|
| Article Access Statistics | | | Viewed | 5971 | | | Printed | 125 | | | Emailed | 3 | | | PDF Downloaded | 0 | | | Comments | [Add] | | |
|
Click on image for details.
|
|
|
|
|
|
| Year : 1982 | Volume
: 28
| Issue : 2 | Page : 64-7 |
Use of lignocaine in bronchoscopy.
Chaudhari LS, Manjrekar RP, Kamat SK, Dasgupta DD
How to cite this article:
Chaudhari L S, Manjrekar R P, Kamat S K, Dasgupta D D. Use of lignocaine in bronchoscopy. J Postgrad Med 1982;28:64 |
The performance of bronchoscopy by proper anaesthesia and/or analgesia is many times required in certain diagnostic methods. However, no ideal method has yet been developed for this purpose. The use of intravenous lignocaine together with sodium thiopentone for this purpose was reported by Blancato et al.[2] These authors based their work on demonstration of depression of cough reflex by intravenous lignocaine by Steinhouse et al.[5] The latter workers demonstrated that lignocaine obtunds pharyngeal and laryngeal reflexes without causing respiratory depression. de Clive-Lowe et al[3] have reported the use of intravenous lignocaine to provide analgesia during surgery. We, therefore, undertook a study of intravenous lignocaine together with sodium thiopentone, nitrous oxide and oxygen to produce analgesia with anaesthesia for bronchoscopy.
Fifty adults (30 males and 20 females) were studied; 32 of these were 20-39 years old, 8 were 40-59 years old and 10, were 60 years and above. Twenty patients had lung abscess, 10 had pulmonary consolidation, 12 had malignancy of the lung and the rest 8 had pulmonary tuberculosis. The patients underwent a thorough clinical examination and the detailed findings were recorded on a proforma. They also had electrocardiogram, X-ray chest, and detailed clinical chemistry profile. Only those patients who could hold their breath for more than 15 seconds were included in the study.
The patients were pre-medicated with 100 mg sodium phenobarbitone, 30 mg of pentazocin and 0.6 mg of atropine sulphate, all given intramuscularly, one hour before the bronchoscopy. They were asked to gargle with 5 ml of 2% lignocaine hydrochloride viscous, 10 minutes before the commencement of the procedure. After this, they were made to spit out the viscous so as to avoid overdosage of lignocaine and bucking. A 5% glucose drip was started. The patient was oxygenated with 100% oxygen for 5 minutes and then anaesthesia was begun with a 3:5 mixture of nitrous oxide and oxygen. One per cent lignocaine solution was injected intravenously in a dose of 2 mg/kg body weight over a period of 3-5 minutes. Then sodium thiopentone was administered intravenously in a dose of 4-5 mg/kg body weight until the desired state of anaesthesia was achieved. As soon as the lower jaw was relaxed, the vocal cords were sprayed with 2 ml of 4% lignocaine hydrochloride. One ml of the same solution was injected through the cricothyroid membrane. Two to three minutes after this injection, bronchoscopy was commenced. During bronchoscopy, the anaesthesia was maintained with a 1:1 mixture of nitrous oxide and oxygen through a side arm of the bronchoscope. Additional sodium thiopentone was injected intravenously as and when required, as indicated by straining; the total dose of sodium thiopentone was kept below 100 mg. During the entire procedure, the pulse rate was monitored by a photocell type of instrument and the blood pressure was measured repeatedly using a mercury manometer. The electrocardiogram was monitored during the procedure using an oscilloscope. Blood gas analysis was done before and immediately after the procedure using the capillary blood.
The bronchoscopy procedure lasted for 10 minutes on an average. After the procedure was over, the patient was oxygenated till he responded to painful stimuli and was then shifted to the recovery room. He was observed for cyanosis, laryngospasm, bronchospasm and coughing.
The results of the technique were considered good if the patient showed no significant changes in the vital signs during bronchoscopy and if the latter could be performed with ease. The result was considered as fair if the patient showed some changes in the vital signs but the bronchoscopy proceeded without difficulty. It was considered as poor if stridor, bucking or laryngospasm prevented successful bronchoscopy.
According to the above criteria, the results were considered good in 32 patients, fair in 16 patients and poor in 2 patients. In these two latter patients, suxamethonium chloride had to be used to permit the completion of bronchoscopy. These two patients had fewer muscle fasciculations than are usually seen with suxamethonium. The post-operative muscle pain in them was also insignificant. This was probably due to the effect of lignocaine injected earlier. All patients showed a slight tachycardia; the average increase in the pulse rate was 15-20 beats per minute. One patient had convulsion during the procedure. Post-operatively, one patient had severe coughing. Blood gas analysis did not reveal any hypercarbia in the post-operative samples.
Passing bronchoscope through the glottis into the trachea and bronchi evokes a series of unpleasant reflexes which may make endoscopic examination impossible. The aim of general and local anaesthesia is to depress these reflexes and permit unhurried examination of the respiratory tract without any physical and/or mental distress to the patient. Vigorous and uncontrolled coughing in an unanaesthetised patient can even rupture the trachea.[4]
The pre-medication with phenobarbitone, pentazocin and atropine sulphate helps to raise the threshold for convulsions, bring about analgesia and narcosis and to dry the oral mucosa respectively. Gargling with lignocaine viscous anaesthetises the oral mucosa and prevents gagging and coughing during bronchoscopy. Intratracheal lignocaine helps to prevent bucking and straining during the scopy. Intravenous lignocaine suppresses the cough reflexes without depressing the respiration.[5] It also provides a certain degree of analgesia.[3] All these permit smooth and easy performance of bronchoscopy. Further, should suxamethonium chloride be required at a later stage, prior lignocaine minimises muscle twitching and post-operative muscle pain due to suxamethonium chloride. However, lignocaine must be injected slowly to prevent convulsions.[7] Plasma levels of lignocaine exceeding 10 ug per ml should be avoided. One patient in this series who got a convulsion received rather rapid intravenous injection of lignocaine and he had to be treated with suxamethonium chloride and intermittent positive pressure ventilation. This patient was one of the earliest cases in our series. Convulsions can also be precipitated by hypoxia and hypercarbia.[7] In this series, hypoxia was avoided by adequate oxygenation. Further, oxygenation helps the rapid hepatic degradation of lignocaine.[1], [6] Wagman et al[7] have demonstrated that hypercarbia lowers the threshold to lignocaine-induced convulsions. We did not notice hypercarbia in any patient of our series. Neither hypotension nor cardiac arrhythmia was seen in this series.
Advantages of lignocaine as an adjunct during bronchoscopy are as follows: suppression of cough reffex; relaxation of larynx; elimination of post-operative cough, nausea and vomiting; adequate relaxation of the patient; anti-arrhythmic and bronchodilator action of lignocaine. As the patient breathes spontaneously, the endoscopist can see the movements of the vocal cords, can see the entire bronchial tree and can collect secretion from any site that he desires. There is no respiratory depression and post-operatively, the normal cough reffex is retained. The use of suxamethonium chloride is eliminated. Intro-operative apnoea and post-operative muscle pain are avoided. This technique is particularly useful where jet ventilators are not available and the apnoeictechnique could be dangerous.
Our thanks are due to Dr. A. J. Dhruva, Professor and Head, Department of Anaesthesiology, Seth G . S . Medical College and K.E.M. Hospital, Parel, Bombay, for his encouragement and guidance in carrying out the present study. We are also thankful to Dr. C. K. Deshpande, Dean, Seth G.S. Medical College and K.E.M. Hospital, Bombay, for allowing us to publish the data.
| 1. | Adriani, J., Zepernick, R. and Hyde, E.: Influence of the status of the patient on the systemic effects of local anaesthetic agents. Anaesth and Analges., 45: 87-92, 1966.  |
| 2. | Blancato, L. S., Peng, A. T. C. and Alonsabe, D.: Intravenous lidocaine as an adjunct to general anaesthesia for endoscopy. Anaesth. and Analges., 48: 224-227, 1969. |
| 3. | de Clive-Lowe, S. G., Desmond, J. and North, J.: Intravenous lignocaine anaesthesia. Anaesthesia, 13: 138-146, 1958. |
| 4. | Mushin, W. W.: "Thoracic Anaesthesia". Blackwell Scientific Publications, Oxford, 1963 p. 239. |
| 5. | Steinhaus, J. E. and Howland, D. E.: Intravenously administered lidocaine as supplement to nitrous oxide thiobarbiturate anaesthesia. Anaesth. and Analges., 37: 40-46, 1958. |
| 6. | Sung, C. Y. and Traunt, A. P.: The physiological disposition of lidocaine and its comparison with procaine. J. Pharmacol. & Eper. Ther., 112: 432-443, 1954. |
| 7. | Wagman, J. H., deJong, R. H. and Prince, D. A.: Effects of lidocaine on the central nervous system. Anaesthesiology, 28: 155-167, 1967. |
 |
 |
|
|
|
|
