Sodium/Water Balance Issues Flashcards
In the 2013 guidelines NICE recommend the following requirements for maintenance fluids (water) ?
25-30 ml/kg/day of water
In the 2013 guidelines NICE recommend the following requirements for maintenance fluids (electrolytes) ?
approximately 1 mmol/kg/day of potassium, sodium and chloride
In the 2013 guidelines NICE recommend the following requirements for maintenance fluids (glucose) ?
approximately 50-100 g/day of glucose to limit starvation ketosis
for a 80kg patient, for a 24 hour period how much maintenence water and potassium would you prescribe?
2 litres of water
80mmol potassium
For the first 24 hours NICE recommend the following (fluid therapy?)
When prescribing for routine maintenance alone, consider using 25-30 ml/kg/day sodium chloride 0.18% in 4% glucose with 27 mmol/l potassium on day 1 (there are other regimens to achieve this).
The amount of fluid patients require obviously varies according to their recent and past medical history.
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Who would require more fluid? Who would require less?
a patient who is post-op and is having significant losses from drains will require more fluid whereas a patient with heart failure should be given less fluid to avoid precipitating pulmonary oedema.
electrolyte concentrations (in millimoles/litre) of plasma
Na+ 135-145 Cl- 98-105 K+ 3.5-5 HCO3- 22-28 Glucose
electrolyte concentrations (in millimoles/litre) of 0.9% saline
Na+ 154
Cl- 154
electrolyte concentrations (in millimoles/litre) of 5% glucose
Glucose 50g
electrolyte concentrations (in millimoles/litre) of 0.18% saline with 4% glucose
Na+ 30
Cl- 30
Glucose 40g
electrolyte concentrations (in millimoles/litre) of Hartmann’s
Na+ 131
Cl- 111
K+ 5
HCO3- 29
0.9% saline
if large volumes are used there is an increased risk of
hyperchloraemic metabolic acidosis
Hartmann’s should not be used in?
contains potassium and therefore should not be used in patients with hyperkalaemia
Which solutions are not reccomended for surgical patients?
5% dextrose and dextrose/saline combinations
excessive administration of normal saline and many oliguric postoperative patients can lead to what? Why?
hyperchloraemic acidosis
With a greater understanding of this potential complication, the use of electrolyte balanced solutions (Ringers lactate/ Hartmans) is now favoured over normal saline
guidance for post op fluids?
Fluids given should be documented clearly and easily available
Assess the patient’s fluid status when they leave theatre
If a patient is haemodynamically stable and euvolaemic, aim to restart oral fluid intake as soon as possible
When should post op patients fluid status be reviewed?
urinary sodium is < 20
If a post op patient is oedematous, what should be treated first?
hypovolaemia if present should be treated first. This should then be followed by a negative balance of sodium and water, monitored using urine Na excretion levels.
What is used in caution in spetic patients and why?
Solutions such as Dextran 70 should be used in caution in patients with sepsis as there is a risk of developing acute renal injury.
What is the water deprivation test?
The water deprivation test is designed to help evaluate patients who have polydipsia.
Method
prevent patient drinking water
ask the patient to empty their bladder
hourly urine and plasma osmolalities
What would you see in water deprivation test for Normal?
Starting plasma osm. Normal
Final urine osm. >600
Urine osm. post-DDAVP >600
What would you see in water deprivation test for Psychogenic polydipsia?
Starting plasma osm. Low
Final urine osm. >400
Urine osm. post-DDAVP >400
What would you see in water deprivation test for Cranial DI?
Starting plasma osm. High
Final urine osm. <300
Urine osm. post-DDAVP >600
What would you see in water deprivation test for Nephrogenic DI?
Starting plasma osm. High
Final urine osm. <300
Urine osm. post-DDAVP <300
Diabetes insipidus (DI) is a condition characterised by
either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
Causes of cranial DI
idiopathic post head injury pituitary surgery craniopharyngiomas histiocytosis X DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome) haemochromatosis
Causes of nephrogenic DI
Genetic Electrolyte abnormalities lithium demeclocycline tubulo-interstitial disease:
Why does lithium cause nephrogenic DI
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
Which electrolyte abnormalities cause nephrogenic DI?
hypercalcaemia, hypokalaemia
What genetic mutations cause nephrogenic DI?
the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
Features of DI
polyuria
polydipsia
Investigation DI
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
Mx nephrogenic diabetes insipidus
thiazides, low salt/protein diet
mx - central diabetes insipidus
can be treated with desmopressin
What is SIADH?
The syndrome of inappropriate ADH secretion (SIADH) is characterised by hyponatraemia secondary to the dilutional effects of excessive water retention.
Causes of SIADH - Malignancy
small cell lung cancer
also: pancreas, prostate
Causes of SIADH - Neurological
stroke
subarachnoid haemorrhage
subdural haemorrhage
meningitis/encephalitis/abscess
Causes of SIADH - Infections
tuberculosis
pneumonia
Causes of SIADH - Drugs
sulfonylureas, *reported with glimepiride and glipizide. SSRIs, tricyclics carbamazepine vincristine cyclophosphamide
Causes of SIADH - other
positive end-expiratory pressure (PEEP)
porphyrias
Management SIADH?
correction must be done slowly to avoid precipitating central pontine myelinolysis
fluid restriction
demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
ADH (vasopressin) receptor antagonists have been developed
Hyponatraemia may be caused by
water excess or sodium depletion
Causes of pseudohyponatraemia include
hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm
What aid making a diagnosis in hyponatraemia
Urinary sodium and osmolarity levels
Urinary sodium > 20 mmol/l causes in hypovolemic patient?
Sodium depletion, renal loss (patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure
Urinary sodium > 20 mmol/l causes in euvolemic patient?
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism
Urinary sodium < 20 mmol/l causes
Sodium depletion, extra-renal loss
diarrhoea, vomiting, sweating
burns, adenoma of rectum
Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia
Management of hyponatremia complicated and primarily based around the following parameters
Duration of hyponatremia: is it acute or chronic?
Severity of hyponatremia: what is the sodium level?
Symptoms: is the patient symptomatic?
Acute hyponatremia:
Develops over a period of
less than 48 hours
Acute hyponatremia usually develops due to
excessive fluid intake, either parenteral or oral. Common examples include post-operative parenteral fluids and athletes.
Acute hyponatremia usually has mild sx
false severe
What is chronic hyponatraemia?
If the duration is unknown or it is present for more than 48 hours.
Symptoms are usually less severe than acute.
Describe mild hyponatraemia?
Serum Na+: 130-134 mmol/l
Sx: Non-specific symptoms such headache, lethargy, nausea, vomiting, dizziness, confusion, and muscle cramps
Describe moderate hyponatraemia?
Serum Na+: 120-129 mmol/l
Sx: Same as mild
Describe severe hyponatraemia?
Serum Na+: Less than 120 mmol/l
Sx: Seizures, coma, and respiratory arrest
Mx mild hyponatraemia?
Fluid restriction (less than 800 mL/day) Loop diuretics
Mx moderate hyponatraemia?
Hypertonic saline in first 3-4 hours to increase Na+ >120 mmol/l
Rest is the same as mild
Mx severe hyponatraemia?
Bolus of hypertonic saline until symptom resolution
With or without conivaptan
Fluids intake should be less than urine output in the following patients?
Oedematous states like heart failure and cirrhosis
SIADH
Renal failure
Psychogenic polydipsia
How do Vasopressin/ADH receptor antagonists (conivaptan) work
These act on V1 and V2 receptors. The V1 receptors cause vasoconstriction while the V2 receptors results in selective water diuresis, sparing the electrolytes.
Vasopressin/ADH receptor antagonists (conivaptan) should be avoided in
patients who have hypovolemic hyponatremia.
Vasopression/ADH receptor antagonists make you thirsty
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Vasopression/ADH receptor antagonists can stimulate the thirst receptors leading to the desire to drink free water.
Vasopression/ADH receptor antagonists should be avoided in
hepatotoxic in patients with underlying liver disease.
Complication of Vasopression/ADH receptor antagonists
Osmotic demyelination syndrome (central pontine myelinolysis)
can occur due to over-correction of severe hyponatremia
to avoid this, Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period
symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma
patients are awake but are unable to move or verbally communicate, also called ‘Locked-in syndrome’
Causes of HYPERnatraemia
dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline
Hypernatraemia should be corrected with great caution.
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Describe effect of lowering sodium on the brain
Although brain tissue can lose sodium and potassium rapidly, lowering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death
NICE or Royal College of Physicians at present, it is generally accepted that a rate of no greater than ? correction is appropriate in hypernatraemia
0.5 mmol/hour
Hyperosmolar hyperglycaemic state (HHS) is?
is a medical emergency which is extremely difficult to manage and has a significant associated mortality. Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies
HHS typically presents in
the elderly with type 2 diabetes mellitus (T2DM), however the incidence in younger adults is increasing. It can be the initial presentation of T2DM.
It is extremely important to differentiate HHS from
HHS from diabetic ketoacidosis (DKA) as the management is different
Firstline for HHS is insulin?
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treatment of HHS with insulin (e.g. as part of a DKA protocol) can result in adverse outcomes
Which unit are HHS pts usually managed in?
The first 24 hours of treatment is very labour intensive so these patients are best managed in either a medical high dependency unit.
DKA or HHS higher mortality?
HHS has a higher mortality than DKA
HHS complications
vascular complications such as myocardial infarction, stroke or peripheral arterial thrombosis. Seizures, cerebral oedema and central pontine myelinolysis (CPM) are uncommon but documented complications of HHS.
Timeframe HHS or DKA?
DKA presents within hours of onset
HHS comes on over many days - therefore dehydration and metabolic disturbances are more extreme.
Pathophysiology of HHS?
Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood.
Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.
Clincial features of HHS?
General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia
Diagnosis of HHS?
- Hypovolaemia
- Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
- Significantly raised serum osmolarity (> 320 mosmol/kg)
Note: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.
The goals of management of HHS can be summarised as follows?
- Normalise the osmolality (gradually)
- Replace fluid and electrolyte losses
- Normalise blood glucose (gradually)
Fluid replacement in HHS?
Caution is needed
Intravenous (IV) 0.9% sodium chloride solution is the first line fluid for restoring total body fluid.
If the serum osmolarity is not declining despite positive balance with 0.9% sodium chloride, then the fluid should be switched to 0.45% sodium chloride solution which is more hypotonic relative to the HHS patients serum osmolarity
Fluid losses in HHS are estimated to be
between 100 - 220 ml/kg (e.g. 10-22 litres in an individual weighing 100 kg).
In HHS The rate of rehydration will be determined by assessing the combination of initial severity and any pre-existing co-morbidities (e.g. heart failure and chronic kidney disease). Caution is needed, particularly in ?
elderly, where too rapid rehydration may precipitate heart failure but insufficient may fail to reverse an acute kidney injury.
isotonic 0.9% sodium chloride solution is already relatively hypotonic/hypertonic compared to the serum in someone with HHS?
hypotonic compared to the serum in someone with HHS. Therefore in most cases it is very effective at restoring normal serum osmolarity.
In HHS IV fluid replacement should aim to achieve
positive balance of 3-6 litres by 12 hours and the remaining replacement of estimated fluid losses within the next 12 hours.
in HHS Existing guidelines encourage vigorous initial fluid replacement and this alone (without insulin) will result in
a gradual decline in plasma glucose and serum osmolarity. A rapid decline is potentially harmful (see below) therefore insulin should NOT be used in the first instance unless there is significant ketonaemia or acidosis
In HHS The aim of treatment should be
replace approximately 50% of estimated fluid loss within the first 12 hours and the remainder in the following 12 hours. However this is just a guide, and clinical judgement should be applied, particularly in patient with co-morbidities such as heart failure and chronic kidney disease (which may limit the speed of correction).
Rapid changes of serum osmolarity are dangerous and can result in
cardiovascular collapse and central pontine myelinolysis (CPM).
Guidelines suggest that what should me monitored hourly in HHS Monitoring response to treatment
serum osmolarity, sodium and glucose levels
In HHS Fluid replacement alone (without insulin) will gradually lower blood glucose which will reduce osmolality
true
Describe the physiological effect of reduction of serum osmolarity in HHS
will cause a shift of water into the intracellular space.
This inevitably results in a rise in serum sodium (a fall in blood glucose of 5.5 mmol/L will result in a 2.4 mmol/L rise in sodium). This is not necessarily an indication to give hypotonic solutions. If the inevitable rise in serum Na+ is much greater than 2.4 mmol/L for each 5.5 mmol/L fall in blood glucose this would suggest insufficient fluid replacement. Rising sodium is only a concern if the osmolality is NOT declining concurrently.
In HHS A safe rate of fall of plasma glucose of? safe target?
4 and 6 mmol/hr is recommended
A target blood glucose of between 10 and 15 mmol/L is a reasonable goal.
In HHS: The rate of fall of plasma sodium should not exceed
10 mmol/L in 24 hours.
Complete normalisation of electrolytes and osmolality may take up to
72 hrs
In HHS Fluid replacement alone with 0.9% sodium chloride solution will result in a gradual decline of blood glucose and osmolarity
true
most patients with HHS are insulin sensitive (e.g. it usually occurs in T2DM), administration of insulin can result in a rapid decline of serum glucose and thus osmolarity.
A steep decline in serum osmolarity may also precipitate CPM.
In HHS insulin treatment prior to adequate fluid replacement may result in?
cardiovascular collapse as the water moves out of the intravascular space, with a resulting decline in intravascular volume.
In HHS Measurement of ? is essential for determining if insulin is required. How does this affect mx
ketones
If significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L) this indicates relative hypoinsulinaemia and insulin should be started at time zero (e.g. mixed DKA / HHS picture). The recommended insulin dose is a fixed rate intravenous insulin infusion given at 0.05 units per kg per hour.
If significant ketonaemia is not present (3β-hydroxy butyrate is less than 1 mmol/L) then do NOT start insulin.
Patients with HHS are potassium what? How should this be mx
Deplete but less acidotic than those with DKA so potassium shifts are less pronounced
Hyperkalaemia can be present with acute kidney injury
Patients on diuretics may be profoundly hypokalaemic
Potassium should be replaced or omitted as required
