Acute quadriplegic myopathy following autologous peripheral blood stem cell transplantation for breast cancer.

Autologous peripheral blood stem cell transplantation (APSCT) is increasingly used in the treatment of breast cancer. We report a patient who experienced septic shock, and after treatment with antibiotics, high-dose corticosteroids and mechanical ventilation due to respiratory insufficiency, developed quadriplegia. Electroneurophysiological examination, as well as a muscle biopsy, showed a typical picture of acute quadriplegic myopathy with loss of thick filament proteins. This is, to the best of our knowledge, the first reported case of this complication following APSCT.

Thoracoabdominal restriction in supine men: CT and lung function measurements.

Thoracoabdominal restriction was brought on by means of a corset, and the subsequent effects on thoracic dimensions and lung tissue were studied by computerized tomography (CT) and by various lung function tests in supine healthy volunteers (mean age 30 yr). Restriction caused reductions in total lung capacity (helium equilibration) from mean 6.84 to 4.80 liters, in functional residual capacity (FRC) from 2.65 to 2.08 liters, and in vital capacity from 5.16 to 3.45 liters. Closing capacity (single-breath N2 washout) fell from 2.42 to 1.88 liters, thus matching the reduction in FRC. The static pressure-lung volume curve was shifted to the right by 1.5 cmH2O at 50% of total lung capacity. However, no change in the slope of the curve was observed. The diaphragm was moved cranially by 1.2 cm, and the thoracic cross-sectional area was reduced by a mean 32 cm2 at a level just above the diaphragm. No changes in the lung tissue were seen on CT scanning. Gas exchange, as assessed by multiple inert gas elimination technique and arterial blood gas analysis, was unaffected by restriction. It is concluded that in supine subjects, thoracoabdominal restriction that reduces FRC by 0.6 liter is not accompanied by atelectasis (normal CT scan). In this respect the result differs from that found in anesthetized supine subjects who show the same fall in FRC and atelectasis in dependent lung regions.

V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans.

Regional ventilation and perfusion were studied in 10 anesthetized paralyzed supine patients by single-photon emission computerized tomography. Atelectasis was estimated from two transaxial computerized tomography scans. The ventilation-perfusion (V/Q) distribution was also evaluated by multiple inert gas elimination. While the patients were awake, inert gas V/Q ration was normal, and shunt did not exceed 1% in any patient. Computerized tomography showed no atelectasis. During anesthesia, shunt ranged from 0.4 to 12.2. Nine patients displayed atelectasis (0.6-7.2% of the intrathoracic area), and shunt correlated with the atelectasis (r = 0.91, P < 0.001). Shunt was located in dependent lung regions corresponding to the atelectatic area. There was considerable V/Q mismatch, with ventilation mainly of ventral lung regions and perfusion of dorsal regions. Little perfusion was seen in the most ventral parts (zone 1) of caudal (diaphragmatic) lung regions. In summary, shunt during anesthesia is due to atelectasis in dependent lung regions. The V/Q distributions differ from those shown earlier in awake subjects.

Atelectasis causes gas exchange impairment in the anaesthetised horse.

The anatomical basis of gas exchange impairment in the anaesthetised horse was studied by computerised tomography (CT; three shetland ponies) and morphological analysis (one pony and three horses). By means of CT, densities were seen in dependent lung regions early during anaesthesia, both with spontaneous breathing and with mechanical ventilation. The densities remained for some time where they had initially been created when the animal was turned from dorsal to sternal recumbency. Deep insufflation of the lungs reduced the dense area. Gas exchange was impaired roughly in proportion to the dense area. On histological analysis, the densities were atelectatic and congested with blood. Gravimetry showed no more extravascular water per unit lung tissue in the atelectatic than in the 'normal' regions, and the blood content was increased only slightly. It is concluded that the horse develops atelectasis in dependent lung regions early during anaesthesia in dorsal recumbency, and that atelectasis is the most likely explanation for the large shunt and impaired arterial oxygenation regularly seen during anaesthesia.

Radiospirometry V/Q.

Single photon emission computerized tomography (SPECT) of the lungs was used for topographical determination of V/Q ratios in anaesthetized-paralyzed subjects. Ventilation and perfusion were estimated from the distribution of an inhaled aerosol containing a radioactive isotope and injected macroaggregates of human albumin tagged with another isotope. There was a prominent gradient of V/Q ratios in the vertical direction. In the horizontal plane there were marked gradients of both ventilation and perfusion of similar appearance with maxima in central lung regions, resulting in only small gradients of V/Q ratios.

Splanchnic blood flow during halothane-relaxant anaesthesia in elderly patients.

We have previously found that halothane-relaxant anaesthesia in elderly patients causes a change towards a hyperkinetic circulation, with a decrease in the arterial-mixed venous oxygen content difference. This could be attributed to vasodilation. In the present study the splanchnic contribution to these changes was investigated. Nine patients were studied during halothane-relaxant anaesthesia prior to surgery. During anaesthesia splanchnic blood flow was markedly reduced, while splanchnic oxygen uptake decreased only moderately compared with the awake level. This resulted in an increase in splanchnic oxygen extraction. It is concluded that the splanchnic vascular bed does not contribute to the "hyperkinetic" circulation during halothane anaesthesia.

Halothane-relaxant anaesthesia in elderly patients.

Twenty-three elderly patients, scheduled for elective cholecystectomy, were studied during halothane-relaxant anaesthesia. Anaesthesia was induced with thiopentone and maintained with halothane in 12 patients, six of whom had also received premedication. Eleven patients were anaesthetized with halothane, without thiopentone induction and with no premedication. Measurements of central haemodynamics were performed awake and during anaesthesia at end-tidal halothane concentrations of 0.5 and 1.0%; at the lower concentration, measurements were also made after addition of nitrous oxide. Premedication and thiopentone had no influence on the subsequent halothane anaesthesia. Halothane caused reductions of cardiac index, mean arterial blood pressure and oxygen uptake. However, neither right atrial nor pulmonary capillary venous pressure increased and the arterio-venous oxygen content difference decreased. These findings differ from those made by others in younger subjects and are probably attributable to a dose-dependent reduction in systemic vascular resistance. The addition of nitrous oxide had only minor effects on central circulation. The results suggest that the age of the patients influences their reaction to halothane anaesthesia.

Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia.

We have studied the effects of anaesthesia on atelectasis formation and gas exchange in 45 patients of both sexes, smokers and nonsmokers, aged 23-69 yr. None of the patients showed clinical signs of pulmonary disease, and preoperative spirometry was normal. In the awake patient, partial pressure of arterial oxygen (PaO2) decreased with increasing age (P less than 0.001) and the alveolar-arterial oxygen partial pressure difference (PAO2-PaO2) increased with age (P less than 0.001). Shunt, assessed by the multiple inert gas elimination technique, was small (mean 0.5%) and uninfluenced by age. However, there was an increasing dispersion (log SD Q) of ventilation/perfusion ratios (VA/Q) and increasing perfusion of regions of low VA/Q (VA/Q less than 0.1) with increasing age (P less than 0.001 and P less than 0.05, respectively). No patient displayed any atelectasis as assessed by computed x-ray tomography of the chest. During inhalation anaesthesia (halothane or enflurane) with mechanical ventilation, 39 of 45 patients developed atelectasis and shunt. There was a strong correlation between the atelectatic area and the magnitude of shunt (r = 0.81, P less than 0.001). Atelectasis and shunt did not increase significantly with age, whereas log SD Q and perfusion of regions with low VA/Q ratios did (r = 0.55, P less than 0.001 and r = 0.35, P less than 0.05, respectively). Awake, the major determinant of PaO2 was perfusion of regions of low VA/Q ratios, which increased with age. During anaesthesia shunt influenced PaO2 most, low VA/Q being a secondary factor which, however, was increasingly important with increasing age, thus explaining the well-known age-dependent deterioration of arterial oxygenation during anaesthesia.

Influence of age on circulation and arterial blood gases in man.

BACKGROUND: Modern data on the influence of age on hemodynamic and blood gas data in healthy subjects are sparse, especially in middle aged or older subjects. Most measurements have been done in patients during major surgery or in intensive care when the patients have one or more failing organ systems. This study reports on hemodynamics, blood gases and blood volume in healthy patients prior to anesthesia and elective surgery. METHODS: A total of 116 subjects (92 males, 24 females) were investigated prior to anesthesia and elective surgery. No one had received any premedication or was taking regular medication. All subjects were in good physical condition, except for their surgical disease, and clinical examination and history did not reveal any sign of cardiopulmonary disease. Measurements were made of systemic and pulmonary vascular pressures, cardiac output, arterial blood gases and blood volume by 131I-Albumin distribution. RESULTS: Cardiac output, stroke volume, and blood volume correlated to body surface. Relating these variables to body size eliminated almost all differences between the male and female groups. These variables, as well as both systemic and pulmonary artery systolic vascular pressures, were affected by increasing age. Pulmonary capillary wedge and right atrial pressures were not influenced by age. PaO2 decreased with age from 14.0 kPa at 20 years to 11.3 kPa at 80, whereas PaCO2 was unaltered. No effect of light smoking was found on pulmonary circulation or arterial blood gases. Significant correlations were found between blood volume on the one hand and body size and age on the other hand, but not in regard to sex.

Oxygen uptake and central circulation during ketamine anaesthesia.

Cardiac output, oxygen uptake and plasma catecholamines were studied in patients when awake and during ketamine anaesthesia prior to and during upper abdominal surgery. Oxygen uptake was determined by using a masspectrometer and cardiac output was measured according to the Fick principle. Plasma catecholamines were analysed by high performance liquid chromatography. Stroke volume had fallen by 27% while heart rate had increased after 15 min of anaesthesia, maintaining cardiac output at the awake level. Concomitantly, the oxygen uptake had fallen by 18%. During the succeeding hour of anaesthesia and surgery, cardiac output displayed a transient decrease and oxygen uptake returned to the awake value. The plasma adrenaline concentration fell during the initial phase of anaesthesia and then returned to the awake level. The noradrenaline concentration was increased during the whole anesthetic period. The data suggest a relationship between oxygen uptake and cardiac output during ketamine anaesthesia, similar to that seen during neurolept-nitrous oxide and halothane anaesthesia, except for the initial hyperkinetic period following the induction. No relationship could be shown between catecholamine concentrations in plasma and the central haemodynamics.

Oxygen uptake, plasma catecholamines and cardiac output during neurolept-nitrous oxide and halothane anaesthesias.

Cardiac output, oxygen uptake and plasma catecholamines were studied in patients both awake and during anaesthesia prior to and during upper abdominal surgery. Two different forms of anaesthesia were used: neurolept-nitrous oxide (NLA) and halothane (HALO) anaesthesia. Oxygen uptake was determined by using a masspectrometer, and cardiac output was measured according to the Fick principle. Plasma catecholamines were analysed by high performance liquid chromatography. Cardiac output fell by 40% during NLA and by 30% during HALO. Concomitantly, the oxygen uptake fell by 40% and 35%, respectively. A linear relationship between cardiac output and oxygen uptake could be established both in the awake state and during anaesthesia, with no significant change in the slope or position of the regression line when anaesthesia was commenced. Ventricular filling pressures fell during both anaesthetic procedures. Adrenaline fell to half the plasma concentrations seen in normal subjects under resting conditions, while noradrenaline returned to normal from an initially 30-40% increased value. Surgery caused no significant changes in either cardiac output or oxygen uptake, whereas plasma adrenaline increased by 20 times and noradrenaline by 60-90%. The findings suggest that the reduced oxygen uptake during anaesthesia causes the fall in cardiac output rather than any cardiodepressant action of the anaesthetic. It is possible that the anaesthetic depresses whole-body metabolism by either blocking the effects of catecholamines or interfering with cellular metabolism.

Lung function after open versus laparoscopic cholecystectomy.

Postoperative lung function and gas exchange were studied in 36 patients after cholecystectomy. Twenty-four of the patients underwent laparoscopic cholecystectomy while the remaining twelve were operated with open technique. Before surgery all patients had normal ventilatory volumes (forced vital capacity, FVC and forced expired volume in 1 s, FEV1) and normal gas exchange. Two hours postoperatively FVC was reduced to 64 +/- 16% (P < 0.05) of the preoperative level in the laparoscopic group and to 45 +/- 23% (P < 0.05) after open cholecystectomy. On the first postoperative day FVC was virtually normal in the laparoscopic patients (77 +/- 17% of preoperative level, NS), whereas the open surgery patients still had a decreased FVC (56 +/- 13% of preoperative, P < 0.05). FEV1 in the postoperative period followed the same course as FVC. Gas exchange was significantly impaired in the early postoperative period in all patients but no difference between the two groups was found. Two hours postoperatively PaO2 was reduced to 85% (P < 0.05) of preoperative value and PaCO2 had increased by 0.5 kPa (P < 0.05). The alveolo-arterial oxygen tension difference (PA-aO2) had increased by approximately 45% to a mean of 3.7 kPa (P < 0.05). On the first postoperative day gas exchange was still significantly impaired in the open surgery patients. Atelectasis detected by computed X-ray tomography of the lungs were found in both groups. However, the amount of atelectasis tended to be smaller in the laparoscopic group than in the open surgery patients.(ABSTRACT TRUNCATED AT 250 WORDS)

CT-assessment of dependent lung densities in man during general anaesthesia.

PURPOSE: We aimed to describe the frequency of atelectasis occurring during anaesthesia, to describe the size and pattern of the atelectasis, and to standardise the method of identifying the atelectasis and calculate its area. MATERIAL AND METHODS: Patients (n = 109) scheduled for elective abdominal surgery were examined with CT of the thorax during anaesthesia. RESULTS: In 95 patients (87%) dependent pulmonary densities were seen, interpreted as atelectasis. Two different types of atelectasis were found-homogeneous (78%) and non-homogeneous (9%). Attenuation values in histograms of the lung and atelectasis were studied using 2 methods of calculating the atelectatic area. CONCLUSION: On the basis of the present findings, we defined atelectasis as pulmonary dependent densities with attenuation values of -100 to +100 HU.

Phrenic nerve stimulation during halothane anesthesia. Effects of atelectasis.

BACKGROUND: Atelectasis formation during anesthesia may be due to loss of respiratory muscle tone, in particular that of the diaphragm. This was tested by tensing the diaphragm by phrenic nerve stimulation (PNS) and observing the effect on atelectasis. METHODS: Twelve patients (mean age 48 yr) without preexisting lung disease were studied during halothane anesthesia. PNS was executed with an external electrode on the right side of the neck. Chest dimensions and area of atelectasis were studied by computed tomography of the chest. RESULTS: Right-sided PNS against an occluded airway at functional residual capacity reduced the atelectatic area in the right lung from 5.1 to 3.8 cm2. The atelectasis was reduced to 1.1 cm2 after application of positive end-expiratory pressure (PEEP) of 10 cmH2O and large tidal volumes but increased to 2.5 cm2 within 1 min after discontinuation of PEEP. Commencement of PNS immediately after PEEP prevented the atelectasis from increasing, the mean area being 0.9 cm2. In seven patients, in whom the trachea was intubated with a double-lumen endobronchial catheter the atelectatic area was smaller during PNS with an open airway than during positive pressure inflation of the lung with the same volume as inspired during PNS (3.5 and 5.2 cm2, respectively. CONCLUSIONS: The findings indicate that contracting the diaphragm in the anesthetized subject reduces the size of atelectasis.

Analysis of lung density by computed tomography before and during general anaesthesia.

Pulmonary structure was analysed by means of computed tomography (CT) in 20 lung-healthy patients, relating tissue density to the attenuation value (AV) of a picture element. Regional density of pulmonary tissue (rlung) was determined using mean lung density in five regions of interest (ROI1-5) (sector method). Vertical and horizontal distributions of x-ray attenuation were analysed by density profiles, relating AV values to evenly distributed and normalised length scales. In group I (n = 12), CT-densitometry was obtained in awake, supine patients and after induction of general anaesthesia. In group II (n = 8), the effect of mechanical ventilation with positive end-expiratory pressure (PEEP, 1.0 kPa [10 cmH2O]) was studied. In the awake state, a vertical tissue density difference between the top and bottom of the lung was found in all patients, accounting for a mean of 0.235 g.cm-3 (right lung) and 0.199 g.cm-3 (left lung). Only minor changes were seen in the horizontal lung density profiles. After induction of anaesthesia, x-ray attenuation of ROI1-4 showed no significant differences when compared with the awake state. The basal lung areas (ROI5) revealed a significantly increased tissue density (P < or = 0.01), reaching mean values of 0.94 g.cm-3 (right lung) and 0.814 g.cm-3 (left lung). Similarly, vertical density profiles showed a markedly enhanced rlung of the bottom of the lung in all patients, interpreted as atelectasis. The amount of atelectasis accounted for 4.8 +/- 2.6% (right lung) and 4.7 +/- 2.1% (left lung) of the intrapulmonary area.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure.

Lung densities (atelectasis) and pulmonary gas exchange were studied in 13 supine patients with no apparent lung disease, the former by transverse computerized tomography (CT) and the latter by a multiple inert gas elimination technique for assessment of the distribution of ventilation/perfusion ratios. In the awake state no patient had clear signs of atelectasis on the CT scan. Lung ventilation and perfusion were well matched in most of the patients. Three patients had shunts corresponding to 2-5% of cardiac output, and in one patient there was low perfusion of poorly ventilated regions. CT scans after 15 min of halothane anesthesia and mechanical ventilation showed densities in dependent lung regions in 11 patients. A shunt was present in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. Ventilation of poorly perfused regions was noted in nine patients, ranging from 1-19% of total ventilation. The magnitude of the shunt significantly correlated to the size of dependent densities (r = 0.84, P less than 0.001). Five patients studied during spontaneous breathing under anesthesia displayed both densities in dependent regions and a shunt, although of fairly small magnitude (1.8% and 3.7%, respectively). Both the density area and the shunt increased after muscle paralysis. PEEP reduced the density area in all patients but did not consistently alter the shunt. It is concluded that the development of atelectasis in dependent lung regions is a major cause of gas exchange impairment during halothane anesthesia, during both spontaneous breathing and mechanical ventilation, and that PEEP diminishes the atelectasis, but not necessarily the shunt.

Constitutional factors promoting development of atelectasis during anaesthesia.

The extent of atelectasis was correlated to constitutional factors in 38 patients who underwent computed tomography prior to and during general anaesthesia with halothane. All patients but two developed atelectasis in dependent regions of both lungs immediately after induction of anaesthesia prior to surgery. The transverse area of the densities ranged from 0 to 27 cm2, and there were no significant differences between patients of different age or sex, or with different smoking habits. A significant linear regression was found between Broca's index weight (kg)/height (cm)-100 and the area of the densities, and also between an index describing the shape of the thorax and the density area. Thus, patients who were overweight and/or had a low and wide thorax tended to develop more extensive atelectasis during anaesthesia. This finding might partly explain why overweight patients develop postoperative pulmonary complications more often than non-obese patients.

Postoperative analgesia with intrapleural administration of bupivacaine-adrenaline.

Twenty-one patients who underwent elective cholecystectomy were studied with regard to the effect of intrapleural administration of bupivacaine-adrenaline solution on postoperative pain and ventilatory capacity. Administration of 10 or 20 ml of 2.5 mg/ml or 5 mg/ml bupivacaine solution resulted in complete analgesia in 143 of 159 administrations. Most patients experienced the maximal pain-relieving effect within 1-2 min and analgesia persisted as a rule for 3-5 h. Forced vital capacity and forced expiratory volume in 1 s increased after intrapleural analgesia on average by 56% and 46%, respectively, on the first postoperative day and by 35% and 51%, respectively, on the second day. There was no significant difference in the analgesic effect or in the effect on the ventilatory capacity between the 2.5 mg/ml or the 5 mg/ml solution, in either the 10 ml or the 20 ml dose. Placebo (NaCl) given intrapleurally had no effect on pain or on the ventilatory capacity. The plasma concentration of bupivacaine after intrapleural administration showed a wide interindividual variation, with considerably higher average values when the 5 mg/ml solution had been used than for the 2.5 mg/ml solution. Although no toxic effects were noted, a 2.5 mg/ml solution, which can be given in an initial dose of 20 ml and top-up doses of 10 ml at 3-6 h intervals, is recommended. In four patients minor pneumothorax developed when the catheter was introduced. The pneumothorax was easily evacuated, but underlines the need for great care when introducing the catheter.

Densities in dependent lung regions during anaesthesia: atelectasis or fluid accumulation?

In previous studied with computed tomography (CT) prior to and during general anaesthesia, we found that densities developed in dependent parts of the lungs immediately after induction of anaesthesia in all examined patients. It was suggested that the densities were atelectases created by compression of lung tissue but an alternative explanation could be accumulation of extravascular fluid in the lung tissue and/or in the pleural space. In the present study the nature of the densities was analysed in further detail. Injections of contrast medium into the pleural space revealed that the densities were located in the lung tissue and not in the pleural space. By injecting contrast medium intravenously and repeating the CT scanning over a 2-min period the passage of contrast through the major vessels and the lung densities could be studied. The transit time of the contrast medium was of the same magnitude in the densities and the major lung vessels. This indicates that there were no regions with an increased amount of extravascular fluid to delay the contrast passage. These findings oppose the idea of fluid accumulation as the cause of the densities, while atelectasis remains the most plausible explanation.