FLUID and ELECTROLYTES
Total body water (TBW), the distribution volume of sodium-free water, approximately 60% of total body weight.
Intracellular volume (ICV) constitutes 40% of total body weight,
Extracellular volume (ECV) constitutes 20% of body weight.
Plasma volume (PV), equals about one fifth of ECV - 4% - (ie about 3 liters), the remainder of which is interstitial fluid (IF).
Red cell volume, approximately 2 liters, is part of ICV.
.
For example, assume that a 70-kg patient has suffered an acute blood loss of 2000 ml, approximately 40% of the predicted 5-liter blood volume. The formula describing the effects of replacement with 5% dextrose in water (D5W), lactated Ringer’s solution, or 5 or 25% human serum albumin is as follows:
To restore blood volume using D5W:
2 liters is the desired PV increment, 42 liters is the TBW in a 70-kg person, and 3 liters is the normal estimated PV.
2 liters x 42 liters/3 liters = 28 liters
To restore blood volume using LR:
14 liters is the ECV in a 70-kg person.
2 liters x 14 liters/3 liters = 9.3 liters
If 5% albumin, which exerts colloid osmotic pressure similar to plasma, are infused, the infused volume initially would remain in the PV, perhaps attracting additional interstitial fluid intravascularly. 25% albumin expands PV by approximately 400 ml for each 100 ml infused.
The half-life of albumin is normally about 16 hours, but it can be as short as 2 to 3 hours in pathologic conditions. Useful when crystalloids fail to sustain plasma volume for more than a few minutes due to a low COP. This will be most appropriate when there is an abnormal loss of protein from the vascular space; e.g., peritonitis, extensive burns.
Hetastarch is an alternative to 5 percent albumin for intravascular volume support. Coagulopathy has not been a clinical problem with less than 1 L or less than 25 ml/kg. The excretion of hetastarch is complex due to the wide range of molecular sizes, although the average is 450,000. Molecules of less than 50,000 are excreted rapidly in the urine, while larger molecules are metabolized by amylase to smaller sizes that are lost in the urine. The initial rate of loss from the body has a half-life of 13 days; thus accumulation occurs if repeated doses are infused
Renal adaptation to hypovolemia (and decreased cardiac output) occurs through three primary mechanisms:
· a reduction in renal blood flow (RBF),
· a reduction in the glomerular filtration rate (GFR), and
· increased tubular reabsorption of sodium and water.
Initially, RBF is maintained (i.e., RBF is autoregulated) as perfusion pressure decreases by reductions in renal afferent arteriolar resistance.
Further decreases in cardiac output may decrease the fraction of cardiac output delivered to the kidneys.
Increases in renal vascular resistance redistribute blood flow from the kidneys in an attempt to preserve perfusion of other tissues.
Renal vasoconstrictive factors (the renal sympathetic nerves, angiotensin II, and catecholamines) and
vasodilatory mechanisms (intrinsic renal auto-regulation and the renal vasodilatory effects of prostaglandins).
Autoregulation may be impaired or lost during severe, acute hypovolemia.
Hypovolemia also redistributes renal perfusion from outer cortical nephrons to inner cortical nephrons, in which longer loops of Henle, which penetrate more deeply into the hypertonic renal medulla, are capable of greater sodium conservation.
To preserve PV, reabsorption of filtered water and sodium is enhanced by changes mediated by the hormonal factors antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), and aldosterone. A 10–20% decrease in blood volume is necessary before ADH secretion from the posterior pituitary increases.
ADH acts primarily on the medullary collecting ducts to increase water reabsorption and cause excretion of smaller volumes of more highly concentrated urine.
Vasopressin release is regulated by intravascular volume and blood pressure.
· The normal osmolar threshold for AVP release is 275 to 290 mOsm/kg. Osmolality is sensed by osmoreceptors in the anterior hypothalamus.
· Intravascular volume depletion greater than 10 percent leads to vasopressin release independent of osmolality and is even more potent in producing release.
· Surgical stimulation and other "stressful" stimuli also release vasopressin.
· Any effect of anesthetics and narcotics to release vasopressin is due to hemodynamic changes.
· Induction of anesthesia without hypotension does not raise vasopressin levels. After hypotension, urine flow may not increase above minimal levels of 0.5 mg/kg/h, for 50 to 60 minutes after resuscitation.
· Vasopressin has a half-life of 10 to 20 minutes.
· Increases urinary concentration, shifts renal blood flow (RBF) from cortex toward medulla, vasoconstriction, and stimulates thirst.
ANP secretion is decreased during hypovolemia. ANP, released from the cardiac atria in response to increased atrial stretch, exerts vasodilatory effects and increases the renal excretion of sodium and water.
Hypoperfusion stimulates the
granular cells of the renal juxtaglomerular apparatus to release renin, which catalyzes the conversion
of angiotensinogen to
The kidney also contains large quantities of vasodilator prostaglandins that may play a crucial role in protecting the kidney from vasoconstrictor hormones and in maintaining RBF during hypovolemia. The protective effect of endogenous renal prostaglandins may be lost if renal circulatory compromise develops in patients receiving nonsteroidal anti-inflammatory drugs.
Sufficient water is required to balance
· gastrointestinal losses of 100–200 ml/day;
· insensible losses of 500–1000 ml/day (half of which is respiratory and half cutaneous);
· urinary losses of 1000 ml/day-. Two simple formulas are used interchangeably to estimate maintenance water
Weight (kg) ml/kg/h ml/kg/day
1–10 4 100
11–20 2 50
> 21 1 20
The predicted daily maintenance fluid requirements for healthy, 70-kg adults is 2500 ml/day of a solution with a [Na+] of 30 mEq/l and a [K+] of 15–20 mEq/l .
Water and Electrolyte Composition of Fluid Losses
· Wound and burn edema and ascitic fluid are protein rich and contain electrolytes in concentrations similar to plasma.
· Substantial loss of gastrointestinal fluids also requires replacement of other electrolytes (i.e., potassium, magnesium, phosphate).
· Gastric losses may produce hypochloremic metabolic alkalosis that can be corrected with 0.9% saline;
· Diarrhea may produce hyperchloremic metabolic acidosis that may be prevented or corrected by infusion of fluid containing bicarbonate or bicarbonate substrate (i.e., lactate).
Average volumes and electrolyte composition of gastrointestinal secretions.
Volume Na+ K+ Cl- HCO3-
Source (ml/day) (mEq/l) (mEq/l) (mEq/l) (mEq/)
Gastric 1500 60 10 130 —
Ileal 3000 140 5 104 30
Pancreatic 400 140 5 75 115
Biliary 400 140 5 100 35
Fluid Shifts During Surgery.
Healthy subjects who received no intraoperative sodium while undergoing gastric or gallbladder surgery demonstrated a decline in ECV of nearly 2 liters and a 13% decline in GFR.
In contrast, patients who received lactated Ringer’s solution maintained ECV and increased GFR by 10%.
During prolonged experimental hemorrhagic shock, both sodium and water accumulate intracellularly, in part because of impaired cellular membrane function. Shock-induced alterations in cellular membrane function and intracellular concentrations of sodium appear to return to normal once systemic hemodynamic stability is restored.
Patients studied during the first 10 days after resuscitation from massive trauma demonstrated a 55% increase in IF volume Because of the reduction of colloid osmotic pressure in traumatized patients, the ratio of IF to blood volume is increased.
Guidelines have been developed for replacement of fluid losses during surgical procedures.
In addition to maintenance fluids and replacement of estimated blood loss,:
4 ml•kg-1•h-1 for procedures involving minimal trauma,
6 ml•kg-1•h-1 for those involving moderate trauma, and
8 ml•kg-1•h-1 for those involving extreme trauma.
20 ml•kg-1•h-1 for a one-day old with gastroschesis (Hughes)
Most general and regional anesthetics cause arteriolar and venous dilation, expanding the venous capacity. The latter reduces peripheral venous pressure and therefore, venous return and CO. Therefore, fluid must be administered to expand the blood volume to compensate for venodilation. Compensatory volume expansion (CVE) with 5 to 7 ml/kg of balanced salt solution must occur prior to, or simultaneous with, the onset of anesthesia.
The maintenance fluid meets ongoing basal needs for water and electrolytes as described earlier. The onset of surgical stimulation and to a smaller extent onset of anesthesia elicits changes in catecholamines, cortisol, and growth hormone. These tend to reduce insulin secretion or to impede its glucose-lowering effect leading to hyperglycemia. If dextrose-containing solutions are infused at the usual 5 percent concentration at the rates required by other fluid requirements, severe hyperglycemia will result. Thus the fluid used for volume maintenance should not contain dextrose.
Redistribution, or so-called 3rd-space losses, are primarily due to tissue edema and transcellular fluid displacement. Functionally this fluid is not available to the vascular space. Colloid enters the injured tissue at a more rapid rate than normal, but at a slower rate than electrolyte. For example, bowel wall edema is lessened by utilizing colloid containing fluids compared with crystalloid. The composition of third-space losses is equivalent to the ECFV electrolyte concentration plus a smaller amount of protein. Therefore, balanced salt solution is the most appropriate replacement fluid.
Description of the fluid management for a 70-kg patient undergoing gastrectomy starting with a hemoglobin of 15 g/dl, who has been fasting for 10 hours. The maintenance rate is 110 ml/h, producing a deficit of 1,100 ml.
During the first and second hours
of intra-abdominal activity, assume that
100 ml of blood was lost and replace it 3:1 with balanced salt solution. By the
fourth hour, the deficit had been replaced and because the abdomen was being
closed during part of that hour the third space (redistribution) losses
estimate was likewise reduced and no further blood loss was noted. The
assumption is made that urine flow was 50 to 80 ml/h and that heart rate, and
arterial blood pressure were in an acceptable range and the central venous
pressure (CVP) remained
350 mls for initial compensatory losses; the deficit is made up over 3 hours ; 110 for maintainance, and 350 mls is given for each hour of surgery for 3rd space losses. 1,000 mls are given over the pre-incision phase. A blood loss of 250 mls is replaced with a total of 750 mls. The total for the preinduction hour plus 3 hours of surgery is 4,000 mls.
An important corollary of IF expansion is the mobilization and return of accumulated fluid to the ECV and the PV, colloquially termed “deresuscitation” In most patients, mobilization occurs on approximately the third postoperative day. If the cardiovascular system and kidneys cannot effectively transport and excrete mobilized fluid, hypervolemia and pulmonary edema may occur.
Osmolality = ([Na+] ´ 2) + (glucose/18) + (BUN/2.3)
Sugars, alcohols, and radiographic dyes increase measured osmolality, generating an increased “osmolal gap” between the measured and calculated values.
A hyperosmolar state occurs whenever the concentration of osmotically active particles is high. Both uremia (increased BUN) and hypernatremia (increased serum sodium) increase serum osmolality. However, because urea distributes throughout TBW, an increase in BUN does not cause hypertonicity. Sodium, largely restricted to the ECV, causes hypertonicity, that is, osmotically mediated redistribution of water from ICV to ECV The term “tonicity” is also used colloquially to compare the osmotic pressure of a parenteral solution to that of plasma.
· If membrane permeability is intact, colloids preferentially expand PV rather than IF volume.
· 25% albumin) may exert sufficient oncotic pressure to translocate substantial volumes of IF into the PV.
· However, exhaustive research has failed to establish the superiority of either colloid-containing or crystalloid-containing fluids.
· In disease states associated with increased alveolar capillary permeability (i.e., sepsis or the adult respiratory distress syndrome), infusion of colloid may aggravate pulmonary edema
· Hypoproteinemia in critically ill patients has been associated with the development of pulmonary edema.
· Either crystalloid or colloid administration may precipitate pulmonary edema in patients who have valvular heart disease, decreased left ventricular compliance, or decreased left ventricular contractility
· In animals infused with E. coli lipopolysaccharide, which mimics some aspects of clinical sepsis, clinically relevant doses of lactated Ringer’s solution or 6.0% hydroxyethyl starch produced comparable effects on the critical end point of oxygen delivery while producing the expected differences in extravascular fluid accumulation
Hyponatremia is nearly always associated with water excess rather than sodium deficiency. Factitious hyponatremia may be seen in hyperlipidemia (chylomicronemia) or hyperproteinemia. Hyperosmolality due to nonsodium molecules (e.g., hyperglycemia, mannitol overdose) draws water from intracellular space, diluting the ECFV sodium.
· SIADH secretion is seen after a variety of pulmonary, central nervous system and malignant conditions.
· The diagnosis must exclude cardiac, liver, kidney, thyroid, or adrenal disease and establish normal intravascular volume and blood pressure.
· Water retention causes the intravascular volume to expand, suppressing sodium reabsorption, so that urine sodium tends to be elevated.
· In the perioperative period, hypovolemia or cardiac compromise is probably more commonly the etiology of the appropriate release of vasopressin causing excess water retention.
The signs and symptoms of hyponatremia include nausea, vomiting, visual disturbances, depressed level of consciousness, agitation, confusion, coma, seizures, muscle cramps, weakness, and myoclonus.
Management
· Eliminate cause.
· Supportive care of the airway and hemodynamics.
· If the sodium is less than 120 mEq/L for less than 48 hours, with mental status changes present, give 0.9 percent NaCl; hypertonic NaCl or NaHCO3 should be administered based on acid-base status and the desired degree of correction.
· Correct at 0.6 to 1 mmol/L/h until the [Na] = 125 mEq/L, then more slowly. Diuresis may be indicated if the intravascular volume is judged to be increased.
· Without mental status changes, correction should be made more slowly, usually by restricting free water administration, by changing all fluids to 0.9 percent NaCl and limiting total water intake to 70 to 75 percent of maintenance rates or less. This rate allows uncompensated water loss via skin and respiratory tracts to slowly increase [Na].
Hypernatremia is most often caused by water deficiency due to excessive loss or inadequate intake. Excessive intake may follow massive intravascular administration of fluids containing high concentrations of sodium (e.g., NaHCO3 therapy during resuscitation). Signs and symptoms include changes in mental status, thirst, shock, hypotension, and myoclonus.
· Diabetes insipidus (DI) may result from deficiency of AVP or inability of the kidney to produce a hypertonic medullary interstitium.
· Vasopressin deficiency is seen following pituitary surgery, basal skull fracture and severe head injury.
· Nephrogenic causes include virtually any systemic or kidney disease that impairs tubular function (e.g., ischemia, aminoglycosides, and amphotericin) or redistributes renal blood flow (RBF).
Criteria for the diagnosis of DI include:
· Presence of an adequate stimulus for vasopressin release (hypernatremia, hypovolemia, hypotension) accompanied by an inappropriately dilute urine.
· After hypernatremia and dilute urine concentration are documented, initial management is based on administration of aqueous vasopressin during the acute phase. A typical starting dose of vasopressin is 5 units, subcutaneously every 4 to 6 hours.
· A common mistake is to administer 5 percent dextrose in water to replace the water deficit by matching urine output. The rate of dextrose administration required quickly leads to hyperglycemia, followed by glycosuria and the development of an osmotic diuresis, in addition to diabetes insipidus.
· Another common mistake is to diagnose a high urine output following pituitary surgery as diabetes insipidus, when the patient is simply excreting fluids that were administered intraoperatively.
·
Potassium functions to maintain transmembrane potentials and electrophysiologic stability. Aldosterone, b-adrenergic stimulation, and insulin regulate the distribution and excretion of potassium. Several factors cause [K] to average 0.4 to 0.5 mEq/L lower when measured on heparinized arterial samples, as compared to clotted venous samples.
Hypokalemia may occur due to an absolute deficiency or redistribution into the intracellular space. Deficiency may be due to inadequate dietary intake or excessive loss, usually due to diuretics. During the perioperative period, a mild deficiency may be unmasked due to redistribution mediated by aldosterone, b-adrenergic stimulation, alkalosis, and carbohydrate administration.
The maximal rate of administration is 0.5 to 1.0 mEq/kg/h (roughly 1 mEq/min), but this must be accompanied by continuous monitoring of the ECG. Doses of 0.25 mEq/kg/h should be administered for asymptomatic moderate to severe hypokalemia (venous serum level < 3.0, or arterial plasma [K] <2.6).
Hyperkalemia causes weakness, paralysis, paresthesia, and ECG changes. As the [K] increases, peaked T waves, prolonged PR interval, loss of P waves, widening of the QRS, and appearance of a sine-wave pattern with loss of contraction occur in sequence. The more rapidly hyperkalemia develops, the lower the absolute [K] at which abnormalities appear.
Management of hyperkalemia starts with administration of calcium to antagonize the electrophysiologic effect when ECG changes appear. Redistribution of potassium from the extracellular to the intracellular space can be encouraged by stopping tissue destruction, administration of b-adrenergic agonists, aldosterone agonists, induction of alkalosis, and insulin administration. Ultimately, excretion must be increased by diuresis, resin exchange (e.g., kayexalate 1 g/kg via the upper or lower GI tract), or dialysis.
Hypomagnesemia due to excess excretion results from diuretics, tubular nephrotoxins (e.g., aminoglycosides, cyclosporine), and postobstructive diuresis, laxative abuse, diarrhea, nasogastric suction, hyperaldosteronism, hyper-thyroidism, hyperparathyroidism, diabetic ketoacidosis, and theophylline toxicity. Decreased intake, malabsorption, and alcoholism also lead to hypomagnesemia.
The signs and symptoms of hypomagnesemia appear when the deficit is 0.5 to 1.0 mmol/kg. Arrhythmias (ventricular, or supraventricular), neuromuscular excitability (exaggerated deep tendon reflexes, stridor, tremor, myoclonic jerks, tetany), mental status changes (apathy, depression, anxiety, restlessness, hallucinations, and Wernicke's encephalopathy), digitalis toxicity, heart failure, hypertension, hypokalemia, and renal potassium wasting all result from hypomagnesemia. It also causes hypocalcemia. In addition, hypomagnesemia is often associated with hyponatremia, and hypophosphatemia.
For acute therapy of arrhythmias,
administer
Hypermagnesemia may result from the use of laxatives and antacids
and from renal dysfunction, adrenal insufficiency, or hypothyroidism. The
threshold for the onset of symptoms is
Management focuses on stopping administration and initiating administration of large doses of calcium, followed by diuresis or dialysis.
Review of magnesium. BJA 83: 202 99
· Primarily works like a Ca antagonist, more like nifedipine than verapamil.
· An effective adrenergic blocker, useful in managing ventricular arrhythmias, particularly Torsade de Pointe, possibly bupivacaine-induced, and those that are refractory to other treatment, or where bretylium might have been used.
· May block response to intubation, especially in pre-eclamptic patients, but its vagal blocking effect makes it less than optimal in patients with ischemic heart disease.
· May have an analgesic effect synergistic with that of morphine by modulating NMDA-induced pain.
· May have some success in improving the outcome from cerebral ischemia.
Review of magnesium. Letter From James, BJA supplement, 86: 594, 01
· Inhibits release of catecholamines from the adrenal medulla
· Inhibits release of catecholamines from peripheral adrenergic nerve endings.
· Direct blockade of catecholamine receptores.
· Vasodilation from a direct effect on vessel walls.
· Antiarrhythmic, particularly with high catecholamine levels.
Glucose Physiology
· Glucose is a crucial fuel source. Insulin facilitates glucose movement into cells in a process that also requires K and PO4.
· RBCs, healing wounds, the brain, and adrenal medulla require glucose for fuel, totaling approximately 2 mg/kg/min.
· Traditionally, glucose-containing intravenous fluids have been given in an effort to prevent hypoglycemia and limit protein catabolism.
· Iatrogenic hyperglycemia can induce an osmotic diuresis and, in animals, may aggravate ischemic neurologic injury,
· Because of the hyperglycemic response associated with surgical stress, only infants and patients receiving insulin or drugs that interfere with glucose synthesis are at risk for hypoglycemia.
Hyperglycemia is most often due to insulin deficiency or to resistance or glucose overadministration.
Hyperglycemia produces osmotic diuresis, exacerbation of brain, spinal cord, and renal damage by ischemia, delayed gastric emptying, hypophosphatemia, delayed wound healing, and impaired WBC function.
Maternal hyperglycemia increases the risk of neonatal brain damage and fetal acidosis if the fetus becomes hypoxic, as well as increasing the risk of neonatal jaundice.
Even with supramaximal levels of insulin, adults can use only 3 to 5 mg/kg/min at rest (approximately 240 ml/h of 5 percent dextrose solutions). The maximal rate of disposition is less in stress states, more with increased metabolic rate. In general, no more than 2 to 3 mg/kg/min (120 to 180 mg/kg/h, i.e., 10 g/h for a 70-kg person, which is supplied by 240 ml of a 5 percent dextrose solution/hour) should be administered. Healthy infants and children become hyperglycemic if 5 percent dextrose is included in maintenance fluids. The maximal rate of glucose disposition in young children is 4 to 8 mg/kg/min, and the optimal rate is less than 5 mg/kg/min. It is not clear that glucose administration is necessary for intraoperative management of most patients.
There are many suggested methods of perioperative glucose management, but all successful approaches rely on careful monitoring. Perioperative management of blood glucose during brief peripheral surgery in the diet-controlled diabetic will generally involve only monitoring of blood glucose immediately preoperatively and every 3 hours until oral intake is resumed. Frequent glucose monitoring and preparation for insulin administration are essential for the diabetic patient (1) requiring less than 50 units of insulin/day or oral hypoglycemic agents for control, and who requires brief peripheral surgery; or (2) the diet-controlled diabetic having major surgery. Recommendations include discontinuation of long acting insulin or oral hypoglycemic agents 1 to 2 days preoperatively, six evenly spaced meals per day, and short-acting insulin every 4 to 6 hours subcutaneously, with the dose adjusted according to glucose levels just before administration. Urine glucose and ketone bodies should be measured periodically.
The typical "sliding scale" is destined to fail because it involves the administration of a fixed dose after documentation of hyperglycemia. A small modification improves control. The selected dose should be administered every 4 to 6 hours, based on response. If the glucose is below 60 mg/dl, the dose should be held for at least an hour, and 50 percent dextrose IV, 0.01 to 0.02 ml/kg/min administered, with blood glucose monitored hourly. When the blood glucose is above 125 mg/dl without supplemental dextrose infusion, the insulin dose should be restarted 20 to 40 percent lower. If the glucose is less than 100 or is less than 125 mg/dl and falling, the scheduled dose should be maintained until the hourly measured glucose is above 125; followed by resumption with a 10 to 20% lower dose. If the glucose level is 100 to 200 mg/dl and stable, the current dose and interval are continued. If the glucose level is 200 to 350 mg/dl, the scheduled dose is increased by 10 to 20 percent. If the glucose level is over 350 mg/dl, the dose is increased by 20 to 40 percent.
On the day of surgery, a fluid infusion is begun at the time a meal would have been ingested, to deliver dextrose at 2 mg/kg/min, and glucose measured preoperatively. An insulin (0.25-U/ml) infusion is begun in those currently receiving insulin at 0.5 to 1.25 U/h, depending on the amount of insulin normally administered and the current glucose level. Blood glucose is monitored hourly and the infusion rate adjusted to maintain glucose 100 to 200 mg/dl. After the blood glucose is stable, urine glucose and ketone bodies are checked to ensure that glycosuria due to a low threshold will not confuse interpretation of urine output.
The insulin-dependent diabetic (1) requiring more than 50 U/day for control, (2) the diabetic whose condition is poorly controlled on a lower dose, or (3) the insulin-treated diabetic undergoing major surgery, are candidates for an intense monitoring and treatment regimen. Long- and intermediate-acting insulin is discontinued and the patient is managed with an intravenous insulin infusion or scheduled subcutaneous insulin preoperatively. Oral intake must be stopped 12 hours before anesthesia, because gastroparesis severely delays stomach emptying. When oral intake stops, maintenance fluids containing dextrose at 2 mg/kg/min are started; this should be continued at a stable rate throughout the procedure. Glucose is measured prior to induction and hourly until stable postoperatively, and urinary ketones are measured every 6 hours. An insulin infusion is started with an initial rate of 1 to 2 U/h, or to match the amount administered hourly the previous day if good control was achieved. Patients with obesity, liver disease, steroid therapy or severe infection require higher doses. An attempt should be made to maintain glucose 100 to 200 mg/dl and urinary ketones negative. Extremely high rates (up to 80 U/h) may be required during stressful procedures (e.g., cardiopulmonary bypass). 30 When the glucose level has remained stable and within the desired range for 3 hours, the frequency of glucose measurement can be decreased.
Diabetic ketoacidosis is an emergent condition that often presents in the diabetic patient with an acute surgical abdominal emergency. The priorities are to restore intravascular volume, clear ketonemia, and control blood glucose, and to correct the underlying problem. Patients with ketoacidosis are dehydrated due to glucosuria and the underlying condition. Because the dehydration is due to water and electrolyte loss, colloids are not indicated. If the patient's osmolality is elevated, 0.45 percent NaCl can be administered. The volume administered should be guided by the hemodynamic response and by urine output. Insulin should be administered intravenously as described above. When the blood glucose falls below 300 mg/dl, dextrose should be added to the fluids. Urine ketones are monitored every 2 hours after the blood glucose is within 100 to 200 mg/dl. If ketones are still present, the rate of glucose infusion should be increased and insulin increased correspondingly. The osmotic diuresis causes wasting of sodium, potassium, magnesium, and phosphate. Despite total body deficiencies, their concentrations may be elevated at the time of presentation due to severe water loss. In contrast, severe hyperglycemia extracts water from the intracellular space, diluting electrolyte concentrations. If the initial potassium level is elevated or the patient is anuric, potassium should not be administered. As hydration improves, and urine output increases, potassium, magnesium, and PO4 should be administered and monitored frequently. In general, the acidosis per se should not be treated with buffers. The ketoacidosis will correct as insulin and glucose levels improve and the lactic acidosis due to poor perfusion will respond to intravascular fluid replacement. If the pHa is less than 7.15 and hypotension fails to respond to intravascular fluid administration, bicarbonate therapy may be required.
Hypoglycemia
Hypoglycemia is dangerous because glucose is the sole fuel source for much of the brain. Symptoms commonly occur at blood glucose concentrations of less than 50 mg/dl or less than 57 mg/dl of plasma for adults, or less than 30 to 50 mg/dl for infants. Symptoms are seen at higher levels in diabetics than normals, and are obscured by general anesthesia. A biochemical stress response occurs at about 70 mg/dl, including sympathetic nervous system (SNS) stimulation, elevated growth hormone, and cortisol levels. Neurologic depression and electroencephalographic (EEG) depression appear at 50 to 55 mg/dl in normals and 70 to 85 mg/dl in diabetics. Selective neuronal necrosis, not infarction, occurs in the caudate, putamen, and cortex. There is a compensatory increase in cerebral blood flow. During labor, maternal starvation-induced ketosis has adverse fetal effects, including fetal ketonemia, hypoxia, and fetal lactic acidosis.
Inadequate gluconeogenesis coupled with absence of intake, or excess insulin cause hypoglycemia. Inadequate gluconeogenesis occurs in liver failure, cortisol deficiency (primary or secondary), inadequate glucagon response, growth hormone deficiency, during b-adrenergic blockade, and in neonates. Fasting in women is likely to produce hypoglycemia in 24 hours, whereas men tolerate 72 hours of fasting. The incidence of hypoglycemia in healthy infants and children is low (2 of 446), with 4 to 8 hours of fasting. Hyperinsulinemia follows sudden cessation of rapid dextrose administration (i.e., total parenteral nutrition [TPN]), with insulinoma, pancreatic islet cell adenoma or carcinoma, and following iatrogenic overadministration. Fetal hypoglycemia occurs if maternal glucose is greater than 150 mg/dl, because glucose crosses the placenta, inducing fetal insulin secretion. When delivery stops placental glucose delivery, hyperinsulinemia produces hypoglycemia. Treatment consists of an intravenous bolus of 5 g followed by increasing the rate of dextrose infusion by 1 to 2 mg/kg/min.
Nonanion gap hyperchloremic metabolic acidosis is managed by correcting the underlying cause or by administering NaHCO3. The calculated HCO3- dose is (HCO3-desired-HCO3-measured) 1 0.2 1 wt, because HCO3- distributes initially in the ECFV, which is 200 ml/kg. The indications for treatment of metabolic acidosis with bicarbonate are becoming fewer. If the underlying condition cannot be corrected, the outcome is not changed by the administration of buffer.
Antacid therapy, incidental administration of citrate with blood products, NaHCO3 administration, gastric drainage, or renal bicarbonate retention due to diuresis, or in compensation for respiratory acidosis, are common causes of perioperative metabolic alkalosis. NaCl or KCl can be administered orally or via a peripheral intravenous catheter or 0.1 normal HCl delivered slowly through a central venous catheter. The required dose is (Cl-desired-Cl-measured) 1 0.2 L 1 Wt in kg.
Hypertonic Saline
Hypertonic saline is not a specific concentration of NaCl. Investigators have studied concentrations ranging from 250 mEq/L and upward. The rationale for their use is that small volumes will expand plasma volume by osmotic translocation of extracellular and intracellular water. This could minimize storage space requirements at remotesites. However, the very high osmolality (some aremore than 900 mOsm/kg H2O) causes hemolysis at thepoint of injection. In addition to space savings, theminimal volume of water injected may reduce edema formation. This could be crucial in patients predisposed to tissue edema (e.g., prolonged bowel surgery, burns, brain injuries). Clinical studies have confirmed that a moderately hypertonic (Na = 250 mEq/L) solution was associated with lower muscle interstitial pressure than lactated Ringer's solution and bowel function returned earlier, but pulmonary shunt fraction was no different. 37 Experimental studies have demonstrated lower intracranial pressures in animals receiving hypertonic as opposed to hypotonic solutions. However, the intravascular half-life of hypertonic sodium is no longer than isotonic solutions of equivalent sodium load. In most studies, sustained plasma volume expansion was only achieved when colloid was present in the resuscitation solution. To date, hypertonic solutions have not gained widespread acceptance as resuscitation or intraoperative maintenance solutions. Thus, their accepted role is in the correction of hyponatremia.
Intravascular volume and hemodynamic resuscitation (cardiac output, oxygen delivery, correction of lactic acidosis) is more rapid, complete, and longer-lasting following administration of colloid containing solutions. Even when given in four times the shed blood volume, balanced salt solutions did not maintain hemodynamic stability. When crystalloid solutions are used for maintenance of intravascular volume, the short intravascular half-life mandates continuous infusion with close monitoring of filling pressures, and frequent measurement of hemoglobin concentration to avoid hemoconcentration. When crystalloid and colloid fluids are administered to attain hemodynamic goals, three to five times the volume of crystalloid are required.
Pulmonary effects of crystalloid as compared to colloid based resuscitation are not significantly different during the first 24 hours. Despite an early report of pulmonary complications following colloid resuscitation, many subsequent studies have failed to confirm this finding. Resuscitation of animals from hemorrhagic shock with 5 percent albumin in lactated Ringer's solution did not increase pulmonary interstitial water. The crucial factor determining the rate of pulmonary fluid accumulation is the pulmonary capillary pressure, determined predominantly by the pulmonary venous pressure as reflected by the pulmonary artery occlusion pressure. It is also clear that the lung will avoid edema at a higher PAOP, the higher the COP (see discussion of Pcrit earlier).
CNS effects of a crystalloid and colloid do not differ when the brain is not injured. This is undoubtedly due to the fact that the blood-brain barrier excludes sodium nearly as effectively as protein. The major determinant of water movement in the brain is the osmotic gradient between the brain and plasma. When plasma osmolality is abruptly decreased, water will move into the brain interstitium and intracellular space, causing edema. When the blood-brain barrier is damaged, colloid would have a theoretical advantage in preventing edema, but clinical confirmation is lacking. The critical factor in preventing brain swelling is to maintain ECFV osmolality with fluids containing sodium at isotonic or higher concentrations (i.e., not 0.45 percent NaCl or even lactated Ringer's solution, but rather 0.9 percent or hypertonic NaCl).
Bowel edema formation is less with colloid than crystalloid solution during bowel resection. It is believed that bowel edema is an important determinant of delayed return of bowel function following illness or injury.
In summary, colloids should be considered when rapid rates of crystalloid administration are required to maintain hemodynamic stability despite minimal external losses, the risks of rapidly changing volume status are high (vasodilator therapy, myocardial ischemia, elevated intracranial pressure [ICP]), the consequences of edema formation are serious, continuous monitoring of filling pressures will be difficult, and pulmonary capillary pressure is increased (e.g., heart failure).
The Pediatric Patient.
Using the same principles as outlined for adults, the neonate requires maintenance fluids of 0.3 percent NaCl with potassium. Dextrose administration should not exceed 5 mg/kg/min. This can generally be met by using 2.5 percent dextrose-containing fluids.
From BJA CEPD Reviews Feb, 2003.
Molecular movement across fluid compartments occurs by:
· Simple diffusion – O2, CO2
· Through protein channels – Na, K, Ca.
· Facilitated though transmembrane carrier proteins, - glucose, amino acids.
Contol of ECF volume.
Sensors:
· Carotid baroreceptors,
· Atrial stretch receptors.
· Juxtaglomerular apparatus.
Thus, contraction of ECF volume causes:
· non-osmotic ADH release,
· stimulation of the sympathetic system,
· release of atrial natriuretic peptide,
· activation of the renin-angiotensin-aldosterone system.
GFR
At birth, 25% normal
4 weeks, 90%
Neonate’s kidney cannot conserve Na, so there is an obligatory water loss, ie limited concentrating power. Thus, neonates should not be without fluid for more than 3 to 4 hours; otherwise, significant dehydration may result. Food should be offered until 6 to 8 hours prior to induction and glucose-containing clear liquids should be given about 4 hours prior to induction
Water and caloric requirements.
Weight kg Daily calories kcal/kg Hourly water ml/kg/hour
0 -10 100 4
10 – 20 1000 + 50 40 + 2
21 – 70 1500 + 20 60 + 1
The Postoperative Patient With Bowel Obstruction
Patients with bowel obstruction are often older with limited reserves in several vital organ systems; estimating the degree of loss of fluids is extremely difficult, because fluid is retained in the bowel lumen where it cannot be measured; the slowly developing volume depletion allows time for full expression of compensatory mechanisms which mask the degree of the deficit; patients will often not have ingested any fluids for many hours before entering the hospital; vomiting often occurs; the patient may have ischemic bowel injury with severe bowel wall edema and continued sequestration of luminal fluid, and formation of ascites. Perioperative fluid intake will be much greater than measured output, leading consultants to suggest diuresis for fluid overload. Nutrition is impaired pre-operatively and protein losses into the bowel are increased, leading to hypoalbuminemia, exacerbating the tendency to lose fluid from the vascular space. The clinical picture is one of ongoing fluid requirement in the absence of external fluid loss, commonly referred to as "third spacing."
The goals of fluid management are similar to other patients and include restoration of the vascular volume, interstitial volume and correcting severe electrolyte depletion, correction of acidosis, decreasing systemic vascular resistance into the normal range and optimization of oxygen delivery and utilization. Initial fluid infusion can restore intravascular volume sufficiently that blood pressure and heart rate improve. Yet, intravascular volume may remain depleted with a low cardiac output and severe arterial and venous vasoconstriction. The ECFV (except for the bowel) will remain dehydrated, continuing to accept fluids from the vascular space. The vasoconstricted patient will fail to perfuse all tissue, limiting the rate at which the ECFV can be replenished. If fluids are infused more rapidly than the rate at which they can enter the ECFV, increased filling pressures may result in pulmonary edema. It is crucial to estimate filling pressures, cardiac output and systemic vascular resistance, while aggressive intravascular fluid replacement with balanced salt solution and colloid is pursued. It may be necessary to administer arterial vasodilators such as nitroprusside to facilitate correction.
Management of a typical patient includes frequent monitoring of arterial blood pressure, heart rate, CVP, pulse pressure and respiratory variation, urine output, and electrolytes. If the above variables indicate stability, hemoglobin and COP should be monitored every 2 to 4 hours, until stable. A rising hemoglobin indicates ongoing loss of plasma water, with or without protein loss. An increasing COP indicates continued loss of plasma water in excess of protein loss. Because maintenance fluid requirements persist, 5 percent dextrose is infused in 0.45 percent NaCl with 20 to 40 mEq of KCl/L at maintenance rate. The fluid lost to the bowel and ECFV is similar to plasma water in electrolyte composition, so a balanced salt solution is a reasonable first choice for the fluid boluses required to sustain plasma volume. The fluid lost also will contain protein, so either albumin or colloid osmotic pressure should be monitored and colloid delivered, if a low COP (< 15 to 18 mmHg) coexists with hemodynamic instability. Replacement should be started at 3 ml/kg/h if the CVP (and PAOP if pulmonary artery catheter (PAC) has been placed) is within the patient's usual range. If it is high, start at 1 to 2 ml/kg/h. If the urine output rises above 1.5 ml/kg/h, one should check for glucosuria. If glucosuria is absent, the fluid infusion rate is reduced by 0.5 ml/kg/h. If the CVP or PAOP rise above the patient's usual values and urine output is 0.5 to 1.5 ml/kg/h, the fluid infusion rate is reduced by 0.5 ml/kg/h. If the CVP (and/or PAOP) decreases less than the patient's usual and urine flow rate is low, balanced salt or colloid solution is administered rapidly (0.5 to 2 ml/kg/min) with close monitoring of filling pressures.
The Liver Failure Patient
Fluid management of the liver failure patient is complicated by several interacting problems. These patients appear to be simultaneously hyper- and hypovolemic. When fluids are infused, most is retained, yet renal function deteriorates while avid sodium retention persists. Two major hypotheses have been advanced to explain these contradictory findings: primary sodium retention and arterial underfilling. Neither explains all the clinical findings, nor does either lead to consistently successful therapy.
According to the arterial underfilling (primary vasodilation) MLID89014632 47 hypothesis, some factor produced or not catabolized by the failing liver causes inappropriate arterial dilation. The relative hypotension leads to activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system, and vasopressin release. These lead to subsequent sodium and water retention resulting in ascites and tissue edema.
In fact, cirrhotic patients have low systemic vascular resistance, high cardiac output, and relative hypotension. Persistent endotoxemia (shunting via portasystemic anastomoses, and enhanced endotoxin absorption from the intestine due to bile salt deficiency) may contribute to the vasodilation via activation of a cascade of secondary mediators beginning with tumor necrosis factor and interleukins. In addition, other vasodilator neurotransmitters may be produced or may not be cleared by the damaged liver.
The primary sodium retention hypothesis explains the avid sodium retention on the basis of hormonal (aldosterone) hyperactivity due to failure of the liver to metabolize aldosterone. Given the ECFV expansion, the distribution into ascites and tissue edema is explained by the abnormally high portal venous pressures and hypoalbuminemia.
More recently, abnormalities of atrial natriuretic peptide (ANP) have been investigated. ANP levels are normal or low in cirrhotic patients, in contrast with expected increases in volume expanded patients. MLID89300870 48 ANP increased with water immersion, or fluid administration, but natriuresis was not closely correlated with ANP levels. (Water immersion of the lower body compresses the venous capacitance system, resulting in centralization of blood volume. This simulates a volume infusion without adding any sodium or water to the body and should cause ANP release.) Water immersion did not increase ANP levels in patients with high baseline renin and aldosterone levels. Additionally, patients with ascites may have blunted responses. Thus, impaired ANP release failed to explain sodium retention. MLID89300870 48 Patients with tense ascites had increased ANP, renin and aldosterone concentrations. After paracentesis, ANP increased, but renin and aldosterone decreased. MLID90184983 49 The reasons for these findings were not clarified, but a reduction in intra-abdominal pressure would have decreased inferior caval pressure, thus facilitating venous return, leading to increased ANP levels. Decreased intraabdominal pressures would also improve renal perfusion pressure, causing a reduction in renin release and subsequent aldosterone generation.
The role of increased intra-abdominal pressure may be important in sustaining sodium retention after ascites develops. Increased intra-abdominal pressure raises caval pressure. This decreases renal blood flow (RBF) and glomerular filtration rate (GFR), because the renal perfusion pressure gradient (mean arterial pressure minus renal venous pressure) is decreased both by systemic hypotention and increased caval pressure. The hypotension and reduction in renal blood flow can lead to renin activation, with aldosterone production. The hypotension, increased aldosterone and the decrease in glomerular filtration rate lead to enhanced sodium reabsorption, and low fractional excretion of sodium.
Hypoalbuminemia results from impaired synthesis by the liver, transudation into ascitic fluid due to portal hypertension, and malnutrition. The low COP favors loss of fluid from the vascular space into the interstitial space, producing intravascular hypovolemia. Ascites results from high portal venous pressure and hypoalbuminemia, markedly increasing the volume of transcellular fluid, which is functionally excluded from rapid exchange with the ECFV.
Splanchnic blood pooling due to increased portal venous resistance plus lower body pooling due to elevated caval pressures from ascites tends to decrease net systemic venous return. Patients are, thus, functionally hypovolemic despite normal or elevated total blood volume. Heart failure due to alcoholic cardiomyopathy may further complicate the clinical picture.
The goals in these patients are to avoid increasing interstitial fluid overload, maintain normal potassium concentration, and maintain intravascular volume. If cardiac failure is present, treatment must include administration of inotropic drugs and diuretics when filling pressures are increased. Restore intravascular COP by infusion of 25 percent albumin when possible. If the patient is acutely hypovolemic, then 5 percent albumin solutions should be preferred to crystalloid which will tend to further expand the already overexpanded ECFV (i.e., produce more edema and ascites). In addition, intra-abdominal pressure should be estimated from urinary bladder pressure and paracentesis performed whenever it increases above 20 to 25 mmHg. Finally, trials of dopamine, norepinephrine, phenylephrine, or vasopressin may be performed in hypotensive patients with low vascular resistance and hypotension in attempts to increase renal perfusion pressure and renal blood flow.
The Heart Failure Patient
Fluid management of the heart failure patient is directed to maintain the optimal cardiac preload, avoid overadministration of sodium, diminish edema content, and correct common electrolyte abnormalities. The goal of maintaining ideal cardiac preload during rapid fluid shifts which occur perioperatively is extremely difficult without direct or indirect measures of both preload (CVP, thermodilution, end-diastolic volume [EDV]), echocardiography, pulmonary artery occlusion pressure, left atrial pressure) and cardiac contractile function (stroke volume, ejection fraction, stroke work). Patients with a history of cardiac failure scheduled for major or prolonged surgery should have monitoring instituted preoperatively and an intravascular fluid challenge (i.e., 500 to 1,000 ml/70 kg of crystalloid) performed to identify the optimal preload. Avoid exacerbating tissue edema by frequent monitoring of preload and arterial blood pressure coupled with support of contractility and control of vascular resistance. These patients have impaired ability to excrete fluids during the fluid mobilization which occurs postoperatively. Because the ECFV is usually already expanded in these patients, the initial rates of fluid infusion intraoperatively should be at the lower ranges of estimates. Similarly, maintenance of intravascular volume without expansion of the interstitial space favors the use of colloid during the immediate perioperative period. Postoperatively, continue close hemodynamic monitoring until the fluid mobilization phase is complete. The objective in managing fluid postoperatively should be to give as little crystalloid as is consistent with maintaining adequate overall cardiovascular performance. It is common to find perioperative patients receiving more than 200 mEq of sodium per day including maintenance fluids, plus saline used to measure cardiac output, administer antibiotics, and infuse vasoactive medications and inotropic agents. Thus, fluid should be maintained at a low maintenance rate and should include flushing fluid and sodium in that consideration. As soon as either urine output begins to increase or filling pressures or diastolic volumes begin to rise, maintenance fluids should be stopped completely. If preload becomes excessive, diuretics are administered.
Patients with heart failure have primary electrolyte problems due to compensatory physiologic mechanisms activated by the impaired cardiac performance. These are then complicated by therapy with diuretics, digitalis, vasodilators, and angiotensin converting enzyme inhibitors. Hyponatremia is common due to excess activation of the vasopressin system despite sodium retention. Treatment is directed at excreting the excess water load with diuretics, which virtually always increase free water excretion more than sodium excretion; sodium administration is not indicated unless volume depletion is documented. Aldosterone activation and diuretics lead to potassium and magnesium wasting. These ions are crucial for maintaining cardiac electrophysiologic stability as well as digitalis and catecholamine effectiveness. Ionized calcium is crucial for cardiac contractility, and hypocalcemia is extremely common during the perioperative period. Ionized calcium must be measured and corrected routinely in these patients. Severe hypophosphatemia often coexists with abnormalities of calcium, potassium and magnesium and will lead to depressed contractility. Pi must be monitored and corrected.
The Patient With Cerebral Edema
Goals:
· maintaining cerebral perfusion pressure, in the normal range, 80 to 90 mmHg.
· avoiding elevations of cerebral venous pressure and hypertension,
· preventing large changes in plasma osmolality (particularly depression of plasma osmolality),
· avoiding hyperglycemia.
Cerebral edema formation is related to capillary pressure, COP, and permeability. The normal brain capillary bed is essentially impermeable to sodium, mannitol and protein, although water freely crosses. The damaged capillary bed becomes excessively permeable with greatest conductivity to the smallest molecules, thus favoring use of colloid.
A degree of water dehydration without hypovolemia is desired to maintain the plasma [Na] between 142 to 148 mEq/L. Thus it is common to provide 75 to 90 percent of maintenance fluids with 0.9 percent NaCl or lactated Ringer's solution, and to minimize water volume required for other medications. Isotonic crystalloid or colloid do not cause edema in normal brain and can be used to sustain intravascular volume.
Parenteral nutrition can be prepared with 15 percent amino acids solutions, 20 percent lipid and 70 percent dextrose to give full protein and caloric support in the minimal volume. Similarly, tube feeding formulations with 2 cal/ml should be prescribed. Hypovolemia must be carefully avoided. Colloid infusion to sustain intravascular volume, guided by hemodynamic monitoring tends to provide better long term control of the intravascular volume than crystalloid. If diuretics or diabetes insipidus cause loss of more than 2 ml/kg/h for more than 2 to 4 hours, consider placement of a pulmonary artery catheter for closer monitoring.
Blood glucose should be maintained at 80 to 175 mg/dl by closely monitoring (initially hourly, decreasing frequency as stability is demonstrated) blood glucose concentration. Fortunately, the indications for steroid use have become fewer in recent years, lessening the problems with hyperglycemia.
The Anuric Renal Failure Patient Undergoing Nontransplant Surgery
Fluid management of the anuric renal failure patient for non-transplant surgery should avoid excessive intravascular fluid administration, ECFV expansion and correct, (at least not worsen) electrolyte and acid base problems. We also attempt to prevent precipitating conditions that would require dialysis during the immediate postoperative period (hyperkalemia, pulmonary edema, metabolic acidosis). Dialysis is difficult or impossible in the hemodynamically unstable patient and anticoagulation may be strongly contraindicated for several hours postoperatively.
Patients with chronic renal failure often present with hypertension, diabetes, and vascular disease. Thus avoidance of hypotension may be indicated to maintain coronary or cerebral perfusion pressure. Patients with acute renal failure are at great risk of recurrent ischemic renal injury should hypotension occur. This contrasts with the lack of concern for an adverse effect on renal function of the chronic renal failure patient. Furthermore, recent dialysis often induces acute electrolyte shifts and hypovolemia, while the patient who has not been dialyzed recently is at risk of fluid overload, hyponatremia, hyperkalemia and acidosis. The best compromise appears to be dialysis 12 to 24 hours preoperatively. If dialysis is performed close to the time of surgery, volume removal should be minimal. Patients with renal failure are often malnourished, with hypoproteinemia and are anemic and have poor glucose tolerance.
Hemodynamics should be closely monitored. If hypovolemia develops, colloid should be used early, but one should avoid producing vascular overexpansion. Likewise, one must avoid interstitial fluid overload, which would require acute postoperative dialysis. Crystalloid replacement of third-space losses should be limited to 1 to 2 ml/kg/h, while blood loss should be replaced with colloid or RBCs. Correction of sodium, potassium, and acidosis can be achieved by the use of isotonic fluid without potassium and with reduced amounts of chloride and increased amount of buffer. Initially, an infusion of 30 percent of calculated maintenance fluid rate is important because approximately 70 percent of normal fluid requirements are used in excreting solute via the kidney, a route no longer available. Na, K, pH, HCO3-, and glucose should be monitored at regular intervals.
Tests of renal function, with regard to sevoflurane toxicity. A&A 90: 505 00
· Creatinine tests GFR
· Proteinuria glomerular leakiness
· Glycosuria also enzymuria, tests of tubular absorptive function.
Compound A affects the tubule.
The Patient With Adult Respiratory Distress Syndrome
Fluid management of the patient with adult respiratory distress syndrome (ARDS) emphasizes keeping the CVP and PAOP as low as possible, consistent with good ventricular function, and maintaining colloid osmotic pressure. Oxygen delivery should be sustained, ideally above 600 ml/min/m2, by increasing cardiac index and hemoglobin concentration. Compensation for hemodynamic effects of increased airway pressure is achieved by maintaining adequate right and left ventricular filling volumes. When airway pressure increases, the lung expands in proportion to its compliance. The intrapleural pressure increases in direct proportion to lung expansion and inversely with chest-diaphragm compliance. The increased intrapleural pressure increases CVP, which reduces the peripheral to CVP gradient. This reduces venous return unless peripheral venous tone increases or fluids are administered. The increased venous pressure increases fluid filtration out of the peripheral capillary bed, tending to produce hypovolemia. The increased pleural pressure is transmitted via the pericardium to reduce the filling pressure gradient for all cardiac chambers. The consequent reduction in end diastolic volume diminishes preload to all chambers. The elevation of intrapulmonary pressure increases pulmonary artery pressure, which leads to augmented right ventricular afterload. The reduced venous return, decreased right ventricular preload, and increased afterload may severely compromise right ventricular stroke volume, cause stiffening of the interventricular septum and reduce preload for the left ventricle. All these consequences can be improved by intravascular volume expansion, except for the increased afterload on the right ventricle. Thus CVP and right ventricular end-diastolic volume are monitored to aid in the decision to institute inotropic therapy. An increase in CVP also compromises lymphatic return from the lung and periphery. Additionally, sepsis, the most common coexisting condition with ARDS, causes increased vascular capacity, vasodilation, decreases COP, and results in tissue edema. The net clinical outcome of these factors is that fluid intake usually exceeds output until the ARDS (and sepsis) begins to subside. There are no good data comparing crystalloid and colloid management over the entire time course of ARDS. However, after 48 hours, pulmonary function may be somewhat better in patients managed with some colloid rather than crystalloids alone.
The Acutely Burned Patient
Fluid management of the acutely burned patient focuses on restoration of plasma volume and a shift of the ECFV into the burned but viable tissue, accompanied by increased losses caused by loss of the normal barrier function of the skin. The tissue injury produced by the burn leads to an abrupt disruption of the capillary bed manifested by local vasodilation, increased permeability, and, presumably, decreased reflection coefficient to proteins. The vasodilation increases the surface area for filtration and tends to increase capillary pressure. The lowered reflection coefficient diminishes the effect of colloids on retaining fluid in the capillary bed. Thus water, electrolyte, and protein enter the burned tissue at the expense of the intravascular volume. Fluid is mobilized from uninjured tissues by reduced filtration due to compensatory arteriolar vasoconstriction and reduced venous pressure, which diminish capillary pressure, and by lymphatic return. The net result is a transfer of fluid from normal tissue into the injured tissue and intravascular hypovolemia. Capillary permeability was formerly thought to increase in all tissues after a serious burn injury, but this is not the currently held view. In addition to the tissue edema, there is a markedly increased loss of water by evaporation from the wound surface, and the metabolic rate increases dramatically, leading to proportionate increases in fluid requirements.
Several formulas have been developed to aid in writing the initial fluid prescription. The key to success is close hemodynamic monitoring, with titration of therapy to the individual patient's physiology. For example, if urine output increases progressively, or if filling pressures increase, fluid administration must be decreased.
The Parkland formula 53 prescribes fluids based on the percentage of the body surface area burned (%BSA-burned): (2 ml/kg)/(%BSA-burned) during the first 8 hours and (2 ml/kg)/(%BSA-burned) during the next 16 hours. The formula prescribes ((0.25 ml/kg)/(%BSA-burned))/h for 8 hours, then ((0.125 ml/kg)/(%BSA-burned))/h for 16 hours, then 5 percent dextrose in water, ((0.8 ml/kg)/(%BSA-burned))/h, plus 5 percent albumin, ((0.015 ml/kg)/(%BSA-burned))/h for 24 hours. For example, a 50 kg person with 50 percent BSA burn should receive (50 kg) 1 (0.25 ml/kg) 1 (50 %BSA-burned), which equals 625 ml/h for 8 hours, followed by (50 kg) 1 (0.125 ml/kg) 1 (50 %BSA-burned), which equals 310 ml/h for 16 hours. During the second 24 hours one should administer (50 kg) 1 (0.08 ml/kg) 1 (50 %BSA-burned), which equals 200 ml/h of 5 percent dextrose in water, plus (50 kg) 1 (0.015 ml/kg) 1 (50 %BSA-burned), which equals 37.5 ml per hour of 5 percent albumin. Colloids are not contraindicated, even during the acute phase of fluid resuscitation. Although they will pass into the injured tissue at an accelerated rate, they have a more sustained effect on plasma volume than does crystalloid alone.
Labor increases energy expenditure, for which glucose may provide calories. Prolonged labor without caloric intake may lead to maternal and fetal hypoglycemia, ketosis, and lactic acidosis. However, controversy surrounds the use of dextrose solutions during labor. All studies do not demonstrate hypoglycemia in parturients receiving no dextrose, perhaps because of the gluconeogenic effects of epinephrine added to epidural anesthetics. In neonates of mothers receiving varying amounts of 5% dextrose, hyperinsulinemia and hypoglycemia developed, prompting a recommendation that parturients not receive more than 6 g/h of dextrose. In patients randomized to receive no dextrose, 1% dextrose, or 5% dextrose, administration of dextrose-free solution resulted in umbilical artery hypoglycemia, 1% dextrose maintained euglycemia in both the mother and neonate, and 5% dextrose was associated with neonatal hypoglycemia. Based on these clinical studies, glucose should be given during labor in a dose of 1–2 g/h (equivalent to 100–200 ml of a 1% dextrose solution); should not exceed 6 g/h; and should be considered especially in patients not receiv