This is an offshoot of another thread that strayed far off its path.
I will be posting questions that spring from situations I see on my quaternary level PICU to test your knowledge of critical care topics that apply to children. As we know, children are not small adults and the reasons they are admitted to ICU are very different from those of adults. For example, PICUs see virtually NO life-style related comorbidities such as COPD from a 2 pack-per-day cigarette habit, cardiovascular disease from a 10 Big-Mac-per-week habit or end-stage cirrhosis from a 6-drink-per-day habit. Congenital anomalies, trauma (accidental and non-accidental), metabolic disorders, ingestions and respiratory infections are our biggest offenders.
Question #1:
Name the 4 main treatments for JET (junctional ectopic tachycardia).
It's been so long that I forget the answer LOL. I believe it was a chemical pneumonitis due to aspiration that caused the pulmonary hypertensive crisis.
The repeat CT showed 3 separate areas of infarct in his brain, the largest being at the temporoparietal junction in the vicinity of Broca's area roughly the size of a walnut. The smaller ones were a left frontal area the size of a dime and the third also the size of a dime at the central sulcus near the interhemispheric fissure. Later an MRI revealed a left basal ganglion hemorrhage of indeterminate age. Because the damage was not visible on the first CT it was decided that the infarcts were thrombotic strokes caused by dehydration and hyperviscosity. Careful questioning of his mother revealed that the boy had been complaining of a headache for several days prior to his collapse, and that he had "lost his balance" two days prior while sitting unsupported in bed watching television. At the time neither of these had been deemed significant.
His stay in the PICU was complicated by ongoing sepsis, fungemia, funguria, pneumonia, pleural effusion, acute renal failure progressing to total anuria and liver failure. It was necessary to hold his immunosuppressants for several days when it reached a toxic level. A liver biospy was suggestive of chronic rejection and his condition was such that he could not be relisted. 3 weeks after his readmission to the PICU he suffered a circulatory collapse and required aggressive resuscitation. He also had sanguinous drainage from his peritoneal drain that led to a laparotomy. 4 days later he had a seizure. The following day the PICU attending, the multidisciplinary team and his primary physician met with the mother, the rest of the family having returned home, to discuss her wishes. After hearing from all parties the mom decided that if his renal function deteriorated to defined limits, the team would withdraw life-sustaining therapies. 27 days after his admission he suddenly began to make urine; his BUN and creatinine peaked just below the threshold that had been set at the meeting. 11 days after that, he was transferred out of the PICU.
By six months post infarcts he was sitting unsupported, feeding himself and attending school. He is now nearly 27 years old, still living with that transplanted liver and in excellent health. He is my son.
Specializes in NICU, PICU, PCVICU and peds oncology.
I consider what happened with my son to be a minor miracle. He should have died, not once but several times. It makes my job difficult sometimes because I know that his story is the exception and that most children with similar issues will not survive.
I've been wracking my brain to come up with another complex test question for y'all and haven't gotten there yet! But here's a short snapper:
List as many negative effects of therapeutic hypothermia that you can think of, with rationale.
hmm I don't have all the rationales...but with the induced cooling in the HIE babies we see a lot of glucose instability, a lot of electrolyte abnormalities, coagulation issues and sinus brady with low blood pressure. I think a lot of the electrolyte/glucose issues is that the body is just so stressed with being cold and metabolic demands change pretty significantly. The bradycardia because the demand on the heart decreases so it slows down no always pumping effectively for all the organs, and I'm not sure what the coagulation issues are from but I know when I've had those kids i've given a lot of platelets and FFP, and they usually have mild to moderate pulmonary hemorrhages as well
Fatty tissue necrosis and subsequent hypercalcification. Hypoperfusion of the surface tissues leads to hypothermia and hypoxia of these tissues. This can promote inflammation and necrosis. Also, due to a higher concentration of saturated fat in the neonatal subcutaneous tissue, it is more likely to crystallize at low temperatures than older child or adult skin. These events are also promoted by the hypoxic event that may have precipitated the cooling also.
Specializes in NICU, PICU, PCVICU and peds oncology.
We're not just talking about neonates, remember, and HIE isn't the only reason for therapeutic hypothermia in children. All good responses so far but there's at least one big one missing.
Dingdingdingdingding! Sepsis is what I was after. But why is sepsis such a problem for these kids? And why do they have arrhythmias?
I assume it's because of their decreased immune function due to the hypothermia in combination with the stress that's been placed on their body due to the events leading up to and including induced hypothermia? Sepsis itself is a huge problem for a kiddo who has had induced hypothermia because their immune system IS decreased and cannot fight off infection and their organs have decreased perfusion due to decreased cardiac output and MAPs.
Also, hypothermia causes electrolyte imbalances which in turn cause cardiac dysrhythmias, but they can also happen because the heart gets irritable from hypothermia.
Specializes in NICU, PICU, PCVICU and peds oncology.
Oh dear... for the last three months all I've done is care for VAD (ventricular assist device) patients... a little beyond the scope of many of our little group. Let me think for a minute...
Let's do a quick arterial blood gas analysis. The patient is an infant wih central hypoventilation admitted with possible pneumonia and receiving BiPAP. Settings were adjusted based on capillary blood gas results over several days. However, the child's condition remains essentially unchanged from admission 5 days prior and her toes are bruised from all the cap gases. So an arterial line is established. The first ABG result looks like this: pH 7.378; pO2 78; pCO2 87; Na 133; K+ 3.8; Cl- 88; HCO3- 50.4; Hgb 124; Hct 0.34
1. What state is the patient in at this point?
2. Which came first - the abnormal pCO2 or the abnormal HCO3- and how could you tell?
Compensated respiratory acidosis. I believe the CO2 was elevated as part of the central hypoventilation with exacerbation and the bicarb is elevated as compensation.
:yeah:
.thumb.jpg.1730911fbf00f611ba1c99c44f0b92b3.jpg){kind=small}
:nurse:
NeoPediRN
945 Posts
It's been so long that I forget the answer LOL. I believe it was a chemical pneumonitis due to aspiration that caused the pulmonary hypertensive crisis.