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
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 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)
Isotonic hyponatremia: Is a spurious hyponatremia normalTotal Serum sodium is normal normalOsmolality is normal It is due to; –hyperlipidemia –hyperlipidemia or –hyperprotienemia –hyperprotienemia(>10g/dl) falsely low serum Na reading. Na plasmaplasma Na
Hypertonic hyponatremia High osmolalityLogically 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) bothDue to loss of both Na and water >Na loss > water loss Causes: –Renal: Diuretics Slat loosing nephropathy Mineralocorticoid deficiency Osmotic diuresis –Extra renal: 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) 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.
Clinical features of hyponatremia 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 ifSerious hyponatremia occurs if: [medical emergency] –Rapid reduction in serum Na –Serum Na < 110 meq/l
Investigations of hyponatremia 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 –Low serum Na –Low serum osmolality –High urine osmolality –Normal or high ECF volume
Offending cause Management of hyponatremia Salineifhypovolumic Water restriction if not hypovolumic +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 slow iv infusion –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 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 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 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: –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: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 –Hyperaldosteronism, Cushing, –Diabetes mellitus –Metabolic alkalosis –Drugs: »Diuretics, corticosteroids, aminoglycosides, carbenoxolone Renal: –Recovery phase of ATN –RTA
Hypokalemia Investigations: –Serum K –ECG: 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 –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)(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: Bleeding into soft tissues Haemolysis Rhabdomyolysis Sever burns Vigorous exercise –Shift of K out of cell: 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:Management: –Exclude spurious hyperkalemia –Stop any K source –Cation exchange resin Sodium polystyrene sulphonate Calcium resonium –Correct underlying cause Urgent treatment: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.