Sodium abnormality

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      Acute, Symptomatic or Severe Hyponatraemia

      Hyponatraemia Vomiting Cardiorespiratory distress Excessive drowsiness GCS < 8 Acute hyponatraemia (< 48 hours) Seizures Sodium < 125

      URGENT ADMISSION

      What are the complications?[NICE – CKS]
      • Cerebral oedema is a potentially life-threatening complication of severe and/or acute hyponatraemia.
        • If hyponatraemia is severe (less than 125 mmol/L) or develops acutely (in less than 48 hours), the brain does not have time to adapt and cerebral oedema occurs.
        • Cerebral oedema and raised intracranial pressure can lead to symptoms of vomiting, headache, drowsiness, seizures, coma, and cardio-respiratory arrest.
      • Complications of chronic hyponatraemia include increased risk of falls, bone fractures, and osteoporosis. Even mild levels of hyponatraemia may predispose to gait disturbances, falls, and concentration and cognitive deficits.
      • Failure to correct hyponatremia can lead to permanent neurologic damage, as can over rapid correction.
        • Myelinolysis (also known as osmotic demyelination syndrome) is a possible consequence of over rapid correction of sodium levels.
        • It is characterized by altered mental status, reduced motor functioning, and/or abnormalities of balance, and can lead to permanent neurological dysfunction. 
      • In hospitalized people, hyponatraemia is associated with an increased mortality, prolonged hospital admission, and higher risk of re-admission compared with people with normal serum sodium concentrations.

      Clinical assessment
      Assessment of recent events, including collateral history if appropriate. Ask about:

      Intercurrent illnesses Food and fluid intake Urine output Falls Cognitive function Symptoms of underlying malignancy

      Review comorbidities and medication history, including recent changes in medication and assess volume status:

      Hyponatraemia + Hypovolaemia CONSIDER URGENT ADMISSION

      The majority of patients with hypovolaemia will need admission for IV fluids

      Review medications (prescription and OTC) and consider risk/benefit of stopping
      e.g. Thiazides, SSRI, anticonvulsants, ACE inhibitors, loop diuretics, PPIs
      NICE > CKS > HYPONATRAEMIA [NICE – CKS]
        Symptoms and when should I suspect hyponatraemia?
        • Hyponatraemia is usually an incidental finding on routine blood tests.
        • Most people are asymptomatic, particularly if hyponatraemia is mild (serum sodium concentration of 130–135 mmol/L) and has developed slowly.
        • When symptoms of hyponatraemia are present, they are often non-specific and are related to the severity of the hyponatraemia, its rate of onset, the intrinsic ability of the central nervous system to adapt to changing osmolar stress, and the range and degree of comorbidities.
          • Rapid changes in sodium levels or severe hyponatraemia can cause symptoms such as vomiting, drowsiness, headache, seizures, coma, and cardio-respiratory arrest due to cerebral oedema and raised intracranial pressure.
          • Chronic mild hyponatraemia can lead to gait instability, falls, and concentration and cognitive deficits.
        • The severity of clinical presentation may not match the degree of hyponatraemia:
          • People with severe hyponatraemia (serum sodium concentration less than 125 mmol/L) may be asymptomatic, while some people with moderate hyponatraemia (serum sodium concentration of 125–129 mmol/L) may have significant neurological symptoms and signs. 
          • Severe symptoms are unlikely with serum sodium greater than 130 mmol/L, and alternative causes of neurological dysfunction should be considered in this context. 

        NICE: CKS –  Hyponatraemia (accessed Feb 2021)

        What causes it?
        • The cause of hyponatraemia is often multifactorial
        • Hypotonic (or true) hyponatraemia can result from a range of clinical conditions that can be categorized by their effect on extracellular fluid volume:
          • Hypovolemic (volume depletion) hyponatraemia occurs when the total body water and sodium content are both decreased but the relative decrease in total body sodium is greater than the decrease in total body water. Causes include:
            • Medications, especially thiazide diuretics.
            • Endocrine disorders (primary adrenal insufficiency).
            • Cerebral salt-wasting (a rare cause of hyponatraemia resulting from a central nervous system insult such as aneurysmal subarachnoid haemorrhage).
            • Severe diarrhoea and/or vomiting (gastrointestinal sodium loss).
            • Sweating (for example during exercise) and extensive skin burns (transdermal sodium loss).
            • Salt-wasting nephropathies, for example tubulopathy after chemotherapy.
            • Third space losses — bowel obstruction, pancreatitis, severe hypoalbuminaemia, sepsis, or muscle trauma.
          • Hypervolemic (volume overload) hyponatraemia occurs when the total body water and sodium content both increase but the relative increase in total body water is greater than the increase in total body sodium, resulting in oedema. Causes include:
          • Euvolemic (normal volume status) hyponatraemia occurs when the total body water increases but the total body sodium remains unchanged, thereby producing a dilutional effect. Causes include:
        • Pseudo-hyponatraemia is an artifactually (falsely) low serum sodium concentration due to hyperproteinaemia (multiple myeloma is the most common cause) or hypertriglyceridaemia .
        • Hypertonic (or hyperosmolar) hyponatraemia can be caused by severe hyperglycaemia (the high levels of glucose draw intracellular water into the extracellular space) or administration of an active osmolyte (such as mannitol).
        How should I assess a person with hyponatraemia? History, Examination and Investigations

        For people with moderate or severe hyponatraemia and/or symptoms:

        For people with asymptomatic, mild hyponatraemia (serum sodium concentration 130–135 mmol/L):

        • Take a history to help identify an underlying cause.
          • The cause of hyponatraemia is often multifactorial and includes drugs (especially thiazide diuretics) and clinical conditions (such as the syndrome of inappropriate antidiuretic hormone secretion [SIADH], heart failure, liver disease, and kidney disease).
          • Ask about any intercurrent illness (such as gastroenteritis) or chronic illness (such as anorexia nervosa).
          • Ask about fluid intake and nocturnal polyuria (suggesting a possible diagnosis of primary polydipsia).
        • Examine the person to determine their volume status. 
          • Assess for pulse rate, postural changes in blood pressure, jugular venous pressure, presence or absence of oedema, and clinical signs of dehydration.
            • Hypovolaemia is characterized by tachycardia, postural hypotension, dry skin and mucous membranes, low urine output, decreased jugular venous pressure, and reduced skin turgor.
            • Hypervolaemia is characterized by peripheral, sacral, and pulmonary oedema, ascites, significant weight gain, and raised jugular venous pressure.
            • Determining the volume status will narrow the differential diagnosis considerably and help identify the cause of hyponatraemia. However, changes may be subtle and difficult to interpret.
        • Arrange investigations as appropriate.
          • Repeat the serum sodium measurement (timescale dependant on clinical judgement) to exclude a rapidly decreasing serum sodium concentration, which will require admission to hospital.
          • Measure serum osmolality to differentiate between hypotonic (true) hyponatraemia, hypertonic hyponatraemia, and pseudo-hyponatraemia. See the section on Interpreting investigation results for more information.
          • Send a urine sample to measure urinary osmolality and sodium concentration.
            • Urinary osmolality provides an estimate of antidiuretic hormone (ADH) activity and can be used to evaluate the cause of hyponatraemia.
            • Urinary sodium concentration in conjunction with the person’s volume status from examination may help differentiate the underlying cause of hyponatraemia.
            • See the section on Interpreting investigation results for more information.
          • If clinically indicated, arrange further tests to identify an underlying cause, for example:
            • Urinalysis for urine protein and blood — if renal disease is suspected. See the CKS topic on Chronic kidney disease for more information.
            • Thyroid function tests — if hypothyroidism is suspected. See the CKS topic on Hypothyroidism for more information.
            • Serum cortisol (morning sample at 8–9 am) — if Addison’s disease is suspected. See the CKS topic on Addison’s disease for more information.
            • B-type natriuretic peptide — if heart failure is suspected.  See the CKS topic on Heart failure – chronic for more information.
            • Liver function tests — if liver disease is suspected. 
        When should I admit or refer a person with hyponatraemia?
        • Admit the person to hospital immediately if they:
          • Have acute onset (duration for less than 48 hours) or severe (serum sodium concentration of less than 125 mmol/L) hyponatraemia.
          • Are symptomatic.
          • Have signs of hypovolaemia.
        • Discuss with an endocrinologist about the need for admission or referral:
          • If the person has asymptomatic, moderate hyponatraemia (serum sodium concentration of 125–129 mmol/L).
        • Arrange an urgent 2-week wait referral to the appropriate specialist:
        • Refer to an endocrinologist, the urgency depending on clinical judgement:
          • If the cause of hyponatraemia is not clear.
          • If SIADH or another endocrine cause is suspected.
            • Hyponatraemia related to an endocrine disorder is uncommon, and will require specialist input to confirm the diagnosis and initiate treatment.
            • If Addison’s disease is suspected, admission or urgent referral may be required. See the CKS topic on Addison’s disease for more information.
          • If reset osmostat syndrome or cerebral salt-wasting is suspected.
        • Refer to an appropriate specialist:
        How should I manage a person with hyponatraemia in primary care?

        People with asymptomatic, mild hyponatraemia (serum sodium concentration of 130–135 mmol/L) may be managed in primary care.

        • In all people, ensure a repeat serum sodium measurement has been taken to exclude a rapidly decreasing serum sodium concentration, which will require admission to hospital.
        • If the person has an acute illness that may be contributing to the hyponatraemia, treat the underlying problem and recheck the serum sodium concentration after 2 weeks or sooner based on clinical judgement.
        • If the person is taking a medication that may be contributing to the hyponatraemia, stop this if appropriate and recheck the serum sodium concentration after 2 weeks.
          • If the person is taking a medication that cannot be stopped (for example an antipsychotic), contact their appropriate specialist to discuss whether to stop the medication, monitor the serum sodium concentration, or refer to an endocrinologist or nephrologist.
          • If the serum sodium concentration remains low after stopping the medication, assess for another underlying cause or refer the person to an endocrinologist.
        • Provide patient information on hyponatraemia.

        NOTE: Failure to correct hyponatremia can lead to permanent neurologic damage, as can over rapid correction.

        • Myelinolysis (also known as osmotic demyelination syndrome) is a possible consequence of over rapid correction of sodium levels.
        • It is characterized by altered mental status, reduced motor functioning, and/or abnormalities of balance, and can lead to permanent neurological dysfunction. 
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The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Considerations for Prescribing SGLT2i Therapy in Type 2 Diabetes Mellitus

The clinical summary below aims to offer practical advice for healthcare professionals when prescribing SGLT2i therapies for the treatment of T2DM. Please refer to the relevant individual SmPC before prescribing any SGLT2i therapy: Canagliflozin | Dapagliflozin | Empagliflozin | Ertugliflozin

Dapagliflozin | Dose | Safety | Side-effects | NICE
Indication: T2D glycaemic control
↓eGFR: ≥ 45 = 10mg| < 45 = not recommended for glycaemic control
Indication: Chronic HFrEF with or without T2D
↓eGFR: ≥ 15 = 10mg| < 15 = Continue but don't initiate
Indication: Chronic Kidney Disease with or without T2D
↓eGFR: ≥ 15 = 10mg| < 15 = Continue but don't initiate

SOURCE: @Visualmedapp

Dapagliflozin | Dose | Safety | Side-effects | NICE
Indication: T2D glycaemic control
↓eGFR: ≥ 45 = 10mg| < 45 = not recommended for glycaemic control
Indication: Chronic HFrEF with or without T2D
↓eGFR: ≥ 15 = 10mg| < 15 = Continue but don't initiate
Indication: Chronic Kidney Disease with or without T2D
↓eGFR: ≥ 15 = 10mg| < 15 = Continue but don't initiate

SOURCE: @Visualmedapp

Canagliflozin | Dose | Safety | Side-effects | NICE
Indication: T2D glycaemic control
↓eGFR: ≥ 60 = 100mg, titrate → 300mg if required | 45 - 59 = Use 100mg only | < 45 = not recommended for glycaemic control
Indication: T2D + Diabetic Kidney Disease
↓eGFR: ≥ 30 = Initiate and continue 100mg | < 30* = Continue but do not initiate 100mg | Dialysis = STOP
*With urinary albumin/creatinine ratio > 30 mg/mol

SOURCE: @Visualmedapp

Empagliflozin | Dose | Safety | Side-effects | NICE
Indication: T2D glycaemic control
↓eGFR: ≥ 60 = Initiate 10mg, titrate → 25mg if required | 45 - 60 = Continue 10mg only but do not initiate | < 45 = STOP
Indication: T2D AND estalished cardiovascular disease
↓eGFR: ≥ 60 = Initiate 10mg, titrate → 25mg if required | 30 - 60 = Initiate or continue 10mg only | < 30 = STOP
Indication: Chronic HFrEF with or without T2D
↓eGFR: ≥ 20 = Initiate or continue 10mg | < 20 = STOP

SOURCE: @Visualmedapp

Ertugliflozin | Dose | Safety | Side-effects | NICE
↓eGFR: Initiate only if eGFR ≥ 60 = 5mg, titrate → 15mg if required | < 45 = STOP

SOURCE: @Visualmedapp

Empagliflozin | Dose | Safety | Side-effects | NICE
Indication: T2D glycaemic control
↓eGFR: ≥ 60 = Initiate 10mg, titrate → 25mg if required | 45 - 60 = Continue 10mg only but do not initiate | < 45 = STOP
Indication: T2D AND estalished cardiovascular disease
↓eGFR: ≥ 60 = Initiate 10mg, titrate → 25mg if required | 30 - 60 = Initiate or continue 10mg only | < 30 = STOP
Indication: Chronic HFrEF with or without T2D
↓eGFR: ≥ 20 = Initiate or continue 10mg | < 20 = STOP

SOURCE: @Visualmedapp

Dapagliflozin | Dose | Safety | Side-effects | NICE
Indication: T2D glycaemic control
↓eGFR: ≥ 45 = 10mg| < 45 = not recommended for glycaemic control
Indication: Chronic HFrEF with or without T2D
↓eGFR: ≥ 15 = 10mg| < 15 = Continue but don't initiate
Indication: Chronic Kidney Disease with or without T2D
↓eGFR: ≥ 15 = 10mg| < 15 = Continue but don't initiate

SOURCE: @Visualmedapp

Canagliflozin | Dose | Safety | Side-effects | NICE
Indication: T2D glycaemic control
↓eGFR: ≥ 60 = 100mg, titrate → 300mg if required | 45 - 59 = Use 100mg only | < 45 = not recommended for glycaemic control
Indication: T2D + Diabetic Kidney Disease
↓eGFR: ≥ 30 = Initiate and continue 100mg | < 30* = Continue but do not initiate 100mg | Dialysis = STOP
*With urinary albumin/creatinine ratio > 30 mg/mol

SOURCE: @Visualmedapp