No abstract

The benefits, risks and resource implications of providing an Acute Pain Service were assessed during the first year of the service. Six hundred and sixty patients recovering from major surgery were treated with patient-controlled analgesia (510 patients) or extradural infusion analgesia (150 patients). The results of a prospective outcome study showed that pain control was good: more than 60% of patients scored their pain as mild during the first 24 h. Only 10% of patients complained of severe postoperative pain. Eight patients developed potentially serious complications including respiratory depression and hypotension; the diagnosis and management of these problems on general wards is discussed. Retrospective analysis of the incidence of postoperative chest infection in surgical patients showed a marked reduction during the first year of the service (1.3% in 1988, 0.4% in 1989-90 (P less than 0.01].

A randomized, double-blind study of 38 patients undergoing total knee replacement was undertaken to compare the efficacy and respiratory effects of low-dose spinal morphine and patient-controlled i.v. morphine against patient-controlled i.v. morphine alone. Patients received either morphine 0.3 mg or saline 0.3 ml with 0.5% heavy spinal bupivacaine 2-2.5 ml. Respiratory effects were measured continuously for 14 h postoperatively with an Edentec 3711 respiratory monitor. There was an improvement in pain relief in the intrathecal morphine group, with significantly lower median VAS pain scores on movement at 4 h (0 (median 0-1.5) vs 5 (1.25-7.75) P < 0.01), 12 h (2 (1-5) vs 6 (3-8) P < 0.01) and 24 h (3 (1-5) vs 5 (3-7) P < 0.05) postoperatively, despite using significantly less patient-controlled morphine (20 mg (10.25-26.25) vs 38.5 mg (27-51) P < 0.01) in the first 24 h. There was a small but statistically significant reduction in the median oxygen saturation (SpO2) in the intrathecal morphine group 97 (95-99)% compared with the placebo group 99 (97-99)% (P < 0.05). Although marked disturbances in respiratory pattern were observed in both groups, none of the patients in the study had severe hypoxaemia (SpO2 < 85% > 6 min h-1) and there was no significant difference in the incidence of mild (SpO2 < 94% > 12 min h-1) or moderate (SpO2 < 90% > 12 min h-1) hypoxaemia or in the incidence of episodes of apnoea or hypopnoea in the two groups.

Arterial oxygen saturation (SaO2) was analysed continuously before and for 24 h after lower abdominal surgery in 30 patients breathing air using one of three postoperative analgesic regimens: i.v. diamorphine using a patient-controlled analgesia system (PCAS), extradural diamorphine or i.m. morphine. Hypoxaemia was defined as SaO2 less than 94% for more than 6 min h-1. Before operation there was no difference between the three analgesia groups assessed by the duration when SaO2 was less than 94%. After operation the pattern of SaO2 vs time distribution was either stable, with little variation from hour to hour with no hypoxaemia, or unstable with large variation with 30% of patients hypoxaemic. Thus three patterns of SaO2 distribution were seen in the postoperative period: stable without hypoxaemia (4/10 PCAS, 0/10 extradural, and 1/10 i.m. patients), unstable without hypoxaemia (4/10 PCAS, 5/10 extradural and 7/10 i.m. patients) and unstable with prolonged nocturnal periods with SaO2 less than 94% for a mean of 17.7 min h-1, 95% confidence limits (CL) 10-25 min h-1, (2/10 PCAS, 2/10 i.m. and 5/10 extradural patients). Before operation, the unstable group with hypoxaemia spent longer at less than 94% SaO2 (mean 4.8 min h-1, 95% CL 1.0-8.6 min h-1) than the stable group (mean 0.4 min h-1, 95% CL 0.17-0.61 min h-1) and this was a predictor of postoperative hypoxaemia. Hypoxaemia occurred in all analgesia groups, but extradural diamorphine tended to cause longer periods. Some patients at risk of postoperative hypoxaemia may be predicted by preoperative monitoring of SaO2 although extradural diamorphine boluses were associated with hypoxaemia in patients with normal preoperative values.

SummaryPostoperative hypoxaemia results predominantly from two mechanisms. Gas exchange is impaired during anaesthesia as a result of reduced tone in the muscles of the chest wall and probably alterations in bronchomotor and vascular tone, and the resulting changes persist into the postoperative period. In addition, there is an abnormality of control of breathing, which results in episodic obstructive apnoea. These episodes continue for several days after operation and are related to sleep pattern and analgesic administration, although the precise effects of different analgesic regimens have not been evaluated. Oxygen administration is effect in reducing the degree of hypoxaemia. Key wordsHypoxia; postoperative. Lung; atelectasis. The role of intra-operative atelectasisIt is widely believed that postoperative respiratory depression after administration of opioid is a rare event.' However, the validity of this belief depends on the criteria used to define respiratory depression. Most investigators have focused on hypercapnia or changes in ventilatory rate as the main indicators of postoperative respiratory depression. We showed recently that 60% of patients who received a morphine infusion after operation had episodes of hypoxaemia (Spo, < 80%). These were associated with obstructive apnoea, occurred exclusively during sleep and were rarely associated with a slow respiratory rate or small tidal volume.* It must be emphasised that hypoxaemia rather than hypercapnia is of the greatest clinical concern, but the degree of hypoxaemia has, until recently, rarely been measured in postoperative patients. General anaesthesia, particularly for surgical procedures on the upper abdomen and thorax, is followed by a decrease in Pao, which may persist for many days postoperatively. This is caused by intrapulmonary shunting and is less frequently accompanied by either a change in Paco, or reduced rate of breathing. An explanation for this postoperative shunting is based on changes in lung function that are induced during anaesthesia and persist postoperatively. Postoperative opioid-induced obstructive apnoea leads to a further decrease in oxygen saturation. The problem is therefore the additive effect of two causes of hypoxaemia, each of which might be harmless, by itself.The recent introduction of pulse oximetry has provided an excellent opportunity to examine in more detail the causes, severity and duration of postoperative hypoxaemia. Mechanisms of impaired gas exchange during and after anaesthesiaOne of the most consistent changes in pulmonary function after induction of anaesthesia is a reduction in functional residual capacity (FRC) due partly to a change in shape of the chest wall and partly to a change in intrathoracic blood volume. A close relationship has been shown between the reduction in FRC and an increase in alveolar-arterial Po, gradient.3 Subsequent research has progressed in two directions: a search for the cause of the abnormality of gas exchange; and the cause of the change in lung volume.The decreases in FRC...