Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.
I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.
Here's the case:
A 6-year-old child with a known h/o craniopharyngioma who has been endocrinologically intact with exception of needing thyroid replacement was admitted to the PICU prior to craniotomy to proceed with further tumor resection as well as the removal of a secondary cyst impacting his brainstem. The patient is receiving Keppra for seizures and per mother, he has recently been significantly more sleepy at school.
On POD Op day 5: the PICU the bedside nurse notices increased urine output (6cc/kg/hr to as high as 10cc/kg/hr). Initially, there was an increase in Na to 157mEq/L within 48-72 hours the serum Na dropped to 128mEq/L
To summarize key elements from this case, this patient has:
In today’s episode, we will be breaking down all things Sodium & the Brain. We will discuss diagnostic & management frameworks related to three pathologies:
These diagnoses can certainly be seen individually inpatients or as a spectrum of diseases — as we go through each of these diagnoses, pay particular attention to patient characteristics and lab abnormalities. Namely, serum sodium, serum osm, and urine osm.
To build the fundamentals, lets first start with classic nephrology saying: Serum Na represents Hydration
This takes us into a brief review of normal physiology — talking about three important hormones:
Let’s go through a quick multiple-choice question.
A patient is recently started on DDAVP for pan-hypopituitarism. The medication acts similarly to a hormone that is physiologically synthesized in which of the following from which are in the body?
A. Paraventricular Nucleus of the Hypothalamus
B. Supraoptic Nucleus of the Hypothalamus
C. Anterior Pituitary
D. Vascular Endothelium
The correct answer here is B the Supraoptic Nucleus of the Hypothalamus. Remember that ADH is synthesized in the hypothalamus and released from the posterior pituitary.
What are the physiologic actions of ADH?
ADH Increases H2O permeability by directing the insertion of aquaporin 2 (AQP2) H2O channels in the luminal membrane of the principal cells. Thus, as we will see with Central Diabetes insipidus, in the absence of ADH, the principal cells are virtually impermeable to water.
Let's talk about our next hormone, aldosterone. What are the important physiologic considerations?
Alright, what about the third hormone, ANP?
As ANP causes natriuresis, diuresis, and inhibition of renin, you can consider this hormone as having a complementary & opposite effect to ADH and aldosterone.
Alright, now that we have the basics, let's talk about our index case presentation, central diabetes insipidus, can you illustrate the key diagnostic features of this disease?
What are common triggers for CDI?
Because patients with CDI can conserve sodium appropriately, they typically do not manifest signs of volume depletion unless the diagnosis is delayed. Thus CDI is a cause of euvolemic hypernatremia.
Absolutely, actually, in CDI the urine osmolality is typically less than the plasma osmolality. These patients have about >4 mL/kg/hr of urine output.
What is the management of CDI?
Alright, so you gave the patient with presumed CDI a dose of DDAVP. What will you expect?
Rahul why do you think in our patient with high UOP and a high serum Na, the serum Na suddenly dropped in 48 hours?
There are two possibilities. Either patient has received DDAVP or more likely patient is having a Triphasic Response as many patients undergoing pituitary surgery do (DI within 2-4 days, followed by SIADH for 2-5 days, and a return to DI), which sometimes can be difficult to treat.
Most patients with CP already have pituitary hormone deficiencies at the time of diagnosis, which is more common in children than adults. Approximately 70% of children had growth hormone (GH) deficiency, followed by gonadotropin deficiency (51.7%), central diabetes insipidus (CDI, 28.6%), and thyroid-stimulating hormone (TSH) deficiency (21.9%), and adrenocorticotrophic hormone (ACTH) deficiency (12.5%).
The course of postoperative CDI can be transient, permanent, or a component of the triphasic pattern.
Pradip, can you highlight the triphasic response a bit more?
Let’s transition to the other extreme, and that is SIADH — syndrome of too much ADH. What are some common etiologies?
We will be reviewing specific electrolyte disorders in future episodes however please remember that hyponatremia like SIADH typically develops when a relative excess of free water is accompanied by an underlying condition that impairs the kidney’s ability to excrete free water. In SIADH, ADH secretion occurs independently of serum osmolality and intravascular volume status.
Interestingly, SIADH is essentially a diagnosis of exclusion. Before SIADH can be diagnosed, diseases causing decreased effective circulating volume, renal impairment, adrenal insufficiency, and hypothyroidism must be excluded.
Clinically, what will we see?
If left uncorrected, SIADH can lead to severe hyponatremia (plasma Na <120 mEq/L) - leading to seizures.
To close out this topic, how would you approach the management of SIADH?
Finally, let’s talk about Cerebral salt wasting. How can we compare and contrast CSW and SIADH?
So to summarize patients with CSW and SIADH can both be hypoNa in the setting of brain injury however patients with CSW are hypovolemic relative to patients with SIADH who have a euvolemic hypoNa.
What is the pathogenesis of CSW?
Pradip, any other clinical pearl regarding CSW?
How do we manage these patients?
Ok, Rahul, do you mind summarizing today’s episode?
This concludes our episode on All Things Sodium & the Brain in the PICU. We hope you found value in our short, case-based podcast. We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by myself Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!