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).




SBA AHMEDABAD NEOCON

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.





NNF PAPER 2008

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

 

 





NNF PAPER HAEMODYNAMICS 2007

 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

 


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