Hyponatremia - Causes, Pathophysiology, Algorithm, Correction, Treatment

Facts about Hyponatremia : Definition

This is a condition characterized by lower-than-normal levels of sodium in the blood. The normal serum sodium concentration in the body is between 135 and 145mEq/L. If the sodium serum levels go below 135mEq/L, you are considered to be suffering from hyponatremia. The condition is said to be severe if the serum levels go below 125mEq/L. The body uses sodium as an electrolyte to regulate water in and around the cells of the tissues. [1, 2, 3,5,8,9, 10, 13,]


  • The sodium concentration in the serum is regulated by secretion of the ADH (antidiuretic hormone), variations of the renal handling of filtered sodium, and the renin-angiotensin-aldosterone system.
  • If the serum osmolality increases over the normal range of 280-300mOsm/kg, there is the stimulation of hypothalamic osmoreceptors that cause an increase in thirst and circulate the ADH.
  • The ADH increase the reabsorption of the water from urine that results in low volume urine with high osmolality but returns the serum osmolality to normal.
  • Aldosterone is also released to curb hypovolemia through renin-angiotensin-aldosterone feedback system. The hormone causes the sodium absorption in the kidney’s renal tubule.
  • The sodium retention causes the retention of water that in turn corrects the hypovolemic problem. The kidney is able to balance the sodium-independent of these two hormones.
  • In a hypovolemic, state such as dehydration or hemorrhage increases the absorption of sodium in the proximal tubule of the kidney.
  • When the vascular volume is increased, tubular sodium reabsorption is suppressed and helps to restore the normal vascular volume. Thus, the sodium balance disorders can be traced to aldosterone, renal sodium transport, ADH, or disturbance water or thirst acquisition.
  • Hyponatremia is said to be physiologically significant when there is the indication of extracellular hyposmolality and the tendency of free water shifting from vascular space to the intracellular space.
  • The body tolerates cellular edema to a greater extent by not at the bony calvarium. Thus, hyponatremia clinical manifestations are primarily on cerebral edema. The rate at which the condition develops is critical to its treatment. [4,6,10, 11]

Hypovolemic Vs Hypervolemic hyponatremia  

A condition is considered hypovolemic hyponatremia if there is a decrease in total body water with the decrease in the total amounts of the body sodium.

Hypervolemic hyponatremia occurs when there is an increase in total body sodium along with the increase in total body water.
If the normal body sodium levels do not change with the increase in total body water, the condition is said to be euvolemic hyponatremia. [1, 2, 3,5,8,9]

There are cases where water shifts from the intercellular to extracellularly environment and results in dilution of sodium. The total body water is not changed in this case.
This condition occurs if one is suffering from hyperglycemia and is referred to as redistributive hyponatremia. [1, 2, 3, 5, 8, 9]

Acute hyponatremia and chronic hyponatremia

Acute hyponatremia is the case where sodium levels fall rapidly in less than 48 hours.
The condition is more dangerous than hyponatremia that occurs over several day or weeks, commonly known as chronic hyponatremia. In the latter, the brain cells adjust to the condition, and there is minimal swelling. [1, 2, 3, 5, 8, 9]

Signs and symptoms of hyponatremia

  • Vomiting
  • Short memory loss
  • Lethargy
  • Fatigue
  • Irritability
  • Loss of appetite
  • Nausea
  • Confusion and muscle weakness.
  • Some patients also complain muscle cramps, seizures, and decreased consciousness.
  • In severe cases, one may fall into a coma. 

Neurological symptoms only occur when sodium levels get very low at quantities below 115mEq/L. At this level of sodium, water enters the brain causing the brain to swell.

The condition later causes pressure in the skull, a condition called hyponatremic encephalopathy. If the condition is not checked at the point, there is squeezing of the brain across the structures of the skull. The physical symptoms of this condition are:

  • Confusion
  • Respiratory arrest
  • Non-cardiogenic fluid accumulation in lungs
  • Brain stem compression. 
The condition is fatal if not treated at once.
The severity of the symptoms is dependent on the severity of the sodium drop and show fast the condition happens. The body may tolerate gradual drop even to levels that are very low. As the body has a neurotic adaptation capability. However, the presence of neurological diseases, seizure disorders, and other non-neurological metabolic abnormalities influence the severity of the condition [1, 2, 3,5,8,9, 13]

Causes of hyponatremia 

Sodium in the body fluid is used to maintain electrolyte balance, blood pressure and for the working of muscles and nerves. If the level of sodium in the fluids outside the cells goes down, the fluids enter the cells causing the cells to swell. Here are the main causes of hyponatremia:

  • Diarrhea
  • The intake of diuretic medicines that increase the urine output
  • Burns that cover large areas of the body
  • Heart failure
  • Vomiting
  • Sweating
  • Vomiting
  • Heart failure
  • Kidney diseases
  • Liver cirrhosis
  • The Syndrome of Inappropriate antidiuretic hormone secretion (SIADH)
  • Hypothyroidism, a condition where there is underperformance of the pituitary glands
  • Deficiency of glucocorticoid, a steroid
  • Congenital adrenal hyperplasia that makes the adrenal glands unable to produce enough steroid 


  • Exercise-associated hyponatremia from prolonged period of exercise while taking water alone
  • Certain medications such as Lasix for treating blood pressure and antidiuretics [1, 2, 3,5,8,9, 13]

Workup : A clinical diagnosis chart used to determine the cause of hyponatremia


Legionnaire’s disease workup

Cases of pneumonia are caused by several pathogens that share similar laboratory findings. Hyponatremia that is secondary to SIADH is common in Legionnaires’ disease that that which is caused by pathogens. However, the condition is not specific to Legionnaires’ disease. [4, 5]


Hyponatremia is also classified according to effective osmolality. It can be said to be: 
  • Hypotonic hyponatremia
  • Hypertonic hyponatremia
  • Isotonic hyponatremia.
During the diagnosis, the patients undergo three tests that when combined with physical examination and history, the doctor is able to establish the etiological mechanism as urinary sodium concentration, urine osmolality, serum osmolality. [1, 2, 5, 6, 9, 13]

Urine osmolality 

This osmolality test is used to differentiate primary polydipsia from free-water excretion. Osmolality that is greater than 100mOsm/kg shows that the kidneys are unable to dilute the urine. . [1,2,5,6,9,13]

Serum osmolality 

Serum osmolality is used for differentiating between pseudo hyponatremias and true hyponatremia. The earlier is secondary to hyperproteinemia or hyperlipidemia or could be hypertonic hyponatremia that is linked to elevated mannitol, glucose, and glycine maltose or sucrose. Symptoms do not appear until the plasma levels drop below 120 mmol per L . [1,2,5,6,9]

The urinary sodium concentration

This test is used to differentiate between the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and hyponatremia that is secondary to hypovolemia. The condition is considered SIADH hyponatremia when the urine sodium is greater than 20-40mEq/L. The typical measurements of urine sodium for hypovolemia patients are usually less than 25mEq/L. However, an SIADH patient taking low sodium will have the values falling below 25mEq/L.  . [1,2,5,6,9,11,13]

Hyponatremia treatment 

  • The treatment of the hyponatremia condition is dependent on the underlying cause. Such a condition should be treated first to correct the condition.
  • Treatment starts with the examination of the condition to determine if one has euvolemic, hypervolemic or hypovolemic condition
  • If the patient is suffering from hypovolemia, the condition is corrected by an intravenous administration of normal salt in a saline solution.
  • Euvolemic hyponatremia is treated by restriction of fluid and abolishment of the stimuli that causes the secretion of the antidiuretic hormone such as nausea.
  • Any drug that the patient is taking that could be causing SADH is also discontinued.
  • Hypervolemic hyponatremia is treated by treating the disease that could be causing the condition. In most cases, the cause is usually liver or heart failure. If this is not resolved, the patient receives the same treatment as that of the euvolemic hypervolemic hyponatremia condition. 
There is a risk of the patient developing severe neurological disorder called Central Pontine Myolysis that breaks down the sheaths covering parts of the nerve cells if hyponatremia is corrected rapidly. As a precautionary measure the salt level in blood, or called sodium serum, should not rise beyond 0.33mmol/l/h during the application of the saline solution. [1,2,4,5,6,8,9,13]

Hyponatremia correction calculator

 Hyponatremia calculator is used for calculating the amount and the intensity of the saline solution that is needed to correct the serum hyponatremia. The formula for calculation of the infusateRate is; 

Infusate Rate = (1000 * Serum Na Change Per Hr * ((Water Fract * Weight) + 1)) / (IVNa + IVK - SerumNa) 

Serum Na Change Per Liter = (IVNa + IVK - SerumNa) / ((Water Fract * Weight) + 1) [12]

ICD-9-CM Diagnosis Code 276.1 

ICD-9-CM Diagnosis Code 276.1 is a billable medical code used to indicate that hyposmolality and hyponatremia were diagnosed for reimbursements. However, the code can only be used for claims for services rendered before October 1, 2015. For claims after the date, the code ICD-10-CM code is used. [7]

  1. Merck Manuals Professional Edition. Hyponatremia - Endocrine and Metabolic Disorders [Internet]. 2015 [cited 22 December 2015]. Available from: http://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-disorders/hyponatremia#sec12-ch156-ch156d-714
  2. Melissa Conrad Stöppler M. Hyponatremia: Get the Facts on Symptoms and Treatment [Internet]. MedicineNet. 2015 [cited 24 December 2015]. Available from: http://www.medicinenet.com/hyponatremia/article.htm
  3. Goh K. Management of Hyponatremia - American Family Physician [Internet]. Aafp.org. 2015 [cited 24 December 2015]. Available from: http://www.aafp.org/afp/2004/0515/p2387.html
  4. Emedicine.medscape.com. Legionnaires Disease Workup: Approach Considerations, Histologic Findings, Laboratory Studies [Internet]. 2015 [cited 24 December 2015]. Available from: http://emedicine.medscape.com/article/220163-workup
  5. Updated by: David C. Dugdale a. Hyponatremia: MedlinePlus Medical Encyclopedia [Internet]. Nlm.nih.gov. 2015 [cited 24 December 2015]. Available from: https://www.nlm.nih.gov/medlineplus/ency/article/000394.htm
  6. Haralampos J. Milionis M. The hyponatremic patient: a systematic approach to laboratory diagnosis. CMAJ: Canadian Medical Association Journal [Internet]. 2002 [cited 24 December 2015];166(8):1056. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC100882/
  7. Icd9data.com. 2012 ICD-9-CM Diagnosis Code 276.1 : Hyposmolality and/or hyponatremia [Internet]. 2015 [cited 24 December 2015]. Available from: http://www.icd9data.com/2012/Volume1/240-279/270-279/276/276.1.htm
  8. Mayoclinic.org. Hyponatremia Symptoms - Mayo Clinic [Internet]. 2015 [cited 24 December 2015]. Available from: http://www.mayoclinic.org/diseases-conditions/hyponatremia/basics/symptoms/con-20031445
  9. Healthline. Low Blood Sodium (Hyponatremia) [Internet]. 2015 [cited 24 December 2015]. Available from: http://www.healthline.com/health/hyponatremia
  10. Moritz M, Ayus J. The pathophysiology and treatment of hyponatraemic encephalopathy: an update. Nephrology Dialysis Transplantation. 2003;18(12):2486-2491.
  11. Encyclopedia Britannica. syndrome of inappropriate antidiuretic hormone (SIADH) | pathology [Internet]. 2014 [cited 24 December 2015]. Available from: http://www.britannica.com/science/syndrome-of-inappropriate-antidiuretic-hormone
  12. Reference.medscape.com. Hyponatremia Correction Infusate Rate [Internet]. 2015 [cited 24 December 2015]. Available from: http://reference.medscape.com/calculator/hyponatremia-correction-infusate-rate
  13. Updated by: David C. Dugdale a. Hyponatremia: MedlinePlus Medical Encyclopedia [Internet]. Nlm.nih.gov. 2015 [cited 24 December 2015]. Available from: https://www.nlm.nih.gov/medlineplus/ency/article/000394.htm
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Paresthesia (Tingling and Numbness) - Causes and Treatment


Meaning : Paresthesia (pronunciation: \ˌpar-əs-ˈthē-zhə\; ICD-10: R20.2; ICD-9-CM: 782.0, 355.1) generally refers to abnormal sensations except pain (vs. dysesthesia). This covers a wide variety of sensations like tingling (pins and needles), itching, pricking, shooting, aching, burning, searing, twisting, or electrical, among others. Most common of these symptoms is the tingling sensation. It is primarily felt on the extremities (hands, feet, arms, and legs) [1, 2, 3].



Causes of Transient Paresthesia

This is the temporary type of paresthesia and is very common because we sometimes tend to position ourselves in a wrong way, like resting your head on your bent forearm over a table or by simply crossing your legs. The following are the other common causes of transient paresthesia [2, 4, 5]:

  • Whiplash injury or injury to the soft tissue of the neck can cause paresthesia of upper extremities after a vehicular accident.
  • Disturbance in sodium ion occurs in hyperventilation syndrome, producing abnormal discharges in the afferent nerves.
  • During panic attacks, an individual may experience paresthesia of the mouth, hands, and feet. Add hyperventilation syndrome to that and it gets worse.
  • After a transient ischemic attack (TIA) or stroke, excess potassium goes out of the cell causing hyperactive muscle contraction, thus paresthesia.
  • Paresthesia during seizures is possible and with its treatment with vagus nerve stimulation, paresthesia is an adverse reaction, thus worsened.
  • Dehydration can also cause paresthesia because of electrolyte imbalance.
  • Insufficient blood supply due to acute arterial occlusion by thrombosis, embolism, or aneurysm can cause paresthesia.
  • Beta-alanine supplements have paresthesia as one of the side effects when the dose reaches 800 mg.

Causes of Chronic Paresthesia

Chronic paresthesia is the type of paresthesia that comes and goes and has been happening periodically, thus its other name intermittent paresthesia. Generally, the causes are neurologic diseases. Specific causes are listed below [2, 4, 5, 6]:

Disorders of the Nervous System

Central Nervous System
  1. Cerebrovascular accident (CVA) or stroke: Poststroke paresthesia, Lacunar infarction
  2. Epidural/Subdural hematoma or Subarachnoid hemorrhage
  3. Head trauma
  4. Brain tumor or metastasis: Cavernous angioma, Trigeminal sensory neuropathy, Syringomyelia
  5. Trigeminal trophic syndrome
  6. Encephalitis
  7. Meningitis
  8. Brain abscess
  9. Multiple sclerosis (MS)
  10. Transverse myelitis
  11. Lumbar spinal stenosis
  12. Pernicious anemia
  13. Lumbar puncture
Peripheral Nervous System
  1. Peripheral neuropathy /Entrapment neuropathy
  2. Carpal tunnel syndrome (CTS)
  3. Thoracic outlet syndrome (TOS)
  4. Cubital tunnel syndrome
  5. Tarsal tunnel syndrome
  6. Lateral femoral cutaneous syndrome
  7. Peroneal palsy
  8. Neuralgia
  9. Chronic nerve compression
  10. Meralgia paresthetica
  11. Disc herniation
  12. Cervical spondylosis
  13. Sciatica
  14. Pressure palsy
  15. Piriformis syndrome
  16. Spinal canal stenosis
  17. Charcot-Marie-Tooth disease
  18. Amyloidosis
  19. Spondylolisthesis
  20. Spinal tumors
Disorders of the Circulatory System
  1. Buerger’s disease or thromboangiitis obliterans
  2. Raynaud’s disease
Metabolic Disorders
  1. Diabetic neuropathy
  2. Alcoholic neuropathy
  3. Electrolyte imbalance in potassium, sodium, calcium
  4. Hypothyroidism
  5. Hypoparathyroidism
  6. Insulinoma
  7. Uremia
  8. Hyperaldosteronism
  9. Porphyria
  10. Hypoestrogenemia
Autoimmune Disorders
  1. Rheumatoid arthritis
  2. Systemic lupus erythematosus (SLE)
  3. Fibromyalgia
  4. Sjogren’s syndrome
  5. Polyarteritis nodosa
  6. Systemic sclerosis
  7. Autoimmune vasculitis
  1. Herpes simplex virus (HSV)
  2. Herpes zoster virus causing shingles
  3. Human immunodeficiency virus (HIV)
  4. Guillain-Barre syndrome (GBS)
  5. Lyme disease
  6. Leprosy
  7. Rabies
  8. Neurosyphilis
Other Causes of Paresthesia
  1. Trauma
  2. Acute idiopathic polyneuritis
  3. Chronic relapsing polyneuropathy
  4. Dental paresthesia
  5. Fabry disease
  6. Refsum syndrome
  7. Drug abuse especially opioids, pyridoxine
  8. HIV medications: Didanosine, Zalcitabine, Stavudine
  9. Heavy metal poisoning: Mercury, lead, arsenic
  10. Exposure to industrial toxins
  11. Carbon monoxide poisoning
  12. Nitrous oxide poisoning
  13. Snake bite
  14. Burns
  15. Frostbite
  16. Pink disease
  17. Tobacco smoking
  18. Ito syndrome
  19. Ciguatera (tropical fish) poisoning
  20. Paraneoplastic syndrome


Picture 1: The Nervous System and How it Works
Image Source: people.eku.edu

Sensations from different parts of the body are detected by receptors on the peripheral nerves. In the illustration above, we focus on the somatic nervous system under peripheral nervous system because it is type related to paresthesia.

The afferent nerves deliver the information to the spinal cord into the brain (mainly to the sensory cortex) through the brainstem and trigeminal nerve. This is now interpreted by the brain and delivers response towards the effectors, in this case, the skeletal muscle, through the spinal cord and efferent nerves. Any disruption in this sensory pathway may cause paresthesia [2, 4, 7].


Diagnosis of the underlying cause of paresthesia requires the patient’s detailed medical history, accurate physical and neurologic examination, and appropriate laboratory tests [8].
Physical examination for paresthesia primarily consists of testing sensations for pain, touch, vibration, temperature and joint position.

Stance and gait, which determine the presence of motor and cerebellar problems, are also included to correctly diagnose the cause of the paresthesia.

The examination begins at the center of the problem and proceeds radially until the sensation is perceived as normal. The root and peripheral nerve territories define the distribution of the abnormality [3].

Picture 2: Anterior Peripheral Nerves and Dermatomes
The left (colored) side of this picture shows the dermatomes and on the right are the corresponding peripheral nerves.
Image Source: www.mysijd.com

Picture 3: Posterior Peripheral Nerves and Dermatomes
The left (colored) side of this picture shows the dermatomes and on the right are the corresponding peripheral nerves.
Image Source: mysijd.com

Picture 4: Diagnosis of Common Nerve Root Lesions
Image Source: McKnight JT & Adcock BB. 

Picture 5: Diagnosis of Common Nerve Entrapment Syndrome
Image Source: McKnight JT & Adcock BB.

Laboratory tests indicated for the diagnosis of underlying cause of paresthesia may include the following [2, 9]:

  • Complete blood count (CBC)
  • Chemistry panel (Chem7)
  • Erythrocyte sedimentation rate (ESR)
  • Urinalysis
  • Thyroid stimulating hormone (TSH)
  • Radiograph of affected extremity
  • CT scan
  • MRI
  • Nerve conduction studies
  • Electromyogram (EMG)
  • Myelography
  • Vitamin B12
  • Serum folate
  • Antinuclear antibody (ANA)
  • Serology for syphilis (VDRL or RPR)
  • Nerve biopsy
  • Muscle biopsy
  • Serum immunoelectrophoresis


Cure for paresthesia lies on the treatment of its underlying cause. For transient paresthesia, massage and exercise of the affected extremity frequently relieves this symptom. For chronic paresthesia, the following treatment may be helpful [5, 10]:

  • Acupuncture and massage with aromatic oils or capsaicin are useful in relieving paresthesia.
  • Anti-inflammatory drugs like ibuprofen or aspirin are used for mild paresthesia.
  • Low dose antidepressants such as amitriptyline are used to alter the patient’s perception for paresthesia.
  • For severe paresthesia, opioids may be used as prescribed by the physician.
  • Human nerve growth factor is controversial for restoring damaged nerves.
  • Vitamin supplements are used if the cause of paresthesia is nutrient deficiency.
  • Avoid exposure to underlying causes like alcohol and tobacco.

  1. Merriam-Webster Dictionary. Available from: http://www.merriam-webster.com/dictionary/paresthesia
  2. McKnight JT & Adcock BB. Paresthesias: A Practical Diagnostic Approach. American Family Physician 1997 (Dec); 56 (9): 2253–2260
  3. Kasper DL, et. al. Harrison’s Principles of Internal Medicine 19th edition. McGraw-Hill Education. 2015.
  4. Alhoseini MS, Movaghar VR, Vaccaro AR. Underlying Causes of Paresthesia, Paresthesia, Dr. Luiz Eduardo Imbelloni (Ed). ISBN: 978-953-51-0085-0. InTech 2012. Available from: http://www.intechopen.com/books/paresthesia/underlying-causes-of-paresthesia
  5. Paresthesia: Causes, Symptoms, Diagnosis & Treatment. Available from: http://www.disabled-world.com/health/neurology/paresthesia.php
  6. Paresthesia Causes. Family Practice Notebook. Available from: http://www.fpnotebook.com/Neuro/Sensory/PrsthsCs.htm
  7. Neurons and the Nervous System Part 2. Available from: http://people.eku.edu/ritchisong/301notes2b.html
  8. NINDS Paresthesia Information Page. National Institute of Neurological Disorders and Stroke. Available from: http://www.ninds.nih.gov/disorders/paresthesia/paresthesia.htm
  9. Paresthesia. Family Practice Notebook. Available from: http://www.fpnotebook.com/neuro/Sensory/Prsths.htm
  10. Paresthesia. New Health Guide. Available from: http://www.newhealthguide.org/Paresthesia.html
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What is Hyperkalemia - Signs and Symptoms, Causes, ECG and Treatment

Defining Hyperkalemia

When the potassium levels in the blood are extremely high, one is said to have the hyperkalemia condition. When these levels exceed measure, one can easily die from abnormal heartbeats. The normal range of potassium in the blood lies between 3.5 to 5.5.mEq/L for adults.

Levels higher than these are likely to interfere with neurological and hemodynamic functions but in extreme cases, cardiac arrest. Even though potassium is a necessary nutrient, it should be consumed in proportions that will ensure it remains in the right measure [1,3,5].


Hyperkalemia Signs and Symptoms 

How do you know you are suffering from Hyperkalemia? Hyperkalemia does not present obvious symptoms and thus most patients are unaware that they have this condition until it is either too late or they are undergoing other tests of which potassium level is tested. However, like most other diseases, there are some tell-a-tale signs that could lead one into more testing [10]. These include
  • Dyspnea, this is the condition where the patient will have trouble breathing, mostly having short breaths even when not carrying out tasks. The patient may become breathless for apparently short walks or climbing stairs, a task previously completed effortlessly. 
  • Chest Pains There is a presence of increased pains along the thoracic region. 
  • Palpitations These are quick and irregular heartbeats usually forceful and are an indicator of something wrong in the body
  • Muscle Weakness Patients exhibit general lethargy claiming of muscle weaknesses and may be unable to carry out simple life tasks.
  • Nausea and vomiting, extreme nausea will be accompanied by vomiting even when those suffering have not had anything to eat, or eaten anything new. This will be prolonged and do not wane even with simple remedies
  • Parenthesis, this is tingling or prickly feeling as though one is being prickled with needles. There will also be a remarkable sensation that is abnormally sensitive usually caused by pressure to the peripheral nerves.


Pathophysiology of hyperkalemia

  • Presence of potassium in the electrolytes, which is part of our blood, plays a unique role in the formulation and circulation of body fluids. As indicated, the normal levels of potassium in adults are 3.5 to 5.5m/Eq/L. beyond 5.5 is referred to as hyperkalemia while below 3.5 is hypokalemia [4]. Both hyper or hypokalemia are life threatening
  • Potassium may be housed in the cells but also form a part of the intercellular fluid such as blood. Therefore, potassium’s presence is essential in that its total concentration determines if it will stick inside the cell or it is a free flow.
  • It also helps in maintaining the cell fluid volume.
  • Potassium is also an ingredient used in transmitting of communication links to the nerves.
  • Foods rich in potassium include tomatoes, meats and bananas, though best when ripe as well the orange fruit.
  • Regulation of this vital nutrient is through determined intakes, relative distribution between the cell region as well as extracellular. Excretion also forms an integral part in maintaining the right potassium volumes.
  • Elimination of excessive potassium is often through the kidneys, sweating as well as through the gastrointestinal tract. Aldosterone hormones are useful in the excreting processes.


Causes of Hyperkalemia

  • Some of the most common causes of genuine hyperkalemia (Sometimes hyperkalemia may be diagnosed due to potassium levels found in a blood sample. The cause of the heightened levels may be caused by the broken cells when piercing is to get the blood sample and thus not truly right. Hyperkalemia should be in conjunction with other related signs and symptoms) is kidney ailments;
  1. Chronic kidney disease
  2. Kidney failure
  • Alcoholism
  • Excessive drugs use
  • Injuries that cause destruction of the red blood cells
  • Body burns that causes acute cell-tissue damages
  • Type 1 diabetes
  • Acidosis
  • Adrenal failure
  • Angiotensin, (a protein when in the blood stream raises the pressure and also advances aldosterone secretion) imbalances


Determining if one has hyperkalemia

Since it is difficult to tell obvious signs of Hyperkalemia, one should therefore request for a check-up if they suspect its presence. Thankfully, potassium level in the blood stream is one of the components of most blood related checkups. This will most likely attract a medical intervention should their levels be elevated beyond normal ranges.

It is however important to note that potassium levels checkups are done repeatedly as homeostasis can present the wrong indications. This is because of the rapturing of the blood cells during the actual drawing of the blood sample. This is referred to as pseudo hyperkalemia. However, other methods of determining hyperkalemia are

Hyperkalemia ECG (EKG)

  • Electrocardiography or ECG, the results of a patient suffering from hyperkalemia will have
  1. Elevated or tall T Waves
  2. QT interval is short.
  3. The PR interval will however be lengthened,
  4. Loss in P waves
  5. Widened QRS will culminate in morphology that takes a sine wave and left unattended, leads to death.

For patients with highly elevated potassium quantities, this brings about palpitations or other cardiac complications that result in fatality. Generally, potassium acts as the general regulator of electrical activities in the heart.

A peaked T wave is one of the obvious elements of the presence of hyperkalemia. However, this alone does not present the severity of the disease and other further examinations are required [9].
  • Medical examinations that may include doctor’s determination of historical occurrences of hyperkalemia related symptoms.
  • Laboratory Investigations, this will include;
  1. Kidney functions checks, 
  2. Urinary tract infections,
  3. Cardiac functions, 
  4. Level amounts of hydration.
  5. Blood Urea Nitrogen as well as Creatinine levels so as to determine the renal status
  6. If there is determined renal failure, confirm the calcium levels
  7. If on digitalis medication, confirm the digoxin levels
  8. Where acidosis is suspected, checks for arterial or any venous blood gas
  9. Where all other above is eliminated, confirm the Cortisol and aldosterone levels


Treatment for Hyperkalemia

Treating hyperkalemia is dependent on the most aggressive symptoms as well as the patient’s present condition and level of tolerance.
  • Elimination of potassium; excretion of urinary potassium is usually impaired by either Chronic Kidney Disease (CKD) or any drugs of disorders that impede renin angiotensin aldosterone axis. At such times, elimination of potassium involves reducing potassium out of the cells even though this may hamper even the necessary potassium levels in the body. This is especially when there is uncontrolled hyperglycemia. The insulin deficiency in this case is the primary determinant in potassium trans-cellular shifting. The potassium moves from the cells to the extracellular fluid [6,7].
  • For such conditions, administration of insulin and fluids reverses the movement of potassium to the extracellular fluids. This process should however be closely monitored to prevent reducing the potassium levels to a point of causing hypokalemia, which is the too much lowering of useful potassium.
  • Administration of Albuterol Sulfate, 0.5mg in chronic renal failure patients is necessary for lowering the potassium. Elimination may be through cation or diuretics for those who have no cardio related complexities or those with no renal complications. Those with renal conditions either about to undergo dialysis or transplanting are better administered orally.
  • Correcting the abnormality in potassium levels, this is done by finding out the cause of the potassium increase and managing it.
  • Calcium is also recommended for enhance and regulate the cardiac toxicity. Administration of calcium is better intravenously.
  • Sodium Bicarbonate is used to correct severe metabolic acidosis, a condition where there is elevated acid content in the body fluids and tissue.
  • Surgery is recommended only on certain cases and as a last result. This is often endorsed for;
    1. Severe acidosis
    2. Rhabdomyolysis hyperkalemia, where the ischemic muscles are swollen
    3. Patients who will need Hemodialysis and are not at the last stages of renal failure


      Prevention of Hyperkalemia 

      Hyperkalemia is largely preventable through [7]
      • Reducing the potassium in your diet or
      • Reducing any medication that may be causing the rise of the potassium levels.
      • Engaging the use of a regular mild diuretic such as furosemide; for the maintenance of ideal levels of potassium.
      1. Pergola PE, DeFronzo R. Clinical disorders of hyperkalemia. In: The Kidney: Physiology and Pathophysiology, Seldin DW, Giebisch G (Eds), Lippincott Williams & Wilkins, 2000. Vol 2, p.1647.
      2. Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869.
      3. Goldfarb S, Strunk B, Singer I, Goldberg M. Paradoxical glucose-induced hyperkalemia. Combined aldosterone-insulin deficiency. Am J Med 1975; 59:744.
      4. Blumberg A, Weidmann P, Shaw S, Gnädinger M. Effect of various therapeutic approaches on plasma potassium and major regulating factors in terminal renal failure. Am J Med 1988; 85:507.
      5. Ettinger, P O, T J Regan, and H A Oldewurtel. 1974. Hyperkalemia, cardiac conduction, and the electrocardiogram: a review. American heart journal, no. 3.http://www.ncbi.nlm.nih.gov/pubmed/4604546.
      6. Weisberg, Lawrence S. 2008. Management of severe hyperkalemia. Critical care medicine, no. 12. doi:10.1097/CCM.0b013e31818f222b.http://www.ncbi.nlm.nih.gov/pubmed/18936701.
      7. Wrenn, K D, C M Slovis, and B S Slovis. 1991. The ability of physicians to predict hyperkalemia from the ECG. Annals of emergency medicine, no. 11.http://www.ncbi.nlm.nih.gov/pubmed/1952310.
      8. Webster A, Brady W, Morris F. Recognising signs of danger: EKG changes resulting from an abnormal serum potassium concentration. Emerg Med J. 2002 Jan 19;19(1):74–7. DOI:http://dx.doi.org/10.1136/emj.19.1.74. [PMC free article] [PubMed]
      9. Diercks DB, Shumaik GM, Harrigan RA, Brady WJ, Chan TC. Electrocardiographic manifestations: electrolyte abnormalities. J Emerg Med. 2004 Aug;27(2):153–60. DOI:http://dx.doi.org/10.1016/j.jemermed.2004.04.006. [PubMed]
      10. Hampton, JR. The ECG in Practice (5th edition), Churchill Livingstone 2008.
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      Hypernatremia - Definition, Symptoms, Causes, Correction and Treatment

      What is Hypernatremia?

      Medical dictionary defines hypernatremia (pronounced: [hahy-per-nuh-tree-mee-uh]) as “a pathological abnormally in which there is high concentration of sodium in the blood” (usually above the value of 145 mmol/L) [1]. Severe cases may register blood sodium values as high as 152mmol/L.

      On the other hand, serum sodium values slightly lower than 145mmol/L constitute mild hypernatremia. While an increase in blood sodium is a sign of hypernatremia, it is, however, as a result of excessive loss of fluids or water in the body. When there is a decline in water level in the blood, a concentration gradient is induced which forces sodium ions to migrate from the body cells into the blood plasma through the process of osmosis.


      Hypernatremia is a common incidence among the elderly, infants and mentally or physically disabled persons since they cannot physically get water on their own whenever they feel thirsty.

      ICD 9 code for hypernatremia is: 276.1 [2]

      Causes of Hypernatremia

      Causes of hypernatremia are typically categorized according to each type.

      Common causes of hypernatremia include:


      This is a false indication of high sodium levels in the blood. It occurs when there is low plasma protein due to an exclusion effect on blood electrolytes thus portraying a rise in sodium in the blood.

      Hypovolemic causes 

      Hypovolemia or hypovolemic shock is a condition that entails decrease in the volume of blood plasma due to prolonged dehydration. Most cases of hypovolemia are due to limited access to regular water intake or excessive loss of fluids from the body. The list below details some of hypovolemic causes of hypernatremia.
      • Severe losses of water via urine: this is due to certain urinary tract disorders like osmotic diuresis which leads to increased urination. Presence of substances like mannitol or isosorbide in the kidney causes impaired reabsorption of water and sodium.
      • Excessive loss of water due to prolonged diarrhea. This is common among the elderly and infants. Water is lost directly through watery stool.
      • Prolonged sweating or perspiration: if a person is exposed to unfavorable weather conditions e.g. dry and hot environment, they will eventually lose a lot of water via sweating causing hypernatremia. Sweat not only leads to direct loss of body water but also important solutes like potassium.
      • Kidney diseases: many kidney diseases like Nephrotic syndrome induce excessive loss of plasma protein into urine due to impaired renal permeability. This may also be depicted by extensive edema in the body.
      • Liver diseases: liver ailments specifically liver cirrhosis lead to impaired loss of free water causing hypernatremia.
      • Heart congestion may also lead to excessive loss of free water
      • Vomiting 

      Euvolemic causes

      As opposed to hypovolemia, euvolemia is a biological condition in which there is a decrease in total body water without an associated decrease in sodium levels (i.e. sodium level remain relatively constant while there is a drop in free water in the body). Such a condition may be cause by one or more of the following:
      • Sweating
      • Nephrogenic diabetes insipidus due to either limited production of vasopressin or slow response to hormone vasopressin
      • Urinary tract water losses

                                              Figure : Illustration of Causes of Hypernatremia

      Other causes 

      • Excessive ingestion of hypertonic fluids such as sea water, resuscitation fluids etc may cause hypervolemic hypernatremia. Such fluids creates unfavorable concentration gradient relative to blood plasma which causes massive loss of free water
      • Potomania: also known as beer drinker’s hyponatremia; a condition caused by excessive beer consumption. Beer is deficient of important electrolytes and solutes like potassium, sodium etc which aids the kidney in reabsorption of water. Severe cases of potomania may lead to massive dehydration.
      • Excessive salt ingestion: this is common infants and may lead to what is called “salt poisoning”. High concentration of salt impairs water intake leading to hypernatremia.
      • Intake of certain steroids/hormones e.g. cortisol, impair electrolyte balances in the body causing impaired absorption of water into blood plasma.
      • Extensive burns on the body leads to direct water loss via damaged tissue and blood vessels.
      • Polydipsia in which the amount electrolytes required to get rid of excess water via urine exceeds what the body can produce. [3,4,5]

      Symptoms of Hypernatremia

      Hypernatremia is portrayed by effects of excessive loss of water or rather lack of adequate intake of water. Some of the symptoms of hypernatremia are listed below.
      • Thirst
      • Edema
      • Sometimes seizures indicate a case of hypernatremia
      • Vomiting: this is signifies eventual loss of total body water.
      • Migraines and headache: excessive amount of sodium in blood causes swellings which in turn agitates brain cells causing mild to severe headaches or migraines
      • Loss of appetite: this is common among the aging group. Acute loss of water (dehydration) causes massive thirst which makes one sad leading to loss of appetite.
      • Confusion: Inadequate free water in the blood impairs normal brain function making one disoriented and unable to think or reason well. Brain cells require both sodium and water to function normally.
      • Fatigue: this is experience because muscles cannot function well without water. Since water is an essential input into metabolic process, a dehydrated people tend to exhibit signs of tiredness [3,4,5]


      Diagnosis of Hypernatremia

      As rule of thumb, a physician must start the diagnosis by establishing patient’s medical history for any past case of hypernatremia or related disorders. Since a rise of blood sodium (above 145mM) is a clear indicator of hypernatremia, it is necessary to obtain a laboratory workup of the following:
      • Blood levels of important electrolytes like sodium, potassium or calcium ions
      • Blood glucose level to establish hypernatremia causes like glycosurina
      • Urea for electrolyte or metabolic agents
      • Urinalysis for any defective hormones and levels of electrolytes/water. Also to get hour-to-hour urine volumes
      • Osmolality of both urine and blood plasma
      • Water deprivation test can be carried out for patients suspected to have diabetes insipidus to establish both renal/pituitary responses.

      Hypernatremia Calculation and Correction

      The following formulas are used to calculate the degree and extend of hypernatremia in a patient: [4]

      The calculated change in serum sodium is used to gauge if a patient has hypernatremia or not.

      The desired sodium in a human body is about 120 meq/L and the insensible water loss should be between 500 and 1500 cc per day.


      Treatment of Hypernatremia 

      General treatment of hypernatremia require cautious uptake of water into the body with an associated decrement in serum sodium. The rate at which hypernatremia can be corrected depends partially on age and weight of the patient, extend of dehydration, and the nature of the cause itself. If hypernatremia is rectified too quickly it may cause seizures or brain damage (edema) which can lead to an eventual death.

      Figure 2: Management of Hypernatremia (Approach and Algorithm)

      The list below details some of the corrections recommended for treatment of hypernatremia:

      • Oral intake of water: this is the case for patients with small water deficit
      • Use of hypotonic fluid: a patient should receive a hypotonic fluid that is lower in the concentration of electrolytes. This method would correct impaired removal of sodium in the kidneys. The fluid administered should be hypotonic to the urine.
      • Administration of insulin: This is used if the primary cause of hypernatremia is diabetes insipidus. Insulin would allow proper production of hormone vasopressin. Therefore, the body can respond timely to vasopressin normalizing sodium/potassium excretion and intake of free water into the body. In addition, any drugs which may cause worsening of diabetes insipidus should be discounted if possible. Such drugs include those that have lithium in them.
      • Dialysis: this may be required to correct such causes of hypernatremia as heart failure and edema (pulmonary).
      • IV therapy: if water deficit very large, a patient may need to have water and other important electrolytes administered through intravenous methods. IV therapy involves two phases: emergency phase and rehydration phase.
      • Emergency phase entails use of a neutral (isotonic) fluid to replenish blood plasma volume. Fluids such as Ringer solutions which contain sodium and other electrolytes can be used as the replenishment fluid. Amount and concentration of the fluid depends on the age and weight of the patient.
      • In the rehydration phases, a hypotonic fluid is used. Such a solution normally contains some dextrose sugar, normal salinity and around 31mM of sodium. In this phase, the body is supposed to replenish its blood free water supply by creating an electrolyte concentration gradient that favor uptake of water into the blood plasma [3,4 and5]
      1. Dictionary.com. the definition of hypernatremia [Internet]. 2015 [cited 14 December 2015]. Available from: http://dictionary.reference.com/browse/hypernatremia
      2. Icd9data.com. 2012 ICD-9-CM Diagnosis Code 276.0 : Hyperosmolality and/or hypernatremia [Internet]. 2015 [cited 14 December 2015]. Available from: http://www.icd9data.com/2012/Volume1/240-279/270-279/276/276.0.htm
      3. Wikipedia. Hypernatremia [Internet]. 2015 [cited 14 December 2015]. Available from: https://en.wikipedia.org/wiki/Hypernatremia
      4. Steve D. Hypernatremia - Symptoms, Causes, Correction, Calculator, Algorithm, Treatment [Internet]. Howshealth.com. 2015 [cited 14 December 2015]. Available from: http://howshealth.com/hypernatremia/
      5. Schwaderer A, Schwartz G. Treating Hypernatremic Dehydration. Pediatrics in Review. 2005;26(4):148-150.
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