PLEURAL EFFUSION COMPLICATING THIOPENTONE ADMINISTRATION

Transcription

1 Brit. J. Anaesth. (1967), 39, 78 A Case Report BY M. W. POTTS AND P. W. R. SMETHURST Department of Anaesthetics, Guy's Hospital, London SUMMARY In a case report concerning a patient with mitral stenosis and mixed aortic valve disease we illustrate and describe the development of and subsequent recovery from, acute interstitial pulmonary oedema together with a large pleural efifusion, following induction of anaesthesia with thiopentone. Attention is drawn to the disproportion between physical signs and radiological appearance and also to the speed of onset and disappearance of both clinical signs and radiological evidence of pulmonary oedema and, more unexpectedly, the pleural effusion. Recorded are the accompanying changes in blood gas and oxygen saturation estimations and details are given of the treatment employed. The induction of anaesthesia with thiopentone can precipitate circulatory collapse with severe consequences (Edwards et al., 1956), this being a particular hazard in patients suffering from severe heart disease, (Dinnick, 1964); furthermore, it has been possible to demonstrate a linear relationship between blood thiopentone concentration and arterial hypotension in man (Price, Dundee and Conner, 1957). There is evidence suggesting that two principal factors are responsible for this hypotension. The first is direct myocardial depression or negative inotropic effect (Prime and Gray, 1952; Goldberg, Maling and Gaffney, 1961); the second a decreased venous return due to peripheral vasodilatation with, in particular, loss of venous tone (Eckstein, Hamilton and McCammond, 1961). A fall in cardiac output due to either or both of the above causes is a likely explanation of how, in a patient with mitral stenosis, acute left ventricular failure with consequent pulmonary oedema can be precipitated by too rapid or too great an administration of intravenous barbiturate. The case described illustrates such a complication and, in addition, the development of a large pleural effusion. CASE REPORT The patient was a married man aged 39 and weighing 67 kg; his previous medical history contained references to rheumatic fever and chorea as a child with an attack of nephritis in adolescence and the subsequent development of valvular heart disease which for some time remained symptomless. However, by 1951 deterioration in health led to a mitral valvotomy being performed; despite embolic complications the result was good. In the preceding 18 months his symptoms had recurred, particularly increasing breathlessness and intermittent bilateral daudication; this led to hospital admission for further investigation and assessment The diagnosis on clinical findings was of mitral restenosis with mixed aortic valve disease and the circulation in the lower limbs was noted to be poor; in addition a series of chest radiographs showed evidence of chronic venous congestion with well marked haemosiderosis. The valve lesions were confirmed by cardiac catheter studies performed without complication under sedation using papaveretum IS mg hyoscine 0.3 mg and promethazine 25 mg with chlorpromazine 10 mg given via the catheter during the procedure. Before proceeding with cardiac surgery it was decided to investigate the cause of his intermittent claudication by translumbar aortography under general anaesthesia. Bed rest in hospital had improved his general condition, there was no overt heart failure although chest radiographs demonstrated marked venous congestion: the only significant drug therapy was chlorothiazide 1 g given on alternate days. A preoperative film, seen by the anaesthetists, was subsequently reported as showing the cardiac configuration indicative of right ventricular and left atrial enlarge-

2 ment due to mitral disease, mainly stenosis. In addition there was some collapse at the right base which might have masked a small amount of pleural fluid: however, the costo-phrenic angle and periphery of the lung was clear and certainly no appreciable amount of fluid was present. The collapse of the right lower lobe with elevation of the diaphragm was not, however, evident pre-operatively either clinically or radiologically to the anaesthetists. Figure 1 shows the radiological appearance of the lungs at this time. Premedication for the proposed aortogram consisted of pethidine 75 mg and atropine 0.6 mg by subcutaneous injection 2 hours before induction of anaesthesia. On arrival in the anaesthetic room the patient appeared calm and although pale his condition gave no cause for concern: induction of anaesthesia was performed with the patient supine, his head supported by one pillow, using a slow intravenous injection of 5 per cent sodium thiopentone; he was still awake after 275 mg and so the injection was continued until a total of 325 mg had been given. Following suxamethonium 60 mg the lungs were ventilated with oxygen and the trachea intubated with a Magill tube (11.0 mm). Cyanosis was noted although ventilation was continued with nitrous oxide and oxygen in 50 per cent mixture; moreover, movement of the chest indicated FIG. 1 Erect postero-anterior chest film. There is chronic venous congestion with well-marked haemosiderosis. This film differs from previous ones in that it shows some collapse at the right base which may be masking a small amount of fluid. The costophrenic angle and periphery of the lung are clear, so there can be no appreciable amount of fluid present. 79 that there was inflation of both lungs and this was confirmed by auscultation; however, even when 100 per cent oxygen was again used the cyanosis persisted and appeared to intensify: the radial pulse felt weak and hypotension (systolic pressure 70 mm Hg) was confirmed. It seemed dear that the relative or absolute overdose of thiopentone had resulted in acute left ventricular failure and so a subcutaneous injection of isoprenaline sulphate 0.1 mg and an intravenous injection of methyl amphetamine 6 mg were given, following which there was an immediate rise in systolic pressure to 100 mm Hg. About 8 minutes had elapsed since induction and cyanosis still persisted, so that in order to establish whether it was of central or peripheral origin an arterial blood sample was taken and found to be obviously desaturated; subsequent measurements gave the following results: Oxyhaemoglobin saturation 68 per cent (Kipp Haemorenector); Paco, 70 mm Hg; Standard bicarbonate 20.5 m.equiv/l; ph (by Micro-Astrup determination). After approximately 12 minutes spontaneous respiration began with the blood pressure having risen to 120 mm Hg systolic and the patient beginning to react to the stimulus of the endotracheal tube, accordingly halothane (0.5 per cent) was introduced. Auscultation of the chest had, at that time, revealed no abnormality except fine crepitations over the right lung field. A supine anteroposterior chest radiograph taken now, 25 minutes after induction (fig. 2), showed FIG. 2 Supine antero-posterior chest film. There is evidence of pulmonary oedema on both sides but particularly on the right where there is, in addition, a large pleural effusion. Although this print is suggestive of a localized left pneumothorax the original film showed lung markings visible to the periphery.

3 BRITISH JOURNAL OF ANAESTHESIA 80 FIG. 3A FIG. 3B (A) Pleura! effusion partially shown in this lateral decubitus film. (B) The effusion, whose lateral limit is not shown, is represented by the black unstippled area in this drawing. The interlobar distribution is particularly evident. mottled oedema, predominantly throughout the right lung where a large pleural effusion was also apparent: on the left side, where oedema was less severe, lung markings were visible to the periphery. Although this film was taken in the supine position the volume of pleural fluid, which extended from apex to bast, appeared much greater than could have b;en concealed in figure 1 (erect). It was noteworthy that, despite the clinical and radiological findings, aspiration of the bronchial tree was at no time productive of any frothy blood-stained fluid; indeed there seemed no evidence of any increase in bronchial aspirate. It was decided to abandon the aortogram on the basis of the clinical and radiological findings although it was clear that steady improvement was occurring, therefore halothane was withdrawn, extubation performed and shortly thereafter the patient regained consciousness. A slow intravenous injection of aminophylline 0.5 g was then given but diuretics were withheld because clinically the pulmonary oedema appeared to be diminishing; the patient was by now co-operative enough for a lateral decubitus film to be taken (fig. 3A, B), in which the large right-sided pleural effusion was more clearly seen than in figure 2, although the lateral chest wall was partially excluded from the picture, which was of poor quality. Clinical examination at this time, with the patient sitting up, confirmed the presence of a pleural effusion, there was dullness to percussion and a reduction in breath sounds over the whole right posterior chest A third film in the supine anteroposterior projection was taken some 10 minutes after the lateral decubitus film and showed considerable improvement in the pulmonary oedema (fig. 4). A second arterial blood sample showed an oxyhaemoglobin saturation of 91 per cent; the patient was fully conscious and rational, with no cyanosis or FIG. 4 Supine antero-posterior chest film. Comparison with fig. 2 shows that there has been considerable improvement in the pulmonary oedema together with some decrease in the pleural fluid.

4 11 respiratory distress, his pulse rate being 90 beats /min and blood pressure 115/90 mm Hg. At this stage he was returned to the ward, l i hours after the induction of anaesthesia, and no further treatment was necessary since there occurred spontaneous re-expansion of the lung with re-absorption of the effusion: closed mitral valve surgery was successfully performed 9 days later, induction being uneventfully accomplished using methohexitone 70 mg. It is perhaps of additional interest to illustrate with one further erect anteroposterior chest radiograph (fig. 5) that by 3 hours after the onset of the episode the radiologist was able to report a remarkable improvement in the extent of the pulmonary oedema on both sides, particularly the right. The pleural effusion also appeared to be smaller although some of the fluid was probably lying medially, adjacent to the collapsed right lower lobe. FIG. 5 Erect postero-anterior chest film. Comparison with fig. 1 does not suggest any residual pulmonary oedema: the pleural effusion is probably smaller but some fluid may be lying medially adjacent to the collapsed right lower lobe. should be directed towards improving the cardiac performance with a drug such as isoprenaline, which has a positive inotropic effect, and simultaneously to reduce peripheral stasis by a vasoconstrictor. Some pressor agents produce constriction of limb veins and this action may result in important circulatory adjustments (Eckstein and Hamilton, 1957; Rashkind et al., 1953), thereby improving venous return to the right heart. In mitral stenosis pulmonary oedema is not infrequently interstitial in location and oedema fluid, as here, tends to accumulate in interlobar septa (Bates and Christie, 1964); the radiological picture, the absence of bronchial aspirate together with the disproportion between physical signs and radiological appearance suggests that such was the situation in this case. Although acute left ventricular failure is expected to result in alveolar oedema, which plainly did not exist here, it seems none the less to be the most likely antecedent cause, since there was no "bucking", straining or other apparent reason for an abrupt rise in pulmonary vascular pressure; moreover, left ventricular revival preceded all other improvement. In this case the relative speed of onset and disappearance of both clinical signs and radiological evidence of pulmonary oedema and pleural effusion is impressive. Since the patient was anaesthetized in the X-ray department it was convenient to take repeated chest films at relatively short intervals; had this not been done the presence of an accompanying pleural effusion might well have passed unrecognized at this stage. It should be emphasized that the blood gas changes which occurred as a result of altered ventilation perfusion ratios and/or venous admixture were severe, despite the relatively trivial auscultatory TABLE I Results. DISCUSSION This case report draws attention to the well-known need for care in the administration of thiopentone to patients with heart disease or those in whom, for any other reason, the powers of circulatory homeostasis are depleted. Should circulatory collapse occur it seems reasonable that treatment Sample Time Oygen Standard sarurapaccn bicarbonate tion ph (mm Hg) (m.equiv/1.) (%) 10 min min hr 30 min days

5 82 BRITISH JOURNAL OF ANAESTHESIA changes, but showed a rapid improvement. The results given in table I comprise blood gas estimations and oxygen saturation values determined from arterial samples, the times of the measurements are indicated, zero time being at induction. It appears more probable that the changes above reported were attributable to the onset and rapid termination of pulmonary oedema rather than to the brief accumulation of a pleural transudate. It should be noted that the oxygen saturation did not achieve a value greater than 94 per cent despite lung re-expansion and fluid re-absorption: this may be due to more long-lasting effects of interstitial pulmonary oedema and atelectasis, to other chronic lung changes secondary to mitral stenosis, or a combination of all, upon ventilation and perfusion. ACKNOWLEDGEMENT We are indebted to Doctor J. D. Dow, Consultant Radiologist, Guy's Hospital, for his interpretation and comments upon the radiographs. REFERENCES Bates, D. V., and Christie, R. V. (1964). Respiratory Function in Disease, p Philadelphia and London: Saunders. Dinnick, O. P. (1964). Deaths associated with anaesthesia: observations on 600 cases. Anaesthesia, 19, 537. Eckstein, J. W., and Hamilton, W. K. (1957). The pressure-volume responses of human forearm veins during epinephrine and norepinephrine infusions. J. din. Invest., 36, McCammond, J. M. (1961). The effect of thiopental on peripheral venous tone. Anesthesiology, 22, 525. Edwards, G., Morton, H. J. V., Pask, E. A., and Wylie, W. D. (1956). Deaths associated with anaesthesia: a report on 1000 cases. Anaesthesia, 11, 194. Goldberg, A. H., Mating, H. M., and Gaffney, T. E. (1961). The effect of digoxin pretreatrnent on heart contractile force during thiopental infusion in dogs. Anesthesiology, 22, 974. Price, H. L., Dundee, J. W., and Conner, E. H. (1957). Rates of uptake and release of thiopental by human brain; relation to kinetics of thiopental anesthesia. Anesthesiology, 18, 171. Prime, F. J., and Gray, T. C. (1952). The effect of certain anaesthetic and relaxant agents on circulatory dynamics. Brit. J. Anaesth., 24, 101. Rashkind, W. J., Lewis, D. H., Henderson, J. B., Heiman, D. F., and Dietrick, R. B. (1953). Venous return as affected by cardiac output and total peripheral resistance. Amer. J. Physiol., 175, 415. EXSUDAT PLEURAL APRES ADMINISTRA- TION DE THIOPENTONE: HISTOIRE D'UN CAS SOMMAIRE Rapportant un cas de stenose mitrale et vice aortique combine, nous illustrons et decrivons le deyeloppement puis la guirison d'un oedeme interstitiel aigu du poumon, associi a un exsudat pleural important, ceci apres induction d'une anesthfaie au thiopentone. Nous attirons l'artention sur la disproportion entre les signes physiques et l'aspect radiologique de mfirne que sur la rapidity d'apparition et disparition tant des signes cliniques que des signes radiologiques d'oedeme pulmonaire et, de maniere plus inattendue, de l'exsudat pleural Les variations des gaz sanguins et de la saturation en oxygene sont enregistres, et des details sont donnes sur le traitement suivi. PLEURAERGUSS ALS KOMPLKATION EINER THIOPENTONE-ANWENDUNG FALLBERICHT ZUSAMMENFASSUNG Wir illustrieren und beschreiben bei einem Fall von Mitralstenose und kombiniertem Aortenvitium die Entwicklung und anschliedende Genesung von einem akuten interstitiellen Lungenodem mit grooem Pleuraergufl, aufgetreten im Anschlufl an eine Narkoseeinleitung mit Thiopentone. Die Aufmerksamkeit wird gelenkt auf das Mifiverhfiltnis zwischen klinischen und radiologischen Zeichen sowie auf die Geschwindigkeit von Entstehen und Verschwinden sowohl der klinischen Zeichen als auch der radiologischen Merkmale des Lungenoderns und, noch unerwarteter, des Pleuraergusses. Mitgeteilt werden die begleitenden Anderungen der Werte von Blutgas- und- sauerstoffsfittigung, ferner werden Einzelheiten uber die acgewandte Therapie mitgeteilt.