[Epiduritis after long-term pain therapy with an epidural catheter--review of the literature with a current case report]. / Epiduritis nach Langzeitschmerz-therapie mit einem Epiduralkatheter--eine Literaturübersicht mit einem aktuellen Fallbericht.

Patients suffering from vascular disease are often a challenge for the acute pain service. Ischaemia, impaired wound healing, stump and phantom limb pain often require a complex analgesic regimen. Invasive measures such as spinal or epidural catheters can be very helpful but carry the risk of infection, as shown by this case report. A 53-year-old woman with a ten-year history of diabetes developed arterial vascular disease. Her right lower leg had been amputated two years previously. She was now admitted with necroses of the left forefoot. A bypass operation was performed under general anaesthesia. Because of intractable ischaemic pain, she was provided with an epidural catheter by the acute pain service. The bypass occluded, however, and a few days later her left lower leg also had to be amputated, this operation being performed under epidural anaesthesia with bupivacaine. The catheter was subsequently used for postoperative pain control and as a means to prevent phantom limb pain. When signs of superficial catheter infection were noticed days later, the catheter was immediately removed. Intractable pain then developed in the left leg which could not be sufficiently controlled with opioids and NSAIDs, and so a second epidural catheter was inserted one segment rostrally. Several days later the infected vascular prosthesis had to be removed followed by amputation of the thigh, this operation also being performed in epidural anaesthesia. Eleven days after insertion of the first epidural catheter, the patient complained of low back pain and headache. Examination by a neurologist revealed no signs of intraspinal infection. The second epidural catheter dislocated at this point in time and it was decided to introduce a third one, this being the only means to treat the otherwise intractable stump pain. Ten days later meningism, Kernig's sign and leucocytosis developed. NMR tomography detected intraspinal fluid in the epidural space at the dorsal border of the spinal canal. A hemilaminectomy was performed. The spinal epidural space showed signs of inflammation of the adipose tissue, but no pus. A little necrotic material and residues of an old haematoma were removed and the epidural space was lavaged. Specimens taken from the epidural material revealed colonisation with staphylococcus epidermidis, which was sensitive to the broad spectrum antibiotics formerly given to the patient to treat the infection in the left stump. By the next day, all signs of epiduritis had disappeared and the patient recovered completely.

[Differential administration of non-opioids in postoperative analgesia, I. Quantification of the analgesic effect of metamizole using patient-controlled analgesia]. / Untersuchungen zum differenzierten Einsatz von Nichtopioiden zur postoperativen Analgesie I. Quantifizierung des analgetischen Effektes von Metamizol mittels der patientenkontrollierten Analgesie.

OBJECTIVE: The aim of this study was to investigate: 1. Whether the perioperative administration of metamizol causes a significant reduction in postoperative opioid requirements within the first 24 h after surgery. 2. The opioid-sparing effect after different types of operations. 3. Whether preoperative application of metamizol causes a significant reduction of the pain-score immediately after operation. METHODS: In a double-blind, randomised, placebo-controlled study, 117 patients, scheduled for minor orthopaedic or laparoscopic surgery or other operations (mainly resection of the thyroid gland and inguinal herniotomies) received either metamizol (1 g/100 ml NaCl 0.9%) or placebo (100 ml NaCl 0.9%) intravenously over 15 min in three separate doses: the first dose was given just before induction and the others 6 h and 12 h later. After surgery all patients were allowed to self-administer buprenorphine from a PCA (patient-controlled analgesia) pump (Bolus: 30 microgram, lockout: 5 min in the recovery room, 30 min on the ward). Every hour for the first 6 h and after 24 h, cumulated doses of buprenorphine, pain scores (0-10), blood pressure, pulse and side effects were recorded. RESULTS: After minor orthopaedic and laparoscopic surgery, metamizol-treated patients had significantly less pain immediately after surgery and used a significantly lower cumulated dose of opioid in the first 24 h after surgery (-20% and -67% respectively) than patients receiving placebo. After the other types of surgery no analgesic effect could be established. CONCLUSIONS: Perioperative administration of metamizol results in better pain relief and significantly lower buprenorphine requirements particularly after laparoscopic operations. To achieve a significant pain reduction immediately after the operation, the first dose should be applied before induction.

Are the effects of noradrenaline, adrenaline and dopamine infusions on VO2 and metabolism transient?

OBJECTIVE: To determine whether noradrenaline, adrenaline and dopamine have persistent actions on VO2 and metabolism. DESIGN: Descriptive laboratory investigation. SETTING: Laboratory of the Department of Anaesthesiology at a University Hospital. SUBJECTS: 9 volunteers. INTERVENTION: VO2 and the plasma concentration of glucose and free fatty acids were measured prior to and during a 4 h infusion of saline (control), noradrenaline (0.14 microgram/kg min) adrenaline (0.08 microgram/kg min) or dopamine (7 micrograms/kg min), n = 9 each. VO2 was measured using an open circuit gas exchange system. MEASUREMENTS AND MAIN RESULTS: VO2 increased from 250 +/- 22 ml/min to 280 +/- 38 ml/min during noradrenaline, to 298 +/- 30 ml/min during adrenaline and to 292 +/- 39 ml/min during dopamine infusion. The plasma glucose concentration increased from 6.2 +/- 0.6 mmol/l to 8.8 +/- 0.8 mmol/l, 13.2 +/- 1.4 and 7.3 +/- 0.4 mmol/l during infusion of noradrenaline, adrenaline or dopamine, respectively. The plasma free fatty acid concentration increased from 0.28 +/- 0.10 mmol/l to 0.79 +/- 0.21 mmol/l during noradrenaline and to 0.52 +/- 0.09 mmol/l during dopamine. In contrast, free fatty acid values averaged baseline values at the end of the adrenaline infusion after an initial increase to 0.72 +/- 0.31 mmol/l. CONCLUSIONS: Administration of noradrenaline, adrenaline or dopamine resulted in persistent increases in VO2 in volunteers. With the exception of the transient adrenaline effect on fatty acids the metabolic actions were steady during 4 h of adrenergic stimulation. Since the adrenergic effect on VO2 is persistent over time a similar action in patients (e.g. septic shock) during treatment with adrenoceptor agonists may be important. Thus, an increase in VO2 during therapy may not only reflect an oxygen debt but also a pharmacodynamic action of adrenoceptor mediated calorigenic and metabolic induction.

Effects of norepinephrine, epinephrine, and dopamine infusions on oxygen consumption in volunteers.

OBJECTIVE: To determine the relationships between plasma concentrations of norepinephrine, epinephrine, and dopamine and oxygen consumption (VO2) during infusion of these catecholamines. DESIGN: Prospective, randomized variable dose, pharmacologic study in which a noncumulative infusion-rate design was used. SETTING: Laboratory of the Department of Anesthesiology at a University Hospital. PATIENTS: Twenty-one normal volunteers. INTERVENTIONS: After a control period of 20 mins, norepinephrine (three infusion rates; 0.06 to 0.2 microgram/kg/min; n = 7), epinephrine (four infusion rates; 0.02 to 0.2 microgram/kg/min; n = 7), or dopamine (three infusion rates; 3 to 12 micrograms/kg/min; n = 7) was administered to normal volunteers (n = 21) for the purpose of constructing plasma concentration/VO2 response curves. MEASUREMENTS AND MAIN RESULTS: Systolic and diastolic blood pressure, heart rate, plasma concentrations of norepinephrine, epinephrine, and dopamine, and VO2 were measured at the end of the control period and at the end of each catecholamine infusion. VO2 was measured using a ventilated canopy system and a differential oxygen sensor. Typical hemodynamic responses to vasopressors were seen during adrenergic receptor agonist infusions. VO2 increased from 132 +/- 7 to 153 +/- 10 mL/min/m2 during the highest infusion rate of norepinephrine, from 133 +/- 7 to 182 +/- 11 mL/min/m2 during the highest infusion rate of epinephrine, and from 132 +/- 13 to 163 +/- 8 mL/min/m2 during the highest infusion rate of dopamine (p < .05; paired t-test). Increases in VO2 were correlated with the logarithms of the corresponding plasma catecholamine concentrations. Effects on VO2 and hemodynamic responses occurred at similar plasma concentrations for each of the three catecholamines. CONCLUSIONS: Administration of norepinephrine, epinephrine, or dopamine results in marked increases in VO2 in volunteers. In patients, the administration of catecholamines or sympathomimetics to attain optimal values of cardiac index, oxygen delivery (DO2), and VO2 may increase the oxygen demand and thus obscure the DO2-VO2 relationship.

Hemodynamic and metabolic effects of epinephrine during cardiopulmonary resuscitation in a pig model.

BACKGROUND AND METHODS: This study was designed to assess the effect of epinephrine during cardiopulmonary resuscitation (CPR) on left ventricular myocardial blood flow, systemic oxygen delivery and consumption, and on plasma glucose and lactate concentrations. Fourteen pigs were allocated to receive either 0.9% saline (n = 7), or 45 micrograms/kg epinephrine (n = 7) after 5 mins of ventricular fibrillation, and 3 mins of open-chest CPR. Left ventricular myocardial blood flow was measured with radiolabeled microspheres. Plasma catecholamine concentrations were measured by high-pressure liquid chromatography. RESULTS: During open-chest CPR, mean (+/- SD) values of left ventricular myocardial blood flow before, 90 secs, and 5 mins following drug administration were 49 +/- 10, 46 +/- 12, 43 +/- 15 mL/min/100 g, respectively, in the control group, and 52 +/- 12, 118 +/- 21, 84 +/- 28 mL/min/100 g, respectively, in the epinephrine group (p less than .05 at 90 secs and 5 mins). At the same time points, mean (+/- SD) oxygen delivery indices were 7.7 +/- 3.0, 6.0 +/- 2.1, 6.5 +/- 2.7 mL/min/kg in the control group and 7.6 +/- 2.5, 5.3 +/- 2.1, 5.5 +/- 1.9 mL/min/kg in the epinephrine group (nonsignificant). Mean oxygen consumption indices were 5.8 +/- 2.4, 4.6 +/- 1.6, 5.2 +/- 2.6 mL/min/kg in the control group and 5.4 +/- 1.6, 4.2 +/- 1.6, 4.4 +/- 1.4 mL/min/kg in the epinephrine group (nonsignificant). During CPR and before epinephrine administration, arterial plasma epinephrine concentrations increased from prearrest values of 0.77 +/- 0.70 to 62.1 +/- 48.7 micrograms/L, and plasma norepinephrine concentrations increased from 0.28 +/- 0.32 to 104.3 +/- 57.1 micrograms/L. After administered epinephrine, there was an additional increase to 271 +/- 83 micrograms/L at 90 secs in arterial plasma epinephrine, but no important alteration in the plasma norepinephrine concentration. At no time point could we find a clinically important difference in plasma glucose or lactate concentrations between the two groups. CONCLUSIONS: At a dose of 45 micrograms/kg, epinephrine caused an increase in left ventricular myocardial blood flow after a total of 8 mins of cardiac arrest, including 3 mins of CPR, while not altering systemic oxygen delivery and consumption, plasma glucose, or lactate concentrations.

Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers.

Noradrenaline and adrenaline were infused IV at 5 different rates (0.01-0.2 micrograms.kg.min-1) for 30 min to volunteers. The plasma catecholamine concentrations were determined by HPLC and electro-chemical detection. At the highest infusion rate, the arterial and venous plasma concentrations of noradrenaline increased from 1.18 to 44.1 nmol.l-1 and from 1.14 to 31.9 nmol.l-1, respectively, and of adrenaline from 0.29 to 23.9 nmol.l-1 and from 0.28 to 19.3 nmol.l-1, respectively. The peripheral venous plasma concentration of noradrenaline averaged 76% of the arterial concentration, and of adrenaline it was 73%. There was a linear relationship between the peripheral venous and arterial plasma noradrenaline and adrenaline concentrations at therapeutic doses.

Concurrent fast and slow synchronized efferent phrenic activities in time and frequency domain.

In urethane-anesthetized or decerebrated vagotomized rabbits efferent multifiber activity of the phrenic nerve was investigated for synchronized activities both in time and frequency domains. When respiratory drive was steadily increased by either an elevation of end-tidal CO2 concentration or i.v. administration of 4-aminopyridine, medium-frequency oscillations (MFO) first increased, then decreased and finally became absent. The power of high-frequency oscillations (HFO) steadily rose with increasing respiratory drive. In contrast to HFO which revealed a unimodal spectral peak of mostly small bandwidth, the MFO spectrum in most cases consisted of a broad complex. This complex in some cases was composed of two distinct peaks, i.e. MFO were heterogenous. The low- and high-frequency fractions of the MFO complex were related predominantly to the first and last third of inspiration, respectively. Examination of the on-going multifiber activity of the phrenic nerve with an expanded time scale revealed that lower frequency MFO probably result from synchronized ramp-like wave activity during early and mid-inspiration. The duration of the observed ramps well matched the corresponding MFO frequency. We suggest that these ramps might result from propagated synchronized waves of high-threshold phrenic motoneurons. During the last part of inspiration, however, MFO, like HFO, resulted from burst-like synchronized discharge of phenic motoneurons. Thus HFO are superimposed on ramp-like and burst-like activity of the MFO. It is assumed that the decline of MFO at high respiratory drive may be due to the increasing strength of HFO bursts which interrupt ramp activity in the MFO range and thus let MFO appear 'invisible' to the recording electrode. Both MFO and HFO were visually detectable in postinspiration.

[Case report: lumen obstruction with a Magill tube]. / Fallbericht: Lumenverlegung bei einem Magill-Tubus.

A case is reported where a reusable red rubber tube was obstructed by a plastic capsule. This capsule was part of a washing machine for cleaning of reusable anaesthetic equipment. As a consequence we recommend the examination for free passage of each endotracheal tube before use.