Endocrine
Critical illness-related adrenal (corticosteroid) insufficiency
Dysfunction of the HPA axis during critical illness
Often seen in vasopressor resistant hypotension/sepsis possibly due to tissue resistance cortisol
Typically have decreased basal cortisol production and inadequate cortisol response to stress (diagnosed with an ACTH stim test)
Treatment:
IV hydrocortisone: 100 mg/m 2/day or 2 mg/kg once
Then, continue to dose 50-100 mg/m2/day divided q6h or 1 mg/kg q6h (if > 25kg, then will be 100 mg daily divided into 4 dose)
Max dose: 100 mg/dose
Short cuts for initial bolus:
25 mg for < 3 years old
50 mg 3-12 years old
100mg > 12 years old
Helpful to obtain a baseline “Random Cortisol” level, but not needed prior to initial therapy
Diabetic Ketoacidosis (DKA)
Definition
Per the International Society of Pediatric and Adolescent Diabetes: must have ALL of the following:
Hyperglycemia > 200 mg/dL
Metabolic Acidosis - Venous pH < 7.3 OR serum bicarbonate < 15 mEq/L
Ketosis, as detected in the blood or urine
Urine – greater than 2+ or moderate ketones
Blood > 3 mmol/L Beta-hydroxybutyrate
Severity of DKA Assessment
Pathophysiology of DKA
Pathophysiology of HHS
https://calgaryguide.ucalgary.ca/wp-content/uploads/2015/05/Hyperosmolar-Hyperglycemic-State-HHS.jpg
Management
Two main goals - correct acidosis (with insulin) and correct hypovolemia/shock (with IVF)
Please see RBC PICU Protocols for specifics (under additional resources tab)
3 distinct protocols:
o PICU DKA
o PICU Mixed DKA/HHS
o PICU HHS
Serum monitoring is vital --> patients need 2 points of vascular access
May need arterial line if profound shock or difficult vascular access for lab
While correcting acidosis and hypovolemia, need to ensure slow decrease in serum osmolality to reduce risk of cerebral edema
Monitor glucose, serum osmolality, pH, and electrolytes
Use IV regular insulin when initiaing treatment for DKA
How do we know when they can transition to subcutaneous insulin/you have reversed the patient's DKA?
o Correction of acidosis = pH > 7.3
o Bicarbonate > 15
o Anion Gap closed < 12
o Underlying etiology for DKA identified
o Back to neurological baseline
Please consult endocrinology when patients are INITIALLY admitted 😊
General Principles, Chart used from UpToDate
Complications
Cerebral edema - occurs most frequently in the first 12h of treatment, in about 0.5- 1% of patients and has about a 25% mortality rate
See more below (Source: UpToDate)
Venous thrombosis -extremities and cerebral venous sinuses
AKI - generally pre-renal in nature but can see intrinsic renal injury
Pancreatitis - elevation in amylase and lipase, sometime sub-clinical
Pathophysiology of Cerebral Edema in DKA
From: Azova S, Rapaport R, Wolfsdorf J. Brain injury in children with diabetic ketoacidosis: Review of the literature and a proposed pathophysiologic pathway for the development of cerebral edema. Pediatr Diabetes. 2021 Mar;22(2):148-160. doi: 10.1111/pedi.13152. Epub 2020 Dec 3. PMID: 33197066; PMCID: PMC10127934.
Graphic Explanation: "A hypothetical schema of the pathways that contribute to the development of cerebral injury in children with diabetic ketoacidosis. Solid arrows indicate pathophysiologic mechanisms that have been observed in humans. Dashed arrows represent hypothesized mechanisms or those that have only been shown in animal studies. The blue arrows signify factors that lead to cytotoxic injury, including upregulation of cytotoxic substances, altered membrane transporter activity, and hypoxic injury. The red arrows depict mechanisms that predispose towards vasogenic injury, characterized by the disruption of the blood–brain barrier. The green arrows denote treatment-related effects that may cause osmotic injury. A combination of these processes causes cerebral edema in high-risk children."