Resp_distress_March02

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Respiratory Distress in the Newborn: Recognition and Treatment:

Respiratory Distress in the Newborn: Recognition and Treatment

Respiratory Distress:

Respiratory Distress 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:

Evaluation of respiratory distress H+P CXR Hematocrit Blood Glucose Blood pressure Blood gas status

Clinical Features aid in diagnosis:

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:

Transient Tachypnea of the Newborn Mild and self-limited Increased RR, no retractions, mild cyanosis FiO 2 < 0.4 Usually term infants, C/S and maternal IV fluids associated CXR with prominent vascular markings

Transient Tachypnea of the Newborn:

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 6

Meconium aspiration syndrome:

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

Meconium Aspiration:

Meconium Aspiration CXR- 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:

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):

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

HMD - Clinical features:

HMD - Clinical features 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

HMD - Pathologic features:

HMD - Pathologic features 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

HMD- Pathophysiology:

HMD- Pathophysiology 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 2) recoil of tissue elasticity

HMD - Pathophysiology:

HMD - Pathophysiology 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:

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 Function in HMD:

Lung Function in HMD Lung Compliance is also reduced: from 1-2 to 0.2 -0.5 ml/cmH 2 O-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

Initial Care:

Initial Care 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:

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

Temperature Control:

Temperature Control First things first: Dry the baby Keep the baby warm Use shields to decrease evaporative and convective losses PUT A HAT ON THE BABY!

Initial Care:

Initial Care 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:

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

Initial Care:

Initial Care Consider other etiologies: INFECTION,INFECTION Evaluate Begin antibiotic therapy as prophylaxis Continue as clinically indicated Anatomic malformations

Clinical features:

Clinical features Risk factors: Prematurity maternal diabetes, maternal bleeding, perinatal asphyxia, C-section without labor White race, male sex Features : Early onset, from birth to four hours uncomplicated clinical course with progressive worsening until day 2-3 and onset of recovery by 72 hours

Clinical features (contd):

Clinical features (contd) Physical Examination Brief but thorough Signs of respiratory distress : Cyanosis Tachypnea ( >60/min, shallow, rapid ) Grunting ( delayed expiration maintains FRC ) Retraction ( Subcostal, substernal, intercostal ) Flaring ( 50% airway resist in nose& pharynx) Temperature, Blood pressure, Skin perfusion

Management:

Management Concepts Respiratory Prevent hypoxia and acidosis Prevent worsening atelectasis, edema Minimize barotrauma and hyperoxia Supportive management Optimize fluid and nutrition management Perfusion, Infection, Temperature control

Surfactant replacement therapy:

Surfactant replacement therapy When : Prophylaxis (prevention) vs. Treatment (rescue) ; Early vs. Late What: Synthetic preparation (Exosurf) vs. Mixed Natural/Synthetic (Survanta) How: Administration : Indications, Dosage, Technique Additives : Antioxidants

Surfactant replacement therapy:

Surfactant replacement therapy Prophylaxis vs Rescue Four major trials so far ( Dunn et al, Kendig et al, Merritt et al, Egberts et al ) No significant difference in mortality, BPD. Possible minor decrease in pneumothorax with prophylaxis Prophylaxis leads to overtreatment, logistics difficult - immediate manipulation in delivery room

Surfactant replacement therapy:

Surfactant replacement therapy Early treatment vs. delayed selective treatment The OSIRIS Collaborative Group 1992 Early (<2hrs age) vs delayed selective treatment :6774 babies, international Early treatment led to a small, but significant reduction in risk of death or O 2 dependence at term-adjusted age (RR 0.84)

Surfactant replacement therapy:

Surfactant replacement therapy Dosage: Survanta 4cc/kg (Max 8cc) q 6-12 ( 100mg/kg phospholipids ) Administer through side-port ETT adapter, do not need to remove from vent or pass catheter Three doses better than one dose ( American Exosurf Neonatal Study ) Two doses as good as 3-4 doses ( OSIRIS ) Minimum two doses; if sick, may give up to 4. Retreatment criteria open to question

Surfactant replacement therapy:

Surfactant replacement therapy Unclear if positioning is required during administration Commonest side effects are transient bradycardia and desaturation Rare association with pulmonary hemorrhage ( temporal association with PDA ) Rapid improvement in PO 2 due to better V/Q matching, slower improvement in PCO 2 and compliance.

CPAP:

CPAP Indication: Significant respiratory distress, FiO2 > 0.40 Start with Nasal prong CPAP , 5 cm H 2 O pressure, flow 5-10 lpm, FiO 2 0.40-0.60 Increase pressure in steps of 1-2 cm H 2 O till 8-9 depending on resp effort and PO 2 . Wean by decreasing FiO 2 in steps of 0.05 till 0.40, then wean CPAP in steps of 1-2 cm H 2 O till 4-5, then discontinue.

CPAP:

CPAP Concept: Prevents atelectasis reduces pulmonary edema shifts infant to breathe on more compliant portion of pressure volume curve Problems: High CPAP may decrease venous return High CPAP may decrease minute ventilation Abdominal distension, open mouth, crying

Mechanical Ventilation:

Mechanical Ventilation Indications: PCO 2 >55 or rapidly increasing / pH<7.25 PO 2 <50 with FiO2 >0.6-1.0 Severe apnea No role for elective intubation, whatever the birth weight Babies grow just as well, whether on the ventilator or not. Risks of intubation and barotrauma considerable. More ET / IMV=More BPD .

Mechanical Ventilation:

Mechanical Ventilation Initial settings PIP 20-25 , PEEP 4-5 cm H 2 O Frequency 20-40/min Ti 0.4-0.5 sec Previously required FiO2 0.5-1.0 Manual ventilation with anesthesia bag and mask will give an idea of pressures required.

Mechanical Ventilation:

Mechanical Ventilation Continuous flow, pressure-limited, time-cycled ventilator conventional Adjustments PO 2 50-80 mmHg PCO 2 45-55 mmHg pH 7.25-7.40 Blood gases q4-6 or more frequently + 15-20 mins following vent changes ET suctioning as required. Chest physiotherapy in acute RDS not required, may be associated with IVH.

Mechanical Ventilation:

Mechanical Ventilation Weaning once infant improves Lower PIP to 30 in steps of 2-4 cmH 2 0 Next reduce FiO 2 to 50-60% by decrements of 5% Then reduce PIP to 20 and PEEP to 5 in steps of 1-2 Decrease FiO 2 to 40% Decrease rate to 10-15/min; then PIP to 15-18, FiO 2 to 30% Extubate tiny premies to NCPAP. May try larger babies on ETCPAP.

Acute Complications:

Acute Complications 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

Acute Complications:

Acute Complications 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

Acute Complications:

Acute Complications 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

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