I second moving the girl over to the PICU.
Now, we still don't know the cause of her illness.
While the low diastolic BP and tachycardia were present at the time she got to the ED, the gallop (assuming there truly is one) is a new finding. Something that happened (or more likely, that we did
) caused stress to the left heart.
Was it a) the oxygen, or b) the fluid boluses, or c) something else?
a) The point J-Rad mentioned earlier about heart defects with a left-to-right shunt would explain this: the size of the shunt e.g. in a VSD depends on the pressure gradient between the chambers and the size of the hole. At a given hole size, if you lower pulmonary vascular resistance by supplying more oxygen to the lungs and thereby dilating the pulmonary vascular bed, the RV will have a lower afterload, and even more blood will flow through the hole towards the right side. An increased shunt volume leads to pulmonary "flooding" and causes stress to the left side of the heart, since the LV has to move forward all the recirculating volume in addition to the systemic output via the aorta. A gallop may then be heard as a sign of LV failure.
So, could this girl have a yet unrecognized congenital heart defect with an L-R shunt? If it's a "post-cardiac" one (a PDA), this would also explain the low diastolic blood pressures. Of course, she would need a second diagnosis of the condition that caused the fever and initial amount of respiratory distress - the reason she got supplemental oxygen in the first place.
b) If you can't deal with two 20 ml/kg fluid boluses over half an hour each after not having had much PO and with a low UOP, there's likely some underlying cardiac pathology. Possibly one that also explains the fever, such as myocarditis or endocarditis (although you would have expected to hear a murmur in the latter).
c) Something else is stressing the heart (a lot), and the low diastolic blood pressure is a sign of low systemic vascular resistance like in the early phase of septic shock (thanks for posting the SIRS/sepsis/... criteria, J-Rad - good reminder). However, if all the extra fluid was getting away into the periphery, I don't see how that would explain a gallop to be heard.
So, I have a few more questions:
- Are you hearing any new murmur along with the gallop, too (e.g. that of a relative pulmonary stenosis from increased pulmonary blood flow)?
- Does the normal BMP include a normal anion gap? With the findings in this patient, an elevated AG from lactic acidosis wouldn't be surprising.
- Or was the "gallop" really something else? Since you hooked up the patient to a cardiorespiratory monitor (and I think that's a good thing to do in any patient you admit with significant cardiorespiratory pathology), you would have seen whether there was a normal ECG rhythm, or if maybe the "gallop" was really an arrhythmic heart beat. A split S2 (heart sounds like a Spanish "D-DR, D-DR, D-DR") may also be confused with a gallop (heart sounds like "DR-D, DR-D, DR-D"). While it's normal to have an S2 split variably with respiration, a fixed split S2 occurs in instances like the ones in a), where there is so much blood that has to go through the pulmonary valve that the valve closes later than the aortic valve does in every heart beat.
- How big is the liver by now (congestive heart failure with a gallop should be significant enough to cause hepatomegaly)?
- How hard is it at your hospital to get an echo? Did you do one?
By the way, my money is on b1) currently
