newborn

1. APNEA IN THE NEWBORN

2. DEFINITION
APNEA IS DEFINED AS:
A] CESSATION OF BREATHING FOR 20 SECONDS OR
B] CESSATION OF BREATHING FOR 15 SECONDS ASSOCIATED WITH
CYANOSIS AND / OR BRADYCARDIA

3. PATHOPHYSIOLOGY
THERE ARE 2 MAJOR MECHANISMS THAT REGULATE PULMONARY
VENTILLATION.
THESE ARE: NEURONAL AND CHEMICALNEURONAL SYSTEM
THE CEREBRAL CORTEX AND BRAINSTEM CONTROL THE NEURONAL
SYSTEM , WHICH REGULATES RESPIRATORY RATE AND RHYTHM..

4. THE PERIPERAL COMPONENTS OF THIS SYSTEM ARE FOUND IN THE
UPPER AIRWAYS AND THE LUNGS.
THE CHEMICAL CONTROL CENTER IS LOCATED IN THE MEDULLA AND
IS SENSITIVE TO CHANGES IN PaCo2.
ALVEOLLAR VENTILLATION IS CONTROLLED CONTROLLED BY THE
CHEMICAL SYSTEM, AND THIS IS THE PRINCIPAL DEFENCE AGAINST
HYPOXIA

5. NEONATE HAVE A UNIQUE RESPONSE TO HYPOXAEMIA AND
CARBON DIOXIDE RETENTION.
THEY GET A BRIEF PERIOD OF INCREASED VENTILLATION FOLLOWED
BY RESPIRATORY DEPRESSION.
THIS IS IN COMPARISON TO ADULTS WHO HAVE A SUSTAINED
INCREASE IN VENTILLATION IN RESPONSE TO HYPOXAEMIA.

6. APNEA OF PREMATURITY
RESPONSIVENESS TO CARBON DIOXIDE IS LESS DEVELOPED IN THE
PRETERM BABY, WHICH MAY BE DUE TO IMATURITY AND DECREASED
SENSITIVITY OF THE CHEMICAL CENTER.
IT MAY ALSO BE DUE TO MECHANICAL FACTORS WHICH PREVENT AN
INCREASE IN VENTILLATION.
** APNEA OF PREMATURITY , ORPRIMARY APNEA IS NOT ASSOCIATED
WITH OTHER ENTITIES.

7. THE YOUNGER THE GESTATIONAL AGE, THE GREATER THE INCIDENCE
OF APNEA
APNEA AND BRADYCARDIA IN THE MICROPREM START IN THE FIRST
WEEK OF LIFE AND RESOLVE BY 36 WEEKS POSTCONCEPTIONAL AGE.
IN INFANTS BORN AT OR LESS THAN 27 WEEKS 60% STILL HAVE
APNEA AT 36 WEEKS POSTCONCEPTIONAL AGE.

8. APNEA MAYBE ASSOCIATED WITH THE FOLLOWING:
• HYPOXAEMIA
• NEURONAL IMMATURITY
• SLEEP
• CATECHOLAMIN DEFICIENCY
• RESPIRATORY MUSCLE FATIGUE

9. ETIOLOGY OF APNEA
• APNEA MAYBE CENTRAL - ABSENCE OF BREATHING EFFORT
• IT MAYBE PERIPHERAL OR OBSTRUCTIVE –THERE IS BREATHING
EFFORT BUT AIRWAY IS BLOCKED
• MIXED APNEA IS MORE COMMON IN WHICH THERE IS AN INNITIAL
CENTRAL APNEA FOLLOWED BY OBSTRUCTION OF THE AIRWAY

10. CAUSES OF APNEA IN PREMATURITY
• THEY ARE USUALLY SECONDARY TO HYPOXIA ± ALTERATION OF THE
SENSITIVITY OF THE PERIPHERAL OR CENTRAL CHEMORECEPTORS,
AND INCLUDE THE FOLLOWING:
INFECTIONS:
SEPSIS
• PNEUMONIA
• MENINGITIS

11. CAUSES OF APNEA OF PREMATURITY
• CVS:
• PDA±CCF
GIT:
• VOMITING
• NEC
• DEGLUTITION SYNCOPE

12. CAUSES OF APNEA OF PREMATURITY
CNS:
• CNS SUPPRESANT DRUGS
• IVH
• SEIZURES
• BILIRUBIN ENCEPHALOPATHY
• INFECTIONS
• TUMOURS
• ISCHAEMIA

13. CAUSES OF APNEA OF PREMATURITY
• ENVIROMENTAL:
• A RAPID RISE IN ENVIROMENTAL TEMPERATURE
• HYPOTHERMIA
• VIGOROUS SUCTIONING
• FEEDING[DIVING REFLEX]
• STRAINING AT STOOLS
• STRETCHING OR OTHER MOVEMENTS
• FATIGUE[EG INCRESED WORK OF BREATHING]
• STRESS[EG NICU PROCEDURES]

14. CAUSES OF APNEA OF PREMATURITY
ENVIROMENTAL:
• EXPOSURE TO CIGARETTE SMOKE [PRENATAL ]
• SLEEP STATE – EG ACTIVE [REM ] RATHER THAN QUIET
• PAIN

15. CAUSES OF APNEA OF PREMATURITY
• HEMATOLOGICAL
• ANAEMIA
• POLYCYTHAEMIA [ MY CAUSE THROMBOSIS AND IT’S
COMPLICATIONS]

16. PRIMARY APNEA
NEURONAL IMMATURITY:
RESPIRATORY EFFORTS ARE MORE UNSTABLE AT YOUNGER
GESTATIONAL AGES.
THIS APPEARS TO BE DUE TO A LACK OF DENDRITIC FORMATION AND
LIMITED SYNAPTIC CONNECTIONS, RESULTING IN A DECREASED
EXCITATORY DRIVE.
APNEA MAY ALSO BE A MANIFESTATION OF SYNAPTIC DISORDERS
WHICH OCCUR WITH A MOTOR COMPONENT
SUCH PHENOMENA HAVE BEEN COMFIRMED ON EEG

17. ALL INFANTS DEPEND ON ALTERNATING EXCITATION AND
INHIBITION OF THE CNS TO ESTABLISH RYTHMIC BREATHING,
THEREFORE IMBALLANCES IN THE ABOVE MAY CAUSE RESPIRATORY
ARREST [EG HYPOXIA, HYPOGLYCAEMIA, HYPOCALCAEMIA ]
SLEEP
APNEA IS MORE COMMON IN SLEEP ESPECIALLY REM SLEEP.
PREM UNDER 32 WEEKS SLEEEP 80% OF THE TIME AND ARE
THEREFORE MORE PRONE TO APNEA.
APNEA IS UNCOMMON IN NON-REM SLEEP BUT PERIODIC
BREATHING MAY BE OBSERVED

18. SLEEP:
REM SLEEP CAUSES :
INHIBITION OF SPINAL MOTOR NUERONES
INCRESAED BRAIN ACTIVITY CAUSING INCREASED EYE MOVEMENTS
MUSCEL TWITCHING
CHANGES IN BRAIN TEMPERATURE AND CEREBRAL BLOOD FLOW
CNS AROUSAL IN REM SLEEP IS SHOWN BY EEG CHANGES.

19. PRETERM INFANTS HAVE A MORE COMPLIANT RIB CAGE AND LESS
COMPLIANT LUNGS, RESULTING IN A GREATER RESPIRATORY
WORKLOAD.THEREFORE RESPIRATORY MUSCLE FATIGUE AND
APNEA OCCUR MORE EASILY ESPECIALLY IN THE ABSENCE OF
FATIGUE-RESISTANT FIBERS

20. SECONDARY APNEA
MAY BE ASSOCIATED WITH A PARTICULAR DISEASE ENTITY OR A
RESPONSE TO PARTICULAR PROCEDURES.
THE MAJORITY OF CAUSES OF SECONDARY APNEA EXERT THEIR
INFLUENCE THROUGH HYPOXAEMIA AND SUBSEQUENT RESPIRATORY
CENTER DEPRESSION.

21. CAUSES OF SECONDARY APNEA-DISEASE
ENTITIES
RDS: IN THIS CASE APNEA IS RELATED TO THE DEGREE OF
PARENCHYMAL DISEASE WHICH DETERMINES DEGREE OF HYPOXIA.
IT MAY ALSO RESULT FROM RESPIRATORY MUSCLE FATIGUE.
SEPSIS: CAUSES APNEA SECONDARY TO CNS DEPRESSION
CNS: HEMORRHAGE, SEIZURES,ASPHYXIA.APNEA ARISES FROM
ASPHYXIA WITH SUBSEQUENT HYPOXAEMIA RESPIRATORY
CENTERDEPRESSION OR ACTUAL BRAIN INJURY.

22. PDA:
DUE TO CARBON DIOXIDE RETENTION AND HYPOXAEMIA
ASSOCIATED WITH A LEFT TO RIGHT SHUNT.
THE ABOVE ARE THE 4 COMMONEST SECONDARY CAUSES OF APNEA
IN THE NEW BORN

23. IATROGENIC CAUSES OF APNEA
• SUDDEN INCREASES IN ENVIROMENTAL TEMPERATURE
• VAGAL RESPONSE DUE TO SUCTION OF THE NASOPHARYNX
VOMITING AND OBSTRUCTION OF THE AIRWAY
• REFLEX APNEA-OCCURS WHEN FOREIGN MATERIALS [MILK OR
SECRETIONS ] ARE PRESENT IN THE OROPHARYNX. THIS LARYNGEAL
CHEMO REFLEX IS PROTECTIVE IN THAT IT PREVENTS ASPIRATION OF
THE FOREIGN SUBSTANCES.
• OBSTRUCTION OF AIRWAY MAYBE DUE TO IMPROPER NECK
POSITION OR ASPIRATION

24. RESULTS OF APNEA
• CEREBRAL BLOOD FLOW DECREASES WITH APNEA AND
BRADYCARDIA, AND IS DIRECTLY CORRELATED WITH THE SEVERITY
OF THE BRADYCARDIA.
• CEREBRAL BLOOD FLOW MAY INCREASE WITH RECOVERY.
• DECREASED OXYGEN SATURATION OCCURS AND ALSO CORRELATES
WITH DURATION OF APNEA IRRESPECTIVE OF CAUSE.
• GREATER XIMUM FALL IN CEREBRAL BLOOD FLOW THAN CENTRAL
OR MIXED APNEAMAOBSTRUCTIVE APNEA IS ASSOCIATED WITH A

25. • BECAUSE ALTERATION OF CEREBRAL BLOOD FLOW MAY CAUSE OR
• EXACERBATE IVH, OBSTRUCTION OF THE UPPER AIRWAYS WITH
• RESULTANT APNEIC EPISODES MUST BE PREVENTED

26. PREVENTION
• ALL NEWBORNS ASSESSED AS BEEING AT HIGH RISK FOR APNEA
SHOULD BE OBSERVED FOR AT LEAST 12 DAYS.
• BOTH HEART AND RESPIRATORY RATE SHOULD BE MONITORED.
• ALARM SYSTEMS SHOULD BE USED ALL THE TIME.
• A QUALIFIED OBSERVER IS ESSENTIAL

27. • APNEA IS FOLLOWED BY BRADYCARDIA AND OXYGEN
DESATURATION,AND THE DEGREE OF THESE CHANGES IS
ASSOCIATED WITH THE EXTENT OF THE APNEIC EPISODE.
• ** CHANGES IN OXYGEN SATURATION ARE DISTINCT FROM
CHANGES IN HEART RATE,SO DESATURATION CANNOT BE
PREDICTED FROM HEART RATE PATTERNS.
• BECAUSE EPISODES OF APNEA AND BRADYCARDIA ARE ASSOCIATED
WITH A DECREASED CEREBRAL BLOOD FLOW, AND OXYGEN
DESATURATION [AS LITTLE AS 5-10% ] IS ALSO ASSOCIATED WITH
ALTERATION IN CEREBRAL BLOOD FLOW,
• OXYGEN MONITORING MUST ACCOMPANY CARDIORESPIRATORY

28. • PULSE-OXYMETRY MONITORS MAY DETECT HYPOXAEMIC EPISODES
THAT CAN LEAD TO APNEIC SPELLS.
CARE SHOULD BE ORGANISED TO REDUCE STRESSFUL HYPOXIC
EPISODES.

29. PREVENTION OR REDUCTION OF APNEA
• REDUCE ENVIROMENTAL STRESS EG MINIMAL HANDLING AND KMC.
• GENTLE TACTILE STIMULUS HAS BEEEN SHOWN TOBE HELPFUL IN
DECREASIG AND PREVENTING APNEIC SPELLS.
• NOXIOUS STIMULI SHOULD BE AVOIDED EG BANGING
VENTILLATORS.

30. MANAGEMENT OF APNEA
• GENTLE TACTILE STIMULUS
• TEMPORARY BAG AND MASK VENTILLATION IF STIMULUS IS
INEFFECTIVE.DO NOT APPLY UNDUE PRESSURE TO CHIN AND NECK,
SO THAT THE AIRWAY REMAINS OPEN.
• VIGOROUS BAGGING MAY ALSO STIMULATE PULMONARY STRETCH
RECEPTORS AND AGGRAVATE APNEA , THEREFORE IT SHOULD BE
AVOIDED.

31. MANAGEMENT OF APNEA
• KINESTHETIC STIMULATION [ EG WATERBED OR OSCILLATING
MATTRESS ARE NOY RECOMMENDED.
• PROPHYLACTIC USE OF METHYLXANTHINES IN INFANT UNDER 1.5
KG [PROPHLACTIC DOSE]
• METHYL XANTHINES MAY ALSO INCREASE THE CHANCE OF
SUCCESSFUL EXTUBATION FROM VENTILLATOR [WITHIN 1 WEEK].

32. PREVENTION
• [CHECK PREVIOUS SLIDES]
• PREVENT SUDDEN INCREASES IN ENVIROMENTAL TEMPERATURE
• KEEP ENVIROMENTAL TEMPERATURE IN THE LOWER ZONE OF
NORMAL.
• REM SLEEP IS ALSO MORE COMMON AT HIGHER TEMPERATURES, SO
LOWER TEMPERATURES ARE ALSO USEFUL IN REDUCING THIS.