Neonatal Resuscitation

Neonatal Resuscitation
By:Mary P. Martinasek, BS, RRT
Director of Clinical Education
Hillsborough Community College

Asphyxia
* Hypoxia + Hypercapnia + Acidosis
* May lead to irreversible brain damage
* The necessity to resuscitate is related to the degree of asphyxia

Causes of fetal asphyxia
* Maternal hypoxia
* Insufficient placental blood flow
* Blockage of umbilical blood flow
* Fetal disorders

Primary vs. Secondary Apnea
* Primary
o Initial asphyxia
o Signs
+ Initial period of rapid breathing
+ Respiratory movements cease
+ Heart rate and bp drop
+ Neuromuscular tone diminishes

Secondary Apnea
* If no resuscitation and apnea continues
* Signs
o Deep gasping respirations
o Heart rate continues to decrease
o Blood pressure begins to fall
o Infant flaccid

* Primary
o Stimulation and oxygen will usually induce respirations

* Secondary
o Infant unresponsive to stimulation – must be resuscitated

Effects of asphyxia on the lungs
* Ineffective respirations cannot open alveoli
* Pulmonary Hypertension
* Pulmonary vasoconstriction
o Hypoxia, hypercarbia, acidosis

Persistent Fetal Circulation
known as PPHN

* Leads to further asphyxia
* Blood shunted
* CO2 remains high despite ventilation
o Indocin
o Ligation of PDA

Preparation for Resuscitation

* Anticipation of high risk delivery
* Proper equipment
* Trained personnel

Purpose of Resuscitation

* Reverse asphyxia before irreparable damage has occurred

ABC’s of Resuscitation

* A – Establish an open airway
o Position infant
o Suction mouth then nose
* B – initiate breathing
o Use tactile stimulation
o Use PPV if necessary

Resuscitation

* C – Maintain circulation
o Stimulate and maintain circulation
+ Chest compressions
+ drugs

Initial steps
* Dry the infant
* Warm the infant
* Position the infant
* Suction the infant
* Stimulate the infant

Next step
* Evaluate respirations
o If none or gasping , provide PPV with 100% O2 for 15-30 seconds
o If spontaneous respirations then evaluate HR
* After 15-30 seconds of PPV or evaluation of spontaneous respirations then:
* EVALUATE HEART RATE
* If HR is above 100 then reevaluate respirations and color
* If HR is less than 60 continue/start PPV and start compressions

Reassess
* After 30 seconds reassess
* HR greater than 60 stop compressions
* HR greater than 100 and breathing stop PPV
* Evaluate infant’s color
o Peripheral vs. central cyanosis
o What is acrocyanosis?

Thermoregulation
* Maintain a neutral thermal environment
* Possible causes of heat loss
o Radiant
o Evaporative
o Convective
o Conductive

Neonatal Resuscitation.ppt

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Global trends of neonatal, infant and child mortality

Global trends of neonatal, infant and child mortality: implications for child survival
By:Dr KANUPRIYA CHATURVEDI & Dr S.K CHATURVEDI

When are child deaths occurring?

What are under-fives dying of?
(excluding neonatal causes of death)

* Pneumonia
* Diarrhoea
* Malaria
* Measles
* HIV/AIDS

Malnutrition contributes to more than half of all under-five deaths
What are neonates dying of?
* Preterm births
* Severe infection
* Asphyxia
* Congenital anomalies
* Tetanus

INDIA’S SHARE OF GLOBAL BURDEN
SOLUTIONS EXIST

* A mix of community and facility-based interventions
* A mix of integrated child health approaches
* Integrated management of neonatal and child hood illnesses is proven tool

Goals of IMNCI
* Standardized case management of sick newborns and children
* Focus on the most common causes of mortality
* Nutrition assessment and counselling for all sick infants and children
* Home care for newborns to
o promote exclusive breastfeeding
o prevent hypothermia
o improve illness recognition & timely care seeking

Essential components of IMNCI
* Improve health and nutrition workers’ skills
* Improve health systems
* Improve family and community practices
Home visits for young infants: Schedule
Colour Coded Case Management Strategy
Other innovations in case
Innovations in therapy
* Single daily dose gentamycin
* How to treat at home when hospital admission is not feasible
* Counselling the mother to give oral drugs at home
* Clear recommendations for follow up
* Negotiated feeding counselling
What does IMNCI not provide at all or fully
* Antenatal care
* Skilled birth attendance
* Birth asphyxia management
* Improved health system management
* What can be rapidly added to IMNCI
* Inpatient care modules for first level referral hospitals
IMNCI Experience--Milestones
* Early 2002, GOI constituted an Adaptation Group
* In joint GOI-UNICEF review meeting in April 2002 GOI requested to experiment IMNCI in BDCS districts
* July 2002, First national 2 days planning meeting
* December 2002, pre-tested 8-days physician course material
* Early 2003 - adaptation of H&N workers module
* May 2003 – First field testing in Osmanabad followed by one in Shivpuri & content & methodology frozen
* Implementation started in Andoor PHC, Osmanabad in June 03 followed by Valsad district
* Follow-up training of supervisors in April 04 in Osmanabad
* Field trial for case registers initiated in late 2004
* Physicians courses from 2005 included community visit, facilitation technique and briefing on Health workers’ course
* First Facilitation technique course in Orissa in June 2005

Training Flow
Training: Strengths -- Contents Doable
Training Limitations: Contents
Key messages

* Maternal and newborn care and support is essential to achieve a substantial reduction in neonatal mortality
* Improving child survival requires coordinated action between maternal and child health, and other programme areas (e.g. EPI, NUT, RBM, HIV)
* IMCI is an effective delivery strategy for multiple child survival interventions (India has already incorporated newborn care)
* For substantive impact, strong community component must accompany the health system strengthening

Global trends of neonatal, infant and child mortality.ppt

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Angioedema

Angioedema

Overview
* Self-Limited, subcutaneous edema resulting from increased vascular permeability
* Generally resolves over 24-48 hours
* Mast Cell / Kinin related etiologies
* Involvement of the lips, pharynx and bowel common (potentially life-threatening)
* Treated with CCS and H1/H2 blockers

Etiology
* Immunologic / IgE mediated
* Hereditary and Acquired (non-mast cell)
Ace-Inhibitors
* ACE (Kininase II) degrades bradykinin
* ACE-I results in inc levels bradykinin
* Pts with genetic deficiencies in bradykinin degradation could be at higher risk
* 0.1-0.7% of patients tx with ACE-I
* Intestinal edema may develop

ACE-I
Hereditary/Acquired
* Kinin-mediated angioedema that may be unmasked with use of ACE-I
* C1-Inh deficiency (level or fx) - Inc BKinin
Summary

* Angioedema is potentially life-threatening
* Associated pruritis and hives points to anaphylaxis
* Absence of pruritis and hives think ACE-I and/or C1-Inh deficiency
* Use caution when switching from an ACE-I to an ARB

Angioedema

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