Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9933898/
Decreased serum sodium levels (less than 135 mmol/L )are occasionally observed in patients with diabetes.
Hyponatremia is usually due to the hyperglycemia [6].
In fact, glucose is an osmotic active substance.
Osmotic pressure is the pressure required to stop the flow of water
Hyponatremia can be the result of illnesses and medications. Some causes that may be related to kidney disease include:
- Kidney failure - the kidneys cannot get rid of extra fluid from the body
- Congestive heart failure - excess fluid builds up in the body
- Diuretics (water pills) - makes the body get rid of more sodium in the urine
- Antidepressants and pain medication - may cause more sweating or urinating than normal
- Severe vomiting or diarrhea - the body loses a lot of fluid and sodium
- Excessive thirst (primary polydipsia) - causes too much fluid intake
- Certain medications. Some medications, such as some water pills (diuretics), antidepressants and pain medications, can interfere with the normal hormonal and kidney processes that keep sodium concentrations within the healthy normal range.
- The recreational drug Ecstasy. This amphetamine increases the risk of severe and even fatal cases of hyponatremia.
- Certain drugs. Medications that increase your risk of hyponatremia include thiazide diuretics as well as some antidepressants and pain medications. In addition, the recreational drug Ecstasy has been linked to fatal cases of hyponatremia.
Complications
In chronic hyponatremia, sodium levels drop gradually over 48 hours or longer — and symptoms and complications are typically more moderate.
In acute hyponatremia, sodium levels drop rapidly — resulting in potentially dangerous effects, such as rapid brain swelling, which can result in a coma and death.
Premenopausal women appear to be at the greatest risk of hyponatremia-related brain damage. This may be related to the effect of women's sex hormones on the body's ability to balance sodium levels.
Hypertonic saline has also been used to treat cerebral edema and is preferred over the diuretics.
Swelling can occur in specific locations or throughout the brain. It depends on the cause. Wherever it occurs, brain swelling increases pressure inside the skull. That's known as intracranial pressure, or ICP.This pressure can prevent blood from flowing to your brain, which deprives it of the oxygen it needs to function. Swelling can also block other fluids from leaving your brain, making the swelling even worse. Damage or death of brain cells may result
- Taking certain medications: These include selective serotonin reuptake inhibitors (SSRIs) and carbamazepine (Tegretol®). SSRIs are commonly used to treat depression and carbamazepine to treat epilepsy and mania.
What Causes Brain Swelling?
Injury, other health problems, infections, tumors, and even high altitudes -- any of these problems can cause brain swelling to occur. The following list explains different ways the brain can swell:
- Traumatic brain injury (TBI): A TBI is also called a head injury, brain injury, or acquired brain injury. In TBI, a sudden event damages the brain. Both the physical contact itself and the quick acceleration and deceleration of the head can cause the injury. The most common causes of TBI include falls, vehicle crashes, being hit with or crashing into an object, and assaults. The initial injury can cause brain tissue to swell. In addition, broken pieces of bone can rupture blood vessels in any part of the head. The body's response to the injury may also increase swelling. Too much swelling may prevent fluids from leaving the brain.
- Ischemic strokes: Ischemic stroke is the most common type of stroke and is caused by a blood clot or blockage in or near the brain. The brain is unable to receive the blood -- and oxygen -- it needs to function. As a result, brain cells start to die and swelling occurs.
- Hemorrhagic strokes: Hemorrhage refers to blood leaking from a blood vessel in the brain (intracerebral). Hemorrhagic strokes are the most common type of stroke. They occur when blood vessels anywhere in the brain rupture. As blood leaks and the body responds, pressure builds inside the brain. High blood pressure is thought to be the most frequent cause of this kind of stroke. Hemorrhages in the brain can also be due to certain medications and unknown malformations present from birth.
- Infections: Illness caused by an infectious organism such as a virus or bacterium can lead to brain swelling. Examples of these illnesses include:
- Meningitis: This is an infection in which the covering of the brain becomes inflamed. It can be caused by bacteria, viruses, other organisms, and some medications.
- Encephalitis: This is an infection in which the brain itself becomes inflamed. It is most often caused by a group of viruses and is sometimes spread through insect bites.
- Subdural abscess: Subdural abscess (empyema) refers to an area of the brain becoming abscessed or filled with pus, usually after another illness such as meningitis or a sinus infection. The infection can spread quickly, causing swelling and blocking other fluid from leaving the brain.
- Tumors: Growths in the brain can cause swelling in several ways. As a tumor develops, it can press against other areas of the brain. Tumors in some parts of the brain may block cerebrospinal fluid from flowing out of the brain. New blood vessels growing in and near the tumor can leak and also lead to swelling.
- High altitudes: Although researchers don't know the exact causes, brain swelling is more likely to occur at altitudes above 4,900 feet. This type of brain edema is usually associated with severe acute mountain sickness (AMS) or high-altitude cerebral edema (HACE).
Hyponatremia is associated with increased plasma glucose concentrations. Higher glucose concentration results in an osmotic force that draws water to the extracellular space.
Many medications commonly used in the management of diabetes result in hyponatremia as well. Tricyclic antidepressants, used in the treatment of diabetic neuropathy, stimulate vasopressin and lead to lower levels. First-generation sulfonylureas and insulin are also known to cause hyponatremia by augmenting the effects of vasopressin at the renal collecting ducts.
Potassium levels are also altered in diabetes. High plasma glucose concentrations lead to potassium efflux to the extracellular space, causing hyperkalemia.
Hyperkalemic renal tubular acidosis can occur in diabetic patients with nephropathy. Nephron dysfunction leads to impaired excretion of potassium and hydrogen, resulting in hyperkalemia and acidosis with hyperchloremia. It can even occur in patients with have mild nephropathy.
Magnesium is a common thread here. Low intake of magnesium is associated with increased risk of diabetes; low serum magnesium levels disrupt glucose uptake and contribute to microvascular complications and end-organ damage.
Overall, diabetic patients are at increased risk of acid-base disorders and electrolyte disturbances
Thus, in cases of hyperglycemia Posm is increased leading to movement of water out of cells and subsequently to a reduction of serum sodium levels (dilutional hyponatremia).
In such cases the corrected, for the degree of hyperglycemia, serum sodium value should be calculated. , The addition of 2.4 mEq/L to the measured concentration for every 100 mg/dl increment in plasma glucose is required.
The most common cause of hypotonic hyponatremia in patients with diabetes is osmotic diuresis-induced hypovolemia( Hypovolemia is the loss of 15% or more of circulating fluids in the body).
Drugs are a common cause of hyponatremia even in individuals with diabetes.
In fact, a number of drugs used in this population could result in a decrease of serum sodium levels [mainly thiazides in combination with SSRIs [16], and first generation sulphonylureas (such as tolbutamide and chlorpropamide)].
Administration of insulin drives glucose and water into the cells, reverses the initial direction of water movement and results in an increment of serum sodium levels.
Diabetic patients frequently develop a constellation of electrolyte disorders. These patients are often potassium-, magnesium- and phosphate-depleted.
Hyperglycemia increases serum osmolality, resulting in movement of water out of the cells and subsequently in a reduction of serum sodium levels ([Na+]) by dilution.
Therefore, in hyperglycemic patients, the corrected [Na+] should be taken into account, which is calculated by adding to measured [Na+] 1.6 mmol/L for every 100 mg/dL (5.55 mmol/L) increment of serum glucose above normal;
A correction factor by 2.4 mmol/L(43.2 mg/dL)[Na+] is used when serum glucose concentrations are higher than 400 mg/dL (22.2 mmol/L). or
A correction factor by /L(54 mg/dL) is used when serum glucose concentrations are 500 mg/dL or
A correction factor by /L(0.108g/dL) is used when serum glucose concentrations are 1g/dL or
A correction factor by /L(108g/dL) is used when serum glucose concentrations are 1000g/dL(1kg) or
Ratio of Sodium and Glucose is 1g:9.25g or
Ratio of Sodium and Glucose is 1 tea spoon salt:22.2g or
Ratio of Sodium and Glucose per day is 3 tea spoon salt:66.6g or
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Hyponatremia, defined as plasma sodium concentration <135 mmol/L,(2430mg/dl=2.43g/dl=1 spoon of table salt)
Every man has 4g Nacl(1.6g Na) per kg
1tea spoon of table salt (6g) has 2.4g Na
So 4g NaCl has 1.6g Na
Salt is 40% sodium, so that’s 3,287mg sodium per teaspoon of table salt.
The weight of one tea spoon of table salt is 6 g. 100 g of salt has 40 g of sodium. Therefore, 6 g of salt meaning 1 spoon of table salt has 40 × 6÷ 100 = 2.4 g =2400 mg of sodium.
Sodium is the major cation of extracellular fluid [ECF2 (1 mmol, or molar equivalent, corresponding to 23 mg of sodium)]. The mean body content of sodium in the adult male is 92 g, half of which (46 g) is located in the ECF at a concentration of 135–145 mmol/L, ∼11 g is found in the intracellular fluid at the concentration of ∼10 mmol/L, and ∼35 g is found in the skeleton.
(1 g of sodium corresponding to ∼2.5 g of salt).
Na+,K+-ATPase is kinetically stimulated by Na+
any decrease in [Na+]i reduces Na+,K+-ATPase activity.
On the extracellular side, Na+,K+-ATPase is stimulated by K+
Normal serum sodium levels are between approximately 135 and 145 mEq/L (135 to 145 mmol/L). A serum sodium level of less than 135 mEq/L qualifies as hyponatremia, which is considered severe when the serum sodium level is below 125 mEq/L.[13][14]
The renin–angiotensin system and the atrial natriuretic peptide indirectly regulate the amount of signal transduction in the human central nervous system, which depends on sodium ion motion across the nerve cell membrane, in all nerves. Sodium is thus important in neuron function and osmoregulation between cells and the extracellular fluid; the distribution of sodium ions are mediated in all animals by sodium–potassium pumps, which are active transporter solute pumps, pumping ions against the gradient, and sodium-potassium channels.[15] Sodium channels are known to be less selective in comparison to potassium channels. Sodium is the most prominent cation in extracellular fluid: in the 15 L of extracellular fluid in a 70 kg human there is around 50 grams of sodium, 90% of the body's total sodium content.
A pinch of salt is somewhere in the region of 100 milligrams and sodium chloride is 40% Na and 60% Cl. So the answer is about 40milligrams.
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Drug-induced hyponatremia due to hypoglycemic agents (chlorpropamide, tolbutamide, insulin) or other medications (e.g., diuretics, amitriptyline for the treatment of diabetic neuropathy) should be considered in every diabetic patient with low [Na+][10,11]. Chlorpropamide, which is now rarely used in the treatment of patients with DM, can induce hyponatremia in approximately 4% to 6% by potentiating the effect of antidiuretic hormone.
Tolbutamide can lead to hyponatremia by decreasing renal free water clearance
HYPOKALEMIA
The causes of hypokalemia in diabetics include:
(1) redistribution of potassium [K+] from the extracellular to the intracellular fluid compartment (shift hypokalemia due to insulin administration);
(2) gastrointestinal loss of K+ due to malabsorption syndromes (diabetic-induced motility disorders, bacterial overgrowth, chronic diarrheal states); and
(3) renal loss of K+ (due to osmotic diuresis and/or coexistent hypomagnesemia). Hypomagnesemia can cause hypokalemia possibly because a low intracellular magnesium [Mg2+] concentration activates the renal outer medullary K+ channel to secrete more K+[38].
Exogenous insulin can induce mild hypokalemia because it promotes the entry of K+ into skeletal muscles and hepatic cells by increasing the activity of the Na+-K+-ATPase pump[39]. The increased secretion of epinephrine due to insulin-induced hypoglycemia may also play a contributory role[40]. The major setting in which insulin administration leads to hypokalemia is during the treatment of severe hyperglycemia. The majority of patients with diabetic ketoacidosis (DKA) and HHS are markedly K+-depleted. The average K+ deficit is 3-5 mEq/kg, but it can exceed 10 mEq/kg in some cases.
The loss of K+ from the cells due to glycogenolysis( by which glycogen, the primary carbohydrate stored in the liver and muscle cells of animals, is broken down into glucose) and proteolysis.
The sodium/glucose cotransporter 2 (SGLT2) is expressed in the proximal tubules of the kidneys and reabsorbs approximately 90% of the filtered glucose [17]. Blockade of SGLT2 with SGLT2 inhibitors (oral antidiabetic drugs) results in renal excretion of glucose [18] and subsequent osmotic diuresis [19]. The SGLT2 inhibitor empagliflozin reduces the risk of major adverse cardiovascular events [20] and heart failure [21] and slows progression of kidney disease in patients with diabetes with high cardiovascular risk
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