Fluid & Electrolytes Imbalance PDF

FLUID & ELECTROLYTES ANHAR KAMARUDIN EMERGENCY DEPARTMENT PPUM COMPARTMENTS As a function of TBW ICF ECF Interstitial fluid Intravascular fluid Total weight 60% 40% 20% 15% 5% Total body water 67% 33% 25% 8% E...

FLUID & ELECTROLYTES ANHAR KAMARUDIN EMERGENCY DEPARTMENT PPUM COMPARTMENTS As a function of TBW ICF ECF Interstitial fluid Intravascular fluid Total weight 60% 40% 20% 15% 5% Total body water 67% 33% 25% 8% ECF compartment 75% 25% IVF IF ECF Total body weight TBW ICF ELECTROLYTES HYPER HYPO Excess total body amount Depleted total body amount Shift between compartments Shift among compartments Relative fluid loss Relative fluid gain Rate of change of electrolyte concentrations rather than absolute concentrations usually determine the severity of symptoms Correction of the disturbance should occur over a time frame similar to the course during which the abnormality developed SODIUM  Total body [Na] content is between 40-50 meq / kg  Predominanlty in ECF space (98%)  Concentration in blood plasma = 140mmol/L (135-145mmol/L)  Concentration intracellular : 20mEq/L  intrinsic renal tubular damage or natriuretic response to hypervolemia Diagnosis  First step : Clinical evaluation of ECF volume status & measured and calculated plasma osmolalitis  Enable us to categorize whether TRUE hyponatremia (low plasma osmolality) or FACTITIOUS hyponatremia (normal or increases plasma osmolality) Hypertonic hyponatremia (Osm pressure >295)  Large quantities of osmotic solute accumulate in ECF space  Net movement of water from ICF -> ECF  dilute ECF [Na]  Most common causes : 1. Hyperglycemia (each 5 mmol/L increase in plasma glucose decreases serum [Na] by 1.6 to 1.8mEq/L 2. Mannitol excess 3. Glycerol therapy Treatment : Reduce the ECF hypertonicity – treat the underlying disorder Isotonic Hyponatremia  Hyponatremia with normal plasma osmolality -> pseudohyponatremia  High levels of plasma proteins and lipis increase the nonaqueous , non-[Na] containing fraction of plasma causing factitous measurements of sodium level  True Na and osmolality of plasma water are actually normal  Causes :  Hyperlipidaemia  Hyperproteinaemia -> multiple myeloma, Waldenstrom macroglobulinaemia No treatment required Hypotonic hyponatremia (Osm pressure Urinary [Na]>20mEq/L : clinical manifestation usually due to volume deficit -> Causes : diuretics, salt-wasting nephropathy(RTA), chronic renal failure, osmotic diuresis( glucose, urea, mannitol), mineralocorticoid deficiency (aldosterone) -> treatment : reexpansion of ECF volume with isotonic saline and appropriate correction of any underlying disorder  Extrarenal losses ->Urinary [Na]contracted ECF and hyponatremia -> causes : volume replacement with hypotonic fluids, GI loss(vomiting,diarrhea,fistula), third space loss(pancreatitis, peritonitis), sweating  Hypotonic - Euvolemic  Combination of normal volume status with hyponatremia  Clinically NOT EDEMATOUS & have nearly normal total body [Na] content despite presence of hyponatremia  Urine Na usually > 20mEq/L  Causes  SIADH (most notable)  Hypothyroidism  Pain,stress, nausea, psychosis  Drugs : ADH, nicotine, sulfonylureas, morphine, barbiturates, NSAIDS, acetaminophen, carbamazempine, TCA, phenothiazines, colchicine, clofibrate, cyclophosphamide, MAO, vincristine  Water intoxication(psychogenic polydipsia, lesion @ thirst center)  Glucocorticoid deficiency( GC required to suppress ADH)  Positive pressure ventilation  Porphyria TREATMENT : Fluid restriction and appropriate diagnosis & management of underlying disorder. Admission warranted Hypotonic - hypervolemic  Total body water in great excess  Manifestations of volume overload -> peripheral / pulmonary edema  Impaired ability to excrete water load result in water retention in excess of [Na] retention.  Divide into 2 a) Generalised edematous states without advanced renal insufficiency – urinary Na 20mEq/L Treatment : Optimize treatment for underlying disorder coupled with salt & water restriction. Diuretics, dialysis Emergency treatment of Severe hyponatremia  Na < 115 mEq/L / symptomatic -> treatment should be initiated  Urine electrolytes useful only before beginning treatment and therefor should be collected in eD  Hypovolemia – calculate Na deficit Total body [Na] deficit = desired plasma [Na] – actual plasma [Na] x TBW Replace with normal saline Severe hyponatremia 0.5mEq/L -> use 3% saline (513mEq/L), with careful observation. The rise in [Na[ should be no greater than 0.5 – 1mEq/L per hour (1-2mEq/L /hour if +seizures) HYPERNATREMIA  [Na] > 150mEq/L  Decrease in TBW or less commonly increase intake / decrease excretion  Main defense against hypernatremia : Thirst. 2% increase in plasma osmolality should stimulate thirst to increase free water intake.  Most hypernatremia in ED -> due to severe volume loss Symptoms  Acute symptoms appear in [Na] >158 mEq/L  Neurologic sx : Irritability, increased muscle tone, seizures, coma, death Massive brain haemorrhage / Cellular fluid loss, brain shrinkage & multiple small haemorrhages & tearing of cerebral blood vessels thromboses  Hypocalcemia frequently seen in hypernatremic patients (mechanism unclear  Clinical signs of hypernatrmiec states related to serum osmolality Osmolality (mOsm/kg) Manifestations 350-375 Restlessness, irritability 375-400 Tremulousness, ataxia 400-430 Hyperreflexia, twitching, spasticity >430 Seizures & death  Causes of Hypernatremia Excessive sodium Inadequate water intake Essential hypernatremia Iatrogenic sodium administration – Inability to obtain/swallow NaHCO3 & hypertonic saline water Accidental /deliberate ingestion of large Impaired thirst drive quantities of sodium -substitution of salt for sugar in infant formula Mineralocorticoid /GC excess Increases insensible loss -Primary aldosteronism, Cushing’s syndrome, Ectopic adrenocorticotropic hormone production Peritoneal dialysis GI – vomiting, diarrhea, intestinal fistula Renal loss – Central diabetes insipidus, impaired renal concentrating ability, osmotic diuresis (nephrogenic DI, hypercalcemia, multiple myeloma) Drugs/medication – lithium, phenytoin, sulfonylureas Skin loss : Burns, sweating Treatment of Hypernatremia  Cornerstone : VOLUME REPLETION  Should first use NS / lactate Ringer’s solution  Some concerned with usage of NS (154mEq/L is > than normal serum [Na] )  However, most hypernatremic stats -> TOTAL BODY [Na] DEFICIT  Restore perfusion with above solution then switch to 0.45% saline / another hypotonic soliution till urine output 0.5ml /kg / hour Calculation free water deficit in adults  Water deficit (L) = 0.6x weight (kg) x measured [Na] - 1  normal [Na]  Reduction in [Na] should not exceed 10-15 mEq/L per day  General rule : Each 1 L of water deficit results in a rise of serum [Na] of 3-5 mEq / L Protective mechanism of brain for hypernatremia  If hypernatremia develops gradually, idiogenic osmoles (amino acids : taurine) form and accumulate in the brain cells in attempt to increase intracellular osmolality.  This attracts water back into brain cells to restore cellular volume and prevent brain cell shrinkage  Rapid rehydration & lowering of serum [Na]  cerebral oedema ,seizures, permanent neurologic sequelae / death  Acute hypernatremia -> serum [Na] levels can be corrected rapidly with little fear of cerebral oedema as the idiogenic molecules are not yet present POTASSIUM Normal Values Parameter Values Intracellular 100-150 mEq/L Extracellular 3.5-5.0 mEq/L Total body store 33-55 mEq/kg or 3500 mEq in healthy 70kg adult Daily intake of K 50-150 mEq Significant & rapid intracellular to extracellular shifting occurs in response to severe injury (surgical stress, trauma / burns), acid-base imbalance, catabolic state, increased EC osmolality, insulin deficiency HYPOKALEMIA  Definition : serum [K] < 3.5 mEq/L  Causes : Intracellular shifts & Increased losses  High pH (alkalotic) ECF -> K shift into cells in exchange for H ions  Rise in pH 0.10 generally causes 0.5mEq/L decrease in serum [K]  Respiratory alkalosis & acidosis minimal effect on K shift  Symptoms appear at levels < 2.5 mEq/L – due to abnormalities of membrane polarization & effect almost every syste,  Symptoms & Signs of hypokalemia System S&S Cardiovascular Hypertension, orthostatic hypotension, potentiation of digitalis toxicity, dysrhythmias (usually tachycarrythmias), ECG : T flattening, U waves, ST depression Neuromuscular Malaise, weakness, fatigue Hyporeflexia Cramps Paresthesias Paralysis Rhabdomyolysis GI Ileus Renal Increased ammonia production, Urinary concentrating defects, Metabolic alkalemia, paradoxical aciduria, nephrogenic diabetes insipidus Endocrine Glucose intolerance  Causes of Hypokalemia Type Example Extracellular to Alkalosis Renal loss Diuretic therapy, intracellular potassium Inc plasma insulin Primary aldosteronism, shitts (treatment of DKA) Secondary Beta-adrenergics aldosteronism, Licorice Hypokalemic periodic ingestion, RTA, Osmotic paralysis diuretics Decreased intake Poor dietary intake, Drugs & toins Carbenicillin, penicillin, geophagia amphotericin B, lithium, thallium, theophylline, dopamine GI loss Vomitting, NG suction, Sweat loss Heavy exercise, heat diarrhea, stroke, febrile illness malabsorption Others Hypomagnesemia, acute leukemia, Treatment of Hypokalemia  Replacement of K Stable patients : ORAL  Advise food rich in K -> baked potatoes, spinach, lima beans, dried prunes, bananas, tomatoes  Salt substitutes : Dose of 20 mEq [K] every 30-60 minutes until desired result is achieved Severe hypokalemia : IV replacement - Administer KCL in 10 mEq – increments over 30-60 minutes, cumulative dose of 20mEq will raise serum K by 0.25mEq/L - No more than 40mEq should be added to each liter of IV fluid and infusion rate no greater than 40mEq/hour - Cardiac monitoring for infusion rates >20mEq/hour Hyperkalemia  K> 5.5 mEq/L  Clinical manifestation result from disordered membrane polarization  Cardiac manifestations most serious  VF , complete heart block, asystole  Death usually due to diastolic arrest / VF  Neuromuscular dysfunctional weakness, paresthesias, arreflexia, ascending paralysis & GI signs : nausea, vomiting, diarrhoea K (mEq/L) ECG changes 6.5 – 7.5 Prolonged PR interval, tall peaked T waves, short QT interval 7.5 – 8.0 Flattened P waves, QRS widening 10-12 QRS complex degradation into a sinusoidal pattern Treatment  Confirm the presence of nonfactitious hyperkalemia -> repeat sample  Immediate cessation of K administration  Asymptommatic patients (5-6 mEq/L) – determine & treat UL cause  Emergent treatment : continuous cardiac monitoring, correction & monitoring of electrolyte disturbance  3 Phases 1. Membrane stabilization 2. Intracellular shift K 3. Removal / excretion of K from the body Therapy Dose & route Onset of action Duration of effect Mechanism Albuterol(neb) 2.5mg in 4 ml NS, 15-30 min 2-4 hrs Upregulate cAMP, neb over 20 min shift K into cell Calcium 5-10ml IV 1-3 min 30-50 min Membrane chloride(10%) stabilization Calcium 10-20ml IV 1-3 min 30-50min Membrane gluconate (10%) stabilization NaHCO3 50-100mEq IV 5-10 min 1-2 h Shift K into cell Insulin & glucose 5-10U regular 30 min 4-6h Shift k into cell insulin IV 1-2 amps D50Q IV Furosemide 40mg IV Varies Varies Renal K excretion Sodium 25-50g PO/PR 1-2h 4-6h GI K excretion polystyrene sulfonate Haemodialysis - Minutes Varies Removes K CALCIUM  Total body Ca = 15g/kg of body weight  99% bound to bone as PO4 and carbonate, remainder in ECF  Normal daily intake 800-3g  1/3 absorbed in small bowel by active (vit D dep) & passive ( concentration dependent) absorption  Excretion : stool  Measured serum Ca 8.5-10.5mg /dL  Lab value reported in mEq/L is equal to half the amount in mg/dL (eg 4.2mg/dL is equal to 2.1 mEq/L or 1.05 mOsm/L) Calcium properties  50% bound to plasma protein  45% free active ion (physiologically active)  5% non ionized  Factors affecting protein binding 1. Serum protein – 0.8mg of Ca bind to 1g of protein 2. Alkalosis produce decrease in ionized fraction with no change in total serum Ca. Each 0.1 rise in pH lowers ionized Ca by 3-8% 3. Acidosis produce an increase in ionized fraction with no change in total serum Ca