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Fluid and electrolyte disorders (Dehydration (HYPERTONIC DEHYDRATION…
Fluid and electrolyte disorders
Disorders of extracellular volume
Disorders of water metabolism
Disorders of potassium metabolism
Disorders of Calcium and Phosphate metabolism
Acid-Base balance and disorders
The body compartments
ECF electrochemical equilibrium
Cations 153 mEq/l: Na+ 144, K+ 4,5, Ca2+ 2,5, Mg2+ 2,0
Anions 153 mEq/l: Cl- 101, HCO3- 26, Protein anions 16, other 10
ANION GAP
AG = Na+ – (Cl- + HCO3-)
Normal range: <12 mEq/l
Anions not assessed in routine practice: Protein, Organic acid, Phosphate, Sulphate
SERUM OSMOLALITY
Osmolality – a measure of the number of dissolved particles per unit of water in serum
CALCULATED:
Total osmolality = 2[Na+(mmol/l)] + [glucose(mmol/l)] + [urea(mmol/l)]
Total osmolality = 2[Na+(mmol/l)] + [glucose (mg/dl)/18] – [BUN (mg/dl)/2,8]
Estimated in pts with normal renal function and no DM: Osmolality = 2[Na+(mmol/l)] + 10
MEASURED:
Measured with the use of osmometer.
Normal range: 280-295 mmol/kg H2O
hypoosmolality – < 280 mmol/kg H2O
hyperosmolality – > 295 mmol/kg H2O
I.V. Replacement fluids in widespread use
Body fluid osmolality-regulatory factors
ADH-vasopressin
hypernatremia hyperglicaemia, DEHYDRATION --> reales ADH--> collecting tubules to reabsorb water
THIRST
Assessment of patient’s hydration
BP, HR, Jugular veins, Skin turgor, Eye bulb turgor
Mucous membranes (dry if dehydrated)
In hospital ward: 24 hrs fluid balance/chart, Weight, CVP (6-10 cm H2O)
SODIUM METABOLISM
Average body sodium content = 4200 mmol
91% of sodium in ECF.
Average Na concentration in ECF = 140 mmol/l
Average Na concentration in ICF = 10-20 mmol/l
Daily sodium intake = 2-4 g (80-160 mmol)
Excretion: 95% urine, 4,5% digestive tract, 0,5% skin/sweat
RENAL SODIUM EXCRETION
Urine Na concentration = 10-400 mmol/l
Excretion regulation: GFR, Aldosterone, Natriuretic peptides: ANP, BNP
Dehydration
CAUSES OF EXCESS WATER LOSSES:
ventilation, Excessive sweating, vomiting, diarrhea, hemorrhage, diuresis
causes of hypovolemia
Reduced cardiac output
Fluid redistribution:
hypoalbuminemia (liver cirrhosis, nephrotic syndrome)
Increased vessel permeability (Acute Pancrestitis, small bowel ischaemia, rabdomyolysis, sepis)
Water deficit estimation
Clinical:
2 liter: faintness, tachycardia, orthostatic RR fall
4 liter: systolic BP recumbent 80-100 mmHg, apathy, vomiting
5-6 liter: systolic BP recumbent < 80 mmHg, loss of consciousness
Laboratory:
[20 x BW (kg)/(1-Ht1) x 100] x [Ht2 – Ht1/Ht2]
Water deficit = (Na+ - 140) / 140 x 0,6 x BW
Ht1 – normal hematocrit
Ht2 – current hematocrit
HYPERTONIC DEHYDRATION
Free water deficit, both ECF and ICF volume reduced.
Etiology
water intake reduced
insensible water losses (sweating/fever, respiration)
diabetic coma,
diabetes insipidous
excessive intake of osmotically active substances (mannitol, glycerol)
SYMPTOMS
Related to dehydration
Related to increased osmolality
-cell dehydration, reduced MCV
-CNS symptoms: delirium, desorientation
-inrtacerebral hemorrhage
TREATMENT
Remove cause
Symptomatic:
rehydration and lowering natremia (1 mEq/l/h when acute and 0,5 mEq/l/h when chronic hipernatremia present)
p.o.: water and electrolyte free fluids
i.v.: 5% glucose, 0,45% NaCl
HYPERNATREMIA
Increase in serum sodium concentration > 145 mmol/l.
Causes: excessive sodium load, Hypotonic fluid loss
Symptoms – dependent on cell dehydration:
-anxiety, desorientation
-muscle cramps, seizures
-Lab tests: decreased MCV
Treatment:
1 mEq/l/h when acute and 0,5 mEq/l/h when chronic hipernatremia present
oral fluids preferred in conscious pts. (NaCl)
Hypervolemic hypernatremia—diuretics and remove excess sodium
Diagnosis
ISOTONIC DEHYDRATION
Concomitant proportional water and sodium loss not leading to changes in serum osmolality
Afects only ECF.
Etiology
Renal: Polyuric phase of ARF, salt losing nephritis
Extrarenal: vomiting, diarrhea, Fluid loss to „third space” (Acute pancreatitis, peritonitis), burns, hemorrhage
TREATMENT
Remove cause
Symptomatic:
-0,9% NaCl, or other fluid replacement similar in composition to ECF (Ringers solution)
-Diarrhea:
I.V. Infusion of (5 g NaCl, 4 g NaHCO3, 1 g KCl)/liter,
oral: glass orange juice, 1 l water, 2 spoons sugar, 1⁄2 teaspoon salt
HYPOTONIC DEHYDRATION
Salt loss > water loss leading to ECF contraction and ICF expansion
Etiology:
Isotonic dehydration treated with electrolyte free i.v. fluids
salt losing nephritis
diuretic use (tiazides)
Symptoms: related to hypovolaemia, related to hyponatremia
Treatment: I.V. electrolyte solutions (NaCl, NaHCO3)
Clinical features
mental status changes, sleepiness, coma
orthostatic hypotension, tachycardia, decreased pulse pressure, decreased central venous pressure (CVP)
Skin: poor skin turgor, hypothermia, pale extremities, dry tongue
Oliguria
OVERHYDRATION
Isotonic Volume Expansion
Increased ECF volume, ICF volume unchanged .
Etiology: CHF, CRF, Liver cirrhosis, Nephrotic syndrome, hypoproteinemia
SYMPTOMS
increased BW
hydrothotax, ascites
edema (also pulmonary edema)
low hematocrit, low urine specific gravity
Jugular venous distention
TREATMENT
Treat underlying cause: e.g. heart failure treatment
Symptomatic:
-fluid and sodium restriction
-diuretics
-in CRF renal replacement therapy
hypotonic volume expansion
Excessive intake of electrolyte free fluids in RF or inadequate ADH secretion
Volume expansion of both ECF and ICF.
Symptoms: related to volume expansion, related to hyponatremia
Treatment options: fluid restriction, osmotic diuretics (20% mannitol), dialysis
HYPONATREMIA
Serum [Na+] < 135 mmol/l.
Possible causes:
-dilution of body fluids with excess water
-sodium deficit (rare):
Excess electrolyte free fluids, SIADH, Adrenal cortex insufficiency (Addison’s desease), Medications e.g.: carbamazepine, cyclophosphamide
Diagnosis
SYMPTOMS
Related to expansion of ICF due to water shift:
High MCV,
CNS cells swelling: general weakness, nausea and vomiting, headache, disorientation, seizures, coma
[Na+ ] 125 mmol/l --> CNS volume increased 10%
TREATMENT
CAU T I O U S LY
When corrected quickly-->pons demyelinization, tetraplegia, decreased respiratory drive
Acute (<48hrs) >>> increase [Na+ ] not more than 20 mml/d
Chronic >>> increase [Na+ ] not more than 10-12 mml/d
I.v. 0,9% NaCl,
10 % NaCl only if: [Na+ ] <125 mmol/l, lub when symptomatic
Hypertonic volume expansion
causes:
Excessive i.v. hypertonic or isotonic sodium chloride in impaired renal function
Leads to ECF expansion and ICF contraction.
Symtoms: edema, CNS dehydration
Treatment: water and salt restriction, diuretics (loop), dialysis
Potassium disorders
Distribution in the Body:
Total body K+ stores: 50-55 meq/kg body weight (3500-4000 meq K+ total)
Extracellular fluid compartment: 2% [K+] = 3.5-5.0 meq/L (50-100 meq K+)
Intracellular fluid compartment: 98% [K+] = 120-150 meq/L
Large cellular K+ (and Na+) concentration gradients are maintained by the Na,K-ATPase
Hypokalemia hyperpolarizes excitable tissues
Hyperkalemia depolarizes excitable tissues
Potassium Homeostasis
External Balance: The regulation of total body potassium content through alterations in potassium intake (e.g. dietary) and excretion (e.g. renal, GI)
Internal Balance: The regulation of the distribution of potassium between intracellular fluid (ICF) and extracellular fluid (ECF) compartments
Intake & Renal K+ Reabsorption
intake
Dietary intake = 50-150 meq/day (3-9 grams KCl/day)
IV KCl, hyperalimentation, drugs
Blood products
Renal potassium reabsorption
Proximal tubule:
• Majority of solute and H2O transport
• Passive processes
• 65% filtered K+ load
Thick ascending limb
• 25% filtered K+ load
• Active + passive processes
• Na-K-2Cl cotransporter
Cortical and medullary collecting ducts
• Intercalated cells (Type A + Type B)
• Active process
• H-K-ATPase
Internal Balance
Physiologic Factors
Insulin
Insulin stimulates the cellular uptake of potassium via an increase in Na+,K+-ATPase activity
Insulin and potassium are components of a regulatory loop
High splanchnic K+ concentration stimulates pancreatic insulin secretion
Insulin stimulates K+ uptake by the liver and muscle returning serum [K+] to normal
Catecholamines
stimulate the cellular uptake of potassium via 2- adrenergic receptors by increasing Na+,K+-ATPase activity
Pathophysiologic
Acid-Base Disturbances
Changes in extracellular pH produce reciprocal shifts in H+ and K+ between extracellular and intracellular fluid compartments
Metabolic acid-base disturbances have a greater effect than respiratory disturbances
Metabolic acidoses due to organic acids (ketoacidosis, lactic acidosis) have smaller effects than do acidoses due to mineral acids
Acidemia: K+ out, H+ in
Alkalemia: K+ in, H+ out
Plasma Tonicity
Increases in plasma tonicity --> fluid shifts from the intracellular to the extracellular compartments and K+ exits the intracellular compartment along with water via solvent drag
Hyperkalemia
Plasma [K+] > 5.0
may be the result of disturbances in external balance (total body K+ excess) or in internal balance (shift of K+ from intracellular to extracellular compartments)
Disorders of External Balance:
Decrease Renal K+ excretion, Excessive K+ intake, Acute & chronic renal failure, Decrease Distal tubular flow, Distal tubular dysfunction, Mineralocorticoid deficiency
Disorders of Internal Balance:
Insulin deficiency, B2-Adrenergic blockade, Hypertonicity, Acidemia, Cell lysis
Clinical Manifestations
result primarily from the depolarization of resting cell membrane potential in myocytes and neurons
Cardiac toxicity: ECG changes, Cardiac conduction defects, Arrhythmias
Neuromuscular changes: Ascending weakness, ileus
EKG
Peaked T-wave, Wide QRS Complex, Shortened QT Interval, Prolonged PR Interval, Further Widening of QRS Complex Absent P-Wave, Sine-Wave Morphology (e.g. Ventricular Tachycardia)
Iatrogenic Hyperkalemia
Multi drug treatment, i.e. Cardiology patients:
ACEI &/OR ARB, ß blockers, Potassium sparing diuretic (Spironolactone), Potassium supplement
Treatment
Membrane Stabilization: IV calcium
Internal Redistribution: IV insulin (+ glucose), ß-adrenergic agonist (albuterol inhaled)
Enhanced Elimination: Kayexalate (sodium polystyrene sulfonate) ion exchange resin, Loop diuretic, Hemodialysis
Glucose + insulin
Glucose : insulin - 3 : 1
500 ml 5% glucose = 5 x 5 = 25 g glucose + 8 j short acting insulin
100 ml 40% glucose = 40 g glucose + 14 j short acting insulin
Hypokalemia
Plasma [K+] < 3.5
may result from disturbances in external balance (total body K+ deficiency) or internal balance (transmembrane K+ shifts)
Disorders of External Balance
Inadequate dietary intake (Malnutrition),
Increased extrarenal K+ losses:
GI: Diarrhea, Enteric fistulas
Cutaneous: Burns
Increased renal K+ losses + Hypertension
Hyperreninemia– Renin excess (renal artery stenosis, renin-secreting tumor)
Primary hyperaldosteronism (Conn’sSyndrome) – Mineralocorticoid excess (adrenal hyperplasia, tumor)
Cushing’s syndrome – Glucocorticoid excess (exogenous, pituitary, adrenal)
Congenital adrenal hyperplasia – Enzymatic defects in cortisol biosynthesis (excess aldosterone precursors)
Increased renal K+ losses - Hypertension
Diuretics
Osmotic diuresis – Glucosuria
Renal tubular acidoses
Prolonged vomiting, nasogastric drainage
Ureteral diversion – Ureteroileostomy, ureterosigmoidostomy
Disorders of Internal Balance
– Insulin excess
– Catecholamine excess
• Myocardial ischemia/infarction
• Delirium tremens
• Pharmacologic agents
– Alkalemia
– Cell proliferation
• Rapidly proliferating leukemia or lymphoma
Manifestations
Cardiac – EKG changes – Arrhythmias
Smooth muscle – Hypertension – Ileus
Skeletal muscle – Weakness – Rhabdomyolysis
Metabolic – Glucose intolerance – Growth retardation
Renal – Increased renal ammoniagenesis – Nephrogenic diabetes insipidus
EKG
Flat T-wave, Prominent U-wave, Depressed ST-segment
Treatment
Potassium Replacement – Oral or IV (kcal)
Potassium-sparing diuretics
– ENaC sodium channel inhibitors • Amiloride, triamterene
– Mineralocorticoid antagonists • Spironolactone
