Reduction of postischemic edema with hyperbaric oxygen

In recent years, reports have shown positive effects of hyperbaric oxygen (HBO) treatment in posttraumatic circulatory insufficiency of the extremities. A tourniquet model for temporary ischemia was used to examine such treatment in rats. The circulation of the rat hindlimb was interrupted for 3 hours, while the contralateral uninjured leg served as control. There was a significant (p less than 0.001) postischemic edema in the tourniquet leg up to 48 hours after restoration of circulation. One group of animals received treatment with hyperbaric oxygen at 2.5 atmospheres absolute (ATA) for 45 minutes after release of the tourniquet. This significantly reduced (p less than 0.001) the postischemic edema, and the reduction persisted for 40 hours after the last treatment. It is concluded that hyperbaric oxygen reduces postischemic edema. Hyperbaric oxygen may therefore be useful as an adjuvant in the treatment of acute ischemic conditions when surgical repair alone fails or is not sufficient to reverse the ischemic process.     

Pulseless electrical activity during electroconvulsive therapy: a case report

Background

Arrhythmias resulting in cardiac arrest during electroconvulsive therapy have been reported. Most reported cases of cardiac arrest had asystole as the initial rhythm. Pulseless electrical activity as an initial rhythm of cardiac arrest during electroconvulsive therapy has never been reported. Also, thromboembolism after inflation of pneumatic tourniquet during lower limb surgery has been reported but never following tourniquet inflation during an electroconvulsive therapy.

Case presentation

We report a case involving an 81- year- old female who presented to us for an electroconvulsive therapy for severe depression and developed pulseless electrical activity immediately after electroconvulsive therapy. She was successfully resuscitated and was later found to have bilateral pulmonary emboli with a complete occlusion of the right lower lobe pulmonary artery. The source of embolus was from her left lower extremity deep venous thrombus, which we believe, got dislodged intraoperatively after inflation of pneumatic tourniquet. Our patient not only survived the massive pulmonary embolus, but also showed significant improvement in her mental status compared to her pre-admission level at the time of discharge to a sub-acute rehabilitation centre.

Conclusion

We recommend that patients who are elderly and at high risk of thromboembolism should selectively undergo a preoperative doppler ultrasound for deep venous thrombosis. Also, selective application of tourniquet in the upper limb, to monitor for seizure activity, would reduce the incidence of pulmonary thrombo-embolism as embolic events are significantly less from deep venous thromboses of upper extremities when compared to lower extremities.     

Effect of the timing of tourniquet release on postoperative hematoma formation: an experimental animal study

There is a controversy over when to release a pneumatic tourniquet after completing a hand surgical procedure. To study this controversy, we performed a standardized operation with tourniquet inflow occlusion on both lower legs of a series of rabbits. Total tourniquet time and the procedure performed, including intraoperative Bovie electrocautery of actual and potential bleeding points identified with 2.5 X loupe magnification, were identical on the two sides, except for the method of tourniquet release. On one leg, the tourniquet was released and all new bleeding points were controlled prior to wound closure. On the other leg, the tourniquet was released after the wound had been closed and dressed. Animals were injected with technetium-99m-labeled red blood cells and scanned to measure hematoma formation. Qualitatively, we observed more label in the leg whose tourniquet was released after wound closure in 17 of the 20 animals (p less than 0.005). Quantitatively, we also measured more mean label in the leg whose tourniquet was released after the wound was closed (p less than 0.001). Tourniquet release after wound closure was associated with greater hematoma formation.     

Generation, in activation and level of blood kinins during tourniquet shock in rabbits

Traumatic shock was induced by the tourniquet method compressing one thigh during 10 hours. Venous blood samples were taken from control animals, as well as twice in the nervous phase of shock - after application and before removal of the tourniquet, and in the humoral-toxic phase - 1, 3 and 5 hours after tourniquet removal, in groups of 10 animals. Determinations included blood kinin level, and plasma kininogen level, and the activity of kallikreins and kininases in the plasma. It was found that during tourniquet shock a significant change occurred in the whole blood kinin system. Proportionally to the severity of shock the level of free kinins and kallikrein activity increased 3-4, times and the level of kininogen and the activity of kininases decreased, especially 3 hours after tourniquet removal.     

Oxygen-Derived Free Radicals Mediate Liver Damage in Rats Subjected to Tourniquet Shock

The placement of rubber band tourniquets upon rat hind-limbs for 5 h followed by reperfusion of the extremities results in a severe form of circulatory shock characterized by hypotension and death within 24 h of tourniquet release. Oxidative damage to muscle tissue is an early consequence of hind-limb reperfusion on tourniquet release, yet this local damage does not explain the lethal hypotensive shock state which evolves within the next 24 h. Multiple system organ failure (MSOF), of as of yet unknown causes, is usually described in relation to several shock states. It has been suggested that injured or necrotic tissue may activate neutrophils, platelets, and the coagulation system leading to embolization in remote tissues. Effective decreases in hepatic blood flow have been observed in several forms of sepsis which precedes the biochemical evidence consistent with an ischemic insult of the liver. In support of our original hypothesis, that organ failure has its genesis in a primary perfusion abnormality with secondary ischemic organ injury, herein we have assessed the possibility that oxygen-derived free radicals are generated in the liver of rats after reperfusion of their hind-limbs on release of the tourniquets. We report on the protective effects of allopurinol (ALLO) and a mixture of superoxide dismutase (SOD) catalase (CAT) and dimethylfulfoxide (DMSO) on liver free sulfhydryl content (SH), thiobarbituric acid-reactive substances (TBARS), and on the release of aspartic acid (AsT) and alanine aminotransferase (AIT) activities, and of alkaline phosphatase during a 5 h tourniquet period and after 2 h of reperfusion of the hind-limbs. During the hind-limb ischemic period hepatis tissue SH levels remained essentially constant during the first hour (6.02 ± 0.36 to 5.65 ± 0.20 μmoles/g wet tissue), and decreased significantly, over and above the normal circadian decrease of liver glutathione levels, to 4.02 ± 0.69 μmoles/g wet tissue after the third hour and remained lowered until tourniquet release. A further significant decrease (3.11 ± 0.49 μmoles/g wet tissue) was observed after 2h of reperfusion. TBARS production remained constant during the 5 h hind-limb ischemic period (168.4 ± 37.3 μmoles/g wet tissue) and rose by 55+ to 261.7 ± 55.8 μmoles/g wet tissue after 2 h of tourniquet release. ALLO, but not the SOD-CAT-DMSO combination, protected hepatic SH loss during the hind-limb ischemic insult, yet both offered protection after 2 h of tournoquet release. With regard to TBARS production, ALLO and the SOD-CAT-DMSO mixture had no effect on basal levels during the ischemic period, but both significantly reduced liver TBARS production after the two hour reperfusion period of hind limb reperfusion. Plasma AsT levels rose 8-fold from 99.4 ± 7.2 to 193 ± 17.0 U/L after the 5-hour tourniquet period, and to 844.8 ± 75.1 U/L two hours after hind-limb reperfusion. The plasma levels of AsT were significantly lower in both the ALLO and SOD-CAT-DMSO pre-treated animals. This was not the case with plasma AIT levels which increased 3-fold during the reperfusion period, but which could not be protected with these same pre-treatment protocols. Alkaline phosphatase plasma levels increased 2-fold during the same period. It is concluded that oxidative stress to the liver, as a result of himd-limb ischemia followed by reperfusion, is partly responsible for the MSOF which leads to circulatory derangements and death of rats subjected to this tourniquet shock model.     

Oxygen-Derived Free Radicals Mediate Liver Damage in Rats Subjected to Tourniquet Shock

The placement of rubber band tourniquets upon rat hind-limbs for 5 h followed by reperfusion of the extremities results in a severe form of circulatory shock characterized by hypotension and death within 24 h of tourniquet release. Oxidative damage to muscle tissue is an early consequence of hind-limb reperfusion on tourniquet release, yet this local damage does not explain the lethal hypotensive shock state which evolves within the next 24 h. Multiple system organ failure (MSOF), of as of yet unknown causes, is usually described in relation to several shock states. It has been suggested that injured or necrotic tissue may activate neutrophils, platelets, and the coagulation system leading to embolization in remote tissues. Effective decreases in hepatic blood flow have been observed in several forms of sepsis which precedes the biochemical evidence consistent with an ischemic insult of the liver. In support of our original hypothesis, that organ failure has its genesis in a primary perfusion abnormality with secondary ischemic organ injury, herein we have assessed the possibility that oxygen-derived free radicals are generated in the liver of rats after reperfusion of their hind-limbs on release of the tourniquets. We report on the protective effects of allopurinol (ALLO) and a mixture of superoxide dismutase (SOD) catalase (CAT) and dimethylfulfoxide (DMSO) on liver free sulfhydryl content (SH), thiobarbituric acid-reactive substances (TBARS), and on the release of aspartic acid (AsT) and alanine aminotransferase (AIT) activities, and of alkaline phosphatase during a 5 h tourniquet period and after 2 h of reperfusion of the hind-limbs. During the hind-limb ischemic period hepatis tissue SH levels remained essentially constant during the first hour (6.02 ± 0.36 to 5.65 ± 0.20 μmoles/g wet tissue), and decreased significantly, over and above the normal circadian decrease of liver glutathione levels, to 4.02 ± 0.69 μmoles/g wet tissue after the third hour and remained lowered until tourniquet release. A further significant decrease (3.11 ± 0.49 μmoles/g wet tissue) was observed after 2h of reperfusion. TBARS production remained constant during the 5 h hind-limb ischemic period (168.4 ± 37.3 μmoles/g wet tissue) and rose by 55+ to 261.7 ± 55.8 μmoles/g wet tissue after 2 h of tourniquet release. ALLO, but not the SOD-CAT-DMSO combination, protected hepatic SH loss during the hind-limb ischemic insult, yet both offered protection after 2 h of tournoquet release. With regard to TBARS production, ALLO and the SOD-CAT-DMSO mixture had no effect on basal levels during the ischemic period, but both significantly reduced liver TBARS production after the two hour reperfusion period of hind limb reperfusion. Plasma AsT levels rose 8-fold from 99.4 ± 7.2 to 193 ± 17.0 U/L after the 5-hour tourniquet period, and to 844.8 ± 75.1 U/L two hours after hind-limb reperfusion. The plasma levels of AsT were significantly lower in both the ALLO and SOD-CAT-DMSO pre-treated animals. This was not the case with plasma AIT levels which increased 3-fold during the reperfusion period, but which could not be protected with these same pre-treatment protocols. Alkaline phosphatase plasma levels increased 2-fold during the same period. It is concluded that oxidative stress to the liver, as a result of himd-limb ischemia followed by reperfusion, is partly responsible for the MSOF which leads to circulatory derangements and death of rats subjected to this tourniquet shock model.     

Dupuytren's fasciectomies in 60 consecutive digits using lidocaine with epinephrine and no tourniquet

Dupuytren's contracture is a common hand problem. Its treatment, other than percutaneous fasciectomy, is an outpatient operation performed with the patient under regional or general anesthesia. If local anesthetics are used, they are used without epinephrine, and an arm or forearm tourniquet is essential. Multiple reviews have described the safety of local anesthetics with epinephrine in the digits. This study is a retrospective review of operations performed by the same surgeon in the hospital (43 digits) versus the office using local anesthetics with epinephrine and no tourniquet (60 digits). Results and complications were compared and tabulated. The hospital and epinephrine groups were comparable regarding preoperative measurements. Postoperative improvement in extension at the metacarpophalangeal and proximal interphalangeal joints was similar in both the hospital and epinephrine groups. Complications, including digital nerve and artery injuries, infections, and hematomas, were similar between the groups. There were no cases of digital necrosis or gangrene in the epinephrine group, even though one patient sustained a transection of a digital artery at the proximal interphalangeal joint. Because of the similarities in results and complications, there does not seem to be an advantage to performing Dupuytren's excisions with full arm tourniquet and outpatient admission in many cases. Local anesthetics with epinephrine are safe in the treatment of Dupuytren's contracture, although both the use of digital epinephrine and the use of mechanical tourniquets carry the potential for complications. Visibility is similar to that for facial or head and neck surgery and is aided by the use of loupe magnification. The old dogma against its use in the fingers is refuted, as seen by the results in these 60 consecutive Dupuytren's fasciectomies and the results of other authors.     

Effects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma.

Proopiomelanocortin (POMC) is expressed in pituitary, central nervous system, and in a few peripheral tissues. This study addresses the hypothesis that metabolic stressors, such as acidosis, may induce the release of POMC derivatives into the cardiovascular system not only from the pituitary but also from other sites of POMC expression. In our study, we investigated the liberation of POMC derivatives from peripheral tissues under a state of acidosis achieved by tourniquet-induced ischemia, alteration of lactate concentration, and base excess. In eight patients undergoing knee arthroplasty under spinal anesthesia, catheters were inserted into the femoral vein proximally to thigh tourniquet location. Blood was drawn from these catheters 5 min before and 40 s, 5 min, and 10 min after tourniquet deflation to measure plasma concentrations of N-acetyl-beta-endorphin immunoreactive material (IRM), beta-endorphin IRM, authentic beta-endorphin, adrenocorticotropin, lactate, pH, and base excess. In five of eight patients, we found a significant increase of beta-endorphin IRM levels 40 s after tourniquet deflation compared with predeflation levels; 5 and 10 min after tourniquet deflation, the beta-endorphin IRM levels were below the detection limit. Thus beta-endorphin IRM was released from ischemic limb tissues into the cardiovascular system. Only a small part of the determined beta-endorphin IRM corresponded to authentic beta-endorphin. Forty seconds after tourniquet deflation, the beta-endorphin IRM concentration correlated with base excess (r < 0.71; P < 0.05); no significant correlations were found with pH or lactate levels. Thus it was shown here for the first time that ischemic stress may induce the release of beta-endorphin IRM from nonpituitary tissues.     

XPD and hOGG1 gene polymorphisms in reperfusion oxidative stress

Knee replacement surgery is an ischemia/reperfusion model, as it uses tourniquet applied to the knee area to stop the blood flow during the operation. Fifty patients that were undergoing elective arthroscopic knee surgery were included in our study. Human 8-oxoguanine glycosylase 1 (hOGG1) is an enzyme to repair specific DNA lesions and a good marker of hydroxyl radical damage to DNA. XPD is another DNA repair gene. We investigated the effect of hOGG1 (Ser326Cys) and XPD (Lys751Gln) polymorphisms on the oxidative stress level after reperfusion. To evaluate oxidative stress conditions, we measured 8-hydroxyguanosine and malondialdehyde (MDA) levels. Polymorphism analyses were done by PCR-RFLP; serum 8-hydroxyguanosine and MDA levels were determined by enzyme-linked immunoassay. There were no significant differences between serum MDA and 8-hydroxyguanosine levels in the samples taken before and after tourniquet application; none of these parameters were related with hOGG1 genotypes. However, we observed increased MDA levels after tourniquet application in M allele carriers for the XPD gene; this could mean that M allele carriers are more prone to DNA damage due to oxidative activity.     

Biomarkers of oxidative stress and endothelial dysfunction after tourniquet release in children

Pneumatic tourniquets are widely used in pediatric extremity surgery to provide a bloodless field and facilitate dissection. This prospective study was carried out to examine possible effect of different anesthesia techniques on oxidative stress and endothelial dysfunction connected with ischemia-reperfusion injury during extremity operations at children's age. Patients were randomized into three groups of 15 patients each: general inhalational anesthesia with sevoflurane (group S), total intravenous anesthesia with propofol (group T) and regional anesthesia (group R). Venous blood samples for determination of the malondialdehyde in plasma and erythrocytes, protein carbonyl groups concentration as well as plasma nitrites and nitrates level and xanthine oxidase activity were obtained at four time points: before peripheral nerve block and induction of general anesthesia (baseline), 1 min before tourniquet release, 5 and 20 min after tourniquet release. This study demonstrates that total intravenous anesthesia with propofol and regional anesthesia techniques provide better antioxidant defense and reduce endothelial dysfunction than general inhalational anesthesia with sevoflurane during tourniquet application in pediatric extremity surgery.     

Effect of proteolytic enzyme inhibitors on lung cell population function in normal mice and in the development of tourniquet shock

Cell populations of mice lungs have been studied for variations in the lavage and lumen of the alveoli. The development of the tourniquet shock induces a decrease in the number of macrophages and lymphocyte and an increase in the number of neutrophils, erythrocytes and epithelium cells. Application of the proteolysis enzyme inhibitors is found to stabilize the bronchoalveolar barrier and to prevent these changes.     

Axisymmetric finite element analysis of tourniquet application on limb

An axisymmetric finite element model of cuff on limb was developed. The model was used to simulate a clinical experiment by others in which the fluid pressure was measured at various points under a blood pressure cuff; the distribution of calculated hydrostatic stress was consistent with the clinical results. Simulations involving varying degrees of rounding at the edges of a tourniquet suggested that ensuring such rounding decreases maximum octahedral shear stress; this finding was consistent with studies by others using a two-dimensional physical model. The calculated stresses were highest at the tourniquet edges; this was consistent with nerve conduction and photomicrographic studies by others of damage caused by tourniquet use.     

Dependence of skeletal muscle fatigue on the membrane polarization of the different types of muscle fibers in tourniquet shock

Fatigue, polarization level and excitability of striated muscle fibers from ischemia zone were studied on experimental rats under the tourniquet shock. It was established that violation-mediated contraction and fatigue of skeletal muscle was associated with a decrease in a number of muscle fibers with high level of MPP. The article discussed the mechanisms of fatigue and depolarization of muscle fibres in tourniquet shock.     

Pharmacological manipulation of gastrocnemius muscle blood flow in an animal model of reperfusion injury

Despite technically satisfactory surgery for acute lower limb ischaemia reperfusion injury may result in failure of limb salvage and the need for amputation. An animal model using the rat hind limb has been developed which demonstrates this complication. A tourniquet was applied to one hind limb for 6 h and then released. Gastrocnemius muscle blood flow in both hind limbs was assessed using radiolabelled microspheres and a perfusion index calculated between the revascularized and normal hind limbs and the results compared with similar measurements in control animals and rats with a tourniquet still in situ (ischaemic). Following 10 min the median perfusion index in reperfused animals was significantly less than that in control animals (0.12 ± 2 inter-quartile range 0.02–0.43) versus 1.05 (0.68–1.18), P < 0.01) but similar to the results in rats with a tourniquet still in situ [0.04 (0.00–0.07), ns], thus demonstrating low reflow following tourniquet release. After 120 min revascularization a phase of relative reperfusion occurred with perfusion indices becoming higher than those in animals with a tourniquet in situ (0.48 (0.11–0.70) versus 0.02 (0.01–0.07), P < 0.05) but remaining lower than those in control rats [0.97 (0.79–1.13), P < 0.05]. Finally after 240 min, reperfusion injury occurred with perfusion being similar to that in animals with a tourniquet applied [0.05 [0.01–0.38) versus 0.03 (0.00–0.07), ns] and less than that in the normal rats [1.01 (0.73–1.16), P < 0.01]. Attempts to modify these reductions in muscle perfusion pharmacologically have demonstrated that a superoxide radical scavenger (superoxide dismutase and catalase) abolished low reflow (0.94 (0.54–1.12) versus 0.12 (0.02–0.43), P < 0.01). In contrast dimethylthiourea, an hydroxyl radical scavenger, prevented the phase of relative reperfusion (0.04 (0.02–0.21) versus 0.48 (0.11–0.70), P < 0.01. Sodium nitroprusside, a vasodilator, increased perfusion at 240 min [0.41 (0.11–1.22] versus 0.05 (0.01–0.38], P < 0.05] with 6 out of 15 rats having a normal perfusion index at the time when reperfusion injury would be expected to occur.     

A pneumatic tourniquet as an aid to release of capsular contracture around a breast implant

The use of a pneumatic tourniquet to release fibrous capsular contracture around a breast implant is described. This method protects the operator's hands and, we believe, is potentially safer for the patient and for the breast prosthesis.     

Varix of the digit

Varix of the digit is a rarely described lesion. Over 3 years, eight patients were diagnosed as having this abnormality. Surgical confirmation of the identity of the lesion was accomplished in six of these patients. Repetitive trauma, mechanical compression, and aging phlebectasia have all been associated with the pathogenesis of a digital varix. Thrombophlebitic and thrombotic changes occurring within the varix may lead to an erroneous assessment and clinical confusion. In such instances, a tourniquet test has been useful in demonstrating the presence of a varix. Excision of a symptomatic lesion has proven to be curative for all six patients. Two patients have been observed for 3 years with little change and no resolution of the varix. It is probable that varix of the digit is a more common lesion than indicated by a review of the literature.     

Effect of the duration of the previous ischemia and of the mass of ischemic tissue on the state of the coagulating and anticoagulating blood systems in tourniquet shock]

In the experiments on 80 rabbits it was shown that the inclusion of the previously ischemized extremities into circulation is accompanied by elevation of coagulating potential of the blood and inhibition of fibrinolysis shortly after the tourniquet removal followed by hypocoagulation and fibrinolysis activation. These changes depend on the duration and mass of previously ischemized tissues. It is suggested that in tourniquet shock these disorders lead either to the danger of intravascular thrombosis or to hypocoagulation with secondary fibrinolysis.     

Near infrared monitoring of human skeletal muscle oxygenation during forearm ischemia

Changes in tissue oxygenation of forearm muscles were measured by near infrared (NIR) spectrophotometry in 10 healthy adults during tourniquet ischemia and venous outflow restriction. Muscle O2 stores were depleted rapidly by forearm ischemia manifest by a progressive decrease in tissue oxyhemoglobin and oxymyoglobin over 4-5 min. Muscle ischemia significantly decreased the oxidation level of cytochrome aa3, to below resting base line after only 1.5 min, and the enzyme became fully reduced after 6.5 min. After 8 min of ischemia, tourniquet release was accompanied by a transient increase in muscle blood volume due to influx of oxyhemoglobin. The cytochrome aa3 oxidation level increased above resting base line within 1 min after tourniquet release. Transcutaneous PO2 measurements recorded simultaneously from the same forearm correlated poorly with the kinetics of O2 availability and cytochrome oxidation in the underlying muscle tissue; this was not unexpected because overlying skin did not contribute significantly to NIR muscle signals. Venous outflow restriction without inflow obstruction increased muscle deoxyhemoglobin and tissue blood volume but did not change muscle O2 stores or cytochrome aa3 oxidation level. The ability of the NIR technique to detect dynamic trends in tissue oxygenation reveals that muscle O2 is rapidly consumed during tourniquet ischemia and rapidly restored by hyperemic responses after brief ischemia.     

Investigation of the role of venous pressure in bone changes during prolonged weightlessness

Several recent studies have suggested roles for venous pressure, intraosseous pressure, and mechanical load in the regulation of bone mass. This paper describes a study conducted during the EuroMIR 95 space mission in which a venous tourniquet system was used to apply intermittent compression to the right ankle of crewmembers. Bone mineral density was then measured using the ultrasonic Bone Densitometer. Hardware development is discussed in detail. Data are in the process of being analyzed and are not presented.