Fluid and electrolyte disturbances

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Transcript Fluid and electrolyte disturbances

Ismail M. Siala
65 Kg healthy man
40 L Water (60% of body wt)
70% ICF (28L)
30% ECF (12L)
75% Interstiatial fluid (9L)
25% Plasma (3L)
Fluid disturbances
• Water passes freely from one compartment
to another
• In a healthy person water distribution
remains constant despite variation in intake.
• Factors determining water distribution:
1. Osmotic (oncotic pressure) draw water in
2. Hydrostatic pressure push water out
Fluid disturbances
• Fluid disturbances could be in form of:
1. Volume depletion
2. Volume overload
• Usually associated with electrolyte
disturbances
Volume Depletion
1-Volume depletion
Dehydration
• Presentation:
– Weight loss, thirst, concentrated urine
– Tachycardia, low blood pressure, dry mucous
membranes, skin turger
– High Hct
Causes of volume depletion
A- Loss of water:
•GIT loss:
– Vomiting
– Aspiration of gastric contents
– Diarrhoea
– Sequestration of fluid in bowel
•Loss in Urine:
– Osmotic diuresis: DM
– Diuretics
– Adrenocortical insufficiency
– Renal disease
– DI
•Profuse sweating:
– Fever, hot environment
•Third space loss:
– Burns, extensive dermatitis
– Ascites, peritonitis, acute pancreaitis
B-Inadequate oral intake in a patient with impaired thirst mechanism
Management of volume depletion
• Aim:
– Restore plasma volume
• What to give:
– Crystalloids: NaCl 0.9%
– Plasma expanders: plasma protein
• Monitor:
– Blood pressure
– JVP/CVP (central venous pressure) specially in
elderly patients and those with heart disease
– Input-output charting
Volume Overload
2-Volume overload
• Clinical features:
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Weight gain,
oedema,
high JVP,
+ Ascites
Low Hct
• Management of volume
overload:
– Dietary sodium restriction
– Diuretics
– Treat the underlying
cause
• Causes:
– CCF
– Chronic and end-stage
Liver disease
– Nephrotic syndrome
– Advanced CRF, acute
oliguric renal failure
– Drugs: ACE, NSAID,
mineralocorticoids,
calcium channel blockers
Sodium Disturbances
Osmolality
• Osmolality:
– Represents solute concentration in ECF
• More solutes  high osmolality  hypertonic state
• Less solutes  low osmolality  hypotonic state
Osmolality = 2(Na meq/l) + glucose mg/dl + BUN mg/dl
18
2.8
N=285-295 mosm/kg
Hyponatremia
• Hyponatremia : serum Na < 130 meq/l
• Types of hyponatremia:
– Isotonic ( Normal osmolality)
– Hypertonic (  osmolality)
– Hypotonic, (  osmolality) with;
• Low ECF (hypovolumic)
• Normal ECF (euvolumic)
• High ECF hypervolumic)
plasma
Na
– hyperlipidemia or
– hyperprotienemia(>10g/dl)
 falsely low serum Na reading.
plasma
Is a spurious hyponatremia
• Total Serum sodium is normal
• Osmolality is normal
• It is due to;
Na
Isotonic hyponatremia:
Hypertonic hyponatremia
• Logically if Na is low osmolality should be
low but, here there is low Na with High
osmolality!
• It is due to other solutes that will increase
the osmolality
• Causes:
– Hyperglycaemia: osmotic diuresis
– Manitol
– Radio contrast agents
• Treatment: that of the underlying cause
Hypotonic hyponatremia
• Low serum Na
• Low osmolality
• Further classified according to ECF status into:
– Hyponatremia with low ECF (Na + Water)
– Hyponatremia with normal ECF (Na + N water)
– Hyponatremia with high ECF (N/ Na +  water)
Hyponatremia with low ECF
(Na + Water)
• Due to loss of both Na and water
• Na loss > water loss
• Causes:
– Renal:
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Diuretics
Slat loosing nephropathy
Mineralocorticoid deficiency
Osmotic diuresis
– Extra renal:
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Vomiting
Diarrhoea
Third space loss: (ascites)
Skin, burns and sever dermatitis
Hyponatremia with low ECF
• The urine Na
– Measurement of urine Na helps differentiating
renal from non-renal causes of hyponatremia
with low ECF
– In renal cause: urine Na > 20 meq/l
– In non-renal cause: urine Na < 10 meq/l
indicating Na retention by the kidney as a
compensation for a loss of Na from outside
the kidneys.
Hyponatremia with normal ECF
(Na + N water)
• Due to pure Na loss
• Causes:
– Nephrotic syndrome
– NSAID
– Hypothyroidism
– Post operative pain and analgesia
– Diuretics
Hyponatremia with high ECF
(N/ Na +  water)
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Low serum Na
Total body Na is increased
Total body water is increased
Total body water > total body Na
Causes:
– Cardiac failure
– Renal failure
– Liver cirrhosis
– SIADH
Appropriate or inappropriate ADH?
• ADH is released in response to
– Reduction of plasma volume
– Increased osmolality
• When there is reduction of plasma volume and
low osmolality what will be the response of
ADH?
• It will respond preferentially to low plasma
volume
• So if plasma volume is normal or increased and
ADH is high we call it inappropriate secretion.
Causes of SIADH
• Neoplasms:
– Carcinoma of bronchus (small cell), pancreas,
lymphoma, mesothelioma, others
• CNS disorders:
– Meningitis, encephalitis, brain abscess, head
injury,cerbral tumours, CVA, etc
• Non-malignant pulmonary diseases:
– TB, pneumonia
• Drugs:
– Narcotics, phenothiazines,TCA, vincristine,
cyclophosmphamide, chlorpropamide, NSAID
• Others:
– Pain, nausea
Clinical features of hyponatremia
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Mild confusional state gross confusion
Sleepiness
Myoclonic jerks generalized seizures
Features of the accompanying ECF status
– Low ECF hypovolemia
– High ECF fluid overload and oedema
• Serious hyponatremia occurs if:
[medical emergency]
– Rapid reduction in serum Na
– Serum Na < 110 meq/l
Investigations of hyponatremia
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Serum Na: low
Osmolality: low
Urea and creatinine
Urinary Na
Urine osmolality
• In volume depletion due to extra renal loss
– Low Na
– Low urinary Na
– High urine osmolality (concentrated urine)
• In SIADH
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Low serum Na
Low serum osmolality
High urine osmolality
Normal or high ECF volume
Management of hyponatremia
Water
restriction
if not
hypovolumic
Saline
if
hypovolumic
Offending cause
+
Diuretics
Management of hyponatremia
• Mild hyponatremia( >120meq/l)
– with normal or high ECF:
• Water restriction to 0.5 L/day
• Demeclocycline could be used if water restriction is
not tolerated or not effective, check Contraindications
• Stop the offending drug
• Correct the underlying cause
– With low ECF:
• 0.9% NaCl
Management of hyponatremia
• Moderate hyponatremia (>110-120meq/l):
– With normal or high ECF:
• Water restriction <0.5l/day
• 0.9%NaCl iv in normal ECF
• Frusemide could be added orally if high ECF
– With low ECF:
• 0.9% NaCl iv
Management of hyponatremia
• Severe hyponatremia:
– Na <110 meq/l
– Symptomatic
– 1.8 or 3% NaCl slow iv infusion, aiming at
• Raise plasma Na by 0.5 meq/l/hr
• Do not exceed plasma Na of 130 meq/l in the first 48 hrs.
– Frusemide 20 mg iv if overloaded or high CVP
Rapid correction to > 135 meq/l in the first 48 hrs or increase of
plasma Na of > 25 meq/l in the firs 24 hrs  osmotically induced
demylination of brain Osmotic Demylination Syndrome (central
pontine myelinolysis) brain damage
Hypernatremia
Hypernatremia
• Definition: serum Na > 145 meq/l due to pure water loss.
• Causes:
– Decreased water intake
• Unavailable
• Coma
– Non-renal
• Increased water loss in presence of impaired thirst mechanism
• Dehydration, fever, hot climate,diarrhea
– Urinary loss
• Diabetes Insipidus
– Cranial
– nephrogenic
• Osmotic diuresis
– Increased salt intake
Hypernatremia
• Clinical features:
– Mild
• Thirst
• Concentrated urine
– Moderate
• Dizzinessconfusion
• oliguria
– Sever
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Confusioncoma
Muscle weakness
Doughy skin
Tachycardia
Low BP
Hypernatremia
• Investigations:
– Raised Na
– Raised osmolality
– Raised Hct
– Raised urea
– Urine osmolality
• If high>400 mosm/kgnon renal loss and kidney is
concentrating urine
• If< 200 mosm/kg  diabetes insipidus
Hypernatremia
• Treatment:
– Mild:
• Water 2 litres over 6-12hrs orally or,
• 5% dextrose iv over 6-12 hrs
– Moderate:
• 5% dextrose 2-4 litres over 24 hrs
– Severe: usually associated with hypovolumia
• 0.9%NaCl 1 litre iv over 1 hr
• 5% dextrose 4L iv over 24 hrs
• 5% dextrose 2-4L iv over 24-48 hrs
– Aim:
• Correct deficit over 48 hrs
• Correction should not be > 1meq/l/hr
• Correct K and phosphate as required
Idiogenic osmoles
Normal
Hypernatremia
Water shift out
Brain cell
dehydration
Formation
of
Idiogenic
Osmoles
Rapid correction
of
Hypernatremia
Water shift to
brain cells
Brain oedema
Hypernatremia
• High osmolalitybrain cells form idiogenic
osmolesincrease the osmotic pressure
in the brain cellsdraw water back to
brain cell and thus prevent dehydrating
brain cells, this usually begins 4-6 hrs after
dehydration.
• Rapid correction of Hypernatremia more
water will go inside brain cells brain
oedema severe neurological damage.
Potassium disturbances
• K is filtered through the glomerular filtrate
• 90% is reabsorbed in the proximal tubule
• The urinary K is mainly derived from excretion
through the distal nephron
• 90% of the eliminated K is through the kidney
and the rest is through faeces.
• Factors affecting shift of K to inside the cell:
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Insulin
B2 agonists
Aldosterone
alkalosis
Hypokalemia
• Def: serum K < 3.5 meq/l, levels < 2.5 meq/l are considered as
severe hypokalemia.
• Causes of hypokalemia:
– Shift to cell:
• B2 agonists, alkalosis, insulin, mineral corticoids, theophyllines.
– Decreased intake
– GIT loss:
• Vomiting/aspiration of gastric contents
• Diarrhoea, villous adenoma
• Sequestration of fluid in bowel, ilius
– Renal loss:
• Extra renal causes
–
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Hyperaldosteronism, Cushing,
Diabetes mellitus
Metabolic alkalosis
Drugs:
» Diuretics, corticosteroids, aminoglycosides, carbenoxolone
• Renal:
– Recovery phase of ATN
– RTA
Hypokalemia
Clinical features:
– Mild to moderate
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Muscular weakness
Muscular cramps
Fatigue
Constipation
– Severe: ( <2.5 meq/l)
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Ilius
Flaccid paralysis
Hyporeflexia
Tetany
Rhabdomyolysis
Hypercapnia
Hypokalemia
• Investigations:
– Serum K
– ECG:
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Low amplitude of T wave
Prominent U
Depression of ST segment
AV block
Cardiac arrest
– Hypokalemia will increase the chance of digitalis
toxicity
– Urinary K
• <20meq/l  extra renal cause
• >30 meq/l  renal cause
Hypokalemia
• Treatment:
– Mild to moderate:
• Oral K
– Rapidly absorbed
– May cause peptic ulcer
– If not tolerated give parentral K
– Severe:
• Parentral K
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10meq/l/hr in a peripheral iv infusion
Concentration should not exceed 40meq/l
Rate should not exceed 40meq/l/h (60meq/l/hr)
Monitor by ECG
Check K every 3-6 hrs
• If K deficiency is refractory to treatment then concomitant
magnesium deficiency could be present
– Treat underlying cause
Hypokalemia
• Prevention:
– Diuretics:
• Additional KCl
• (Do not give with K sparing diuretics, ACE)
– Corticosteroids:
• Monitor K level on prolonged use
– Parentral therapy:
• Add K to parentral therapy protocol
Hyperkalemia
• A serum K of >5 meq/l
• Causes:
– Spurious:
• Lysis of RBCs in tube
• Thrombocytosis
• Repeated fist clenching
during phlebotomy
– Increased intake:
• Iv fluids containing K salts
– Impaired excretion:
• Renal failure
• Adrenocortical
insufficiency
• Hyporeninemic
hypoaldosteronism
• Drugs: spironolactone,
ACE, NSAID, amiloride,
– Tissue breakdown:
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Bleeding into soft tissues
Haemolysis
Rhabdomyolysis
Sever burns
Vigorous exercise
– Shift of K out of cell:
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Acidosis
Insulin deficiency
Aldosterone deficiency
B-receptor antagonists
Hyperkalemia
• Clinical features:
– Symptoms are rare
– Weakness, flaccid paralysis, ilius, lost tendon
jerks, abdominal distension, diarrhoea
– Cardiac arrest is expected when K level is
>7meq/l
– Patients usually present with collapse due to
bradyarrythmia
Hyperkalemia
• Investigations:
– Serum K >5 meq/l
– ECG:
Changes occur with high levels >6.5meq/l
• Peaked T
• Prolonged PR interval
• Wide QRS
• Atrial arrest
• Biphasic QRS-T
• Slowing of HR
• VF
• Cardiac arrest
Hyperkalemia
• Management:
– Exclude spurious hyperkalemia
– Stop any K source
– Cation exchange resin
• Sodium polystyrene sulphonate
• Calcium resonium
– Correct underlying cause
• Urgent treatment:
– Indications:
• Cardiac toxicity
• Muscular paralysis
• Severe hyperkalemia>6.5meq/l
Hyperkalemia
• Urgent treatment:
– 50 ml of 50% dextrose iv with insulin 1 unit for each 5
grams of dextrose , monitor serum K after half an
hour.
– Calcium gluconate 10%, give 10 ml over 10 min iv, to
antagonise cardiac effect
– Salbutamol iv in 5%dextrose over 15 min.
– Na Bicarbonate 1.26%, give 500 ml over 6-8 hrs only
if there is metabolic acidosis.
– Hemodialysis or hemofiltraion or peritoneal dialysis if
above fails or in patient with renal failure.