Article info

Authors

Deligianni M.
Fortounis K.
Fyntanidou B.
Gkarmiri S.
Grosomanidis V.
Kotzampassi K.
Kyparissa M.
Ourailoglou V.

DOI

The Greek E-Journal of Perioperative Medicine 2022;21(b): 37-54

PDF


Language

EN

POSTED: 09/5/22 2:50 PM
ARCHIVED AS: 2022, 2022b, Case Reports
KEYWORDS: , ,
COMMENTS FEED: RSS 2.0

DOI: The Greek E-Journal of Perioperative Medicine 2022;21(b): 37-54

Authors: Fyntanidou B.1a*, Kotzampassi K.2b, Fortounis K.3c, Ourailoglou V.2dGkarmiri S.3a, Deligianni M.4b, Kyparissa M.2e, Grosomanidis V.2e

1, MD, PhD, MSc
2, MD, PhD
3, MD
4, RN, MSc

a Emergency Department, AHEPA Hospital, Thessaloniki, Greece.
b1stPropaedeutic Department of Surgery, AHEPA University Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece
cDepartment of Surgery, Papageorgiou General Hospital Thessaloniki Greece
dICU, General Hospital of Halkidiki, Polygyros, Greece
eClinic of Anesthesiology and Intensive Care, School of Medicine, Aristotle University of Thessaloniki, AHEPA Hospital, Thessaloniki, Greece

*Corresponding Author: Emergency Department AHEPA University Hospital, Kautatzoglou 14A, 54639, Thessaloniki, Greece, Tel: 0030 6977427336, e-mail:

 

 ABSTRACT

Four patients (♂/♀: 1/3), aged 51, 52, 50 and 58 years old, who underwent general surgery procedures, suffered acute major blood loss intraoperatively. For the management of acute hemorrhage, 4ml/kg NaCl 7.5% were administered in each patient at the fastest possible rate through the existing intravenous line. Both standard monitoring and Oesophageal Doppler Monitoring (ODM) were applied and heart rate (HR), mean arterial pressure (BPmean), stroke volume (SV), peak velocity (PV), mean acceleration (MA) and corrected flow time (FTc) were recorded at six different phases, before blood loss (Phase 1), before and after completion of NaCl 7.5% administration (Phases 2 & 3), 10min and 20min after NaCl 7.5% administration (Phases 4 and 5) and at the end of the surgical procedure (Phase 6). After completion of NaCl 7.5% infusion, all patients received Lactated Ringers, vasoactive drugs and packed red blood cells (pRBCs). All recorded parameters showed significant deterioration after blood loss, they improved after NaCl 7.5% infusion and remained stable until the end of the surgery. Infusion of NaCl 7.5% was completed in 5min, 4.2min, 6min and 5.3min respectively. Lowest Hb values were 7.6g/dL, 4g/dL, 5g/dL and 6.6g/dL and the corresponding patients received 3, 5, 4 and 3 units pRBCs respectively. Bleeding was surgically controlled, noradrenaline was discontinued before the end of the surgery and all patients were transferred intubated to the Intensive Care Unit (ICU) after the end of the surgery. Three of them were extubated on the same day and the fourth patient on the next. During their ICU stay patients were hemodynamically stable and were discharged from the ICU on the 1st postoperative day. Outcome was overall positive and all patients were discharged home at a good physical status. Based on our results, it seems that hemodynamic instability can be treated with safety by NaCl 7.5% infusion, provided that bleeding can be managed surgically.

 

Introduction

Perioperative fluid administration is the cornerstone for the establishment of hemodynamic stability and homeostasis during the perioperative period and is correlated with the outcome1. Since several years the type and volume of the administered fluid remains a matter of scientific debate2,3. Isotonic crystalloids, normal saline and lactated Ringer (RL) are the most common used solutions for the restoration of the intravascular fluid volume during the perioperative period4.

Hypertonic saline solutions (HSS) are crystalloids which contain high NaCl5.

The main mechanism of action of hypertonic salt solutions is that they create an excessive osmotic gradient which drives fluid from the interstitial (mainly the intracellular) space into the intravascular space. This action has an immediate clinical impact after fluid administration6,7.

The efficiency of HSS in the acute treatment of major blood loss has been documented in several experimental and clinical studies. In an experimental study in 1919, Penfiled et al restored low blood pressure, which was induced by acute blood loss, by administration of hypertonic NaCl 1.8%. In an another experimental study in 1980, Velasco et al restored immediately both cardiac output and blood pressure after administration of 4ml/kg BW NaCl 7.5%8,9. This study of Velasco et al has been the catalytic agent into promoting further scientific research in this field, investigating the clinical impact and usefulness of HSS in the management of hemorrhagic shock10-12. All those studies, both clinical and experimental, proved that administration of a small amount of HSS can restore hemodynamics after major blood loss.

Nakayama suggested in 1984 to use the term small volume resuscitation because the administered amount of fluid is lower to the blood volume loss and this term has been used ever since13,14.

Hypertonic NaCl 7,5% contains 1284meq Na+ and 1284meqCl and its osmolarity is 2568 mOsm /l15. Rapid intravenous administration creates an osmotic gradient due to the excessive increase of plasma sodium concentration. This osmotic shift drives fluid into the intravascular space and results in a transient but significant increase of the intravascular volume15,16. On average, 1ml of HSS raises the intravascular volume by 2-4ml, whereas isotonic crystalloids result to an intravascular volume increase, which is no more than 1/3 of the infused fluid volume17-21.

It has been calculated that approximately a fourfold volume of fluids (depending on the administration rate) should be infused for the restoration of intravascular volume after acute blood loss. On the contrary, intravascular volume can be restored quickly and efficiently by small volume infusion of hypertonic solutions. This is the concept of small volume resuscitation22,23.

Hypertonic resuscitation restores blood pressure and improves cardiac output. Those effects are not only attributed to the expansion of the intravascular volume, but also to circulation enhancement due to vasodilation and to direct positive inotropic effects6,24. Moreover, it improves microcirculation by causing endothelial edema decrease25 and has anti-inflammatory properties26.

The effect of HSS on the circulatory system is of limited duration due to osmotic equilibrium between the intravascular and interstitial fluid compartment. Several researchers have recommended the use of colloids in an effort to postpone its effect 22,27,28. The advantages and disadvantages of HSS solutions are presented in table 15,21,29.

 

Table 1. Advantages and disadvantages of HSS solutions.

Advantages Disadvantages
· Rapid increase of the intravascular volume
· Intracranial pressure decrease
· Endothelial edema decrease
· Low risk of fluid volume overload
· Low incidence of adverse effects
· Positive effects last for a short time period
· Positive clinical impact has not yet been proven

Several methods have been used for intravascular volume assessment and prediction of fluid responsiveness, some of which are difficult to be applied in the operation theatre30,31.

Static parameters, such as Central Venous Pressure (CVP), Pulmonary Artery Occlusion Pressure (PAOP) Right Ventricular End Diastolic Volume (RVEDV), have not been proven to be reliable for intravascular volume assessment32. However, dynamic parameters, such as stroke volume, pulse pressure, diameter of inferior vena cava, which correlate with intrathoracic pressure during spontaneous breathing and under mechanical ventilation have been used for this cause32-34.

Since 1870, when Adolf Fick first described a method for the measurement of cardiac output (CO), several other methods have been discovered35,36.

Development of non-invasive methods for CO determination allowed continuous intraoperative CO monitoring37.

CO is the main determinant of oxygen transport to the tissues. However, standard normal values do not exist. Nevertheless, low values are associated with poor outcome. In clinical practice, there is still no agreement in which CO alterations should be considered as clinically important38.

One patient might have a “normal” CO value and still be suffering from circulatory shock because CO at that specific time phase can meet metabolic needs of the body. In most operations, CO monitoring is not considered as standard monitoring.CO increase following fluid administration is a reliable indicator of fluid responsiveness39.

Oesophageal Doppler Monitor (ODM) is a non-invasive monitoring device, which is designed to measure blood flow by using Doppler technology in the descending thoracic aorta and to calculate stroke volume and CO by a specific algorithm40-42.

Altogether, ODM can measure or calculate following parameters, Stroke Volume (SV), Cardiac Output (CO), Peak Velocity in the descending thoracic aorta (PV), Flow Time Corrected (FTc) and Mean Acceleration (MA)40,41.

Therefore, ODM provides a good estimate of preload, afterload and left ventricular contractility41. Namely, FTc is inversely related to afterload and directly to preload. Low FTc values could be an indicator of hypovolemia and/or increase of resistance/afterload increase. PV is an indicator of contractility and is inversely related to afterload. Low PV values may be caused by decreased contractility or increased resistance/afterload. MA is directly correlated to contractility40,43,44.

Nevertheless, none of those parameters alone is specific to draw any conclusions regarding preload, afterload or contractility. In clinical practice, alterations of one parameter might cause compensatory alterations of another parameter. Combination of different parameters and their assessment in relation to the result of treatment interventions might provide a complete picture of patient’s hemodynamic status at a certain time point.

Material and Methods

Four patients (♂/♀: 1/3), aged 51, 52, 50 and 58 years old, ASA-PS: 2-3, who underwent general surgery procedures, suffered acute major blood loss intraoperatively. For the management of acute hemorrhage, 4ml/kg NaCl 7.5% were administered in each patient at the fastest possible rate through the existing intravenous line.

After completion of NaCl 7.5% infusion, all patients received Lactated Ringers (RL), vasoactive drugs and packed red blood cells (pRBCs).

Applied monitoring consisted of ECG, direct arterial pressure monitoring, capnography, pulse oxymetry and Oesophageal Doppler Monitoring (ODM) (ODM II, Abbot Laboratories) and following parameters were recorded:

  • HR: Heart Rate (b/min),
  • SAPs: Systemic Arterial Pressure, systolic (mmHg),
  • SAPd: Systemic Arterial Pressure, diastolic (mmHg),
  • SAPm: Systemic Arterial Pressure, mean (mmHg),
  • CO: Cardiac output (L/mim),
  • SV: Stroke Volume (ml),
  • PV: Peak Velocity (cm/sec),
  • MA: Mean Acceleration (m/sec2),
  • FTc: Flow time corrected(s).

Study parameters were recorded at six different phases:

  • Before blood loss (Phase 1),
  • Before and After completion of NaCl 7.5% administration (Phases 2 & 3),
  • 10min and 20min after NaCl 7.5% administration (Phases 4 and 5),
  • End of the surgical procedure (Phase 6)

All patients were transferred intubated to the Intensive Care Unit (ICU) after the end of the surgery.

RESULTS

All recorded parameters showed significant deterioration after blood loss. At the time of hemorrhage patients were euvolemic/normovolemic, since fluids had already been administered to them in order to compensate preoperative fasting and any negative hemodynamic effects of anesthesia induction and mechanical ventilation.

The cause of hemodynamic collapse was clinically obvious without any doubt and it was managed immediately.

All patients received 4ml/kg NaCl 7,5% and its infusion was completed in 5min, 4.2min, 6min and 5.3min respectively.

Alterations of recorded parameters are depicted on Table 2.

 

Table 2. Alterations of recorded parameters at the six study phases.

Study phases 1 2 3 4 5 6
HR (b/min) 70

62

72

75

112

95

92

120

86

88

85

83

75

80

83

78

80

82

78

80

75

80

76

75

BP(mean) (mmHg) 99

100

90

95

37

45

43

40

65

70

65

70

100

96

95

85

105

100

96

95

103

102

98

97

SV (ml) 68

70

65

75

18

31

23

20

47

54

77

70

99

78

88

90

75

70

82

85

80

68

81

80

CO (L/min) 4,8

4,3

4,7

5,3

2,1

2,8

2,1

2,4

4,1

4,7

6,5

5,9

7,4

4,7

6,5

5,9

6

5,7

6,4

6,8

6

5,4

6,2

6

PV (cm/sec) 60

65,7

56

70

31,3

38.9

35

35

65

65

64

65

74

66

71

75

73

62

76

76

62

60

73

73

FTc (msec) 0,391

0,382

0,365

0,410

0,268

0,265

0,23

0,220

0,368

0,303

0,406

0,305

0,361

0,320

0,401

0,402

0,349

0,315

0,387

0.370

0,360

0,310

0,376

0,386

MA (cm/sec2) 6,5

6,2

5,7

5,4

3,8

4,24

4,5

3,5

7,8

6,2

7,5

7,4

7,34

6,1

7,2

6,9

7,4

5,8

6,5

6,5

7,5

5,5

6,2

6,8

Heart rate (HR), mean arterial pressure (SAPm), stroke volume (SV), cardiac output (CO), peak velocity (PV),flow time corrected (FTc), and mean acceleration (MA).

 

HR increased immediately after blood loss, it was restored after NaCl 7.5% infusion and remained stable until the end of the surgery (Fig. 1).

Systemic arterial pressure (systolic, diastolic and mean) decreased dramatically after blood loss, it improved immediately after NaCl 7.5%

infusion and remained at acceptable levels until the end of the surgery (Fig 1).

Stroke Volume, Cardiac Output, Peak Velocity, Mean Acceleration and Flow Time corrected decreased after blood loss and increased after NaCl 7.5% infusion (Fig. 2, 3 & 4). All measured parameters remained increased until the end of the study.

 

 

Figure 1. HR and mean BP alterations at the six study phases.

 

Figure 2. SV and CO alterations at the six study phases

Figure 3. PV and MA alterations at the six study phases

 

Figure 4. FTc alterations at the six study phases.

 

Measured parameters significantly improved before completion of NaCl 7.5% infusion (Image 1).

BIS changes in response to acute blood loss were characteristic. BIS decreased immediately after blood loss and remained decreased for a prolonged time period, whereas the hemodynamic status had improved (Image 2).

 

Image 1. The velocity-time Doppler waveform of one of the patients.
A: Basic measurement, B: Initiation of NaCl 7.5% administration, C: Administration of half of the NaCl 7.5%volume, D: Completion of administration, E: 20min after administration, F: End of the surgery.

 

Image 2. BIS alterations in one patient at the six study phases.

Lowest intraoperative Hb values were 7.6g/dL, 4g/dL, 5g/dL and 6.6g/dL and the corresponding patients received 3, 5, 4 and 3 pRBCs units respectively.In addition to HSS, patients also received 3.5L, 3.3L, 4.5L and 5.1L RL. Diuresis remained at an acceptable level throughout the operation.

Bleeding was surgically controlled, operation was completed uneventfully (in one of the 4 cases there was a change of surgical plan) and vasoactive drugs were discontinued before the end of the surgery.

During ICU stay patients were hemodynamic-cally stable without any need for vasoactive medication, three of them were extubated a few hours after the end of the surgery and one of them on the next day. All 4 patients were discharged to a ward on the 1st postoperative day, and overall outcome was positive. All of them were discharged home at a good physical status.

DISCUSSION

Maintenance of hemodynamic stability is one of the most important and challenging aspects of anesthesia since hypotension is associated with injury of organs such as kidneys and heart45-47. Intraoperative hypotension is common and its actual occurrence mainly depends on its definition since there is no universal definition. In a systematic review of the literature, Bijker et al identified 140 definitions for hypotension in 130 anesthesia articles48.

Acute hemodynamic collapse is not as common as hypotension and can be attributed to several causes, which are not always obvious despite the applied monitoring. The most frequent cause is acute major bleeding. Its occurrence may lead to tissue hypoperfusion and increases the risk of sepsis and multimodal organ failure49.

In the present study we present four patients, who suffered acute major blood loss intraoperatively, which led to hemodynamic collapse. For their management 4ml/kg NaCl 7.5% were administered in each patient and thereafter all patients received LR, pRBCs to correct low hemoglobin levels and vasoactive drugs for as long as necessary.

Fluid administration for intravascular volume restoration is the first line treatment after blood loss and crystalloids are widely used since they are already available50. Infusion of small volumes of HSS has been used for animal resuscitation in the setting of experimental hemorrhagic shock but also in clinical studies, which were mainly focusing on prehospital or intrahospital trauma management16,51. Small volume resuscitation has also been used in some surgical operations, such as aorta and cardiac surgery and before spinal anesthesia52. Furthermore, it has been used in the ICU, where it has been proved to have similar results as in hypovolemic patients53. All those studies have documented the efficacy of HSS for restoration of hemodynamics and microcirculation normalization.

Blood loss in our patients resulted in a dramatic decrease of SV, CO, BP and in HR increase. Those alterations are expected after acute volume loss because there is no time for compensatory mechanism to respond54,55.

Hemodynamic response to bleeding is related both to the amount and speed of blood loss, but also to the volemic status at that specific time point. Body’s response to hypovolemia is well described and documented in classic physiology handbooks. One of the commonest methods used for intraoperative blood loss estimation is visual estimation; however this is not very reliable56.

Both SV and CO increased immediately after NaCl 7.5% administration. CO increase after hypertonic infusion is already known and has been described in previous studies6,9,15,23. The main mechanism of action of hypertonic salt solutions is that they create an excessive osmotic gradient that drives fluid into the intravascular space7. BP increased after NaCl 7.5% administration. In the existing literature it is mentioned that rapid NaCl 7.5% administration might cause hypotension in normovolemic patients.57,58. SV, CO, BP alterations are efficacy indicators of administered fluids and vasoactive drugs59. PV, MA and FTc also showed a remarkable increase. Those parameters are related to preload and contractility of the left ventricle40-42. NaCl 7.5% administration had a double positive effect by both increasing the intravascular volume and improving circulation. The transient positive effects of HSS can be prolonged by addition of colloids22,27,28. All crystalloids have an impact on volume expansion for a restricted time period60.

In the present study the beneficial effects of HSS remained until the end of the operation. This prolonged action is attributed to the administration of RL, pRBCs, to vasoactive support of the circulation and surgical control of the bleeding. Fluid administration is aiming to restoration of the intravascular volume and is only one of several suggested treatments according to the management algorithm of the hemodynamically unstable patient. Early catecholamine administration is vital for the support of circulation61,62. Record of hemodynamic parameters revealed that the administration of HSS immediately restored the intravascular volume and contributed to good outcome63.However, NaCl 7.5% administration alone would not be capable of maintaining the beneficial effect. Rapid and efficient surgical control of the bleeding played a determinant role without which outcome would not be good despite any other management interventions.

According to existing literature, it seems that HSS administration with or without colloids results to immediate hemodynamic improvement of patients in shock. However, those studies have not proved whether HSS are superior to isotonic crystalloids as far as final outcome is concerned.

Wu et al conducted a meta-analysis of 12 randomized controlled clinical trials in trauma patients with hemorrhagic shock, in 6 of which hypertonic saline 7.5% was compared to 0.9% saline or RL and in 11 studies 7.5% hypertonic saline with dextran was compared to isotonic saline or RL. Authors did not find any differences as far as overall mortality, mortality in 28 days, survival to discharge, complication rate and acute respiratory distress syndrome free survival are concerned11. In another review by Dornelles et al, authors concluded that HSS could be beneficial in specific clinical settings despite the fact that they have no impact on mortality64.

Blanchard et al compared prehospital administration of 250ml NaCl 7.5% to normal saline or RL in a meta-analysis of 5 studies which enrolled 1162 trauma hypotensive patients (systolic BP below 100mmHg). Authors concluded that there were no clinical significant differences related to outcome65.

Pfortmueller and Schefold conducted another systematic review of 25 clinical trials in which all patients received HSS. Authors concluded that its administration might have positive effects in carefully selected patients66.

Based on our results and on existing literature it seems that NaCl 7.5% administration can be beneficial in correcting hypovolemia and in restoring hemodynamic stability.      

The limitations of this study concerned the facts that due to the limited number of patients included and the lack of control group, we could not generalize our results. Moreover, despite the fact that bleeding was significant, it lasted only for a short time period and it was rapidly controlled by the surgeon.

Conclusion

NaCl 7.5% administration was successful in restoring hemodynamics in our patients, who suffered hemodynamic shock due to acute major blood loss. NaCl 7.5% administration along with all other treatment interventions has been shown to be beneficial to achieving a good outcome.


Addittional materials: No


Acknowledgements:

Not applicable

Authors’ contributions:

FB contributed to planning and is the lead author, KK contributed to the critical revision of the paper. FK contributed to the critical revision of the paper. OV contributed to the critical revision of the paper. GS contributed to the critical revision of the paper. DM contributed to the critical revision of the paper. KM contributed to the critical revision of the paper. GV contributed to the critical revision of the paper. All authors read and approved the final manuscript.

Funding:

Not applicable.

Availability of supporting data:

Not applicable.

Ethical approval and consent to participate:

No IRB approval required

Competing interests:

The authors declare that they have no competing interests.

Received: August 2022, Accepted: September 2022, Published: September 2022.


REFERENCES

  1. Shin Ch, Long D, McLean D, et al. Effects of Intraoperative Fluid Management on Postoperative Outcomes A Hospital Registry Study. Ann Surg 2018; 267: 1084–92. doi. 1097/ SLA.0000000000002220
  2. Bellamy M. Wet, dry or something else? Br J Anaesth 2006; 97:755–7. https://doi.org/10.1093/bja/ael290
  3. Bellomo M, Forbes C, Peyton P, et al. Restrictive versus Liberal Fluid Therapy for MajorAbdominal Surgery. N Engl J Med 2018; 378: 2263 – 74. 10.1056/NEJMoa1801601
  4. Myburgh J, Mythen M. Resuscitation fluids. N Engl J Med 2013;369:1243-51. doi. 1056/ NEJMra1208627
  5. Smith J, Hall M. Hypertonic Saline. J R Army Med Corps 2004; 150: 239-43. 10.1136/jramc-150-04-03
  6. Rocha Silva M, Poli de Figueiredo L. Small volume hypertonic resuscitation of circulatory shock. Clinics. 2005;60:159. 10.1590/s1807-59322005000200013
  7. Rocha Silva M. Hypertonic saline for treatment of shock: have we looked for everything? Medical Express. 2014:14-21. https://doi.org/10.5935/MedicalExpress.2014.01.04
  8. Penfield W. The treatment of severe and progressive hemorrhage by intravenous injections. Am J Physiol 1919;48:121-8. https://doi.org/10.1152 /ajplegacy.1919.48.1.121
  9. Velasco I, Pontieri V, Rocha Silva M, et al. Hyperosmotic NaCl and severe hemorrhagic shock. Am J Physiol. 1980;239:664–73. 10.1152 /ajheart.1980.239.H664
  10. Traverso L, Bellamy RF, Hollenbach S, et al. Hypertonic sodium chloride solutions: Effect on hemodynamics and survival after hemorrhage in swine. J Trauma 1987;27: 32–39. PMID: 3806709
  11. Wu M Ch, Liao T-Y, Lee E, et al Administration of Hypertonic Solutions for Hemorrhagic Shock: A Systematic Review and Meta-analysis of Clinical Trials. Anesth Analg 2017;125:1549–57.doi. 1213/ANE. 0000000000002451
  12. De FelippeJ, Timoner J, Velasco I, et al. Treatment of refractory hypovolaemic shock by 7.5% sodium chloride injections. Lancet 1980;ii:1002–1004. https://doi.org /10.1016/S0140-6736(80) 92157-1
  13. Nakayama S, Sibley L, Gunther R. Small-volume resuscitation with hypertonic saline (2,400 mosm/liter) during hemorrhagic shock. Circ Shock 1984: 13: 149–159. PMID: 6744520
  14. Kreimeier U, Frey L, Messmer K. Small-volume resuscitation. Curr Opinion Anaesth1993: 6: 400–408. 10.1007/s001010050406
  15. Kramer G, Elgjo G, Poli de Figueiredo L, et al. Hyperosmotic- hyperoncotic solutions. Baillieres Clin Anaesth1997 ;11: 143–60. https://doi.org/10.1016 /S0950-3501(97)80009-8
  16. Kreimeier U, Messmer K. Small-volume resuscitation: from experimental evidence to clinical routine. Advantages and disadvantages of hypertonic solutions. Acta Anaesthesiol Scand 2002; 46: 625–38.10.1034/j. 1399-6576.2002. 460601.x
  17. Watenpaugh D, Gaffney F. Measurement of the net whole-body transcapillary fluid transport and effective vascular compliance in humans. J Trauma 1998 ;45: 1062–68. doi.10.109/0005373-199812000
  18. Kramer G. Hypertonic resuscitation: physiologic mechanisms and recommendations for trauma care. J Trauma 2003; 54: 89-99. 10. 1097/01.TA.0000065609.82142.F1
  19. SvensonC, Hahn RG. Volume kinetics of Ringer solution, dextran 70, and hypertonic saline in male volunteers. Anesthesiol 1997; 87:204-212. doi. 10.1097/00000542-199708000-00006
  20. Drobin D, Hahn RG. Volume kinetics of Ringer’s solution in hypovolemic volunteers. Anesthesiol 1999; 90:81-91. 10.1097/00000542-199901000 -00013
  21. Drobin D, Hahn R. Kinetics of Isotonic and Hypertonic Plasma Volume Expanders. Anesthesiol 2002; 96: 1371–80. doi. 10.1097/00000542200 206000-00016
  22. Smith G, Kramer G, Perron P, et al. A comparison of several hypertonic solutions for resuscitation of bled sheep. J Surg Res 1985;39:517-28. 10. 1016/0022-4804(8 5)90120-9
  23. Velasco I, Silva M, Oliveira M, et al. Hypertonic and hyperoncotic resuscitation from severe hemorrhagic shock in dogs: a comparative study. Crit Care Med 1989;17:261-4. 10. 1097/00003246-198903000-00012
  24. Frithiof R, Eriksson S, Bayard F, et al. Intravenous hypertonic NaCl acts via cerebral sodium-sensitive and angiotensinergic mechanisms to improve cardiac function in haemorrhaged conscious sheep. J Physiol. 2007;583: 1129 –43. 10.1113/jphysiol. 2001 139592
  25. Rocha Silva M. Hypertonic saline resuscitation: a new concept. Baillieres Clin Anaesth 1997;11: 127–42. https:// doi.org/10.1016/S0950-3501(97)800 08 -6
  26. Junger W, RHind S, Rizoli S, et al. Resuscitation of traumatic hemorrhagic shock patients with hypertonic saline without dextran – inhibits neutrophil and endothelial activation. Shock 2012, 38:341–50. 10.1097/SHK. 0b013e3182635aca
  27. KreimeierU, Pruecknera S. Small-volume resuscitation from hemorrhagic shock by hypertonic saline dextran –conceptional basis and historical background. Eur Surg Res 2002;34: 138–144. 10.1159 /000048900
  28. Kramer G, Walsh J, Perron P, et al. Comparison of resuscitation of hypovolemia using hypertonic saline-dextran and hypertonic saline-hetastarch. Braz J Med Biol Res 1989; 22: 279-82. PMID: 2477094
  29. Coppola S, Froio S, Chiumello D. Fluid resuscitation in trauma patients: what should we know? Curr Opin Crit Care 2014, 20:444–50. 10.1097/ MCC.0000000000000115
  30. Bentzer P, Griesdale D, Boyd J et al. Will This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? JAMA. 2016;316:1298-1309. 10.1001/ jama.2016.12310
  31. Zochios V, Wilkinson J. Assessment of intravascular fluid status and fluid responsiveness during mechanical ventilation in surgical and intensive care patients. JICS 2011;12: 295-300. https://doi.org/10.1177/175114371101200410
  32. Kalantari K, Chang J, Ronco C, et al. Assessment of intravascular volume status andvolume responsiveness in critically ill patients. Kidney International 2013;83: 1017–28. doi.10.1038/ki.2012.424
  33. Perel Α. Using Dynamic Variables to Guide Perioperative Fluid Management. Anesthesiol 2020; 133: 929-35. 10.1097/ALN.0000000000003408
  34. Teboul J, Monnet X, Chemla D, et al. Arterial pulse pressure variation with mechanical ventilation. Am J Respir Crit Care Med 2019; 199:22–31. doi.:1164/rccm.201801-0088CI
  35. Fick A. On the measurement of blood mass in the heart ventricules. Sitzber Physik Med Ges Wurzburg 1870:36: 16-28.
  36. Kobe J, Mishra N, Arya V, et al. Cardiac Output Monitoring: Technology and Choice. Ann Card Anaesth. 2019; 22: 6–17. doi.4103/aca.ACA_4118
  37. Saugel Β, CCecconi Μ, Wagner Ζ, et al. Noninvasive continuous cardiac output monitoring in perioperative and intensive care medicine. BJA2015; 114: 562–75. doi.10.1093/bja/aeu447
  38. Pinsky M. Why measure cardiac output? Crit Care 2003, 7:114-16. doi.1186/cc1863
  39. Schulz L, Geri G, Vieillard‐Baron, et al. Assessment of volume status and volume responsiveness in the ICU: Protocol for an observational, multicentre cohort study Schulz L, Geri G, Vieillard‐Baron et al. Acta Anaesthesiol Scand 2019;00: 1–7. https ://doi.org/10.1111/aas.13385
  40. Prentice D, Sona C. Esophageal Doppler Monitoring forHemodynamic Assessment. Crit Care Nurs Clin N Am 2006; 8: 189 – 93. doi.1016/j.ccell.2006.02.004
  41. SchoberP, Loer S, Schwarte L. Perioperative hemodynamic monitoring with transesophageal Doppler technology. Anesth Analg 2009; 109: 340–53. 10.1213/ane. 0b013e3181 aa0af3
  42. Singer M. Oesophageal Doppler. Curr Opin Crit Care 2009;15:244–8. doi. 1097/MCC.0b013e32832b7083
  43. King S, Lim M. The use of the oesophageal Doppler monitor in the intensive care unit. Crit Care Resusc 2004; 6: 113–22. PMID: 16566698
  44. Schober P, Loer S, Schwarte L. Haemodynamic monitoring of critically ill patients with transoesophageal Doppler technology. Neth J Crit Care 2010;14: 388-94.
  45. Salmasi V, Maheshwari K, Yang D, et al. Relationship between Intraoperative Hypotension, Defined by Either Reduction from Baseline or Absolute Thresholds, and Acute Kidney and Myocardial Injury after Noncardiac Surgery A Retrospective Cohort Analysis. Anesthesiol 2017; 126:47-65. 10.1097/ALN.0000000 000001432
  46. Walsh M, Devereaux P, Garg AX, et al. Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: Toward an empirical definition of hypotension. Anesthesiol 2013; 119:507–15. 10.1097/ ALN.0b013e3182a10e26
  47. vanWaes J, van Klei W, Wijeysundera D, et al. Association between intraoperative hypotension and myocardial injury after vascular surgery. Anesthesiol 2016; 124:35–44. https://doi.org/10.1097/ ALN.00000 00000000922
  48. Bijker J, van Klei W, Kappen T, et al. Incidence of intraoperative hypotension as a function of the chosen definition: Literature definitions applied to a retrospective cohort using automated data collection. Anesthesiology 2007; 107:213–20. doi.1097/01. anes.0000270724.40897.8e
  49. Thacker J, Mountford W, Ernst F, et al. Perioperative fluid utilization variability and association with outcomes: Considerations for enhanced recovery efforts in sample US surgical populations. Ann Surg 2016; 263:502–10. 10.1097/ SLA.0000000000001402
  50. SemlerΜ, Rice Τ. Saline Is Not the First Choice for Crystalloid Resuscitation Fluids. Critical Care Medicine 2016 ; 44 : 1541- 4. 10.1097/CCM.0000000000001941
  51. Heath Μ. Hypertonic Saline: A Review of the Literature and Evaluation of its Role inResuscitation of Traumatic Hypovolaemic Shock. J R Med Corps 1994; 140: 37-41. DOI: 1136/jramc-140-01-09
  52. Azoubel G, Nascimento B, Ferri M, et al. Operating room use of hypertonic solutions: a clinical review. CLINICS 2008 ; 63 :833-40. doi.1590/S1807-59322008000600021
  53. Oliveira R, Velasco I, Soriano F, et al. Clinical review: Hypertonic saline resuscitation in sepsis. Critical Care 2002; 6:418-23. doi.1186/cc1541
  54. Schiller Α, Howard J, Convertino V. The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage. Exper Biol Med 2017; 242: 874–83. 10.1177/1535370217694099
  55. PernerΑ, Backer D. Understanding hypovolaemia. Intensive Care Med 2014; 40: 613 5. doi.: 1007/s00134-014-3223-x
  56. Gerdessen L, Meybohm P, Choorapoikayil S, et al. Comparison of common perioperative blood loss estimation techniques: a systematic review and meta‑analysis. J Clin Monitor Comput 2021; 35:245–58. 10.1007/s10877-020-00579-8
  57. Ken N, Kramer G, White D. Acute hypotension caused by rapid hypertonic saline infusion in anesthetized dogs. Anesth Analg 1991;73:597-602. PMID:1952141
  58. Bead B, Johnson J, Vick J, et al. Vascular effects of hypertonic solutions. Circul Res 1960;8: 538–48. https://doi.org/1161/01.RES.8.3. 5.3
  59. Doherty M, Buggy DJ: Intraoperative fluids: how much is too much? Br J Anaesth 2012, 109:69–79. 10.1093/bja/aes171
  60. NunesΤ, Ladeira R, BafiA et al. Duration of hemodynamic effects of crystalloids in patients with circulatory shock after initial resuscitation. Annals of Intensive Care 2014;4:25. doi.1186/s13613-014-0025-9
  61. Funk D, Jacobsohn E, Kumar A. The role of venous return in critical illness and shock. I. Physiology. Crit Care Med 2013;41:255-62. 10.1097/ CCM.0b013e3182772ab6
  62. De Backer D, Aissaoui N, Cecconi M, et al. How can assesing hemodynamics help to assess volume status? Intensive Care Med 2022. 10.1007/s00134-022-06808-9
  63. Funk D, Jacobsohn E, Kumar A. Role of the venous return in critical illness and shock: part II-shock and mechanical ventilation. Crit Care Med 2013;41:573-9. 10.1097/CCM.0b013e31827bfc25
  64. Dornelles Μ, DornellesΕ, Dornelles L. Hypertonic saline in ICU setting: what is its position? A systematic review and empirical analysis. Ain-Shams J Anesthes 2022; 14:55. https://doi.org/1186/s42077-022-00254-x
  65. Blanchard I, Ahmad A, Tang K, et al.The effectiveness of prehospital hypertonic saline for hypotensive trauma patients: a systematic review and meta analysis. BMC Emergency Medicine 2017;17: 35. doi.10.1186 /s12873-017-0146-1
  66. Pfortmueller C, Schefold J. Hypertonic saline in critical illness – A systematic review. J Crit Care 2017;42; 168–77. 10.1016 /j.jcrc. 2017.06.019

 

Publisher’s Note

The publisher remains neutral with regard to jurisdictional claims in published maps and institutional afliations.

Citation: Fyntanidou B, Kotzampassi K, Fortounis K, Ourailoglou V, Gkarmiri S, Deligianni M, Kyparissa M, Grosomanidis V.Hypertonic saline resuscitation in acute intraoperative hemorrhage: Case Series presentation. Greek e j Perioper Med. 2022;21(b): 37-54.

 

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution – ShareAlike 4.0 International license (CC BY-SA 4.0) (https://creativecommons.org/licenses/by-sa/4.0/)
Language
Αναβάθμιση του Impact Factor

Archives
ATOM Feed
RSS Feed
RDF Feed
Creative Commons License