Approach to the neonatal cyanosis

12,398 views 52 slides Sep 23, 2015
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About This Presentation

Approach to the neonatal cyanosis topic presentation


Slide Content

Approach to the
neonatal cyanosis
Topic presentation
By Ext. Sripada Kriangkhajorn
Faculty of Medicine, Srinakharinwirot University

Objective
•Definition, presentation, and abnormalities in cyanotic
newborn
•Approach cause of neonatal cyanosis; include history, risk, and
initial evaluation
•Initial management in neonatal cyanosis disease; pulmonary,
cardiac cause

Cyanosis
•A physical sign causing bluish discoloration of the skin
and mucous membranes
•Three factor causes cyanosis are
•Total amount of Hb in blood
•The degree of Hb saturation
•State of circulation.

Central cyanosis
•Increase in arterial deoxyhemoglobin, associated with
decreased PaO
2 and Hb oxygen saturation (SaO
2)
•Present when deoxyhemoglobin in blood reaches 3-5
g/dL.

Peripheral cyanosis
•Discoloration of skin but sparing in mucous membrane,
tongue. Usually normal in PaO
2.
•Peripheral vascular instability, cold exposure are common
cause in the cyanosis

Differential Cyanosis
•Asymmetrical cyanosis between upper and lower extremities,
usually lower limbs more than the upper limbs.
•This finding suggested of Rt.-to-Lt. Shunt from PDA
Differential Cyanosis Cause
1
-PPHN with PDA
-PDA with severe pulmonary hypertension (Eisenmenger Syndrome)
-Interrupted aortic arch
-Severe coarchtation of aorta with VSD and PDA

Differential Cyanosis
•Usually lower limbs more cyanosis than the upper limbs.

Reversed differential cyanosis
•Cyanosis that appear in upper limbs more than lower limbs.
•Found in complete TGA with severe pulmonary hypertension,
D-TGA with VSD ,or Interrupted aortic arch or severe
coarctation of aorta
http://journal.frontiersin.org/article/10.3389/fphar.2013.00070/full

APPROACH TO A CYANOTIC NEONATE

1. Identify kind of cyanosis
Cyanosis
Peripheral
Cyanosis
Central
Cyanosis
•Pink tongue, conjunctiva
•Normal PaO
2
•Cold peripheral Ext.
•Cap. Refill > 2 sec.
•Discoloration all skin and
mucous
•Decrease PaO
2 ,SpO
2
•Capillary refill <2 sec.

2. Identify possible cause
•Three common causes of central cyanosis are Cardiac
disease,Respiratory disease, Central nervous system
•Another cause is hematologic cause such as
methemoglobinemia

Central Cyanosis
CNS
Pulmonary disease
Cardiac disease

CNS
Causes and clinical finding of Central Cyanosis
5
System Causes Clinical Findings
CNS depression
Perinatal asphyxia
Hypoventilation
Heavy maternal
sedation
Intrauterine fetal
distress
Shallow irregular
respiration
Poor muscle tone
Cyanosis resolved when
given oxygen or
stimulated the patient

Pulmonary System
Causes and clinical finding of Central Cyanosis
5
System

Causes Clinical Findings
Pulmonary
disease
Parenchymal lung
diseases
Pneumonia
Pneumothorax or
pleural effusion


Congenital lung
abnormalities
Persistent
pulmonary
hypertention
Tachypnea, respiratory
distress with chest
retraction, or expiratory
grunting
Crackles,or decreased
breath sound
X-ray films may show some
lung abnormalities
Oxygen giving may
improved cyanosis

Cardiac System
Causes and clinical finding of Central Cyanosis
5
System Causes Clinical Findings
Cardiac
disease
Cyanosis CHD
with right to left
shunt (5 ‘T’s)
Tachypnea, but not
respiration effort
Normal breath sound unless
severe CHF
A continuous murmur may
present.
X-ray may shows
cardiomegaly, increased or
decreased lung markings.
Little or no improved in
oxygen giving.

3. History & risks evaluation Risk assessment in initial evaluation
5,6
History Possible risks
Maternal Diabetic
Heart disease
GBS and infectious
screening
PROM
CHD, sepsis, fetal
asphyxia, pneumonia
Oligohydramnios Hypoplastic lung
disease
Polyhydramnios Airway, esophageal,
neurological disorder
Perinatal Difficult delivery Neurological cause; birth
trauma, ICH, phrenic
nerve paralysis
Postnatal Polycythemia
Hypoglycemia
Hypoventilation

4. Physical Examination
•Complete examination but also pay focus on pulmonary,
cardiac, and neurologic system
•Growth curve for SGA, LGA which are prone for
polycythemia, and associated congenital anomaly

Cardiac Examination
•In cardiac auscultation, focus on S
2, which will be loud
and single (or narrowly split) in PPHN, TGA, PA
•Heart murmurs is often not helpful to detect serious
lesions such as TGA
•Loud murmurs are frequently benign lesion such as a
small VSD.

5. Special Tests
•Hyperoxia test
•Hyperoxia-hyperventilation Test
•Pre-/postductal PaO2 Test
•Echocardiography

Hyperoxia test
•Perform by given 100% oxygen for 5-10 minutes, then
measure the before and after oxygen saturation Changes after performed Hyperoxia Test
1
PaO2 SpO2
Pulmonary disease
Pneumonia
RDS, Hyaline membrane
disease etc,.
> 150-200
mmHg
Up to 99%
Rt.-to-Lt. Shunt Disease
Congenital cyanosis
heart disease
PPHN
Pulmonary AV Fistula
< 50-150
mmHg
< 80%

Hyperoxia-hyperventilation Test
•Given the 100% O
2 through ET-tube or oxygen bag,
•Perform the patient hyperventilation, start at 100
times/min then keep monitor PaCO
2 at 20-30 mmHg Changes after performed Hyperoxia-Hyperventilation Test
Rt.-to-Lt. Shunt PaO2 SpO2
Congenital cyanosis
heart disease
< 50-150
mmHg
< 80%, no improve
PPHN > 100 mmHg Up to 95%

Pre-/postductal PaO
2 Test

Pre-/postductal PaO
2 Test
Pre-/postductal PPHN CHD
PaO
2 difference > 15-2o mmHg <15mmHg
SpO
2 difference > 10% <10%

6. Investigation
•Chest X-ray
•Help differentiate lung parenchymal diseases, some
congenital anomaly, and some congenital heart
diseases
•EKG
•Useful to detect cardiac arrhythmias, but is not useful
to detected serious neonatal cardiac condition such as
TGA

Identify possible cause
3

Central Cyanosis
CNS
Cardiac disease
Cyanosis not improve when crying
No respiratory effort
+/- murmurs
+SpO
2, PaO
2 do not improve
after O
2 support
Abnormal S
2 sound
+/- CRX abnormal
+/- EKG annormal
Cyanosis improve when crying
Respiratory effort; grunting,
chest wall retraction, RR>60/min
Normal cardiac examination
+SpO2, PaO2 do improve after O
2 support
Normal CRX, EKG

Perinatal asphyxia
Hypoventilation
Heavy maternal sedation
Intrauterine fetal distress
Difficult delivery
Pulmonary disease

TREATMENT BY SPECIFIC CAUSE

Respiratory distress in the
neonates
Common abnormalities in the Neonatal Respiratory Distress
2
Initial management Specific treatment
RDS

On O2 support, with
CPAP , or ET-tube

Keep normal BT at
36.5-37.5c

Correct metabolic
disturbance
IV fluid support
Surfactant,mechanical
ventilation

MAS
Keep PaO2 60-80
mmHg, adequate O2,
ventilation
Sepsis/Pneumonia Antibiotic
Pneumothorax Pleural tapping
Congenital
diaphragmatic
hernia
Retain OG tube,
definitive surgery
Airway obstruction Definitive surgery

Cardiac cause of neonatal CHD
Congenital Heart Disease
7,1
Pulmonary BloodFlow Cyanotic Acyanotic
High flow
TA
TGA
TAPVR
Common Atrium
Common Ventricle
ASD
VSD
PDA
AVC
Low flow
TOF
Tricuspid atresia
Ebstein’s anomaly
Pulmonary
stenosis

Normal

-
Coarctation
of Aorta
Aortic
stenosis

CYANOTIC CONGENITAL HEART
DISEASE

Fetal and neonatal circulation
•Structure and Function: The Heart Before and After Birth
Source aviva.co.uk

ที่มา ภาวะวิกฤติทางหัวใจในเด็ก; มูลนิธิเพื่อสนับสนุนการผ่าตัดหัวใจในเด็ก; กรกฎาคม 2551

Cyanotic Congenital heart disease
Common finding cyanotic
congenital heart disease
ที่มา ภาวะวิกฤติทางหัวใจในเด็ก; มูลนิธิเพื่อสนับสนุนการผ่าตัดหัวใจในเด็ก; กรกฎาคม 2551

Ductal Dependent Cardiac Lesions
•Congenital cardiac abnormality that need the remain opening
ductus arteriosus to maintain vital circulation.
•Must be considered in any neonate (<28day) with sudden
onset shock should be treated as having ductal dependent
lesions until proved otherwise
•PGE1 infusion, by maintaining patency of ductus arteriosus is
life-saving in infants

Ductal Dependent Cardiac Lesions
•Lt. to Rt. shunt pulmonary vascular resistance is lower than
systemic vascular resistance.
•Rt. to Lt. shunt pulmonary vascular resistance is
suprasystemic.

Patent Ductus Arteiosus
8,7,1,9
Dependent non-Dependent Initial Management
Pulmonary Systemic Confirm cardiac cause of
cyanosis.
Initial resuscitation; ABC’s,
but limit O2 support in
preterm
Identify whether it is
ductal dependent lesion
if possible
Medication
PGE1 IV continuous drip
0.05-0.1mcg,
prefer start with 0.1mcg,
then taper down
Side effect; apnea, flushing,
diarrhea. Intubation may be
used in some patient
Correct metabolic
disturbance(acidosis)
PA e IVS
TGA e IVS
TOF e PA
Critical PS
TA e PS/PA
Severe
Ebstein’s
anomaly

Univentricular Heart
Coarctation of
aorta

Critical AS
HLHS
IAA
TAPVR If can’t rule out the non-
ductal dependent lesion,
and the patient became
more deteriorate, PGE1 may
be used
Truncus
arterosus

TOF
•Most common cyanosis CHD, 14% of all CHD
•PE; Loud single S2, systolic ejection murmur Lt. mid-upper
sternal border, clubbing of finger
•Cyanosis with decrease pulmonary blood flow, no CHF
•TOF with PA has early onset
of cyanosis, ductal dependent
lesion, no murmur

Source Swatchz’s principal of surgery edition 10th

TOF

TGA
•3rd common cyanotic heart disease, associated with another
CHD
Source Swatchz’s principal of surgery edition 10th

TGA
•A. The heart is enlarged with a narrow "pedicle" giving the so
called "egg on a string" appearance.
•The superior mediastinum appears narrow due to the antero-
posterior relationship of the transposed great vessels and
"radiologic-absence of the thymus".

Ebstein anomaly
•an uncommon congenital cardiac anomaly, characterised by a
variable developmental anomaly of the tricuspid valve

TAPVR(Total anomalous pulmonary venous return)
•Mixing blood circulation with increase pulmonary blood flow
•Pulmonary vein obstruction is key to determine severity of
disease

TAPVR

TAPVR (Supracardiac)

Finding mild cardiomegaly, increased pulmonary vascular markings and
"snowman" appearance

TAPVR(infradiaphragmatic-obstructed)
• The heart is normal sized with increased pulmonary venous
pattern preferentially in the right upper lobe
https://www.bcm.edu/radiology/cases/pediatric/text/2e-desc.htm

Truncus arteriosus
•Single great vessel exit from heart, mixing blood circulation,
rare, 0.9% of all cyanotic CHD
•Present with late cyanosis, with congestive heart failure, or
URI on top
Source Swatchz’s principal of surgery edition 10th

Univentricular Heart
•Group of abnormality such as; tricuspid atresia, pulmonary
atresia, HPLS, single ventricle
•2
nd
most common with 10% of all CHD
•Mixing blood lesion, variable severity

Tricuspid atresia
•Complete absence of the communication between the right
atrium and ventricle. This lesion occurs in approximately
1:15,000 live births

HPLS
•Most severe cyanotic CHD

Univentricular Heart
•Pulmonary atresia
Source Swatchz’s principal of surgery edition 10th

Cyanosis neonate in cardiac
disease
•Most common cyanosis CHD in neonate is TOF
•Most of early cyanosis in newborn <1wk is cyanosis CHD
with ductal dependent lesion
•Subacute cyanosis with CHF usually come from decrease
pulmonary vascular resistant present at > 2wk of life
•Hypercyanotic spell from TOF mostly present late, at
2mo.-6mo.

Before refer to specialist
•If possible, identify ductal dependent lesion
•Resuscitation; ABC’s, but limit O
2 support in preterm
•Medication;
•PGE
1 IV continuous drip 0.05-0.1mcg, prefer start with
0.1mcg, then taper down
•Side effect; apnea, flushing, diarrhea
•Correct metabolic disturbance(acidosis)

Save Blue Heart Project

THANK YOU

References
1.ภาวะวิกฤติทางหัวใจในเด็ก; มูลนิธิเพื่อสนับสนุนการผ่าตัดหัวใจในเด็ก; กรกฎาคม 2551
2.Cyanosis in neonate; คู่มือกุมารเวชศาสตร์ฉุกเฉิน; คณะแพทยศาสตร์ รามาธิบดี กันยายน 2554
3.Fetal Asphyxia; คู่มือทารกแรกเกิด; คณะแพทยศาสตร์ มหาวิทยาลัยของแก่น
4.Evaluation and management of the cyanotic neonate;Clin Pediatr Emerg Med. ;Pubmed;Author
manuscript; PMC 2009 Sep 1.
5.Pediatric cardiology;
6.Swatchz’s principal of surgery edition 10th
7.โรคหัวใจตั้งแต่ก าเนิด; ต ารากุมารเวชศาสตร์; คณะแพทยศาสตร์ มหาวิทยาลัยศรีนคริทรวิโรฒ
8.Identification and Management of Ductal Dependant Cardiac Defects in the Transport Setting - Robyn
Neely Funk, RN, BS/BSN, PHRN, CMTE
9.Ductal-dependent cardiac lesions/Hyperplastic left heart syndrome; Atlas of pediatric emergency medicine;
McGrawHill; second edition
10.Patent Ductus Arteriosus Aortopulmonary Window; George A. Gibson9
11.https://www.bcm.edu/radiology/cases/pediatric/text/2e-desc.htm