Qualitative analysis of unanticipated difficult airway management.

BACKGROUND: Unanticipated difficult airway management (DAM) is a major challenge for the anaesthesiologist and is associated with a risk of severe patient damage. We analysed 24 cases of unanticipated DAM for actual case management and anaesthesiologists knowledge, technical and non-technical skills. Anaesthesiologists' opinions, as well as environmental factors of importance for DAM proficiency, were also assessed. METHODS: Departments of Anaesthesiology in three Copenhagen University Hospitals participated in a prospective study of unanticipated DAM. Anaesthesiologists recorded the details of the cases on a data sheet. Qualitative data were collected in a semi-structured interview if the value of the Intubation Difficulty Score (IDS) was more than five, if the value of the visual analogue scale score for mask ventilation was more than five or in the case of a registered complication. Transcripts were theme analysed independently by two analysts. Data sheets and interviews were used in the final evaluation. RESULTS: All 24 cases concerned difficult tracheal intubation, and this was associated with difficult mask ventilation on four occasions. Management in three cases demonstrated strict adherence to a DAM practice guideline. Anaesthesiologists lacked standards for DAM. Inadequate knowledge, training and training facilities were documented. Sudden re-allocation of personnel and change of anaesthetic technique were potential risk factors for DAM. Insufficient airway assessment, insufficient patient information and registration of difficulties were demonstrated. Ethical issues were raised concerning the use of patients for skills practice. CONCLUSIONS: Both personal and system failures resulted in unanticipated DAM. There was insufficient knowledge of DAM and anaesthesiologists lacked DAM training. Standards for DAM and curricula for continuing education in DAM are needed.

Attenuated hepatosplanchnic uptake of lactate during intense exercise in humans.

We evaluated whether the increase in blood lactate with intense exercise is influenced by a low hepatosplanchnic blood flow as assessed by indocyanine green dye elimination and blood sampling from an artery and the hepatic vein in eight men. The hepatosplanchnic blood flow decreased from a resting value of 1.6 +/- 0.1 to 0.7 +/- 0.1 (SE) l/min during exercise. Yet the hepatosplanchnic O2 uptake increased from 67 +/- 3 to 93 +/- 13 ml/min, and the output of glucose increased from 1.1 +/- 0.1 to 2.1 +/- 0.3 mmol/min (P < 0.05). Even at the lowest hepatosplanchnic venous hemoglobin O2 saturation during exercise of 6%, the average concentration of glucose in arterial blood was maintained close to the resting level (5.2 +/- 0.2 vs. 5.5 +/- 0.2 mmol/l), whereas the difference between arterial and hepatic venous blood glucose increased to a maximum of 22 mmol/l. In arterial blood, the concentration of lactate increased from 1.1 +/- 0.2 to 6.0 +/- 1.0 mmol/l, and the hepatosplanchnic uptake of lactate was elevated from 0.4 +/- 0.06 to 1.0 +/- 0.05 mmol/min during exercise (P < 0.05). However, when the hepatosplanchnic venous hemoglobin O2 saturation became low, the arterial and hepatosplanchnic venous blood lactate difference approached zero. Even with a marked reduction in its blood flow, exercise did not challenge the ability of the liver to maintain blood glucose homeostasis. However, it appeared that the contribution of the Cori cycle decreased, and the accumulation of lactate in blood became influenced by the reduced hepatosplanchnic blood flow.

Interference of cerebral near-infrared oximetry in patients with icterus.

UNLABELLED: Near-infrared spectrophotometry assesses cerebral oxygen saturation (ScO(2)) based on the absorption spectra of oxygenated and deoxygenated hemoglobin and the translucency of biological tissue in the near-infrared band. In patients with icterus, however, bilirubin can potentially hinder cerebral oximetry. In 48 patients undergoing orthotopic liver transplantation, we related total plasma bilirubin to ScO(2) as determined from spectrophotometry with wavelengths of 733 and 809 nm. Before surgery, ScO(2) was 59% (15%-78%) (median with range) and bilirubin was 71 (6-619) micromol/L with a negative correlation (r = -0.72; P < 0.05). The 95% prediction interval included the lowest measurable ScO(2) of 15% at a bilirubin level of 370 micromol/L. During reperfusion of the grafted liver, the ScO(2) increased by 7% (-8% to 17%) (P < 0.05), and bilirubin did not influence this increase. In one patient, the ScO(2) remained below 15% despite a decrease in bilirubin from 619 to 125 micromol/L, suggesting that tissue pigmentation deposits also absorb light. In conclusion, bilirubin dampens the spectrophotometry-determined cerebral oxygen saturation at 733 and 809 nm. A bilirubin level of 370 micromol/L, tissue pigment deposits, or both, may render determination of cerebral oxygen saturation impossible. Even at high bilirubin values, changes in cerebral perfusion may be visible. IMPLICATIONS: In 48 patients undergoing liver transplantation, the interference of icterus on cerebral oximetry by near-infrared light was investigated. Bilirubin absorbed the near-infrared light and lowered the measured cerebral oxygen saturation. Even at high bilirubin values, changes in cerebral oxygenation, as seen during reperfusion of the grafted liver, may be visible.

The effect of increasing blood pressure with dopamine on systemic, splanchnic, and lower extremity hemodynamics in patients with acute liver failure.

BACKGROUND: Arterial hypotension occurs frequently in patients with acute liver failure (ALF). Treatment with epinephrine and norepinephrine in patients with ALF has been associated with a decrease in whole-body (systemic) oxygen consumption. We aimed to investigate the effect of increasing blood pressure with dopamine on whole-body (systemic), splanchnic, and lower extremity hemodynamics and oxygen consumption in patients with acute liver failure and hepatic encephalopathy grade III or IV. METHODS: In seven patients with ALF cardiac output (CO) was measured with the thermodilution technique, and hepatic blood flow (HBF) was estimated with infusion of sorbitol as test compound, liver vein catheterization, and calculations on the basis of Fick's principle. Lower-extremity blood flow was measured with strain-gauge plethysmography. RESULTS: During infusion of dopamine (5 +/- 2 microg kg(-1) min(-1)) mean arterial pressure (MAP) increased from 68 +/- 5 to 85 +/- 8 mmHg. CO increased from 6.8 +/- 0.8 to 9.0 +/- 2.4 l/min (P < 0.05), systemic oxygen delivery from 45 +/- 7 to 63 +/- 19 mmol/min (P < 0.05), systemic oxygen consumption from 10.2 +/- 2.0 to 11.5 +/- 3.3 mmol/min (NS). HBF increased from 2.2 +/- 0.7 to 2.7 +/- 1.0 l/ min (P < 0.05), splanchnic oxygen delivery from 14.4 +/- 5.3 to 18.5 +/- 7.2 mmol/min (P < 0.01), and splanchnic oxygen consumption decreased from 3.9 +/- 1.1 to 2.9 +/- 0.6 mmol/min (P < 0.05). No significant changes in lower extremity flow and oxygenation variables were found. CONCLUSIONS: The use of dopamine in patients with ALF to increase MAP was associated with increases in systemic and splanchnic oxygen delivery. A concomitant decrease in splanchnic oxygen consumption was observed.

Preserved arterial flow secures hepatic oxygenation during haemorrhage in the pig.

1. This study examined the extent of liver perfusion and its oxygenation during progressive haemorrhage. We examined hepatic arterial flow and hepatic oxygenation following the reduced portal flow during haemorrhage in 18 pigs. The hepatic surface oxygenation was assessed by near-infrared spectroscopy and the hepatic metabolism of oxygen, lactate and catecholamines determined the adequacy of the hepatic flow. 2. Stepwise haemorrhage until circulatory collapse resulted in proportional reductions in cardiac output and in arterial, central venous and pulmonary wedge pressures. While heart rate increased, pulmonary arterial pressure remained stable. In addition, renal blood flow decreased, renal vascular resistance increased and there was elevated noradrenaline spill-over. Further, renal surface oxygenation was lowered from the onset of haemorrhage. 3. Similarly, the portal blood flow was reduced in response to haemorrhage, and, as for the renal flow, the reduced splanchnic blood flow was associated with an elevated noradrenaline spill-over. In contrast, hepatic arterial blood flow was only slightly reduced by haemorrhage, and surface oxygenation did not change. The hepatic oxygen uptake was maintained until the blood loss represented more than 30 % of the estimated blood volume. At 30 % reduced blood volume, hepatic catecholamine uptake was reduced, and the lactate uptake approached zero. 4. Subsequent reduction of cardiac output and portal blood flow elicited a selective dilatation of the hepatic arterial vascular bed. Due to this dilatation liver blood flow and hepatic cell oxygenation and metabolism were preserved prior to circulatory collapse.

Hepatic blood flow and splanchnic oxygen consumption in patients with liver failure. Effect of high-volume plasmapheresis.

Liver failure represents a major therapeutic challenge, and yet basic pathophysiological questions about hepatic perfusion and oxygenation in this condition have been poorly investigated. In this study, hepatic blood flow (HBF) and splanchnic oxygen delivery (DO2, sp) and oxygen consumption (VO2,sp) were assessed in patients with liver failure defined as hepatic encephalopathy grade II or more. Measurements were repeated after high-volume plasmapheresis (HVP) with exchange of 8 to 10 L of plasma. HBF was estimated by use of constant infusion of D-sorbitol and calculated according to Fick's principle from peripheral artery and hepatic vein concentrations. In 14 patients with acute liver failure (ALF), HBF (1.78 +/- 0.78 L/min) and VO2,sp (3.9 +/- 0.9 mmol/min) were higher than in 11 patients without liver disease (1.07 +/- 0.19 L/min, P <.01) and (2.3 +/- 0.7 mmol/min, P <.001). In 9 patients with acute on chronic liver disease (AOCLD), HBF (1.96 +/- 1.19 L/min) and VO2,sp (3.9 +/- 2.3 mmol/min) were higher than in 18 patients with stable cirrhosis (1.00 +/- 0.36 L/min, P <.005; and 2.0 +/- 0.6 mmol/min, P <.005). During HVP, HBF increased from 1.67 +/- 0.72 to 2.07 +/- 1.11 L/min (n=11) in ALF, and from 1.89 +/- 1.32 to 2.34 +/- 1.54 L/min (n=7) in AOCLD, P <.05 in both cases. In patients with ALF, cardiac output (thermodilution) was unchanged (6.7 +/- 2.5 vs. 6.6 +/- 2.2 L/min, NS) during HVP. Blood flow was redirected to the liver as the systemic vascular resistance index increased (1,587 +/- 650 vs. 2, 020 +/- 806 Dyne. s. cm-5. m2, P <.01) whereas splanchnic vascular resistance was unchanged. In AOCLD, neither systemic nor splanchnic vascular resistance was affected by HVP, but as cardiac output increased from 9.1 +/- 2.8 to 10.1 +/- 2.9 L/min (P <.01) more blood was directed to the splanchnic region. In all liver failure patients treated with HVP (n=18), DO2,sp increased by 15% (P <.05) whereas VO2,sp was unchanged. Endothelin-1 (ET-1) and ET-3 were determined before and after HVP. Changes of ET-1 were positively correlated with changes in HBF (P <.005) and VO2,sp (P <.05), indicating a role for ET-1 in splanchnic circulation and oxygenation. ET-3 was negatively correlated with systemic vascular resistance index before HVP (P <.05) but changes during HVP did not correlate. Our data suggest that liver failure is associated with increased HBF and VO2, sp. HVP further increased HBF and DO2,sp but VO2,sp was unchanged, indicating that splanchnic hypoxia was not present.

Mesenteric, coeliac and splanchnic blood flow in humans during exercise.

1. Exercise reduces splanchnic blood flow, but the mesenteric contribution to this response is uncertain. 2. In nineteen humans, superior mesenteric and coeliac artery flows were determined by duplex ultrasonography during fasting and postprandial submaximal cycling and compared with the splanchnic blood flow as assessed by the Indocyanine Green dye-elimination technique. 3. Cycling increased arterial pressure, heart rate and cardiac output, while it reduced total vascular resistance. These responses were not altered in the postprandial state. During fasting, cycling increased mesenteric, coeliac and splanchnic resistances by 76, 165 and 126 %, respectively, and it reduced corresponding blood flows by 32, 50 and 43 % (by 0.18 +/- 0.04, 0.42 +/- 0.03 and 0.60 +/- 0.04 l min-1). Postprandially, mesenteric and splanchnic vascular resistances decreased, thereby elevating regional blood flow, while the coeliac circulation was not influenced. Postprandial cycling did not influence the mesenteric resistance significantly, but its blood flow decreased by 22 % (0.46 +/- 0.28 l min-1). Coeliac and splanchnic resistance increased by 150 and 63 %, respectively, and the corresponding regional blood flow decreased by 51 and 31 % (0.49 +/- 0.07 and 0.96 +/- 0.28 l min-1). Splanchnic blood flow values assessed by duplex ultrasound and by dye-elimination techniques were correlated (r = 0.70; P < 0.01). 4. During submaximal exercise in humans, splanchnic resistance increases and blood flow is reduced following a 50 % reduction in the hepato-splenic and a 25 % reduction in the mesenteric blood flow.

Age dependency of resistance to cerebrospinal fluid outflow.

OBJECT: Resistance to cerebrospinal fluid (CSF) outflow (Rout)is an important parameter in assessing the need for CSF shunt placement in patients with hydrocephalus. The normal lower limit of Rout has been estimated on the basis of the clinical effect of shunt placement in patients with varying values of Rout and in young healthy volunteers. The lack of clinical effect from CSF shunts in some elderly patients, despite elevated Rout,suggests that the normal value of Rout increases with age and may be higher in elderly persons. The aim of the present study was to examine the relationship between Rout and age in patients without known CSF dynamic disturbances. METHOD: Fifty-two patients ranging from 20 to 88 years of age and with no known CSF dynamic disorders were examined. The Rout was measured using a lumbar computerized infusion test. The correlation between Rout and age was analyzed by performing linear regression. The Rout increased significantly with patient age. The Rout in a patient in the eighth decade will be approximately 5 mm Hg/ml/minute higher than in a young patient. CONCLUSIONS: The present study shows a small but critical increase in Rout with increased patient age. A notable residual variation was present and borderline values of Rout should be regarded and used with caution.

Cerebral oxygen saturation and blood flow during liver transplantation.

After reperfusion of a liver graft, transcranial Doppler determined middle cerebral artery flow velocity, increases more than expected from the arterial carbon dioxide tension (PaCO2). We evaluated if this indication of cerebral hyperperfusion is reflected in the jugular oxygen saturation (SjO2) (n = 31) and oxygen saturation (ScO2) (near-infrared spectrophotometry, n = 22). From the dissection phase to the anhepatic phase SjO2 71.0% (range 62.3%-78.5%), ScO2 70% (range 65%-77%), and PaCO2 34.9 mm Hg (range 30.8-38.3) remained statistically unchanged. In contrast, during the early reperfusion phase, SjO2 increased to 77.0% (71.4%-83.0%) (P < 0.01) and the ScO2 to 75% (68%-80%) (P < 0.05) as PaCO2 increased to 37.5 mm Hg (34.8-41.9) (P < 0.001). Notably, SjO2 also increased at reperfusion from 71.6% (66.5%-78.0% mm Hg) to 80.0% (76.8%-84.8%) in the four patients in whom PaCO2 decreased at reperfusion from 37.6 mm Hg (36.8-39.5) to 34.0 mm Hg (32.3-36.8). If the changes in SjO2 after reperfusion of the grafted liver should be explained as a reflection of changes in cerebral blood flow, in response to PaCO2, it would indicate a highly accentuated CO2 reactivity of 13%/mm Hg. The results support that cerebral blood flow and, in turn, oxygenation increase after reperfusion because the grafted liver liberates a vasodilating substance(s).

Lower body impedance for the evaluation of venovenous bypass flow.

Inferior vena cava (IVC) clamping during liver transplantation causes venous congestion in the splanchnic and IVC beds. A venovenous bypass relieves congestion and improves cardiac output (CO), but the bypass flow required for adequate drainage of the vascular beds is controversial. In this study we evaluated the bypass flow necessary to compensate for the IVC clamping. Lower body impedance (BI) is inversely related to tissue fluid content and was used to reflect congestion. A venovenous bypass was successfully applied to 59 of 62 patients. BI was measured across the left buttock and related to bypass flow, CO, bypass flow ratio (bypass flow/CO before IVC clamping; n = 62), and right femoral venous pressure (n = 8). The bypass flow was 1.7 (0.0-3.0) L.min-1 (median and range). BI decreased (delta BI; -2.2 [-10.3-1.1)] omega) as the femoral venous pressure increased (29 [21-49] mm Hg; r = -0.81; P < .05), and the femoral venous pressure correlated inversely to bypass flow (r = -0.35; P < .01). The change in CO at IVC clamping (delta CO; -2.3 [-6.3-1.6] L.min-1) related to bypass flow ratio (0.25 [0-0.51]; r = 0.57, P < .01), whereas delta BI related only minimally to bypass flow or bypass flow ratio (r = 0.37; P < .05). In conclusion the median bypass flow of 1.7 L.min-1 was too small to prevent fluid accumulation in the lower caval region, and extrapolation of data suggests that bypass flow should have approached 3.5 L.min-1 or 50% of CO in order to prevent fluid accumulation in the lower caval region. However the minimal correlation between lower BI and bypass flow indicates that bypass flow per se is not the only determinant of lower body fluid accumulation.

Plasma magnesium during human liver transplantation.

Patients with severe liver disease and accompanying malnutrition may exhibit electrolyte disturbances including the magnesium balance. In 18 patients plasma magnesium (p-Mg) was determined at the start of the liver transplantation and during the anhepatic and reperfusion phases of the operation. The blood loss was 6.9 (2.5-8.8) 1 (median and range) and the cumulative transfusion volume was 10.2 (5.0-17.2) 1 of which 5.9 (2.5-14.2) 1 was with fresh frozen plasma. p-Mg was 0.72 (0.58-0.88) mmol.l-1 and it did not change significantly during the operation. Thus, in 4 patients it was at or below the lower reference value of 0.67 mmol.l-1. In 11 patients it changed less than 0.05 mmol.l-1, while in 4 patients the concentration was rose, and in 3 patients we noted a fall in each of 0.08 mmol.l-1. There was no correlation between p-Mg and the blood loss or the administered volume of fresh frozen plasma. In 10 randomly chosen fresh frozen plasma units, the p-Mg was 0.64 (0.61-0.71) mmol.l-1. These observations do not support a need for close monitoring or substitution of magnesium during human liver transplantation. On the other hand, the finding of a low value in 4 of 18 patients suggests that plasma magnesium should be monitored and eventually corrected while the patient is on the waiting list.

[Time consumption at an orthopedic operating theatre. Physicians' ability to predict their own time consumption]. / Tidsforbrug på en ortopaedkirurgisk operationsstue. Loegers evne til at forudsige eget tidsforbrug.

The aim of the study was to investigate the time spent on different procedures in an orthopaedic operating theatre, and to evaluate the ability of doctors to predict their own time consumption. Time schedules were registered for 146 operations, of these 104 were either knee or hip replacements. Sixty percent of the total time was spent on surgery. The median misjudgment was 15 minutes for surgeons and five minutes for anaesthetists. An improvement in the doctors' ability to predict their own time consumption in the course of the study period could not be demonstrated. Comparing the study period with the similar period the year before it was not possible to demonstrate a change in the number of cancelled operations or the number of days with overtime. Epidural anaesthesia with bupivacaine was the most time consuming anaesthesia, the differences between the other forms of anaesthesia used were insignificant.

Methodological limitations of the use of intrinsic hepatic clearance of ICG as a measure of liver cell function.

Negligible extra-hepatic elimination of indocyanine green (ICG) makes it well suited as a liver test substance. The liver blood flow rate (Q) is estimated from concentration measurements in peripheral (A) and hepatic venous (V) blood during a constant ICG infusion rate (Inf), as Q = Inf/(A-V). Intrinsic hepatic clearance of ICG, Cli = Inf/((A-V)/ln(A/V)), is interesting because it should give a flow-independent quantitative estimate of liver cell function, utilizing the same concentration measurements. The present study was aimed to investigate possible limitations involved in the estimation and use of Cli of ICG in 41 liver patients and 20 controls. Time-dependence was studied by means of two successive 40-min infusion periods (with no significant change in Q). Cli of ICG decreased 6% per hour +/- 3% (mean +/- SD, n = 6, P less than 0.01) due to a small but significant increase of the concentrations during the infusion period. Flow-dependence was studied by measurements before and after an increment of flow of on average 51%, induced by the intake of a meal. This caused no significant change in Cli of ICG (P greater than 0.5, n = 5, Student's paired t-test). The intrinsic hepatic clearance of ICG was on average 0.75 +/- 0.26 l plasma min-1 (+/- SD, n = 20) in controls and 0.39 +/- 0.18 l plasma min-1 in liver patients (n = 41), P less than 0.001. It was positively correlated to the galactose elimination capacity, although the scatter was large (P less than 0.05, n = 56).(ABSTRACT TRUNCATED AT 250 WORDS)

Methodological problems in the use of indocyanine green to estimate hepatic blood flow and ICG clearance in man.

Liver blood flow (Q) is often measured by constant infusion of ICG (i), concentration measurements in an artery (A) and a hepatic vein (V): Q = (A-V)/A. Some authors use ICG clearance, Cl = i/A, as a measure of Q assuming complete hepatic extraction. During the infusion, the ICG concentration often increases. The importance of this for calculated values of Q and Cl was examined, and the use of Cl as a measure of Q was reevaluated. ICG was given as 0.06-0.20 mumol/min to 52 subjects with liver disease, and about 0.20 mumol/min to 86 subjects with no liver disease. ICG concentration increased steeply during the first 90 min after start of the infusion; thereafter the increment was constant as evaluated in successive 40-min periods in eleven 320-min studies (analysis of variance P greater than 0.5); on average, 6 +/- 1% per hour (+/- SD). Q was not time-dependent (P greater than 0.5). ICG clearance decreased significantly, on average 5 +/- 2% per hour (+/- SD). Hepatic extraction fraction, (A-V)/A, (measurement period 90-130 min) was 0.34 +/- 0.21 in liver patients (+/- SD) and 0.61 +/- 0.80 in controls. Cl and Q were positively correlated in both groups but with substantial scatter. Thus, not only is the calculated ICG clearance time-dependent but the extraction fraction is further so low and variable, that any use of ICG clearance as a measure of liver flow is not justified.