Changing pattern of the intraoperative blood pressure during endoscopic adrenalectomy in patients with Conn's syndrome.

BACKGROUND: Primary hyperaldosteronism caused by an aldosterone-producing adenoma of the adrenal gland is regarded as the most common type of endocrine hypertension. The aim of this study was to analyze the changing pattern of the intraoperative blood pressure during endoscopic adrenalectomy recorded in patients with Conn's syndrome compared to patients with hormone-inactive incidentaloma and its possible influence by the surgical approach. METHODS: From February 1994 to March 2004, 40 patients underwent endoscopic adrenalectomy for Conn's syndrome. All patients had arterial hypertension over a median period of 84 (5-240) months and were pretreated with an aldosterone antagonist in 76.3% and with specific antihypertensive medication in 85%. Over the same period of time, endoscopic adrenalectomy was carried out in 80 patients with incidentaloma. Of these, 41 (53.2%) displayed arterial hypertension requiring drug therapy. RESULTS: The adrenal gland was resected using the retroperitoneal in 25 and the transperitoneal approach in 15 patients with Conn's syndrome. Conversion to an open procedure was required in two patients. Intraoperative increases in blood pressure necessitating antihypertensive therapy were observed in 17 of 40 patients (44.7%), in 11 of 40 patients (28.9%) blood pressure peaks of >200 mmHg (> 1 min) were noted. Differences between the preoperative and maximum intraoperative blood pressure were significant for the retroperitoneal approach only (systolic: p = 0.0001; diastolic: p = 0.0005), but not for the transperitoneal technique. The increase in intraoperative blood pressure in patients with Conn's syndrome was significantly higher, for both systolic (p < 0.0001) and diastolic (p = 0.0037) readings, compared to that in patients with incidentaloma undergoing endoscopic adrenalectomy during the same period of time. CONCLUSION: Our results demonstrate that relevant intraoperative increases in blood pressure occur in patients with Conn's syndrome despite prior therapy with an aldosterone antagonist, necessitating specific precautionary measures during anesthesia. Intraoperative blood pressure was significantly higher for the retroperitoneal than for the transperitoneal procedure, which leads us to advocate the latter approach for endoscopic adrenalectomy.

[Paraneoplastic lupus anticoagulans syndrome]. / Paraneoplastisches Lupus antikoagulans Syndrom. Eine seltene Gerinnungsstörung.

The antiphospholipid antibody syndrome (Lupus anticoagulans syndrome) is a rare form of coagulopathy due to the presence of autoantibodies against phospholipids or phospholipid-binding protein cofactors that can lead to vascular thrombosis. We report the case of a 57-year-old female patient presenting with decompensated duodenal stenosis due to a pancreatic tumor. Perioperative testing of coagulation markers revealed with 26 % a strongly decreased Quick-Test and with 81.4 s a prolonged partial thromboplastin time that persisted despite intravenous application of 80 mg vitamin K (Konakion) and 10 units of fresh frozen plasma. Subsequent screening for common causes of thrombophilia revealed antiphospholipid antibodies. Consequently, low molecular weight heparin (Dalteparin-Natrium) was administered perioperatively while a gastroenterostomy with entero-enterostomy was performed with uneventful postoperative course. With this presentation and an analysis of the contemporary literature we would like to discuss different aspects of Lupus anticoagulans syndrome.

Fructose-1,6-bisphosphate and MK-801 by aortic arch flush for cerebral preservation during exsanguination cardiac arrest of 20 min in dogs. An exploratory study.

In our exsanguination cardiac arrest (CA) outcome model in dogs we are systematically exploring suspended animation (SA), i.e. preservation of brain and heart immediately after the onset of CA to enable transport and resuscitative surgery during CA, followed by delayed resuscitation. We have shown in dogs that inducing moderate cerebral hypothermia with an aortic arch flush of 500 ml normal saline solution at 4 degrees C, at start of CA 20 min no-flow, leads to normal functional outcome. We hypothesized that, using the same model, but with the saline flush at 24 degrees C inducing minimal cerebral hypothermia (which would be more readily available in the field), adding either fructose-1,6-bisphosphate (FBP, a more efficient energy substrate) or MK-801 (an N-methyl-D-aspartate (NMDA) receptor blocker) would also achieve normal functional outcome. Dogs (range 19-30 kg) were exsanguinated over 5 min to CA of 20 min no-flow, and resuscitated by closed-chest cardiopulmonary bypass (CPB). They received assisted circulation to 2 h, mild systemic hypothermia (34 degrees C) post-CA to 12 h, controlled ventilation to 20 h, and intensive care to 72 h. At CA 2 min, the dogs received an aortic arch flush of 500 ml saline at 24 degrees C by a balloon-tipped catheter, inserted through the femoral artery (control group, n=6). In the FBP group (n=5), FBP (total 1440 or 4090 mg/kg) was given by flush and with reperfusion. In the MK-801 group (n=5), MK-801 (2, 4, or 8 mg/kg) was given by flush and with reperfusion. Outcome was assessed in terms of overall performance categories (OPC 1, normal; 2, moderate disability; 3, severe disability; 4, coma; 5, brain death or death), neurologic deficit scores (NDS 0-10%, normal; 100%, brain death), and brain histologic damage scores (HDS, total HDS 0, no damage; >100, extensive damage; 1064, maximal damage). In the control group, one dog achieved OPC 2, one OPC 3, and four OPC 4; in the FBP group, two dogs achieved OPC 3, and three OPC 4; in the MK-801 group, two dogs achieved OPC 3, and three OPC 4 (P=1.0). Median NDS were 62% (range 8-67) in the control group; 55% (range 34-66) in the FBP group; and 50% (range 26-59) in the MK-801 group (P=0.2). Median total HDS were 130 (range 56-140) in the control group; 96 (range 64-104) in the FBP group; and 80 (range 34-122) in the MK-801 group (P=0.2). There was no difference in regional HDS between groups. We conclude that neither FBP nor MK-801 by aortic arch flush at the start of CA, plus an additional i.v. infusion of the same drug during reperfusion, can provide cerebral preservation during CA 20 min no-flow. Other drugs and drug-combinations should be tested with this model in search for a breakthrough effect.

Intraperitoneal, but not enteric, adenosine administration improves survival after volume-controlled hemorrhagic shock in rats.

OBJECTIVE: To circumvent the potential adverse systemic side effects of adenosine, this study explored the potential benefit of intraperitoneal or enteric adenosine on survival and inflammatory responses after volume-controlled hemorrhagic shock. DESIGN: Prospective, randomized, and blinded. A three-phase, volume-controlled hemorrhagic shock model was used: hemorrhagic shock phase (120 mins), resuscitation phase (60 mins), and observation phase (72 hrs). Three groups were compared: controls, intraperitoneal adenosine, and enteric adenosine. SETTING: Animal research facility. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Starting at 20 mins of hemorrhagic shock and continuing through the resuscitation phase, all three groups received both intraperitoneal lavage and repeated bolus injections into the ileum of vehicle (normal saline) or adenosine. In the intraperitoneal adenosine group (n = 10), adenosine solution (0.1 mM) was used for intraperitoneal lavage. In the enteric adenosine group (n = 10), adenosine (1.0 mM) was injected into the ileum. Blood cytokine concentrations and leukocyte infiltration in lungs and liver were studied in 12 separate rats (control and intraperitoneal adenosine, n = 6 each) with the same hemorrhagic shock model at resuscitation time 1 hr or 4 hrs. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure and heart rate were similar between the three groups during hemorrhagic shock and resuscitation. Potassium, lactate, and blood urea nitrogen concentrations were lower and arterial pH was higher in the intraperitoneal and enteric adenosine groups compared with the control group (both p <.05). Survival time to 72 hrs was longer in the intraperitoneal adenosine group than in the control group(p <.05). Neither plasma interleukin-1beta, interleukin-6, interleukin-10, and tumor necrosis factor-alpha concentrations nor leukocyte infiltration in the lungs and liver was different between the control and intraperitoneal adenosine groups. CONCLUSIONS: The administration of adenosine via the intraperitoneal route improves survival time after severe volume-controlled hemorrhagic shock in rats without worsening hypotension or bradycardia. This beneficial effect may not be attributable to effects of adenosine on the inflammatory response.

Thiopental and phenytoin by aortic arch flush for cerebral preservation during exsanguination cardiac arrest of 20 minutes in dogs. An exploratory study.

We are systematically exploring in our exsanguination cardiac arrest (CA) outcome model in dogs suspended animation (SA), i.e. immediate preservation of brain and heart for resuscitative surgery during CA, with delayed resuscitation. We have shown in dogs that inducing moderate cerebral hypothermia with an aortic arch flush of 500 ml normal saline solution of 4 degrees C, at start of CA 20 min no-flow, leads to normal functional outcome. We hypothesized that, using the same model, adding thiopental (or even better thiopental plus phenytoin) to the flush at ambient temperature (24 degrees C), which would be more readily available in the field, will also achieve normal functional outcome. Thirty dogs (20-28 kg) were exsanguinated over 5 min to CA of 20 min no-flow, and resuscitated by closed-chest cardiopulmonary bypass. They received assisted circulation to 2 h, 34 degrees C post-CA to 12 h, controlled ventilation to 20 h, and intensive care to 72 h. At CA 2 min, the dogs received an aortic arch flush of 500 ml saline at 24 degrees C by a balloon-tipped catheter, inserted through the femoral artery (control group 1, n=14). In group 2 (n=9), thiopental (variable total doses of 15-120 mg/kg) was added to the flush and given with reperfusion. In group 3 (n=7), thiopental (15 or 45 mg/kg) plus phenytoin (10, 20, or 30 mg/kg) was given by flush and with reperfusion. Outcome was assessed in terms of overall performance categories (OPC 1, normal; 2, moderate disability; 3, severe disability; 4, coma; 5, brain death), neurologic deficit scores (NDS 0-10%, normal; 100%, brain death), and histologic deficit scores (HDS, total and regional). The flush reduced tympanic temperature to about 36 degrees C in all groups. In control group 1, one dog achieved OPC 1, three OPC 2, six OPC 3, and four OPC 4. In thiopental group 2, two dogs achieved OPC 1, two OPC 3, and five OPC 4. In thiopental/phenytoin group 3, one dog achieved OPC 1, two OPC 3, and four OPC 4 (p=0.5). Median NDS were 36% (IQR 22-62%) in group 1; 51% (IQR 22-56%) in group 2; and 55% (IQR 38-59%) in group 3 (p=0.7). Median total HDS were 67 (IQR 56-127) in group 1; 60 (IQR 52-138) in group 2; and 76 (IQR 48-132) in group 3 (p=1.0). Thiopental and thiopental/phenytoin dogs achieved significantly lower HDS only in the putamen. Thiopental in large doses caused side effects. We conclude that neither thiopental alone nor thiopental plus phenytoin by flush, with or without additional intravenous infusion, can consistently provide 'clinically significant' cerebral preservation for 20 min no-flow. Other drugs and drug-combinations should be tested with this model in search for a breakthrough effect.

Mild hypothermia increases survival from severe pressure-controlled hemorrhagic shock in rats.

BACKGROUND: In previous studies, mild hypothermia (34 degrees C) during uncontrolled hemorrhagic shock (HS) increased survival. Hypothermia also increased mean arterial pressure (MAP), which may have contributed to its beneficial effect. We hypothesized that hypothermia would improve survival in a pressure-controlled HS model and that prolonged hypothermia would further improve survival. METHODS: Thirty rats were prepared under light nitrous oxide/halothane anesthesia with spontaneous breathing. The rats underwent HS with an initial blood withdrawal of 2 mL/100 g over 10 minutes and pressure-controlled HS at a MAP of 40 mm Hg over 90 minutes (without anticoagulation), followed by return of shed blood and additional lactated Ringer's solution to achieve normotension. Hemodynamic monitoring and anesthesia were continued to 1 hour, temperature control to 12 hours, and observation without anesthesia to 72 hours. After HS of 15 minutes, 10 rats each were randomized to group 1, with normothermia (38 degrees C) throughout; group 2, with brief mild hypothermia (34 degrees C during HS 15-90 minutes plus 30 minutes after reperfusion); and group 3, with prolonged mild hypothermia (same as group 2, then 35 degrees C [possible without shivering] from 30 minutes after reperfusion to 12 hours). RESULTS: MAP during HS and initial resuscitation was the same in all three groups, but was higher in the hypothermia groups 2 and 3, compared with the normothermia group 1, at 45 and 60 minutes after reperfusion. Group 1 required less blood withdrawal to maintain MAP 40 mm Hg during HS and more lactated Ringer's solution for resuscitation. At end of HS, lactate levels were higher in group 1 than in groups 2 and 3 (p < 0.02). Temperatures were according to protocol. Survival to 72 hours was achieved in group 1 by 3 of 10 rats, in group 2 by 7 of 10 rats (p = 0.18 vs. group 1), and in group 3 by 9 of 10 rats (p = 0.02 vs. group 1, p = 0.58 vs. group 2). Survival time was longer in group 2 (p = 0.09) and group 3 (p = 0.007) compared with group 1. CONCLUSION: Brief hypothermia had physiologic benefit and a trend toward improved survival. Prolonged mild hypothermia significantly increased survival after severe HS even with controlled MAP. Extending the duration of hypothermia beyond the acute phases of shock and resuscitation may be needed to ensure improved outcome after prolonged HS.

Gut damage during hemorrhagic shock: effects on survival of oral or enteral interleukin-6.

It has been reported that oral interleukin (IL)-6, without deleterious systemic side effects, prevents bacteremia and gut epithelial apoptosis after hemorrhagic shock (HS) in rodents. The goal of this study was to explore potential benefit of oral or enteral IL-6 on the gut and, consequently, on survival in a long-term outcome model of HS in rats. In Study A, 20 rats (control and IL-6, n = 10 per group) were anesthetized by spontaneous breathing of halothane and N2O. The left femoral vein and artery were cannulated. HS was initiated with withdrawal of 3 mL of blood per 100 g body weight over 15 min, and mean arterial pressure was maintained at 40 to 50 mmHg for another 75 min (total HS 90 min) by blood withdrawal or infusion of Ringer's solution. At HS 90 min, resuscitation included reinfusion of shed blood and additional Ringer's solution to restore normotension for 30 min. After awakening at resuscitation time 30 min, the rats received either 300 units IL-6 or the same volume of vehicle (controls) injected into the stomach via a feeding cannula. In Study B, 20 rats (control and IL-6, n = 10 per group), fasted overnight, were prepared and treated as in Study A, except that HS was initiated with withdrawal of 2 mL blood per 100 g over 10 min, and mean arterial pressure was maintained at 35-40 mmHg. IL-6 rats received 3,000 units IL-6 in 5 mL of normal saline injected directly into the ileum lumen 20 min after induction of shock and again at resuscitation time 60 min. Control rats received normal saline alone. In both studies, survival was observed to 72 h. In Study A, 7 of 10 rats in the control group and 5 of 10 in the IL-6 group survived to 72 h (NS). Macroscopic assessment of gut injury was not different between the two groups. In Study B, 6 of 10 rats survived to 72 h in each group. Frequency of bacteria growth in liver tissue of 72 h survivors was not different between the two groups. IL-6, administered into the stomach or directly injected into the small intestine lumen, did not protect the gut from ischemic injury, nor did it improve survival following severe HS in rats.

Rapid induction of mild cerebral hypothermia by cold aortic flush achieves normal recovery in a dog outcome model with 20-minute exsanguination cardiac arrest.

OBJECTIVES: Resuscitation attempts in trauma victims who suffer cardiac arrest (CA) from exsanguination almost always fail. The authors hypothesized that an aortic arch flush with cold normal saline solution (NSS) at the start of exsanguination CA can preserve cerebral viability during 20-minute no-flow. METHODS: Twelve dogs were exsanguinated over 5 minutes to CA of 20-minute no-flow, resuscitated by cardiopulmonary bypass, followed by post-CA mild hypothermia (34 degrees C) continued to 12 hours, controlled ventilation to 20 hours, and intensive care to 72 hours. At CA 2 minutes, the dogs received a 500-mL flush of NSS at either 24 degrees C (group 1, n = 6) or 4 degrees C (group 2, n = 6), using a balloon-tipped catheter inserted via the femoral artery into the descending thoracic aorta. RESULTS: The flush at 24 degrees C (group 1) decreased tympanic membrane temperature [mean (+/-SD)] from 37.5 degrees C (+/-0.1) to 35.7 degrees C (+/-0.2); the flush at 4 degrees C (group 2) to 34.0 degrees C (+/-1.1) (p = 0.005). In group 1, one dog achieved overall performance category (OPC) 2 (moderate disability), one OPC 3 (severe disability), and four OPC 4 (coma). In group 2, four dogs achieved OPC 1 (normal), one OPC 2, and one OPC 3 (p = 0.008). Neurologic deficit scores (0-10% normal, 100% brain death) [median (25th-75th percentile)] were 62% (40-66) in group 1 and 5% (0-19) in group 2 (p = 0.01). Total brain histologic damage scores were 130 (62-137) in group 1 and 24 (10-55) in group 2 (p = 0.008). CONCLUSIONS: Aortic arch flush of 4 degrees C at the start of CA of 20 minutes rapidly induces mild cerebral hypothermia and can lead to normal functional recovery with minimal histologic brain damage. The same model with aortic arch flush of 24 degrees C results in survival with brain damage in all dogs, which makes it suitable for testing other (e.g., pharmacologic) preservation potentials.

Rapid hypothermic aortic flush can achieve survival without brain damage after 30 minutes cardiac arrest in dogs.

BACKGROUND: Neither exsanguination to pulselessness nor cardiac arrest of 30 min duration can be reversed with complete neurologic recovery using conventional resuscitation methods. Techniques that might buy time for transport, surgical hemostasis, and initiation of cardiopulmonary bypass or other resuscitation methods would be valuable. We hypothesized that an aortic flush with high-volume cold normal saline solution at the start of exsanguination cardiac arrest could rapidly preserve cerebral viability during 30 min of complete global ischemia and achieve good outcome. METHODS: Sixteen dogs weighing 20-25 kg were exsanguinated to pulselessness over 5 min, and circulatory arrest was maintained for another 30 min. They were then resuscitated using closed-chest cardiopulmonary bypass and had assisted circulation for 2 h, mild hypothermia (34 degrees C) for 12 h, controlled ventilation for 20 h, and intensive care to outcome evaluation at 72 h. Two minutes after the onset of circulatory arrest, the dogs received a flush of normal saline solution at 4 degrees C into the aorta (cephalad) via a balloon catheter. Group I (n = 6) received a flush of 25 ml/kg saline with the balloon in the thoracic aorta; group II (n = 7) received a flush of 100 ml/kg saline with the balloon in the abdominal aorta. RESULTS: The aortic flush decreased mean tympanic membrane temperature (Tty) in group I from 37.6 +/- 0.1 to 33.3 +/- 1.6 degrees C and in group II from 37.5 +/- 0.1 to 28.3 +/- 2.4 degrees C (P = 0.001). In group 1, four dogs achieved overall performance category (OPC) 4 (coma), and 2 dogs achieved OPC 5 (brain death). In group II, 4 dogs achieved OPC 1 (normal), and 3 dogs achieved OPC 2 (moderate disability). Median (interquartile range [IQR]) neurologic deficit scores (NDS 0-10% = normal; NDS 100% = brain death) were 69% (56-99%) in group I versus 4% (0-15%) in group II (P = 0.003). Median total brain histologic damage scores (HDS 0 = no damage; > 100 = extensive damage; 1,064 = maximal damage) were 144 (74-168) in group I versus 18 (3-36) in group II (P = 0.004); in three dogs from group II, the brain was histologically normal (HDS 0-5). CONCLUSIONS: A single high-volume flush of cold saline (4 degrees C) into the abdominal aorta given 2 min after the onset of cardiac arrest rapidly induces moderate-to-deep cerebral hypothermia and can result in survival without functional or histologic brain damage, even after 30 min of no blood flow.

Pharmacokinetics and pharmacodynamics of hydroxyethyl starch in hypovolemic pigs; a comparison of peripheral and intraosseous infusion.

Intraosseous (i.o.) infusion is considered a useful technique for the administration of medications and fluids in emergency situations when peripheral intravascular access is not possible. This study investigated the effectiveness of i.o. versus intravenous (i.v.) infusion of hydroxyethyl starch (HES 200/0.5) in hypovolemic pigs. Twenty-three pigs (8- to 9-week-old) were anaesthesized, instrumented and blood was withdrawn (25-30 ml/kg) to < 50 mmHg mean arterial pressure (MAP). The animals were left untreated in haemorrhage for 30 min. Relevant haemodynamic parameters were monitored and blood samples were collected for blood gas and HES concentration analysis. Infusion of HES via i.v. or i.o. line (20 ml/kg per h) carried out over a period of 30 min for volume resuscitation and measurements were taken every 5 min. Infusion was discontinued after 30 min and the animals were monitored for 1 h. Analysis of HES-pharmacokinetics and pharmacodynamics revealed no significant differences between i.o. and the i.v. administration. The results demonstrate i.o. infusion of HES to be a rapid and effective method for fluid resuscitation in hypovolemic shock.

[Resistance to vecuronium--a case report]. / Resistenz gegen Vecuronium--ein Fallbericht.

We observed that a female patient aged 52 undergoing elective surgery (microscopic laryngoscopy and laser resection) was markedly resistant to the action of the neuromuscular blocking drug vecuronium. During induction of anaesthesia with propofol and alfentanil no effect of neuromuscular relaxation was observed even after a total dose of more than 0.15 mg/kg vecuronium. Accelerography was used for monitoring neuromuscular function. Only with small doses of succinylcholine was clinically sufficient relaxation achievable. The patient had no drugs or diseases with known interaction on neuromuscular blocking agents, but a suspected hypothyroidism could be the reason for the resistance.

[The effect of preischemic blood sugar concentration on hemodynamics and regional organ blood flow during and following cardiopulmonary resuscitation (CPR) in swine]. / Zum Einfluss der präischämischen Blutzuckerkonzentration auf Hämodynamik und regionale Organdurchblutung während und nach kardiopulmonaler Reanimation (CPR) beim Schwein.

UNLABELLED: Blood glucose alterations prior to cerebral ischaemia are associated with poor neurologic outcome, possibly due to extensive lactic acidosis or energy failure. Cerebral effects of hyper- or hypoglycaemia during cardiopulmonary resuscitation (CPR) are less well known. In addition, little information is available concerning cardiac effects of blood glucose alterations. The aim of this study was to evaluate the effects of pre-cardiac-arrest hypo- or hyper-glycaemia compared to normoglycaemia upon haemodynamics, cerebral blood flow (CBF) and metabolism (CMRO2), and regional cardiac blood flow during CPR subsequent to 3 min of cardiac and respiratory arrest and after restoration of spontaneous circulation. METHODS: After approval by the State Animal Investigation Committee, 29 mechanically ventilated, anaesthetised pigs were instrumented for haemodynamic monitoring and blood flow determination by the radiolabeled microsphere technique. The animals were randomly assigned to one of three groups: in group 1 (n = 9) blood glucose was not manipulated; in group II (n = 10) blood glucose was increased by slow infusion of 40% glucose to 319 +/- 13 mg/dl; in group III (n = 10) blood glucose was lowered by careful titration with insulin to 34 +/- 2 mg/dl. After 3 min of untreated ventricular fibrillation and respiratory arrest, CPR (chest compressor/ventilator (Thumper) and epinephrine infusion) was commenced and continued for 8 min. Thereafter, defibrillation was attempted, and if successful, the animals were observed for another 240 min. Cerebral perfusion pressure (CPP), CBF, CMRO2, coronary perfusion pressure (CorPP), and regional cardiac blood flow were determined at control, after 3 min of CPR, and at 10.30, and 240 min post-CPR. RESULTS: In group 1. 4/9 animals (44%) could be successfully resuscitated; in group II 4/10 (40%); and in group III 0/10 (0%). Prior to cardiac arrest, mean arterial pressure, CPP, and CorPP in group III were significantly lower compared to groups I and II. In group I. CPP during CPR was 26 +/- 6 mmHg; CBF 31 +/- 9 ml/ min/100g CMRO2 3.8 +/- 1.2 ml/ min/100 g; CorPP 18 +/- 5 mmHg; and left ventricular (LV) flow 35 +/- 15 ml/min/100 g. In group II; CPP = 21 +/- 5; CBF 21 +/- 7; CMRO2 1.8 +/- 0.8; CorPP 16 +/- 6; and LV flow 22 +/- 9; and in group III: CPP 15 +/- 3; CBF 11 +/- 8; CMRO2 1.5 +/- 1.1; CorPP 4 +/- 2; and LV flow 19 +/- 10. During the 240-min post-resuscitation period, there were no differences in CBF, CMRO2, or LV flow between groups I and II. CONCLUSION: Hypoglycaemia prior to cardiac arrest appears to be predictive for a poor cardiac outcome, whereas hyperglycaemia does not impair resuscitability compared to normoglycaemia. In addition, hyperglycaemia did not affect LV flow, CBF, or CMRO2. However, it has to be kept in mind that haemodynamics and organ blood flow do not permit conclusions with respect to functional neurologic recovery or histopathologic damage to the brain, which is very likely to be associated with hyperglycaemia.

[Combination of intravenous patient-controlled analgesia with epidural anesthesia for postoperative pain therapy]. / Kombination einer intravenösen Patientenkontrollierten Analgesie mit Epiduralanästhesie zur postoperativen Schmerztherapie.

The aim of this study was to prove the hypothesis that a combination of epidural anaesthesia with intravenous patient-controlled analgesia (PCA) could improve perioperative pain management. Patients of the urological department undergoing lower abdominal surgery were randomized for two different pain managements. Patients of group 1 (n = 37) were narcotized, intubated and ventilated for the operation; arriving at the recovery room, they were given a PCA-pump, the drug used was piritramide and the parameters were bolus 2.5 mg, blocking time 20 minutes and no basal infusion rate. In group 2 (n = 37) an epidural catheter was inserted preoperatively followed by narcosis with intubation and ventilation. Additionally, epidural anaesthesia was performed intraoperatively using bupivacaine 0.5%. For postoperative pain management, patients of group 2 were also given a PCA-pump (same parameters as mentioned above) and a continuous epidural infusion was started additionally (bupivacaine 0.1875%, infusion rate 8 ml/h). Patients were monitored at the urological ICU for 36 hours. Assessment of pain (6-degree scale), grade of sedation (4-degree scale), cumulative doses of piritramide, heart rate, blood pressure, respiratory rate, in group 2 additional motoric function (Bromage) and degree of epidural anaesthesia were recorded at fixed time intervals: 0, 1, 2, 3, 5, 8, 11, 15, 19, 24, 28, 32, 36 hours. There was no difference regarding age of patients or type of operation. Assessment of pain showed a significant pain reduction in group 2 compared to group 1 during the first 8 hours. This result was underlined by a significantly smaller dose of piritramide. All other parameters showed no differences except lower blood pressure and heart rate in group 2 for the first three hours. The benefits of better pain management contrast with the risks resulting from combining the two techniques. In our patients we found an improvement of pain management in the early postoperative period. The combination of epidural anaesthesia with intravenous patient-controlled analgesia can be regarded as a further possibility for treating postoperative pain in the sense of "balanced pain management".