Extracellular fluid deficit following operation and its correction with Ringer''s lactate. A reassessment.

The changes in extracellular fluid volume (ECV) in two groups of surgical patients, one receiving Ringer's lactate solution intraoperatively and the other receiving only dextrose and water, were assessed. A deficit in the ECV, as measured by radioactive sulfate, of 1.9 +/- 0.8 l (p less than 0.003) compared to the preoperative volume was found in the dextrose group. This was accompanied by a decrease in the mean creatinine clearance (-13% p less than 0.01), the mean urinary sodium excretion (-57% p less than 0.05), and the mean rate of clearance of the sulfate tracer (-18% p less than 0.01). The use of intraoperative Ringer's lactate (1660 cc +/- 96 cc) resulted in no change in the ECV, an increase in the mean creatinine clearance (+10% p less than 0.05), and no change in sodium excretion or tracer clearance. As a result of these findings, it appears that postoperative sodium retention is a physiologic response to a decreased ECV, which can be prevented by the administration of Ringer's lactate.     

Inhibition of CD18-dependent neutrophil adherence reduces organ injury after hemorrhagic shock in primates

Neutrophil adherence or aggregation may be important in the development of organ injury after hemorrhagic shock. Monoclonal antibody (MAb) 60.3 prevents both adherence and aggregation. Therefore we investigated MAb 60.3 treatment in prevention of organ injury after hemorrhagic shock in rhesus monkeys (Macaca mulatta). We performed esophagogastroscopy and placed catheters to measure cardiac output, mean arterial pressure, arterial blood gases, and urine output. Blood was removed to decrease CO to 30% of baseline for 90 minutes. Just before resuscitation, MAb 60.3 (2 mg/kg) or saline solution (control) was administered intravenously. Monitoring and fluid resuscitation continued for 24 hours, with lactated Ringer's solution given as a maintenance infusion (4 ml/kg/hr) plus additional lactated Ringer's solution to maintain CO at preshock levels. Esophagogastroscopy was repeated 24 hours after shock. There were two deaths in the control group at about 72 hours and none in the MAb 60.3 group. MAb 60.3-treated animals required less fluid (9.6 +/- 8.8 ml/kg vs 263.8 +/- 225.7 ml/kg), gained less weight (0.08 +/- 0.11 kg vs 0.70 +/- 0.37 kg), and maintained a higher hematocrit level (35.0% +/- 1.0% vs 26.9% +/- 4.9%). All five control animals had gastritis; MAb 60.3-treated animals had none (p less than 0.05; Fisher's exact test). Inhibition of neutrophil adherence or aggregation with MAb 60.3 at the time of resuscitation reduces fluid requirements and gastric injury in monkeys after hemorrhagic shock.     

The effects of dextrose infusion and head position on neurologic outcome after complete cerebral ischemia in primates: examination of a model

The hypothesis that iv dextrose infusion prior to--and head position during--cerebral ischemia would influence the severity and pattern of neurologic injury was tested in primates. Fifteen pigtail monkeys weighing 3.3 +/- 0.2 kg (mean +/- SE) were subjected to 17 min complete cerebral ischemia followed by 24 h intensive care treatment and neurologic assessment for an additional 72 h. Monkeys were given 50 ml iv infusions of either dextrose 5% in 0.45% saline solution (n = 8) or lactated Ringer's solution (n = 7) during the preparatory period. This volume corresponds to approximately 1 1/70 kg individual. These same monkeys were placed in either the lateral (n = 3), prone (n = 5), or supine (n = 7) position during the ischemic period. Two monkeys failed to meet preestablished protocol criteria and were excluded from data analysis. Blood glucose immediately preischemia in the dextrose-treated group (181 +/- 19 mg X dl-1) was not significantly greater than in the group given lactated Ringer's solution (140 +/- 6 mg X dl-1; P = 0.07). Dextrose infusion resulted in significantly greater cerebral injury at 96 h postischemia when comparing both neurologic (P less than 0.05) and histopathology (P less than 0.05) scores. Specifically, dextrose administration resulted in the greatest injury to the insular cortex, thalamus, Purkinje cells, and substantia nigra. Although blood glucose was less than 250 mg X dl-1 in all monkeys at the time of complete cerebral ischemia, there was a high correlation between blood glucose rank and neurologic function rank (rs = 0.76; P less than 0.005). The authors were unable to note any effect of head position on the distribution of histopathologic lesions. Prior to removing the brain for histopathologic studies, four monkeys were given repeat infusions of 50 ml dextrose 5% in 0.45% saline solution over 11 +/- 1 min. These infusions produced increases in blood glucose from 56.7 +/- 7.6 to 244 +/- 24.9 mg X dl-1 (P less than 0.01) and increases in brain glucose from 1.64 +/- 0.22 to 5.11 +/- 0.48 mumol X g-1 (P less than 0.01).     

Effect of a hypertonic lactated Ringer's solution on intracranial pressure and cerebral water content in a model of traumatic brain injury

There has recently been an increased interest in the use of hypertonic solutions for fluid resuscitation of trauma victims. In this study, we examined the acute cerebral effects of a hypertonic lactated Ringer's solution (measured osmolality = 469 mOsm/kg) in an animal model of traumatic brain injury. Following the production of a cerebral cryogenic lesion, eight New Zealand white rabbits were randomized to undergo hemodilution with either lactated Ringer's (measured osmolality = 254 mOsm/kg) or hypertonic lactated Ringer's. Over the course of the experiment the lactated Ringer's group required significantly more fluid than the hypertonic group to maintain stable central venous and mean arterial pressure (245 +/- 5 ml vs. 132 +/- 20 ml; p less than 0.0001). Osmolality increased in the hypertonic group by 13.5 +/- 3.3 mOsm/kg whereas it decreased in the lactated Ringer's group by 5.5 +/- 2.6 mOsm/kg. Intracranial pressure increased in both groups over the course of the experiment but the increase in pressure was greater in the lactated Ringer's group than the hypertonic group (9.5 +/- 2.4 mm Hg vs. 1.7 +/- 1.5 mm Hg; p less than 0.001). Brain water content was significantly increased in the region of the lesion as assayed by both the wet/dry weight method and cortical specific gravity determinations, but there was no difference between the two treatment groups. Water content of the nonlesioned hemisphere was significantly less in the hypertonic group. This study suggests that hypertonic saline solutions may be useful for the resuscitation of hypovolemic patients with localized brain injury.     

Hypertonic saline fluid therapy following surgery: a prospective study

Successful resuscitation of the injured may be achieved more rapidly and with less fluid using hypertonic crystalloid solutions than with isotonic solutions. This randomized, double-blind study compared 0.9% normal saline (NS) to 1.8% hypertonic saline (HS) in 20 postoperative coronary artery bypass patients suffering uniform injury. Study solutions were administered to maintain physiologic endpoints: heart rate, blood pressure, and pulmonary capillary wedge pressure. The groups were similar with respect to age, body surface area, operative procedure, intraoperative fluid status, and intraoperative and postoperative red cell transfusion requirements. HS patients required 30% less fluid than NS patients and were in negative fluid balance during the study (-1,715 +/- 732 ml/24 hr, HS, vs. +266 +/- 825 ml/24 hr, NS; p less than 0.01). In contrast, NS patients were in positive fluid balance after 8 hours. Moreover, HS patients experienced less chest tube drainage than NS patients (981 +/- 88 ml, HS, vs. 1,700 +/- 285 ml, NS; p less than 0.01). Systemic and pulmonary hemodynamic measurements, oxygen delivery, oxygen consumption, and shunt fraction did not differ between the two groups. Serum sodium and osmolality increased in the HS group and peaked at 12 hours (145.4 +/- 1.4 mEq/L and 308.7 +/- 2.0 mOsm/kg, respectively) and correlated with the volume of HS infused (correlation coefficient = 0.81). No deaths occurred and no complication was attributed the hypertonicity of the solution. We conclude that 1.8% hypertonic saline is a safe alternative to isotonic crystalloid therapy in the fluid management of postoperative patients. Decreased third-space losses may occur with HS as suggested by the lower thoracic losses in the HS group; 1.8% NaCl may be the preferred solution in situations where excess free water administration is not desired, and where interstitial edema is detrimental to function and/or survival.     

Renal concentration defect induced by cisplatin. The role of thick ascending limb and papillary collecting duct

The effects of cisplatin (5 mg/kg BW given intraperitoneally) on renal concentration mechanism were evaluated initially by clearance studies in rats 5-7 days after cisplatin administration and compared to normal rats. During hypotonic saline infusion, cisplatin rats showed a lower inulin clearance (0.56 +/- 0.07 vs. 1.12 +/- 0.09 ml/min/100 g BW, p less than 0.01), a higher fractional distal delivery (CNa + CH2O/Cin) (36.3 +/- 4.4 vs. 22.8 +/- 4.5%, p less than 0.05), and lower CH2O/CNa + CH2O (33.6 +/- 5.8 vs. 56.5 +/- 5.0%, p less than 0.01). During hypertonic saline infusion the TcH2O/Cosm was lower in cisplatin (18.3 +/- 1.1%) than in normal rats (33.4 +/- 3.5%, p less than 0.01). These results suggest a defect in NaCl transport in the thick ascending limb of Henle and proximal tubule. In order to characterize these tubular defects, we measured Na-K-ATPase activity (microM Pi/mg protein/h). In the renal cortex of cisplatin rats the ATPase activity was lower (18.1 +/- 3.2) than in normal rats (33.4 +/- 6.4, p less than 0.05), also in the inner strip of the outer medulla of cisplatin rats Na-K-ATPase was reduced (26.0 +/- 5.7) when compared with normal rats (67.3 +/- 9.2, p less than 0.01), presumably representing a decrease in enzyme activity in the thick ascending limb.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantitative measurement of bleeding following hypertonic saline therapy in 'uncontrolled' hemorrhagic shock

The effect of small volume hypertonic saline in "uncontrolled" hemorrhagic shock (UCHS) induced by partial resection of the tail was studied in rats. The rats were divided into three groups: in group 1 (n = 15) 10% of the terminal portion of the animal's tail was resected to induce UCHS. In group 2 (n = 14) UCHS was induced as in group 1 and after 5 min 5 ml/kg NaCl 0.9% (NS) was infused intravenously. In group 3 (n = 22) UCHS was induced as in group 1 and after 5 min, 5 ml/kg NaCl 7.5% (HTS) was infused intravenously. Resection of the animal's tail was followed by bleeding of 3.5 +/- 0.3 ml within 5 min, fall in MAP to 63 +/- 4 torr (p less than 0.001) and pulse to 300 +/- 18 per min (p less than 0.05). The amount of bleeding, fall in MAP, and pulse after 5 min were similar in the three groups. Further blood loss after 60 min in group 1 was 3.7 +/- 0.8 ml, in group 2, 2.9 +/- 0.5 ml, and in group 3, 6.5 +/- 0.8 (p less than 0.01). Increased bleeding in group 3 showed two peaks: an early peak of 1.3 +/- 0.2 ml after 15 min (p less than 0.05) and a late peak of 1.2 +/- 0.4 ml at 45 min (p less than 0.05) and 1.7 +/- 0.5 ml at 60 min (p less than 0.01). MAP fell after 60 min to 54 +/- 7 torr in group 1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypertonic saline resuscitation of head injury: effects on cerebral water content

Ideal resuscitation would simultaneously replete intravascular volume and minimize cerebral edema. We assessed the effects of hypertonic saline (HS) shock resuscitation on cerebral edema after head injury. Rats were subjected to hemorrhagic shock (40 mm Hg for 1 hour) in the presence or absence of mechanical brain injury, followed by 1 hour of resuscitation with either hypertonic saline (6.5%) or lactated Ringer's (LR). After resuscitation, animals were sacrificed and brain water contents determined. Results: Less HS than LR was needed for resuscitation both in animals without brain injury (7 +/- 2 ml/kg vs. 97 +/- 16 ml/kg; p less than 0.0003) and with brain injury (10 +/- 1 ml/kg vs. 68 +/- 6 ml/kg; p less than 0.0001). Brain water content (ml H2O/gm dry wt) after HS resuscitation was decreased compared to LR resuscitation in animals without brain injury (3.36 +/- 0.12 vs. 3.74 +/- 0.08; p less than 0.025) and in the uninjured hemisphere of head-injured animals (3.29 +/- 0.11 vs. 3.78 +/- 0.09; p less than 0.025). Brain water content was increased in injured brain in both resuscitation groups, but the increase was the same (HS 4.10 +/- 0.13; LR 4.25 +/- 0.17; p greater than 0.05). Conclusions: HS resuscitation of hemorrhagic shock decreases brain water content in uninjured but not injured brain. HS may be useful in resuscitation of combined hemorrhagic shock and head injury.     

Myocardial protection during prolonged aortic cross-clamping. Comparison of blood and crystalloid cardioplegia

We compared the ability of blood and crystalloid cardioplegia to protect the myocardium during prolonged arrest. Twelve dogs underwent 180 minutes of continuous arrest. Group I (six dogs) received 750 ml of blood cardioplegic solution (potassium chloride 30 mEq/L) initially and every 30 minutes. Group II (six dogs) received an identical amount of crystalloid cardioplegic solution (potassium chloride 30 mEq, methylprednisolone 1 gm, and 50% dextrose in water 16 ml/L of electrolyte solution). Temperature was 10 degrees C and pH 8.0 in both groups. Studies of myocardial biochemistry, physiology, and ultrastructure were completed before arrest and 30 minutes after normothermic reperfusion. Biopsy specimens for determination of adenosine triphosphate were obtained before, during, and after the arrest interval. Regional myocardial blood flow, total coronary blood flow, and myocardial oxygen consumption were statistically unchanged in Group I (p greater than 0.05). Total coronary blood flow rose 196% +/- 49% in Group II (p less than 0.005), and left ventricular endocardial/epicardial flow ratio fell significantly in this group from 1.51 +/- 0.18 to 0.8 +/- 0.09, p less than 0.01 (mean +/- standard error of the mean. The rise in myocardial oxygen consumption was not significant in this group (34% +/- 36%, p greater than 0.05). Ventricular function and compliance were statistically unchanged in both groups. In Group II, adenosine triphosphate fell 18% +/- 3.4% (p less than 0.005) after 30 minutes of reperfusion; it was unchanged in Group I. Ultrastructural appearance in both groups correlated with these changes. We conclude that blood cardioplegia offers several distinct advantages over crystalloid cardioplegia during prolonged arrest.     

Benefits of a glucose-containing priming solution for cardiopulmonary bypass

Benefits from the use of glucose-containing intravenous and priming solutions during coronary artery bypass operation have not been documented, but an increased risk of postoperative neurologic deficit by hyperglycemia has been suggested. To determine benefits, 107 patients undergoing coronary artery bypass operation were managed identically except that one group (n = 54) received 5% dextrose in lactated Ringer's solution (D5LR) as the sole intravenous and priming solution during operation and a second group (n = 53) received the same solution without glucose (LR). During cardiopulmonary bypass, the D5LR group required significantly less additional crystalloid to maintain safe oxygenator levels and flow (1.8 +/- 3.3 vs 15.8 +/- 20.9 mL.kg-1.h-1) and produced more urine (3.5 +/- 3.2 vs 1.2 +/- 1.4 mL.kg-1.h-1). By 24 h after operation, fluid balance in the LR group was approximately 2 L more positive than in the D5LR group. Five days after operation, the D5LR group weighed less than preoperatively (-0.8 +/- 2.6 kg), whereas the LR group gained weight (+1.0 +/- 2.8 kg). We conclude that use of glucose-containing solutions during coronary artery bypass operation benefits patients by decreasing perioperative fluid requirements and postoperative fluid retention. Because embolism is the cause of most postoperative neurologic deficits, any increased risk by hyperglycemia is small.     

Massive Ringer's lactate infusion: comparison with dextrose 5% and whole blood.

The objectives of this study were to compare in dogs the effects of massive infusion of Ringer's lactate, 5% dextrose in water, and whole blood. Special interest centered upon lung function, central venous pressure, and dilutional effects upon the blood components. Three groups of 5 healthy dogs each received respectively Ringer's lactate, 5% dextrose, or whole blood over 60 minutes in the amount of 135 ml/kg. Arterial blood gases and pH, right atrial and systemic arterial pressures, hemoglobin and hematocrit values, and plasma sodium, chloride, potassium and protein levels were determined. Coagulograms and serum osmolality were examined in the early experiments. The purpose of the whole blood infusion was primarily to serve for comparison in the study of dilutional effects upon blood components. There was no statistically significant change in the arterial blood gas values or pH following Ringer's lactate infusion. The infusion of 5% dextrose in water produced moderate decline in arterial Pco2 and a temporary, slight fall in blood pH. Ringer's lactate infusion produced a prompt and statistically significant rise in central venous pressure. The infusion of 5% dextrose was followed by a late moderate decline in arterial blood pressure, possibly due to marked dilution of plasma sodium, chloride and potassium. It is concluded that massive Ringer's lactate infusion is capable of increasing right atrial pressure and presumably cardiac output. In healthy dogs, lung function was not impaired sufficiently to alter arterial blood gas values. However, where other previous or concomitant factors have diminished pulmonary reserve, fluid overload may impose a serious additional burden upon cardiopulmonary function.     

Fluid distribution and pulmonary dysfunction following burn shock

Respiratory function and body fluid changes were measured in 46 burned patients for up to 7 days postburn (DPB). The patients in this prospective study were divided into an HLS group [n = 17, burn size 61 +/- 0.5% BSA (mean +/- SEM), resuscitated with hypertonic lactated saline] and an iso-Na group (n = 29, burn size 60 +/- 4.5% BSA, resuscitated with lactated Ringer's solution). During DPB 3 to 5, the Respiratory Index (A-aDO2/PaO2), functional extracellular fluid volume (f-ECFV), an ratio of plasma volume to interstitial fluid volume (PV/ISFV) were increased in the iso-Na group compared with the HLS group. During the same period, the Respiratory Index and PV/ISFV correlated significantly; respiratory dysfunction was less in the HLS group. Nearly 50% of the iso-Na group required endotracheal intubation. Sodium loads were the same in both groups; the HLS group required less water. These results suggest that extracellular fluid distribution differs between the two treatments; HLS may be associated with ameliorated respiratory function not only because of less volume loading during resuscitation, but also because the PV/ISFV ratio is less than when lactated Ringer's is administered.     

Maternal and fetal effects of prophylactic hydration with crystalloids or colloids before epidural anesthesia

Prophylactic intravenous hydration decreases the incidence and severity of hypotension due to obstetric epidural anesthesia. This study assesses whether infusion of normal serum albumin (NSA) offers any advantages over Ringer's lactate (RL) solution. Sixty patients scheduled for elective cesarean sections were divided into three equal groups. Group 1 received 1200 ml of RL; group 2, 700 ml of RL plus 500 ml of 5% NSA; and group 3, 1000 ml of RL plus 200 ml of 25% NSA. In group 1, the concentrations of serum albumin (SA) decreased from 3.5 +/- 0.3 (mean +/- SD) to 3 +/- 0.2 g/dL (P less than 0.01) and plasma oncotic pressure (POP) from 20 +/- 3 to 17 +/- 3 torr (P less than 0.005) immediately after hydration. In group 2, SA remained unchanged, but POP decreased from 21 +/- 2 to 19 +/- 2 torr (P less than 0.005). In group 3, SA increased from 3.6 +/- 0.5 to 3.9 +/- 0.3 g/dL (P less than 0.01) and POP from 19 +/- 2 to 21 +/- 2 torr (P less than 0.0025). Neither SA nor POP levels differed among the groups 24 h later; however, both SA and POP were significantly lower than preinfusion values in all groups at 24 h. The incidence of maternal hypotension, neonatal Apgar scores, and acid-base status also were comparable among the groups (X2 analysis). Because low POP may predispose to postoperative pulmonary morbidity, the incidence of this complication was studied in the mothers by using a point scoring system (based on the presence of symptoms and physical signs) and also by measuring AaDO2 gradients. Neither pulmonary morbidity scores nor AaDO2 gradients differed significantly in the three groups. It is concluded that both crystalloid and colloid prehydration produce equally satisfactory maternal and fetal outcomes.     

The effects of muscle-building exercise on vitamin D and mineral metabolism

Exercise and muscle strength are important determinants of bone mass. Studies were carried out in normal young adult white males to determine the effects of exercise on vitamin D and mineral metabolism. Fourteen men who had engaged in regular muscle-building exercises for at least 1 year and 14 age-matched controls (age range, 19-36 year) were hospitalized on a metabolic ward and were given a constant daily diet estimated to contain 400 mg of calcium, 900 mg of phosphorus, 110 mEq of sodium, 65 mEq of potassium, and 18 mEq of magnesium. Body weight averaged 78 +/- 3 kg in the exercisers and 72 +/- 2 kg in the controls (NS). Serum calcium, ionized calcium, phosphate, magnesium, somatomedin-C, and immunoreactive parathyroid hormone (PTH) were not different in the two groups, whereas serum Gla-protein (39 +/- 5 vs. 24 +/- 2 ng/ml, p less than 0.01), 25-hydroxyvitamin D (23 +/- 2 vs. 16 +/- 2, p less than 0.05) and 1,25-dihydroxyvitamin D [1,25(OH)2D] (40 +/- 2 vs. 29 +/- 2 pg/ml, p less than 0.01) were higher in the exercisers than in the controls. Urinary calcium, phosphorus, sodium, potassium, creatinine clearance, and norepinephrine were not different in the two groups, whereas urinary magnesium (12.6 +/- 1.0 vs. 9.4 +/- 0.5 mEq/d, p less than 0.01) and urinary cyclic adenosine 3',5'-monophosphate (cyclic AMP) (2.52 +/- 0.19 vs. 1.72 +/- 0.20 nM/dl glomerular filtrate, p less than 0.01) were higher in the exercisers than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inability of University of Wisconsin solution to reduce postoperative peritoneal adhesions in rats.

OBJECTIVE: To examine the effect of University of Wisconsin solution (UWS) on the formation of postoperative peritoneal adhesions. DESIGN: Laboratory experiment. SETTING: University hospital, Italy. ANIMALS: 42 Sprague-Dawley rats. INTERVENTIONS: A standard lesion was made consisting of serosal trauma of the caecum and a parietal peritoneal defect. Rats were randomly divided into seven groups (n = 6 each): the first group acted as controls; the second had instilled normal saline 6 ml; the third Ringer's lactate 6 ml; the fourth UWS 6 ml; the fifth normal saline 12 ml; the sixth Ringer's lactate 12 ml; and the seventh UWS 12 ml. MAIN OUTCOME MEASURES: Adhesions were scored two weeks later for extent (0 to 4) and type (0 to 4). Adhesion strength was measured by a tensiometer. RESULTS: The mean (SEM) scores for extent and type of adhesions were significantly lower (p < 0.05) after instillation of Ringer's lactate 12 ml [1.0 (0.4) and 1.2 (0.4), respectively] than controls [3.5 (0.3) and 2.7 (0.2), respectively]. Adhesions were also significantly weaken (p < 0.05) [101 (33) g] than in controls [207 (6) g]. CONCLUSIONS: Intraperitoneal instillation of normal saline and UWS were ineffective in reducing the extent and type of adhesions. Although Ringer's lactate produced a significant reduction in severity, the effect was strongly volume related. This amount of fluid may be detrimental to a patient's postoperative course.     

The effect of albumin or crystalloid resuscitation on bacterial translocation and endotoxin absorption following experimental burn injury.

Burn injury induces immune suppression and increases susceptibility to infection. Hypoalbuminemia is an early and consistent finding following thermal injury and is independently associated with gastrointestinal dysfunction and increased rates of infectious morbidity. This study assessed the effects of albumin resuscitation on burn-induced immunosuppression, bacterial translocation, and absorption of gut endotoxin. Male Sprague-Dawley rats, presensitized to keyhole limpet hemocyanin (KLH), underwent a 20% dorsal scald burn injury, followed by laparotomy and IVC catheterization for fluid resuscitation. Animals were randomized to one of three resuscitative regimens: Ringer's lactate 3 ml/kg/% burn, Ringer's lactate 9 ml/kg/% burn, or 5% human albumin 3 ml/kg/% burn. Delayed hypersensitivity (DTH) responses to KLH were depressed 24 hr following injury (preburn 8.9 +/- 0.2 mm, post-burn 3.1 +/- 0.3 mm, P less than 0.001) and were significantly lower in animals in whom gram-negative bacterial translocation had occurred (2.3 +/- 0.4 vs 3.6 +/- 0.2 mm, P less than 0.005). Serum albumin levels were lower and rates of gram-negative bacterial translocation higher for those animals receiving low volume crystalloid resuscitation; animals resuscitated with albumin or high volume crystalloid experienced similar degrees of postinjury hypoalbuminemia and bacterial translocation. Uptake of radiolabeled endotoxin was maximal in animals resuscitated with albumin. Bacterial translocation is believed to be responsible for a significant number of late nosocomial infections following trauma. These data suggest that the adequacy of early resuscitation rather than the type of resuscitative solution is the more important factor in minimizing translocation.     

Hypertonic sodium resuscitation is associated with renal failure and death.

OBJECTIVE: The use of hypertonic sodium solutions (HSS) and lactated Ringer's (LR) solution in the resuscitation of patients with major burns was compared. SUMMARY BACKGROUND DATA: Hypertonic sodium solutions have been recommended for burn resuscitation to reduce the large total volumes required with isotonic LR solution and their attendant complications. METHODS: To evaluate the efficacy of this therapy in our adult burn center, we resuscitated 65 consecutive patients with HSS (290 mEq/L Na) between July 1991 and June 1993 and compared them with 109 burn patients resuscitated with LR (130 mEq/L Na) between July 1986 and June 1988 (LR-1). A subsequent 39 patients were resuscitated with LR between September 1993 and August 1994 (LR-2). RESULTS: Patients receiving hypertonic sodium solutions versus LR-1 were similar with respect to age (46.0 vs. 43.6 years), total burn size (39.2% vs. 39.9%), incidence of inhalation injury (41.5% vs. 47.7%), and predicted mortality (34.6% vs. 30.2%). Total resuscitation volumes during the first 24 hours were lower among patients treated with HSS than those in the LR-1 group (3.9 +/- 0.3 vs. 5.3 +/- 0.2 mL/kg/% body surface area [BSA], p < 0.05). After 48 hours, however, cumulative fluid loads were similar (6.6 +/- 0.6 vs. 7.5 +/- 0.3 mL/kg/%BSA), and total sodium load was greater with the HSS group (1.3 +/- 0.1 vs. 0.9 +/- 0.1 mEq/kg/%BSA, p < 0.002). During the first 3 days after burn, serum sodium concentrations were moderately elevated in the HSS patients (153 +/- 2 vs. 135 +/- 1 mEq/L, p < 0.001). Patients resuscitated with HSS had a fourfold increase in renal failure (40.0 vs. 10.1%, p < 0.001) and twice the mortality of LR-1 patients (53.8 vs. 26.6%, p < 0.001). In patients resuscitated with HSS, renal failure was an independent risk factor (p < 0.001, by logistic regression). Analysis of these results prompted a return to LR resuscitation (LR-2). Age (41.6 +/- 2.9 years), burn size (37.8 +/- 3.9 %BSA), and incidence of inhalation injury (51.3%) were similar to the earlier groups. Total sodium load was less among LR-2 patients than the HSS group (0.7 +/- 0.1 mEq/kg/%BSA, p < 0.01), but similar to the LR-1 patients. Renal failure developed in only 15.4%, and 33.3% died, similar to the LR-1 group and significantly lower than patients treated with HSS (p < 0.001 and p < 0.05, respectively). CONCLUSION: Hypertonic sodium solution resuscitation of burn patients did not reduce the total resuscitation volume required. Furthermore, it was associated with an increased incidence of renal failure and death. The use of HSS for burn resuscitation may be ill advised.     

Effect of high vs. low arterial blood oxygen content on cerebral energy metabolite levels during hypoxia with normothermia and hypothermia in the rat

The effects of different levels of arterial blood oxygen content (CaO2) on brain tissue adenosine triphosphate (ATP), phosphocreatine (PCr), lactate, and reduced nicotinamide adenine dinucleotide (NADH) were studied during cerebral hypoxia in normothermic and hypothermic male Wistar rats with unilateral carotid ligation. Animals were exposed to hypoxia (PaO2 19--26 torr) for 25 min, and brain tissue metabolite values measured microfluorometrically were compared with those of normothermic normoxic controls. CaO2 was 4.0 +/- 0.2 ml/dl (mean +/- SEM) at PaO2 26 torr in normothermic animals. CaO2 was increased to 8.2 +/- 0.3 ml/dl at PaO2 26 torr by means of bicarbonate infusion producing a leftward shift of the oxyhemoglobin-dissociation curve in one normothermic hypoxic group. In all normothermic hypoxic groups ATP and PCr decreased and lactate and NADH increased significantly compared with control values. There was no significant difference in brain tissue metabolite values among these groups despite an increase in CaO2 by twofold in one group. Hypothermia (32 C) resulted in CaO2 8.4 +/- 0.2 ml/dl at PaO2 26 torr. This was decreased to 4.0 +/- 0.2 ml/dl by decreasing PaO2 to 19 torr in another group at the same temperature. ATP and PCr were well preserved in both groups despite the difference in CaO2s. Although the lactate and NADH levels were increased in the hypothermic group with CaO2 4.0 +/- 0.2 ml/dl, they were significantly lower than those values in normothermic hypoxic groups. These results indicate that the increase in CaO2 produced by hypothermia is not a major determinant in hypothermic protection during cerebral hypoxia.     

A comparison of 5% dextrose in 0.9% normal saline versus non-dextrose-containing crystalloids as the initial intravenous replacement fluid in elective surgery

Intravenous fluid replacement in adult elective surgery is often initiated with dextrose-containing fluids. We sought to determine if this practice resulted in significant hyperglycaemia and if there was a risk of hypoglycaemia if non-dextrose-containing crystalloids were used instead. We conducted a randomized controlled trial in 50 non-diabetic adult patients undergoing elective surgery which did not involve entry into major body cavities, large fluid shifts, or require administration of >500 ml of intravenous fluid in the first two hours of peri-operative care. Patients received 500 ml of either 5% dextrose in 0.9% normal saline, lactated Ringer's solution, or 0.9% normal saline over 45 to 60 minutes. Plasma glucose, electrolytes and osmolarity were measured prior to infusion, and at 15 minutes and one hour after completion of infusion. None of the patients had preoperative hypoglycaemia despite average fasting times of almost 13 hours. Patients receiving lactated Ringer's and normal saline remained normoglycaemic throughout the study period. Patients receiving dextrose saline had significantly elevated plasma glucose 15 minutes after completion of infusion (11.1 (9.9-12.2, 95% CI) mmol/l). Plasma glucose exceeded 10 mmol/l in 72% of patients receiving dextrose saline. There was no significant difference in plasma glucose between the groups at one hour after infusion, but 33% of patients receiving DS had plasma glucose > or = 8 mmol/l. We conclude that initiation of intravenous fluid replacement with dextrose-containing solutions is not required to prevent hypoglycaemia in elective surgery. On the contrary, a relatively small volume of 500 ml causes significant, albeit transient, hyperglycaemia, even in non-diabetic patients.     

Fluid management and plasma renin activity in organ donors

Fluid management and assessment of organ perfusion in organ donors with hypotonic polyuria remain poorly investigated problems. In our protocol, urinary losses (565 +/- 202 ml/h) were replaced volume for volume by 3.3% dextrose/0.3% natrium chloride solution (Baxter) with 20 mmol/l potassium chloride. Concentrated red blood cells were administered to maintain hematocrit at about 30%, and volume expansion (central venous pressure above 6 mmHg) was obtained by gelatin (haemaccel) infusion. In all donors (n = 9), plasma electrolytes remained within normal limits despite hypotonic polyuria. Suppression of initial plasma renin activity (PRA: 9.7 +/- 3.6 ng/ml per hour) was obtained by subacute volume expansion. In eight donors the hemodynamic status improved, dopamine administration, when used, was discontinued, and PRA decreased (2.3 +/- 0.7 ng/ml per hour; P less than 0.05). The only donor who failed to respond to fluid therapy had increased PRA (24.2 ng/ml per hour). During fluid challenge, an inverse relationship was demonstrated between mean arterial pressure and PRA in all nine donors (r = -0.61; P less than 0.001), while there were no significant changes in blood urea. creatinine, or urine output. It is concluded that in organ donors, proper maintenance of the hemodynamic status and suppression of the renin stress response may be obtained by an adequate fluid management, involving both qualitative restoration and expansion of intravascular volume.