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FLUID AND ELECTROLYTE DISORDERS Dr. Chandra Kant Pandey1 Dr. R. B. Singh2 Preoperative dehydration is common in surgical patients, and is primarily attributed to prolonged fasting period and bowel preparation. The symptoms of dehydration in post-operative fluid may be most evident in minor surgical procedures, where intraoperative fluid requirements are low. This is opposed to major surgical procedures, where large amounts of fluid are often administered intraoperatively, and therefore may compensate for an initial fluid deficit. Preoperative fasting of 12 hours or more may result in a fluid deficit of about one litre in an adult patient consisting primarily of free water as well as a small quantity of electrolytes.1,2 The symptoms from this fluid deficit have not been defined, but may include thirst, drowsiness and dizziness.3 Apart from subjective patient’s discomfort, these symptoms of mild dehydration may contribute to prolonged hospital stay in a review of 17638 patients, where postoperative dizziness and drowsiness were independent predictors of prolonged hospital stay after ambulatory surgery.4 The anatomy of body fluids Fluid balance is often thought of in terms of the external balance of water and electrolytes between the body and it s environment. However, it is important to consider the balance between the fluid compartments within the body and how these change with diseases. The Table 1 represents the body fluid compartment in a 70 kg man. It can be seen that total body water is approximately 60% of the body weight, and that roughly one third of this is extra-cellular and two third intra- cellular. The two intra-cellular and extra-cellular are divided by the cell membrane which, through its sodium pump, maintains the integrity of the two compartments in which sodium is the main extra-cellular and potassium the main intracellular cation, balancing the negative charges on protein and other molecules within the cells. It is also seen from diagram that the plasma volume is roughly a quarter of the total extra cellular fluid volume, the two being separated by the capillary membrane which, with its restricted pore size, slows the passage of the large protein molecules from the vascular to the interstitial space.5 The integrity of the intravascular volume is therefore maintained by the oncotic 1. M.D., Anaesthesiology, Associate Professor 2. M.D., P.D.C.C. Ex. Senior Resident Correspond to : E-mail :
[email protected]
pressure of the plasma proteins and the functions of the capillary membrane. Any condition, therefore, which alters the permeability of the vascular membrane or the level of plasma proteins, will affect the distribution of fluid between the intravascular and the interstitial space.5 The integrity of the intravascular volume is therefore maintained by the oncotic pressure of the plasma proteins, will affect the distribution of fluid between the intravascular and the interstitial space. The intestinal space can be further divided. Approximately one litre may be transcellular, i.e. secreted into the gut, and 3-4 litres may be rapidly exchangeable, the reminder being bound in the matrix of connective tissue. Table - 1 : Total body water (70 kg adult) is 60% of the body weight= 70 × 60/100=42 litres. Extracellular fluid volume comprises interstitial fluid and blood volume (20% body weight= 14 litres) Blood volume is approximately 5 litres (of which 5% of body weight is plasma volume equal to 3 litres)
Intracellular water = 40% body weight = 28 litres. Na+ 10 meql-1 K+ 150 meql-1
Interstitial fluid = Extracellular fluid volume – plasma volume (14-3)=11 litres Na+ 140 meql-1 K+ 4.0 meql-1
The flux of the body fluids : Through the gut Approximately 8-9 litres of fluid a day pass the duodenum, although only 150 ml of water may eventually appear in the faeces. The reabsorptive capacity of the gut may fail in various diarrhoeal diseases or with short bowel or fistulae. In the presence of ileus or intestinal obstruction, more than 6 litres of water may be pooled in the gastrointestinal tract and be therefore lost from the extracellular fluid. It is important therefore, when designing nutritional support regimens, to be aware of the electrolytes content of the various gastrointestinal fluids. Through the kidneys and extracellular fluid volume regulation Hundred and eighty litres of water, 25200 mmol of sodium and 720 mmol of potassium are filtered daily, but more than 99% of the water and sodium and 86% of the potassium filtered are reabsorbed. The normal kidney responds to water or sodium excess or deficit, via osmolality and volume receptors, acting through anti-diuretic-hormone
PANDEY, SINGH : FLUID AND ELECTROLYTE DISORDERS
(ADH) and the rennin-angiotensin system to restore normal volume and osmolality of the extracellular fluid. Maintenance of volume will always override maintenance of osmolality if hypovolumaemia and hypo-osmolality coincide. In the presence of starvation or illness, however, these normal responses may be altered. Unless such changes are well understood, the therapeutic errors will be madefrequently. Renal adaptation to hypovolumia occurs through three primary mechanisms: a reduction in renal blood flow, a reduction in glomerular filtration rate, and increased tubular reabsorption of sodium and water.6 Initial, renal blood flow is maintained as perfusion pressure decreases by decreases in renal afferent arteriolar resistance. Furthermore decrease in cardiac output may result in increased renal vascular resistance as blood flow is redistributed from the kidney to preserve cardiac and cerebral perfusion. Renal perfusion during hypovolumia is determined by balance between renal vasoconstrictor factors and vasodialtaory mechanism. Autoregualtion may be impaired or lost during severe acute hypovolumia and may be lost in the inner-medulla with even reduction in perfusion pressure7,8 Renal sympathetic stimulation with secretion of alpha-adrenergic catecholamine and angiotensin II increases renal vascular resistance. To preserve plasma volume, reabsorption of filtered water and sodium is enhanced by antidiuretic hormone and aldosterone and by reduced secretion of atrial natriuretic peptide. A 10-20% decrease in blood volume is necessary before ADH secretion from the posterior pituitary increases.9 ADH acts primarily on the medullary collecting ducts to increase water reabsorption and causes excretion of smaller volumes of more highly concentrated urine. Sodium conservation results from both decreased filtration and increased distal tubular reabsorption of sodium, mediated by aldosterone. Hypoperfusion stimulates glomerular cells of the renal juxtaglomerular apparatus to release rennin, which catalyses the conversion of angiotensionogen to angiotensin I. Angiotensin converting enzyme converts angiotensin I to angiotensin II, which stimulates the adrenal cortex to synthesise and release aldosterone.10 Atrial natriuretic peptide (ANP), which exerts vasodilatory effects and increases the renal excretion of sodium and water, is released from the cardiac atria in smaller quantities in hypovolumia.11 Kidney also synthesizes vasodilatory prostaglandins that play a critical role in protecting the kidney from vasoconstrictor hormones and in maintaining RBF during hypovolumia. The protective effect of endogenous renal prostaglandin may be
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antagonized by nonsteriodal anti-inflammatory drugs.12 Response to starvation Food deprivation and refeeding oedema have been described. In the semi-starvation in normal volunteers, it has been shown that although the fat and lean compartments of the body tissues shrink, the extracellular fluid volume remains either at its pre-starvation level or decreased very slightly. In relative terms, therefore, the extracellular fluid volume occupies an increasing proportion of the body mass as starvation progress. The degree of oedema may be related to access to sodium and water and may of course be exacerbated by refeeding. The sodium and water balance may also be affected by the diarrhoea which cause problems in food deprived victims, as well as the cardiovascular decompensation associated with the effect of starvation on the myocardium.13 Response to injury and acute illness It was observed that anaesthesia and surgery produce oliguria, postoperative patients were unable to excrete the large amounts of salt and water administered intravenously. This effect was highlighted by Wilkinson et al who showed that postoperatively patients were unable to excrete an excess salt and water load whereas the infusion of saline solution intravenously into normal subjects resulted in a diuresis and a restoration of normal salt and water balance within hours, those suffering from trauma, surgery, or acute illness were unable to do so. The injudicious administration of fluids, therefore, results in an increasingly positive salt and water balance and gross interstitial overload, manifest as oedema. The presence of oedema in such patients signify a salt and water overload of at least 3 litres and often much more. The consequent oedema of tissue may impair function as well as wound healing.14 The capacity to diurese an excess fluid load returns as the phase of the injury gives way to the recovery or anabolic phase. The two terms, sodium retention phase and sodium diuresis phase has been used to describe two periods of response to trauma or illness. In fact these responses are non-specific and occur equally in acute medical illness and in surgical patients. This is also common to find a low sodium concentration in sick patients. This is not, of course, equivalent to salt deficiency, but merely to the changed proportion of water and sodium in extracellular space. It often occurs in the presence of increased body sodium, where hypotonic fluids have often occurs in the presence of increased body sodium, where hypotonic fluids have been given in excess to cause dilution. A limited to dilute the urine may persist until the convalescence or recovery phase of injury.
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The table 2 shows daily plasma and urine osmolality for 5 days postoperatively in a series of patients who had undergone uncomplicated abdominal surgery and received hypotonic fluid postoperatively. Despite increasing hypotonicity persisting to the seventh day and beyond, the urine remained relatively concentrated. Severely ill patients may develop defective cell membrane function such that sodium may accumulate within the cell. This has been called the sick cell syndrome.14 Table - 2 : Mean daily plasma and urine osmolalities in 10 patients undergoing abdominal surgery and receiving hypotonic crystalloids (Allison SP. Metabolic aspect of intensive care Br I Hosp Med 1974; 661-72). Osmolalities (in mosmolkg-1) day after operation Fluid
Day 0
Day 1
Day 2
Day 3
Day 4
Day 5
Plasma Urine
282579
279696
273610
273358
270489
270611
The importance of potassium Although potassium is lost from the cells as protein is catabolised, the losses of potassium in the urine may be disproportionately greater, probably through mineralcorticoid effects. Even though the total body potassium may decrease, the serum potassium concentration may be normal or increase in the catabolic patients, depending on the presence of other sources of loss, e.g. urine, fistulae, diarrhoea or nasogastric aspirate. Once refeeding starts, however, the cells begin to take up potassium as glycogen and protein are resynthesised. This may result in abrupt drops in serum potassium concentration, revealing the underlying potassium deficit. Careful monitoring of serum potassium and adequate potassium replacement are important aspect for nutritional management for such patients. A rise in blood pH or the use of insulin may precipitate a rapid fall in serum potassium concentration, not only in the management of diabetic ketoacidosis, but also in the care of catabolic and unstable patients. Effects of feeding In a series of elegant studies, it has been shown that starved rabbits tend to retain salt and water when refed intravenously and that this may lead to increased lung water.15 This overload was not seen when a low volume, low sodium feed was given. It was also demonstrated that a regimen with sole non-protein energy source was glucose, caused greater water retention than when half the energy was supplied as fat. Although water is retained intracellualy as glycogen is reformed, there was also, in these studies, an increase in extracellular
water and a dilution of serum albumin concentration.15 Startker et al had reported a series of malnourished patients who were fed preoperatively. Those who retained fluid and became hypoalbuminaemic had more complications postoperatively than those who were able to diurese the excess fluid and maintain a higher albumin concentration.16 Sitges Serra devised a no sodium, low volume feed for such patients and showed that this protected against extracellular fluid expansion and dilution of serum albumin. This regimen is now used extensively in patients who have already been overloaded, and restores normal balance over a period of a week to ten days, with gradual loss of oedema. Dissociation between compartmental changes Feeding of the patients who are unable to eat and have considerable oedema and hypoalbuminaemia 600 mlmin-1m-2 demonstrated a decrease in mortality and in the number of complications in the patient managed the higher level of oxygen delivery.18 These data suggest that aggressive, goal directed haemodynamic support in certain high risk surgical patients may limit the mortality and morbidity that results from clinically inapparent hypoperfusion. The aims to be achieved with fluid administration The goals of perioperative fluid administration are to: 1. Maintain adequate oxygen delivery 2. Normal body electrolyte concentrations 3. Normoglycemia. The total fluid requirements are made up of: 1. Compensatory intra-vascular volume expansion (CVE) 2. Deficit displacement 3. Maintenance fluids 4. Restoration of losses 5. Substitution for fluid redistribution (third space losses).
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1. Compensatory intra-vascular volume expansion (CVE) Most general and regional anaesthetics cause arteriolar and venous dilatation, expanding venous capacity and leading to a reduction in venous return and preload, and therefore a reduction in cardiac output. Infusing fluids to increase the preload will most often return the stroke volume to an acceptable range. CVE requires 5 to 7 mlkg-1 of balanced salt solution just before or during induction of anaesthesia. 2. Deficits Fluid deficit is the maintenance fluid requirement that is 1 to 2 mlkg-1hr-1 multiplied by hours since last intake PLUS unreplaced PREOPERATIVE external and third space loss. When hypovolemia is present, infuse sufficient fluid to restore mean arterial pressure, heart rate and filling pressure (preload or CVP) prior to induction. It is also desirable to establish a normal urine flow rate if time permits. 3. Maintenance fluids. Maintenance fluids meet the ongoing basal needs for water and electrolytes. The surgical stress response tends to reduce insulin production and leads to hyperglycemia , therefore fluid use for volume maintenance should NOT contain dextrose. There are however certain high risk patients who are in danger of developing hypoglycemia: premature infants, neonates who are receiving glucose containing or hyperalimentation solutions preoperatively, infants of diabetic mothers, neonates who are small for gestational age and children and adults who are diabetic. These patients should have their glucose solution continued in the peri-operative period. They also require peri-operative blood glucose monitoring. There is no reason to administer glucose in the routine clinical situation and there are potential hazards. After surgery, when the danger of hypoxia and cerebral ischemia is over or less, glucose solutions can be started. 4. Fluid losses Any external losses such as blood and ascitic fluid should be replaced to maintain the normal intravascular blood volume and composition of the extracellular fluid. Blood loss is replaced initially with either 3 ml of balanced salt solution or 1 ml of colloid solution for each ml of blood loss. Packed red blood cell infusions are used roughly one ml for each 2 ml of blood loss plus either crystalloid or colloid as described. Blood transfusion is associated with certain risks. In patients with reasonable cardiac and respiratory reserve and without compromised regional
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circulation (e.g. coronary, cerebral, renal and intestinal) haemoglobin levels of 7.5 gdL-1 and above are usually well tolerated provided the intravascular volume is sufficient (i.e. the CO is maintained). If intravascular volume and myocardial function are normal, the cardiac output (specially stroke volume) will increase to maintain the oxygen delivery. Neonates and small infants are less able to increase their stroke volume, and are therefore less able to compensate for a low arterial oxygen content (which is associated with low haemoglobin). 5. Third space losses This is primarily caused by tissue oedema and transcellular fluid displacement. Functionally, this fluid is not available to the vascular space. The composition of third space losses is equivalent to the extracellular fluid and electrolyte composition plus a small amount of protein. Therefore balanced salt solution is the most appropriate replacement for third space loss. The volume distributed correlates roughly with the degree of tissue damage and manipulation. Intra-abdominal procedures with small incisions (example hysterectomy) may require 2 mlkg-1hr-1 while major bowel resection will require 4 to 6 mlkg-1hr-1. Post-operative fluid therapy Haemoglobin should be maintained at an acceptable level. Urine output should be above 0.5 mlkg-1hr-1 and administration of 1.5 mlkg-1hr-1 of balanced salt solution will provide replacement of insensible loss, and maintain urine output. Which fluids? Hypotonic intravenous fluid in the immediate postoperative period, coupled with the loss of sodium that is not being replaced by intravenous fluid, potentially leads to the development of dilutional hyponatremia. This may occur 2 to 24 hours after surgery. Acute dilutional hyponatremia is a potential problem in almost every post-operative patient who has undergone any degree of tissue trauma or has been placed on hypotonic fluids postoperatively. Vomiting results in loss of fluid which is high in sodium i.e. balanced salt solution. Vomiting, coupled with small bowel losses and / or third space losses can result in the need for post-operative sodium. Sodium in hypotonic solutions is often inadequate and acute dilutional hyponatremia results. The problem is that while the extracellular fluid becomes hypotonic, the intracellular fluid remains isotonic, so there is a transfer of water from the extracellular fluid to the intracellular fluid, resulting in cerebral edema. This leads to central nervous system depression, irritability, and vomiting and seizure activity.
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
Hyponatremia is the most frequent electrolyte disorder in the perioperative period. Acute symptomatic hyponatremia is a medical emergency which requires immediate therapy. Because of its availability, 4.2 % NaHCO3, which is 3 % sodium solution is the drug of choice to correct the problem. The empirical dose is 2 ml per kilogram of 4.2 % NaHCO3 over 1 to 2 hours. This should raise the serum sodium by 6 meqL-1. NaHCO3 should be administered to any patient with seizures who is receiving a hypotonic solution post-operatively, along with the normal treatment of the seizure. When the seizure has abated, balanced salt solutions can be given as the appropriate fluid.19 Duration of intravenous therapy This should be continued as long as gastrointestinal function is inadequate to meet metabolic and caloric requirements. Fluid management in perioperative period Trauma and surgery alters the volumes and composition of the intracellular and extra cellular spaces. Therapeutic infusion of fluids further alters compartmental volumes and composition. Appropriate management of fluid may limit surgical morbidity and mortality. Accurate replacement of fluid deficits requires an understanding of the distribution spaces of water, sodium, and colloid. Sodium concentration is equal in plasma volume and interstitial fluid. Albumin is unequally distributed in plasma volume (4g mdL-1) and IF (1g mdL-1). The IF concentration of albumin varies greatly among tissues. ECV is the distribution volume for colloid, although the concentration in PV and IF are unequal. Physiology and pharmacology of colloid, crystalloids, and hypertonic solutions and its clinical implication Osmotically active particles attract water across semipermeable membranes until equilibrium is attained. If membrane permeability is intact, colloids such as albumin or hydroxyl starch preferentially expand plasma volume rather than interstitial fluid volume. Concentrated colloid solutions may translocate interstitial fluid into the plasma. Plasma expansion unaccompanied by interstitial expansion offers apparent advantages: lower fluid requirements, less peripheral and pulmonary oedema accumulation, and reduced concern about later fluid mobilization. Exhaustive research has failed to establish the superiority of either colloid-containing or crystalloid containing fluids. Much of the debate has centred on the relative risk of pulmonary oedema. Crystalloid solutions are associated with pulmonary oedema. In disease states associated with increased pulmonary capillary permeability, infusion of colloids may aggravate pulmonary oedema. In
PANDEY, SINGH : FLUID AND ELECTROLYTE DISORDERS
the absence of oncotic pressure gradient, small increase in the hydrostatic gradient can result in pulmonary oedema. Hypoproteinaemia in critically ill patients has been associated with development of pulmonary oedema and with increased mortality. However either crystalloid or colloid administration may precipitate pulmonary oedema in patients who have valvular heart diseases and decreased left ventricular compliance. After experimentally increasing microvascular permeability, no difference was found between increase in extravascular lung water induced by colloid or crystalloid.20 In surgical patients at risk for the development of pulmonary oedema, pulmonary artery catheterisation may facilitate management. Part of the difficulty in defining the superiority of crystalloid or colloid fluids is directly attributable to the difficulty of defining comparable end points in clinically relevant experimental models21. More recently developed models replicate clinical situations, permitting more accurate comparison of crystalloid and colloid solutions. In animals infused with E.coli lipopolysaccharide, which mimics some aspects of clinical sepsis, lactated ringers solutions 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.22 Fluid replacement therapy Two simple formulas are used interchangeably to estimate maintenance water requirement. Combining the predicted daily maintenance requirement for water, sodium, and potassium in healthy, 70 kg adult results in an estimated 2500 mlday-1 of a solution containing a Na of 30 meqL-1 and K of 15-20 meqL-1 intraoperatively, fluids containing sodium free water are rarely employed in adults because most surgical losses are isotonic. Postoperatively, lactated Ringer’s solution or 0.9% saline commonly is used until patients are haemodynamically stable. Subsequently, patients can tolerate fluids containing either more free water or containing Na+ in excess for maintenance requirements if cardiac and renal function is satisfactory.19 Dextrose Traditionally, physicians have infused glucosecontaining intravenous fluids perioperatively in an effort to prevent hypoglycemia and limit protein catabolism. However, due to 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. Iatrogenic hyperglycemia can induce an osmotic diuresis and may aggravate ischemic and traumatic brain injury. 23,24 The type of fluid administered may be of importance because preoperative administration of glucose-containing fluid has in several
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studies been found to reduce postoperative insulin resistance25. In one randomized study, administration of 1200 ml 12.5% glucose solution preoperatively led to improvements in preoperative hunger, thirst and anxiety.22 Another study compared administration of 20 mlkg-1 lactated ringer with 20 mlkg-1 lactate/glucose intra operatively in minor gynaecological surgery and the improvements in the fitness for discharge, and the late outcome evaluations dizziness, faintness, headache, drowsiness and throat pain were only seen in the patients receiving solutions containing glucose.20 Further studies are needed with regard to postoperative effects of pre and intraoperative glucose administration. Surgical fluid requirements Surgical patients require replacement of plasma volume and extracellular losses secondary to wound or burn oedema, ascitis and gastrointestinal secretions. Wound and burn oedema and ascetic fluid are protein rich and contain electrolytes in concentrations similar to those found in plasma. If extracellular volume is adequate and renal and cardiovascular functions are normal, all gastrointestinal secretions can be replaced using lactated ringer’s solution or 0.9% saline; if renal or cardiovascular function is compromised, more precise replacement is necessary. Substantial loss of gastrointestinal fluids requires replacement of other electrolytes. Chronic gastric losses may produce hypochloremic metabolic alkalosis that can be corrected with 0.9% saline; chronic diarrhoea may produce hyperchloremic metabolic acidosis that may be prevented or corrected by infusion of fluid containing bicarbonate or bicarbonate substrate. Guidelines have been developed for replacement of fluid shift during surgical procedures. The simplest formula provides, in addition to maintenance fluids and replacement of estimated blood loss, 4 mlkg-1hr-1 of lactated ringer’s solution or 0.9% saline for procedures involving minimal trauma, 6 mlkg-1hr-1 for those involving moderate trauma, and 8 mlkg-1hr-1 for those involving extreme trauma. Clinical implications of hypertonic fluid administration An ideal alternative to conventional crystalloid and colloid fluid would be hypertonic fluid which is inexpensive, produce minimal peripheral or pulmonary oedema, generate sustained hemodynamic effects, and be effective even if administered in small volumes. Hypertonic, hypernatremic solutions combined with colloid appear to fulfil some of these criteria. In an experimental study small volumes 6 mlkg-1 of 7.5 hypertonic saline restored blood pressure and cardiac output and increased mesenteric blood flow to greater than control values in haemorrhaged dogs and all animals survived.26 Although posttreatment serum
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osmolality exceeded 330 mmolkg-1, no animal showed adverse effects. Hypertonic solutions exerts favourable effects on cerebral haemodynamics because the in-permeability of sodium to the blood-brain barrier in uninjured brain causes the brain to shrink in response to acute increases in serum sodium. In dogs with intracranial mass lesions and haemorrahgic shock, intracranial pressure increased during resuscitation from with 0.8% saline but remained unchanged if 7.2% saline was infused in a sufficient volume to a comparably improved systemic haemodynamics.27 Hypertonic solutions restored regional cerebral blood flow better than did slightly hypotonic solutions. 26 In haemorrhaged rats subjected to mechanical brain injury, brain water content was lower in uninjured brain after resuscitation with hypertonic saline. If fluid resuscitation continues after immediate stabilization, difference between fluids of varying tonicity become negligible.28,29 Conclusion Careful fluid management is essential in limiting morbidity and mortality in critically ill surgical patients. Maintenance of systemic perfusion is a critical strategy in avoiding shock and the late consequences of the multiple system organ failure syndromes. Acknowledgement We acknowledge and thanks for the efforts and support provided by Dr. Mehdi Raza, Dr. Devendra Gupta, Dr. Sanjay Dhiraj and Dr. Sandeep Pawar in preparation of this manuscript. References 1. Holte K, Kehlet H. Compensatory fluid administration for preoperative dehydration-does it improve outcome? Acta Anaesthesiol Scand 2002; 46: 1089-93. 2. Keane PW, Murray PF. Intravenous fluids in minor surgery. Their effect on recovery from anaesthesia. Anaesthesia 1986; 41: 635-7. 3. Yogendran S, Asokumar B, Cheng DC, Chung F. A prospective randomized double-blinded study of the effect of intravenous fluid therapy on adverse outcomes on out patient’s surgery. Anesth Analg 1995; 80: 682-6. 4. Chung F, Mezei G. Factors contributing to a prolonged stay after ambulatory surgery. Anesth Analg 1999; 89: 1352-9. 5. Allison SP. Dehydration. In: Macrae R, Robinson RK, Sadler MJ (eds). Encyclopedia of food science, food technology ad nutrition. London Academic Press 1993; 457-72. 6. Badr KF, Ichikawa I. Prerenal failure: a deleterious shift from renal compensation to decompensation. N Eng J Med 1988; 319: 623-9. 7. Henrich WL, Pettinger WA, Cronin RE. The influence of circulating catecholamine and prostaglandins on canine renal hemodynamics during hemorrhage. Circ Res 1981; 48: 424-9.
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003 8. Lerman LO, Bentley MD, Fiksen-Olsen MJ, Strick DM, Ritman EL, Romero JC. Pressure dependency of canine intrarenal blood flow within the range of autoregulation. Am J Physiol 1995; 268: F 404-9. 9. Hall J, Robertson G. Diabetes insipidus. Problems in Critical Care 1990; 4: 342-54. 10. Laragh JH. The endocrine control of blood volume, blood pressure and sodium balance: atrial hormone and rennin system interactions. J Hypertens 1986; 4(suppl 2): S143-56. 11. Needleman P, Greenwald JE. Atriopeptin: a cardiac hormone initimately involved in fluid, electrolyte, and blood pressure homeostasis. N Eng J Med 1986; 314: 828-34. 12. Murray MD, Brater DC. Adverse effect of nonsteriodal antiinflammatory drugs on renal function. Ann Intern Med 1990; 112: 559-60. 13. Winick M (ed). Hunger disease: studies by the Jewish Physicians in the Warsaw Ghetto. New York, Wiley 1979. 14. Allison SP. Metabolic aspect of injury. In: Tubbs N, London PS (eds). Topical reviews in accident surgery. Bristol, John Wright 1980; 1: 11-32. 15. Stiges SA, Arcas G, Guirao X, Garcia-Dominho M, Gil MJ. Extracellular fluid expansion during parenteral feeding. Clin Nutr 1992: 11: 63-8. 16. Starker PM, Lasala PA, Forse RA, Askanzi J, Elwyn DH, Kinney JM. Response to total parenteral nutrition in the extremely malnourished patient. JPEN 1985; 9: 300-302. 17. Shoemaker WC, Appel PL, Kram HB, Waxman K, Lee TS. Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest 1988; 94: 1176-86. 18. Boyd O, Grounds RM, Bennett ED. A randomized clinical trail of the effect of deliberate perioperative increase of oxygen delivery on mortality in high risk surgical patients. JAMA 1993; 270: 2699-2707. 19. Prough DS, Mathru M. Fluid management in critically ill patients. In: Murray MJ, Coursin DB, Pearl RG, Prough DS, editors. Critical Care Medicine: Perioperative management. Philadelphia, Lippincott-Raven, 1997: 99-108. 20. Pearl RG, Halperin BD, Mihm FG, Rosenthal MH. Pulmonary effects of crystalloid and colloid resuscitation from hemorrhagic shock in the presence of oleic acid-induced pulmonary capillary injury in the dog. Anesthesiology 1988; 68: 12-20. 21. Prough DS, Johnston WE. Fluid resuscitation in septic shock: no solution yet. Anesth Analg 1989; 69: 699-704. 22. Baum TD, Wang H, Rothschild HR, Gang DL, Fink MP. Mesentric oxygen metabolism, ileal mucosal hydrogen ion concentration, and tissue edema after crystalloid or colloid resuscitation in porcine endotoxic shock: comparison of Ringer’s lactate and 6% hetastarch. Circ Shock 1990; 30: 385-97. 23. Lanier WL, Stangland KJ, Scheithauer BW, Milde JH, Michenfelder JD. The effects of dextrose infusion and head position on neurologic outcome after complete cerebral ischemia in primates: examination of a model. Anesthesiology
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24. Lam AM, Winn HR, Cullen BF, Sundling N. Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg 1991; 75: 545-51.
27. Prough DS, Whitley JM, Taylor CL, Deal DD, DeWitt DS. Regional cerebral blood flow following resuscitation from hemorrhagic shock with hypertonic saline. Influence of a subdural mass. Anesthesiology 1991; 75: 319-27.
25. Traber LD, Brazeal BA, Achmitz M, et al. Pentafraction reduces the lung lymph response after endotoxin administration in the ovine model. Circ Shock 1992; 36: 93-103.
28. Wisner DH, Schster L, Quinn C. hypertonic saline resuscitation of head injury: effects on cerebral water content. J Trauma 1990; 30: 75-8.
26. Velasco IT, Pontieri V, Rocha e Silva M Jr, Lopes OU. Hyperosmotic NaCl and severe hemorrhagic shock. Am J Physiol 1980; 239: H664-73.
29. Whitley JM, Prough DS, Brockschmidt JK, Vines SM< DeWitt DS. Cerebral hemodynamic effects of fluid resuscitation in the presence of an experimental intracranial mass. Surgery 1991; 110: 514-22.
CONFERENCE CALENDER 2003 - 2004 1) 25th Annual UP State Chapter 1st and 2nd November 2003 Contact : Dr. Mukesh Tripathi Organising Secretary UPISACON-2003 Dept. of Anaesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow – 226 014. E-mail:
[email protected] 2) Post-Graduate Assembly, Anaesthesiology & Critical Care, 2003 8th–15th November 2003 Contact : Prof. A. K. Sethi Organizing Chairman Head, Dept. of Anaesthesiology & Critical Care, University College of Medical Sciences & GTB Hospital, Shahdara, Delhi-110 095 3) Asian Society of Paediatric Anaesthesiologists of ISA. 22-23rd November 2003 Contact : Dr. Dilip Pawar Dept. of Anaesthesiology, All India Institute of Medical Sciences, New Delhi – 110 029. Email:
[email protected] 4) 51st Annual Conference of ISA ISACON 2003 26th- 30th December. 2003 Contact : Dr. Narayan Acharya Organising Secretary IMA House Medical Road, Ranihat, Cuttack – 753 007 Orissa. Mobile.: 0-9437053586 / 0-9861053586 Email.: drnacharya@isacon2003.
5) XIX Annual Conference of the Indian Society for study of pain (IASP–Indian Chapter) ISSPCON 2004, 23rd, 24th, 25th January 2004 Contact : Dr. S. Sen Pacific Point-57/14, Ballygunj Circular Road, Kolkata – 700 019. Email :
[email protected] 6) 5th Annual Conference of Indian Society of Neuroanaesthesiology and Critical Care 6th 8th February 2004. Contact : Dr. G.S. Umamaheshwara Rao Organising Secretary 5th Annual Conference of Mental Health and Neurosciences (NIMHANS) Bangalore – 560 029 KARNATAKA E-mail:
[email protected] 7) 7th Annual Conference of Indian Association of Cardiovascular and Thoracic Anaesthesiologists (IACTA) 19th and 21st February 2004. Contact : Dr. Suresh G. Nair Oranising Secretary Anaesthesia House, Shopping Complex, Panampilly Nagar, Cochin – 682 036 Tel : 0484-2322251 E-mail :
[email protected] 8)
13th World Congress of Anaesthesiologists 2004 Paris (France) 18th -23rd April, 2004 Contact : Prof. Philippe Scherpereel President, WCA 2004 Congress Office, COLLOQUIM-12 Reu-dela-Croix-Faubin – 75557, Paris-cedex-11-France Tel. : 33(0)144-64-1515 E-mail:
[email protected] 