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Many thousands of dacryocystorhinostomies (DCRs) are performed by ophthalmologists routinely without problems. Postoperative pain and nausea may wrongly be attributed to wound pain and post-anaesthetic nausea. Medical and nursing staff need to be aware of the potential for intranasal cocaine to precipitate acute angle closure glaucoma (AACG). We report two cases of AACG following the use of intranasal cocaine and subcutaneous lignocaine (lidocaine) with adrenaline during DCR surgery. We believe this to be the second report of such cases.
Two women, a 67 year old and a 75 year old, developed right sided AACG immediately after ipsilateral DCR surgery. Both patients were treated successfully for AACG. Cocaine is a known mydriatic and can induce angle closure glaucoma in predisposed individuals. Adrenaline in the local anaesthetic solution and intravenous atropine sometimes used during general anaesthesia are also known mydriatics.
We performed right sided external DCR surgery under general anaesthesia on both females. Regional preparation included a cocaine nasal pack (5% solution) and infiltration with lignocaine and adrenaline 1:200 000 at the proposed incision site subcutaneously. Preoperative intraocular pressures were within normal limits and there was no history of previous attacks of AACG or subacute angle closure glaucoma in either patient.
Overnight, both developed right eye pain and nausea and each was given analgesia and an antiemetic. Medical staff were not called to review the patients. The following morning, dressings were removed and a diagnosis of right sided AACG was made. Each patient had corneal oedema, a mid-dilated and non-reactive pupil, anterior chamber flare, and 360 degrees of angle closure on gonioscopy.
In the 67 year old, the intraocular pressure measured 18 mm Hg in the right eye. This may be explained by spontaneous termination of the attack as a result of ciliary body ischaemia and suppression of aqueous secretion secondary to a high intraocular pressure overnight.1 In the left eye the intraocular pressure was 15 mm Hg and gonioscopy revealed 270 degrees of grade I open angle, and 90 degrees of complete angle closure. Uneventful bilateral YAG iridotomy was performed.
In the 75 year old, the pressure was recorded as 57 mm Hg in the right eye and only dropped to 39 after two doses of intravenous mannitol. Gonioscopy of the left eye revealed a 360 degree closable angle, grade 0-I. Uneventful bilateral YAG iridotomy was performed. The corneal oedema resolved over the following week in both patients and visual field testing revealed no glaucomatous defect. Both patients require ongoing antiglaucoma therapy.
Cocaine is the only local anaesthetic to block noradrenaline re-uptake at the presynaptic adrenergic receptors.2 This single agent provides anaesthesia and haemostasis, making the use of cocaine desirable in lacrimal drainage surgery. Its use in DCR surgery was first described by Dupuy-Dutemps and Bourgener in 1922.3 We have routinely used cocaine for our DCR surgery, and emphasise the need to remain cognisant of its possible local and systemic side effects.
Cocaine is well absorbed from mucosal surfaces, reaching plasma levels similar to those achieved with intravenous administration.4 In adults, 50–95 mg is a psychoactive dose.5 The maximum allowable dose is 3 mg/kg; 1 g or 10 ml of a 10% solution represents a fatal dose for an adult.6 Usually, 80–200 mg of cocaine is administered intranasally in DCR surgery. Systemic cocaine toxicity has been reported in patients undergoing DCR surgery under general anaesthesia.6
AACG was described in the early 20th century with the use of cocaine as a corneal anaesthetic. More recently, a case of AACG associated with ipsilateral intranasal cocaine abuse was reported.7 In 1999, Hari et al described a single case of AACG following the use of cocaine in DCR surgery.8 Our two case reports strongly suggest that the use of intranasal cocaine to aid DCR surgery may precipitate AACG.
It is highly probable that the mydriasis which precipitated the attack of AACG was caused by the intranasal cocaine rather than the low concentration of subcutaneous adrenaline (1:200 000). There are two possible mechanisms of cocaine entry into the eye during DCR. Inadvertent transfer of cocaine from the surgeon’s glove to the patient’s conjunctival sac is possible if fresh gloves are not used between cocaine nasal packing and the infiltration of local anaesthetic. Alternatively, residual cocaine in the nasal cavity has direct access to the conjunctival sac after the lacrimal sac anastomosis in the DCR procedure.
Other potential causes of AACG include the mydriatic effect of the adrenaline in the lignocaine 1%, 1:200 000 adrenaline, and atropine given intravenously during general anaesthesia.
At this concentration, subcutaneously administered adrenaline is unlikely to have precipitated the acute angle closure glaucoma. Atropine was not used during anaesthesia in either patient.
Given the apparent rarity of this proposed event, we cannot definitively conclude that lacrimal surgeons should change their approach to patients undergoing DCR surgery. However, it is important to remain cognisant of this potential complication and educate both nursing staff and medical trainees in ophthalmology and otolaryngology as to this potential complication. In addition, it would be reasonable to pad only the wound and not occlude the eye, which may have allowed the origin of the pain in our cases to be more readily identified. Postoperative pain and nausea following DCR surgery should not be automatically attributed to wound pain and post-anaesthetic nausea: AACG needs to be excluded. It may be prudent to assess routinely anterior chamber depth in high risk eyes before DCR surgery. If there is any suspicion of an eye anatomically predisposed to AACG both nursing and medical staff should be made aware of the potential complication. A prophylactic peripheral iridectomy may be indicated.
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