302 Indian J. Anaesth. 2003; 47 (4) : 302-303
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PULMONARY EDEMA FOLLOWING CONCOMITANT ADMINISTRATION OF OXYTOCIN AND VASOPRESSOR DURING LSCS UNDER SUBARACHNOID BLOCK Dr. A. K. Wahal 1 Dr. V. K. Kapoor 2
Dr. M. Venugopal 3
SUMMARY The syndrome of pulmonary edema of noncardiac origin is encountered by the anaesthesiolgist quite frequently and contributes both for morbidity and mortality associated with anaesthesia. Timely recognition and proper management are of paramount importance for a successful outcome. A case encountered during conduct of LSCS under subarachnoid block is presented.
Non-cardiogenic pulmonary edema may be caused by upper airway obstruction due to post-extubation laryngospasm. The clinical syndrome of negative pressure pulmonary edema is well known among anaesthesiologists but not by other specialists.1 The literature suggests that it occurs more commonly than is generally thought, with a frequency of 0.05% to 0.1% of all anaesthetics and is often unrecognized or misdiagnosed.2 We report our experience with pulmonary edema during subarachnoid block for LSCS following concomitant use of oxytocic and vasopressor drugs. Case report A 28-year, ASA-I female, full term gravida III weighing 52 kg was admitted for induction of labour. The ultrasonographic report of abdomen revealed, single large size anencephalic fetus with breech presentation. She was nondiabetic. Her blood group was O, Rh +ve and hemoglobin 11gmdl-1. Induction of labour was initiated with one unit of oxytocin in 5% dextrose in water and increments there on. A total dose of 20 units of oxytocin and 2.5 L of 5%dextrose were administered in 36 hours. The induction of labour was abandoned and LSCS was decided because the anencephalic dead foetus could not be delivered in spite of full dilation of cervix for more than two hours. The woman was in maternal physical exhaustion of labour. The patient was counseled and she agreed for subarachnoid block. On pre-anaesthetic assessment her pulse 1. Supertime Gr.II 2. Sr. Specialist & Head 3. Sr. Specialist & Medical Suprintendent Department of Anesthesiology, Swami Dayanand Hospital, New Delhi-110095 Correspond to : Dr. A. K. WAHAL E-138-A, Dilshad Garden, Shahdara-Delhi-110095 Ph: o12o-4626869. Mobile: 9810124600 E-mail:
[email protected]
and blood pressure were found to be 86 beats min-1. and 120/80 mmHg respectively. Chest and cardiovascular system were clinically normal. Two intravenous lines were secured. Prior to the block she was hydrated with crystalloid solution up to a liter (inclusive of 250 ml of 5% dextrose with 5 units of oxytocin infused rapidly in 25 to 30 min, 20min prior to institution of subarachnoid block). With all aseptic precautions, the subarachnoid block was induced with 2 ml of 0.5% bupivacaine heavy in the left lateral position at L3-4 SAS using 25 SWG spinal needle. The patient was positioned supine with pelvic wedge. Oxygen was administered via a facemask throughout surgery. Level of analgesia was ensured adequate up to T4-5 prior to start of surgery. Extraction of anencephalic foetus was difficult and complete in five minutes. Methylergotamine 0.2mg was administered intravenously. 20 units of oxytocin in 5% dextrose infused at the behest of the obstetricians for effective management of III stage of labour. Systolic BP of the patient dropped to 70 mmHg. Infusion of fluid was enhanced with polygeline (Haemaccel). Atropine sulphate 0.6mg and increments of mephentermine sulphate 10,7.5,5 (total 22.5mg) were given i.v over a period of 10 minutes. Systolic BP rose to 100mmHg. However the patient developed mild tachypnoea and cough. Bronchospasm was detected. By this time 150 to 200 ml of Haemaccel had been infused. Patient was not considered to be over hydrated at any stage. Injection of etophyllin and theophyllin 4ml (each ml contains etophyllin 84.7mg and theophyllin 25.3 mg) was injected slowly and hydrocortisone 200 mg injected I.V stat. On auscultation initially basal then generalized crepitations were found. This was soon followed by blood tinged frothy sputum. Pulmonary edema was suspected. Inj. frusemide 80 mg I.V was given as increments of 40 mg at an interval of 3-4 minutes. Aminophylline 250 mg was administered in infusion and the rate of infusion was adjusted at 0.6mgkg-1hr-1. High flow oxygen was administered through facemask. The patient was persuaded to take deep breaths. She did not need ventilatory support to sustain oxygen
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saturation. The pulmonary edema reversed within 20 minutes of onset. By the time surgery was over (skin to skin duration 40 min), patient was fully conscious though exhausted. There were no spasm or crepitations. Her respiration was adequate. At this stage systolic BP stabilized at 110 mmHg with pulse rate 110 beats min-1 regular. She was shifted to postoperative recovery room after one hour. Postoperative recovery was uneventful. Six hours later she was fully awake, comfortable, conversing. Her vitals were stable at pulse 88 beats min-1, systolic BP 110 mmHg, chest clinically clear and urine output 1000 ml.
We conclude that peripartum use of oxytocics and vasopressors can precipitate pulmonary edema, without any evidence of vascular overloading or any occult cardiac disease.
On regular follow up of the patient there wasn’t any residual effect of the incident. At 3rd postoperative week echocardiography was done and found to be normal. The left ventricular ejection fraction was 70%.
2. McConkey, PP. Postobstructive Pulmonary oedema – case series and review. Anaesth Intensive Care 2000; 28(1): 72-76.
Discussion Hypotension during centroneuraxis blockade occurs due to decrease in venous return (due to posture, caval compression, blood loss), vasodilatation and decreased cardiac output. Bladder distention and vagal overactivity may also contribute.3 Standard preventive measures include preinfusion up to one litre of crystalloid, prevention of high levels of block, correction of hypovolaemia, elevation of lower limbs, use of vasopressers4 and sedation. In the patients with full term gravid uterus, the most important maneuver is left lateral tilt. Volume loading does not always guarantee arterial pressure and overloading can be harmful in patients at the risk of pulmonary edema. Vasopressors have to be administered to maintain optimal level of arterial pressure.5 In the present case,usual measures were taken. Incremental mephentermine sulphate 10,7.5,5 (total 22.5 mg) administered intravenous to correct hypotention.6 Methylergotamine 0.2 mg I.V. stat and oxytocin 20 units were administered in infusion to ensure effective contraction of uterus. This reduced the incidence and extent of post partum haemorrhage. 7,8 Both mephentermine sulphate and methylergotamine maleate are alfa agonists. Concomitant use of these two vasopressor agents may have caused severe widespread vasoconstriction causing marked increase in the afterload to heart.9 Clinch fist effect of mephentermine sulphate on heart10 with the markedly increased afterload prevent forward pumping action of heart resulting in pulmonary vascular leak and pulmonary edema. Antidiuretic action of oxytocin7,11 might have been contributory.
High index of suspicion and prompt treatment is mandatory. We believe that oxytocin and vasopressors must be used judiciously. References 1. Lathan, SR; Silverman, ME; Thomas, BE; waters, Wc; 4th. Postoperative pulmonary edema. South Med J 1999; 92(3): 313-315.
3. McCrae, AF; Wildsmith, JA. Prevention and treatment of hypotension during central neural block. Br J Anaesth 1993; 70(6): 672-800. 4. Shinder, SM; Livingson, G. Anaesthesia for Obstetrics In : Millar RD, ed. Anaesthesia 4th Edition, New York: Churchill Livingstone 1994; 2057. 5. Park, GE; Hauch, MA; Curlin, F; Dutta, S; Bader, M. The effect of varying volumes of Crystalloid administration before cesarean delivery on maternal hemodynamics and Colloid osmotic pressure. Anesth Analg 1996; 83(2): 299-303. 6. Brain, B; Hoffman; Lefkowitz, RJ. Catecholamines, Sympathomimetic drugs, and Adrenergic receptor antagonist In: Goodman and Gillman eds. The Pharmacological Basis of Therapeutics 9th Edition, New york: Mc Graw-Hill 1996; 216-17. 7. Percival, R; Holland; Brews. Normal labour In: Daftary, SN; Chakravarti, S eds. Manual of obstetrics 5th edition, New Delhi; India: B.I.Churchill Livingstone 1993; 325-328. 8. Graves; Cornelia, R. Agents that cause contraction or relaxation of the uterus In : Goodman and Gillman eds. The pharmacological Basis of therapeutics 9th Edition, New York: Mc Graw-Hill 1996; 944. 9. Atkinson, RS; Rushman, GB; Davies, NJH. Surgical operation and choice of anaesthetic In : Lee’s Synopsis of Anaesthesia 11th Edition, Lundon: Butterwerth Heinemann 1993; 525. 10. Collins, VJ. Pressor Drugs In : Collins, VJ ed. Principals of Anesthesiology 2nd edition, Philadelphia: Lea and Febiger 1976; 1572-75. 11. Graves; Cornelia, R. Agents that cause contraction and relaxation of the uterus In : Goodman and GillMan eds. The Pharmacological Basis of Therapeutics 9th Edition, New York : MC Graw-Hill 1996; 941.
