Neonatal shock in
SBA
Key words:
(Hb level, oxygen
content, compensated and uncompensated shock and cerebral
circulation) In cases of
severe birth asphyxia, we noticed the following in our NICU:
We already know:
?
Nature tries to maintain
oxygen delivery to all cells through circulation. Failure to supply needed oxygen to cells
is shock.
?
Initially to preserve
circulation & prevent shock, nature tries vasoconstriction and there
by maintains blood pressure and HR. (because circulating volume is maintained
till a limit)
?
Late Effect of hypoxia in the
arterioles is change in diameter due to vasodilatation which leads to change in
flow of ml/kg/ min.
?
In SBA if we do haemodynamic
studies :
1.
most frequent findings are
low RIGHT VENTRICULAR OUT PUT(RVO) and increased SUPERIOR VENACAVA FLOW(SVF)
& collapsing INFERIOR VENACAVA(
IVC).
2.
low LEFT VENTRICULAR OUT PUT(
LVCO)
3.
PATENT DUCTUS ARTERIOSUS(PDA)
without murmur AD SMALL LEFT ATRIUM(LA). These findings suggest
hypovolemia.
v
In cerebral circulation, while monitoring anterior cerebral
artery(ACA),middle cerebral artery(MCA) and basilar artery (BA) we observed:
?
High systolic flow &
resistence index (RI)? with normal pulsatality index(PI) with low total cerebral
flow or
?
Low systolic flow and
decreased RI & PI with low
total cerebral flow or
?
Absent diastolic or reversal
of flow with very low RI & very low PI-stage of end
dilatation.
?
Normal HR & BP with low cardiac
output and collapsing IVC
(hypovolaemia)is compensated Shock and
low cardiac out put with tachycardia and decreased BP is uncompensated
shock, the later being more terminal event.
?
Low cardiac output with
normal BP and HR i.e. compensated shock correlates with increased peak systolic
velocity, increased RI, higher diastolic velocity and normal or high PI in
cerebral arteries with low total cerebral flow .
?
Low cardiac output with
increased HR and decreased BP- Uncompensated shock correlates with low PSV, low
or absent or reversal of diastolic flow, low RI and PI. & very
low cerebral flow. Immediate Cord
clamping in SBA situation by restricting the flow of placental blood leads to
further hypovolaemia in baby. Late cord clamping with intact cord resuscitation
is good for SBA babies (intact cord resuscitation).
?
When SBA is associated with
low Hb i.e. <14.5gms at birth, we see very low oxygen content of blood which
might lead to decreased oncotic pressure with hypovolaemia leading to decreased
oxygen extraction and shock. If this persists beyond window period i.e. 6 to 8
hrs of life, the changes in arterioles and venules are irreversible. When we try
to recover this stage and shock by pushing volume and vasopressors, the damaged arterioles give way and
intracranial hemorrhage occurs and in periphery venous stasis leads to irreversible
shock.
?
Also we noticed the stages of
cerebral arterial Circulation in ACA, MCA & basilar artery and if it is in
stage one (high PSV & high EDV
with slightly reduced total cerebral flow-less than 30ml/100gms/min, high RI and
near normal PI) or stage two [low
PSV low EDV very low flow (20 to 25ml/100gms/min)]i.e. slightly lower RI up to
65, lower PI up to 0.90.we can reverse it by giving PCV or FFP as needed for
correcting the volume near normal and vasopressures to improve venous return and
their by save cerebral damage to great extent.
?
If cerebral circulation is in
stage three very low RI, PI &
very low flow les than 20 ml/100gms/min or absent or reversal of diastolic flow
with uncompensated shock, hemorrhage is inevitable and we shall fail to save the
brain damage and hence no option then to have HIE II or III depending on degree
of damage.
We also know these facts about placental and foetal
circulation:
?
Placental circulation is the
main stay of foetal growth and foetal hamodynamics.75% of circulating blood
stays in venous side of circulating system and rest 25% in arterial side.
Umbilical vein is indirect indicator of placental circulation and umbilical
artery ? the indicator of foetal circulaton.We know the changes related to
umbilical artery and its reflection in foetus. We also know right side of heart
? RV, RA, IVC, SVC etc. are dominating circulation in foetal life. So if we know
the size of umbilical vein i.e. diameter and if we know the VTI (Velocity time
interval) of umbilical venous flow we can calculate the venous blood flow in
ml/kg/min.
?
The venous flow is continuous
flow in Doppler examination but there has to be a change in characteristic of
flow as well as ml/kg/min of flow. (volume)If we try to plot the diameter in UV
and correlate with UA diameter and flow we may get a correlation which can tell
us which side of placental pool- Placental arterioles in foetus side of placenta
or venules in the same side is early to show changes. (Our
hypothesis).
?
Hypoxia causes arterioles to
contrict and venules to dilate. So there has to be a
correlation.
Additional effects of Asphyxia (viruses solely hypoxemia
or ischemia or both- page 256, chapter 6, the neurology of new born- volpe ?
5th edition)
At least four
major factors are added to constellation of biochemical features controlling out
come of asphyxia, with its attendant increase in PaCo2. The first
three of these effects appear to be beneficial, at least initially, and the
fourth of these, deleterious.
First, the
hypercapnia acts to maintain or even augment CBF through and increase in
perivascular H+ concentration in brain, which may be beneficial early in
asphyxia.
Second, the
hypercapnia may be associated with a diminution in cerebral metabolic rate.
Moderate hypercapnia has been shown to cause diminution in cerebral metabolic
rate in adult rat brain, adult monkey brain & developing rat
brain.
Third, an increase
in PaCo2 leads to acidemia, which is accompanied by a shift in
the oxygen hemoglobin dissociation curve such that affinity of hemoglobin for
oxygen is decreased. The result is an increase in the delivery of oxygen to
cells. The operation of one or more of these three factors could underline the
protective effect of moderate hypercapnia in immature rats subjected to
hypoxia-ischemia.
Fourth, important
factor relative to hypercapnia & the outcome with asphyxia may be
deleterious; intracellular PH falls more drastically for a given amount of
lactate formed when the effect of elevated PaCo2 is added by
asphyxia. Thus extreme acidosis & consequent tissue injury could result.
Future studies directed at defining the relative roles these four factors in the
genesis of the biochemical & physiological derangements associated with
asphyxia in the perinatal animal will be of great
interest.
With Our intervention we did
following:
?
Ventilation: - remove
excessive PaCo2.
?
If Hb is less than 14.5gm% -Red cell
concentrate transfusion increase, total oxygen content of blood (in anaemic infants) &
buffering capacity of blood & raises the volume.
?
Fresha frozen plasma (FFP) if
Hb is > 14.5 gm % -also does the roll of preventing hypovolamia.increasing
the volume always increased cerebral circulation.
?
Vasopressors may be
responsible for maintaining of haemodynamics by increase in cardiac output,
cerebral blood flow, urine output & there by preventing HIE to a great
extent.
What clinical
effects we see in SBA babies with compensated shock with our strategy of
intervention?
?
Cardiac output becomes normal
& the effect of hypoxia on myocardium recover to normal by 48 hrs, cerebral
circulation becomes normal i.e. RI & PI becomes normal with in 36 to 48 hrs,
total cerebral flow decreased initially (PSV & EDV ) & then stabilizes
with in 36 to 48 hrs, so is the clinical & heamatological
recovery.
?
Consciousness of SBA baby is
directly related to total cerebral flow . If the flow is more than 30
ml/100gm/min then baby becomes conscious & active. No convulsion is seen in SBA babies if SBA
babies are taken care as follows:
Our strategy for Treatment of SBA
babies
?
if baby is clinically in
Shock ,treat it with 10 to20ml/kg of N. saline bolus immediately after birth or
as soon as admitted within 30 minutes by infusion pump.( pale look, prolonged CRT
and mild to moderate degree of respiratory distress and low spo2 is considered shock, BP may
be normal so is heart rate.)
?
Simultaneously we do f echo
to estimate LVCO,RVCO, IVC size, superior venacava flow, PDA and PFO flow and
also flow in anterior and middle cerebral arteries and basilar artery there by
estimating total cerebral flow per 100 gms per minute. We there by conclude it
to say baby is in compensated or uncompensated shock.
?
We send for investigations
like blood gas, serum electrolyte, haemogram with platelet and blood culture
sensitivity.( pl. note blood investigations are done from sample collected by
umbilical venous catheter. If the total oxygen content of blood is low (below
20) and haemoglobin is below 14.5 gms/dl. We give red cell concentrate
transfusion 10ml/kg as quickly as possible always with in 6-8 hrs of birth of
baby i.e. window period in SBA babies.
?
Baby with SBA is put on ventilator if
required.
?
All the babies with SBA with
shock are put on vasopressures dopamine + dobutamin in dose of 5 to 10 microgram
as needed in order to improve venous blood return and improve renal circulation and hypoxic myocardial
dysfunction for first 24- 48 hrs..
?
We continue doing f echo and cerebral flow monitoring at
least 3 times in first 48 hrs and then s.o.s. and there by monitor the progress
and reperfusion injury . If we find
that baby is still having hypovolaemia than we give fresh frozen plasma 10ml/kg
to these babies.
?
If haemoglobin level and
oxygen content of blood is not low than we give fresh frozen plasma (FFP)10ml/kg
and improve cardiac out puts along with total cerebral flow.
?
Clinically we find the majority of babies who are in
compensated shock urine out put improves dramatically to 3ml/kg/min and stays
around that thereafter, Urine out put increases significantly if we use FFP or
packed red blood cells as needed in compensated shock, oliguria does not happen.
If we use N. saline bolus for treating compensated shock, if at all urine output
increases, it is for temporary period & then again oliguria sets in. it is
known that N.saline stays in circulation & maximum period of 6 hrs only.
where as FFP & RCC stages longer.if left atrial size is small (also seen
with more than 2.1mm size ?silent PDA, there by a dercreased pre load
significant respiratory distress is present. If LA size is increased by volume
replacement (RCC OR FPP) the respiratory distress improves to a great extent and
gasping if present disappears.
?
baby becomes conscious by 18 to 24 hrs ,
respiratory distress improves dramatically with replacement of volumes by red
cell concentrate or fresh frozen plasma as needed. It did not happen when we
used only normal saline bolus for correction of volume.
?
Non of the babies had
convulsion and if any had it before never did it again when hypovolemia is
corrected by N.saline bolus 10 to 20 ml/kg dose or RCC or FFP. Anticonvulsants
are not needed in any of the babies who recovered. Low cardiac output,
collapsing IVC are better sign of hypovolemia then HR & BP in newborn
babies.
?
Many of the surviving baies
go in HIE stage ii or iii.
?
Neurological recovery is
remarkably good in surviving babies on follow up of 3 months to 3
yrs.
? Author believes that this is superior method of treatment of SBA babies with compensated shock as compared with head or total body cooling (not practical in our country).
CATEGORY: NEONATAL CARDIOLOGY
MODE OF PRESENTATION: POSTER PRESENTATION.
TITLE: CORRELATION OF HEMODYNAMIC STUDIES IN SEVERE BIRTH ASPHYXIA BABIES WITH SHOCK AND THEIR CLINICAL OUT COME.
AUTHER NAME AND PLACE: ANIL PATEL, RAJKOT.
AFFILIATES: UNIQUE NURSING HOME PVT. LTD. NEONATAL UNIT.
WORD COUNT : 325
BACK GROUND: BABIES. VERY LITTLE IS KNOWN ABOUT COMPANSATED AND UNCOMPANSATED SHOCK,ITS CORRELATION WITH ANTERIOR CEREBRAL ARTERY FLOW AND CLINICAL OUT COME IN SEVERE BIRTH ASPHYXIA
OBJECTIVE AND DESIGN: IN THIS PROSPECTIVE SYDY WITH THE HELP OF FUNCTIONAL ECHOCARDIOGRAPHY( f ECHO) AND ANTERIOR CEREBRAL ARTERY FLOW(ACA FLOW)STUDIES,SYSTEMIC BLOOD FLOW ,WE ASSESED UPPER BODY SYSTEMIC VASCULAR RESISTANCE,CATAGORISED THEM IN TO COMPENSATED AND UNCOMPANSATED SHOCK .FINALLY WE CORRELATED THIS WITH CLINICAL OUT COME. FOR THIS ACA FLOW STUDIES AND f ECHO WAS DONE AT LEAST 3-4 TIME IN FIRST 48 HRS.
SETTINGS: TERTIARY NEONATAL CARE UNIT IN SAURASHTRA ,GUJRAT.
SUBJECT AND INTERVENTION: CONSECUTIVELY ADMITTED 21 FULL TERM NEONATES WITH SEVERE BIRTH SAPHYXIA IN OUR LEVEL 3 CARE NICU FROM 24.11.07 TO 16.7.2008 WERE INVESTIGATED WITH STANDARD PROTOCOL AND IN SPECIAL WITH f ECHO AND ACA FLOW SIMULTANEOUSELY WITH DIGITAL COLOR DOPPLER AND NEONATAL MICRO CONVEX 4-9 MHZ PROBE WITH ONE HOUR OF ADMISSION.THEY WERE THAN GROUPED IN TO COMPANSATED AND UNCOMPANASATED SHOCK AND VARIOUS CATAGORIES OF ANTERIOR CEREBRAL ARTERY FLOW.THESE WERE THAN CORRELATED WITH CLINICAL OUT COME .EACH CASE WAS FOLLOWED UP FOR A MINIMUM PERIOD OF 6 MONTHS TO ASSES THE NEUROLOGICAL DEVELOPMENT.
RESULT: COMPANSATED SHOCK (LOW SYSTEMIC BLOOD FLOW & NORMAL BLOOD PRESSURE FOR THE WEIGHT AND HR) WAS SEEN IN 80.94% CASES OUT WHICH 14.28% CASES DIED.UNCOMPANSATED SHOCK WAS SEEN IN 19.04% CASES AND ALL OF THEM DIED.TREATMENT GIVEN TO THESE BABIES ARE REDCELL CONCENTRATE,FRESH FROZEN PLASMA,VASOPRESSORS,VENTILATION AND OTHER NEEDED THERAPY AS PER PROTOCOL.ALL THE BABIES HAD ONE OF THE THREE f ECHO i.e LOW RVCO,LOW LVCO OR HIGH SUPERIOR VENACAVA FLOW WITH BRAIN SPARING EFFECT WITH ANY TWO OF THESE i.e. HIGH PSV, HIGH OR LOW EDV,ABSENT OR NO DIASTOLIC FLOW, LOW OR HIGH RI, INCREASED SUPERIOR VENACAVA FLOW .CINICALLY URINE OUT PUT STATRTED WITH IN ONE HOUR OF INTERVENTION IN 90.40% CASES AND WAS MORE THAN 3ML/KH/HOUR IN FIRST 24 HRS IN 80.95% CASES.HYPOXIC ISCHAEMIC ENCEPHALOPATHY(HIE) STAGE I WAS SEEN IN 7.14% AND NO HIE IN 92.85% CASES WHO SURVIVED AND WERE TREATED .NO DEVELOPMENTAL MOTOR OR SENSORY DELAY WAS SEEN IN ANY CASE EXCEPT ONE WHO WAS TREATED WITH NORMAL SALINE BOLUS (NOT GIVEN RCC WITH IN 12 HRS OF BIRTH)
CONCLUSION: f ECHOCARDIOGRAPHY AND ANTERIOR CEREBRAL ARTERY FLOW STUDIES CAN BE OF IMMENSE HELP IN CATAGORISING THE SBA BAIES WITH COMPANSATED AND UNCOMPANSATED SHOCK AND FURTHER ASSESING WHICH BABIES WITH COMPANSATED SHOCK ARE AT VERY HIGH MORTALITY RISK.INTERFERENCE WITH 10ML/KG OF REDCELL CONCENTRATE WITH IN WINDOW PERIOD AND 10ML/KG OF FRESH FROZEN PLASMA WITH IN FIRST 36 HRS IF BLOOD PRESSURE IS AGAIN LOW CAN INCREASE SYSTEMIC BLOOD FLOW AND ALTER ANTERIOR CEREBRAL ARTERY FLOWAND OXYGEN CONTENT OF BLOOD AND THERE BY OXYGENATION OF PERIPHERAL CELLS OF ENTIRE BODY.THIS MIGHT BE THE REASON FOR NO HIE OR NEONATAL ENCEPHALOPATHY IN 92.85% CASES OF SBA BABIES IN OUR SERIES. LIKE HYPERDYNAMIC SEPSIS, SYSTEMIC VASCULAR RESISTANCE IN 76.47% CASES i.e UPPER BODY VASCULAR RESISTANCE OF LESS THAN 0.5 MMHG PER ML/KG/MIN. .
KEY WORDS: SBA-TYPES OF SHOCK-TYPES OF ANTERIOR CEREBRAL ARTERY FLOW & THEIR OUT COME IF TREATED IN WINDOW PERIOD.
CATEGORY: NEONATAL CARDIOLOGY
MODE OF PRESENTATION: POSTER PRESENTATION.
TITLE: BIRTH ASPHYXIA ,ANTERIOR CERBRAL ARTERY FLOW ,CARDIAC FUNCTIONS & ITS CLINICAL CORRELATION.
AUTHER NAME & PLACE: ANIL R. PATEL RAJKOT GUJRAT
AFFILIATION: UNIQUE NURSING HOME PVT. LTD.
WORD COUNT : 324 .
BACK GROUND : VERY LITTLE IS KNOWN ABOUT ANTERIOR CERBRAL ARTERY FLOW IN BIRTH ASPHYXIA AND ITS CLINICAL CORRELATION.
OBJECTIVE AND DESIGN: IN THIS PROSPECTIVE STUDY WE ANALYSED ON ADMISSION DOPPLER ANTERIOR CEREBRAL ARTERY FLOW,LEFT VENTRICULAR OUT PUT,RIGHT VENTRICULAR OUT PUT,SUPERIROR VENACAVA FLOW,INFERIOR VENACAVA FLOW, PATENT DUCTUS ARTERIOSUS FLOW, FORAMEN OVALE FLOW, VARIOUS CARDIAC FUNCTIONS IN DETAIL IN FULL TERM NEONATES WITH SEVERE BIRTH ASPHYXIA THE STUDY WAS CARRIED OUT AT LEAST FOUR TIMES ONCE BEFORE AND THEN AFTER INTERVENTIONS WHERE SO EVER POSSIBLE.
SETTINGS: TERTIARY CARE NEONATAL UNIT IN SAURASHTRA ,GUJRAT.
SUBJECT AND
INTERVENTIONS:
CONSECUTIVELY ADMITTED 21 FULL TERM NEONATES WITH SEVERE BIRTH ASPHYXIA TO OUR LEVEL THREE NICU FROM 24.11.2007
TO 16-07-2008 ANTERIOR CEREBRAL ARTERY FLOW AND CARDIAC FUNCTIONS STUDY WAS DONE BY DIGITAL COLOR DOPPLER WITH
4-9 MHZ MICRO CONVEX NEONATAL PROBE ..CARDIAC FUNCTIONS AND ANTERIOR CEREBRAL ARETRY FLOW WERE THAN CORRELATED WITH CLINICAL OUT COME i.e. URINE OUT PUT,STAGES OF HYPOXIC ISCHAEMIC ENCEPHALOPATHY,AVERAGE VENTILATION HOURS,
BLOOD PRESSURE, CAPILLARY REFIL TIME, LEVEL OF CONSCIOUSNESS AND DEATH IN NEONATES.ALL OTHER INVESTIGATIONS WERE DONE AS PER PROTOCOL .
RESULT : IN SEVERE BIRTH ASPHYXIA BABIES ANTERIOR CEREBRAL ARTERY FLOW STUDIES SHOWED HIGH (> 29CMS/SEC) AND LOW (<17CMS/SEC)PEAK SYSTOLIC VELOCITY IN 57.14% CASES AND 9.52% CASES.. HIGH (> 6CMS/SEC) AND LOW (<2CMS/SEC)END DIASTOLIC VELOCITY WERE SEEN IN 61.90% CASES AND 9.52% ,. HIGH (>0.86) AND LOW(<0.74)RESISTANCE INDEX WERE SEEN IN 19.04% AND 71.40% CASES RESPECTIVELY. LOW (<140ML/KG/MIN) AND HIGH (270ML/KG/MIN) LVCO WAS SEEN IN 58.82% AND 0% CASES.. LOW (<130ML/KG/MIN) AND HIGH (265ML/KG/MIN) RVCO SEEN IN 52.94% & 5.88% CASES, HIGH (120ML/KG/MIN) AND LOW (<40ML/KG/MIN) SUPERIOR VENA CAVA FLOW SEEN IN 76.42% AND 5.08% CASES..INFERIOR VENACAVA SIZE<20MM AND COLLAPSING WALLS SEEN IN 95.23% CASES.
ANTERIOR CEREBRAL ARTERY FLOW RETURNS TO NORMAL IF INTERVENED WITH IN 3-8 HRS OF BIRTH WITH VOLUME REPLACEMENT BY RED CELL CONCENTRATE OR FRESH FROZEN PLASMA WITH IN 36 HRS. SUPERIOR VENACAVA FLOW RETURNS TO NORMAL IN 48-72 HRS WHERE AS CARDIAC OUT PUTS TAKE MORE THAN 72 HRS TO BECOME NORMAL IF FOUND INITIALLY LOW IN BABIES SURVIVED IN OUR SERIES.
URINE OUT PUT STARTED WITH IN 1 HOUR OF INTERVENTION IN 90.47% CASES & WAS MORE THAN 3ML/KG/HOUR IN FIRST 24 HRS IN 80.95% CASES. WHEN COMPARED RETROSPECTIVELY WITH SBA BABIES WITHOUT HAEMODYNAMIC MONITORING .IT WAS SIGNIFICANT FINDING.HYPOXIC ISCHEMIC ENCEPHALOPATHY STAGE I WAS SEEN IN 7.14% CASES AND NO HIE IN 92.85% SURVIVED CASES. FRANK TONIC AND CLONIC CONVULSION WAS NOTED IN 1 OUT OF 14 CASES SURVIVED(7.14%) IN FIRST 12 HRS OTHER 3 (21.42%) HAD JITTERY MOVEMENTS IN FIRST 12 HOURS.NO CONVULSION WAS NOTED IN ANY OF THE SURVIVED BABIES AFTER 12 HRS OF LIFE..NORMAL MOTOR AND SENSORY MILE STONES WERE NOTED IN 13 OUT OF 14 SURVIVED BABIES AT 3 TO 6 MONTHS OF FOLLOW UP. AVERAGE VENTILATION HOURS IN SURVIVED GROUP (14 OUT OF 21 CASES) 51.14 HOURS . IN BABIES WHO DIED 71.42% CASES WERE ADMITTED AFTER 18 HOURS OF BIRTH, 14.28% CASES HAD SEVERE PULMONARY ARTERY HYPERTESNION,AND 1 ADMITTED WITH IN 2 HRS DIED HAD SEVERE GRAM NEGATIVE SEPSIS.
CONCLUSION: MAJOR FACTOR CAUSING BRAIN DAMAGE IN SBA BABIES- HYPOVOLEMIA WITH BRAIN SPARING EFFECT CAN BE WELL MONITORED BY MEASURING CARDIAC OUT PUTS AND ANTERIOR CEREBRAL ARTERY FLOW.. IF INTERVENED WITH IN WINDOW PERIOD (WITH IN 8 HRS OF BIRTH) CEREBRAL PALSY AND HIE COULD BE PREVENTED IN GREAT MAJOTITY OF CASES.
KEY WORDS: HAEMODYNAMICS,SEVERE BIRTH ASPHYXIA,
INTERVENTION IN WINDOW PERIOD.
Dear Dr. Anil R.
Patel,
We have received your abstract for the free paper session
during the XXVIII Annual convention being held at Kolkata between 11-14th
Dec`2008. The paper entitled ?Birth Asphyxia ,Anterior Cerbral Artery Flow
,Cardiac Functions & its Clinical Correlation? was received on 9/19/2008 in
Cardio category. The final date, time and mode of presentation will be informed
after screening of the abstracts, by end October, 2008.
Looking forward to
seeing you at Kolkata.
With warm regards
Dr. Harish
Chellani
Secretary NNF
CATEGORY: NEONATAL CARDIOLOGY
MODE OF PRESENTATION: POSTER
TITLE: SICK NEONATES AND THEIR HEMODYNAMICS.
AUTH0R NAME &PLACE : ANIL.R.PATEL . RAJKOT ,GUJRAT
AFFILIATION: UNIQUE NURSING HOME PVT.LTD. RAJKOT
WORD COUNT : 325.
BACK GROUND: VERY LITTLE IS KNOWN ABOUT HEMODYNAMICS
ASSESED BY DOPPLER ECHOCARDIOGRAPHY IN SICK
NEONATES.AND ITS CORRELATION WITH CLINICAL
CONDITIONS .
OBJECTIVE AND DESIGN: IN THIS PROSPECTIVE STUDY WE ANALYSED DOPPLER LEFT VENTRICULAR AND RIGHT VENTRICULAR OUT PUT ,SUPERIOR VENACAVAFLOW,INFERIOR VENACAVA DIAMETRE AND FLOW,EJECTION FRACTION,PATENT DUCTUS ARTERIOSUS DIAMETER AND FLOW,FORAMEN OVALE FLOW IN SEVERE BIRTH ASPHYXIA,MECONEUM ASPIRATION,INTRAUTERINE PNEUMONIAS,SEPTICEMIA CASES .VARIOUS CARDIAC OUT PUTS WERE CORRELATED WITH CAPILLARY REFIL TIME,BLOOD PRESSURE, PULMONARY ARTERY PRESSURE ANDDEATH IN NEONATES .
SETTINGS: TERTIARY CARE NEONATAL UNIT IN SAURASHTRA,GUJRAT.
SUBJECTS AND INTERVENTION: CONSEQUENTLY ADMITTED NEONATES FROM 1.2.06 TO 1.7.07 WITH MECONEUM ASPIRATION SYNDROME,SEVERE BIRTH ASPHYXIA,,INTRAUTERINE PNEUMONIAS,SEPTICEMIA WERE INVESTIGATED FOR THEIR CARDIAC FUNCTION WITH JDS MEDISON DIGITAL COLOR DOPPLER WITH 4-9 MHZ NEONATAL CARDIAC PROBE IN DETAIL .THE CARDIAC FUNCTIONS WERE THAN ANALYSED IN DETAILS AND CORRELATED WITH THEIR CLINICAL CONDITION i.e. CAPILLARY REFIL TIME,BLOOD PRESSURE, INCIDENCE OF PDA SIZE IN VARIOUS CONDITIONAND DEATH IN NEONATES.
RESULTS: IN FOUR GROUP OF BABIES i.e. MECONEUM ASPIRATION SYNDROME(15),SEVERE BIRTH ASPHYXIA(15),,INTRAUTERINE PNEUMONIAS(23),SEPTICEMIA(27) DETAILED CARDIAC FUNCTIONS-HAEMODYNAMICS WERE STUDIED .BOTH TERM AND PRETERM BABIES
WERE INCLUDED.
LOW LEFT VENTRICULAR OUTPUT WAS SEEN IN 40%,53.33%,43.47% AND 41.44% CASES WITH MECONEUM ASPIRATION SYNDROME,SEVERE BIRTH ASPHYXIA,,INTRAUTERINE PNEUMONIAS,SEPTICEMIA RESPECTIVELY.
LOW RIGHT VENTRICULAR OUT PUT WAS SEEN IN 33.3%,66.66%,43.47% AND 25.92% CASES WITH MECONEUM ASPIRATION SYNDROME,SEVERE BIRTH ASPHYXIA,,INTRAUTERINE PNEUMONIAS,SEPTICEMIA RESPECTIVELY.
LOW SPOERIOR VENA CAVA FLOW WAS SEN IN 46.66%,0%,4.34% AND 25.92% CASES WITH MECONEUM ASPIRATION SYNDROME,SEVERE BIRTH ASPHYXIA,,INTRAUTERINE PNEUMONIAS,SEPTICEMIA RESPECTIVELY.
NORMALOR PROLONGED CAPILLARY REFIL TIME HAD NO CORRELATION WITH HIGH OR LOW OUT PUT IN ANY GROUPS.
INCIDENCE OF PATENT DUCTUS ARTERIOSUS WITHOUT CLINICAL MUMRMER WAS SEEN IN 61.66%,80%,82.60,50% CASE WITH MECONEUM ASPIRATION SYNDROME,SEVERE BIRTH ASPHYXIA,,INTRAUTERINE PNEUMONIAS,SEPTICEMIA RESPECTIVELY.
INCIDENCE OF MORE THAN 40MMHG PULMONARY ATERY PRESSURE
WAS SEEN IN 53.33%,46.66%,30.43% AND 25.92% CASE WITH MECONEUM ASPIRATION SYNDROME,SEVERE BIRTH ASPHYXIA,,INTRAUTERINE PNEUMONIAS,SEPTICEMIA RESPECTIVELY.IN NON OF THE ABOVE CASES HIGH RIGHT VENTRICULAR OUT PUT WAS ASSOCITED WITH RAISED PULMONAR ARTERY PRESSURE.EITHER IT WAS LOW OR NORMAL,WHILE
SUPERIOR VENACAVA FLOW WAS HIGH IN 68.98% CASES. DEATH RATE IN CASES WITH HIGH PULMONARY ARTERY PRESSURE VARIED FROM 14.28% TO 57.14% IN ABOVE CONDITIONS.
OVER ALL DEATH RATE WHEN BOTH LEFT AND RIGH VENTRICULAR OUT PUT WAS LOW IS 60%,20%,40%,66.60% IN MECONEUM ASPIRATION SYNDROME,SEVERE BIRTH ASPHYXIA,,INTRAUTERINE PNEUMONIAS,SEPTICEMIA RESPECTIVELY. LEFT ATRIUM TO AORTA SIZE RATIO OF 1.3:1 HAS NO CORRELATION WITH SIZE OF PDA IN ANY CASE.
CONCLUSION: ESTIMATION OF VARIOUS CARDIAC OUT PUTS,PA PRESSURE,AND CORRELATION WITH CAPILARY REFIL TIME AND DEATH GIVES US BETTER INSIGHT TO HAEMODYNAMICS IN SICK BABIES AND ITS MANAGEMENT.IT MAY HELP US TO PREVENT THE MORBIDITY AND MORTALITY IN MANY SICK BABIES IN FUTURE.
KEY WORDS: HAEMODYNAMICS,PULMONARY ARTERY PRESSURE,CAPILLARY REFIL TIME,SICK NEONATES.
WON THE BEST POSTER PAPER PRIZE AT
NATIONAL NEONATOLOGY CONFERENCE 2007
HELD AT PUNE IN DECEMBER 2007