6. PAST HISTORY OF ILLNESS
H/o PULMONARY TUBERCULOSIS
AND EXTENSIVE
BROCHOPNEUMONIA since 5 yr
MEDICATION
She take AKT upto 6 month coarse
Stop AKT as per MEDICAL ADVOICE
7. FAMILY HISTORY
HAVING A NUCLEUS FAMILY AND 5
PERSON IS THEIR
*GRANDMOTHER
*FATHER
*MOTHER
*BROTHER
8. IMMUNIZATION
TAKEN
BCG,HEP-B,’0’POLIO …NOT TAKE STAT OR
WHENEVR AT HOSPITALIZATION AT TIME OF
LABOUR …..SHE TAKE AT 21 DAYS IN
ANGANWADI
AFTER OPV1/2/3,DPT1/2/3,HEP-B1/2/3,DPT
BOOSTER ,POLIO BOOSTER,MEASCLE AND
BOOSTER ,VITAMIN 1 AND 2 TAKE AS PER
UNIVERSAL SHEDULE
VITAMIN 3 TO 9 DOSE AND DT 5 YEAR ARE
NOT TAKEN
9. ECONOMIC STATUS
TOTAL INCOME OF FAMILY IS UPTO
10,000/month FROM LABOUR IN FARM
AND CELLING GOAT,BIRDS.THEY ARE
VERY MUCH POOR AND UNHYGENIC
FAMILY.
EXPENDITURE ON HEALTH
SPEND ONLY 20%,NEARLY 2000 FOR
SHOPING VEGITABLE ,OIL,AND KITCHEN
NECESSORY MATERIAL AND SO ON FROM
WEEKLY MARKET.
THEIR HOUSE IS ‘KACCHA”.
10. DIET PLAN
THEY TAKE BOTH VEG AND NONVEG DIET.
RUPALI WANT NEARLY 1500 Kcal DAILY IN
HER DIET PLAN
SHE TAKE DIALY
MILK 300ml AT MORNING
TAKE BRAKFAST WITH 1 CHAPATI AND TEA
LUNCH BEFOUR SHOOL 2 CHAPATI ½ CUP
RISE ½ SABJI(dal) OR NONVEG LIKE EGG
LUNCH IN SCHOOL TAKE ½ CUP KHICHADI
DINNER 2 CHAPATI ½ CUP DAL OR
NONVEG ATEMS LIKE BIRDS,FISH,CHIKEN etc
11. CHILD PERSONAL DATA
PRENATAL HISTORY
MOTHER OF CHILD HAVING TAKE ALL
TRATMENT AS PER GOI WITH RESPECTIVE
NEARER P.H.C
NO.ANY COMPLICATION REGARDING FTND
AT HOME DELIVERY BY TRAIN DAI.
13. POSTNATAL
IN NEONATAL AND INFANT PERIOD
PROVIDED EXCLUSIVE BREAST FEEDING
UPTO 6 MONTH AND WEANING FOOD
STARTD FROM THEM
14. GROWTH AND DEVELOPMENT
S
R
ANTHRO. IN
BOOK
IN
PATIE
NT
INTER
ACTIO
N
1 HEIGHT 133 132 1 cm less
2 WEIGHT 28 18 VERY LESS
3 H.C - - -
4 C.C - - -
15. Developm
ant
IN BOOK IN PATIENT
Gross
motor
Enjoying all
physical
activity
LESS Enjoying
physical activity
Fights may
Occur
Fights
Occur in patient
Continues to
collection
eg hobbies
Continues to
collection ALSO
eg hobbies
30. CONGENITAL CAUSES
2Kartagener syndrome
2 primary immunodeficiencies
2 Williams-Campbell syndrome and Marfan’s
syndrome.
2 Patients with alpha 1-antitrypsin deficiency
have been found to be particularly
susceptible to bronchiectasis,
32. INFECTIVE CAUSES ASSOCIATED WITH
BRONCHIECTASIS INCLUDE
2 infections caused by
the Staphylococcus,
Klebsiella, or
Bordetella pertussis,
the causative agent of
whooping cough.
33. ASPIRATION OF AMMONIA AND OTHER TOXIC
GASES,
2 pulmonary aspiration,
2alcoholism, heroin (drug use),
2 various allergies all appear to be linked
to the development of Bronchiectasis
34. 3Childhood Acquired Immune Deficiency
Syndrome (AIDS), which predisposes patients
to a variety of pulmonary ailments, such as
pneumonia and other opportunistic infections.
3 Inflammatory bowel disease, especially
ulcerative colitis.
3 A Hiatal hernia can cause Bronchiectasis when
the stomach acid that is aspirated into the
lungs causes tissue damage.
35. CLINICAL MANIFESTATION
The production of large quantities of purulent
and often foul-smelling sputum.
The volume of sputum can be used for
estimating the severity of the disease
2 Mild < 10 mL
2 Moderate 10~150 mL
2 Severe >150 mL
36. OTHER
2 Some people with bronchiectasis may
produce frequent green/yellow sputum (up to
240ml daily.
2 Bronchiectasis may also present with
hemoptysis
2 Pneumonia
2 Bad breath indicative of active infection.
2 Frequent bronchial infections and
breathlessness are two possible indicators of
37. 2. Chronic cough
3.Hemoptysis:
Frequent
More commonly in dryvariety
Usually mild (blood streaking ofpurulent
sputum)
Massive hemoptysis is usually from
dilated bronchial arteries or bronchial-
pulmonary anastomoses under systemic
pressure
41. Due to etiological factor
Inflammation of bronchial wall
causing
Loss of supporting structure
Result in
Thick sputum that obstruct the bronchi
The bronchial wall become
permanently dialated and distorted
47. INVESTIGATION
3 History and physical examination
3 Chest x-ray
3 CT (computerised tomography) scan
3 Blood tests
3 Testing of the mucus to identify any bacteria
present
3 Checking oxygen levels in the blood
3 Lung function tests (spirometry).
48. Spirometry and Arterial
Blood Gas Analysis
Supportive evidence of airway disease (Obstructive
defect) Severity assessment (Severe impairment =
poor prognosis) Bronchodilator therapy (Positive
bronchodilator response) Oxygen therapy
(Hypoxemia)
53. TREATMENT
Therapy has several major goals:
(1)Treatment of infection, particularly during acute
exacerbations
(2) Improved clearance of tracheobronchial secretions
(3) Reduction of inflammation
(4) Treatment of an identifiable underlying problem
54. TREATMENT
2 Treatment of bronchiectasis includes
2 controlling infections and bronchial
secretions,
2 relieving airway obstructions,
2 removal of affected portions of lung by
surgical removal or artery embolization
2 preventing complications.
56. 2. Antibiotic
The choice of antibiotics should be
accurately by the results of sputum
culture and drug sensitivity test.
Empirical therapy ---
antipseudomonal antibiotics.
57. ANTIBIOTICSARETHE OF BRONCHIECTASIS
MANAGEMENT
2 Antibiotics are used only during acute
episodes
2 Choice of an antibiotic should be guided by
gram's stain and culture of sputum
2 Empiric coverage (amoxicillin, co-
trimoxazole,levofloxacin) is often given
initially
58. BRONCHODILATER
Bronchodilators to improve
obstruction and aid clearance
of secretions are useful in
patients with airway
hyperreactivity and reversible
airflow obstruction
60. Surgical management is indicated
1. Recurrent and refractory clinical
symptoms are due to a focal area
of disease involvement.
2. Massive hemoptysis
Management of hemoptysis
61. NURSING MANAGEMENT:
2 History and physical examination
2 Obtain history regarding amount
and characteristics of sputum
produced, including haemoptysis.
2 Auscultate lungs for diffuse rhonchi
64. Bronchiectasis: Summary
Abnormal irreversibly dilated and often
thick-walledbronchi
Pathogenesis related to one or more
defects ofmucociliary clearance, cellular
and immunity defense mechanism or
presence of associated conditions
“The vicious cycle”and P aeruginosa
contributes progression and severity of
disease
Imaging greatly helps in diagnosis: Tram
line, honeycombing, cystic, signet ring sign
Additional test may be required in specific
clinical settings
Microbiology of the diseased
airway may aidproper
antimicrobial therapy
