When I was in middle school chemistry class our teacher thought he’d be a wise guy and tell us about this terrifying chemical called dihydrogen monoxide that could kill us by accidental inhalation, wipe out whole cities, or burn us in its gaseous state. After convincing a bunch of students that the chemical should be banned he revealed that it was water. A chemical none of us, or life as we know it, could live without. But too much of a good thing can be dangerous.
But water intoxication? Really?
Humans need to drink water every day to stay hydrated but it’s a balancing act with our body’s electrolytes, like sodium. If the blood becomes too diluted we can get very sick. “Water intoxication is a rare phenomenon that occurs due to an excessive intake of water, and when the amount of water intake exceeds that of water excretion in the kidney. As a result, the sodium concentration in the blood is diluted, and hyponatremia develops,” (Joo and Kim, 2013).
Hyponatremia [hypo (low) natr (sodium) emia (blood] is when there isn’t enough sodium in the blood due to low sodium intake and/or high water intake. A healthy range for blood sodium is 135-145mmol/L (millimoles per liter) and hyponatremia is sodium below 135mmol/L. For perspective, 1 tsp salt = 6 g salt ≈ 2,400 mg sodium = 104 mmol sodium (CDC, 2016). That means for every liter of blood in your body, you should have around 1 1/3 tsp of salt. An average-sized adult has around 4.5-5.5 liters of blood in them, so that’s 6 -7 1/3 tsp of salt (note: this isn’t dietary advice). Anyone can develop hyponatremia but it’s common for people with spinal cord damage for a few reasons.
Neurological:
The kidneys aren’t working properly due to issues in the brain’s osmostat (located in the hypothalamus) which tells the kidneys when and how much sodium to filter out of the blood and how much diuretic hormone to release, which tells the body how much to urinate (Soni, 1994). “Around 10% of quadriplegics have mild hyponatremia due to a reset osmostat ” (Gibbs, 1994).
Lifestyle:
People with spinal cord injuries have an increased fluid intake, potentially because it is easier for people with limited mobility to consume liquids than solids and due to the neurological issues in the osmostat increasing thirst. When combined with a low sodium diet, especially common in a medical setting, the increased fluid intake can result in low blood sodium levels.
Medical:
Because people with spinal injuries tend to have limited mobility, diuretics (which cause you to urinate) to prevent edema (swelling of the legs) are commonly used and can cause increased thirst and interfere with the body’s own release of diuretic hormones. Intravenous therapies using hypotonic (low sodium) fluids can also cause diluted blood sodium.
Many quadriplegic people use some form of a catheter; with the use of catheters, there is an increase in UTI’s because the urine isn’t completely emptied from the bladder. UTI’s can become chronic and asymptomatic. Asymptomatic kidney infections combined with the neurological issues interfering with kidney function can cause increased sodium loss through the urine (Gibbs, 1994)
The water in our cells is approximately .9% sodium. This is the same concentration as the saline used in IVs, so it’s referred to as an isotonic [iso (equal) tonic (fluid)] because it’s equal to the saline solution in our body. An osmotic gradient occurs when water flows towards a higher concentration of sodium in order to equalize itself. So when a person drinks a bunch of water and the blood sodium level is diluted, the water is going to move into the cells of the organs that still have a .9% sodium concentration, causing swelling.
What are the symptoms of hyponatremia?
Unfortunately, many people don’t show symptoms at first and many people with spinal cord injuries live in a mild state of hyponatremia without cause for concern (Gibbs, 1994; Moore, 1997). In a study done in 1994, the majority of the participants were asymptomatic, only discovered to be hyponatremic due to routine blood tests. When symptoms are present they can include confusion, headache, nausea, vomiting, irritability, drowsiness or restlessness, muscle spasms or cramps, and even seizures and coma. These symptoms occur because of the osmotic gradient, causing the brain to swell– while other organs have room to swell, the brain is encased in bone.
Treatment for Hyponatremia:
The treatment is fluid restriction and time. Treating hyponatremia too quickly can cause further neurological damage, for example, central pontine myelinolysis (CPM) or osmotic demyelination syndrome (ODS) meaning that the myelin sheaths that insulate brain cells in the pons (an area of the brain stem) are damaged. Depending on the severity of the hyponatremia (how low the blood sodium is based on blood tests) the patient may be given hypertonic IV fluids to encourage the excess fluids in the organs and tissues to flow towards the higher sodium in the bloodstream and get flushed out as urine. Hyponatremia may be accompanied by hypokalemia, low potassium, which is another electrolyte. This can complicate treatment and may be a risk factor for developing ODS (Koul, 2013). The best treatment is prevention.
How to prevent hyponatremia if you are at risk:
Unless specifically recommended to you by your doctor, don’t limit sodium intake in your diet. (This doesn’t mean go HAM with the fast food either; whole food, home cooking, please. Leafy greens like spinach and swiss chard have naturally occurring high sodium content.) Adults with normal blood pressure should consume anywhere from 3000-5000 mg of sodium a day, and for people with low blood pressur– common with spinal cord injuries– potentially higher amounts. This is very different from the previous recommendations of 1,500-2,300 mg of sodium a day which have been shown to have negative impacts on health.
Don’t drink plain water, always use an electrolyte mix when drinking water. Tucker uses Propel packets in his Camelback water bottle throughout the day. This ensures that he’s consuming an isotonic fluid and will not dilute his blood levels of electrolytes, including potassium, without adding additional calories.
Monitor and limit water intake. Once you’ve had your eight glasses, stop. According to an article on The Hospitalist, “hyponatremia is not a salt problem, it’s a water problem” was the theme of a session on the condition hosted by the Society of Hospital Medicine. The most important thing in preventing hyponatremia is to limit water intake. Don’t drink more than 33 oz or 1 liter per hour (that is the most the body can get rid of per hour) and don’t drink more than 2.7 – 3.7 liters per day depending on your body weight and physical activity/ sweating.
Pay attention to your pee. The amount of water you’re putting in should be equivalent to the water you’re putting out. Low urine output is a sign that what you drank has gone into your organs, ala the osmotic gradient. And the color is important too– aim for a pale yellow color.
ChubbyEmu is a Youtuber who shares rare medical case studies, in this episode he shares a story of a woman who developed hyponatremia after drinking distilled water to win a Nintendo Wii.
If you like these kinds of posts, please consider supporting this blog on Patreon.
Sources and More Information:
CDC. 2016. “Sodium Reduction Toolkit.” CDC. (open source)
Gibbs CJ, HA Lee. 1994. “Severe hyponatraemia in a quadriplegic.” Br J Clin Pract. 48(1):53-4.
Koul P, U Khan, R Jan, S Shah, A Qadri, and B Wani. 2013. “Osmotic demyelination syndrome following slow correction of hyponatremia: possible role of hypokalemia.” Indian Journal of Critical Care Medicine. 17(4):231. (open source)
Leehey DJ, AA Picache, GL Robertson. 1988. “Hyponatraemia in quadriplegic patients.” Clin Sci (Lond). (4):441-4.
Mayo Clinic Staff. 2018. “Hyponatremia.” Mayo Clinic. (open source)
McKnight, Whitney. 2017. “Hyponatremia: Watch the water, not the salt.” The Hospitalist. Society of Hospital Medicine. (open source)
Moore K, M Midha. 1997. “Extra pontine myelinolysis in a tetraplegic patient: case report.” Spinal Cord. 53: 332-334. (open source)
Peng, Kian. 2004. “Management of Hyponatremia.” Am Fam Phys. 69(10): 2387-2394. (open link)
Peruzzi WT, BA Shapiro, PR Meyer Jr, F Krumlovsky, BW Seo. 1994. “Hyponatremia in acute spinal cord injury.” Critical Care Medicine. 22(2):252-258
Salazar LRM, A Agrawal, et. al. 2018. “Hyponatremia in the acute phase of spinal cord trauma: review.” J Acute Dis. 7(3): 103-107. (open source)
Sica DA, RM Culpepper. 1989. “Case Study: Severe hyponatremia in spinal cord injury.” Am J Med Sci. 298(5):331-3.
Sica DA, M Midha, E Zawada, et. al. 1990. “Hyponatremia in Spinal Cord Injury.” The Journal of The American Paraplegia Society. 13(4):78-83
Soni BM, S Vaidyanthan, JW Watt, and KR Krishnan. 1994. “A retrospective study of hyponatremia in tetraplegic/paraplegic patients with a review of the literature.” Paraplegia. 32(9):597-607. (open source)
Watson ID, S Nathanayan, B Soni, M Fraser, WD Fraser, and KR Krishnan. 1999. “Profound hyponatremia in quadriplegia.” Ann Clin Biochem. 36:673-676. (open source)
Tucker Cassidy 