Ellen Ejlersen

A comparison between preincisional and postincisional lidocaine infiltration and postoperative pain.

We conducted a randomized, double-blind trial to compare the efficacy of preincisional and postincisional wound infiltration with 1% lidocaine (40 mL) on the postoperative pain of 37 patients scheduled for elective inguinal herniotomy. The demand for additional postoperative analgesics occurred earlier in those who received lidocaine infiltration after incision (165 min) than in those who received preincisional lidocaine (225 min, P less than 0.05). The preincisional lidocaine infiltration group also had fewer patients requiring supplemental analgesics (58%) than the postincisional group (94%) (P less than 0.05). We conclude that preincisional infiltration of the surgical wound with lidocaine is a more effective method of providing postoperative analgesia than is postincisional infiltration.

Preoperative wound infiltration with bupivacaine reduces early and late opioid requirement after hysterectomy.

We conducted a randomized, double-blind trial to evaluate the early and late analgesic effect of preoperative wound infiltration with bupivacaine 0.25% (40 mL) compared to placebo (NaCl 0.9%, 40 mL) in patients undergoing major surgery. Forty-one patients scheduled for elective hysterectomy during general anesthesia were included. The pain management focused on pain prevention, including preoperative administration of nonsteroidal antiinflammatory drugs (NSAIDs), and peroperative administration of opioids. Postoperatively patients received buprenorphine and/or acetaminophen on demand. A significant difference between treatments was evident in the 3-day postoperative trial period. With identical pain scores in the two groups, the requested total amount of buprenorphine was greater in the placebo group (2.0 [0-5.1] mg) (median and [range]) than in the bupivacaine group (0.8 [0-2.8] mg) (P < 0.05). The demand for analgesics occurred earlier in those who received placebo (225 min) than in those who received bupivacaine (345 min), but did not reach the level of significance. In conclusion, preoperative wound infiltration with bupivacaine improved immediate and late postoperative pain management after hysterectomy compared to placebo. (Anesth Analg 1996;83:376-81)

Dissociated cerebral vasoparalysis in acute liver failure A hypothesis of gradual cerebral hyperaemia

BACKGROUND/AIMS Normally, cerebral blood flow responds to changes in the arterial carbon dioxide tension (PaCO2) but not to changes in mean arterial pressure, commonly referred to as the cerebral CO2-reactivity and autoregulation. In patients with fulminant hepatic failure and in the rat with thioacetamide-induced liver failure, autoregulation is absent, presumably due to cerebral vasoparalysis. Since also CO2-reactivity may then be compromised, it was studied in patients with fulminant hepatic failure and rats with thioacetamide-induced liver failure. METHODS In ten patients (median age 32 (range 20-48) years)) and in ten age-matched volunteers, cerebral perfusion was elevated by transcranial Doppler assessed mean flow velocity (V(mean)) in the middle cerebral artery during hypo- and hyper-capnia. In six rats with liver failure and in six control rats, cerebral blood flow was measured repeatedly by the intracarotid 133 Xenon injection technique. RESULTS In the patients and volunteers, PaCO2 was lowered from 33 (23-44) to 28 (23-39) mmHg by hypocapnia and raised to 40 (34-48) mmHg by hypercapnia or 5% CO2 inhalation. During hypocapnia, the CO2-reactivity did not differ significantly between patients and volunteers, 4.0 (1.1-7.4) vs. 3.0 (1.7-5.0)% mmHg(-1), while it was reduced during hypercapnia in the patients, 2.2 (1.8-5.2) vs. 4.6 (3.0-8.0)% mmHg(-1) (p < 0.05). In the rats, PaCO2 was reduced from 39 (37-40) to 30 (29-31) mmHg and then raised to 51 (41-55) mmHg. During hypocapnia, CO2-reactivity was similar in rats with liver failure and in control rats, 2.3 vs 2.7% mmhg(21), respectively. In all rats with liver failure CO2-reactivity was abolished during hypercapnia, while it was 1.5% mmHg(-1) in the control rats (p < 0.01). CONCLUSIONS The finding that cerebral CO2 reactivity is reduced in hypercapnia, while it is preserved in hypocapnia, suggests that gradual dilation of the cerebral resistance vessels develops in fulminant hepatic failure and connects previous morphological studies with changes in the regulation of cerebral blood flow, i.e. impaired cerebral autoregulation and blunted CO2-reactivity.

Epidural clonidine enhances postoperative analgesia from a combined low-dose epidural bupivacaine and morphine regimen

In a randomized, double-blind, placebo-controlled trial, the value of adding clonidine to a low-dose epidural regimen for postoperative pain treatment was assessed. Twenty-four patients scheduled for hysterectomy during combined thoracic epidural (bupivacaine and morphine) and general anesthesia were studied. Postoperative analgesia consisted of epidural bupivacaine (5 mg/h) and morphine (0.1 mg/h) for 12 h. In addition, the patients randomly received clonidine (75 micrograms), followed by an infusion of 18.75 micrograms/h or saline solution (placebo) epidurally. Pain was evaluated at rest, during cough, and during mobilization every hour. Sensory level of analgesia was evaluated by pinprick. We found no significant difference in pain scores at rest between the clonidine and placebo groups but an enhanced analgesic effect by clonidine during cough and mobilization (P less than 0.05). Arterial blood pressure decreased significantly during clonidine infusion and remained lower than in the control group throughout the study. We conclude that a continuous low-dose epidural clonidine infusion enhances analgesia from a combined low-dose epidural bupivacaine and morphine regimen after hysterectomy; however, the concomitant decrease in arterial blood pressure during epidural clonidine deserves further study before such a regimen can be recommended.

Cerebral blood flow, oxygen metabolism and transcranial Doppler sonography during high-volume plasmapheresis in fulminant hepatic failure.

Objective: The effect of high-volume plasmapheresis on hepatic encephalopathy, cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) was investigated in patients with fulminant hepatic failure (FHF). Methods: Twelve consecutive patients (8 women, 4 men, median age 34 years (range 19–51)) were studied before and after high-volume plasmapheresis with 10–16 litres fresh frozen plasma, while PaCO2 and body temperature were maintained at 30 (23–34) mmHg and 37.6°C (36.6–38.4), respectively. Blood samples from the internal jugular vein and a radial artery allowed calculation of the cerebral arteriovenous oxygen difference (AVDO2) and oxygen extraction (AVDO2 divided by arterial oxygen content). CBF was determined by a xenon-133 clearance method in eight patients and CMRO2 calculated as AVDO2 times CBF. Cerebral perfusion pressure (CPP) was determined as the difference between mean arterial and subdural pressures in eight patients. Results: High-volume plasmapheresis was initiated 22 (6–168) h after the development of hepatic encephalopathy and 11 patients had grade 4 encephalopathy. Following high-volume plasmapheresis the grade of encephalopathy improved in four patients. The CBF increased from a median of 31 (16–86) to 45 (18–97) ml/100 g/min and as oxygen extraction remained unchanged (32 (9–41) vs. 29 (7–39)%), CMRO2 increased from 1.24 (0.96–1.82) to 1.86 (1.00–2.07) ml/100 g/min (P<0.05). The CPP increased from 62 (19–76) to 92 (50–105) mmHg (P<0.01), whereas the intracranial pressure remained unchanged (19 (3–45) vs. 11 (5–33) mmHg). No statistical difference was found between the relative changes in the above parameters in survivors compared to non-survivors. Conclusion: Although the clinical status did not improve in all patients, both CBF and CMRO2 increased after high-volume plasmapheresis. The alleviation of brain oxygen metabolism by high-volume plasmapheresis may reflect partial removal of neuroinhibitory plasma factors.

Haemodynamic changes after high-volume plasmapheresis in patients with chronic and acute liver failure

Objective: To evaluate the haemodynamic changes during treatment with highvolume plasmapheresis in patients with chronic liver failure compared to patients with acute liver failure. Methods: Haemodynamic measurements were performed with a Swan‐Ganz catheter and thermodilution technique. High‐volume plasmapheresis (mean plasma exchange of 8.6 litres) was performed in 11 patients with chronic and 16 patients with acute liver failure. Results: In patients with chronic liver failure, systemic vascular resistance index was unaltered: 1193 ± 494 dynscm‐5m2 before treatment versus 1180±399 dynscm‐5m2 after. Mean arterial pressure increased from 69±11 mmHg to 78±13 mmHg (P<0.05) and cardiac output increased from 8.1 ±2.4l/min to 8.9±2.4 l/min (P<0.05) during highvolume plasmapheresis. In patients with acute liver failure, systemic vascular resistance index increased from 1154±628 dyns cm‐5m2 to 1614±738dynscm‐5m2 (P<0.001). In this group mean arterial pressure increased from 78±16mmHg to 95±10mmHg (P< 0.001) and cardiac output decreased from 9.6±3.7l/min to 8.2±2.9 l/min (P<0.01). Conclusion: The hyperkinetic circulation in chronic and acute patients was differently affected by high‐volume plasmapheresis. We suggest that in chronic liver failure both portosystemic shunting and chronic peripheral vasodilation may contribute to the hyperkinetic syndrome, whereas in acute liver failure a humoral factor which can be removed by high‐volume plasmapheresis is a main contributor.

A maximal central venous oxygen saturation (SvO2max) for the surgical patient

Before induction of anaesthesia, 23 patients scheduled for major abdominal surgery had blood samples drawn from a central venous catheter for oxygen saturation (SvO2) after graded infusion of isotonic saline. The infusion of saline was continued until further administration resulted in a stable SvO2 (SvO2max). The SvO2 increased from 69 (53–83) to 72 (66–83) % (median and range; P < 0. 0001), when the patients received 10 (0–26) mL‐ kg‐1, average 500 mL, of saline. At the same time central venous haematocrit decreased from 38 (32–47) to 36 (23–47) % which suggests that the intravascular volume was expanded by 420 (180–3070) mL or by 72 (18–174) % of the administered volume. The results demonstrate that volume expansion by saline can establish a maximal venous oxygen saturation in the surgical patient.

Cerebrovascular metabolic autoregulation is impaired during liver transplantation.

BACKGROUND We determined whether the coupling between cerebral blood flow (CBF) and oxygen metabolism (CMRO2) is preserved during liver transplantation. Because of cerebrovascular dilatation, we hypothesized that cerebral metabolic autoregulation is impaired, because CBF becomes uncoupled from CMRO2 during the reperfusion phase of the operation. MATERIALS AND METHODS In a prospective study, 13 patients (8 women, median age 46, range 21-6) with liver failure (10 with end-stage chronic liver disease and 3 with acute liver failure) were enrolled. Catheters were placed in a femoral artery and in the internal jugular vein for calculation of the cerebral arteriovenous oxygen content difference (AVDO2). CBF was recorded by the 133Xenon injection technique, and by transcranial Doppler sonography determined mean flow velocity (Vmean) in the middle cerebral artery. The CMRO2 was calculated as the AVDO2 times CBF and the cerebrovascular resistance (CVR) as the mean arterial pressure to CBF ratio. An index of large cerebral artery diameter was expressed by the CBF to Vmean ratio. RESULTS From induction of anesthesia to the anhepatic period, CBF decreased from a median of 47 (interquartiles 31-55) to 41 (37-48) ml 100 g(-1) min(-1), whereas the CMRO2 remained unchanged (1.3 [0.9-2.5] vs. 1.7 [0.9-2.3] ml 100 g(-1) min(-1)). In the reperfusion phase, the CBF increased to 51 (45-54) ml 100 g(-1) min(-1), whereas the CMRO2 remained unchanged at 1.1 (1.0-2.5) ml 100 g(-1) min(-1). The CVR decreased from 2.0 mm Hg (1.4-2.1) to 1.4 (1.1-1.8) mm Hg(-1) min 100 g ml. In the anhepatic phase, mean arterial pressure decreased from 92 mm Hg (84-98) to 85 (80-92) mm Hg and at reperfusion it was 80 (71-105) mm Hg. From the anhepatic to the reperfusion phase, the CBF increased 7% (0 to 26) for each mm Hg concomitant increase in PaCO2. The CBF to Vmean ratio remained stable (1.0 [0.8-1.2] vs. 0.9 [0.7-1.1] ml 100 g(-1) min(-1) cm(-1) sec). CONCLUSION During the reperfusion phase of liver transplantations, cerebrovascular dilatation uncouples cerebral oxidative metabolism from blood flow. The increase in CBF is beyond what can be explained by changes in arterial carbon dioxide tension and arterial pressure.