PULMONARY OEDEMA FOLLOWING TOPICAL PHENYLEPHRINE ADMINISTRATION IN A CHILD ANAESTHETISED FOR CATARACT EXTRACTION.

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Author: Dr.Preeti Goyal Varshney, Dr.Kirti N. Saxena, Dr.Anjali Sethi, Dr. Manu Varshney, Dr.Pallavi.

An 8 years old boy weighing 24 Kg was admitted for traumatic cataract extraction of the right eye. His physical examination appeared normal and there was no evidence of pulmonary or cardiac disease. The patient had no significant past medical or family history. In the operation theatre, monitors (ECG, blood pressure cuff and pulse oximeter) were applied for general anaesthesia. Preoperative vital signs were as follows: heart rate 88 beats per minute, BP 120/72 mm Hg, SpO2 98% on room air. Following insertion of a 22G intravenous cannula, the patient received intravenous pethidine 12mg. Anaesthesia was induced with administration of propofol 30mg, vecuronium 2.5mg and halothane 1% by mask in a mixture of oxygen and nitrous oxide (fiO2 0.3). After tracheal intubation with a 5.5mm ID endotracheal tube with low pressure cuff and confirming bilateral regular breath sounds by auscultation, patient was placed under mechanical ventilation on pressure control mode to maintain peak airway pressure below 15cm H2O with a respiratory rate of 12 per minute. End tidal CO2 was maintained between 30 and 40mmHg. On the operating table, before incision the operating surgeon noticed that the pupil was not dilated. A well soaked cotton pledget was placed in the eye without informing the anaesthesiologist. While the surgeons were waiting for pupillary dilatation, the heart rate rose from 72 bpm to 180- 190 bpm, and the non invasive systolic arterial pressure from 105 mmHg to 200 mmHg. The ECG showed frequent ventricular ectopic beats. Halothane was stopped and propofol 10 mg was given intravenously to increase the depth of anaesthesia. Preservative free lignocaine 40mg was also given intravenously. On asking the surgeon, which drug he had used for pupillary dilatation, it was found to be a solution of 0.8% tropicamide with 5% phenylephrine. The pledget was removed and the eye was flushed with saline. A few minutes later, the monitors displayed a reduced tidal volume with unchanged airway pressures. With an inspired oxygen concentration of 30%, SpO2 decreased to 88%. Auscultation revealed crepitations which were heard throughout the chest, and a blood stained frothy fluid was suctioned from the trachea via the endotracheal tube. A tentative diagnosis of pulmonary oedema was made and frusemide (10mg) and morphine (3mg) was administered intravenously. Patient was ventilated manually with a fiO2 of 1.0 and the SpO2 increased to 97% after 15 minutes. HR and BP were 130 bpm and 126/78 mmHg respectively. Following insertion of a Foley's catheter, urine output was measured in the operating room which was 300 ml. The amount of intravenous normal saline administered was 350 ml over past one hour. Surgery was postponed and the patient was transferred to the intensive care unit (ICU) on mechanical ventilation with the endotracheal tube in situ after giving a topup of vecuronium. In the ICU, chest radiography taken immediately after transfer, showed a diffuse homogenous alveolar infiltrate. Ventilation was controlled using a ventilator in the synchronized intermittent mandatory ventilation (SIMV) mode with a positive end expiratory pressure (PEEP) of 5 cm H2O and fiO2 of 0.5 respectively. Midazolam was administered for sedation in the ICU during ventilatory care.Six hours after being transferred to the ICU, there were no crepitations on chest auscultation, radiographic abnormalities had almost completely resolved, HR and BP settled to 86 bpm and 110/70 mmHg respectively with a SpO2 of 99% on fiO2 0.4 Extubation was done at this stage and no further problems were encountered.

DISCUSSION:

The case described appears to be one of pulmonary oedema in a paediatric patient following an iatrogenic hypertensive crisis with cardiac arrhythmias. The drug most likely to have been responsible was ocular phenylephrine. Phenylephrine is a selective á1- agonist with a relatively short duration of action (20 minutes when administered intravenously). It is metabolized in the liver by the monoamine oxidase. The maximum serum concentration occurs after 10 minutes, whereas a sufficient topical effect can be observed at the earliest in 30 minutes. It has potential arterial and venous vasoconstrictor effect promoting blood shift from peripheral to pulmonary circulation which is less sensitive to vasoconstrictor effects and promotes increased left ventricular filling pressure.5 The increase in systemic vascular resistance induced by phenylephrine increases left ventricular ejection impedance as well as end diastolic pressure and volume.6 The ability to increase heart rate and contractility are important compensatory mechanisms to preserve cardiac output under these circumstances7, failing which, cardiac congestion and left heart failure leading to pulmonary oedema can occur. Myocardial dysfunction associated with vasoconstrictor administration can be detected by echocardiography even 12-48 hours after the resolution of hypertensive effects of á-agonists, in the form of reduced ventricular ejection fraction.6 Mild to moderate hypertension resulting from phenylephrine use in a healthy individual, should be closely monitored for 10-15 minutes before antihypertensive medications are given. Severe hypertension as well as its adverse effects such as ECG changes or pulmonary oedema must be treated immediately. Antihypertensive agents that are direct vasodilators or á-receptor antagonists are appropriate treatments.6 Significant systemic absorption can occur after topical application of phenylephrine. The systemic absorption of locally applied ocular drugs depends on dosage, application route, aqueous or viscous characteristics, dilution by lacrimation, and uptake through the lacrimal duct by the nasal mucosa which is a major absorption site.8 Several techniques have been advocated for achieving effective mydriasis with ocular phenylephrine while reducing systemic absorption and associated hemodynamic effects. These include the use of 2.5% solution rather than 5% or 10% solution,9 8-10 ìl rather than 30-32 ìl drops,10,11,12 eyelid closure,12 punctuate occlusion and blotting away excess drops after administration of the drug.13 The initial topical phenylephrine dose should not exceed 0.5 mg in adults and 20 ìg/ kg in children upto 25 kg.6 In our case, an uncalculated dose of phenylephrine was administered in the form of a soaked pledget of 5% phenylephrine solution leading to prolonged absorption as well as over dosage of the drug. To prevent future occurrence of the type of cardiopulmonary compromise witnessed in this case, it is important to recognize the possibility of abnormal absorption of topical á-agonists and to anticipate hypertensive events. Topical phenylephrine should be cautiously administered, especially in elderly patient and in those with risk factors for myocardial or brain ischaemia, because they are less tolerant to the effects of its systemic absorption.14 We also recommend that intraoperative administration of ocular drugs by the surgeon should be conducted only after consulting the anaesthesiologist.

REFERENCES:

1. Baldwin FJ, Morley AP - Intraoperative pulmonary oedema in a child following systemic absorption of phenylephrine eyedrops. Br J Anaesth, 2002;88:440-442. 2. Solosko D, Smith RB. Hypertension following 10 percent phenylephrine ophthalmic. Anesthesiology 1972; 36: 187-9 3. Vaughan RW. Ventricular arrhythmias after topical vasoconstrictors. Anesth Analg 1973; 52: 161-5 4. Wesley RE. Phenylephrine eyedrops and cardiovascular accidents after fluoroscein angiography. J Ocul Ther Surg 1983; 2:212-4 5. Wanamaker HH, Arandi HY - Epinephrine hypersensitivity-induced cardiovascular crisis in otologic surgery. Arch Otolaryngol Head Neck Surg, 1985;111:841-84 6. Groudine SB, Hollinger I, Jones J et al - New York State guideline on the topical use of phenylephrine in the operation room. Anesthesiology, 2000;92:859-864. 7. Ji- Seon Son, Sang- Kyi Lee. Pulmonary edema following intranasal spray administration during the induction of general anaesthesia in a child. Yonsei Medical Journal 2005; 46(2): 305-308. 8. Greher M, Hartmann T, Winkler M et al - Hypertension and pulmonary edema associated with subconjuntival phenylephrine in a 2-month-old child during cataract extraction. Anesthesiology, 1998;88:1394-1396 9. Mydriatics and cycloplegics. In British National Formulatory, 39th Edn. London: British medical Association and Royal Pharmaceutical Society of great Britain,2000; 477-8 10. Brown RH, Wood TS, Lynch MG, Schoenwald RD, Chien DS, Jennings LW. Improving the therapeutic index of topical phenylephrine by reducing drop volume. Ophthalmology 1987; 94: 847-850 11. Lynch MG,Brown RH, Goode SM, Schoenwald RD, Chien DS. Reduction of phenylephrine drop size in infants achieves equal dilation with decreased systemic absorption. Arch Ophthalmol 1987; 105: 1364-5. 12. Whitson JT, Love R, Brown RH, Lynch MG, Schoenwald RD. The effect of reduced eyedrop size and eyelid closure on the therapeutic index of phenylephrine. Am J Ophthalmol 1993; 115: 357-9 13. Palmer EA. How safe are ocular drugs in paediatrics? Ophthalmology 1986;93: 1038-40. 14. Fisher Maria de Fatima Savioli, Moro Eduardo Toshiyuki, Guasti Valter Moreno et al. Pulmonary edema after topical phenylephrine absorption during pediatric eye surgery. Case report. Rev. Bras. Anestesiol. 2004; 54(6): 815-820.