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8 جمادي الاولى 1435 هـ Ped.Lec. by Dr.Ala'a Alhussaini
10/3/2014
Respiratory Distress in the Newborn:
Recognition and Treatment
Hyaline Membrane Disease- major cause
Pathophysiology
Surfactant and ventilator therapy
Must distinguish from other causes:
Transient Tachypnea of the Newborn
Pneumonia/sepsis
Evaluation of respiratory distress:::
H+P
CXR and ant.fontanelle US
Hematocrit
Blood Glucose
Blood pressure, urea and electrolyte
Blood gas status (ABG)
Clinical Features aid in diagnosis:
Gestational age
Historical risk factors for infection
Type of distress- grunting,flaring, retractions, tachypnea
Associated anomalies
Radiographs


Transient Tachypnea of the Newborn:::
Mild and self-limited
Increased RR, no retractions, mild cyanosis
FiO2 < 0.4
Usually term infants, C/S and maternal IV fluids associated
CXR with prominent vascular markings
Transient Tachypnea of the Newborn
Delayed resorption of fetal lung fluid
Must consider, and rule out pneumonia
Treat with antibiotics if
diagnosis is uncertain
Oxygen need beyond six hours
Oxygen need increasing
Worsening symptoms

Meconium aspiration syndrome:::

MSF in 10-15% of births
Rare before 34 weeks gestation
More likely with thick staining or particulate MSF
Thin staining in vigorous infant requires no special Rx
Can’t prevent all MAS
CXR show
increased density, irregular infiltrates
areas of hyper-expansion, areas of collapse
Fluffy non-homogeneous infiltrates
May be hard to distinguish from retained fluid, pneumonia


Neonatal Respiratory Disease:::
Not every infant with respiratory symptoms has respiratory disease
Consider Extra-pulmonary causes:
Heart disease
Hypovolemia, polycythemia, anemia
Acidosis, hypoglycemia, hypothermia
CNS hemorrhage, drugs, muscle disease

Hyaline Membrane Disease (HMD(:::

Once the major cause of mortality in premature infants
Progress in treatment mirrors advances in neonatal medicine
Effective treatment has improved survival at gestational ages as low as 24 weeks

Clinical features of HMD:

Disorder of premature infants
Respiratory distress: tachypnea, grunting, flaring, retractions
Difficult to distinguish from pneumonia
Severity peaks at 24-48 hours, resolution by 72-96 hours (without surfactant therapy)
Recovery prolonged by barotrauma or oxidative injury

Pathologic features of HMD:

Characteristic injury to terminal airways beginning within the first few breaths
Lungs are solid, congested, with destruction of epithelium of terminal conducting airways
Hyaline membranes: coagulum of sloughed cells and exudate,plastered against epithelial basement membrane


Pathophysiology of HMD:
Instability of terminal airspaces due to elevated surface forces at liquid-gas interfaces
Stable alveolar volume depends on a balance between:
1) Surface tension at the liquid-gas interface, and
2) Recoil of tissue elasticity
Terminal airspaces are not uniform throughout the lung
There is a range of critical opening and critical closing pressures in various alveoli
Some alveoli remain collapsed, some are ventilated but collapse during expiration, and some remain ventilated during inspiration and expiration (the goal(

Lung Function in HMD:

Reduction in FRC from 30 ml/kg, to as low as 4-5 ml/kg. Caused by loss of volume and interstitial edema.
FRC mirrors changes in oxygenation. Improvements can be due to distending pressure, surfactant replacement, or clinical resolution
Lung Compliance is also reduced: from 1-2 to 0.2 -0.5 ml/cmH2O-kg
Reduction due to decreased number of ventilated alveoli, and increase in recoil pressure of ventilated airspaces
Lung resistance is significantly increased
Usually, impairment in ventilation is less pronounced than altered oxygenation

Clinical Presentation in HMD:

Tachypnea may be initial symptom- especially at gestational age closer to full term
Grunting, Flaring, and Retractions (sub costal, substernal) are hallmark clinical signs
Remember: Always consider other causes of respiratory distress


Acute Complications of HMD:
Air Leak Syndromes
Consider with sudden change in condition
More common if baby receiving ventilatory support
Pneumothorax most common
Therapy
None if stable
Oxygen 100%
Thorocentesis: Needle or tube

Intracranial Hemorrhage

High risk if HMD is severe
More common at lower gestational ages
Rare above 33 weeks gestation
Suspect if there is a sudden change in condition
May coincide with development of air leak
Signs: change in Fontanel, perfusion

Patent Ductus arteriosus

Usually evident during resolution phase
Signs of Congestive Heart Failure
Increased oxygen need
Cardiomegaly
Acidosis, decreased urine output
Therapy:
Decrease fluid intake
Indomethacin


Anatomic abnormalities
Major
Congenital Diaphragmatic hernia
Airway obstruction
Lung malformations, cysts
Other
Choanal Atresia

Initial Care of HMD:

Maintain warmth- cold stress will mimic other causes of distress
Monitor blood glucose levels- assure they are normal
Provide enough oxygen to keep the baby pink

Temperature Control:

Body Temperature that is too high or too low will increase metabolic demands
When oxygen uptake is further compromised by disease, increased demand can not be met
Servo controlled warmers are very helpful, but can be mimicked by frequent assessment
First things first:
Dry the baby
Keep the baby warm
Use shields to decrease evaporative and convective losses
PUT A HAT ON THE BABY!


Ensure adequate hydration:
Start fluids at 70-80 ml/kg/d 10% glucose solution
Smaller babies may need more fluid
Add electrolytes by the second day
On day 3-4 watch for diuresis

Assess circulation

Monitor heart rate
Assess Blood pressure
Check peripheral perfusion and capillary refill
Avoid excessive blood sampling

Consider other etiologies:

INFECTION,INFECTION
Evaluate
Begin antibiotic therapy as prophylaxis
Continue as clinically indicated
Anatomic malformations

Additional Support of HMD:

Oxygen is key- as much as it takes
Continuous Positive Airway Pressure
Usually 5-7 cm H2O
Variety of delivery devices
Simplicity is good-Water bottles
Mechanical Ventilation
Bag and mask / endotracheal tube
Ventilator if available


CPAP for HMD::
Indications:
FiO2 above 0.3 with clinical distress
FiO2 above 0.4
Significant retractions after extubation
Hypoventilation: CPAP may be helpful

Risks

Hard to control in spontaneously breathing baby, especially if vigorous or close to term
Potential for airleak
Can’t give surfactant
May rarely worsen ventilation

Mechanical Ventilation for HMD:

FiO2 more than 0.35 -0.4 on CPAP
Early treatment if condition is deteriorating
Decreasing “work of breathing”
Frequent apnea
Plan to give surfactant therapy
Absolutely: for prolonged apnea or hypoxemia in absence of heart disease
Risks:
May require sedation, reducing spontaneous respiration
Air leaks , especially as compliance improves
Baro-Volutrauma and risk of chronic lung injury


Treatment of HMD:
Oxygen: enhances oxygenation directly, and by decreasing intrapulmonary shunting
Distending pressure: through grunting, CPAP (Continuous positive airway pressure), or mechanical ventilation
CPAP easily provided by simple apparatus

Continuous Positive Airway Pressure (CPAP(:::

Can correct ventilatory insufficiency by;
Diminishing atelectasis
Improving Functional residual capacity
Correcting ventilation-perfusion abnormalities
Decreasing pulmonary edema
Reducing intrapulmonary shunting

CPAP Delivery

Endotracheal tube: simple and efficient, but increased work of breathing
Face mask: Easy to apply, inexpensive, but difficult to regulate, causes abdominal distention
Nasal Prongs: Simple to apply and use, minimal cost, mouth leaks prevents excess but hampers efficacy. Usually the preferred method

Conclusions:::

The understanding of the root cause and pathophysiology of hyaline membrane disease has made successful treatment a reality
CPAP and mechanical ventilation have been refined to provide support while minimizing complications
Antenatal steroids minimize incidence and severity
Surfactant and survival
CPAP is a key part of the treatment array
Delivery can be accomplished by simple, easily made devices
Many babies, especially those 1800 gm and above can be helped by CPAP
Continued progress begins with these basic steps
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الحقيقة أن الإنسان كلما إرتقى بدأ يخاف بعقله،
وكلما هبط مستواه خاف بعينه.
الحيوان يخاف بعينه والإنسان الذي أنكر إنسانيته وعطل عقله لا يخاف إلا بعينه،
فالكافر متى يفزع؟ حينما يأتيه ملك الموت
ومتى يخاف؟ حينما يقترب أجله
ومتى يضطرب؟ حينما تأتيه المصيبة.
أما و هو في بحبوحة العيش والرخاء فلا يبالي إطلاقا بهذا الحق، لذلك الذي يخاف بعينه أقل مرتبة من الإنسان الذي يخاف بعقله أما الذي يخاف بعقله فهذا هو الإنسان العاقل
قال تعالى: (( إن الذين حقت عليهم كلمة ربك لا يؤمنون ولو جاءتهم كل آية، حتى يروا العذاب الأليم )) :: سورة يونس/ الآية 97

د.محمد راتب النابلسي




رفعت المحاضرة من قبل: عادل احمد هلال الجميلي
المشاهدات: لقد قام 23 عضواً و 123 زائراً بقراءة هذه المحاضرة








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