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Case #46 My Baby Is Having Trouble Feeding


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#1 STPEMTP

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Posted 01 December 2008 - 02:09 PM

Today you are working on a ground unit due to icing conditions that have been present all day. While you are in a rural ED, you see an RN coming running into the ED yelling for help. You note that the child looks limp and the color doesn't look the best.

Quick assessment of the child shows:
Cap refill around 5 secs
Resp Rate 40's and labored
Pt Very Pale
pt age 7 days old
Pt weight 3.5kg

Parents of the child are in the ED room also. The RN that brought the child down to the ED stated that the parents brought the child up due to difficulty with feeding.

Now what?
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#2 mjcfrn

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Posted 01 December 2008 - 03:07 PM

Initial Differential:

SVT
Congenital heart defect
Sepsis
Inborn Error(s) of Metabolism
"Shaken" baby

ABC's....
What are the sats? if <88, supplement up to 92-94.
Lung sounds? assess WOB. Positioning - upright, sniffing. Need to nasally sxn? Doesn't take much to obstruct those tiny nares.
HR? peripheral perfusion?
LOC? glucose? temp? fontanel?
Abd exam? Liver enlarged? Decompression if distention may be impeding resps.
PIV (try scalp, saphenous, hand veins) or IO.
With a cap refill of 5sec, even if pt is in heart failure, it is still probably appropriate to fluid resuscitate, maybe 5mL/kg or 10mL/kg increments until CXR available.
Pallor makes me concerned for acidosis - ABG/VBG/CBG. also CBC (manual diff if possible), Lytes, BUN, creat, iCa++, lactate, ammonia....
maybe EKG, echo if avail?
assess for any signs of trauma? head boggy? consider head or head/chest/abd CT if avail. Infants are so cartilagenous that innocuous marks can overlie serious injury...

Hx: term? complications? pre-natal care? birth history? meds? breast/formula? any siblings? ill contacts? Family hx of CHD or deaths in infancy? any possibility of trauma?

Call the tertiary NICU-PICU. They can offer info and advice over the phone even if travel is contraindicated.

Prayer and/or cursing under your breath (or even out loud) both seem to help........
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#3 vtach1010

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Posted 01 December 2008 - 05:13 PM

Besides the above stuff I would like to know if the child was born at home or in a hospital? Vag delivery or c-section? Did the child recieve all the normal shots and treatments associeated with new borns? Some parents opts out of even simple things like Vit. K.
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#4 medicerik

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Posted 01 December 2008 - 05:29 PM

We've got the initial component of the resuscitation covered. Where I would differ is the fluid bolus. Assuming a normal frank-starling curve, you need a 25 percent increase in end-diastolic volume to see a clinically significant improvement in cardiac output, hence the typical 20 cc/kg bolus in kids. My initial bolus would be 20 cc/kg. I can adjust from there as we get more information. Supplemental oxygen is also important. If the patient suddenly decompensates after the oxygen, that gets dramatically decreased and we look to PGE1 for a ductal dependent heart lesion.

I'm also concerned about congenital GI issues. How long have the parents noted trouble feeding? Is the baby refusing to feed or his the baby not keeping feeds down? Has the child vomitted? If so, what color? Has the child moved his/her bowels yet? If we attempt gastric decompression, can the tube be passed? This info, plus the previous history requested by other posters, a the previous labs, and a baby gram would be helpful.

Erik
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Erik Glassman, BS, CCEMT-P, FP-C, EMT-T

#5 Flightgypsy

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Posted 01 December 2008 - 05:30 PM

Good start mjcfrn.

I agree with your differentials.

I would start with intubation. Being cautious with the oxygen. Depending on what the sats are now and how he responds to O2 will guide the O2 administration. If you give him oxygen and he either doesn't improve or gets worse than only use 21%. Start a prostaglandin infusion at 0.05 - 0.1mcg/kg/min to start up to 0.2mcg/kg/min.

Check BP if you can in all extremities. Any cardiac murmurs? Start with a 5ml/kg NS fluid bolus and see how he responds. If he improves give him further fluid boluses as needed. If he deteriorates stop the fluid bolus.
May need lots of dextrose so replace as needed with 10-12% dextrose boluses of 2ml/kg and start maintenance fluids as soon as possible with D5 1/4NS.

Deal with other labs as required. Depends on what his blood gas is like what ventilator settings and fluid and drug resuscitation management you do.

Get him on a warming table. Warm him up and keep him warm. I would insert a continuous rectal probe in this baby.

Treat the VS. If in SVT go straight to cardioversion.

What are all the VS, lab results, echo etc? Get a quick I-stat to start with.

Get the baby to a tertiary care facility ASAP.

Waiting for further info.
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#6 FlyingScot

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Posted 02 December 2008 - 03:25 AM

I'm sure there's a zebra in the room but I'll throw in my two cents. With the info at hand I think I'd go with late onset GBS sepsis. Although a congenital heart defect could very well be possible, one that presents with an infant in extremis would most certainly be a ductal dependent lesion. In the case of a ductal dependent lesion this child would be extremely cyanotic, not pale. In my experience the infants I have seen with undiagnosed DDL's have presented with the most hideous shade of purple one could imagine and are usually Transpos or Co-Arcs. If this is a cardiac issue I agree, mostly, with the plan of care. My experience has been that fluid boluses in the neonatal period are generally initiated at 10ml/kg. An oxygen challenge is certainly worth a try but if there is no improvement or, indeed, worsening in status then the oxygen isn't weaned it is rapidly removed. Just a little FYI, since I doubt many adult programs actually carry PGE and many small hospitals don't either there is a place where it can be found...in penile implant trays. Yep, you read this correctly. Saved my a$$ on a trip where we went for a peds patient and ended up transporting a hypoplastic left ventricle. It was the exact same vial we normally carried. If worse comes to worse a cardiologist for whom I have a ton of respect told me to really pump the fluid into the kid to "blow the ductus open". She said we could deal with the ensuing pulmonary edema when we got back. You're in a rural ER, forget the echo-huge waste of time and probably won't have anybody to read it properly. EKG-helpful in grownups but will be of no diagnostic value with this neonate. SVT extremely unlikely but again there is that zebra thing. Oh, one more thing. If after you have stabilized you have a good BP, cap refill and heart rate but the sats are in the 50's...don't sweat it. These kids do not have normal saturations-they shunt all over the place. As I said before I'm leaning more toward sepsis than anything else with perhaps the exception of trauma. Baby needs blood cultures and antibiotics (Amp 100mg/kg and Gent 5mg/kg although some may replace the Gent with Ceftriaxone) after initial resuscitation is completed. As with any pediatric case if the respiratory status can be stabilized you will be ahead of the game. We need to know mom's GBS status and if there was PROM. That will help make the differential diagnosis. We really need some more information to move forward with this case.
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#7 LWTRF14

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Posted 02 December 2008 - 04:29 AM

Hey FlyingScot....just throwing this out there, only because I have no idea and I just learned all this pedi stuff...my brain still hurts....what about an A-cyanotic Heart defect... ASD, VSD, etc...isn't that the one where the kid fatigues when feeding (left to right shunting) and the cyanotic Heart defect (right to left shunting), the kid gets diaphoretic when feeding? Maybe you could shed some light...I just thought I would throw that out there..


I'm sure there's a zebra in the room but I'll throw in my two cents. With the info at hand I think I'd go with late onset GBS sepsis. Although a congenital heart defect could very well be possible, one that presents with an infant in extremis would most certainly be a ductal dependent lesion. In the case of a ductal dependent lesion this child would be extremely cyanotic, not pale. In my experience the infants I have seen with undiagnosed DDL's have presented with the most hideous shade of purple one could imagine and are usually Transpos or Co-Arcs. If this is a cardiac issue I agree, mostly, with the plan of care. My experience has been that fluid boluses in the neonatal period are generally initiated at 10ml/kg. An oxygen challenge is certainly worth a try but if there is no improvement or, indeed, worsening in status then the oxygen isn't weaned it is rapidly removed. Just a little FYI, since I doubt many adult programs actually carry PGE and many small hospitals don't either there is a place where it can be found...in penile implant trays. Yep, you read this correctly. Saved my a$$ on a trip where we went for a peds patient and ended up transporting a hypoplastic left ventricle. It was the exact same vial we normally carried. If worse comes to worse a cardiologist for whom I have a ton of respect told me to really pump the fluid into the kid to "blow the ductus open". She said we could deal with the ensuing pulmonary edema when we got back. You're in a rural ER, forget the echo-huge waste of time and probably won't have anybody to read it properly. EKG-helpful in grownups but will be of no diagnostic value with this neonate. SVT extremely unlikely but again there is that zebra thing. Oh, one more thing. If after you have stabilized you have a good BP, cap refill and heart rate but the sats are in the 50's...don't sweat it. These kids do not have normal saturations-they shunt all over the place. As I said before I'm leaning more toward sepsis than anything else with perhaps the exception of trauma. Baby needs blood cultures and antibiotics (Amp 100mg/kg and Gent 5mg/kg although some may replace the Gent with Ceftriaxone) after initial resuscitation is completed. As with any pediatric case if the respiratory status can be stabilized you will be ahead of the game. We need to know mom's GBS status and if there was PROM. That will help make the differential diagnosis. We really need some more information to move forward with this case.


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Earl F Bakke III, NR-EMT-P, CC-EMT-P, PNCCT

#8 mjcfrn

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Posted 02 December 2008 - 12:25 PM

Have to agree with 'most everything you said, Flying Scot.

The reason I proposed an EKG is that sometimes it can point you to a CHD in the absence of an echo (which as you point out very correctly, there may be no one to interpret, tech is probably outside the hospital and has to be called in but would be delayed due to weather, etc, etc. But I have been in a couple of rural hospitals where the echo machine is in the corner and the ED doc rolls it over himself/herself and takes two minutes to UNofficially take a look and we form a pretty good guess of what the defect is. I have wondered if FAST could ever be useful in this context but have not had the opportunity to find out) Poor R-wave progression in the V leads could suggest hypoplastic left heart, or large bi/tri/quadriphasic P waves might suggest large ASD or AVSD, for example. Most congenital third degree blocks are usually asymptomatic, but I have seen them present symptomatically when the kid is otherwise under stress, like in sepsis. Also, agree about your statement about cyanosis - I really hate that eggplant shade of purple - but have seen Coarcts and HLHS present very very pale, which my docs have attributed to the degree of acidosis - pH 6.8 or so - which the infant presents in.

I had no idea about the penile implant trays having PGE1 but I will definitely keep that in mind.....Wow!
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#9 FlyingScot

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Posted 02 December 2008 - 01:17 PM

Hey FlyingScot....just throwing this out there, only because I have no idea and I just learned all this pedi stuff...my brain still hurts....what about an A-cyanotic Heart defect... ASD, VSD, etc...isn't that the one where the kid fatigues when feeding (left to right shunting) and the cyanotic Heart defect (right to left shunting), the kid gets diaphoretic when feeding? Maybe you could shed some light...I just thought I would throw that out there..



You are correct that an acyanotic defect will often present as an infant with a history of poor feeding but they usually do not present in severe distress and usually not as early as one week of age. In this particular case with the information we have I really don't think an acyanotic defect is the culprit, however, with these scenarios you never know what's going to be thrown at you. I'm at work at the moment but I'll try to pull up some info for you and post it later. We need some more info.
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#10 FlyingScot

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Posted 02 December 2008 - 01:56 PM

Have to agree with 'most everything you said, Flying Scot.

The reason I proposed an EKG is that sometimes it can point you to a CHD in the absence of an echo (which as you point out very correctly, there may be no one to interpret, tech is probably outside the hospital and has to be called in but would be delayed due to weather, etc, etc. But I have been in a couple of rural hospitals where the echo machine is in the corner and the ED doc rolls it over himself/herself and takes two minutes to UNofficially take a look and we form a pretty good guess of what the defect is. I have wondered if FAST could ever be useful in this context but have not had the opportunity to find out) Poor R-wave progression in the V leads could suggest hypoplastic left heart, or large bi/tri/quadriphasic P waves might suggest large ASD or AVSD, for example. Most congenital third degree blocks are usually asymptomatic, but I have seen them present symptomatically when the kid is otherwise under stress, like in sepsis. Also, agree about your statement about cyanosis - I really hate that eggplant shade of purple - but have seen Coarcts and HLHS present very very pale, which my docs have attributed to the degree of acidosis - pH 6.8 or so - which the infant presents in.

I had no idea about the penile implant trays having PGE1 but I will definitely keep that in mind.....Wow!


Being the idiot that I am I don't know how to do multiple quotes in one post...sorry. Your point is well taken. I guess what I am thinking is that cardiac arrhythmias in the neonate are so extremely rare (zebra?) to the point that if you see even one in your career you will be very lucky. All you really need is a standard monitor, if there is an arrhythmia you will see it. In this instance time is of the essence. An EKG that "might" or "could" suggest some sort of defect really isn't going to change your plan of care that much and finding someone to interpret this is going to delay departure. A CXR will be extremely helpful and easy to interpret. If the heart is taking up more than 2/3's of the chest than "Houston,you have a problem". If you really think the kid has a DDL and you start Prostin but no improvement is gained (because no DDL is actually present) you aren't going to cause any harm to the child nor will you be castigated by the receiving hospital.
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#11 STPEMTP

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Posted 02 December 2008 - 06:59 PM

ABC's....
What are the sats? if <88, supplement up to 92-94.
Lung sounds? assess WOB. Positioning - upright, sniffing. Need to nasally sxn? Doesn't take much to obstruct those tiny nares.
HR? peripheral perfusion?
LOC? glucose? temp? fontanel?
Abd exam? Liver enlarged? Decompression if distention may be impeding resps.
PIV (try scalp, saphenous, hand veins) or IO.
With a cap refill of 5sec, even if pt is in heart failure, it is still probably appropriate to fluid resuscitate, maybe 5mL/kg or 10mL/kg increments until CXR available.
Pallor makes me concerned for acidosis - ABG/VBG/CBG. also CBC (manual diff if possible), Lytes, BUN, creat, iCa++, lactate, ammonia....
maybe EKG, echo if avail?
assess for any signs of trauma? head boggy? consider head or head/chest/abd CT if avail. Infants are so cartilagenous that innocuous marks can overlie serious injury...

Hx: term? complications? pre-natal care? birth history? meds? breast/formula? any siblings? ill contacts? Family hx of CHD or deaths in infancy? any possibility of trauma?

Call the tertiary NICU-PICU. They can offer info and advice over the phone even if travel is contraindicated.

Prayer and/or cursing under your breath (or even out loud) both seem to help........



Besides the above stuff I would like to know if the child was born at home or in a hospital? Vag delivery or c-section? Did the child recieve all the normal shots and treatments associeated with new borns? Some parents opts out of even simple things like Vit. K.


As you start the resuscitation here are the vitals
HR: 150's sinus tach w/o ectopy or prolonged qrs (sorry, no copy of strip available)
BP: not obtained, unable to locate cuff to fit patient.
RR: 46 and labored
SAO2: Difficult to obtain, get glimses of 70's%. Intermittently picking up
Cap Refill 5 secs.

Lung sounds are clear, Pt is supine on hospital cart with towel under shoulders. No obstruction in nares, nothing removed with suction attempt
Heart rate only felt at apical location, unable to locate brachial pulse.
LOC: pt has intermittent cry that is not related to any stimuli. Pt limp on bed.
Fontanel is normal, temp is 98F
Exam: no obvious trauma noted. Pupils are 3mm and sluggish. Chest =rise, murmur noted listening to heart tones. Abd: normal, no distension, no noted liver distension. No marks noted on head, no "boggy" areas identified.

Speaking with the parents, child was in for a well baby check at day 5 and no problems detected at that time. No problems with pregnancy. This is second child, first no problems. Pt born at full term. Pt born at hospital, vaginal. Parents mention that on day 6 pt started having some difficulty feeding. Today child was not able to feed at all. Parents brought child up to L&D to talk with the nurses about possible problems with breast feeding. When L&D RN's saw child they ran down. Reviewing pediatrician's record, no mention of murmur at that time.

O2 started at 2lpm---> pt becoming cyanotic
Attempts to gain PIV unsuccessful, no flash or bleeding from sticks. EZ-IO placed in R tibia, no reaction from child from placement. No marrow returned, fluid infuses easily without swelling of calf.
IO bolus started at 10ml/kg
Unable to obtain labwork due to unable to get any blood from child
Infant warmer on it's way from L&D (3rd floor, gonna be a little bit)
Of note, respiratory distress increasing since o2 started, appears pt is having difficulty with expiration (almost like a grunting expiration).
No echo taken at this this time.
MD electing to defer intubation at the moment, unsure if that may make situation worse.

Vitals now:
Cap refill improving at 4sec
HR 150's still sinus tach
RR 50 and labored
SAO2 50-70% when able to get accurate reading
pt is becoming VERY cyanotic.

What now???

p.s. might be a couple days before I can post next segment on this case. Hopefully I can add next part on Fri.
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#12 Flightgypsy

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Posted 02 December 2008 - 09:58 PM

Start the PGE1 at 0.1mcg/kg/min if it is available. Do a rapid stabilization (and do whatever you can en route) and transport as fast as possible especially if there is no PGE1 available.
Put the infant under a head hood at least if one is available if you can't intubate. Use the lowest O2 concentration necessary to maintain best sats. (could be only 60-70%). Use hypoxic ventilation if you are a specialty team and have the capability. The baby is grunting so he really needs intubation. Grunting is a baby's way of maintaining PEEP.

Insert an OGT to improve respiratory status.
Check chemstick (heelstick) and give dextrose as necessary. This baby will be chewing through the glucose.
Maintain the baby's temperature to decrease the stress on him and decrease his glucose requirements.
Start dopamine or epinephrine drip if needed for BP.
If possible do at least a capillary I-stat and may need to give some bicarb (discuss with MD first) for extreme acidosis not responding to fluid.
Give Ca gluconate per I-stat results.
Be cautious with the fluid - if he is responding repeat the boluses but if it is making his respiratory status worse (grunting, worse sats) then just use maintenance fluids. Use smaller volumes 5-10mls/kg and reassess with each bolus. He may even need some lasix instead of fluid to help his respiratory status.

From the information given to us I am going with a ductal dependent lesion.
If the infant is anemic they will not always present with cyanosis just pallor. And this baby is probably mottled as well further confusing the exact color. I would never base treatment on whether or not they are cyanotic versus extremely pale. If they are cyanotic it just makes the possible diagnosis easier.

Just my pennies worth.

Blue skies and keep safe All.
And Happy Holidays!
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#13 FlyingScot

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Posted 03 December 2008 - 01:34 AM

From the information given to us I am going with a ductal dependent lesion.
If the infant is anemic they will not always present with cyanosis just pallor. And this baby is probably mottled as well further confusing the exact color. I would never base treatment on whether or not they are cyanotic versus extremely pale. If they are cyanotic it just makes the possible diagnosis easier.

Just my pennies worth.

Blue skies and keep safe All.
And Happy Holidays!


Infant seen just 2 days prior for well baby visit and assumed no signs of pallor noted. There is no basis for a sudden drop in Hgb to the point of being so severe that cyanosis is not possible. I NEVER said to base treatment on the patient's color alone but noted that a baby crashing from a DDL usually is cyanotic.. The info given in the first post was not specific to a cyanotic defect and could very well have been and may still be a sepsis picture, or perhaps Eisenmenger's syndrome. I don't want to miss something because I've narrowed my focus. After the post with updated info of course this looks like a probable cyanotic heart or is the patient just getting worse and the timing of the O2 just coincidental (zebra)? I don't know and won't know until the patient is at the tertiary center with an echo probe on his chest. PGE1 is obviously the way to go but it's onset is variable so we might not see an immediate result. I'd still treat for sepsis with antibiotics. Screw the blood cultures for now...they can worry about that later. Take the O2 off and see what happens. A Transpo usually tolerates and even needs O2 but an infant with HLHS is the exact opposite and symptomatically this is sounding more and more like a hypoplast or is it sepsis :blink: (just poking you with a stick FG ;) ). O2 acts as a potent pulmonary vasodilator in infants and we actually WANT to keep his PVR high so to avoid flooding his lungs and worsening his presumed failure. Unfortunately this is going to suck if the kid doesn't have a DDL. The pucker factor here is about 10!
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#14 Flightgypsy

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Posted 03 December 2008 - 07:04 AM

I was also just commenting on not getting too narrow focused on whether or not a baby is cyanotic or just pale to rule out a possible diagnosis. (I can handle a little poke if you can FlyingScot!). My initial treatments were broad enough to cover most of the diagnoses but I didn't mention antibiotics which are a given to me whether it is possible sepsis or cardiac since neonates are so susceptible to infection. (My bad!). I agree we didn't have enough of the picture to start with to narrow it down to a DDL versus sepsis.

The 2 main things to consider besides starting PGE1 and rapid transport are whether to give lots of fluids for a baby in septic shock or less fluids for a baby with too much pulmonary blood flow and how much O2 to give.
Both are based on how he responds to treatment. If the treatment makes him worse then stop it and possibly reverse it (i.e. give a test dose of lasix and see if it helps). Give just enough O2 to improve his sats if it does. If it makes him worse than take it away. In this baby though I am definitely leaning towards the DDL. (Possibly HLHS but could be a good old FUBAR heart too).

Just one more little poke FlyingScot from a Flying Gypsy....the signs and symptoms of Eisenmengers usually don't show until the child is a older as it takes a while for the irreversible damage (scar tissue) to occur. I've never seen a neonate with Eisenmengers unless you are thinking of PPHN?

My pucker factor was at a 10 with the first post!

Cheers!
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#15 FlyingScot

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Posted 03 December 2008 - 03:21 PM

Just one more little poke FlyingScot from a Flying Gypsy....the signs and symptoms of Eisenmengers usually don't show until the child is a older as it takes a while for the irreversible damage (scar tissue) to occur. I've never seen a neonate with Eisenmengers unless you are thinking of PPHN?

My pucker factor was at a 10 with the first post!

Cheers!


It can happen from platelets clumping at the site of the lesion as well although I agree that this is a highly unlikely scenario. I threw it out there wondering if I was going to hit the zebra. At any rate we are in a Catch 22: treat for sepsis and kill the cardiac kid, treat for cardiac and kill the sepsis kid. So we have to find a middle ground to at least stabilize but maybe not improve. So we try an intervention, see what happens and then adjust our plan, just as you said. This is going to be an ugly ride either way and looks like it's going to be by ground. I would kill for a UAC at this point which isn't out of the question at 7 days of age but will take too much time. The referral doc needs to put on his big boy pants and intubate this baby-yeah it might cause some other issues but the intensivist at the Big Children's Hospital should be able to help him with ventilator strategies. Another Swamp A$$ moment!
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#16 MSDeltaFlt

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Posted 05 December 2008 - 04:51 AM

As you start the resuscitation here are the vitals
HR: 150's sinus tach w/o ectopy or prolonged qrs (sorry, no copy of strip available)
BP: not obtained, unable to locate cuff to fit patient.
RR: 46 and labored
SAO2: Difficult to obtain, get glimses of 70's%. Intermittently picking up
Cap Refill 5 secs.

Lung sounds are clear, Pt is supine on hospital cart with towel under shoulders. No obstruction in nares, nothing removed with suction attempt
Heart rate only felt at apical location, unable to locate brachial pulse.
LOC: pt has intermittent cry that is not related to any stimuli. Pt limp on bed.
Fontanel is normal, temp is 98F
Exam: no obvious trauma noted. Pupils are 3mm and sluggish. Chest =rise, murmur noted listening to heart tones. Abd: normal, no distension, no noted liver distension. No marks noted on head, no "boggy" areas identified.

Speaking with the parents, child was in for a well baby check at day 5 and no problems detected at that time. No problems with pregnancy. This is second child, first no problems. Pt born at full term. Pt born at hospital, vaginal. Parents mention that on day 6 pt started having some difficulty feeding. Today child was not able to feed at all. Parents brought child up to L&D to talk with the nurses about possible problems with breast feeding. When L&D RN's saw child they ran down. Reviewing pediatrician's record, no mention of murmur at that time.

O2 started at 2lpm---> pt becoming cyanotic
Attempts to gain PIV unsuccessful, no flash or bleeding from sticks. EZ-IO placed in R tibia, no reaction from child from placement. No marrow returned, fluid infuses easily without swelling of calf.
IO bolus started at 10ml/kg
Unable to obtain labwork due to unable to get any blood from child
Infant warmer on it's way from L&D (3rd floor, gonna be a little bit)
Of note, respiratory distress increasing since o2 started, appears pt is having difficulty with expiration (almost like a grunting expiration).
No echo taken at this this time.
MD electing to defer intubation at the moment, unsure if that may make situation worse.
Vitals now:
Cap refill improving at 4sec
HR 150's still sinus tach
RR 50 and labored
SAO2 50-70% when able to get accurate reading
pt is becoming VERY cyanotic.


What now???

p.s. might be a couple days before I can post next segment on this case. Hopefully I can add next part on Fri.


What are the odds of this child developing clinically significant PDA; at the very least some sort of congenital heart defect? I say this because of the euthermia, clear lung sounds, nondistended abd, along with the murmur, wide QRS, and the complete lack of a BP for no apparent reason.

I also believe the good doctor could either tube the child now or tube the child during chest compressions. Labs were stated to be unable to get due to unable to get PIV. That means absolutely nothing unless you are also unable to get ABG's. If we can get some gases, we can get blood for everybody. Can we get ABG's? I don't like the intermitent Sats.

Also, if the SpO2's are actually that low, 50% is too freaking low. Anoxic brain injury is not supposed to happen. That child needs to be sucking plastic soon.
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Mike Hester, RRT/NRP/FP-C
Courage is resistance to fear, mastery of fear - not absence of fear -- Mark Twain

#17 Flightgypsy

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Posted 05 December 2008 - 06:53 AM

MSDelta we are thinking this child has a congenital heart defect that is ductal dependant meaning they are totally dependant on a patent ductus arteriosus (PDA) for survival and once the ductus starts to close usually within the first few weeks of life they start getting into serious trouble and present pretty much like this infant. Usually they have no other way of getting blood to the body except through the ductus. In some instances they just have very limited blood flow through the aorta which is often nearly as bad. Some of the possible culprits are Hypoplastic Left Heart Syndrome (HLHS), Transposition of the Great Vessels (or arteries), Co-arctation of the aorta, Interrupted aortic arch, Double Outlet Right Ventricle and the list goes on... and there are a lot of kids that don't just have one of these defects but any number and variation you can think of.

If you can get Sats of 60-70% on some of these kids that may be the best you will get until they have palliative or corrective surgery done. O2 in a ductal dependant kid not only closes the ductus more rapidly but it decreases the pulmonary vascular resistance and increases the left to right shunt and consequently "floods" the lungs. Then you end up with even lower sats.

The treatments of PGE1 and decreasing the O2 level actually are aimed at keeping the ductus open until they can get to a cath lab or surgery. It may be their only chance of survival.

You can get a Capillary blood gas from a heelstick and as long as you know the numbers are slightly different from an ABG (In between venous and arterial levels) it will give us an idea of where we are at until we can get an ABG and help us guide treatment.

Waiting to hear more info and response to treatments.

P.s FlyingScot, my understanding is that O2 would be beneficial for Eisenmengers not make it worse but I understand being on the lookout for the zebra. Thank you for your tip on the PGE1 in the penile implant trays. I will try to remember that if I am ever in that situation (hopefully never).

Cheers.
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#18 FlyingScot

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Posted 05 December 2008 - 02:31 PM

Nicely stated FG. MSDeltaFlight one of the reasons we think really hard about intubating suspected cardiac patients is with their already "fubar'd' plumbing once you add intra-thoracic positive pressure and PEEP to the mix you can actually worsen the situation by, in some cases, significantly decreasing systemic vascular return and left ventricular filling (if they have a left ventricle at all) in infants who likely have decreased systemic circulation to begin with-hence the lack of distal pulses, obtainable blood pressure or consistent saturations. Even if this patient was not in acute respiratory distress (and some cardiac patients can present shocky but with what we refer to as "happy tachypnea" that is breathing in the 100's without grunting, flaring or retracting) he will require intubation as the major side-effect of PGE1 is apnea. It is seen most frequently at higher doses 0.1mg/kg and up. Some infants with DDLs present only in mild shock and the PGE can be started at a lower dose so intubation may not be absolutely required. This will not be the case with this child. Your confusion regarding the term PDA is warranted because there is also a condition often referred to as PDA when an infant with a structurally normal heart has a ductus that remains open. When the pulmonary vascular resistance decreases to physiologic this causes a left to right shunt through the ductus into the pulmonary vasculature and ensuing right-sided failure. But we are not talking about structurally normal hearts here. Ductal dependent lesions can be broken into three major categories: lesions that require a PDA for systemic blood flow via a right-to left shunt (Co-Arc, Critical Aortic Stenosis, TAPVR and HLHS), lesions that require a PDA for pulmonary blood flow via a left-to-right shunt (Pulmonary Atresia, Critical Pulmonary Stenosis, Tricuspid Atresia, ToF) and those that require a PDA for circulation anywhere (Transposition of the Great Vessels with intact septum). If you take a look at the direction of the shunts you will begin to understand why it is so critical to be able to balance what you are doing. If you give an infant with HLHS oxygen you will decrease his PVR and stand the chance of reversing the shunt so you will flood the lungs and further decrease systemic circulation. (by the way FG I don't think I said anything about O2 and Eisenmengers and I don't see it any of my posts to what are you referring? :huh: ) So the initial goal with them is to keep their sats around 70% although some may require them to be lower (I've seen as low as the 50% range). Remember, these kids probably have never had sats much above 80 to begin with. This is so important that in the PICU/NICU they are put on what is called sub-ambient O2 down to the 17-19% range. So as we have discussed this baby has severely decreased systemic circulation...the chances of being successful in getting an ABG are probably pretty slim. A CBG will tell us what we need to know. Once the PGE has taken effect we should be able to get consistent pulse oximetry readings and we can get a Ph and pCO2 from the CBG. I'm not entirely sure that the pulse ox readings in this scenario are all that accurate given the patient has absent peripheral pulses. It might be beneficial, once pulses are re-established, to place 2 pulse oximeters-one pre-ductal and one post-ductal to monitor the shunting. Anxiously waiting for further info.
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#19 RoadieRN

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Posted 05 December 2008 - 09:18 PM

I looked up CHD in my APLS book and this is what I found. In essence what has happened here is a hyperoxia test. What I mean by that, is that by placing this infant on 100% oxygen we've seen little to no improvement, actually the exact opposite. This infant is deteriorating quite quickly. What the hyperoxia test is, is a diagnostic test for cyanotic heart disease. In lieu of an echo tech that is skilled in infant/peds echos, it is another way to diagnose cyanotic heart disease. Also, if our CXR shows a boot shaped heart it is indicative of Tetralogy of Fallot. If it doesn't show that boot shape, then x that one off the DD list. A 12 lead is not useless with this patient. What it may show is an abnormal axis, QRS or ST segment changes.
It is not unusual for these kids to have multiple defects. This kid could have a VSD and/or ASD(giving you your murmur, non cyanotic defect) with some kind of cyanotic defect(take your pick of the litany). Either way, this kid is in a seriously bad way. I'm not a 100% convinced that this is CHD, but in addition to meningitis or a group beta strep infection that would be on my short list. However with poor to absent peripheral pulses, difficulty breathing, weak cry, CHD is probably number one on my list.
As far as management of this kid goes, I'd try every trick in the book to get labs out of this kid. Just cause your SpO2 is in the 70s doesn't say a thing about your pO2. Also, NRP says to give 10ml/kg of isotonic IVF for fluid boluses. I"d consider PGE and Dobutamine, instead of Dopa or Epi(don't rule those out, but not first line.) If you do use PGE, elective intubation might be warranted.
That's what I got for now. Curious to see where this goes.
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Nick Crusius RN, BSN

Keep the rubber(or skid, if it applies) side down!

#20 FlyingScot

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Posted 05 December 2008 - 10:02 PM

A 12 lead is not useless with this patient. What it may show is an abnormal axis, QRS or ST segment changes.


Perhaps I was bit too definitive in my statement. What I should have said is an EKG would be useless unless somebody in this small rural facility is skilled in interpreting neonatal EKGS particularly when a defect is suspected. Really it isn't going to give you enough information to make an absolute diagnosis and/or change your plan of care so why waste the time? Seriously, if you got an EKG on this kid and it showed an abnormal axis what would you do differently than has already been discussed? Would you know exactly what it meant? I'm not trying to bust your chops it's just we don't have the luxury of loads of time to perform tests that ultimately won't change anything. Even tertiary pediatric centers don't routinely use them. Regardless of what the defect is the treatment is the same.
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