Monday 21 May 2007

Week 12 (PCL 10) Hoping For The Best

Definition:
Hyponaturemia

Hyponatremia is defined as a serum level of less than 135 mmol/L and is considered severe when the serum level is below 125 mEq/L. (The normal serum sodium level is 135-145 mmol/L)

From emedicine (Hyponatremia, Author: Eric E Simon, MD)

13 comments:

Anonymous said...

SIGNS AND SYMPTOMS OF HYPONATRAEMIA

Salt-Deficient Hyponatraemia: clinical picture is usually similar to volume depletion:

Symptoms: thirst, muscle cramps, nausea, vomiting, postural dizziness.
If severe: hypotension, confusion, eventual coma.

Signs:
Loss of interstitial fluid: decreased skin elasticity
Loss of circulating volume: postural hypotension, low jugular venous pressure, tachycardia, peripheral venoconstriction (cold, clammy skin)
Losses due to renal/adrenocortical disease are suggested by a urinary sodium concentration of more than 20mmol/L in the presence of clinically evident volume depletion.
Losses as high as 50mmol/L of sodium and 2500mL total fluid loss from the stomach alone may be occurring.

Dilutional Hyponatraemia: due to water excess

Symptoms are principally neurological due to water movement into brain cells (hyponatraemic encephalopathy).

EG. Headache, confusion, restlessness, drowsiness, myoclonic jerks, generalised convulsions and eventually coma.

Source: Kumar and Clark
Ang.

Anonymous said...

Management of Hyponatraemia

• Treatment of hyponatraemia depends on the type, cause and severity.
• Obviously we treat the underlying cause if possible.

Mild Hyponatraemia
• If the patient is normovolaemic, asymptomatic or the hyponatraemia is mild, fluid restriction should be sufficient.
- Usually <1L/day
- Demeclocycline (an ADH antagonist) may also be given to aid diuresis
• If the patient is hypovolaemic, isotonic saline (0.9% NaCl) is infused to replace the lost fluid volume
- If they hypovolaemia is secondary to diuretic use, potassium may also need to be given

Severe Acute Hyponatraemia
• The patient is at risk of cerebral oedema, and must be treated urgently
• Treatment is as above

Severe Chronic Hyponatraemia
• This is more difficult to treat as there has been adaptation
• Sudden reversal of hyponatraemia is more dangerous than the hyponatraemia itself
- May cause osmotic demyelination
• The plasma sodium level is brought up only to about 120mEq/L, rather than the normal range. This limits the change in sodium required, while still bringing the patient to a safe level.
• The rate of correction should not exceed 1mEd/L/h, and the maximum amount of correction is 12mEq/l/day
• Either hypertonic saline (3% NaCl) or isotonic saline plus a diuretic is used
• The serum electrolytes should be measured every 2 hours to avoid overcorrection
• Also monitor for neurological symptoms

Severe Hyponatraemia, unknown timescale
• Assume that it is chronic, and treat accordingly

References
E. Simon, Hyponatremia, eMedicine 4th May 2007

Anonymous said...

Hey guys,

Here's the part I said I would do last Friday. Sorry if it's really confusing, especially the part on Diabetic Nephropathy.

Regards
Pat

------------------------------
Causes of Glomerular Diseases

Causes of glomerulopathy (i.e. glomerular disease of any type) can be

(i) immune mediated

(ii) hemodynamic

(iii) metabolic

(iv) hereditary

Nephritic syndrome is: the clinical symptoms of acute glomerulonephritis

Glomerulonephritis is: Renal disease characterized by inflammatory changes in glomeruli that are not the result of infection of the kidneys. Syn: glomerular nephritis

Glomerulonephritis is always (i) immune-mediated (read:inflammatory changes). May be after an infection somewhere else in the body (not kidney infection itself) or Autoimmune.

Nephrotic syndrome has a much more complicated definition. Basically: the cause is congenital or degenerative - symptoms are caused by increased permeability of glomerular basement membrane. Aetiology may be unknown, congenital, secondary to Glomerulonephritis, Amyloidosis or Diabetes, due to exposure to toxic agents or have autoimmune or viral causes such as SLE or Hep C. There are many conditions that are mixed nephrotic/nephritic.
------------------------------

------------------------------
Diabetic Nephropathy has both (ii) haemodynamic and (iii) metabolic causes.

Important haemodynamic changes are hyperfiltration and hyperperfusion. Different factors are known to influence this including prostanoids, nitrogen oxide (NO), atrial natriuretic factor, growth hormone, glucagon, insulin and angiotensin II (AngII). Basically, the key mechanisms are

a) The Renin-Angiotensin-Aldosterone System (RAAS)

High glucose stimulates production of AngII directly or via the macula-densa mechanism. Ang II exerts haemodynamic, trophic, inflammatory and profibrogenic effects on renal cells.

b) Oxidative Stress

Increased uptake of glucose into cells leads to stimulated mitochondrial Reactive Oxygen Species (ROS) which leads to oxidative stress. Oxidative stress activates different pathways including stimulation of AngII synthesis.

Wolf G. New insights into the pathophysiology of diabetic nephropathy: from haemodynamics to molecular pathology. Eur J Clin Invest. 2004 Dec;34(12):785-96. PMID: 15606719
------------------------------

Elliot said...

Investigations
If low sodium concentration is found, must determine if it is true hypoosmolar hyponatraemia or pseudohyponatraemia.

Consider the following causes of a pseudohyponatraemia:
• Serum hyperglycaemia
o Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space
o Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia
o This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is re-established
• A similar phenomenon to above is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing
• Hyperlipidemia or hyperproteinemia

Serum sodium concentration and osmolarity
• Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia
Urine sodium concentration and osmolarity
• Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from non-renal causes
o Non-renal cause: urine sodium levels < 20 mEq/L (milliequivalents of solute per litre of solvent)
o Renal causes: urine sodium levels > 20 mEq/L

Investigations required to:
• Exclude liver disease – liver function test
• Exclude Addison’s disease – adrenal function test - random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test
• Exclude hypothyroidism – thyroid function test - Serum thyroid-stimulating hormone (TSH)
• Consider SIADH (syndrome of inappropriate ADH secretion) – urine osmolarity - indicates SIADH if > 100 mOsm/L

Imaging studies to rule to determine or rule out possible causes of the hyponatraemia symptoms . For example, a head CT scan in patients with altered mental state to ensure no other underlying cause is present.

Important Terms
Osmoles – number of impermeable particles dissolved in a solution regardless of charge. 1 osmole = 1 mole of solute particles.
Osmolarity (osmoles/litre) – A simple count of the number of dissolved particles or total solute concentration in a fluid compartment that can measure the effective gradient for water assuming that all osmotic solute is completely impermeable.
Osmolality (osmoles/kg) – same concept as osmolarity but different units: osmoles/kg
Tonicity – the combined ability of solutes to produce and osmotic pressure that causes water to move from one compartment to another. It is a functional term to describe the tendency of a solution to resist expansion of the intracellular volume – the ability of a solution to alter the fluid volume within a cell.
Hypertonic – a solution with a higher concentration of impermeant solutes than the ICF causing water to move out of the cell.
Hypotonic – a solution with a lower concentration of impermeant solutes than the ICF causing water to move into the cell.
Isotonic – a solution with the same concentration of impermeant solutes as the ICF causing no movement of water. Dextrose and saline are isotonic.

Elliot said...

Forgot to add:
References:
http://www.emedicine.com/emerg/topic275.htm
http://www.clinicalanswers.nhs.uk/index.cfm?question=269
Kumar and Clark
http://physioweb.med.uvm.edu/bodyfluids/calculat.htm

Anonymous said...

CAUSES AND PATHOPHYSIOLOGY OF HYPONATREMIA:

Antidiuretic Hormone: ADH is produced in the hypothalamus and secreted down the posterior pituitary gland. It is secreted in response to an increase in blood osmolarity, most commonly with dehydration. When dehydrated, sodium plasma concentration levels are increased because not as much water is in the system to 'dilute' the sodium levels, increasing blood osmolarity.
Antidiuretic hormone acts on the renal distal tubule. It induces the renal tubule cells to synthesize aquaporines (water-channel proteins) and install them in the plasma membrane, so more water can pass through the epithelial cells. The collecting duct then reabsorbs more water, which is carried away by the peritubular capillaries. Urine output is consequently reduced and more concentrated.

Causes of Hyponatremia:

Most cases of hyponatremia are associated with reduced plasma osmolarity.


1. Hypovolemic hyponatremia

Gut: vomiting, diarrhoea, haemorrhage
Kidney: excessive use of diuretics, adrenocortical insufficiency, tubulo- interstitial renal disease, unilateral renal artery stenosis, recovery phase of acute tubular necrosis

In this situation, ADH secretion is initially suppressed via the hypothalamic osmoreceptors. However, as fluid volume further declines, the volume receptors override the osmoreceptors and therefore stimulate thirst and the release of ADH.

2. Hyponatremia due to excess water intake

This results from an intake of water in excess of the kidney's ability to excrete it. The most common cause of this is overgenerous infusion of 5% glucose.
To prevent this kind of hyponatremia, avoid using hypotonic fluids and instead administer isotonic saline.

3. Hyponatremia in patients with a normal blood volume

Decreased Na+ concentration in the blood may be due to "physiological" releases of ADH such as pain or nausea.
This may also be due to a side effect of certain medications, lung problems such as pneumonia or abscess, brain disease or certain cancers (lung carcinoma). These things may cause a sustained, non-physiological release of ADH.


3. Hypervolemic Hyponatremia
These patients are identified by the presence of oedema. However, the term 'hypervolemia' is actually misleading. The oedema represents the fact that fluid has left the circulation, stimulating ADH release and causing water to be excessively retained. This can be caused by problems such as heart failure or liver cirrhosis.

4. Hyponatremia can result from a dysfunctional decrease in aldosterone production. Aldosterone is responsible for Sodium reabsorption, with water passively following. If there is a decrease in aldosterone production, then blood volume is compromised. Therefore, to maintain adequate blood-volume levels, there is an increase in ADH production. However, since ADH doesn't promote Na+ reabsorption, there plasma Na+ is diluted by the reabsorbed water, resulting in a decreased plasma Na+ concentration.

5. Diuretic use, such as frusemide (a thiazide acting on the distal tubule) can cause the patient to become volume depleted. If severely volume depleted and then immediately taken off their medication, ADH will be immediately stimulated in these patients. This in turn will increase water reabsorption to increase blood-volume, thereby decreasing Na+ plasma concentration.

6. Ecstasy use (Methylenedioxymethamphetamine) has been attributed to many deaths. Along with dehydration at parties, ecstasy can promote the release of ADH. People over-consuming water, along with an increase in water retention, can both result in a decrease in sodium concentration in the body.
7. Pseudohyponatremia
This describes a normal or high plasma osmolarity and may occur if extraordinarily high plasma lipid or protein levels interfere with the sodium assay.

References: Saladin: Antidiuretic Hormone
Kumar and Clark: Hyponatremia

-->BY KATIE

(& JESS - to do presentation in PCL)

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