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OBJECTIVE: To investigate health gain and its predictors during inpatient and associated day patient treatment. METHOD: Consecutive admissions to two inpatient units for children and young adolescents in northwest England were studied (N = 55). Ascertainments were made from multiple perspectives, including family, teacher, clinician, and an independent researcher. Measures were taken at referral, admission, discharge, and 6-month follow-up; health gain was inferred from change scores on measures. Recruitment lasted from late 1995 to 1997; follow-up was completed during 1998. Independent variables tested as predictors included assessments of presenting symptoms, therapeutic alliance, and family functioning. RESULTS: Significant health gain during hospitalization was found on most measures and sustained to follow-up. There was no symptom change during the waiting-list control condition. Health gain was predicted independently by child and parental therapeutic alliance with the unit early in hospitalization and by preadmission family functioning. Externalizing problems did well if accompanied by good alliance. CONCLUSIONS: Assessment of health gain from multiple perspectives is possible and valuable. Inpatient treatment has significant therapeutic effect. Predictors for health gain lie in process variables of therapeutic alliance and family functioning rather than presenting symptoms. The results are discussed in relation to clinical practice and future research.

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PURPOSE: Intrathecal morphine administered prior to coronary artery revascularization (CABG) surgery was studied to determine its effects on the stress response. METHODS: In a single centre, open, randomized clinical trial, first time elective CABG surgery patients, < 75 yr, were studied. Control subjects (n=12) received a standardized anesthetic consisting of fentanyl (maximum cumulative dose of 35 microg x kg(-1)), propofol, and pancuronium. In addition, spinal subjects (n=13) received 1.0 mg (age > 60 yr) or 1.5 mg (age < or = 59 yr) intrathecal morphine prior to induction of anesthesia. Control subjects received continuous i.v. morphine at 2 mg x hr(-1) on arrival in the ICU with i.v. bolus morphine supplementation as required while spinal subjects received bolus i.v. morphine as required. Changes in plasma cortisol and catecholamine concentrations were measured preoperatively, poststernotomy, on admission to ICU, following tracheal extubation, at 0800 hr on the first postoperative day, and 24 and 48 hr after ICU admission. RESULTS: No differences between groups were detected for demographic variables. The percent change in cortisol concentration relative to preoperative values (control vs spinal; (38 (87) vs -41 (46)%: P < 0.05)) was lower in the spinal group on admission to ICU. The percent change in plasma epinephrine levels (control vs spinal) on admission to ICU (285 (337) vs -10 (37)%) and 0800 hr after surgery (314 (341) vs -4 (37)%) was also significantly different. CONCLUSION: Intrathecal morphine only partially attenuated the postsurgical stress response in CABG surgical patients.

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A recently developed detection principle for gamma rays offers the prospect of improving the performance of positron emission tomographic scanners. This detection principle is based on the use of BaF2 scintillator and photosensitive wire chambers. We present technical results obtained with a prototype detector. It is shown that the impact point of the gamma ray can be determined with a precision of a few mm and that the detection efficiency is 60% with a time resolution of 10 ns (FWHM). A scanner based on the new principle is described and its anticipated performance discussed.

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Isoflurane-oxygen was given for induction and maintenance of anesthesia to ten patients having coronary artery bypass grafts. All had preserved ventricular function without hypertension or other cardiac lesions; treatment with beta-blocking drugs was maintained until the operation in all patients. Cardiac output, arterial and central pressures, coronary sinus (CS) blood flow, arterial and CS oxygen, Hb, and lactate contents were measured before, six times during, and twice after anesthesia. On induction, systolic arterial pressure was purposely reduced 33% along with systemic resistance by increasing the concentration of isoflurane; cardiac index, heart rate, and coronary flow did not change. Coronary resistance decreased 23% and CS oxygen content increased 56%; but in three of ten patients myocardial lactate production took place, evidence of global ischemia. Induction of anesthesia was not smooth in three patients. Controlled hemodynamic depression could be maintained with isoflurane-oxygen, but the frequency of myocardial lactate production before and after perfusion was greater than with other general anesthetics. Isoflurane dilated portions of the coronary bed but, because anaerobic metabolism occurred concomitantly, the theory that redistribution of flow can take place resulting in ischemic areas of ventricle is supported.

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Ten patients for coronary vein grafting had induction of anesthesia with fentanyl (30 micrograms/kg), followed by enflurane-oxygen sufficient to decrease systolic blood pressure by 27% before intubation. Enflurane was continued in concentrations to maintain blood pressure below that with patients awake. All patients had preserved ventricular function and effective beta-blockade. Studies of hemodynamic functions and myocardial blood flow and oxygenation were done before induction, six times during anesthesia, and twice postoperatively. The blood pressure decrease on induction and before bypass was due to reduced cardiac index without decreased heart rate or systemic resistance. Stroke work index decreased 47% on induction and remained below awake level throughout. Coronary sinus blood flow decreased 26% after intubation and remained so before bypass. Without change in coronary resistance, coronary sinus oxygen content increased 30% on induction and stayed elevated before bypass. Normal lactate extraction continued after induction and increased before bypass; mean extraction decreased after bypass, with one or two hearts producing lactate in the first 24 postoperative hr. Fentanyl-enflurane-oxygen maintained a steady mild hemodynamic depression during the operation and soon afterward, which preserved myocardial oxygenation.

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Twenty patients about to have coronary artery bypass grafts were studied before and after 15 min of 50% nitrous oxide added to either fentanyl (75 micrograms/kg) or enflurane (0.5%) anesthesia. Arterial and central pressures and cardiac output were measured, plus coronary sinus blood flow and arterio-coronary sinus differences in oxygen, hemoglobin, and lactate contents. Fentanyl-N2O and enflurane-N2O both decreased systemic resistance, heart rate, cardiac output, and hence arterial pressure. Stroke work decreased significantly with little or no change in wedge pressure: ventricular function was impaired. Coronary flow and myocardial O2 consumption decreased with fentanyl-N2O. Oxygen extraction increased with enflurane-N2O, as did lactate contents of coronary sinus blood. Hemodynamic depression occurred from the combined effects of nitrous oxide and fentanyl or enflurane. The beta-blocked myocardia of nonstimulated coronary patients were becoming ischemic globally on 50% oxygen, after significant hypotension. From this and other evidence, we conclude that nitrous oxide may not be benign in patients with coronary arterial disease.

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Ten patients were studied before, during and after enflurane anaesthesia for coronary vein grafting. All had good ventricular function and nine were receiving effective beta blockade. Cardiac output and vascular pressures were measured, plus coronary sinus blood flow (CBF), myocardial oxygen consumption (MVO2) and lactate extraction (MLE). Enflurane induction (10 minutes, mean 1.72 per cent end tidal) reduced blood pressure (MAP), due to decreased cardiac index (CI), with no change in heart rate or systemic resistance. Intubation returned MAP and CI to control level but the heart rate increased. Subsequently, enflurane kept MAP, CI and stroke work below the awake level. CBF decreased on induction, rose again on intubation and remained normal before bypass. MVO2 fell on induction from an increase in CS oxygen content, which remained elevated. Normal MLE continued in every patient. There was no evidence of myocardial ischaemia in patients on beta blockade, when haemodynamics were maintained at or below those of the sedated, awake state.

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A system was evaluated of measuring Pao2 and Pao2 by an inline sensor in the brachial artery and gas chromatography. Eight patients having coronary artery vein grafts were studied during anaesthesia, operation, perfusion and for 24 hours afterward. Compared to conventional blood gas analysis by polarography (electrodes), the chromatographic method gave readings for Pao2 which were not significantly different during normothermia. During hypothermic perfusion, the chromatographic system read significantly higher than the bench electrode, due at least in part to a difference in temperature correction. For Pao2 the correlation between the two methods was close and differences were clinically insignificant. The Sentorr blood-gas analyser provides a sensitive, accurate indicator of changes in oxygenation, ventilation and circulation during anaesthesia and in the intensive care unit.

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A simple mathematical model has been developed which is able to fit the impedance waveform produced by normal and abnormal subjects throughout the cardiac cycle with reasonable precision. Contributions from both the aorta and vena cava are significant. Fitted values of model parameters offer potentially useful clinical information. Estimates of the stroke volume obtained from the model correlate will with values derived from the maximum rate of change of the thoracic impedance during systole, but are in poorer agreement with values obtained using tracer dilution techniques.

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In a patient with a solitary pheochromocytoma severe hypoglycemia developed following excision of the tumour. The possible causative mechanism was thought to be a reactive relative increase in insulin production secondary to increased endogenous production of glucose, induced by the large amounts of epinephrine produced by the tumour. Alternatively, epinephrine withdrawal following removal of the tumour under phentolamine infusion may have induced increased insulin production and hence potentiated the development of hypoglycemia. Careful monitoring of the blood glucose concentration during and after the operation is recommended to obviate this potentially fatal complication.

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