Editing Sodium

== '''Summary:''' ==

* Acute hyponatraemia post-op in general surgical patients would mostly be extra-renal fluid losses (hypovolaemic), SIADH/physiological stress (euvolaemic) or renal/liver/heart failure (hypervolaemic)
** Sodium 126-130: monitor daily electrolytes and review medications if chronic.
** Sodium 120-125: send urine and serum osmolality and sodium levels, and fluid restrict to 500mL less than daily urine output. Identify cause.
** Sodium <120 '''or''' any symptoms: refer ICU for consideration of monitoring and hypertonic saline.
* Acute hypernatraemia in surgical patients is usually due to dehydration from loss of hypotonic body fluids
** Sodium 145-150: volume resuscitate with crystalloid and PO water; identify and fix fluid loss
** Sodium >150: review aetiology, consider medical referral

== '''Pathophysiology''' ==

* The underlying problem is a change in cell volume, but it presents as a change in the plasma sodium concentration (hypernatraemia or hyponatraemia)
* They should be approached in terms of a single variable: the extracellular volume (which consists of both extravascular (interstitial) fluid and intravascular (plasma) fluid compartments).
** Note that plasma volume is about 25% of interstitial fluid volume
** '''Sodium itself equilibrates through both interstitial fluid and plasma'''
** 75% of infused saline solutions will distribute in the interstitial fluid, and 25% in plasma
*
* '''Osmotic activity'''
** The property that determines movement of water between fluid compartments, and is a reflection of the number of solute particles per unit volume of solvent. Osmotic activity depends only on the NUMBER of solute particles in a fluid, and not the electrical charge/size/chemical behaviour of solutes.
** The unit of measurement for osmotic activity is the osmole (osm), which is defined as one gram molecular weight (one mole) of a non-dissociable substance, and is equivalent to Avogadro's number. It can be expressed in two different ways:
*** Osmotic activity per volume of solution - ''osmolarity'' mOsm/L
*** Osmotic activity per volume of water - ''osmolality'' mOsm/kg H2O
** Plasma is mostly (93%) water, so the osmotic activity of plasma solutes is typically expressed as osmolality. For ECF in general, either osmolality or osmolarity can be used, as they will be almost identical (unless a toxin has accumulated to increase the 'osmolal gap', which is the difference between measured and calculated osmolality).
*** Plasma osmolality can be either calculated or measured. Note that sodium accounts for 98% of effective osmotic activity of ECF - '''sodium concentration in ECF is the principal determinant of the distribution of total body water in the intracellular and extracellular fluid compartments.'''
****

*
* 'Effective plasma osmolality' will be almost identical to 'total plasma osmolality', and you can just omit the urea
*

* Water and solutes will rearrange themselves between fluid compartments to reach equilibrium: osmotic activity, based on ''osmotic pressure''. The fluid with the higher osmotic activity is called hypertonic, and the fluid with the lower osmotic activity is called hypotonic.
*

* Impact of osmotic activity
** A change in the relative osmotic activity of ECF produces a transcellular water shift
** When the ECF is hypertonic, water moves out of cells
** When the ECF is hypotonic, water moves into cells
* Anti-diuretic hormone (ADH)
** Released by the posterior pituitary in response to an increase in the osmolality of ECF, promoting water reabsorption in the distal renal tubules
** Normally suppressed at plasma sodium < 135
** Also released in response to non-osmotic factors - hypotension (via baroreceptors), physiological stress (along with ACTH release from anterior pituitary)
** '''SIADH''' occurs when these non-osmotic release triggers persist despite a sodium level < 135, and is an important factor in the development of severe and sustained hyponatraemia. The hallmarks are euvolaemia, hypotonic plasma, inappropriately concentrated urine (urine osmolality >100mosm/kg H2O), and a high urine sodium level.

== '''Hypernatraemia''' ==

* '''Definition'''
** Plasma sodium concentration >145mEq/L
* '''Aetiology''' (see algorithm below)
** '''Loss of sodium and water, with water loss > sodium loss (hypotonic fluid loss)'''
*** The most common cause of community-acquired hypernatraemia
*** Pretty much any body fluid loss is hypotonic, and will lead to hypernatraemia if lost excessively and not replaced
*** This should normally be managed by thirst response, so if this has not taken place it is an indicator of significant pathology
*** Plasma volume is often maintained due to colloid osmotic pressure drawing fluid from interstitial compartment into plasma
***
** '''Free water loss'''
*** Common in ICU patients with hypernatraemia, and usually occurs when sodium losses are replaced, leaving a net free water deficit
*** Diabetes insipidus - loss of urine that is largely devoid of solute
**** Central DI (failure of ADH release from posterior pituitary) - traumatic brain injury, anoxic encephalopathy, meningitis, brain death.
**** Nephrogenic DI (impaired end-organ responsiveness to ADH) - amphotericin, aminoglycosides, radiocontrast dyes, dopamine, lithium, hypokalaemia, and the recovery (polyuric) phase of ATN. Usually less severe than central DI.
**** The hallmark is dilute urine in the face of hypertonic plasma. <200mosm/L in central DI and 200-500mosm/L in nephrogenic DI. Failure of the urine osmolarity to increase in the first few hours of fluid restriction is diagnostic of DI.
**** Response to vasopressin will differentiate central from nephrogenic DI.
** '''Gain of sodium and free water, with sodium gain > free water gain (gain of hypertonic fluid)'''
*** Uncommon, usually the result of sodium bicarbonate infusions for metabolic acidosis, or aggressive use of hypertonic saline to treat increased ICP
*** Excessive ingestion of table salt in patients with psychiatric disorders
* '''Consequences'''
** Hypertonicity moves fluid out of cells, which is most evident in the CNS
** Hypernatraemic encephalopathy - ranges from agitation and lethargy to coma and seizures
* '''Approach'''
**
* '''Hypovolaemic hypernatraemia'''
** Correct the two consequences of hypotonic fluid loss:
**# ''Sodium has been lost'', which reduces ECV -> volume resuscitation with isotonic saline if any evidence of low-flow state. Does not usually lead to hypovolaemic shock.
**# ''Free water deficit'' (water has been lost in excess of sodium) -> correct with some sort of water or hypotonic fluid slowly. Aim to replace about half the free water deficit in the first 12-24 hours. There are some complicated calculators for ICU to play with.
* '''Hypernatraemia without hypovolaemia'''
** DI - replace free water deficits and correct sodium slowly
** Vasopressin is required in central DI to prevent ongoing free water losses.
* '''Hypertonic hypernatraemia'''
** Excess sodium and water are excreted rapidly if renal function is normal
** If renal function is impaired, diuretics may be necessary

== '''Hyponatraemia''' ==

* '''Definition'''
** Plasma sodium concentration < 135mEq/L
** Typically a hypotonic condition, but there are instances of isotonic hyponatraemia and hypertonic hyponatraemia
* '''Aetiology'''
** '''Isotonic'''
*** Pseudohyponatraemia - difference between the measured and actual concentration of sodium. Marked increases in plasma lipids or proteins. Needs to have lipids >1500mg/dL or protein > 12-15 g/dL.
** '''Hypotonic''' 
*** '''Hypovolaemic hyponatraemia - s'''odium loss with excess free water retention.
**** Sodium loss decreases ECV, which triggers baroreceptor-mediated ADH release, and excess free water retention then decreases the extracellular sodium concentration
**** Free water intake worsens the problem
**** Causes:
***** Renal loss - thiazide diuretics, cerebral salt wasting (TBI, neurosurgery, subarachnoid haemorrhage), primary adrenal insufficiency
***** Extra-renal loss - GIT losses
**** The source of sodium loss is usually apparent, but can be elicited with urine sodium concentration
*** '''Euvolaemic hyponatraemia''' - excess water intake or excess water retention from non-osmotic ADH release.
**** ADH-related - SIADH (see above under pathophysiology), physiological stress (post-op patients), severe hypothyroidism
**** SIADH - CNS disturbance, malignancies especially SCLC, drugs (see list at bottom of page), surgery, pulmonary disease, hormone deficiencies or administration, HIV infection, or hereditary SIADH
**** Not ADH-related - primary polydipsia in schizophrenics
**** Differentiate between the two groups with urine osmolality
*** '''Hypervolaemic hyponatraemia''' - sodium and water retention, with water retention exceeding sodium retention.
**** Cirrhosis, heart failure, renal failure (eGFR <15)
**** Differentiate with urine osmolality, but diuretic therapy can increase the osmolality of urine
** '''Hypertonic'''
* '''Clinical features'''
** Severe hypotonic hyponatraemia causes a life-threatening encephalopathy - cerebral oedema, increased ICP, risk of brain herniation. Symptoms start as headache, nausea and vomiting, and confusion, and finish with seizures, coma and death. Much higher risk with <48 hour course of acute hyponatraemia'''.'''
** '''Symptomatic hyponatraemia usually occurs with a sodium of <120'''
* '''Approach'''
**
**
** '''Low ECV'''
*** Isotonic saline to restore euvolaemia
*** If symptomatic, hypertonic saline could be used
** '''Normal ECV'''
*** Furosemide could be used in symptomatic hyponatraemia if there is a concern for fluid overload, like in patients with heart failure, could give 20-40mg IV
*** If fluid restriction is intolerable or ineffective, consider drug therapies
** '''High ECV'''
*** ICU-level decision
*** Hypertonic saline could be used for severely symptomatic patients
*** Otherwise, fluid restrict and furosemide diurese
* '''Infusion rate'''
** Infusion rate of hypertonic saline = body weight * desired rate of increase in sodium
** This gives the infusion rate in mL/hr of 3% hypertonic saline.
** Needs to be corrected at a similar rate to that which it developed to avoid cerebral fluid shifts and osmotic demyelinating syndrome (central pontine myelinolysis) - dysarthria, quadriparesis, and loss of consciousness. 
*** For chronic - raise sodium by 0.5 per hour, and stop rapid correction when you get to 120
*** For acute - raise sodium by 4-6 in the first 1-2 hours, and stop rapid correction when you get to 120
** 3% saline can be safely administered in a peripheral vein according to UTD. If central access is needed, establishing it shouldn't delay starting therapy.
* '''Pharmacotherapy'''
** Vasopressin antagonists - vaptans - alternative to fluid restriction in patients with euvolaemic or hypervolaemic hyponatraemia, except renal failure
** Demelocycline - tetracycline derivative that blocks ADH in renal tubules


'''Non-ketotic hyperglycaemia (Hyperosomlar Hyperglycaemic State - HHS)'''

* See separate topic under 'peri-op diabetes'


Drugs causing SIADH:
{| class="wikitable"
|'''Antidepressants'''
|-
|SSRIs
|-
|Tricyclic
|-
|MAOI
|-
|Venlafaxine
|-
|'''Antiseizure medications'''
|-
|Carbamazepine
|-
|Sodium valproate
|-
|Lamotrigine
|-
|'''Antipsychotics'''
|-
|Phenothiazines
|-
|Butyrophenones
|-
|'''Anticancer drugs'''
|-
|Vinca alkaloids
|-
|Platinum compounds
|-
|Ifosfamide
|-
|Melphalan
|-
|Cyclophosphamide
|-
|Methotrexate
|-
|Pentostatin
|-
|'''Antidiabetic drugs'''
|-
|Chlorpropamide
|-
|Tolbutamide
|-
|'''Vasopressin analogues'''
|-
|Desmopressin
|-
|Oxytocin
|-
|Terlipressin
|-
|Vasopressin
|-
|'''Miscellaneous'''
|-
|Opiates
|-
|MDMA (ecstasy)
|-
|Levamisole
|-
|Interferon
|-
|NSAIDs
|-
|Clofibrate
|-
|Nicotine
|-
|Amiodarone
|-
|Proton pump inhibitors
|-
|Monoclonal antibodies
|-
|Linezolid
|}
[[Category:Nutrition]]
[[Category:Intern education]]