apnea ss

Chairperson: Dr.Harish

Presenter: Dr.Mohan.T.Shenoy

APNEA IN THE NEWBORN

AIIMS-NICU protocols 2

REFERENCESo NELSON textbook of Pediatrics -18th editiono AVERY’s textbook of Neonatology - 6th editiono JOHN.P.CLOHERTY M Manual of Neonatal Careo MEHERBAN SINGH Care of Newborn 6th editiono Internet Journal of Neonatology- Vol. 21, No. 1,

Jan. - Mar. 2007 Drug Therapy of Apnea in Neonate

by G.Guruprasado AIIMS - NICU protocols 2008o www.newbornwhocc.org


DEFINITION

pathological cessation of breathing that results in hemodynamic disturbances

“…cessation of breathing for longer than 20 sec, resulting in pathological changes in heart rate and oxygen saturation...”


Most common problem of ventilatory control in premature

Frequently prolonging hospitalization

Needing cardiopulmonary monitoring.


Types of apnea•Central apnea: (40%)

Total cessation of inspiratory efforts No evidence of obstruction.

•Obstructive apnea: (10%)

Tries to breathe against an obstructed upper airway

Absent airflow but persistent chest wall motion throughout entire apneic episode

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Mixed apnea: (50%) obstructed respiratory efforts usually following central pauses.

Short episodes of apnea are usually central, whereas prolonged ones are often mixed

Purely obstructive apnea in the absence of a positional problem is probably uncommon.


Primary apnea may occur in utero,thus apnea present after birth may be either primary or secondary

Primary apnea is responsive to tactile stimulation; however, secondary apnea does not

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Periodic breathing

“Periods of regular respiration for as long as

20 seconds followed by apneic periods of

5-10 seconds or less that occur at least

3 times in succession without change of

heart rate or color.”

normal event reflective of immaturity of

respiratory control system does not merit any treatment.


Subtle seizures

Apnea is an uncommon presentation of a neonatal seizure in preterm.

Sudden alteration in muscle tone, twitching movts., vacant stare and uprolling of eyes

Tachycardia preceding/accompanying an apneic episode.


Apneic spells are almost never a seizure manifestation unless associated with

tonic deviation of the eyes, tonic stiffening of the body, or characteristic limb movements.

However, prolonged apnea without bradycardia, and especially with tachycardia, is a seizure until proven otherwise

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PATHOGENESIS

A. Developmental immaturity of central respiratory drive

B. Chemoreceptor response

C. Reflexes.

D. Respiratory muscles

E.Gastroesophageal reflux


ANS Control of Respiration


Pre-Bötzinger Complex (preBötC)

Cluster of interneurons in ventrolateral medulla of the brainstem essential to the generation of respiratory rhythm


Sleep state dependent Frequency increases during active (rapid eye movement) sleep.

Increased negative pressure during paradoxical breathing

Fall in Pao2 because of ventilation-perfusion defects. Inhibition of pharyngeal muscle tone


HERING BREUER(HB) REFLEX

It is a ‘Volume’ reflex.

Receptors are located in between the smooth muscles of the small airways.

These receptors are unmyelinated nerve endings; stimulated by the change of shape of the Airways.


HB INFLATION REFLEXA NEGATIVE FEEDBACK SERVOCONTROL SYSTEM

INSPIRATION

TIDAL VOLUME >1lt

STRETCH OF THE AIRWAYS

INCREASED RESPIRATORY RATE

DECREASED TIME FOR INSPIRATION

Immaturity of the central nervous system.

Usually presents after 1-2 days of life but within the first 7 days

AOP is a diagnosis of exclusion and should be considered only after secondary causes of apnea have been excluded.

Common causes of secondary apnea include sepsis, pneumonia,asphyxia, temperature instability and anemia.

25Incidence of AOP is inversely proportional to gestational age


Precipitating factors


Bradycardia follows apnea by 1–2 sec in > 95% of cases -Most often sinus, but on occasion can be nodal.

Vagal responses and, rarely, heart block are causes of bradycardia

without apnea.


Evaluation of Apneic Infant


Short episodes of apnea do not require intervention.

Apneic spells of 10 to 15 seconds

are detectable at some time in

almost all premature and

some full-term newborns.

Apneic spells of 10 to 20 seconds usually associated with a 20% reduction in heart rate

Longer episodes of apnea almost invariably associated with a 40% or greater reduction in heart rate.


Apneic spells in an otherwise normal-appearing newborn is a sign of brainstem immaturity and not a pathological condition.

Sudden onset of apnea & states of decreased consciousness, especially in premature newborns, suggests an intracranial hemorrhage with brainstem compression


A. General measures

1. Specific therapy should be directed at an underlying cause, if one is identified.

2. In general, oxygen saturation should be maintained between 85% and 95%, with supplemental oxygen provided if needed.

3. Care should be taken to avoid reflexes that may trigger apnea. Suctioning of the pharynx should be done carefully, and oral feedings should be avoided.

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4. Avoid Positions of extreme flexion or extension of the neck to reduce the likelihood of airway obstruction.

5. Decreasing the environmental temperature to the low end of the neutral thermal environment range.

6.It is controversial whether blood transfusion reduces the frequency of apneic spells.

7. Treat the underlying cause : Sepsis, anemia, polycythemia, hypoglycemia, hypocalcemia, respiratory distress syndrome (RDS).


Medications

Intubation

Chest Compressions

BVM Ventilations

Oxygen

Drying, Warming, Positioning, Suction, Tactile Stimulation

Triangle of Resuscitation

Least common treatment

Most common


Most apneic spells in premature infants respond to tactile stimulation.

Infants who fail to respond to stimulation should be ventilated during the spell with bag and mask, generally with Fio2 of < 0.40 before the spell to avoid marked elevations in arterial oxygen tension (Po2).

After the first apneic spell, the infant should be evaluated for a possible underlying cause


Evaluation Emergency treatment Clinical examination Investigations

Definitive treatment General measures Specific measures Pharmacotherapy Continuous positive airway pressure Mechanical Ventilation

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Apnea monitors Pulse oximeters

Other apnea monitors

Movement sensors(i) Ripple type mattress(ii) Mattress with sensory pad(iii) Pressure sensitive capsule

Thoracic impedence based monitors Respiratory inductive plethysmography Magnatometer


APNEA MONITOR

When a monitor alarm sounds, remember to respond to the infant, not the monitor, checking for

bradycardia, cyanosis, and airway obstruction


Check for bradycardia, cyanosis, airway obstruction.

Maintain saturation between 90-93% Neck should be positioned in slight extension; Oro-pharynx gently suctioned if required Tactile stimulation should be given.

Ventilation with bag and mask using 100% O2 should be initiated.

If no response, managed with positive pressure ventilation.


Resuscitation With Bag & Mask

Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Pediatrics and Child Health and Royal College of Obstetricians and Gynecologists. London: BMJ Publishing, 1997)


INVESTIGATIONS Exclude common causes of secondary apnea.

Consider:

Blood glucose, Hematocrit, Electrolytes, Septic screen, blood culture Arterial blood gas, Chest x-ray, abdominal x-ray, Cranial Ultrasound Other investigations depending on history and

physical examination


TREATMENT

Treatment should be initiated in order of increasing invasiveness and risk

When apneic spells are

repeated and prolonged (i.e., > 2-3/hr) or require frequent bag and mask

ventilation

.


Methylxanthines =Mainstay of Rx

markedly reduces the number of apneic spells and the need for mechanical ventilation.

Mechanisms

(i) antagonism of adenosine, a neurotransmitter that can cause respiratory depression;

(ii) respiratory center stimulation;

(iii) improvement of diaphragmatic contractility.


Xanthine therapy

increases minute ventilation, improves CO2 sensitivity, decreases hypoxic depression of

breathing, enhances diaphragmatic contractility, and decreases periodic breathing.

Neonates exhibit hypoxic respiratory depression

Ability of methylxanthines to block this response may contribute to their effect on apnea.


Loading dose of intravenous aminophylline is 5 to 6 mg/kg, followed by 1.5 to 3 mg/kg every 8 to 12 hours.

Oral theophylline can be administered once the infant becomes stable in the same dose.

Elimination of methylxanthines is prolonged in infants especially in preterm neonates.


No role for prophylactic use of methylxanthines for prevention of apnea, bradycardia, or desaturation in premature infants.

Injection: Aminophylline ampoule 250 mg per 10-ml ampoule.

Oral: Theophylline 50 mg/5 ml in Theoped syrup


CaffeineHigher therapeutic index More reliable enteral absorptionLonger half-life.

Loading dose of 20 mg/kg slow infusion over 1 hour followed in 24 hrs by 5 to 8 mg/kg per dose, once every 24 hrs.


Aminophylline should be continued till 34 weeks corrected gestational age and stopped thereafter if no episodes of apnea have occurred in the last 7 days.

Caffeine especially to be discontinued at least 1 to 2 weeks prior to discharge, because of its longer half-life

Do not discharge baby until methylxanthines have been stopped.

Side-effects Recommended therapeutic levels :

5 to 10 μg/ml for aminophylline 8 to 20 μg/ml for caffeine.

With Theophylline,

tachycardia

signs of gastrointestinal dysfunctionAbdominal distention, feeding intolerance, vomiting;


Jitteriness and irritability

Diuresis and urinary calcium excretion occur with both drugs.

Metabolic changes, including increased glucose and insulin levels, occur following a theophylline loading dose in some infants

Caffeine appears to be less toxic than theophylline and is well tolerated

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DOXAPRAM Failure to respond to both methylxanthine and CPAP therapy

Acts predominantly on peripheral chemoreceptors

The loading dose is preferably avoided.

Infusion started at 0.5 mg/kg/hr, increased gradually to a maximum of 2-2.5 mg/kg/hr.

Methylxanthine should be continued during doxapram infusion.


DOXAPRAM Side-effects

Hyperactivity, Jitteriness, abdominal distension Seizures, Hyperglycemia, mild liver dysfunction, and hypertension.

Avoided in the 1st wk of life or if High S. Bilirubin

In addition, 0.9% benzyl alcohol is used as a preservative can result in “gasping syndrome”

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WHICH DRUG TO USE ??? Present evidence shows that aminophylline, caffeine and

doxapram are equally effective in the treatment of AOP.

However their clinical use is dependent upon adverse effects.

The ideal drug of choice would be caffeine

AIIMS prefer to use aminophylline as the drug of choice in the management of AOP.


SUMMARY OF PHARMACOTHERAPY


Nasal continuous positive airway pressure

•At moderate levels (4-6 cm H2O)

•Especially useful in

•infants <32 to 34 weeks' gestational age

•residual lung disease


Continuous positive airway pressure

If clinically significant episodes persist despite optimal methylxanthine therapy

Esp. in obstructive and mixed apneas

May also be used to reduce post-extubation apnea in preterm infants.

Delivery through Nasal prongs or nasopharyngeal tube.

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Splinting open of the upper airways by the positive airway pressure of 5 cm water

No role in prophylaxis against apnea of prematurity

Adverse effects of CPAP include barotrauma, abdominal distension, feeding intolerance and local nasal irritation.

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Mechanical Ventilation

If both pharmacotherapy and CPAP have been tried and significant apneas continue to occur

Minimal pressures (PIP 10-12 cm & PEEP 3-5 cm)

Low rate (20-25/min)Short Ti (0.35-0.40 seconds)Low FiO2 (0.3-0.5)


Kinesthetic stimulation

Water bedoscillating bed mattress

Present evidence does not support any role for this mode of therapy either in the prevention or treatment of apnea.


Persistent apneaIf persist beyond 37-40 weeks esp. in

infants before 28 weeks of gestation

Continue MethylXanthine therapy if beyond 34 wks of corrected gestational age.

Reevaluate for secondary causes especially neurological problems and gastro-esophageal reflux.


Criterion for discharge

Resolution of recurrent apnea and bradycardia episodes and

Completion of an "apnea-free" period of 5 to 10 days


“an episode in infant that frightens the caretaker.”

Apnea

Color change (cyanosis, pallor, erythema, plethora)

Marked change in muscle tone (limpness)

Choking or gagging

Apparent Life-Threatening Event (ALTE)

These events can involve any of the following:

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SUDDEN INFANT DEATH SYNDROME (SIDS)

“Sudden death of any infant or young child

which is unexplained by history

and in which a thorough post mortem fails to demonstrate an adequate cause of death.”

Taken from the NIH Consensus Development Conference on Infantile Apnea and Home Monitoring


Sudden Infant Death Syndrome (SIDS) and Apnea

AOP not found to be an independent risk factor for SIDS.

Only 2-4% of patients with SIDS have a history of AOP.


Neurodevelopment outcome Most reports have found little evidence of any

neurodevelopment risk directly attributed to a history of AOP.

• Precisely measured • predischarge apnea related to AOP, however, has been reported to be predictive of

lower developmental indices at 2 yrs.


THANK

YOU

AIIMS-NICU protocols04/08/23

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The resuscitation flow diagram

AIIMS-NICU protocols04/08/23

The resuscitation flow diagram

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Evaluation

Evaluation

Evaluation

Assessment


References American Academy of Pediatrics Committee on Drugs.Emergency Drug Doses for Infants & Children.Pediatrics.1988;81:462

American Academy of Pediatrics.Use & Abuse of the Apgar Score.Pediatrics.1996;98:141-142

Apgar,V.A Proposal for New Method for Evaluation of the Newborn Infant.Anesth.Analg.1953:32:260-267

Ballard R.A.Schaffer & Avery's Diseases of the Newborn-6th Ed.1991; 193-206

British Pediatric Association. Neonatal Resuscitation. London: BPA, 1993

Bloom R.S, Cropley C.S. Textbook of Neonatal Resuscitation. American Heart Association, American Academy of Pediatrics,1987;1-37

Hamilton P.Care of the Newborn in the Delivery Room.BMJ 1999;318:1403-1406

Royal College of Obstetricians and Gynecologists. Working Party Report on Maternity Care in Obstetrics and Gynecology. London: Royal College of Obstetricians and Gynecologists, 1990

Roberton N.R.C.Resuscitation of the Newborn.Textbook of Neonatology 2nd Edn.Churchill Livingstone.1992;173-198


NEOPUFF


ApneaPRIMARY APNEA HR>80,good peripheral perfusion,tone & reflexes Apgar score usually 4-7 The onset of gasping & regular respiration can be

established by peripheral(tactile) stimulation

TERMINAL (SECONDARY) APNEA HR<60, pale,apneic,poor tone & reflexes, Apgar score usually 1-3 Spontaneous respiration is never established

unless actively resuscitated by intubation & PPV


C.Persistent Apnea,Hypotonia,good Cardiovascular Response•Severe terminal apnea

•Structural CNS or muscle disorder•Severe antenatal brain damage

•Fracture cervical spine or cord

•Dystropia myotonica

•Congenital myopathies

•Werdnig-Hoffman disease

•Brain tumor

•Degenerative brain disorder

•Ondine’s curse

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