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I recently took care of a five year old in our ED with a chief complaint of
vomiting that had started 1 day previously. The child had no prior
significant medical history and had previously been healthy.
On exam she was afebrile with a heart rate of 160. She exhibited Kussmall
breathing. She was ill appearing, but was awake and alert. Capillary refill
time was increased and her extremities were cool. Heart and lung exam
unremarkable except the tachycardia. Neuro was normal.
ABG revealed pH=7.07 with HCO3=4. Glucose was in the 700's. The lab was
unable to measure her electrolytes as her serum was so lipemic. CBC showed
Hb of 24. She weighed 20 kg and was given 400 ml bolus of NS over 1hr. She
was given 2u insulin IV and started on infusion. She was reassesed after her
first bolus of fluids. She remained tachycardic and had increased cappillary
refill with cool extremities. A second bolus was started to be given over
1hr. Transfer arrangements were made to a tertiary care center as I felt she
needed a pediatric intensivist. During her stay it was noted that she was
becoming more difficult to arouse. The patient was transferred to PICU
approximately 30 minutes away and had respiratory arrest approximately 5
minutes prior to arrival. CT scan revealed cerebral edema and herniation.
Would appreciate your comments.
Chuck Baxter M.D.
From: Dale Steele <[log in to unmask]>
To: Multiple recipients of list PED-EM-L <[log in to unmask]>
Date: Wednesday, March 11, 1998 3:58 PM
Subject: Initial fluid management in severe DKA
> We recently debated the initial fluid management of children
>presenting with severe diabetic ketoacidosis (DKA). A hypothetical case
>--an 8 month-old male infant with new onset DKA, a heart rate of 190 with
>poor peripheral perfusion, but not hypotensive. Glucose 1054 mg/dL, pH
>(arterial) 7.03, pCO2 10, serum Na 145 meq/L, chloride 113, potassium 3.3,
>HCO3 less than 5, BUN 35 mg/dL, creatinine 1.7 mg/dL, lactate 2.1 meq/L.
> Discussion centered around two issues.
> I. Which components of the evaluation predict intravascular volume
>depletion (compensated shock) in the setting of concurrent acidosis and
> II. What are the risks, if any, of rapid infusions of normal saline
>in pediatric patients with severe DKA? Which patients need rapid expansion
>of intravascular volume? How much?
>Which respect to these issues, how would you respond to the following
>Capillary refill time is primarily increased secondary to acidosis and does
>not imply compensated shock in this setting.
>Tachycardia results from increased epinephrine as part of the excess of
>counter-regulatory hormones, and therefore may not imply volume depletion.
>A normal lactate implies the absence of significant intravascular volume
>depletion, therefore, if lactate is normal, a normal saline bolus not
>The rapid initial decline in serum glucose associated with improved renal
>perfusion increases the risk of cerebral edema.
>Too vigorous initial fluid resuscitation with "isotonic" fluids given in
>the ED predisposes patients with DKA and other hyperosmolar states to
> I look forward to your learned replies...
>- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
>Dale Steele, M.D. Assistant Prof. of Pediatrics
>Pediatric Emergency Medicine Brown University
>Potter 212, Rhode Island Hospital Voice: (401)444-6236
>593 Eddy St. Fax: (401)444-4569
>Providence, RI 02903 USA
>For more information, send mail to [log in to unmask] with the
message: info PED-EM-L
>The URL for the PED-EM-L Web Page is:
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