Meconium Aspiration Syndrome

This assignment describes my own reflective experience while caring for a sick neonate with Respiratory Distress Syndrome (RDS) in the neonatal unit. This has enabled me to explore the meaning and significance of my clinical practice and to recognise the complexities within it. The experience raises a number of issues frequently encountered in daily nursing practice. Within this assignment, I will be discussing a particular pre term baby with RDS and critically analyse the use of nasal continuous positive airways pressure (NCPAP) and surfactant therapy and possible effects on baby’s outcome. Pseudonyms will be used to maintain patient confidentiality in order to keep in with the nursing and midwifery council code of conduct. (NMC 2004)The

Although when it happens, there can be a devastating impact on patients as well as to the multidisciplinary theatre team involved. Consequently, the DAS has produced a consensus set of guidelines for managing failed intubations in adult and paediatric patients, but there are as yet no such nationally-agreed guidelines in obstetrics, therefore each obstetric unit should have their own flowchart with regards to management of failed intubation (Brien and Conlon, 2013). Furthermore, in light of the latest DAS guidelines, several aspects of clinical anaesthetic practise have changed over recent years (Frerk at al, 2015). Amongst the changes are the use of new drugs such as rocuronium and suggamadex and using electronic video-laryngoscopes (Frerk et al, 2015). Further work had also looked at extending the period of apnoea without causing desaturation by optimising the preoxygenation process and adequate patient positioning (Frerk et al, 2015). As a result, updated guidelines for difficult intubations in adult patients were published in 2015; these guidelines provide a flowchart to be used when endotracheal intubation proves difficult or impossible and focus on the central importance of oxygenation while reducing the amount of airway interventions in order to minimize trauma to the delicate airway (Frerk et al, 2015). The main message of the revised guidelines is

Premature babies sometimes have apnea. It may happen together with a slow heart rate. Respiratory distress syndrome or RDS is a breathing problem most common in babies born before 34 weeks of pregnancy.” Babies with RDS don’t have a protein called surfactant that keeps small air sacs in the lungs from collapsing. “Intraventricular hemorrhage or IVH is bleeding in the brain. It usually happens near the ventricles in the center of the brain. A ventricles is a space in the brain that’s filled with fluid. Patent ductus ateriosus or PDA is a heart problem that happens in the connection between two major blood vessels near the heart. If the ductus do not close properly after birth, a baby can have breathing problems or heart failure. Heart failure is when enough blood can’t get pumped into the heart causing it to shut down. Necrotizing enter colitis (NEC) is a problem with a baby’s intestines. It causes feeding problems, a swollen belly and diarrhea. It sometimes happens 2 to 3 weeks after a premature bay has been born. Retinopathy of prematurity (ROP) is an abnormal growth of blood vessels in the eye. ROP can lead to vision loss. Jaundice is when a baby's eyes and skin look yellow. A baby has jaundice when his liver isn't fully developed or isn't working well. Anemia is when a baby doesn’t have enough healthy red blood cells to carry oxygen to the rest of the body. Bronchopulmonary dysplasia (BPD) is a lung condition that can develop in premature babies as well as babies who have treatment with a breathing machine. Babies with BPD sometimes develop fluid in the lungs, scarring and lung damage. Premature babies often have trouble fighting off germs because their immune systems are not fully formed. Infections that may affect a premature baby include pneumonia, a lung infection; sepsis, a blood infection; and meningitis, an infection in the fluid around the brain and

Some of the progressive signs of respiratory distress exhibited by this infant after birth are; nasal flaring, grunting, coarse breath sounds, increase respiratory rate of 100 and irregular, acrocyanosis, his appearance of being pale, circumoral cyanosis, and him developing jaundice as a result of his increased work of breathing and hypoxia which causes an increase in erythropoietin to be released from the kidneys resulting in polycythemia as a result of low levels of oxygen in the body. Subsequently, as a result of an increase or red blood cell production the body will develop jaundice due to an increase in red blood cell breakdown which causes an increase of bilirubin in the blood to accumulate, therefore, causing jaundice to develop.

The main priority for all the pediatric patient was to make sure they are getting enough air. They needed an open airway. Without an open airway nothing else matters. To help with the patients airways we monitored their O2 sats and if they were low we made sure to apply oxygen, and continue to monitor their sats. Once oxygen was applied we worked on

Lungs: Mild end-expiratory wheezing. Pursed-lip breathing noted and has a prolonged expiratory phase. Chest x-ray shows pulmonary hyperinflation, flattening of the diaphragm; Pulmonary function test (after bronchodilation with 2 puffs albuterol—FEV1/FVC ratio 0.60 FEV1 60% of predicted value)

After earning his doctor of medicine from the Medical College of Georgia, Dr. Allen Cherer undertook an internship and a residency in pediatrics through the University of Louisville School of Medicine/Kosair Children's Hospital. He holds certification through the American Board of Pediatrics and the Sub-Board of Neonatal-Perinatal Medicine. Dr. Allen Cherer is also official educational provider through the Neonatal Resuscitation Program (NRP).

At this point I would anticipate the HCP to order bed rest on the left side to hence placental perfusion, monitoring the fetus heart rate through an external monitor and monitoring vital signs. Also, limiting vaginal examination to prevent infection, monitor both fetus and mother for adverse effects tocolytic drugs and measurement of intake and output and prepare Elinah for birth (Ricci el., 2017. Pg. 813)

Lungs: Clear to auscultation bilaterally. No wheezes, rales, or rhonchi. Symmetric chest expansion. Breathing nonlabored. Diminished breath sounds in all lung fields. Resonant to percussion.

The list of proposed chronic abnormalities is lengthy. To this date, research has confirmed the following: 1) SIDS is due to a dysfunction of the cardiac and/or respiratory systems, and 2) the death of the infant is due to hypo-ventilation of the lungs and periods of complete cessation of breathing or apnea. Hypo-ventilation and apnea cause hypo-perfusion of the tissues with necessary oxygen. Ischemia of tissues results and eventually causes death. Research now centers around discovering the cause of infant hypo-ventilation and apnea.

Inability for the baby's body to detect a build-up of carbon dioxide in the blood

The last major theory examined is that the infants that fall victim to SIDS have congenital defects in the brainstem. The brainstem controls breathing and heart rate functions in the body, so it would make sense that instability in this area would cause negative side effects, such as lung failure. Mr. Goldwater reviews this possibility in his article, stating that autopsies done to infants post-mortem indicate “possible, chronic low-grade hypoxemia, attributed to sleep-related hypoventilation.” In layman's terms, the infants received less than normal oxygen in the blood because their breaths were too few or too

Necrosis of the cells in the small, lower airways occurs, and mucous secretions are increased (Conquest, Cremonesini, & Neill, 2013). Because of the ciliary damage in the infants’ lungs, it is almost impossible for the secretions to be cleared. Bronchiolar level obstruction is caused by these mucosusal secretions, as is desquamation of the dead skin cells and edema (Conquest, Cremonesini, & Neill, 2013). Plugs of soughed, necrotic epithelium and fibrin in the airways will cause partial or total obstruction to airflow, making it very difficult for he infant to exhale which will consequently result in air becoming trapped and will reduce gaseous exchange (Conquest, Cremonesini, & Neill, 2013).

G.M. was then immediately transferred to Rady Children’s hospital Emergency Room by her parents. Upon nursing assessment she presented with vital signs within the same range from her clinic visit. These were repeated every fifteen minutes until stable. Her skin was flushed and diaphoretic. Mucous membranes appeared dry with significant skin cracking around the mouth. Patient was alert and oriented times three and pupils were equal, round, and reactive to light and accommodation. Her breath sounds were clear and equal bilaterally, with no adventitious sounds noted. However, patient G.M. appeared to have

Respiratory distress syndrome (RDS) is a common lung disorder that mostly affects preterm infants. RDS is caused by insufficient surfactant production and structural immaturity of the lungs leading to alveolar collapse. Clinically, RDS presents soon after birth with tachypnea, nasal flaring, grunting, retractions, hypercapnia, and/or an oxygen need. The usual course is clinical worsening followed by recovery in 3 to 5 days as adequate surfactant production occurs. Research in the prevention and treatment of this disease has led to major improvements in the care of preterm infants with RDS and increased survival. However, RDS remains an important cause of morbidity and mortality especially in the most preterm infants. This chapter reviews the most current evidence-based management of RDS, including prevention, delivery room stabilization, respiratory management, and supportive care.