CASE PRESENTATION

RESPIRATORY DISTRESS SYNDROME

PREPARED BY ARUNIMA ANN(NICU)

DEMOGRAPHIC DATA

Case number : 326Age: newbornDate of birth : 11-12-201Sex :femaleA.O.G: 28wksWeight: 1.1kgDiagnosis: preterm, respiratory distress

syndrome

Vital signsTemperature is 36.2 0c. Baby is in incubator

with humidity of 70%Heart rateHeart rate is 164bpmRespiration 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.

PHYSICAL ASSESSMENT

Head circumference : 26cm.Chest circumference : 24cm.Weight : 1.1kg. Length : 37cm.

GENERAL MEASUREMENT

SKINAcrocyanosis 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.

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 .

PATIENT HISTORY

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

INTRODUCTION OF RDS

ANATOMY AND PHYSIOLOGY

ANATOMY AND PHYSIOLOGY

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.

DISEASE DISCUSSION

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

Hypoxemia atelectasis

Respiratory Acidosis

Increased alveoli surface tension

Co2 retention

Pulmonary vasoconstriction

Capillary damage

Fibrin exudate

respiratory distress

syndrome/hyaline

membrane disease

Bluish color of the skin and mucus membraneApneaDecrees urine out put Grunting Nasal flaring Hypothermia Shallow breathing and rapid breathing

SIGNS AND SYMTOMS

 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

 

DIAGNOSTIC EVALUVATION

 Promoting adequate gas exchange Maintain thermoregulationPromoting adequate nutrition and

hydrationEncouraging parental attachment

NURSING INTERVENSTIONS

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 acidityA treatment with C-PAP delivers slightly

pressurized air through nose and can help the airway open

Antibiotics

TREATMENT

Condition worsens for 2-4 days some infants will die due to RDS during 2-7 days of life

COMPLICATIONS OF RDSPneumothoraxSepticemiaBPDPDAPulmonary hemorrhageNECRetinopathy of prematurity(ROP)

PROGNOSIS

INFANT WITH RDS

MANAGEMENT OF NEONATAL RESPIRATORY DISTRESS

Severe grunting

suggest

resuscitate

Clinical improvement

no

Ventilation,nicu,lab test

Mild tache/grunting

Observe for10-20mt

Resolve spontaneouslyyesno

Chest x-ray

o2

Nicu

Infant with RDS

Assessment Planning implementation Rationale Evaluation

Vital signs:Tem:36.6RR:68/mtsPR:160/mtsSpo2:80%ABG:PH:7.28PCO2:68PO2:70HCO3:28BE:-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

AdministeredVentilator support

To maintain patient airway

ABG show pco2 &PH level

To prevent hypoxia

RR-52/mnt O2 saturation

98% ABG: PH-7.28 PCO2-39 HCO3-23 BE-1.1

IMPAIRED GAS EXCHANGE RELATED TO DISEASE PROCESS

INEFFECTIVE THERMOREGULATION RELATED TO IMMATURETY

Assessment Planning implementation Rationale Evaluation

Subjective data Baby is crying continuously and seems to be irritableobjective data Temperature 36.4c

To maintain the temperature within the normal range

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

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

Instruct the parents about,Kangaroo care,Breast FeedingProper 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

NURSING HEALTH TEACHING

Presented a case of preterm new born baby with respiratory distress

Baby relived from signs and symptoms of RDS

Thermoregulation maintainedBaby discharged after good care with Mixavit

and iron drops

CONCLUSION

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  

BIBLIOGRAPHY