DR .ALI A. ALLAWI CONSULTANT INTERNIST NEPHROLOGIST & RENAL TRANSPLANT PHYSCIAN
* Fluid and Electrolyte Imbalances
** Body Fluid Compartments
2/3 (65%) of TBW is intracellular (ICF)1/3 extracellular water25 % interstitial fluid (ISF) 5- 8 % in plasma (IVF intravascular fluid)1- 2 % in transcellular fluids – CSF, intraocular fluids, serous membranes, and in GI, respiratory and urinary tracts (third space)*
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* Fluid compartments are separated by membranes that are freely permeable to water. Movement of fluids due to: hydrostatic pressure osmotic pressure\ Capillary filtration (hydrostatic) pressure Capillary colloid osmotic pressure Interstitial hydrostatic pressure Tissue colloid osmotic pressure
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* Balance
Fluid and electrolyte homeostasis is maintained in the body Neutral balance: input = output Positive balance: input > output Negative balance: input < output*
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* Solutes – dissolved particles Electrolytes – charged particlesCations – positively charged ionsNa+, K+ , Ca++, H+Anions – negatively charged ionsCl-, HCO3- , PO43-Non-electrolytes - Uncharged Proteins, urea, glucose, O2, CO2
* Body fluids are: Electrically neutral Osmotically maintained Specific number of particles per volume of fluid
* Homeostasis maintained by:
Ion transport Water movement Kidney function* MW (Molecular Weight) = sum of the weights of atoms in a molecule mEq (milliequivalents) = MW (in mg)/ valence mOsm (milliosmoles) = number of particles in a solution
* Tonicity Isotonic Hypertonic Hypotonic
** Cell in a hypertonic solution
* Cell in a hypotonic solution
* Movement of body fluids “ Where sodium goes, water follows.”Diffusion – movement of particles down a concentration gradient.Osmosis – diffusion of water across a selectively permeable membraneActive transport – movement of particles up a concentration gradient ; requires energy* ICF to ECF – osmolality changes in ICF not rapidIVF → ISF → IVF happens constantly due to changes in fluid pressures and osmotic forces at the arterial and venous ends of capillaries
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* Regulation of body water
ADH – antidiuretic hormone + thirstDecreased amount of water in bodyIncreased amount of Na+ in the bodyIncreased blood osmolalityDecreased circulating blood volumeStimulate osmoreceptors in hypothalamusADH released from posterior pituitaryIncreased thirst*
* Result: increased water consumption increased water conservation Increased water in body, increased volume and decreased Na+ concentration
* Dysfunction or trauma can cause: Decreased amount of water in body Increased amount of Na+ in the body Increased blood osmolality Decreased circulating blood volume
* Edema is the accumulation of fluid within the interstitial spaces. Causes: increased hydrostatic pressure lowered plasma osmotic pressure increased capillary membrane permeability lymphatic channel obstruction
* Hydrostatic pressure increases due to: Venous obstruction: thrombophlebitis (inflammation of veins) hepatic obstruction tight clothing on extremities prolonged standing Salt or water retention congestive heart failure renal failure
* Decreased plasma osmotic pressure: ↓ plasma albumin (liver disease or protein malnutrition)plasma proteins lost in :glomerular diseases of kidneyhemorrhage, burns, open wounds and cirrhosis of liver
* Increased capillary permeability: Inflammation immune responses Lymphatic channels blocked: surgical removal infection involving lymphatics lymphedema
* Fluid accumulation: increases distance for diffusion may impair blood flow = slower healing increased risk of infection pressure sores over bony prominences Psychological effects
* Edema of specific organs can be life threatening (larynx, brain, lung) Water is trapped, unavailable for metabolic processes. Can result in dehydration and shock. (severe burns)
* Electrolyte balance
Na + (Sodium) 90 % of total ECF cations 136 -145 mEq / L Pairs with Cl- , HCO3- to neutralize charge Low in ICF Most important ion in regulating water balance Important in nerve and muscle function*
* Regulation of Sodium
Renal tubule reabsorption affected by hormones: Aldosterone Renin/angiotensin Atrial Natriuretic Peptide (ANP)* Potassium
Major intracellular cation ICF conc. = 150- 160 mEq/ L Resting membrane potential Regulates fluid, ion balance inside cell pH balance* Regulation of Potassium
Through kidney Aldosterone Insulin* Isotonic alterations in water balance
Occur when TBW changes are accompanied by = changes in electrolytesLoses plasma or ECFIsotonic fluid loss ↓ECF volume, weight loss, dry skin and mucous membranes, ↓ urine output, and hypovolemia ( rapid heart rate, flattened neck veins, and normal or ↓ B.P. – shock)* Isotonic fluid excessExcess IV fluidsHypersecretion of aldosteroneEffect of drugs – cortisoneGet hypervolemia – weight gain, decreased hematocrit, diluted plasma proteins, distended neck veins, ↑ B.P.Can lead to edema (↑ capillary hydrostatic pressure) pulmonary edema and heart failure
* Electrolyte imbalances: Sodium
Hypernatremia (high levels of sodium)Plasma Na+ > 145 mEq / LDue to ↑ Na + or ↓ waterWater moves from ICF → ECFCells dehydrate*
* Hypernatremia Due to:Hypertonic IV soln.Oversecretion of aldosteroneLoss of pure waterLong term sweating with chronic feverRespiratory infection → water vapor lossDiabetes – polyuriaInsufficient intake of water (hypodipsia)
Causes of hypernatraemia ADH deficiency Diabetes insipidus latrogenic Administration of hypertonic sodium solutions Insensitivity to ADH (nephrogenic diabetes insipidus) Lithium ,Tetracyclines, Amphotericin B Acute tubular necrosis Osmotic diuresis Total parenteral nutrition Hyperosmolar diabetic coma PLUS Deficient water intake
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* Clinical manifestations of Hypernatremia
Thirst Lethargy Neurological dysfunction due to dehydration of brain cells Decreased vascular volume
* Treatment of Hypernatremia
in ADH deficiency, replace ADH in the form of desmopressin, a stable non-pressor analogue of ADH remember to withdraw nephrogenic drugs where possible and replace water either orally or, if necessary, intravenously. In severe (> 170 mmol/L) hypernatraemia, 0.9% saline (150 mmol/L) should be used initially. Avoid too rapid a drop in serum sodium concentration; the aim is correction over 48 hours, as over-rapid correction may lead to cerebral oedema. In less severe (e.g. > 150 mmol/L) hypernatraemia, the treatment is 5% dextrose or 0.45% saline; the latter is obviously preferable in hyperosmolar diabetic coma. Very large volumes - 5 L a day or more - may need to be given in diabetes insipidus. .* Hyponatremia
Overall decrease in Na+ in ECF Two types: depletional and dilutional Depletional Hyponatremia Na+ loss: diuretics, chronic vomiting Chronic diarrhea Decreased aldosterone Decreased Na+ intake* Dilutional Hyponatremia:Renal dysfunction with ↑ intake of hypotonic fluidsExcessive sweating→ increased thirst → intake of excessive amounts of pure waterSyndrome of Inappropriate ADH (SIADH) or oliguric renal failure, severe congestive heart failure, cirrhosis all lead to:Impaired renal excretion of waterHyperglycemia – attracts water
Causes of hyponatraemia with normal extracellular volume
Abnormal ADH release Vagal neuropathy (failure of inhibition of ADH release) Deficiency of adrenocorticotrophic hormone (ACTH) or glucocorticoids (Addison's disease) Hypothyroidism Severe potassium depletionSyndrome of inappropriate antidiuretic hormone Major psychiatric illness 'Psychogenic polydipsia‘ Nonosmotic ADH release? Antidepressant therapyIncreased sensitivity to ADH Chlorpropamide, TolbutamideADH-like substances Oxytocin Desmopressin *Unmeasured osmotically active substances stimulating osmotic ADH release Glucose Chronic alcohol abuse Mannitol Sick-cell syndrome (leakage of intracellular ions)
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Causes of hyponatraemia with decreased extracellular volume
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Causes of hyponatraemia with increased extracellular volume Heart failure Liver failure Oliguric renal failure Hypoalbuminaemia
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* Clinical manifestations of Hyponatremia
Neurological symptomsLethargy, headache, confusion, apprehension, depressed reflexes, seizures and comaMuscle symptoms Cramps, weakness, fatigueGastrointestinal symptomsNausea, vomiting, abdominal cramps, and diarrheaTx – limit water intake or discontinue medsDISORDERS OF POTASSIUM CONTENT AND CONCENTRATION
The usual dietary intake varies between 80 and 150 mmol daily, depending upon fruit and vegetable intake. Most of the body's potassium (3500 mmol in an adult man) is intracellular. Serum potassium levels are controlled by: uptake of K+ into cells renal excretion extrarenal losses (e.g. gastrointestinal). Uptake of potassium into cells is governed by the activity of the Na+/K+-ATPase in the cell membrane and by H+ concentration. Uptake is stimulated by: insulin β-adrenergic stimulation theophyllines. Uptake is decreased by: α-adrenergic stimulation acidosis - K+ exchanged for H+ across cell membrane cell damage or cell death - resulting in massive K+ release ** Hypokalemia
Serum K+ < 3.5 mEq /LBeware if diabeticInsulin gets K+ into cellKetoacidosis – H+ replaces K+, which is lost in urineβ – adrenergic drugs or epinephrineCauses of hypokalaemia
*Reduced intake
Intravenous fluids without K+ Dietary deficiencyRedistribution into cellsβ-Adrenergic stimulation / Acute myocardial infarction Beta-agonists: e.g. fenoterol, salbutamol / Insulin treatment, e.g. treatment of diabetic ketoacidosis /Correction of megaloblastic anaemia, e.g. B12 deficiency Alkalosis/ Hypokalaemic periodic paralysisGastrointestinal lossesVomiting / Severe diarrhoea /Purgative abuse / Villous adenoma /Ileostomy or uterosigmoidostomy / Fistulae / Ileus/intestinal obstruction ** Clinical manifestations of Hypokalemia
Neuromuscular disordersWeakness, flaccid paralysis, respiratory arrest, constipationDysrhythmias, appearance of U wavePostural hypotensionCardiac arrestOthers – table 6-5Treatment-Increase K+ intake, but slowly, preferably by foods
Treatment of hypokalaemia
Cause dietary deficiency Increase intake of fresh fruit/vegetables or oral potassium supplements (20-40 mmol daily) (Potassium supplements can cause gastrointestinal irritation Hyperaldosteronism, e.g. cirrhosis, thiazide therapy Spironolactone Co-prescription of a potassium-sparing diuretic with a similar onset and duration of action Intravenous fluid replacement Add 20 mmol/L of K+ with monitoring*
* Hyperkalemia
Serum K+ > 5.5 mEq / LCheck for renal diseaseMassive cellular traumaInsulin deficiencyAddison’s disease Potassium sparing diureticsDecreased blood pHExercise causes K+ to move out of cellsCauses of hyperkalaemia
Decreased excretion Renal failure /* Drug:* direct effect on potassium handling /Amiloride / Triamterene / Spironolactone /Aldosterone deficiency/ Hyporeninaemic hypoaldosteronism (RTA type 4)/ Addison's disease/ ACE inhibitors*/ NSAIDs/ Cyclosporin treatment/ Heparin treatment Acidosis/* Gordon's syndromeIncreased release from cells (decreased Na+/K+-ATPase activity Acidosis/ Diabetic ketoacidosis/ Rhabdomyolysis/tissue damage /Tumour lysis /Succinylcholine (amplified by muscle denervation)/ Digoxin poisoning Vigorous exercise (α-adrenergic; transient ) Increased extraneous load Potassium chloride Salt substitutes Transfusion of stored blood*Spurious Increased in vitro release from abnormal cells Leukaemia / Infectious mononucleosis / Thrombocytosis / Familial pseudohyperkalaemia / haemolysis in syringeIncreased release from muscles Vigorous fist clenching during phlebotomy ** Clinical manifestations of Hyperkalemia
Early – hyperactive muscles , paresthesiaLate - Muscle weakness, flaccid paralysisChange in ECG patternDysrhythmiasBradycardia , heart block, cardiac arrest* Treatment of Hyperkalemia
Correction of severe hyperkalaemia IMMEDIATE Attach ECG monitor and IV access Protect myocardium 10 mL of 10% calcium gluconate IV over 5 mins Effect is temporary but dose can be repeated after 15 mins Drive K+ into cells Insulin 10 units + 50 mL of 50% glucose IV over 10-15 mins followed by regular checks of blood glucose and plasma K+ Repeat as necessary and/or correction of severe acidosis (pH < 6.9) - infuse NaHCO3 (1.26%) and/or salbutamol 0.5 mg in 100 mL of 5% glucose over 15 min (rarely used LATER Deplete body K+ (to decrease plasma K+ over next 24 h) Polystyrene sulphonate resins 15 g orally up to three times daily with laxatives 30 g rectally followed 3-6 hours later by an enema Haemodialysis or peritoneal dialysis if the above fails* Calcium Imbalances
Most in ECFRegulated by:Parathyroid hormone↑Blood Ca++ by stimulating osteoclasts↑GI absorption and renal retentionCalcitonin from the thyroid glandPromotes bone formation↑ renal excretion* Hypercalcemia
Results from:Hyperparathyroidism Hypothyroid statesRenal diseaseExcessive intake of vitamin DMilk-alkali syndromeCertain drugsMalignant tumors – hypercalcemia of malignancyTumor products promote bone breakdownTumor growth in bone causing Ca++ release