reintubated after administration of midazolam. 10 mg i.v. and vecuronium 12 mg i.v. She was sedated with midazolam 4-6 mg h"1 and the lungs ventilated with a ...
PULMONARY OEDEMA AND [Orn8]-VP
FIG. 1. Postoperative chest x-ray.
>-SEP-89 1 7 53 •09 DU£ = 904 SCAN 4
TI 4 KV 1£5 HS . 31 •5I_
2
FIG. 2. Postoperative thoracic body scan.
reintubated after administration of midazolam 10 mg i.v. and vecuronium 12 mg i.v. She was sedated with midazolam 4-6 mg h"1 and the lungs ventilated with a tidal volume of 750 ml at a rate of lOb.p.m. PEEP was applied (10cmH 2 O). Blood-gas analysis ( F I O J 0 . 5 ) was: pH 7.36, PcOj 5.95 kPa and Po2 10.2 kPa. Moderate water restriction (Ringer lactate 1500 ml 24 b"1) was ordered. The patient improved dramatically. Chest x-ray on the following day was normal (fig. 3).
The trachea was extubated 18 h after admission to the SICU and the patient was transferred to the general ward the same day. The remainder of her hospital stay was uneventful. Serial ECG showed no signs of ischaemia, right or left ventricular overload and no rhythm or conduction disturbances. Blood tests were all in the normal range; in particular there was no increase in concentrations of cardiac enzymes (CK, CK-MB), no eosinophilia and no increase in IgE concentration. The search for specific IgE
BRITISH JOURNAL OF ANAESTHESIA
550
FIG. 3. Chest x-ray 18 h after that in figure 1.
anticholine antibodies was negative. Skin prick tests 6 weeks later with suxamethonium (0.1 ml of a 1-ugml"1 solution), vecuronium, propofol, alfentanil, atropine and neostigmine were also negative. The Q esterase inhibitor (24 mg %) was within the normal range (11-26 mg%). All the components of complement (Cj/C^ were also within the physiological range. DISCUSSION
Acute pulmonary oedema in a previously healthy patient following an uneventful short anaesthesia and surgical procedure was unexpected. The absence of fever, chills, hypotension, the unremarkable WBC count and rapid resolution of the problem make sepsis unlikely. Failure of the left ventricle may be excluded in the face of normal haemodynamic variables and absence of heart murmur, gallop rhythm, ECG changes or increased concentrations of cardiac enzymes. The occurrence of a silent aspiration would have been diagnosed by changes in oxygen saturation, increased airway pressure and modification of the end-tidal carbon dioxide concentration curve. Obviously there was no major bleeding and the
patient received only 1500 ml of Ringer lactate during the operation, excluding overload. The absence of fever, leucocytosis and signs of pulmonary infection makes the diagnosis of postextubation aspiration of stomach contents unlikely. The differential diagnoses, therefore, include hereditary angioneurotic oedema (Q esterase inhibitor deficiency), anaphylactoid reaction to suxamethonium and a side effect secondary to injection of ornithine-8-vasopressin. The C t esterase inhibitor was present in normal concentration (24 mg %) and had normal activity. The absence of a familial history is also an argument against hereditary angioneurotic oedema. Anaphylactic or anaphylactoid reactions to suxamethonium are unlikely in the presence of normal intradermal skin tests, the absence of eosinophilia and specific IgE anticholine antibodies; moreover, the lack of any personal or familial allergic history associated with the paucity of systemic effects and the rapid clinical resolution also argue against such a diagnosis [6]. All drugs used during the surgical procedure gave negative skin tests, making allergic reaction unlikely. Pulmonary oedema is a common clinical emergency. According to Starling's equation, causes
PULMONARY OEDEMA AND [Orn8]-VP include increased pulmonary capillary pressure, decreased oncotic pressure, altered permeability or lymphatic insufficiency [7]. Non-cardiogenic pulmonary oedema is usually secondary to increased pulmonary vascular permeability and may also be caused by volume overload or, less commonly, by increased pulmonary capillary pressure secondary to pulmonary venous disease. The latter is compatible with the physiological actions of [Orn8]-VP. Indeed, this synthetic polypeptide has a specific potent vasoconstrictor action on capillaries and veins [3]. Pharmacological features of [Orn8]-VP include maximal effect in about 10-15 min and duration of action more than 90 min [8], and these are also compatible with a direct causal effect of [Om8]-VP in inducing acute pulmonary oedema in this patient. The manufacturers suggest administration of [Orn8]-VP in a concentration of 1 iu per 10 ml. They also state that 5 iu (maximum recommended dose) in 50-60 ml gives excellent results. However, no absolute or body weight limits are recommended. In burned children, Lamont and Yorke [9] suggested 0.5 iu kg"1 as the maximum dose, with an upper limit of 15 iu/30 kg. No such data are available for adults. Nevertheless, the local infiltration of 12 iu (0.15 iu kg"1) for a perineal block in a healthy adult may be associated with serious pulmonary complications. In our patient, inadvertent i.v. injection may have been
551
a factor contributing to severe venopulmonary vasoconstriction. Despite the lack of data in the literature on the maximum safe dose of ornithine8-vasopressin for adults, it would seem reasonable to administer no more than 0.1 iu kg"1 by local infiltration. REFERENCES 1. Guzman A, Boada J. Acute pressor response to locally injected ornipressine in gynecological surgery. Farmaco Edizione Pratica 1979; 34: 651-655. 2. Muenker G. Ornithin-8-vasopressin (POR 8) als vasokonstriktrosicher Zusatz zur lokal AnSsthesie bei Tonsillektomien. Monatsschrift Ohrenheikde Laryngo-RMnologie 1973; 107: 289-296. 3. Collins IS. Multicentric clinical trial of a vasocorutrictoromithine vasopressin (POR 8 Sandoz). New Zealand Medical Journal 1972; 76: 77-81. 4. Adcndorff DJ, Davies D. A comparison of ornipressin and adrenalin for local vasoconstriction. South African Medical Journal 1977; 51: 131-132. 5. Corliss RJ, McKenna DH, Sialer S, O'Brien GS, Rowe GG. Systemic and coronary hemodynamics effects of vasopressin. American Journal of Medical Science 1968; 256: 293-299. 6. Stoelting RK. Allergic reactions during anesthesia. Anesthctia and Analgesia 1983; 61: 341-356. 7. Robin ED, Cross CE, Zelis R. Pulmonary oedema. New England Journal of Medicine 1973; 188: 239-246, 292-304. 8. Pirorta T. POR 8 versus adrenaline as a vasoconstrictor in scalp surgery. Australian and New Zealand Journal of Surgery 1972; 2: 762-763. 9. Lamont AS, Yorke P. Maximum safe dose of POR-8. Anaesthesia and Intensive Care 1987; 15: 467.
