Sodium Imbalance
Dr Mohammad Yasin
Diploma(Endocrinology and Metabolism)
BIRDEM General Hospital
Basic daily requirement
Sodium: 1.5-2 mmol/kg
( 105-140 mmol/day in 70 kg adult)
Ref: Davidson’s Principles & Practice of Medicine
Ref: Davidson’s Principles & Practice of Medicine
Disorder in Sodium Balance
A.Hyponatremia
B. Hypernatremia
A. Hyponatraemia:
Hyponatraemia is defined as a serum
Na< 135 mmol/L
Severity Serum Sodium Symptoms
Mild 130-135 mmol/L None
Moderate 125-129 mmol/L Nausea, Delirium,
Headache
Severe < 125 mmol/L Vomiting,
Somnolence,
Seizures, Coma,
Cardiorespiratory
arrest
Causes of Hyponatremia
Volume status Examples
Hypovolaemic
.Renal sodium losses:
.Diuretic therapy (Especially
thiazides)
.Adrenocortical failure
.Gastrointestinal losses:
.Vomiting .Diarrhoea
.Skin Losses: Burns
Volume status Examples
Euvolaemic
. Primary polydipsia
. Excessive electrolyte -free water infusion
. SIADH
. Hypothyroidism
Hypervolaemic
. CCF . Cirrhosis
. Nephrotic syndrome
. CKD(Free water intake)
Ref: Davidson’s Principles & Practice of Medicine
Ref: Davidson’s Principles & Practice of Medicine
Diagnostic criteria of SIADH :
. Low plasma Sodium Conc.( Typically <130 mmol/L)
. Low plasma osmolarity (<275 mOsmol/kg)
. Urine osmolarity not minimally low
(typically >100 mOsmol/kg)
. Urine sodium conc. not minimally low
(>30 mmol/L)
• Diagnostic criteria(Cont.):
. Low-normal plasma urea, creatinine, uric acid
. Clinical Euvolaemia
. Absence of adrenal, thyroid, pituitary or renal
insufficiency
. No recent use of diuretics
. Exclusion of other causes of hyponatremia
. Appropriate clinical context
Ref: Davidson’s Principles & Practice of Medicine
Approach to Hyponatremia
Cont.
Ref: Davidson’s Principles & Practice of Medicine
Ref: Davidson’s Principles & Practice of Medicine
*** That’s why rate of correction of plasma Na
concentration in chronic asymptomatic
hyponatremia should not exceed 10 mmol/L/24
hrs and a slower rate is generally safer.
B. Hypernatremia
Hypernatremia is defined as serum sodium
> 145 mmol/L.
Pathophysiology:
-- Failure to generate an adequate medullary
concentration gradient in kidney due to low
GFR or loop diuretic therapy or,
-- Failure of vasopressin system
(Cranial/ Nephrogenic Diabetes Insipidus)
Ref: Davidson’s Principles & Practise of Medicine
Figure:Etiologies of Hypernatremia Ref:Oxford handbook of Nephrology
Causes of Hypernatremia
Clinical feature:
. Generally this patients have reduced cerebral
function which result in dehydration of neurons &
brain shrinkage
. Usually as this patients have intact thirst
mechanism, hypernatremia may not progress far
. If protective mechanism is impaired sequence of
events may occur:
Weakness, Delirium, Dizziness ComaDeath
Ref: Davidson’s Principles & Practise of Medicine
Management
• Treatment of Hypernatremia depends on
-- Rate of development
-- Underlying cause
• If the condition has developed rapidly relatively
rapid correction may be attempted because
there may be acute neuronal shrinkage
This can be achieved by infusing isotonic 5%
Dextrose or hypotonic 0.45% Normal saline
• In older patients, it is likely that the disorder
has developed slowly and extreme caution is
required in lowering plasma sodium to avoid
the risk of cerebral oedema
• If possible the underlying cause should be
addressed irrespective of the fact that
whether it is acute or chronic
Ref: Davidson’s Principles & Practise of Medicine
Sodium Correction formula
** Na deficit=0.6 Weight(kg) (desired Na-actual Na)
(In case of female use 0.5)
** Change in serum Na with 1 L infusate
Infusate Na- Serum Na
Total Body Water+ 1
Ref: Davidson’s Principles & Practise of
Medicine
Pseudohyponatremia
• It is a condition where serum Na+ is < 135
mmol/L but serum Osmolarity is normal(280-
300 mOsm/kg)
• Occurs dur to presence of osmotically active
substance in plasma leading to intracellular
shift of Sodium
Cont.
• Causes:
-- Severely elevated levels of cholesterol
-- Abnormally high levels of protein in
conditions such as . Chronic infectious
disease(Hepatitis C, HIV etc) . Multiple
Myeloma . Malignant lymphoproliferative
disorder . Heavy/ Light chain disease . IV IG
therapy
-- Hyperglycemia
Ref: Oxford Handbook Of Nephrology
Osmotic Demyelination Syndrome
• Also known as central pontine myelinolysis
• Causes:
-- Overly rapid correction of Hyponatremia
(Most common)
-- Hypokalemia
-- Burn victims
-- Patients on dialysis
-- Anorexia nervosa(when feeding is started)
Cont.
• Symptoms:
Initially patient may have features related to
hyponatremia( Nausea, Vomiting, Confusion,
Headache, Seizure etc.) These symptoms may
subside with normalization of serum Na+ 3-5 days
later patient may present with Gait disturbance,
Decreased consciousness level, Seizure, difficulty in
respiration etc.
• Signs:
Progressive development of
-- Spastic quadriparesis
-- Pseudobulbar palsy
-- Emotional lability etc.
Cont.
• Risk factors:
-- Liver cirrhosis
-- Liver transplant
-- Alcoholism
-- Malnutrition
-- HIV
-- Hyperemesis gravidarum etc.
Cont.
• Treatment:
-- Once osmotic demyelination has begun,
there is no cure or specific treatment
-- Care is mainly supportive
-- Alcoholics should have vitamin supplement
Factors favoring favourable outcome:
-- Concurrent treatment of all electrolyte
imbalance
-- Early ICU involvement
-- Early introduction of feeding including
thiamine supplement
Ref:Harrison’s Nephrology
TAKE HOME MESSAGE
• During evaluation of sodium imbalance
volume status of the patient must be
perceived
• In treating acute severe hyponatremia a rapid
approach should be made but the rate of
cooection must not exceed 10 mmol/day
• Acute hypernatremic cases should be treated
rapidly to prevent acute neuronal shrinkage
electrolyte।।।।।।।।।।।।।।।।।।।।।।।।।।।।।.pptx

electrolyte।।।।।।।।।।।।।।।।।।।।।।।।।।।।।.pptx

  • 1.
    Sodium Imbalance Dr MohammadYasin Diploma(Endocrinology and Metabolism) BIRDEM General Hospital
  • 2.
    Basic daily requirement Sodium:1.5-2 mmol/kg ( 105-140 mmol/day in 70 kg adult) Ref: Davidson’s Principles & Practice of Medicine
  • 3.
    Ref: Davidson’s Principles& Practice of Medicine
  • 4.
    Disorder in SodiumBalance A.Hyponatremia B. Hypernatremia
  • 5.
    A. Hyponatraemia: Hyponatraemia isdefined as a serum Na< 135 mmol/L Severity Serum Sodium Symptoms Mild 130-135 mmol/L None Moderate 125-129 mmol/L Nausea, Delirium, Headache Severe < 125 mmol/L Vomiting, Somnolence, Seizures, Coma, Cardiorespiratory arrest
  • 6.
    Causes of Hyponatremia Volumestatus Examples Hypovolaemic .Renal sodium losses: .Diuretic therapy (Especially thiazides) .Adrenocortical failure .Gastrointestinal losses: .Vomiting .Diarrhoea .Skin Losses: Burns
  • 7.
    Volume status Examples Euvolaemic .Primary polydipsia . Excessive electrolyte -free water infusion . SIADH . Hypothyroidism Hypervolaemic . CCF . Cirrhosis . Nephrotic syndrome . CKD(Free water intake) Ref: Davidson’s Principles & Practice of Medicine
  • 8.
    Ref: Davidson’s Principles& Practice of Medicine
  • 9.
    Diagnostic criteria ofSIADH : . Low plasma Sodium Conc.( Typically <130 mmol/L) . Low plasma osmolarity (<275 mOsmol/kg) . Urine osmolarity not minimally low (typically >100 mOsmol/kg) . Urine sodium conc. not minimally low (>30 mmol/L)
  • 10.
    • Diagnostic criteria(Cont.): .Low-normal plasma urea, creatinine, uric acid . Clinical Euvolaemia . Absence of adrenal, thyroid, pituitary or renal insufficiency . No recent use of diuretics . Exclusion of other causes of hyponatremia . Appropriate clinical context Ref: Davidson’s Principles & Practice of Medicine
  • 11.
  • 12.
    Cont. Ref: Davidson’s Principles& Practice of Medicine
  • 16.
    Ref: Davidson’s Principles& Practice of Medicine
  • 17.
    *** That’s whyrate of correction of plasma Na concentration in chronic asymptomatic hyponatremia should not exceed 10 mmol/L/24 hrs and a slower rate is generally safer.
  • 18.
    B. Hypernatremia Hypernatremia isdefined as serum sodium > 145 mmol/L. Pathophysiology: -- Failure to generate an adequate medullary concentration gradient in kidney due to low GFR or loop diuretic therapy or, -- Failure of vasopressin system (Cranial/ Nephrogenic Diabetes Insipidus) Ref: Davidson’s Principles & Practise of Medicine
  • 19.
    Figure:Etiologies of HypernatremiaRef:Oxford handbook of Nephrology
  • 20.
  • 21.
    Clinical feature: . Generallythis patients have reduced cerebral function which result in dehydration of neurons & brain shrinkage . Usually as this patients have intact thirst mechanism, hypernatremia may not progress far . If protective mechanism is impaired sequence of events may occur: Weakness, Delirium, Dizziness ComaDeath Ref: Davidson’s Principles & Practise of Medicine
  • 22.
    Management • Treatment ofHypernatremia depends on -- Rate of development -- Underlying cause
  • 23.
    • If thecondition has developed rapidly relatively rapid correction may be attempted because there may be acute neuronal shrinkage This can be achieved by infusing isotonic 5% Dextrose or hypotonic 0.45% Normal saline
  • 24.
    • In olderpatients, it is likely that the disorder has developed slowly and extreme caution is required in lowering plasma sodium to avoid the risk of cerebral oedema • If possible the underlying cause should be addressed irrespective of the fact that whether it is acute or chronic Ref: Davidson’s Principles & Practise of Medicine
  • 25.
    Sodium Correction formula **Na deficit=0.6 Weight(kg) (desired Na-actual Na) (In case of female use 0.5) ** Change in serum Na with 1 L infusate Infusate Na- Serum Na Total Body Water+ 1 Ref: Davidson’s Principles & Practise of Medicine
  • 26.
    Pseudohyponatremia • It isa condition where serum Na+ is < 135 mmol/L but serum Osmolarity is normal(280- 300 mOsm/kg) • Occurs dur to presence of osmotically active substance in plasma leading to intracellular shift of Sodium
  • 27.
    Cont. • Causes: -- Severelyelevated levels of cholesterol -- Abnormally high levels of protein in conditions such as . Chronic infectious disease(Hepatitis C, HIV etc) . Multiple Myeloma . Malignant lymphoproliferative disorder . Heavy/ Light chain disease . IV IG therapy -- Hyperglycemia Ref: Oxford Handbook Of Nephrology
  • 28.
    Osmotic Demyelination Syndrome •Also known as central pontine myelinolysis • Causes: -- Overly rapid correction of Hyponatremia (Most common) -- Hypokalemia -- Burn victims -- Patients on dialysis -- Anorexia nervosa(when feeding is started)
  • 29.
    Cont. • Symptoms: Initially patientmay have features related to hyponatremia( Nausea, Vomiting, Confusion, Headache, Seizure etc.) These symptoms may subside with normalization of serum Na+ 3-5 days later patient may present with Gait disturbance, Decreased consciousness level, Seizure, difficulty in respiration etc. • Signs: Progressive development of -- Spastic quadriparesis -- Pseudobulbar palsy -- Emotional lability etc.
  • 30.
    Cont. • Risk factors: --Liver cirrhosis -- Liver transplant -- Alcoholism -- Malnutrition -- HIV -- Hyperemesis gravidarum etc.
  • 31.
    Cont. • Treatment: -- Onceosmotic demyelination has begun, there is no cure or specific treatment -- Care is mainly supportive -- Alcoholics should have vitamin supplement Factors favoring favourable outcome: -- Concurrent treatment of all electrolyte imbalance -- Early ICU involvement -- Early introduction of feeding including thiamine supplement Ref:Harrison’s Nephrology
  • 32.
    TAKE HOME MESSAGE •During evaluation of sodium imbalance volume status of the patient must be perceived • In treating acute severe hyponatremia a rapid approach should be made but the rate of cooection must not exceed 10 mmol/day • Acute hypernatremic cases should be treated rapidly to prevent acute neuronal shrinkage