Transcript Slide 1
CASE PRESENTATION
RESPIRATORY DISTRESS SYNDROME
PREPARED BY ARUNIMA ANN
(NICU)
DEMOGRAPHIC DATA
Case number : 326
Age: newborn
Date of birth : 11-12-201
Sex
:female
A.O.G: 28wks
Weight: 1.1kg
Diagnosis: preterm, respiratory distress syndrome
PHYSICAL ASSESSMENT
Vital signs
Temperature is 36.2 0c. Baby is in incubator with humidity of 70%
Heart rate
Heart rate is 164bpm
Respiration
Baby is on SIMV mode with PIP18, PEEP5, & rate of 40,Fio2 is 25%.
One dose of Survanta given. CXR shows mild RDS. Baby is tachypnic.
GENERAL MEASUREMENT
Head circumference : 26cm.
Chest circumference : 24cm.
Weight : 1.1kg.
Length : 37cm.
SKIN
Acrocyanosis at birth. Skin reddened and thin so blood vessels early
seen. Lanugo is present all over the body. UVC is present on the umbilicus.
Umbilicus is drying.
HEAD: Head appears large in proportion to the body.A.F is soft and flat
EYES: Eyes are symmetrical in position. No abnormal discharge.
NOSE: Nostrils are patent bilaterally. Nasal flaring are present. No nasal
discharge. Obligate nose breathers
MOUTH AND THROAT: Uvula midline. Oral secretion is present Mucosa is
moist. Tongue moves freely and does not protrude.
NECK: Turns to side to side. clavicle intact. evident xiphoid process
CHEST: nipples symmetrical
ABDOMEN: dome shape, soft to palpate,UVC present, cord dry at base,
bowel sound present on auscultation
GENITALIA: clitoris and labia minora slightly large voiding ad equating me
conium passed with in 24 hrs
BACK: Intact spine without masses or opening.
EXTRIMITERS: Full range of motion. ten fingers and toes .creases are
located only in front of the sole.
PATIENT HISTORY
Maternal medical history: 36 old mother with G2P1A0 and LSCS was done
due to PET and HELLP syndrome
PATIENT HISTORY:
Present medical history: Baby girl 28 weeks gestational age was delved
in KING KAHLID HOSPITAL by LSCS due to severe PET and HELLP
syndrome
APGAR score was 5/1 and 7/5.baby was intubated immediately and given
the first dose of Survanta and connected to mechanical ventilator with
setting of PIP18,PEEP5 and RR 60/mt .
INTRODUCTION OF RDS
RDS also known as hyaline membrane disease. It occurs almost extremely premature
infants .incidence and severity of RDS are related inversely to gestational age of the
newborns
ETIOLOGY :
Preterm babies
LSCS
Multiple pregnancy
Maternal diabetics
Delivery complications
Me conium stained
Infections
Rapid labor
ANATOMY AND PHYSIOLOGY
ANATOMY AND PHYSIOLOGY
DISEASE DISCUSSION
The lungs are developmentally deficient in a material called surfactant,
which allows the alveoli to remain open throughout the normal cycle of
inhalation and exhalation
Surfactant is a complex system of lipids, proteins and glycoprotein’s
which are produced in specialized lung cells called Type II cells or Type II
pneumocytes. The surfactant is packaged by the cell in structures called
lamellar bodies, and extruded into the alveoli. The lamellar bodies then
unfold into a complex lining of the alveoli. This layer reduces the surface
tension of the fluid that lines the alveolar walls.
During exhalation the walls of the alveoli come in contact and surface
tension tends to cause them to stick together, preventing re-inflation. By
reducing surface tension, surfactant allows the alveoli to re-expand with
inspiration. Without adequate amounts of surfactant, the alveoli collapse
and are very difficult to expand.
Microscopically, a surfactant deficient lung is characterized by collapsed
alveoli alternating with hyper aerated alveoli, vascular congestion and,
in time, hyaline membranes.
Hyaline membranes are composed of fibrin, cellular debries, red blood
cells, rare neutrophils and macrophages. They appear as an eosinophilic,
amorphous material, lining or filing the alveolar space and blocking gas
exchange.
As a result, blood passing through the lungs is unable to pick up oxygen
and unload carbon dioxide from the alveolar spaces . Blood oxygen levels
fall and carbon dioxide rises, resulting in rising blood acid levels and
hypoxia . Structural immaturity , as manifest by low numbers of alveoli,
also contributes to the disease process.
PATHOPHYSIOLOGY
PREMATURITY
Decreased surfactant
Increased alveoli surface
tension
Hypoxemia
atelectasis
Respiratory Acidosis
Pulmonary vasoconstriction
Capillary damage
Fibrin exudate
respiratory
distress
syndrome/hya
line
membrane
disease
Co2 retention
SIGNS AND SYMTOMS
Bluish color of the skin and mucus membrane
Apnea
Decrees urine out put
Grunting
Nasal flaring
Hypothermia
Shallow breathing and rapid breathing
DIAGNOSTIC EVALUVATION
ABG: shows low O2 and excess acid in the body fluid
Chest x-ray: shows lungs have a characteristic ground glass appearance
with often develops 6-12 after birth
Lab test: at birth PH-7.40,PCO2-68,HCO3-25.4,BE—1
NURSING INTERVENSTIONS
Promoting adequate gas exchange
Maintain thermoregulation
Promoting adequate nutrition and hydration
Encouraging parental attachment
TREATMENT
Infant will be given warm, moist o2 intubated a breathing machine
can be life saving especially
High level of co2 in arteries
Low blood o2 in arteries
Low blood PH acidity
A treatment with C-PAP delivers slightly pressurized air through
nose and can help the airway open
Antibiotics
PROGNOSIS
Condition worsens for 2-4 days some infants will die due to RDS during 2-
7 days of life
COMPLICATIONS OF RDS
Pneumothorax
Septicemia
BPD
PDA
Pulmonary hemorrhage
NEC
Retinopathy of prematurity(ROP)
MANAGEMENT OF NEONATAL
RESPIRATORY DISTRESS
INFANT WITH RDS
Infant with
RDS
Mild tache/grunting
Severe grunting
Observe for10-20mt
suggest
resuscitate
Clinical improvement
no
Ventilation,nicu,lab test
yes
Resolve spontaneously
Chest x-ray
o2
Nicu
no
IMPAIRED GAS EXCHANGE RELATED TO DISEASE PROCESS
Assessment
Planning
implementation
Vital signs:
Tem:36.6
RR:68/mts
PR:160/mts
Spo2:80%
ABG:
PH:7.28
PCO2:68
PO2:70
HCO3:28
BE:-2.5
+nasal flaring
+Acrocyanosis
T o maintain the normal
parameters of respiration
including saturation co2 and
respiratory rate
Cleaned the airway by
proper suctioning when
there is secretions
Kept the head in sniffing
position
Properly monitored all
vital signs and saturation
Elevated the head end
Checked the ABG level
Administered
Ventilator support
Rationale
To maintain patient airway
ABG show pco2 &PH level
To prevent hypoxia
Evaluation
RR-52/mnt
O2 saturation 98%
ABG:
PH-7.28
PCO2-39
HCO3-23
BE-1.1
INEFFECTIVE THERMOREGULATION RELATED TO IMMATURETY
Assessment
Subjective data
Baby is crying continuously and
seems to be irritable
objective data
Temperature 36.4c
Planning
implementation
To maintain the temperature within
the normal range
Rationale
Received baby in pre-
warm radiant warmer
Adjusted incubator or
radiant warmer to obtain
desired skin temperature
Provided kangaroo care
[skin-skin contact]
Put the pre warmed
gloves
around the nest
To prevent water loss&
potential for hypoglycemia
To prevent hypothermia
which may result in
vasoconstriction &
acidosis
Evaluation
After 1 hour of nursing
intervention the goals
were fully met as
manifested by:
Temperature:
T= 36.7 c
Absence of bluish
discoloration present in
extremities
Warm to touch
NURSING HEALTH TEACHING
Instruct the parents about,
Kangaroo care,
Breast Feeding
Proper covering of the baby[warm blanket]
Ensure that the family receives information on routine well baby care.
Before discharge, parents should feel comfortable in their abilities to
care for the infant.
Educate them,importance of regular health care, periodic eye
examinations, and developmental follow up with the parents
CONCLUSION
Presented a case of preterm new born baby with respiratory distress
Baby relived from signs and symptoms of RDS
Thermoregulation maintained
Baby discharged after good care with Mixavit and iron drops
BIBLIOGRAPHY
Maternal and Child Health Nursing by Adele Pillitteri 5th edition; volume 1
page 426- 433;page 329-332
Lippincott Manual of Nursing Practice 9th edition
Lange clinical manual neonatology fifth edition-by Gomella,Douglas,Fabien
Neonatal resuscitation 5th edition