[Fulminant acute pancreatitis caused by a large parathyroid adenoma. Hyperparathyroidism was diagnosed after 5 years].
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Adenoma↗
Biomedical subjects
C J Wickerts
Publications and source records attributed to C J Wickerts.
A retrospective analysis of nitric oxide inhalation in patients with severe acute lung injury in Sweden and Norway 1991-1994.
BACKGROUND: Patients with severe acute lung injury (ALI) have been treated compassionately on doctors' initiative with inhaled nitric oxide (INO) in Sweden and Norway since 1991. In 1994 the previously used technical grade nitric oxide was replaced by medical grade nitric oxide. METHODS: We have carried out a retrospective data collection on all identified adult patients treated with INO for >4 h during the period 1991-1994 focusing on safety aspects and patient outcome. We used the following exclusion criteria (1) Age <18 years, (2) Simultaneous treatment with extracorporeal removal of CO2 (3) NO inhalation period <4 h, (4) Incomplete or missing patient charts, (5) Use of INO in order to treat pulmonary hypertension following cardiac surgery, with little or no acute lung injury. RESULTS: Inclusion criteria were met by 56 out of 73 identified patients. Mean age was 48+/-19 years and the median duration of INO treatment was 102 h. PaO2/FIO2 ratio at start of treatment was 85 +/- 33 mm Hg with a lung injury score (LIS) of 3.2+/-0.8. The aetiology of the lung injury was pneumonia (n= 27), sepsis (n=12) and trauma (n=8). Survival to hospital discharge was 41% and survival after 180 d was 38%. Three serious adverse events were identified, two from technical failures of the INO delivery device and one withdrawal reaction necessitating slow weaning from INO. No methaemoglobin values >5% were reported during treatment. CONCLUSION: The overall mortality did not differ dramatically from historical controls with high mortality. Only a randomised study may determine whether INO as an adjunct to treatment alters the outcome in severe ALI. One cannot at present advocate the routine use of INO in patients with ALI outside such studies.
Administration, Inhalation↗
Hypertonic-hyperoncotic solution increases canine lymph flows.
BACKGROUND: Hypertonic-hyperoncotic solutions (HHS) have attracted a lot of interest in the treatment of various forms of hypovolaemic conditions during the last decade. It has been speculated that HHS might even be of therapeutic value in normo- and hypervolaemic conditions by mobilising extravascular fluid. METHODS: We studied thoracic and abdominal lymphatic flows and circulatory response following the administration of a single bolus injection of hypertonic-hyperoncotic solution, 10% dextran 60 in 7.2% saline (HHS), in a nonhypovolaemic canine model. A modified surgical procedure for collecting thoracic lymph is also presented. RESULTS: Both thoracic and abdominal lymph flow increased significantly by approximately 50% after administration of HHS. Cardiac output and calculated pulmonary capillary hydrostatic pressure increased. CONCLUSION: Hypertonic-hyperoncotic solution given intravenously as a single injection increased both thoracic and abdominal lymph flows in the initially normovolaemic animal.
Animals↗
Plasma levels of cytokines in primary septic shock in humans: correlation with disease severity.
Thirteen patients (median age, 20 years) with life-threatening primary septic shock (10 meningococcal, 3 pneumococcal infections) were studied prospectively. All had a short history of sepsis (< or = 24 h) and no severe underlying disease. Two (15%) died. The logarithm of the initial plasma levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6, IL-1 receptor antagonist (ra), and plasminogen activator inhibitor (PAI)-1 correlated significantly with APACHE II scores (r2 = .67, .57, .68, .81, and .68, respectively). The plasma levels of endotoxin, TNF-alpha, IL-1 beta, and PAI-1 decreased toward normal levels within the first 24 h of treatment, but IL-6 and IL-1ra levels remained high until clinical recovery. On admission, the molar excess of IL-1ra to IL-1 beta was > 2000-fold in 11 of the 13 patients. Acute plasmapheresis in 11 of the 13 patients significantly increased the plasma clearance of TNF-alpha (P = .02).
Adolescent↗
Clinical application of differential ventilation with selective positive end-expiratory pressure in adult respiratory distress syndrome.
Differential ventilation in the lateral position with positive end-expiratory pressure (PEEP) selectively applied to the dependent lung (DVSP) has been shown to reduce venous admixture and improve oxygenation without compromising cardiac output in short term studies of patients with acute respiratory failure. We have applied this ventilation technique as a long-term treatment in severe adult respiratory distress syndrome (ARDS) in an open clinical trial. Eleven patients with ARDS of varying aetiology were treated with DVSP for a total of 34 days. Median duration of conventional ventilatory therapy before start of DVSP was 5 days (1 to 18 days), inspiratory oxygen fraction (FIO2) was 0.61 +/- 0.16 (mean +/- s.d.), resulting in a mean arterial oxygen tension (PaO2) of 7.1 +/- 2.1 kPa (PaO2/FIO2 = 11 +/- 4 kPa). A gradual improvement in gas exchange was seen during the first 24 h of DVSP such that PaO2 increased to 8.4 +/- 1.4 with a decreased FIO2 (0.52 +/- 0.14) resulting in an increased PaO2/FIO2 (16 +/- 5 kPa). Five out of the eleven patients survived. No major complication was noted using DVSP as a method. We found a steady improvement in gas exchange over the first 24 hours in most patients. However, mortality rate was no lower than expected. Drawbacks with DVSP were increased demand on staff and difficulties with adequate endo-bronchial suctioning.
Adolescent↗
[Case report. Thrombolysis of pulmonary embolism during heart massage].
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Aged↗
Enhanced pneumonia resolution by inhalation of nitric oxide?
We present a patient with severe bacteraemic pneumococcal pneumonia associated with severe hypoxaemia, where nitric oxide (NO) 15-40 ppm was added to the inspired gas. Nitric oxide therapy improved gas exchange, reduced pulmonary vasoconstriction and peak airway pressure. The patient survived. We observed an unexpected rapid and complete disappearance of bilateral pulmonary infiltrates during the first 120 h of the 7-day NO inhalation period.
Administration, Inhalation↗
Plasmapheresis in the treatment of primary septic shock in humans.
14 patients (mean age 25.5 yrs) with life-threatening primary septic shock were eligible for treatment with acute plasmapheresis in a prospective study. They had a short history of sepsis and had no severe underlying disease. 10/14 patients had systemic meningococcal disease. All patients were severely ill with a mean APACHE II score of 25.0. 12/14 patients were treated with plasmapheresis exchanging 1 plasma volume within hours of admission. 11/14 patients survived without major sequelae and 3 (21%) died of irreversible septic shock. This mortality is lower than that predicted from the APACHE II scores (55.2%). A subgroup of plasmapheresis-treated patients with septic shock and extensive petechiae were compared to a historical control group. The mortality in the treatment group was 1/7 (14%) versus 8/21 (38%) in the control group. We conclude that acute plasmapheresis may be a therapeutic option in the early stages of severe primary non-surgical septic shock.
Adolescent↗
Influence of positive end-expiratory pressure on extravascular lung water during the formation of experimental hydrostatic pulmonary oedema.
The influence of positive end-expiratory pressure (PEEP) on extravascular lung water measured with the double-indicator dilution technique (EVLWi) has been studied during formation of hydrostatic pulmonary oedema in a canine model. The oedema was created by elevating the mean pulmonary artery pressure (PAP) to 30 mmHg (4.0 kPa) by inflation of a left atrial balloon, and a simultaneous intravenous saline infusion of 15 ml.kg-1.h-1. All dogs were ventilated with zero end-expiratory pressure (ZEEP) until the initial EVLWi had increased by 50%. In one group (n = 5) a PEEP of 10 cmH2O (1.0 kPa) was applied and the dogs were studied for a further 4 h and in the other group (n = 5) ZEEP was maintained throughout the study. During the first 2 h after ZEEP/PEEP application EVLWi increased from 13.7 +/- 2.1 to 20.2 +/- 1.2 ml.kg-1 with ZEEP ventilation and from 13.6 +/- 1.2 to 18.6 +/- 1.9 ml.kg-1 with PEEP ventilation. EVLWi remained unchanged during the last 2 h in both groups. The gas exchange improved with PEEP, arterial oxygen tension increased from 30.4 +/- 8.9 kPa to 38.6 +/- 2.5 kPa (P less than 0.01), and the shunt fraction decreased from 6.0 +/- 3.8% to 1.2 +/- 0.8% (P less than 0.001). There were significant differences (P less than 0.01) in both PaO2 and shunt fraction between the ZEEP and PEEP groups throughout the study. In conclusion, positive end-expiratory pressure improves gas exchange but does not protect against increasing extravascular lung water during the creation of hydrostatic pulmonary oedema.
Animals↗
Influence of hypertonic-hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.
1. This study aimed at enhancing the clearance of experimental hydrostatic pulmonary oedema in dogs using hypertonic-hyperoncotic solution (HHS) and furosemide. 2. Anaesthetized dogs (n = 20) were mechanically ventilated with a positive end-expiratory pressure of 10 cmH2O (1.0 kPa). 3. Hydrostatic pulmonary oedema was induced by inflating a balloon inserted into the left atrium and simultaneously infusing isotonic saline rapidly. Oedema formation was terminated by deflating the balloon and reducing the infusion rate. 4. Four groups were studied: A, control; B, furosemide; C, HHS and D, HHS+furosemide. HHS, 6 ml kg-1, was given as a bolus injection and furosemide, 1 mg kg-1, intravenously as a bolus followed by an infusion of 0.5 mg kg-1 h-1. All dogs were studied for 4 h. 5. Serum osmolarity, plasma colloid oncotic pressure and diuresis in groups C and D (HHS groups) substantially increased; haemoglobin concentration decreased and pulmonary arterial wedge pressure remained constant. 6. Despite the combination of these factors favouring fluid flux from the extravascular to the intravascular compartment, extravascular lung water measured with the double indicator dilution technique decreased no faster in the HHS groups than in the two other groups (from over 26 to approximately 19 ml kg-1 in groups A, C and D and to 14.7 in group B (only furosemide)). 7. This was confirmed by postmortem gravimetric measurements of extravascular lung water; A, 11.0 +/- 5.7; B, 9.7 +/- 3.3; C, 10.5 +/- 3.1 and D, 10.6 +/- 1.8 g kg-1. 8. We speculate that mechanisms other than effective Starling gradients and enhanced diuresis might define a maximal rate of pulmonary oedema clearance.
Animals↗
Thoracic lymph drainage in the dog: evaluation of a new model.
A new model for selective sampling of thoracic lymph flow (TLF) and abdominal lymph flow (TDA) in the dog was assessed to ascertain whether there were extrathoracic contributions of lymph to the TLF. Inflating a right atrial balloon in 4 dogs and a left atrial balloon in 2 dogs indicated good separation between TLF and TDA. Data on total lymph protein and albumin clearance before and after oleic acid induced pulmonary oedema in an additional 5 dogs indicated that TLF and TDA drained two differing regions. Our data demonstrate that this lymph preparation provides a sample of thoracic lymph flow with no major extrathoracic lymph contamination. We also propose an alternative method to test for extrathoracic contributions to thoracic lymph, by the application of positive end-expiratory pressure, thereby replacing right atrial balloon inflation.
Albumins↗
Effects of pleural fluid and positive end-expiratory pressure on the measurement of extravascular lung water by the double-indicator dilution technique.
The reliability of the double-indicator dilution technique (dye/cold) for measuring extravascular lung water (EVLW) has been studied in lung-healthy dogs after pleural fluid injection of saline (up to 20 ml/kg) during mechanical ventilation at zero and 10 cmH2O (1.0 kPa) end-expiratory pressure (ZEEP and PEEP, respectively). Pleural fluid injection had no effect on EVLW at either ZEEP or PEEP. PEEP induced changes in cardiac output, and reduced both the intravascular (dye) and the thermal indicator volumes, but with no effect on the calculated EVLW. It is concluded that pleural fluid up to 20 ml/kg and ventilation with PEEP of 10 cmH2O (1.0 kPa) do not affect the reliability of the double-indicator dilution technique for measuring extravascular lung water in the dog.
Animals↗
Furosemide, when used in combination with positive end-expiratory pressure, facilitates the resorption of extravascular lung water in experimental hydrostatic pulmonary oedema.
The study aimed to establish whether furosemide given intravenously improved resorption of hydrostatic pulmonary oedema in 14 dogs mechanically ventilated with positive end-expiratory pressure (PEEP). Hydrostatic pulmonary oedema was created by simultaneous inflation of a left atrial balloon and rapid intravenous infusion of isotonic saline. The hydrostatic process was terminated by deflating the balloon and reducing the infusion rate. A PEEP of 10 cmH2O (1.0 kPa) was applied in all animals; in seven, furosemide was administered (diuretic group), 1 mg/kg intravenously as a bolus followed by an infusion of 0.5 mg/kg per hour, while the remaining seven dogs served as a control group. All dogs were studied for a period of 4 h. The extravascular lung water measured with the double indicator dilution technique was 28.3 +/- 3.8 (diuretic group) and 28.2 +/- 6.8 ml/kg (control group) during maximum oedema. It was reduced to 16.4 +/- 2.2 (diuretic group) vs 19.8 +/- 3.7 ml/kg (control group) after 4 h of resorption, P less than 0.05. Postmortem gravimetric values of extravascular lung water were 9.1 +/- 3.4 (diuretic group) vs 12.6 +/- 5.0 g/kg (control group). In the diuretic group the urinary output increased threefold, and haemoglobin and serum protein concentrations were higher than in the control group. There was a significantly greater decrease in cardiac output and central blood volume in the diuretic group. In conclusion, furosemide given intravenously improved lung fluid resorption in hydrostatic pulmonary oedema, probably by increasing the plasma colloid osmotic pressure.
Animals↗
Does PEEP facilitate the resolution of extravascular lung water after experimental hydrostatic pulmonary oedema?
The effect of mechanical ventilation with positive end-expiratory pressure on the resolution of hydrostatic pulmonary oedema created by temporary left atrial balloon inflation was studied in mechanically ventilated dogs. Immediately after the hydrostatic process was terminated, by deflating the left atrial balloon, the animals were ventilated for 4 h with zero end-expiratory pressure (ZEEP, n = 6) or with a positive end-expiratory pressure (PEEP, n = 6) of 1.0 kPa (10 cmH2O). Gas exchange and extravascular lung water content (EVLW) with the double indicator dilution technique (dye/cold) were studied and gravimetric determination of lung water was made postmortem. EVLW decreased from 31.6 +/- 7.3 mean +/- SD ml.kg.1 during maximal oedema to 14.5 +/- 2.1 ml.kg.1 (p less than 0.001) 4 h after deflation of the left atrial balloon in dogs ventilated with ZEEP. The corresponding values in dogs ventilated with PEEP were a reduction in EVLW from 28.0 +/- 4.1 to 20.7 +/- 4.0 ml.kg.1 (p less than 0.01) (mean decrease 7.3 +/- 4.0 ml.kg.1). EVLW was significantly higher after 4 h on PEEP than after ZEEP (p less than 0.01). Gravimetric values at the end of the experiment were 12.4 +/- 2.8 ml.kg.1 (ZEEP) and 14.7 +/- 4.5 ml.kg.1 (PEEP) (NS). Oxygenation improved in both groups during the resolution of oedema with a more evident and early effect in the PEEP group. It is concluded that mechanical ventilation with PEEP of 1.0 kPa (10 cmH2O) in the resolution phase after experimental hydrostatic oedema improves oxygenation but retards the resolution of oedema.
Animals↗
Measurement of extravascular lung water by thermal-dye dilution technique: mechanisms of cardiac output dependence.
The extent to which extravascular lung water (EVLW) is dependent on cardiac output was analysed in anaesthetized and mechanically ventilated pigs. EVLW was measured by thermal-dye dilution technique, by a fibreoptic thermistor catheter system (system 1), and by a thermistor catheter-external optical cuvette system (system 2). During baseline conditions, at which cardiac output was 3.65 l/min, and EVLW was 11.7 and 7.7 ml/kg b.w. with systems 1 and 2 respectively. A reduction of cardiac output to a mean of 1.90 l/min by the addition of halothane to the inspired gas did not significantly affect EVLW with system 1 (-5%) but increased EVLW by 39% (p less than 0.05) with system 2. An increase of cardiac output to a mean of 4.78 l/min by intravenous infusion of isoproterenol caused a small increase in EVLW with system 1 (14%; p less than 0.05) and a decrease with system 2 (10%; p less than 0.05). The dependence on cardiac output was the same whether the catheters were positioned centrally (aortic root) or peripherally (abdominal aorta). With system 1 the CO dependence was due to different time constants in thermistor and optical systems, and with appropriate phasing the dependence could be eliminated. With system 2 a large overestimation of the mean transit time difference between the two indicators was seen when cardiac output was low, resulting in overestimation of EVLW. It is concluded that the dependence of EVLW volume on cardiac output is an artefact due to technical problems in the design of the recording equipment rather than a reflection of pulmonary or vascular effects.
Animals↗
Lung fluid balance evaluated by the rate of change of extravascular lung water content.
Lung fluid balance was studied in 27 mongrel dogs by measuring changes in extravascular lung water content (EVLW). The expression delta EVLWi, which is the difference in EVLWi per kilo bodyweight per hour between two measurement occasions, was used as an estimate of the rate of change of EVLW. EVLW was measured by a double-indicator dilution technique (EVLWi) using iced glucose and indocyanine green. In addition, EVLW was determined at the end of each experiment with gravimetric technique (EVLWg), which enabled the calculation of a regression equation between EVLWi and EVLWg. Delta EVLWi was calculated repeatedly during an 8-h period of mechanical ventilation (MV) with no application of a positive end-expiratory pressure (n = 5), during an 8-h period with a positive end-expiratory pressure (PEEP) of 10 cmH2O (1.0 kPa) (n = 5), during the development of oleic acid (OA)-induced pulmonary oedema (n = 7), and hydrostatic pulmonary oedema (left atrial balloon inflation) (n = 9). An increase of EVLW was seen during PEEP 8 h (mean 35%) and after induction of OA and hydrostatic oedema (mean 300%), but no change was found during MV without PEEP. The regression equation was EVLWi = 5.5 + 0.97 x EVLWg (P = 0.001, r = 0.90). OA-induced oedema caused a mean maximum delta EVLWi of 5.1 ml/kg/h, indicating capillary leakage which, however, was self-limiting within 2 h after OA injection. In hydrostatic oedema there was a maximum delta EVLWi of 16.0 ml/kg/h. Delta EVLWi was negative after deflation of the left atrial balloon, indicating reabsorption of oedema.
Animals↗
Net fluid leakage (LN) in experimental pulmonary oedema in the dog.
Net fluid leakage (LN) from the intravascular to the extravascular pulmonary space was estimated in anaesthetised dogs after injection of oleic acid (OA) (n = 8), or after hydrostatic pressure elevation by inflation of a left atrial balloon (n = 5). LN was calculated as the sum of: (i) rate of change in extravascular lung water (delta EVLW), (ii) thoracic lymph flow, and (iii) pleural fluid formation per time unit. Pleural fluid formation was measured in five dogs with hydrostatic or OA induced pulmonary oedema and was 1.8 +/- 0.9 ml/kg/h. In OA-induced pulmonary oedema, LN increased to a peak of 9.2 ml/kg/h within 2 h after OA injection. Thereafter LN fell and was 2-4 ml/kg/h during the succeeding 2-4 h. During hydrostatic pulmonary oedema LN was increased to as much as 13 ml/kg/h, but it became negative, -5 to -8 ml/kg/h (reabsorption of extravascular fluid) as soon as pulmonary vascular pressures returned to normal following deflation of the left atrial balloon. We conclude that in both forms of oedema there is an initial rapid leakage. In OA-induced oedema this leakage continues, although at a slower rate, whereas in hydrostatic oedema there is a considerable net fluid absorption from the pulmonary extravascular to the intravascular space as soon as vascular pressures are brought to normal levels.
Animals↗
Effects of PEEP on extravascular lung water and central blood volume in the dog.
Twenty-four mongrel dogs were anaesthetized and ventilated mechanically in the supine position. Extravascular lung water (EVLW) and central blood volume (CBV) were measured with a double indicator (dye/cold) dilution technique. Both indicators were detected intravascularly in the aortic root with a fibreoptic thermistor catheter. Seven dogs ventilated with a positive end-expiratory pressure (PEEP) of 1.0 kPa (10 cmH2O) for a short period of time (less than 20 min) displayed no significant change in EVLW as measured with the indicator dilution technique (= EVLWi), while reductions were seen in both CBV (15%, P less than 0.01) and cardiac output (CO-thermodilution technique) (10%, P less than 0.05). Another seven dogs ventilated with a PEEP of 1.0 kPa for 8 h showed a gradual increase in EVLWi. After 8 h, a mean increase of 34% (P less than 0.01) was recorded, and the increase was also verified by post-mortem gravimetric determination of EVLW (= EVLWg), displaying an increase of 61% (P less than 0.01). In five dogs ventilated with zero end-expiratory pressure (ZEEP) for 8 h, no changes in EVLWi, CO, and CBV were observed, and EVLWg was mean 4.39 g/kg body weight (BW). Five additional dogs were sacrificed after 15 min of anaesthesia without catheterization and EVLWg was found to be 4.24 g/kg BW. It is concluded that EVLWi does not change measurably during ZEEP or short periods of PEEP. However, long periods (8 h) of PEEP result in elevated EVLWi values. Gravimetry supports these conclusions.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗