Fluids and Electrolytes. Presley Regional Trauma Center Department of Surgery University of Tennessee Health Science Center Memphis, Tennessee

Transcription

1 Fluids and Electrolytes Presley Regional Trauma Center Department of Surgery University of Tennessee Health Science Center Memphis, Tennessee

2 Body Fluid Compartments

3 Total Body Water Approximates 60% of total body weight Composed of the intracellular and extracellular compartments The intracellular compartment or intracellular volume (ICV) constitutes 40% of total body weight Extracellular volume (ECV) makes up the remaining 20%

4 ECV Composed of interstitial fluid (IF) and the intravascular or plasma volume (PV) The PV constitutes 25% of ECV (5% of total body weight) remainder is IF Red cell volume, approximately 2 to 3% of TBW, is part of the ICV Total blood volume is approximately 7 to 8% of total body weight

5 Requirements Sufficient water is required to replace obligatory GU losses of approximately 1L/day and GI losses of ml/day Insensible water losses must also be considered in estimating maintenance fluid - Amount to 8 to 12ml/kg/day - Equally divided into respiratory and cutaneous water loss - Cutaneous losses increase by 10% for each degree of temperature greater than 37 C

6 Electrolytes Daily sodium intake approaches 100 to 250mEq/day Balanced by sodium losses in sweat, stool, and urine Renal conservation of sodium is extraordinary In cases of profound volume depletion, urinary losses of sodium may be less than 1mEq/day

7 Electrolytes In the perioperative period, adequate maintenance of sodium may be achieved with an intake of 1 to 2mEq/kg/day Normal potassium intake is approximately 40 to 120mEq/day 10-15% is excreted as normal urinary losses With normal renal function, body potassium stores can be maintained with an intake of approximately 0.5 to 1.0mEq/kg/day

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10 Perioperative Fluid Requirements

11 Perioperative Appropriate management of fluids and electrolytes in the perioperative period requires a flexible yet systematic approach Ensures that fluid administration is appropriately tailored to the patient's changing requirements

12 Perioperative The amount of fluids administered in the immediate post-op period must take into account the existing deficit, maintenance requirements, and any ongoing losses Estimation of the existing deficit must incorporate an approximation of intra-op blood loss as well as fluid losses from evaporative and third-space fluid sequestration

13 Losses Extravascular fluid sequestration represents an important source of intra-op fluid loss Extensive dissection at the operative site induces a localized capillary leak, resulting in extravasation of intravascular fluid into the interstitium with edema formation The loss of intravascular volume via this route depends on the extent of exposure and degree of dissection

14 Losses For example, estimated intravascular fluid losses associated with IHR are 4ml/kg/h, while losses during AAA repair may be as high as 8ml/kg/h This capillary leak may persist as long as 24h into the post-op period and should be considered as part of ongoing losses in the immediate post-op period

15 Losses GI losses (stomas, tubes/drains, or fistulae) comprise ongoing fluid losses These losses may be accurately estimated by closely following recorded hourly outputs The electrolyte composition of the output depends on the source of effluent Replacement fluids should be chosen to best approximate the composition of the ongoing losses

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17 Post-op Post-op fluid orders should take into account the overall fluid balance in the OR as an estimate of the existing deficit along with maintenance fluid requirements and any ongoing losses The preferred approach is to reassess the patient frequently to determine volume status

18 Post-op Evaluation of heart rate, blood pressure, and most importantly, hourly urine output provides an excellent measure of intravascular volume status Orders for IVF should be rewritten frequently to maintain a normal heart rate, a urine output of approximately 1ml/kg/h, and adequate blood pressure

19 Disorders of Sodium Homeostasis

20 Sodium Maintenance of a normal serum [sodium] is intimately associated with control of plasma osmolarity P osm = 2 Plasma [Na + ] + [Gluc]/20 + [BUN]/3 Plasma [Na + ] alone provides no information about the total content of sodium in the body but simply provides an estimate of the relative amounts of free water and sodium

21 Osmolarity Maintenance of the plasma osmolarity within normal limits depends on the ability of the kidneys to excrete water, thus preventing hypoosmolarity, and on a normal thirst mechanism with access to water to prevent hypernatremia The ability to excrete maximally dilute urine (<100mOsm/kg) allows the kidneys to excrete in excess of 18L of water per day

22 Osmolarity In the presence of normal renal perfusion and intact renal function, ADH is the principal regulator of serum osmolarity 1-2% reduction in P osm maximally inhibits ADH release maximally dilute urine 1-2% increase in P osm or a 5-10% decrease in blood volume or pressure stimulates ADH With both a low P osm and blood volume or pressure, the latter effect will dominate

23 Hyponatremia Begins with an assessment of the serum osmolarity if serum osmolarity is high, then it is important to consider the possibility of other effective plasma osmoles Hyperglycemia shifts H 2 O from cells, leading to dilutional hyponatremia f or every 100mg/dl rise in glucose the [Na + ] falls by 1.3mEq/l

24 Pseudohyponatremia In rare cases, the serum osmolarity may be normal This phenomenon is referred to as pseudohyponatremia and is caused by hyperlipidemia or hyperproteinemia It is an artifact of the laboratory assay

25 Hyponatremia More frequently, a low [Na + ] will be associated with reduced plasma osmolarity The etiology and treatment of hypoosmolar hyponatremia may be classified into 3 groups depending on the ECV status of the patient

26 Hypovolemic Hyponatremia Most common causes are Na + loss A reduction in ECV leads to an increase in ADH secretion, impairing the kidney's ability to excrete free water Either administration of Na + -free solutions or the ingestion of free water induced by thirst aggravates the resulting hyponatremia

27 Hypovolemic Hyponatremia Typically, perioperative isotonic losses (plasma, gastric losses) are replaced with hypotonic solutions in the face of mild hypovolemia Treatment involves replenishing the extravascular volume with isotonic fluids in concert with restriction of free water

28 Hypervolemic Hyponatremia Hyponatremia in the presence of an increased extravascular volume Represents the next most common scenario in the perioperative period Edematous states in which there is a reduction in the effective circulating volume Low CO states, cirrhosis, and other hypoalbuminemic states are the more common etiologies

29 Hypervolemic Hyponatremia Both water restriction and Na + restriction are necessary Depending on the severity of the hyponatremia, a loop diuretic may be required to increase both Na + and water loss In most cases, this induces an excess of urinary water loss over Na + loss and should correct the hyponatremia

30 Euvolemic Hyponatremia Patients with a normal ECV status and hypoosmolar hyponatremia SIADH Nausea, pain, and narcotics, all of which are common in the post-op period, may result in SIADH and contribute to post-op hyponatremia

31 SIADH Diagnosis is confirmed by demonstrating a low plasma osmolarity, a less than maximally dilute urine (U osm. > 100mOsm/l), and renal salt wasting (U Na. > 20mEq/l) Treatment includes management of the underlying cause and water restriction Isotonic (0.9%) saline should not be administered to patients with SIADH as it may cause the plasma [Na + ] to fall

32 Treatment The presence of Sx depends on the rate at which hyponatremia occurred Sx of increased ICP from cerebral edema are the most prominent features and may be present at plasma [Na + ] < 125mEq/l if the development of hyponatremia was rapid If the reduction in [Na + ] occurs slowly, then symptoms may not be evident until plasma [Na + ] drops to as low as 110mEq/l

33 Treatment Too rapid correction may result in CPM If the patient is asx or mildly symptomatic, then the goal should be to raise the [Na + ] by approximately 0.5mEq/h If the patient is Sx with coma or convulsions, then more rapid correction is necessary Goal is to administer sufficient Na + until either the symptoms have improved or the plasma [Na + ] has increased by 5mEq/l

34 Treatment The following formula may be used to estimate the amount of Na + required to raise the [Na + ] to a safe level (approximately 120mEq/l) - Na + deficit = 0.60 Lean body weight (kg) (120 - Measured plasma Na + )

35 Hypernatremia Far less common than is hyponatremia Cellular shrinkage caused by fluid shifts from the intracellular space to the extracellular compartment may cause confusion, coma, and intracranial hemorrhage Symptoms are usually not evident below a plasma [Na + ] of 160mEq/l

36 Hypernatremia Occurs as a result of excessive free HOH loss Frequently associated with hypovolemia Excessive insensible losses caused by fever, hyperventilation, and burns or hypotonic fluid losses due to perspiration or severe diarrhea are the principal causes

37 Treatment If hypovolemia is sufficiently severe that tissue perfusion is compromised, then initial therapy should be isotonic saline until tissue perfusion is restored If perfusion is adequate, then 0.5 NS or D5W is sufficient to return plasma [Na + ] to normal

38 Treatment Rapid correction of severe hypernatremia may cause irreversible neurological deficits - Should not be corrected at a rate faster than 0.5 to 1.0mEq/l per hour In the presence of Sx, free water should be administered either to return the plasma [Na] to that documented before the Sx or to reduce the [Na] by about 6mmol/l - Water deficit = TBW {(Plasma [Na] Desired plasma [Na]) - 1}

39 Disorders of Potassium Homeostasis

40 Potassium The major intracellular cation Only 2% is located in the extracellular fluid Slight alterations in plasma [K + ] may have dramatic effects on muscle contraction and nerve conduction as the [gradient] across the plasma membrane is the main determinant of membrane excitability Abnormalities in plasma [K + ] should be treated expeditiously

41 Hypokalemia Usually from GI, kidney or skin losses Cardiac arrhythmias exacerbated with metabolic alkalosis, dig or hypercalcemia ECG = T-wave flattening or inversion and depressed ST segments, followed by U waves and a prolonged QT interval Replacement should be geared toward rapid correction of plasma [K + ], followed by slower repletion of the total body K + deficit

42 Hyperkalemia Main risks are weakness and myocardial irritability ECG = increase in T-wave amplitude, leading to a narrow, peaked symmetrical T wave, followed by reduced P-waves and widening of the QRS If untreated, may eventually cause a sinusoidal ECG complex and ultimately ventricular fibrillation

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44 Disorders of Mineral Homeostasis

45 Calcium Total body stores are approximately 1000g Almost 99% is in bone The remainder is located within the ECF Either free (40%) or bound to albumin (50%) or other anions such as citrate, lactate, and sulfate Only the free or ionized component is biologically active

46 Calcium Acid-base alterations affect the binding of calcium to albumin Similarly, changes in serum protein levels affect total serum calcium The ionized calcium level can be estimated using the following formula - Ionized calcium (mg/dl) = Total serum calcium (mg/dl) Serum albumin (mg/dl)

47 Hypocalcemia Most frequent cause = low serum albumin In this case, the ionized fraction remains normal, and no treatment is indicated Other causes include acute pancreatitis, massive soft tissue infection, small-bowel fistulae, hypoparathyroidism and massive blood transfusion

48 Hypocalcemia Earliest Sx include numbness or tingling in the circumoral region or at the tips of the fingers Tetany or seizures may arise at more profound levels A positive Trousseau's sign or Chvostek's sign may be suggestive of it Alters myocardial repolarization and results in a prolonged QT interval

49 Hypercalcemia Primary hyperparathyroidism and malignant disease account for 90% of cases Sx include confusion, lethargy, coma, muscle weakness, anorexia, nausea, vomiting, pancreatitis, constipation, renal stones, nephrogenic DI and polyuria ECG = shortened QT interval

50 Magnesium The principal intracellular divalent cation Approximately 50% of total body magnesium is found in bone and is not readily exchangeable Absorption occurs throughout the small intestine and is reabsorbed effectively in the renal tubules

51 Hypomagnesemia May occur because of poor nutritional intake, malabsorption, or increased renal excretion Characterized by neuromuscular and CNS irritability Low serum magnesium levels appear to impair PTH excretion and may induce hypocalcemia refractory to calcium supplementation unless corrected

52 Phosphate The most abundant intracellular anion Only 0.1% of total body phosphorus is in the extracellular fluid compartment As a result, circulating plasma levels do not reflect total body stores

53 Hypophosphatemia May occur as the result of impaired intestinal absorption or increased renal excretion Hyperparathyroidism may induce a drop in serum phosphate levels through an increase in renal excretion Careful monitoring of phosphate should also occur with the administration of parenteral nutrition after prolonged starvation because profound hypophosphatemia may result

54 Hyperphosphatemia Most commonly seen in the setting of impaired renal phosphate excretion In this scenario is frequently associated with hypocalcemia. Similarly, hypoparathyroidism reduces renal phosphate excretion, leading to an increase in serum phosphate levels

55 Acid-Base Abnormalities

56 Metabolic Acidosis Arises as a result of retention (or administration) of fixed acids or the loss of bicarbonate Categorized by the presence or absence of an anion gap (AG) - Addition of fixed acids results in an AG metabolic acidosis - Bicarbonate loss results in a nonag metabolic acidosis

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58 Metabolic Alkalosis Characterized by an elevated plasma [HCO 3- ] May occur as a result of one of three mechanisms - Loss of acid from the GI tract or urine - Administration of HCO 3- or a precursor, such as citrate (as occurs following massive blood transfusions) - Loss of fluid with a high chloride/bicarb ratio

59 Classification Either chloride sensitive or chloride resistant to the extent that they are reversed by the administration of NS Treatment should be directed toward the underlying cause

60 Summary Surgical patients undergo acute alterations in the volume and composition of fluids in the intracellular and extracellular spaces To a great extent, these changes occur as a result of the patient's underlying disease These alterations are not limited to patients requiring urgent operative intervention

61 Summary Elective surgery may result in dramatic fluid shifts without significant blood loss In addition to changes in fluid volume, surgical patients may develop potentially dangerous fluctuations in concentrations and total body content of important lytes Precise peri-op management of fluids and electrolytes is required to minimize peri-op morbidity and mortality