Anesthesiology MD

Primer on aneshesia for liposuction

2007-12-22T09:45:00.000-08:00

There are several techniques used to perform liposuction. See table.1

The wet technique was introduced in the 1980s, and the superwet technique was introduced in 1980 and advocated by fodor. With this technique, infiltration was injected in equal volume to aspirated liposuction. In the same year, the tumescent technique, introduced by Klein, was described and the injectate volume was now 2 to 3.1 to 12 part aspirated and required only local anesthesia.3 Some have liberalized the tumescent technique using ratios from 3-7:1.6 Blood loss was minimal with the tumescent technique and deemed safe.4 While these techniques have been accepted by surgeons, there is still controversy regarding the resuscitation of these patients, typified by the stances of Klein and Pitman. Klein considers (for the tumescent technique) the fluid injected into the tissues sufficient for volume resuscitation hypothesizing that this fluid makes its way into the intravascular space.5 In fact, this process is known as hypodermoclysis. Hypodermoclysis is the mechanism described by which SQ fluid migrates to the intravascular space. This process is estimated to take around 2 ½ hours for 1 liter of fluid infiltrated into medial thigh.11 Unfortunately, this data is from only one study and therefore, the true rate may be quite different. Authors have tried to quantify how much of the infiltrate is removed in the aspirate and have estimated that only 2212 to 29%13 of the aspirated fluid contains the original fluid infiltrated. This view contrasts with Pitman, who advocates a 2:1 ratio (IV + injected SQ:aspirate).7 Neither author reports complications from fluid overload, and there is only one reported case of fluid overload.8 Other reports of death have been documented.9-10
A prospective observational trial of 53 patients who underwent USG liposuction using a superwet technique, where the ratio was 1:1 (infiltrate:aspirate) was used.1 Fluid was replaced per preoperative deficits, and then given to maintain VS and UO WNL, and finally per protocol of 1:1 ratio of infused crystalloid:aspirate after >4L of aspirate. Infiltrate solution contained 0.03% lidocaine plus 0.01% epinephrine (1:1,000,000), and given to maximum of 4,000 mL (lidocaine 1200 mg=17 mg/kg assuming 70kg). In this study the average aspirated volume was ~4.5 L (range 300 mL to 15.5 L). The average UO for both small volume (<4l)>4L) aspirate liposuction was > 1.5cc/kg/hr. There were 3 episodes of transient hypotension responsive to fluid in the PACU and 3 more on the floor. See table 2.

average volume used on per kg per hour basis.
The authors for this study used a reference for fluid replacement of 5 to 6 cc/kg/hr based on the stoelting and miller textbooks of anesthesia stating this type of surgery represented moderate trauma. Based on this study the authors gave the following recommendations based on the fact that the large volume patients seemed to be slightly over resuscitated by virtue of the UO all greater than 1 cc/kg/hr in OR and PACU.
1. Pre op deficits as needed.
2. IVF per VS and UO
3. infiltrate solution
4. 0.25 mL per mL infiltrated after 4 L aspirated.

This same group followed up their first study with a review of 89 patients14 using their own recommendations for IVF therapy from the previous study in an attempt to avoid the slight over resuscitation that occurred. They did modify the regimen only slightly by not starting to give IVF 0.25 mL/mL aspirated until after 5 L of aspirate. Of these 89 pts only 21 underwent large volume liposuction (>5 L aspiration). This group used a super wet technique with a similar lidocaine + epinephrine mixture as detailed in their first study, but this was given up to a total of 5 L of infiltrate after which lidocaine was removed from the LR. See table for volume resuscitation:
The average intraop fluid ratio (total volume in/total volume aspirated) was 1.8 for the small volume group (<5l)>5L). UO ave was 1.5 cc/kg/hr and 1.7 cc/kg/hr for the small and large volume groups respectively. In the PACU, UO was 1.6 and 1.7 for the small and large volume groups respectively, while fluid given was 3.8 and 4.4 mL/kg/hr for the small and large volume groups respectively. On the floor, fluid was required for 10 hrs and 16 hrs for the small and large volume groups respectively, while fluid given was 1.6 and 1.3 mL/kg/hr for the small and large volume groups respectively. UO was 2.9 and 2.5 mL/kg/hr for the small and large volume groups respectively.
They did not have any major complications in this study, and no transfusion was given. This group reports that they have never had pulmonary edema as a complication in over 700 patients, but are still yet wary of this complication.
The graphs below depict comparison from the first cohort on 1st protocol (1 mL IVF given for each mL of aspiration after 4000 mL) compared to the current protocol. The original protocol is blue and revised protocol in purple.
the original protocol is represented by the yellow, and revised by the light blue. The authors note that in the second graph, UO peaked in the RR in the original protocol, which could represent a more sudden and abrupt IV volume shift as compared to the more delayed and gradual shift as occurred with the current protocol. They also note that UO was still high representing a slight over resuscitation which might be modified by not replacing aspirate with IVF therapy at all.
Although this group does not report morbidity from high volumes of fluid, the tumescent technique has potential for harm. Gilliland reports a case of pulmonary edema in a 55 year old ASA 1 male who returned for a 3rd liposuction surgery.8 He received a 7900 mL SQ and 2200 mL IV. He develop hypoxemia in the PACU and required 2 doses of lasix after which he urinated approximately 5 L over the ensuing several hours improving saturations from the 80s to 100. Pitman submitted a response to this case report stating that he believes the imminent cause of this patient’s pulmonary edema to be the 2200 mL of IV fluid.15 He then describes a formula that has been shown to be safe for tumescent liposuction of up to 6 L. He suggests limiting IVF intraop to KVO max 100 to 300 cc. He uses 0.5% lidocaine + 1:1,000,000 epinephrine for the injectate solution and typically gives up to 40 mg/kg. see fig from pitman.

At the conclusion of surgery the aspirate is measure and compared to the total injectate seeking a 2:1 ratio for injectate (infiltrate):aspirate. If this ratio is <2:1,>2:1, then no IVF are given. He states that he has experienced no adverse events in over 1000 patients using this formula. Pitman also states that for his procedures using the tumescent technique, he has calculated blood loss at 7.8% of aspirate volume (78cc blood per 1000cc aspirated).
Grazer has written about the dangers associated with the tumescent technique and reports that most morbidity and mortality is associated with poorly trained physicians performing very large aspiration (~10L) in office type settings. Furthermore, large amounts of lidocaine (40 to 70 mg/kg) are being used in these procedures resulting in toxicity of both lidocaine and epinephrine. He also emphasized pulmonary edema as a problem. In another review, Grazer discussed lidocaine toxicity. He points out that therapeutic plasma lidocaine levels are between 1.5 mcg/mL and 5 mcg/mL total lidocaine, and this is different from reported levels that only measure active drug (unbound) which is 0.5 to 1.5 mcg/mL. Lidocaine is only active when unbound, and 60 to 70% is bound in healthy individuals: to alpha 1 glycoprotein (50%), albumin 25%, and other miscellaneous proteins (25%). Grazer notes that patients undergoing liposuction have increased FFA levels which displace lidocaine from its binding sites on proteins, which will increase the unbound active fraction, increasing the potential for toxicity. They also note that with lidocaine dosages in the tumescent technique, they have measured total lidocaine plasma levels at <1 mcg/mL when up to 35 mg/kg were used. Other factors to consider are metabolites of lidocaine which include MEGX and GX, where MEGX is the active metabolite and is not measured in serum assays. The author concludes by making the following recommendations regarding the tumescent technique. 1) Limit the volume of fluid injected to 3 to 5 L, 2) limit total lidocaine dose to 35 mg/kg.. 3) The volume of injectate should be modified down in patients with one comorbid condition, or may be modified up in the occasional healthy patient. 4) Pts taking dietary medications should be cleared by a medical specialist.
Grazer, in another paper,16 states that the most common cause of mortality from liposuction is PE, thus spawning the practice of giving 5% etOH in D5W although this is only supported by anecdotal evidence.

In summary, the approach to a patient who is to undergo liposuction under anesthesia care requires consideration of more than the standard preoperative history and physical, intraoperative monitoring and post operative care. There should be awareness of the liposuction technique used (superwet, tumescent) and more importantly an understanding of the injectate to aspirate ratio to expect during the procedure since this is critical in determining the volume status of your patient. A clear awareness of expected and actual aspirate volumes is necessary as well to determine fluid requirements and foresee potential risks to the patient. Also, a general understanding of L.A. toxicity is necessary as well as the amount of lidocaine your patient receives on a per kg basis. In addition the amount of epinephrine is important since this is almost universally used in wetting solutions. Finally, some surgeons may ask for a 5% alcohol in dextrose solution be used. Extensive searches in pub med and on the web by myself have proven futile in turning up any articles dedicated to the use of this technique in liposuction. Only peripheral mention of this technique is made in several articles which discuss liposuction and it is noted in each of the articles that there is no evidence to suggest that it is beneficial. Nevertheless, if the surgeon requests this infusion, (in hopes to reduce the risk of fat embolism or pulmonary embolism), it

1. Trott SA, Beran SJ, Rohrich RJ, Kenkel JM et al. Safety considerations and fluid resuscitation in liposuction: An analysis of 53 consecutive patients Plast Reconst Surg. 1998; 102: 2220-29.
Klein, J. A. Tumescent technique for local anesthesia improves safety in large-volume liposuction. Plast. Reconstr. Surg. 92: 1085, 1993
Klein, J. A. The tumescent technique: Anesthesia and modified liposuction technique. Dermatol. Clin. 8: 425, 1990
Lillis, P. The tumescent technique for liposuction surgery. Dermatol. Clin. 8: 439, 1990
Klein, J. A. Tumescent technique for regional anesthesia permits lidocaine doses of 35 mg/kg for liposuction. J. Dermatol. Surg. Oncol. 16: 248, 1990
Fodor, P. B. Wetting solutions in aspirate lipoplasty: A plea for safety in liposuction (Editorial). Aesthetic Plast. Surg. 19: 379, 1995.
Pitman, G. H. The role of subcutaneous infiltration in suction-assisted lipoplasty: A review (Discussion). Plast. Reconstr. Surg. 99: 520, 1997.
Gilliland MD, and Coates N. Tumescent liposuction complicated by pulmonary edema. Plast. Reconstr. Surg. 99: 215, 1997.
Grazer FM, and Meister FL. Complications of the tumescent formula for liposuction (Editorial). Plast. Reconstr. Surg. 100: 1893, 1997.
Grazer, F. M., and Meister, F. L. Factors contributing to adverse effects of the tumescent technique (surgical strategies). Aesthetic Surg. J. 17: 411, 1997
Finley, R. K. and Shaffer, J. M. Parenteral fluid administration beneath the fascia lata. Am. J. Surg. 63: 337, 1944
Pitman, G. H., Aker, J. S., and Tripp, Z. D. Tumescent liposuction. Clin. Plast. Surg. 23: 633, 1996.
Samdal, F., Amland, P. F., and Bugge, J. F. Blood loss during liposuction using the tumescent technique. Aesthetic Plast. Surg. 18: 157, 1994.
Rohrich RJ, Leedy JE, Swamy RBA, Brown SA, Coleman J. Fluid resuscitation in liposuction: A retrospective Review of 89 consecutive patients. Plast Reconstr Surg. 2006; 117: 431-5.
Rohrich RJ, Leedy JE, Swamy RBA, Brown SA, Coleman J. Fluid resuscitation in liposuction: A retrospective Review of 89 consecutive patients. Plast Reconstr Surg. 2006; 117: 431-5.
Grazer FM, De Jong RH. Perioperative management of Cosmetic liposuction. Plast Reconstr Surg. 2001; april.

The anesthesiologist and surgical site infection!

2007-12-15T14:41:00.000-08:00

A 65 year old male for emergent hemicolectomy secondary to massive bleeding. Pt has remote history of testicular cancer (age 30), now with HTN, DM and obesity (BMI 32). Current BP is 100/70, HR is 85, AF, RR 27. Plan is GETA w/ RSI and Cricoid Pressure.The anesthesiologist often does not consider surgical site infection as a main theme or criteria when deciding what medications to give or in developing the anesthetic plan. In many cases, issues of surgical site infection (SSI) are simply to give preop antibiotics and go no further. However, there are special cases as the one above, where your patient has an above average potential for developing a surgical site infection and the anesthesiologists role is directly relevant to this outcome. Although, maintaining normothermia, adminstering effective prophylactic antimicrobials prior to incision, and maintaining blood flow to tissues are obvious and well known to be critical in reducing the risk of surgical site infections, there are other methods that are important, particularly in higher risk patients that are less known and understand by many anesthesia providers who have a great amount of experience.The first step in playing an active role in reducing the probability of a SSI post op is estimating your patients risks which implies understanding those factors that increase risk.the following is a general list of risk factors but does not quantify how much each factor increases risk:

hypovolemia

diabetes

obesity

malnourishment

blood trasnfusion

inadequate pain control

antibiotic prophylaxis

prolonged surgical time

host immune system

air in OR (ultraclean, negative pressure)

hypothermia

low SC Oxygen tension

This article will focus on the few modifiable risk factors that exist with an emphasis on those that are predominantly under the control of the anesthesiologist. These will include:

pain control-brief

antibiotic prophylaxis-brief

patient temp-brief

Sub Q oxygen tension- emphasis

Pain Control: at this point I will limit my comments to a simple better pain control is better. The 'why' will be touched upon under the heading of Sub Q oxygen tension (improved w/ pain control).

Antibiotic prophylaxis: appropriate antibiotics should be given within one hour of surgical incision. Giving antibiotics after incision is has questionable benefit.

Patient temp: normothermia is critical. This is often very difficult in a scenario as described above because patients come to the OR emergently and time is spent placing lines in a pt who is not being warmed in a cold OR. Often by the time the drapes go up and surgery commences the patient has become hypothermic. Evidence for the importance of normothermia comes from a RCT published in the NEJM demonstrating an absolute risk reduction (ARR) of 13% by maintaining normothermia (37C vs. 34.5C)(1).
Sub Q oxygen tension: Most anesthesiologists do not consider this data when performing anesthesia. Indeed, it is usually not important information for the vast majority of anesthetics. However, as arterial lines are appropriate to place in some patients, the information gained from sub q oxygen tension can be quite important. Unfortunately there is no clinical method available to monitor this parameter. Nevertheless, it is important to understand what is normal, what is abnormal, and how this will affect your patient. In a normal volunteer breathing room air, it sits around 65 mmHg. Surgical patients when measured average about 49 mmHg with large variability. Post surgical patients breathing oxygen through NC (~0.4 to 0.6 FiO2) average around 69 mmHg, whereas a normal volunteer given the same amount of oxygen will increase their TsqO2 to ~130 mmHg (2). This is important to understand because it turns out that tissue healing and bacteria killing are dependent on an oxygen tension in the tissues and vary in direct proportion to the tissue oxygen tension (PsqO2). In fact it has been experimentally verified that oxidative killing is oxygen dependent from 0 to 150 mmHg PsqO2 (3). Furthermore, when bacteria are introduced and phagocytes begin utilizing NADPH to reduce O2, this results in a dramatic reduction in PsqO2, that is from the normal of ~60 mmHg down to 0-10 mmHg. Bacterial contamination also alters PsqO2 by altering perfusion of tissues independently of oxygen utilization. In rats where lesions have been experimentally created and then inoculated it has was demonstrated that low FiO2 compared to high FiO2 was an independent variable in determining infection size and was no less important than giving prophylactic antibiotics. In other words, utilizing a FiO2 after bacterial inoculation was just as effect maintaining normal (0.21) FiO2 but giving antibiotics (4,5).
So who do we give oxygen to and in what dose? The first step that should be taken in any patient going to the OR where a surgical incision will be made is to make a valid determination of the risk of SSI to the patient. Although the above risk factors as listed are pertinent, considering them provides no quantitative probability of a particular patient developing a SSI post operatively. A crude, but simple tool that has been used in research is the SENIC scoring system. See below:
1 pt: intraperitoneal abdominal surgery
1 pt: duration of surgery >2 hrs.
1 pt: 3 or more co morbidities (i.e. hypertension, pulmonary disease, diabetes)
1 pt: contaminated wound/surgery- (i.e. abscess, colon surgery non prepped)
Predicted infections rates are as follows depending on score:
0=1% 1pt=3.6% risk 2pts.=9% 3pts.=17% 4pts.=27%
However, in 1997 Hopf and colleagues published a paper in the Archives of Surgery demonstrating that this scoring system was not nearly as effective at predicting the risk for SSI as was measuring the PsqO2 on patients(6). Among their findings were the following:
· If baseline PsqO2 was >70 mmHg, no SSI occurred.
· If baseline PsqO2 was 40 mmHg or less, SSI rate was 40%
· Rate of infection varied inversely with both baseline PsqO2 and with post operative maximal PsqO2.
There are three main factors which determine PsqO2, two of which are under the control of the anesthesiologist. These are vascular anatomy at the site of inoculation (surgical site), vasomotor control (vasoconstricted vs. vasodilated), and PaO2 which varies directly w/ PsqO2 assuming normal blood flow to tissues.
The first factor is beyond our control, however, vasomotor control and the PaO2 can be manipulated by us to a much greater degree.
Controlling PaO2: Two large RCTs in colon surgery patients both demonstrated that indeed, by providing a FiO2 (80% vs. 30%), and therefore increasing PsqO2, indeed decreases the rate of SSI in colon surgical patients although the decrease was modest (7,8). Patients in both of these large studies had significantly lower SSI rates when given 80% FiO2 both during surgery and afterwards for 2 or 6 hours depending on the study.
Vasomotor state: Okca et al(9) demonstrated that in patients undergoing surgery w/ FiO2 of 0.4 received an average increase of ~30 mmHg (from 63 to 89 mmHg) if the etCO2 was maintained at 45 mmHg vs. 30 mmHg. Note that is quite common for the etCO2 to be maintained at ~30 mmHg in patients who are paralyzed and mechanically ventilated. Patients already receiving FiO2 of 0.8 also benefit however(10), going from PsqO2 of 84 mmHg to 116 mmHg and more importantly, an intestinal oxygen tension went from 53 mmHg to 107 mmHg.
Hypovolemia is detrimental to PsqO2. In fact, if you give provide a higher FiO2 to a patient with goal of raising PsqO2 and thus decreasing chance of SSI, but do not adequately resuscitate your patient, it has been shown that despite your good intentions, the PsqO2 will not increase. It’s only after adequate volume status has been restored that raising FiO2 will prove beneficial (11). Others have shown that indeed an aggressive fluid regimen can augment PsqO2 in abdominal surgical patients (12), but a follow up study on this same cohort of patients found that this increase in PsqO2 did not result in a decrease in the rate of SSI (13). Despite these findings, hypovolemia must be avoided and fluid therapy should be adequate to ensure this. In the above study looking at an aggressive fluid regimen vs. a standard protocol of 8 to 10 mL/kg/hr a balanced crystalloid solution was used. However, Lang et al (14). showed that LR in large volumes (11L) caused a 59% decrease in the PsqO2, however, giving a HES in addition to the LR at lower volumens (3 L each) PsqO2 was increased by 23%. The take home message from these studies is avoid hypovolemia, but caution she be used when this requires large volumes of crystalloid (i.e. >8 or 9 L) and consideration should be given to other fluid types.
Inadequate pain control has been shown to have a significant effect on decreasing the PsqO2 by around ~24 mmHg (15). Morphine and its derivatives effective at reducing pain, however, they also can cause respiratory depression and lead to decreased PaO2 which reduces PsqO2. Furthermore, meta analyses have shown that PCA with narcotic pain medications are inferior to PCEA after many different kinds of surgery with regard to pain scores (16, 17). Therefore, whenever appropriate regional anesthesia should be considered as a method not only for pain control but also as an intervention with the goal of decreasing SSI risk. In addition to the improvement provided by improved pain control to the PsqO2 of nearly 24 mmHg as shown, the vasodiliation that results from the sympathectomy of regional anesthesia induces a further increase in PsqO2 of from 9 mmHg to 31 mmHg depending on the method and study (18, 19, 20, & 21).
Obesity is associated with a greater risk of post op SSI. Studies looking at the PsqO2 in obese patients (BMI >30), showed that to no one’s surprise, a much greater FiO2 was required to maintain a certain PaO2 (22, 23). However, more surprising was the studies findings that once obese and non obese patients achieved an equal PaO2, PsqO2 were still much lower in the obese patient by approximately 20 to 30 mmHg depending on the PaO2 that was used as the starting measurement. Both studies indicated that obese patients require FiO2 of >0.95) in order to maintain PsqO2 around ~47 mmHg, which is still low enough to be associated with risk. Furthermore, simply raising FiO2 in this population results in an underwhelming increase of PsqO2 of 13 mmHg, which is half the benefit their non obese counterparts experience. Adding PEEP may be necessary if tolerated in order to increase PaO2 to >300 mmHg, the maximum tested in these studies.
Although PsqO2 is an excellent predictor of risk of SSI, and two RCT have demonstrated benefit to hyperoxia, the practice of delivering high FiO2 is not standard of care. Many cite a study showing that hyperoxia was associated with worse outcome in a study of general surgical patients (24). This study however suffered from methodological flaws: the experimental group (hyperoxia) had a greater number of obese patients, were more likely to be intubated at the end of surgery (likely sicker) and underwent longer and more complicated surgery. Simply put, the groups were not equal. Nevertheless, performing a metanalysis of the three studies shows that hyperoxia is beneficial. Another common concern among clinicians is that of absorption atelectasis resulting in post operative pulmonary complications. Although, this is a known feature of high FiO2, a study looking specifically at this problem in a clinical setting demonstrated that this concern is likely unfounded (25).
In conclusion, it is my current practice to utilize every maneuver possible to maximize PaO2 in at risk patients who present to the OR. I generally estimate risk utilizing a combination of factors including the SCENIC score (although I do not necessarily chart of format pt value for each patient), surgical setting (emergent/elective), type of operation (bowell vs. highly vascular site) surgical duration etc. In most cases FiO2 for short duration is harmless, and therefore that is my default. I typically avoid Nitrous (not necessarily because N2O has been shown to be a risk factor for SSI itself [26], but because it requires FiO2< 1.0. I assiduously avoid hypovolemia in at risk cases (large abdominal case) and use hespan is necessary. I am careful to maintain etCO2 of 45 mmHg in at risk cases per the studies mentioned above. I always offer epidural anesthesia and discuss the risks and benefits with those patients what would benefit. SSI can be devastating for patients, results in greater mortality, and cost to our healthcare system. The anesthesiologist is plays a critical role in this outcome since it has been demonstrated that the critical or decisive period is within two hours of inoculation, for antibiotics and up to 6 hours with regards to oxygen therapy.
I want to conclude with a note on blood transfusion. It is well known that blood transfusion results in immunosuppression and therefore should be avoided in those patients who are at risk for SSI. Some may be tempted to transfuse blood to someone who with a decreased Hbg in order to improved oxygen delivery (DO2) to the tissues so that neutrophils can have substrate to perform their bactericidal duties. However, while DO2 is certainly a function of Hgb, this is only true in vessel rich tissues, but is not at all the case in wounds where intercapillary distances are large. At these sites, oxygen delivery is more a function of adequate perfusion and oxygen tension (i.e. PaO2 and PsqO2). Therefore, transfusions of blood should only be considered if DO2 to critical organs is deemed inadequate.
1. Kurz A et al. Perioperative Normothermia to reduce the incidence of surgical wound infection and shorten hospitalization. NEJM Vol 334, No. 19, 1996
2. Hopk HW, Hunt TK, West JM et al. Wound tissue oxygen tension predicts the risk of wound infection in surgical patients. Arch Surg. 1997;132:997-1005
3. Allen DB, Maguire JJ et al. Wound hypoxia and acidosis limit neutrophil bacterial killing mechanisms. Arch Surg. 1997 Sep;132(9):991-6.
4. Knighton DR, Halliday B, Hunt TK. Oxygen as an antibiotic: the effect of inspired oxygen on infection. Arch Surg. 1984; 119:199-204.
5. Knighton DR, Halliday B, Hunt TK. Oxygen as an antibiotic: a comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg. 1986. 121:191-195.
6. Hopk HW, Hunt TK, West JM et al. Wound tissue oxygen tension predicts the risk of wound infection in surgical patients. Arch Surg. 1997;132:997-1005.
7. Greif R, Akca O, et al. Supplemental Perioperative Oxygen to Reduce the Incidence of Surgical-Wound Infection. N Engl J Med. 2000 Jan 20;342(3):161-7.
8. Dellinger PE. Increasing Inspired Oxygen to Decrease Surgical Site Infection. JAMA. V. 294, N. 16 Oct 2005.
9. Okca O, et al. Effect of intraoperative End tidal CO2 on oxygen tension. Anesthesia, V. 58, 2003.
10. Edith F, Friedrich H et al. Mild Hypercapnia Increases SQ and Colonic oxygen tension in pts given 80% FiO2 during abdominal surgery. Anesthesiology. 2006 V 104: 944.
11. Jonsson K et al. Assessment of perfusion in postoperative patients using tissue oxygen measurements. Br J Surg. 1987 Apr;74(4):263-7.
12. Arkilic C. Supplemental perioperative fluid administration increases tissue oxygen pressure. Surgery Jan 2003
13. Kabon B, Akca O, Taguchi A. Supplemental IV Crystalloid administration Does Not Reduce the Risk of Surgical Wound Infection. Anes Analg. 2005;101:1546
14. Lang K, et al. Colloids vs. Crystalloids and Tissue Oxygen Tension in Patients undergoing Major Abdominal Surgery. Anesth Analg 2001; 93:405
15. Akca O et al. Post-operative Pain and SQ oxygen tension. Lancet 1999; vol 354: 42
16. Block BM, Liu SS, Rowlingson AJ, Cowan AR, Cowan JA Jr, Wu CL. JAMA. 2003 Nov 12;290(18):2455-63.
17. Wu CL, Cohen SR, Richman JM, Rowlingson AJ, Courpas GE, Cheung K, Lin EE, Liu SS.Anesthesiology. 2005 Nov;103(5):1079-88; quiz 1109-10.
18. Treschan TA et al. Effects of Epidural and General Anesthsia on Tissue Oxygenation. Anesth Analg 2003; 96: 1553
19. Buggy DJ. Paraveterbral anesthesia increases post op flap tissue oxygen tension….compared to IV opioids analgesia. Anesthesiology 2004; 100;375
20. Buggy DJ, Dougherty DL. Postoperative Wound oxygenation with epidural or intravenous Analgesia. Anesthesiology 2002; 97:952.
21. Kabon B et al. Thoracic Epidural Anesthesia Increases Tissue Oxygenation During Major Abdominal Surgery. Anesth Analg 2003; 97:1812 .
22. Fleischman E. et al. Tissue oxygenation in obese and non-obese patients during laparoscopy. Obes Surg. 2005 Jun-Jul;15(6):813-9
23. Kabon B, Nagele A, Reddy D, Eagon C, Fleshman JW, Sessler DI, Kurz A. Obesity decreases perioperative tissue oxygenation Anesthesiology. 2004 Feb;100(2):274-80.
24. Pryor KO, Fahe TJ et al. Surgical Site infectin and the Routine Use of Perioperative Hyperoxia in a General Surgical Population: RCT. JAMA. Vol 291, No.1 Jan 2004.
25. Akca O, Podolsky A, Eisen huber E et al. Comparable postoperative pulmonary atelectasis in patient given 30% or 80% oxygen during and 2 hours after colon resection. Anesthesiology 1999;91:991-8.
26. Fleischmann E. Et al. Lancet 2005;366:1101-1107