The notification phone rings.
A thrill runs up your spine as your talented intern picks up the phone.
“Mhmm…Mhmm…,” she mutters as you hear the faint voice of the EMS dispatcher on the line. Your intern summarizes, “20 year old male – found unresponsive at a party– tachycardic, hypertensive – ETA five minutes.”
Moments later, EMS rolls in with a young man and two of his friends. Your patient seems to have the same level of neurological function as the stretcher upon which he lays. His friends are pale and diaphoretic.
“What happened?” you inquire.
“He was just doing shots!” friend A replies.
'Shots of what?' you ask.
“Uhhh. . . . soy sauce . . . about one quart of the stuff,” . . . friend B mutters. He pulls out his phone, already queued up to youtube.com with the following inspirational video:
“Holy ****, that is a lot of sodium chloride! He’s got raisin brain!” You proclaim to everyone in the room. They turn and look at you, impressed with your diagnostic acumen.
“Please intubate the patient, establish dual large-bore IV access, place the patient on the monitor, and send labs.”
As your team hustles to carry out the first steps of the resuscitation, you begin to sweat a little bit but then calm yourself down – and think.
Your internal monologue is as follows:
OK, the patient has severe CNS dysfunction secondary to acute hypernatremia caused by sodium chloride ingestion.
I usually volume resuscitate with normal saline before giving D5W because hypernatremic patients are usually dehydrated.
This is not usual hypernatremia; this is not dehydration.
He does not need more volume, and certainly does not need more sodium.
This patient needs dilution.
Lowering tonicity too quickly can cause cerebral edema.
But why is that? In chronic and subacute hypernatremia the brain synthesizes idiogenic osmoles – reducing tonicity can lead to free water moving intracellularly resulting in cerebral edema.
Here, in this acute illness, there has not been enough time for the synthesis of idiogenic osmoles.
The risk of cerebral edema from rapid infusion of free water is low.
You have your plan and you address the room:
“Alright team, we need to rapidly lower this patient’s sodium. Spike two bags of D5W, run them wide open under pressure – use the level one if need be. Keep changing the bags until he wakes up!”
On the sixth liter of D5W a call comes through from the blood gas laboratory to report a critical value. As your intern dashes into the resuscitation room to inform you that the serum sodium is 196 mEq/L, your patient opens his eyes.
Real life case
This fictionalized case is based on a case report of a 19 year-old man who drank 1 liter of soy sauce and presented to an ED comatose with seizure activity. His serum sodium was measured at 196 mEq/L, and he received six liters of D5W in 30 minutes. He survived without neurological sequelae!
There are many similar cases of acute sodium ingestions involving shoya (soy sauce), salt water gargles, and sea water during near-drownings. Acute hypernatremia with serum sodium above 160 mEq/L has a mortality rate upwards of 50%.
Science and math
Management of hypernatremia usually involves calculating the free water deficit via the formula:
This formula does not apply to an acute ingestion of sodium because there is no loss of free water.
Instead, we must dilute the additional salt water by converting it from a hypertonic to an isotonic solution.
Normal (0.9%) saline contains 9 grams of salt per liter of water.
One liter of soy sauce contains 60 – 90 grams of salt per liter, i.e. 6-9% saline solution.
It would take 6 – 10 liters of water to transform such a solution into normal saline.
Reports exist of hypernatremia associated with dural sinus thrombosis, cerebral hemorrhage, and pulmonary edema.
Questions for discussion
1. Given the lack of high quality evidence to address the treatment of acute hypernatremia, how would you determine the quantity and rate of D5W infusion? What are your clinical endpoints?
2. What is the role for emergent hemodialysis in a situation like this? Would you place a dialysis catheter empirically?
3. What is the role, if any, for GI decontamination in acute sodium ingestion?
Special thanks to Drs. Jackie Shibata and Sage Wiener
Survival of Acute Hypernatremia Due to Massive Soy Sauce Ingestion
Carlberg, David J. et al.
Journal of Emergency Medicine , Volume 45 , Issue 2 , 228 – 231
Goldfrank’s Manual of Toxicologic Emergencies, 7th edition
Chapter 17: Fluid, Electrolyte, and Acid Base principles p. 157
Tintinalli’s Emergency Medicine, 7th edition
Chapter 21: Fluids and electrolytes
Rosen’s Emergency Medicine, 7th edition
Chapter 123: Electrolyte disturbances p. 1618
Fatal hypernatremia due to drinking a large quantity of shoyu (Japanese soy sauce).
J Forensic Leg Med. 2011 Feb;18(2):91-2. doi: 10.1016/j.jflm.2010.11.011. Epub 2011 Jan 15.
Treatment of salt poisoning due to soy sauce ingestion with hemodialysis
Chudoku Kenkyu. 2004 Jan;17(1):61-3.
Fatal hypernatremia from exogenous salt intake: report of a case and review of the literature.
Mayo Clin Proc. 1990 Dec;65(12):1587-94.
Severe hypernatremia due to sea water ingestion in a child
Arch Pediatr. 2015 Jan;22(1):39-42. doi: 10.1016/j.arcped.2014.08.008. Epub 2014 Oct 2.
This is a photograph of Mycroft Javert Blumenberg. He is named after the brother of a fictional detective. In what short story about this detective is a terrier poisoned?
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