Description

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine.

Welcome to our Episode of a 9 year old girl with worsening seizures in the setting of an electrolyte abnormality.

Here's the case:

A 9 year old girl presents to the ED with increased frequency of seizures, dehydration and listlessness. She has h/o of global developmental delay, congenital hydrocephalous (with VP shunt in place with her last revision 3 years prior, and seizure d/o treated with Leviteracetam. She usually has one or two focal seizures per day but on day of admission she had multiple prolonged seizures which were also generalized tonic clonic in semiology. Per her caregiver, the patient usually eats by mouth and mother typically gives her 3 cups of water daily. There is no history of diarrhea but patient has had 2-3 bouts of non-bloody non-bilous emesis on day of presentation. Looking at her growth chart, the patient has also lost ~ 2KG of her weight in the last 3 months and has had poor follow up with her PCP. In the ED she has a hypovolemic shock picture as she is hypothermic, tachycardic, tachpneic, and hypotensive with appropriate saturations. Blood gas is notable for a mild metabolic acidosis. Patient receives abortive seizure rescue. A head CT showed no increased in hydrocephalus, no mass or hemorrhage and a shunt series confirms patency of her VP shunt. Most pertinently to this case, her serum sodium on her RFP was undetectable at a value of = >200mEQ/dL; this was confirmed by a repeat lab draw and POC value. Other notable findings included an elevated Cr for age, an elevated BUN and a microcytic anemia. Patient was given a NS bolus, had cultures drawn, was started on broad spectrum abx therapy, stabilized and sent to the PICU.

To summarize key elements from this case, this patient has:

• A history of GDD with epilepsy and shunted hydrocephalus.
• A stigmata of cachexia.
• And a presentation of hypovolemic shock secondary to decreased intake, increased loss, and potential underlying concern for sepsis.
• The most important element of this case is her extreme hypernatremia
• All of these factors in this case point to our topic of discussion today → the approach to hypovloemic hypernatremia 2/2 to dehydration.
• Let's transition into some history and physical exam components of hypovolemic hypernatremia?

1. Key history features in patients who present with Hypovolemic HyperNa include:

• Increased losses such as emesis
• Decreased intake, and in this setting potentially lack of access to free water
• Listlessness which could be related to cerebral hypoperfusion
• Increase in seizure frequency due to increased rapid depolarization of Na channels in the brain and fluid shifts
• And weight loss → all of these factors were seen in our case.
• Of note if this patient was a neonate considering a high-pitched cry in the setting of hyperNa & dehydration could be a subtle history finding.

1. Are there some red-flag symptoms or physical exam components which you could highlight?

• Our patient is Non verbal and has global delay secondary to a remote neurological insult
• She may not have intact ability to communicate or vocalize thirst.
• Apart from her mucous membranes, dry cracked lips, decreased skin turgor that can be described as doughy, and prolonged capillary refill, I think it is important to highlight her hypotension - as BP is one of the last vital signs in pediatrics to be abnormal in intravascular volume depletion. To me, this really stratifies this patient into severe dehydration and potentially septic shock.

This is a great point — understanding % volume loss and its correlation to vital sign and PE anomalies is key. Remember a sensitive marker for dehydration in pediatrics is tachycardia and a late finding if you are primarily dealing with dehydration is hypotension. This indicates that counter-regulatory responses are unable to maintain adequate systemic vascular resistance (SVR) and that there is a significant loss of intravascular volume. In our patient, we also noticed her weight loss on presentation which not only brings up the concern for malnutrition but it also serves as an adjunct measure of dehydration. In fact, in a 2009 paper assessing dehydration in pediatrics it was noted that the gold standard for confirming the diagnosis of hypovolemia in children is comparison of body weight before and after rehydration.

• To continue with our case, the patients labs were consistent with:
• Severe Hypernatremia
• Elevated BUN and Cr which point to an AKI
• And interestingly mild anemia → this could be a nutritional aberrancy such as iron deficiency anemia or anemia of chronic disease in the setting of her complex underlying condition but it also brings up the concern for hypovolemic shock secondary to bleeding. Pertinently she had no signs of external or internal bleeding, but it is important to stratify this element as your resuscitation efforts — i.e. whether you would give crystalloid or colloid can be guided by this subtlety.

Correct, it is important to highlight that in the setting of dehydration Hct values would be increased. In a 2006 Study in Transfusion, Valeri and colleagues concluded that the Hct values in hypovolemic anemic patients are elevated because the plasma volume does not increase to achieve the normovolemic anemic state.

OK to summarize, we have:

• 9 year old with global developmental delay who has emesis, dehydration and a serum Na of 200 mEq/L. This brings to the topic of our discussion today namely hypernatremia in the PICU.
• Let's start with a short multiple choice question: 15 year old with h/o diabetes insipidus presents with a serum Na of 175mEq/L. 4 months ago his serum Na was 140mEq/L. Currently patient is obtunded with decreased skin turgor, fever and a blood pressure of 140/80 mmHg. Patient has been stressed due to school work and been non compliant with his DDAVP resulting in polyuria for almost 5 days.
• Treatment goal for this patient is

a. Reduce serum sodium concentration to normal in first 12 hours

b. Reduce serum sodium concentration to normal in 24 hours

c. Reduce serum sodium concentration to 150 mEq/L in 24 hours

d. Reduce serum sodium concentration by 10 mEq/L in 24 hours

The correct answer is d. Reduce serum concentration by 10-12 mEq/L in first 24 hours; you can also think of this as not correcting the sodium more than 0.5 meQ/L per hour → thus in 24 hrs you should not lower the sodium by more than 12. I think listeners should remember that it is important to gradually lower the sodium in patients who have developed hypernatremia slowly over a period of days especially when Na is > 165mEq/L. Pradip, why is this?

• Patients with hypernatremia develop idiogenic osmoles to protect the brain from dehydration within hours. Numerous fatal cases of cerebral edema and herniation have occurred with rapid correction over a 24-hour period, leading to recommendations for correction over no less than 48 hours. General trend is for slow correction over 48 hours.

A mnemonic that can be useful is high to low the brain will blow; i.e. if a patient has chronic hypernatremia that is corrected too acutely,...