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Anesth Analg 2002;95:294-298
© 2002 International Anesthesia Research Society


CARDIOVASCULAR ANESTHESIA

Early Postoperative Respiratory Acidosis After Large Intravascular Volume Infusion of Lactated Ringer’s Solution During Major Spine Surgery

Arzu Takil, MD, Zeynep Eti, MD, Pinar Irmak, MD, and F. Yilmaz Gögüs, MD

Department of Anesthesiology, Medical Faculty of Marmara University, Istanbul, Turkey

Address correspondence and reprint requests to Dr. Arzu Takil, Atakent Burç cad. Burç apt. N0: 1B/45 81240 Ümraniye, Istanbul, Türkiye. Address e-mail to takilarzu{at}hotmail.com


    Abstract
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
In this study, we compared the effects of large intravascular volume infusion of 0.9% saline (NS) or lactated Ringer’s (LR) solution on electrolytes and acid base balance during major spine surgery and evaluated the postoperative effects. Thirty patients aged 18–70 yr were included in the study. General anesthesia was induced with 5 mg/kg thiopental and 0.1 mg/kg vecuronium IV. Anesthesia was maintained with oxygen in 70% nitrous oxide and 1.5%–2% sevoflurane. In Group I, the NS solution, and in Group II, the LR solution were infused 20 mL · kg-1 · h-1 during the operation and 2.5 mL · kg-1 · h-1, postoperatively. Electrolytes (Na+, K+, Cl-) and arterial blood gases were measured preoperatively, every hour intraoperatively and at the 1st, 2nd, 4th, 6th, and 12th hours postoperatively. In the NS group, pHa, HCO3 and base excess decreased, and Cl- values increased significantly at the 2nd hour and Na+ values increased at the 4th hour intraoperatively (P < 0.001). The values returned to normal ranges at the 12th hour postoperatively. In the LR group, blood gas analysis and electrolyte values did not show any significant difference intraoperatively, but the increase in PaCO2 and the decrease in pHa and serum Na+ was significant at the 1st hour postoperatively. Although intraoperative 20 mL · kg-1 · h-1 LR infusion does not cause hyperchloremic metabolic acidosis as does NS infusion, it leads to postoperative respiratory acidosis and mild hyponatremia.

IMPLICATIONS: The infusion of large-volume lactated Ringer’s solution does not cause hyperchloremic metabolic acidosis as does 0.9% saline during major surgery, but leads to postoperative mild hyponatremia and respiratory acidosis.


    Introduction
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
In perioperative management during major surgery with blood loss and fluid shifts, maintenance of normovolemia and hemodynamic stability is an important task for anesthesiologists (1). Crystalloid solutions, satisfying basic fluid requirements and compensating for insensible loses are commonly used in large volumes to support circulation during periods of large fluid shifts (2). Sodium chloride 0.9% solution (NS) is commonly used because it is isotonic with plasma and has no effect on serum osmolality. However, experimental data and case reports support the occurrence of hyperchloremic metabolic acidosis in the course of large NS infusion (313). Although the interpretations of the detrimental effect of this metabolic acidosis are debatable, most authors suggested using lactated Ringer’s solution (LR) instead of NS (3,9). However, neither the duration of the acidotic effect of NS nor the postoperative effects of NS and LR infusion on arterial blood gases and electrolytes were evaluated.

The aim of our study was to compare the intraoperative effects of large-volume infusion of NS or LR on electrolytes and acid base balance during major spine surgery and to evaluate the duration of these effects and whether they had any other effects postoperatively.


    Methods
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
After Institutional Ethics Committee approval and patients’ written consent, 30 patients, ASA physical status I and II, aged 18–70 yr, undergoing elective major spine surgery (Cotrel-Dubousset posterior spinal instrumentation) were enrolled in the study. Patients were randomized by using sealed envelopes to receive either NS or LR during and after the operation.

All patients were premedicated with atropine 0.5 mg and midazolam 0.07 mg/kg IM preoperatively. General anesthesia was induced with thiopental 5 mg/kg and vecuronium 0.1 mg/kg IV. After endotracheal intubation, anesthesia was maintained with oxygen in 70% nitrous oxide and 1.5%–2% sevoflurane.

In Group I, NS solution, and in Group II, LR solution were infused 20 mL · kg · -1h-1 intraoperatively (15 patients in each group). The patients with >20% blood loss received blood transfusions. For the first 500-mL blood loss, 500 mL of colloid solution (Gelofusine) was administered to all patients.

After the induction of anesthesia, radial arterial and central venous catheters were inserted. Mechanical ventilation was performed to maintain PaCO2 as close as possible to 40 mm Hg.

Intraoperative monitoring included continuous mean arterial blood pressure, heart rate, oxygen saturation, end-tidal carbon dioxide pressure, central venous pressure, and esophageal temperature in all patients, and the values were recorded every 15 min. Intraoperative crystalloid infusion volumes, urinary output, blood loss, and blood transfusion volumes were recorded hourly.

Electrolytes (Na+, K+, Cl-) and arterial blood gases were measured preoperatively, every hour intraoperatively and at the 1st, 2nd, 4th, 6th, and 12th hours postoperatively. Also, serum albumin values were measured and anion gaps (Na+ - [Cl- + HCO3]) calculated preoperatively and at the end of the surgery.

Postoperatively, the same solutions were infused at 2.5 mL · kg -1 · h-1 for 12 h and IV patient-controlled analgesia with morphine was administered to all patients.

The length of intensive care unit and hospital stay of all patients were also recorded.

All data were compared with two-way repeated measures of analysis of variance and post hoc testing was performed according to Tukey-Kramer test statistically. Student’s t-test was performed for unpaired data and a P < 0.05 was considered significant.


    Results
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
The two groups were similar with regard to demographic patient characteristics and duration of surgery (P > 0.05) (Table 1).


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Table 1. Table 1. Demographic Characteristics and Duration of Surgery
 
There were no significant differences between crystalloid infusion volumes, urinary output, blood loss, and blood transfusion volumes between groups (P > 0.05) (Table 2).


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Table 2. Table 2. Intraoperative Crystalloid Volume, Blood Transfusion Volume, Blood Loss, and Urinary Output
 
The increase in serum sodium concentration was significant at the 4th hour intraoperatively and returned to initial values at the 2nd hour postoperatively in the NS group. A significant decrease in Na+ was observed at the 2nd,4th, and 6th hours postoperatively in the LR group. The difference between groups was significant at the 3rd hour intraoperatively and the 1st and 6th hours postoperatively (Table 3).


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Table 3. Table 3. Serum Sodium and Chloride Concentration
 
Serum chloride concentration was increased significantly at the 2nd hour intraoperatively in the NS group. In comparison with the LR group, the difference was significant at the 3rd hour intraoperatively and persisted until the 12th hour postoperatively (Table 3).

pHa decreased significantly at the 2nd hour intraoperatively and returned to normal ranges at the 12th hour postoperatively in the NS group. No major pHa difference was observed in the LR group intraoperatively but it was decreased significantly at the 1st hour postoperatively. The difference in pHa between groups was significant at the 2nd hour intraoperatively and persisted until the 6th hour postoperatively (Table 4).


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Table 4. Table 4. pHa Values
 
Bicarbonate concentrations decreased significantly at the 2nd hour intraoperatively and returned to normal ranges at the 12th hour postoperatively in the NS group. The difference between groups was significant at the 2nd hour intraoperatively and persisted until the 6th hour postoperatively (Table 5)


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Table 5. Table 5. Bicarbonate Concentration and Base Deficit Values
 
Base excess values decreased significantly at the 2nd hour intraoperatively and returned to normal ranges at the 12th hour postoperatively in the NS group. In comparison with the LR group, the difference was significant at the 2nd hour intraoperatively and persisted until the 12th hour postoperatively (Table 5).

No significant difference was observed in HCO3, Cl-, or base excess values in the LR group during the study period.

During the postoperative period, although there was no difference in respiratory rate between groups, PaCO2 increased significantly at the 1st hour in the LR group and remained increased for 12 h (Table 6).


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Table 6. Table 6. Paco2 Values
 
No differences were observed in hemodynamic variables (mean arterial blood pressure, heart rate), oxygen saturation, end-tidal carbon dioxide pressure, central venous pressure, body temperature and PaO2, SaO2, hemoglobin concentration, and serum K+ concentration between the groups.

The anion gap and albumin concentration showed similar changes in both groups with an insignificant decrease after crystalloid infusions.

There were no significant differences in intensive care unit (ICU) time (42 ± 18 h for NS and 47 ± 23 h for LR) and discharge time (10 ± 2 days for NS and 11 ± 2 days for LR) between the groups.


    Discussion
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
The main results of this study indicate that large intravascular volume infusion of LR solution does not cause hyperchloremic metabolic acidosis intra- or postoperatively as does NS infusion, but leads to early postoperative respiratory acidosis and mild hyponatremia.

Hyperchloremic metabolic acidosis is a consequence of large volumes of chloride-rich crystalloid solutions during surgery (3,4). Although the acidifying potential of large volumes of sodium chloride solutions on plasma has been discussed by McFarlane and Lee (4) in 1994 and recognized in another randomized controlled trial (3) and a series of case reports and letters (613), the etiology and clinical relevance of this metabolic acidosis remains controversial. Some investigators call this "dilutional acidosis," which implies that plasma expansion and dilutional reduction of plasma bicarbonate concentration are the underlying mechanism (3,5). In contrast, the Stewart model emphasizes the importance of hyperchloremia resulting in a reduction of the strong ion difference (6,8,1013).

Most of these studies, other than those by Williams et al. (7) and McFarlane and Lee (4), did not evaluate the duration of acidosis. McFarlane and Lee reported that plasma chloride concentrations after large-volume administration of NS returned to baseline values by 24 hours postoperatively because they made plasma biochemistry measurements only before and after and at 24 hours postoperatively. One of the main implications of our study is that the increase in Na+ and Cl- concentrations and the decrease in HCO3, base excess and pH with 20 mL · kg -1 · h-1 NS infusion, returned to baseline values at the 12th hour postoperatively in patients continuing to receive NS infusion at a rate of 2.5 mL · kg -1 · h-1. This can be explained by the fact that a relatively slow infusion rate was coupled with an appropriate cellular buffering effect of increasing extracellular HCO3 and hyperchloremia was corrected by subsequent chloriduria (5,6,11).

Most of the authors suggested that hyperchloremic acidosis does not have major pathophysiologic implications in the clinical setting unless it is confused with hypoperfusion and leads to further large-volume infusions (35). However, hyperchloremic metabolic acidosis may impair end organ perfusion and interfere with cellular exchange mechanisms (7,9,14). Williams et al. (7) found a significantly increased time to first urination and an increased frequency of abdominal discomfort in healthy volunteers who developed metabolic acidosis with 50 mL/kg NS infusion. Hyperchloremia alone has a negative effect on renal blood flow and glomerular filtration rate (14). Also Wilkes et al. (9) studied the effects of LR and NS infusions on gastric mucosal pH in elderly surgical patients and concluded that the use of balanced IV solutions can prevent the development of metabolic acidosis and is associated with better indices of gastric mucosal perfusion than saline-based solutions. In a recent outcome study done by Waters et al. (15), it was concluded that an acid-base imbalance occurred in the NS group with the development of a hyperchloremic metabolic acidosis but with this acidosis, no difference was seen in the postoperative complications, in the ventilator time, in ICU time, or hospital stay. However, more blood products were transfused in the group receiving NS, although no statistical difference in blood loss was found. In our study, we observed that the LR group had less estimated blood loss but, similar to Waters et al. (15), we found no statistically significant difference. Also, there were no significant differences in blood transfusion volumes, or in ICU and hospital stay of our patients.

In all the studies evaluating the acidotic effect of NS, the authors advocated the use of balanced IV solutions such as LR for large-volume infusion. During the infusion of LR, the removal of lactate from circulation will increase the strong ion difference and reduce acidosis. This effect may be supplemented by a further increase in the strong ion difference associated with lactate metabolism (11). According to the results of controlled trials and our study, large-volume LR infusions do not cause hyperchloremic metabolic acidosis. However, the possible deleterious postoperative effects of lactate load in spontaneously breathing patients were not evaluated in these controlled trials (3,9,15). Another important implication of our study, not previously mentioned, was that intraoperative 20 mL · kg-1 · h-1 LR infusion leads to early postoperative respiratory acidosis as a result of lactate metabolism to CO2. Although the mean PaCO2 was 45 ± 4 mm Hg at the postoperative 2nd hour, in one patient, PaCO2 increased to 52 mm Hg and pH decreased to 7.25. The postoperative increase in PaCO2 can be misinterpreted as a side effect of opioid analgesics and can lead to inadequate postoperative pain treatment or can be clinically significant in patients with pulmonary disease. The clinical effects of this hypercarbia after LR should be evaluated in patients with severe pulmonary disease. The major limitation of our study is that we evaluated ASA physical status I and II patients with intact compensatory mechanisms.

There was a significant decrease in postoperative Na+ concentrations in our patients treated with LR intraoperatively. Although the mean Na+ concentration at the postoperative 6th hour was 136 ± 4 mEq/L in the LR group and this decrease has no clinical relevance in healthy patients, in one patient it decreased to 126 mEq/L. Williams et al. (7) investigated the effect of large volumes of IV LR or NS on serum osmolality and concluded that although the decrease in osmolality (4 ± 3 mOsm/kg) after LR did not cause any clinical signs of increased intracranial pressure in healthy volunteers in the presence of compensatory mechanisms, these mechanisms may not be intact in patients with intracranial pathology. The decrease in Na+ concentration and serum osmolality will tend to increase brain water and it may be clinically significant in patients at risk for intracranial hypertension (7,10).

We conclude that 20 mL · kg-1 · h-1 LR infusion does not cause hyperchloremic metabolic acidosis as does NS infusion; however, it may lead to early postoperative respiratory acidosis. Although this hypercarbia did not have any significant clinical effect, it can be misinterpreted as opioid overdose, leading to inadequate analgesia, or it can have clinical significance in patients with severe pulmonary disease. The combination of LR and NS infusions (such as switching between the two solutions every other liter) during major surgery may be a better choice, but the effects of this combination await confirmation with further clinical trials.


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Tollofsrud S, Elgjo GI, Prough DS, et al. The dynamics of vascular volume and fluid shifts of lactated Ringer’s solution and hypertonic-saline-dextran solutions infused in normovolemic sheep. Anesth Analg 2001; 93: 823–31.[Abstract/Free Full Text]
  2. Olthof CG, de Vries JPPM, de Vries PMJM, et al. The influence of Ringer’s lactate and gelatin infusion on the internal fluid balance of healthy volunteers measured by non-invasive conductivity technique. Eur J Anaesthesiol 1993; 10: 397–402.[Medline]
  3. Scheingraber S, Rehm M, Sehmisch C, Finsterer U. Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. Anesthesiology 1999; 90: 1265–70.[Web of Science][Medline]
  4. McFarlane C, Lee A. A comparison of Plasmalyte 148 and 0.9% saline for intraoperative fluid replacement. Anaesthesia 1994; 49: 779–81.[Web of Science][Medline]
  5. Mathes DD, Morell RC, Rohr MS. Dilutional acidosis: is it a real clinical entity? Anesthesiology 1997; 86: 501–3.[Web of Science][Medline]
  6. Waters JH, Miller LR, Clark S, Kim JV. Cause of metabolic acidosis in prolonged surgery. Crit Care Med 1999; 27: 2142–6.[Web of Science][Medline]
  7. Williams EL, Hildebrand KL, McCormick SA, Bedel MJ. The effect of intravenous lactated Ringer’s solution versus 0.9% sodium chloride solution on serum osmolality in human volunteers. Anesth Analg 1999; 88: 999–1003.[Abstract/Free Full Text]
  8. Skellett S, Mayer A, Durward A, et al. Chasing the base deficit: hyperchloremic acidosis following 0.9% saline fluid resuscitation. Arch Dis Child 2000; 83: 514–6.[Abstract/Free Full Text]
  9. Wilkes NJ, Woolf R, Mutch M, et al. The effect of balanced versus saline-based hetastarch and crystalloid solutions on acid-base and electrolyte status and gastric mucosal perfusion in elderly surgical patients. Anesth Analg 2001; 93: 811–6.[Abstract/Free Full Text]
  10. Prough DS, Bidani A. Hyperchloremic metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline. Anesthesiology 1999; 90: 1247–9.[Web of Science][Medline]
  11. Story DA, Liskaser F, Bellomo R. Saline infusion, acidosis and the Stewart approach. Anesthesiology 2000; 92: 624.
  12. Miller LR, Waters JH. Mechanism of hyperchloremic nonanion gap acidosis. Anesthesiology 1997; 87: 1009–10.[Medline]
  13. Miller LR, Waters JH, Provost C. Mechanism of hyperchloremic metabolic acidosis. Anesthesiology 1996; 84: 482–3.[Medline]
  14. Wilcox CS. Regulation of renal blood flow by plasma chloride. J Clin Invest 1983; 71: 726–35.
  15. Waters JH, Gottlieb A, Schoenwald P, et al. Normal saline versus lactated Ringer’s solution for intraoperative fluid management in patients undergoing abdominal aortic aneurysm repair: an outcome study. Anesth Analg 2001; 93: 817–22.[Abstract/Free Full Text]
Accepted for publication April 2, 2002.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press