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Cocaine or phenylephrine/lignocaine for nasal fibreoptic intubation?

Latorre, F.; Otter, W.; Kleemann, P. P.; Dick, W.; Jage, J.

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European Journal of Anaesthesiology: November 1996 - Volume 13 - Issue 6 - p 577-581



Nasotracheal intubation by means of flexible fibreoptic endoscopy is the method of choice if a difficult intubation is anticipated [1]. Airway management is facilitated in the awake and co-operative patient. In order to reduce or even blunt stressfull reactions, adequate topical analgesia of the nasal mucosa is essential [2]. Bleeding from the nasal mucosa should be prevented, since it impedes the performance of endoscopic intubation. Both objectives can be achieved with the use of cocaine, which is therefore recommended prior to nasal intubation [3-5].

However, cocaine has been shown to inhibit presynaptic noradrenaline and dopamine uptake which leads to their increased availability [6]. The use of cocaine in hypertensive patients, in patients with coronary artery disease or hyperthyroidism could therefore be dangerous. Furthermore, cocaine has a potential for substance abuse. In view of these factors the availability of a viable alternative to cocaine would be desirable.

The present study was designed to investigate whether topical analgesia of the nose for endoscopy with phenylephrine/lignocaine is comparable to topical analgesia with cocaine in terms of vasoconstriction, analgesia and side effects.

Patients and methods

Ninety-nine patients (ASA I, II), requiring nasotracheal intubation for maxillofacial surgery participated in this randomized double-blind study after signing the appropriate informed consent forms and with the approval of the study by the Regional Medical Council Ethics Committee. Patients with history of epistaxis, bleeding disorders, deviation of the nasal septum or adenoids were excluded from the study.

Patients were premedicated with flunitrazepam 1-2 mg orally 1 h before induction and allocated to one of two groups on a random basis to receive into each naris either 0.5 mL 10% cocaine (n=52) or 0.5 mL of 0.25% phenylephrine and 3% lignocaine (1% phenylephrine and 4% lignocaine at a mixing ratio of 1:3) (n=47) respectively.

Following fentanyl 0.1-0.15 mg i.v., both nares were inspected with a flexible fibreoptic endoscope (Olympus BF-P20D, Olympus, Tokyo, Japan). While one naris was chosen for intubation, oxygen was administered to the other nasal opening via a catheter. A flexible spiral tube (Rüscheli i.d. 7.0 mm for men, 6.5 mm for women; Rüsch, Waiblingen, Germany) was attached to the endoscope which was subsequently inserted through the chosen naris. The larynx and glottis were sprayed under fibreoptic vision through the biopsy channel with 5 mL 2% lignocaine, and 2 min later the trachea was sprayed with the same amount of lignocaine.

After topical analgesia was established and with the fibrescope positioned in the trachea, anaesthesia was induced with etomidate 0.2-0.3 mg kg−1. After loss of the eyelid reflex the tube was fibreoptically advanced through the nose into the trachea.

Anaesthesia was then maintained with 70% N2O in oxygen with enflurane.

Reaction of the nasal mucosa was classified as follows: 0 = no epistaxis, 1 = epistaxis during endoscopy, 2 = epistaxis during insertion of the nasotracheal tube, 3 = profuse epistaxis because of 1 and 2 resulting in a visible accumulation of blood in the oral part of the pharynx or the posterior pharyngeal wall (confirmed by laryngoscopy after conclusion of the investigation).

Pain was also assessed during transnasal endoscopy according to a verbal analogue scale which had been explained to the patient on the day prior to surgery: 0 = no pain, 1 = mild pain, 2 = moderate pain, 3 = severe pain.

Heart rate, systolic, diastolic and mean arterial pressure were recorded 5 min after a rest period (control), 3 and 6 min after nasal application of the solution, immediately after intubation, 5 and 10 min later. SpO2 and ST-segment analysis of ECG leads II and V5 were continuously performed (Siemens Siredoc 1280, Siemens, Erlangen, Germany) (0 = no change, 1 = horizontal depression >0.1 mV, 2 = descending depression >0.1 mV, 3 = other observations, all events over a minimum of 10 consecutive heart actions).

Statistical evaluation of the haemodynamic data used the Wilcoxon rank sum test at a level of significance of P<0.05.


The two treatment groups were comparable with regard to demographic data (Table 1).

Table 1
Table 1:
Patient characteristics (mean (SD))

There was no difference in the intensity of pain during endoscopy between the groups (Table 2).

Table 2
Table 2:
Pain during nasal endoscopy

Epistaxis was observed in five patients in the cocaine group, while profuse epistaxis occurred in one patient in the phenylephrine/lignocaine group (not significant) (Table 3).

Table 3
Table 3:
Epistaxis during endoscopy and intubation. 0 = no epistaxis, 1 = epistaxis during endoscopy, 2 = epistaxis during advancement of the tracheal tube, 3 = profuse epistaxis because of 1 and 2 resulting in a visible accumulation of blood in the nasopharynx or the posterior pharyngeal wall

Blood pressure and heart rate were not significantly different (P=0.36) between the groups throughout the study (Table 4).

Table 4
Table 4:
Haemodynamic data in the two treatment groups (mean (SD))

A horizontal ST-segment depression was observed at different measurement points in three patients in the group receiving cocaine and in two patients in the phenylephrine/lignocaine group; there were no differences between groups (Table 5).

Table 5
Table 5:
ST-segment changes. Type of event: 0=no ST-segment change; 1=horizontal ST-segment change

Intubation could be performed in all patients without difficulty.


Awake nasal fibreoptic intubation has been used increasingly over the past few years. It is indicated when direct laryngoscopy is precluded, in patients with anomalies of the upper airways, larynx or trachea and in patients who require an endoscopic investigation prior to tracheal intubation [1].

Cocaine abuse is associated with serious negative side effects [7-11]. This questions the safety of cocaine used under clinically controlled conditions, particularly in combination with lignocaine, which has been shown in animals to potentiate cocaine toxicity [12].

The low incidence of pain in the two treatment groups during endoscopy confirms the similarity in the effect of both substances.

With regard to the incidence of epistaxis, the results confirm those of other authors [13,14]. They did not find differences between patients who received topically vasoactive drugs or placebo. This is of particular interest since the vasoconstrictive effect of vasoactive substances was confirmed by computerized tomography [15]. Furthermore, the pneumotachographically measured resistance of the nares was significantly reduced following the application of lignocaine/phenylephrine as well as after cocaine [16].

Despite pronounced nasal vasoconstriction, a marked increase in the plasma concentration of cocaine can occur following topical administration [17,18]. Resnik et al.[19] reported the onset of acute systemic effects within 2 min and peak effects after 15-20 min independent of the cocaine plasma concentration.

Cocaine increases the concentration of noradrenaline at the receptor level, thus inducing tachycardia, rise in blood pressure, coronary vasoconstriction, and has lead to myocardial infarction [20].

Phenylephrine mainly acts directly on alpha-receptors. The cardiovascular effects consist of a rise in blood pressure and reflex bradycardia may occur [21]. In animals, phenylephrine produces coronary vaso-constriction [22].

The patients reported here did not show the significant rise in heart rate or blood pressure reported elsewhere [23]. Other authors [24] found different results, maybe because of the absence of topical analgesia of larynx, glottis and trachea. The systemic effects of lignocaine after absorption may have contributed to an increase in the depth of anaesthesia [25].

Lange et al.[9] failed to demonstrate electrocardiographic signs of myocardial ischaemia even with a decreased diameter of the coronary arteries following nasal cocaine. In the present study, transient alterations in the ST-segment were observed in four patients. These ceased spontaneously without any pharmacological intervention and in the post-operative period no patient showed signs or symptoms of myocardial ischaemia.

The authors suggest that the mixture of phenylephrine and lignocaine is a suitable alternative to cocaine for nasal fibreoptic intubation.


1 Randell T, Hakala P. Fibreoptic intubation and bronchofibrescopy in anaesthesia and intensive care. Acta Anaesthesiol Scand 1995; 39: 3-16.
2 Latorre F, Hofmann M, Kleemann PP, Dick W. Stress response to nasotracheal intubation. A comparative evaluation of fibreendoscopic vs. laryngoscopic intubation with and without topical anaesthesia of the larynx. Anaesthesist 1993; 42: 423-426.
3 Latto JP, Rosen M. Difficulties in Tracheal Intubation. London: Ballière Tindall, 1985: 90-93.
4 Ovassapian A. Fiberoptic Airway in Anesthesia and Critical Care. New York: Ravens Press, 1990: 45-50.
5 Patil V, Stehling L, Zauder H. Fiberoptic Endoscopy in Anesthesia. Chicago: Year Book Medical Publishers, 1983: 37-41.
6 Ritchie JM, Greene NM. Local anesthetics. In: Gilman AG, Goodman LS, Rall TW, Murad F, eds. Goodman and Gilman's Pharmacologic Basis of Therapeutics, 7th Edn. New York: Macmillan, 1985: 302-321.
7 Fleming JA, Byck R, Barash PG. Pharmacology and therapeutic applications of cocaine. Anesthesiology 1990; 73: 518-531.
8 Schachne JS, Roberts BH, Thompson PD. Coronary-artery spasm and myocardial infarction associated with cocaine use. N Engl J Med 1984; 310: 1665-1666.
9 Lange RA, Cigarroa RG, Yancy Jr CW et al. Cocaine-induced coronary-artery vasoconstriction. N Engl J Med 1989; 321: 1557-1562.
10 Cregler LL. Cocaine: the newest risk factor for cardiovascular disease. Clin Cardiol 1991; 14: 449-456.
11 Minor RL, Scott BD, Brown DD, Winniford MD. Cocaineinduced myocardial infarction in patients with normal coronary arteries. Ann Intern Med 1991; 115: 797-806.
12 Derlet RW, Albertson TE, Tharratt RS. Lidocaine potentiation of cocaine toxicity. Ann Intern Med 1991; 20: 135-138.
13 Mitchell RL, DeNuccio DJ, Alden MA. A comparison of nasal spray with cocaine, lidocaine/phenylephrine and saline for nasal intubation. Anesthesiology 1984; 61: A217.
14 Rector FTR, DeNuccio DJ, Alden MA. A comparison of cocaine, oxymetazoline and saline for nasotracheal intubation. AANA J 1987; 55: 49-54.
15 Cole P, Haight JSJ, Cooper PW, Kassel EE. A computed tomographic study of nasal mucosa: effects of vasoactive substances. J Otolaryngol 1983; 12: 58-60.
16 Sessler CN, Vitaliti JC, Cooper KR, Jones JR, Powell KD, Pesko LJ. Comparison of 4% lidocaine/0.5% phenylephrine with 5% cocaine: Which dilates the nasal passages better? Anesthesiology 1986; 64: 274-277.
17 Van Dyke C, Barash PG, Jatlow P, Byck R. Cocaine: plasma concentrations after intranasal application in man. Science 1976; 191: 859-861.
18 Wilkinson P, Van Dyke C, Jatlow P, Barash P, Byck R. Intranasal and oral cocaine kinetics. Clin Pharmacol Ther 1980; 27: 386-394.
19 Resnik RB, Kestenbaum RS. Acute systemic effects of cocaine in man: a controlled study by intranasal and intravenous routes. Science 1977; 195: 696-698.
20 Chiu YC, Brecht K, DasGupta DS, Mhoon E. Myocardial infarction with topical cocaine anesthesia for nasal surgery. Arch Otolaryngol Head Neck Surg 1986; 112: 988-990.
21 Stoelting KS. Pharmacology and Physiology in Anesthetic Practice. London: Lippincott, 1987: 251-268.
22 Gwirtz PA, Stone HL. Coronary blood flow changes following activation of adrenergic receptors in the conscious dog. Am J Physiol 1982; 243: H13-H19.
23 Katz RI, Hovagim AR, Finkelstein HS, Grinberg Y, Boccio RV, Poppers PJ. A comparison of cocaine, lidocaine with epinephrine, and oxymetazoline for prevention of epistaxis on nasotracheal intubation. J Clin Anesth 1990; 2: 16-20.
24 Gross JB, Hartigan ML, Schaffer DW. A suitable substitute for 4% cocaine before blind nasotracheal intubation: 3% lidocaine-0.25% phenylephrine nasal spray. Anesth Analg 1984; 63: 915-918.
25 Davidson JAH, Gillespie JA. Tracheal intubation after induction of anaesthesia with propofol, alfentanil and i.v. lignocaine. Br J Anaesth 1993; 70: 163-166.


© 1996 European Academy of Anaesthesiology