Electrolyte imbalance and Fluid replacement. Dr. HO, kai leung Kelvin Honorary Consultant in Nephrology Hong Kong Sanatorium and Hospital

Transcription

1 Electrolyte imbalance and Fluid replacement Dr. HO, kai leung Kelvin Honorary Consultant in Nephrology Hong Kong Sanatorium and Hospital

2 Electrolyte imbalance Sodium (Na): Hyponatraemia and hypernatraemia Potassium (K): Hypokalaemia and hyperkalaemia Calcium (Ca): Hypocalcaemia and hypercalcaemia Phosphate (PO4): Hypophosphataemia and hyperphosphataemia

3 Sodium Under physiological conditions: plasma Na concnetration is kept in a very range between mmol/l (meq per L). It is the predominant cation in extracellular fluid (ECF) contributing to osmolality. Equally narrow range of osmolality of body fluid between mosm per kg P(osm)= 2[Na] + [blood urea nitrogen (mg/dl)/2.8]+[glucose (mg/dl)/18]

4 Plasma sodium Serum Na concentration and plasma osmolality are maintained by an osmoreceptor which controls the secretion of antidiuretic hormone (ADH) ADH controls the water excretion in renal tubules by allowing urinary dilution in its absence, and urinary concentration in its presence. Hyponatraemic disorders supervene when the intake of water exceeds the patient s renal diluting capacity Hypernatraemia supervene when there are renal concentrating defects accompanied by inadequate water intake

5 Hyponatraemia Definition : when < 135 meq per L Frequently found in 10% - 15% hospitalised patients Presence in chronically diseased outpatients

6 Hyponatraemia - Signs and Symptoms: Lethargy, apathy Disorientation Muscle cramps Anorexia, nausea Agitation Signs Abnormal sensorium Depressed tendon reflexes Cheyne-Stokes respiration Seizures Death in acute cases symptoms

7 Hyponatraemia Approach It is important to interpret serum Na and osmolality of the patient simultaneously Hyponatreamia with normal osmotic state Hyponatraemia with hypo-osmotic state

8 Hyponatraemia with normal Na level and normal osmotic state Translocational hyponatraemia: the presence of osmotically active solutes moves water from intracellular to extracellular compartment causing a decrease in serum Na concentration Hyperglycaemia in diabetes mellitus (hyponatraemia corrected when treated hyperglycaemia with insulin) Mannitol Pseudohyponatraemia: when solid phase of plasma is greatly increased in Severe hypertriglyceridaemia Paraproteinaemia (e.g. myeloma)

9 Hypo-osmolar hyponatraemia patient In the absence of osmotically active solutes or excessive high lipids or protein -> assess the fluid status of patient allows classification of hyponatraemic patients into 3 catagories: 1. Oedema -> excess water and total body Na 2. Dehydrate -> deficit of water and total body Na 3. Euvolumic -> near-normal total body Na

10 Dehydration

11 Pitted edema Fluid overload

12 Hypervolaemic (Oedematous) hyponatraemic patient Increased total body water more than increase of Na: 1. Cardiac failure & cirrhosis active renal tubular reabsorption of Na, & urinary sodium is low (<10 meq/l) 2. Nephrotic syndrome & Renal failure presence of renal tubular dysfunction, urinary Na concentration is higher (>20 meq/l)

13 Hypovolaemic hyponatraemic patient Signs of dehydration A spot urine Na concentration is useful: 1. Normal function kidney with a low urine Na concentration (<10 meq/l): 1. G.I.: vomiting or diarrhoea, or both 2. Into abdominal cavity in peritonitis, pancreatitis 3. Into bowel lumen in ileus or pseudomembranous colitis 4. Excessive use of laxatives

14 Hypovolaemic hyponatraemic patient 2. Spot urinary Na concentration is higher (>20 meq/l): suggesting renal loss of Na & water: 1. Excessive use of thiazide diuretics: the presence hyponatraemia, hypokalaemia, and metabolic alkalosis 2. Salt-lossing nephritis: medullary cystic disease, polycystic kidney disease, chronic interstitial nephritis, analgesic nephropathy 3. Mineralocorticoid deficiency: Addison s disease (i.e. primary adrenal insufficiency) 4. Osmotic diuresis: hyperglycaemia in uncontrolled diabetes, urea diuresis after relief of urinary tract obstruction

15 Euvolaemic hyponatraemia A common form of hyponatraemia in hospitalised patients Urinary Na concentration is > 20 meq/l Causes: Hypothyroidism Secondary adrenal insufficiency (glucocorticoid deficiency) due to prolonged steroid treatment low cortisol; raised ACTH, normal sex hormone Syndrome of inappropriate antidiuretic hormone (SIADH) in infections, neoplastic disease in lung and CNS

16 Hypernatraemia Definition: Plasma Na > 150 meq/l Always associate with a hypertonic state (hyper-osmolar) Approach: Hypovolaemia hypernatraemia Hypervolaemic hypernatraemia Euvolaemic hypernatraemia

17 Hypovolaemia hypernatraemia Volume depletion Either renal or extra-renal losses Extra-renal losses: GI: hypotonic diarrhoea (G.E. or lactulose)-> urine Na concentration <10 meq/l & hypertonic urine, hypotonic urine (if fluid replacement with normal saline) Renal losses: Loop diuretics and osmotic diuresis (diabetic ketoacidosis) -> hypotonic urine, and urine Na concentration > 20mEq/L

18 Hypervolaemic hypernatraemia Usually due to excessive amounts of hypertonic NaCl or sodium bicarbonate Raised JVP and pulmonary congestion, not much peripheral oedema

19 Euvolaemic hypernatraemia 1. Extra-renal loss of fluid in: Febrile or hypermetabolic states, exercises: loss from skin and lung usually with normal or near normal total boy fluid volume due to normal osmoreceptorvasopressin-renal response induce thirst Patients with normal access to fluid Urine osmolality is usually very high Urine Na varies with sodium intake

20 Euvolaemic hypernatraemia 2. Renal losses of water: 1. Central diabetes insipidus (defects in vasopressin production or release): 50% no detectable underlying cause Pituitary or hypothalamus lesions trauma, surgical, neoplasms, infection 2. Nephrogenic diabetes insipidus (failure of the collecting duct to response to vasopressin): Congenital: X-linked, autosomal recessive forms Acquired causes: Chronic renal diseases: PKD, medullary cystic disease, analgesic nephropathy, pyelonephritis, ureteric obstruction Electrolyte imbalance: hypercalcaemia, hypokalaemia Drugs: lithium, colchicine, amphotericin Dietary: excessive water intake (compulsive), low salt and protein diet Others: multiple myeloma, amyloidosis, sickle cell disease, Sjogren s syndrome 3. Gestational: Vasopressinase excessive rapid degradation of vasopressin Combinations of central and nephrogenic DI

21 Water deprivation test To differentiate the various forms of diabetes insipidus from primary polydipsia in patients presented with polyuria

22 Therapy fluid replacement Correction of ECF volume depletion (dehydration): Isotonic saline (0.9% NS) until restoration of ECF correct volume Hypotonic (0.45% NS) or 5% glucose solution correct plasma osmolality

23 Therapy fluid replacement Correction of ECF volume expension: Diuretics (furosemide) Dialysis in patients with advanced renal failure Correction of euvolaemic patients: Oral fluid i.v. 5% dextrsoe

24 Potassium Intracellular cation Regulate Neuromuscular and cardiovascular excitability Intracellular enzyme function Within narrow range of meq/l

25 Hypokalaemia Causes: 1. Cell shifts of K: Insulin use, catecholamine-mediated (e.g. MI, angina, COPD exacerbation) 2. Decrease in total body potassium: Decrease intake Increase renal and non-renal losses: Non-renal losses: low urinary K excretion level <20 meq/l (24-hour or spot urine measurement) GI losses (laxative abuse, infection) presence of metabolic acidosis; laxative induced with metabolic alkalosis

26 Hypokalaemia 3. Renal losses: Urinary K excretion > 20mEq/L or 20 meq per day Metabolic acidosis renal tubular acidosis (type I&II), diabetic ketoacidosis (osmolal diuresis), ureterosigmoidostomy, or carbonic anhydrase inhibitor use Metabolic alkalosis: Low urinary chloride concentration (< 20 meq/l) upper GI losses (e.g. vomiting), diuretic use High urinary chloride concentration:» Normotensive patient -> diuretic use (loop)» Hypertensive patients -> aldosterone related diseases

27 Hypokalaemia Manifestations Paresis Parapalysis Cardiac: SVT, VT

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29 Hypokalaemia

30 Hypokalaemia Treatment Replacement: 10 meq per hour into peripheral vein Oral supplement

31 Hyperkalaemia Causes: 1. Shift of K from cellular to extracellular- Red blood cell haemolysis, extreme leucocytosis and thrombocytosis Metabolic acidosis Exercise Muscle breakdown (rhabdomyolysis) Drug intoxication e.g. digitalis 2. Decreased K transfer into cells- Decrease in insulin (diabetic patients) Beta-adrenergic blocker thearpy

32 Hyperkalaemia 3. Renal impairment (reduced GFR): increased K intake: fruits, green vegetables, salt substitutes, drugs (KCl, potassium citrate) increased endogenous production: blood from GI bleed, resolving haematoma, rhabdomyolysis, tumor lysis, catabolic state reduced K excretion by drugs: potassium-sparing diuretics, angiotensin converting enzyme inhibitor (ACEIs), angiotensin receptor blockers (ARBs), nonsteroidal anti-inflammatory drugs 4. Normal renal function: Addison s disease (primary adrenal insufficiency decreased mineralocorticoid and glucocorticoid secretion)

33 Hyperkalaemia Clinical manifestations: Vague GI symptoms Nonspecific feelsings of not feeling well Weakness, paralysis, constipation ECG abnormalities: loss on p waves, peak T waves, widen QRS complexes, asystole

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36 Calcium 99% in the form of hydroxyapatite in bone A small fraction in ECF as ionised Ca which is physiologically active and regulated 50% ionised Ca 10% complexed to citrate, PO4, sulfate, and bicarbonate 40% bound to protein (mainly albumin) 200mg/day absorbed from intestine (out of 1000mg) 200mg/day excreted by kidneys (10,600mg out of 10,800mg filtered daily is reabsorbed) Regulated by interplay of PTH, Vit D3 (calcitriol) in intestine, kidney and bone.

37 Hypercalcaemia Increased Ca absorption from GI tract Milk-alkali syndrome Vitamin D intoxication Consume excessive amount of calcium bicarbonate for treatment of osteoporosis Hypercalcaemia in renal failure Treated with excessive amount of Ca supplement and Vit D

38 Hypercalcaemia Increased absorption of Ca from bone Hyperparathyroidism (primary and secondary) Malignancy: high PTH, calcitriol, local bone reabsorption Hyperthyroidism: increase bone turnover, hypercalciuria Immobilisation Vit A toxicity Paget s disease

39 Hyperparathyroidism Primary Adenoma Diffuse hyperplasia MEN I pituitary adenoma and islet cell tumours MEN II medullary carcinoma of thyroid and phaeochromocytoma Sympotms: mild, asymptomatic, incidental finding, women in 50 and 60 s, postmanopausal

40 Hyperparathyroidism Secondary Post renal transplant PTH secretion remains high after correction of Ca, PO4, Vit D metabolism, and renal function Hypercalcaemia resolves within the first year after transplantation

41 Hypercalcaemia Diagnosis Primary hyperpth Malignancies CXR pulmonary tumour & granulomatous disease (e.g. TB) History: Ca & Vit supplements Treatment: Loop diuretic and volume expansion Bisphosphonate (etidronate) Pamidronate Calcitonin mg hydrocortisone i.v. q.d. for 3-5 days Corticosteroid in malignancies

42 Hypocalcaemia Decreased Ca absorption from GI Decreased Ca absorption from bone PTH & Vid D (calcitriol) related Diagnosis True hypocalcaemia is present only when the ionised Ca concentration is reduced

43 Hypocalcaemia Hypoparathyroidism Acquired: Parathyroidectomy for 2nd or 3rd hyperparathyroidism Thyroid surgery Severe hypomagnesaemia Inherited: HAM syndrome (hypoparathyrodism, adrenal insufficiency, and mucotaneous candidiasis)

44 Hypocalcaemia Defects in Vit D metabolism Decrease intake Malabsorption Drugs anticonvulsants (phenobarbital) Renal failure: fail to convert calcidiol to calcitriol Liver disease: HCC disease fail to convert Vit D to calcidiol

45 Phosphate Hyperphosphataemia Renal failure: GFR<30ml/min PO4 reabsorption is suppressed and reduce renal excretion Tumor lysis syndrome or rhabdomyolysis

46 Hyperphosphataemia Treatment Renal failure: Treat high PO4 first prior to hypocalcaemia to avoid metastatic calcification Treat secondary hyperparathyroidism with Calcitriol Dietary restriction sufficient for mild renal failure Phosphate binders Aluminium-containing binders long term side effects of Al to CNS, osteoporosis, anaemia Calcium-containing binders still using extensively, e.g. calcium carbonate & calcium citrate & calcium acetate (watch cardiovascular calcification)

47 hyperphosphataemia Phosphate binders: Sevelamer (Renagel) Can be used with Ca binders Lanthanum (Fosrenol) Nocturnal haemodialysis Normal renal function: Enhanced renal excretion with volume expansion and loop diuretic

48 Hypophosphataemia Shift of PO4 from ECF to intracellular fluid Respiratory alkalosis Treatment of diabetic ketoacidosis Hungry bone syndrome Increased urinary excretion Primary & secondary hyperparathyrodism Signs & symptoms Failure to wean from ventilation (impaired diaphragmatic function) Reversible myocardial dysfunction (failure to response to pressor)

49 Fluid and electrolyte balance is extremely important and complicated

50 Differential Assessment of ECF Volume Differential Assessment of ECF Volume

51 Intravenous volume replacement solutions Hypotonic D5: More water than electrolytes, provides 170 cal/l free water moves from ECF to ICF by osmosis Isotonic Normal saline (NS) No calories, more NaCl than ECF Lactated Ringer s solution More similar to plasma than NS, less NaCl K, Ca, PO 4 3, lactate (metabolized to HCO 3 ) Expands ECF Hypertonic D10W Provides 340 kcal/l, limit of dextrose concentration may be infused peripherally Plasma Expanders albumin

52 It is important because: We need to take a decision regarding fluids in almost every hospitalized patient. Fluid administration can save lives in certain conditions. Acute or chronic loss of body water may cause a range of problems from mild headache, to dizziness, to convulsions, to coma and in some cases to death. Fluid administration can be very harmful if not done properly.

53 Kinds of IV Fluid solutions Hypotonic -½NS (0.45%) Isotonic -NS (0.9%), albumin Hypertonic - Hypertonic saline (3%). 2 categories: Crystalloid Colloid

54 Crystalloid vs Colloid Type of particles (large or small) Fluids with small crystalizable particles like NaCl are called crystalloids Fluids with large particles like albumin are called colloids because they don t pass quickly through the vascular pores and they stay stick longer in the circulation. Much smaller amounts of colloids can be used for same volume expansion: 250ml Albumin = 4 lt NS For the same reason edema resulting from colloids tends to stay longer. Albumin can cause severe allergic reactions.

55 Fluid therapy Fluid therapy can be divided into 2 components: Maintenance therapy which replaces the normal ongoing losses Replacement therapy which corrects water and electrolyte deficits.

56 1 st Part Maintenance therapy Is usually undertaken when a patient is not expected to eat or drink normally for some time (perioperatively or on a ventilator). Note: Patients who won t eat for one to two weeks should be considered for parenteral nutrition. Maintenance therapy

57 Maintenance Requirements Maintenance Requirements: 1. water 2. electrolytes Maintenance therapy

58 Water In eating patients (adults) Most of the necessary water derives from the water content of food and from the water of oxidation It has been estimated that only 500ml of water is necessary to be given in normal diet patients without increased losses. These sources of are markedly reduced in patients who are not eating and so water must be replaced by maintenance fluids. Maintenance therapy

59 Water Requirements water requirements increase with: fever, sweating, burns, tachypnea, surgical drains, polyuria, significant gastrointestinal losses,etc. Example: water requirements increase by 100 to 150 ml/day for each C degree of elevation in body temperature. Maintenance therapy

60 Several formulas can be used to calculate maintenance fluid rates. Maintenance therapy

61 4/2/1 rule 4 ml/kg/hr for first 10 kg (=40ml/hr) then 2 ml/kg/hr for next 10 kg (=20ml/hr) then 1 ml/kg/hr for any kgs over that This always gives 60ml/hr for first 20 kg then you add 1 ml/kg/hr for each kg over 20 kg This results in: Weight in kg + 40 = Maintenance IV rate/hour. (For any person weighing more than 20kg) Maintenance therapy

62 4/2/1 rule (Weight in Kg + 40) 4/2/1 rule: it is the same in adults and children over 20 kg of b.w. Top Limit: 120 ml/hr Maintenance therapy

63 To remember Different formulas produce a variety of fluid recommendations Fluid needs, no matter what formula is used, are at best an estimation. Maintenance therapy

64 What to put in the fluids Maintenance therapy

65 Start: D5% ½NS+20 meq rate: Wt+40/hr a reasonable approach is to start ½ normal saline to which 20 meq of potassium chloride is added per liter (½NS+20 Meq Kcl/lt). Glucose in the form of dextrose (D5%) can be added to provide some calories while the patient is NPO. So,start: D5% ½NS+20 meq Kcl/lt at a rate equal to their weight + 40ml/hr, but not greater than 120ml/hr. then adjust as needed. Maintenance therapy

66 Start D5% ½NS+20 meq Kcl/lt, then adjust: If sodium falls, increase the concentration (to NS) If sodium rises, decrease the concentration (to ¼NS) If the plasma potassium falls add more potassium. If the plasma potassium rises add less potassium. If things are good, leave as they are. Maintenance therapy

67 2 nd part: Replacement therapy Hypovolemia or Fluid Volume Deficit (FVD) is a result of water and electrolyte loss Compensatory mechanisms include: 1. Increased sympathetic nervous system stimulation with an increase in heart rate & cardiac contraction 2. Increased thirst 3. Increased release of ADH & Aldosterone Severe condition may result in hypovolemic shock and prolonged condition may cause acute renal failure Replacement therapy

68 Hypovolaemic shock A variety of disorders may lead to fluid losses that deplete the extracellular space. This can lead to a potentially fatal decrease in tissue perfusion. Fortunately, early diagnosis and treatment can restore normovolemia in almost all cases. Replacement therapy

69 Hypovolaemia and Hypovolaemic shock There is no easy formula for assessing the degree of hypovolaemia. Hypovolaemic Shock, the most severe form of hypolaemia, is characterized by tachycardia, cold clammy extremities, cyanosis, a low urine output (usually less than 15 ml/h), and agitation and confusion due to reduced cerebral blood flow. This needs rapid treatment with isotonic fluid boluses (1-2lt NS), and assessment and treatment of the underlying cause. Replacement therapy

70 Basic Signs of Fluid Volume Excess (FVE) Orthopnoea Oedema & weight gain Distended neck veins & tachycardia Increased blood pressure Crackles & wheezes pleural effusion

71 Thank you