congenital syphilis snuffle
3. Sinusitis
4. Adenoiditis and foreign body in nose
5. Streptococcal pharyngitis
6. Infectious mononucleosis
49. Complication
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1. Respiratory tract obstruction by pseudomembranes:
bronchoscopy or intubation and mechanical ventilation
2. Toxic Cardiomyopathy:
-in 10-25% of patients
-responsible for 50-60% of deaths
-the risk for significant complications correlates directly
with the extent and severity of exudative local
oropharyngeal disease as well as delay in administration
of antitoxin
-Tachycardia out of proportion to fever
-prolonged PR interval and changes in the ST-T wave
50. Complication
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3. Toxic Neuropathy:
Acutely or 2-3 wk after: hypoesthesia and soft palate
paralysis
Afterwards weakness of the posterior pharyngeal,
laryngeal, and facial nerves : a nasal quality in the voice,
difficulty in swallowing and risk for aspiration
Cranial neuropathies (5th wk): oculomotor and ciliary
paralysis- strabismus, blurred vision, or difficulty with
accommodation
Recovery from the neuritis is often slow but usually
complete. Corticosteroids are not recommended.
51. Treatment
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1. Diphtheria antitoxin
2. Erythromycin for 2 weeks but 1 week for
cutaneous form or
3. Procaine penicillin for 14 days or single
dose of Benzathin penicillin Primary goal of
antibiotic therapy for patients or carriers is to
eradicate C. diphtheriae and prevent
transmission from the patient to susceptible
contacts.
53. Prevention and control
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1. Educate the public, and particularly the parents of
young children, of the hazards of diphtheria and the
necessity for active immunization.
2. Immunization of infants with diphtheria toxoid.
3. Concurrent and terminal disinfection of articles in
contact with patient and soiled by discharges of
patient.
4. Single dose of penicillin (IM) or 7-10 days course of
Erythromycin (PO) is recommended for all persons
exposed to diphtheria.
54. Prevention and control Cont …d
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4. Single dose of penicillin (IM) or 7-10 days course of
Erythromycin (PO) is recommended for all persons
exposed to diphtheria.
Erythromycin (40-50 mg/kg/day divided qid PO for
10 days) or a single injection of benzathine
penicillin G (600,000U IM for patients <30 kg,
1,200,000U IM for patients ≥30 kg)
55. Nursing Management
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1.Nursing assessment
History
Physical exam
2. Nursing diagnosis
Hyperthermia related to the release of an exotoxin,
Imbalanced nutrition less than body requirements
related to painful swallowing.
Ineffective air way clearance related to
pseudomembrane blocking the air way.
56. Nursing Management
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3. Nursing care planning and Goals:-
The nursing care planning goals includes:
The client will be able to maintain a clear air
way.
The client will be able to maintain a normal
body temperature
The client will be able to demonstrate &
maintain a normal body weight.
4. Nursing Interventions
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BY ABDI WAKJIRA (BSc, MSc) 59
FOR POST BASIC NURSING
STUDENTS
TITLE: NURSING MANAGEMENT
OF PATIENT
WITH
PERTUSSIS (WHOOPING
60. Pertusis (whooping cough)
Definition:
An acute bacterial disease involving the respiratory
tract.
Cough of 100 days
Whooping cough: whooping sound made when gasping for
air after a fit of coughing
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61. Pertusis (whooping cough)
Infectious agent:
Bordetella pertusis – is aerobic gram-negative
coccobacilli
Produces toxins namely pertussis toxin,
filamentous hemagglutinin, hemolysin,
adenylate cyclase toxin, dermonecrotic toxin
and tracheal cytotoxin- responsible for
clinical features (toxin mediated disease) and
the immunity
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62. Pertusis (whooping cough)
Epidemiology
Occurrence- An endemic disease common to
children especially young children everywhere in
the world.
A marked decline has occurred in incidence
and mortality rates during the past four
decades.
Outbreaks occur periodically.
Endemic in developing world and 90% of
attacks occur in children under 6 years of age.
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63. PATHOGENESIS
-This exudate predisposes to atelectasis, cough, cyanosis and
pneumonia -Organism causes local tissue damage and systemic
effects mediated through its toxin
The organism get attached to the respiratory cilia and toxin
causes paralysis of cilia
mucopurulent-sanguineous exudate forms in the
respiratory tract
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64. Pertussis cont…d
Mode of transmission- Primarily by direct
contact with discharges from respiratory
mucus membranes of infected persons by
airborne route, probably by droplets.
Indirectly by handling objects freshly solid
with nasopharyngeal secretions.
Incubation period- 1-3 weeks
Infection lasts for 6 weeks – 10 weeks
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65. Pertussis cont…d
Period of communicability:
Highly communicable in early catarrhal stage
before the paroxysmal cough stage.
The most contagious disease with an attack rate
of 75-90%. Gradually decreases and becomes
negligible in about 3 weeks.
When treated with erythromycin, infectiousness is
usually 5 days or less after onset of therapy.
Susceptibility and resistance- Susceptibility to
non immunized individuals is universal.
One attack usually confers prolonged immunity
but may not be lifelong.
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66. Clinical manifestation
The disease has insidious onset and 3 phases:
1. Catarrhal phase
Lasts 1-2 weeks
Cough and rhinorrhea
2. Paroxysmal phase
Explosive, repetitive and prolonged cough
Child usually vomits at the end of paroxysm
Expulsion of clear tenacious mucus often followed
by vomiting
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67. Clinical manifestation cont… d
2. Paroxysmal phase cont…d
Whoop (inspiratory whoop against closed
glottis) between paroxysms.
Child looks healthy between paroxysms
Paroxysm of cough interferes with nutrition
and cough
Cyanosis and sub conjunctiva hemorrhage
due to violent cough.
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68. 2. Paroxysmal phase cont…d
Cough increase for next 2-3 weeks and
decreases over next 10 weeks
Absence of whoop and/or post-tussive
vomiting does not rule out clinical
diagnosis of pertussis
paroxysmal cough>2 weeks with or
without whoop and/or post-tussive
vomiting is the hallmark feature of
pertussis
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69. 3. Convalescent phase
The cough may diminish slowly or may last
long time.
period of gradual recovery even up to 6
months
After improvement the disease may recur.
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70. Diagnosis
Difficult to distinguish it from other URTI
1. History and physical examination at phase two
(paroxysmal phase) ensure the diagnosis.
is confirmed by culture, genomics or serology
2. Elevated WBC count with lymphocytosis. The absolute
lymphocyte count of ≥20,000 is highly suggestive
3. Culture: gold standard specially in the catarrhal stage.
A saline nasal swab or swab from the posterior pharynx is
preferred and the swab should be taken using dacron or
calcium alginate and has to be plated on to the selective
medium
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71. Diagnosis
However, culture are not recommended in
clinical practice as the yield is poor because
of previous vaccination, antibiotic use, diluted
specimen and faulty collection and
transportation of specimen.
4. PCR: most sensitive to diagnose; can be
done even after antibiotic exposure. It should
always be used in addition with cultures.
5. Direct fluorescent antibody testing: low
sensitivity and variable specificity.
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72. Differential Diagnosis
1. Bordetella parapertussis, adenovirus,
mycoplasma pneumonia, and
chlamydia trachomatis
2. Foreign body aspiration,
endobronchial tuberculosis and a mass
pressing on the airway.
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73. Differential Diagnosis
1. Secondary pneumonia (1 in 5) and apneic
spells (50%; neonates and infant<6 months
of age)
2. Neurological complications: seizures (1 in
100) and encephalopathy (1 in 300) due to
the toxin or hypoxia or cerebral hemorrhage
3. Otitis media, anorexia and dehydration, rib
fructure, pneumothorax, subdural
hematoma, hernia and rectal prolapse
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74. Treatment
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1. Avoidance of irritants, smoke, noise and other cough
promoting factors
2. Antibiotics: effective only if started early in the course of
illness.
Antibiotics for super infections like pneumonia because of
bacterial invasion due to damage to cilia.
Erythromycin- to treat the infection in phase one but to
decrease transmission in phase two
Erythromycin (40-50 mg/kg/day 6 hrly orally for 2 weeks or
Azithromycin 10 mg/kg for 5 days in children<6 months and
for children>6 months 10 mg/kg on day 1, followed by 5mg/kg
from day2-5 or Clarithromycin 15 mg/kg 12 hrly for 7 days
3. Supplemental oxygen, hydration, cough mixtures and
bronchodilators (in individual cases)
75. Prevention
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All household contacts should be given
erythromycin for 2 weeks
Children <7 years of age not completed the four
primary dose should complete the same at the
earliest ( CDC catch-up schedule).
Children <7 years of age completed primary
vaccination but not received the booster in the last
3 years have to be given a single booster dose
VACCINE
76. Prevention Cont…d
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1. Educate the public about the dangers of whooping
cough and the advantages of initiating
immunization at 6 weeks of age
2. Consider protection of health workers at high risk
of exposure by using erythromycin for 14 days.
77. Nursing care
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1. Proper feeding of the child.
2. Encourage breastfeeding immediately after an
attack (each paroxysm).
3. Proper ventilation- continuous well humidified
oxygen administration.
4. Reassurance of the mother (care giver),
80. Definition
• Chickenpox - also known as varicella, is a highly
contagious viral infection caused by the varicella-
zoster virus (VZV).
• VZV is a DNA virus that is a member of the herpes
virus family.
• After the primary infection, VZV stays in the body
(in the sensory nerve ganglia) as a latent
infection.
81. Pathophysiology
• After initial inhalation of contaminated
respiratory droplets, the virus infects
the conjunctivae or the mucosae of the
upper respiratory tract.
• Viral proliferation occurs in
regional lymph nodes of the upper
respiratory tract 2-4 days after initial
infection; this is followed by primary
viremia on postinfection days 4-6.
82. Pathophysiology Cont …d
• A second round of viral replication occurs in
the body’s internal organs,
• most notably the liver and the spleen, followed
by a secondary viremia 14-16 days post-
infection.
• This secondary viremia is characterized by
diffuse viral invasion of capillary endothelial
cells and the epidermis.
83. Pathophysiology Cont …d
• VZV infection of cells of the malpighian
layer produces both
intercellular edema and intracellular
edema, resulting in the characteristic
vesicle.
• Exposure to VZV in a healthy child
initiates the production of host
immunoglobulin G (IgG), immunoglobulin
M (IgM), and immunoglobulin A (IgA)
antibodies; IgG antibodies persist for life
and confer immunity.
84. Pathophysiology Cont …d
• After primary infection, VZV is
hypothesized to spread from mucosal
and epidermal lesions to local
sensory nerves.
• VZV then remains latent in the dorsal
ganglion cells of the sensory nerves.
• Reactivation of VZV results in the
clinically distinct syndrome of herpes
zoster (shingles).
85. Incubation period
7-21 days
Causative organism
Caused by varicella zoster virus also called
human (alpha)herpes.
86. Sign & symptoms
In Children
• Itchy rash appearance on the head &
spreads down to the trunk & other body
parts
• The rash becomes raised, & blisters
form.
• Blisters may also form on
mucousmemebranes, such as inside the
mouth, nose, throat, & vagina.
87. In Children cont…d
• The blister crust over & disappear within
about 10-14 days.
• Children may also have fever & tiredness
along with rash.
88. Sign & symptoms in adults
Pre-eruptive stage:
At the onset, low or moderate fever, feeling cold,
restlessness, backache etc.
Eruptive phase:
The rash are found on the body which are less on
the face & hands.
Different stages of rashes are ( macular, papular,
vesicular & scabal) found together. This is the
special characteristics of the disease.
The eruptive stage lasts for 4-7 days.
More severe in adults than in children
92. Diagnosis
• S &S, typical spread of rash
• Polymerase chain reaction (PCR) testing. The most
sensitive method for confirming a diagnosis of
varicella is the use of PCR to detect VZV in skin lesions
(vesicles, scabs, maculopapular lesions).
• IgM testing. IgM testing is considerably less sensitive
than PCR testing of skin lesions;
• Blood testing. Most children with varicella have
leukopenia in the first 3 days, followed by
leukocytosis; marked leukocytosis may indicate a
secondary bacterial infection but is not a dependable
sign;
93. Medical Management
• Antiviral therapy. The routine use of
acyclovir or valacyclovir in healthy children if
it can be given within 24 hours after the rash
first appears in children older than 12 years,
• Varicella zoster immune globulin. Varicella
zoster immune globulin
• it is indicated for high-risk individuals within
10 days (ideally within 4 days) of chickenpox
exposure;
• this agent reduces complications and the
mortality rate of varicella, not its incidence.
94. Medical Management Cont….d
• Antibiotic therapy. Suspicion of a
secondary bacterial infection should
prompt the early institution of
empirical antibiotic therapy until the
results of culture studies become
available.
95. Nursing Management
Treatment approaches include:
• supportive measures,
• antiviral therapy,
• administration of varicella-zoster
immune globulin (VZIG), and
• management of secondary bacterial
infection.
96. Nursing Management
Nursing Assessment
• Assessment of a child with chicken pox
includes the following:
• History taking. if any exposure to varicella at
school, daycare, or among family
members has occurred.
• Immunizations - immunocompromised
children often have severe and complicated
varicella, and their mortality rate is higher than
that of immunocompetent children.
97. Nursing Assessment cont..d
Vaccine is available as a single vaccine, also
as part of the MMRV vaccine (measles,
Mumps. Rubella and Varicella vaccine).
Route: Subcutaneous
98. Nursing Diagnosis
Based on the assessment data, the major nursing
diagnoses are:
• Hyperthermia related to viral infection.
• Impaired skin integrity related to mechanical
factors (eg stress, scratch, friction).
• Disturbed body image related to lesions on the
skin.
• Deficient knowledge about the condition and
treatment needs.
• Risk for infection related to damaged skin tissue.
99. Nursing Care Planning and Goals
Desired outcomes for a child with chicken
pox include:
• Client will be comfortable and able to rest.
• Client or caregiver will verbalize needed
information regarding the disease, signs and
symptoms, treatment, and possible
complications of varicella zoster.
• Client will remain free of secondary infection,
and intact skin without redness or lesions.
100. Nursing Care Planning and Goals …
• Client will have minimal risk for disease
transmission through the use of
universal precautions.
• Client will demonstrate positive body
image,
101. Nursing Interventions
Interventions for a child with chicken pox
include:
• Patient education. Educate parents
about the importance and safety of the
Varicella Zoster vaccine.
• Manage pruritus. in patients with
varicella with cool compresses and
regular bathing; warm soaks and
oatmeal or cornstarch baths may reduce
itching and provide comfort.
102. Nursing Interventions …
Trim fingernails. Trimming the child’s
fingernails and having the child wear
mittens while sleeping may reduce
scratching.
Dietary measures. Advise parents to
provide a full and unrestricted diet to the
child; some children with varicella have
reduced appetite and should be
encouraged to take sufficient fluids to
maintain hydration.
103. Evaluation
• The Nurse evaluate whether all goals are met
or not.
Documentation
Documenting all the assessment findings,
Plan of care, current or recent medical therapy,
response to the managements, attainment or
progress toward the desired out come,
modification to plan of care.
106. Influenza
Definition
An acute viral disease of the respiratory tract
Infectious agent
Three types of influenza virus (A,B and C)
Epidemiology
Occurrence: In pandemics, epidemics and
localized outbreaks.
Reservoir- Humans are the primary reservoirs
for human infection.
107. Influenza cont…d
Definition
An acute viral disease of the respiratory tract
Are RNA viruses of orthomyxoviridae family.
Infectious agent
Three types of influenza virus (A,B and C)
Epidemiology
Occurrence: In pandemics, epidemics and
localized outbreaks.
Reservoir- Humans are the primary
reservoirs for human infection.
108. Influenza cont…d
Mode of transmission- Airborne spread
predominates among crowded populations in closed
places such as school buses.
Incubation period- short, usually 1-3 days
Period of communicability- 3-5 days from clinical
onset in adults; up to 7 days in young children.
Susceptibility and resistance- when a new sub-type
appears, all children and adults are equally
susceptible.
Infection produces immunity to the specific infecting
agent.
109. PATHOGENESIS OF INFLUENZA
•
• Influeza Virus
Enter the Respiratory system from an infected individual through
respiratory droplets
• The virus attaches to & replicates in columnar epithelial cells
The virus replicates in cells of both upper & lower respiratory tract
The viral replication combines with the immune response (both humoral
& cell mediated) to infection.
Release of cytokines Leads to destructions & loss of cells lining of the
respiratory tract.
Symptoms such as sore throat, runny nose, cough
110. PATHOPHYSIOLOGY
Influeza Virus
Enter the Respiratory system from an infected individual through
respiratory droplets
The virus attaches to & replicates in columnar epithelial cells
The virus replicates in cells of both upper & lower respiratory tract
The viral replication combines with the immune response (both
humoral & cell mediated) to infection.
Release of cytokines Leads to destructions & loss of cells lining of the respiratory tract.
Symptoms such as sore throat, runny nose, cough
111. Influenza Cont …d
Risk for complication:
Birth to years old
Pregnant women
> 65years old
Long term aspirin therapy
Disorders of the pulmonary or cardiovascular
system
Metabolic disease
112. Influenza Cont …d
Clinical Manifestation
Fever, head ache, mayalgia, prostration, sore
throat and cough
Cough is often severe and protracted, but other
manifestations are self-limited with recovery in 2-
7days
113. Influenza Cont …d
Diagnosis
ƒBased on clinical ground
Treatment
1. Same as common cold, namely:
ƒAnti-pain and antipyretic
ƒHigh fluid intake
ƒBed rest
ƒBalanced diet intake
114. Influenza Cont …d
Prevention and control
1. Educate the public in basic personal hygiene,
especially the danger of unprotected coughs and
sneezes and hand to mucus membrane
transmission.
2. Immunization with available killed virus vaccines
may provide 70-80% protection.
3. Amantadize hydrochloride is effective in the
chemprophylaxis of type A virus but not others.
