Epidural blockades in treatment of patients with bronchial asthma

Constantine P. Zhidkov

The first information on application of epidural blockades ( EB) in patients with bronchial asthma (BA) was reported in the famous book of P.Bromage "Spinal Epidural Analgesia" (1). S. Filippov (2) was the first who performed EB at upper thoracic level in three BA patients with status asthmaticus (SA) in Russia. The bronchodilating effect was obvious and impressive. The positive result of application of EB in asthmatic patients was also reported in multiple studies(3,4). Application of EB in BA patients logically originated from the multiple clinical trials which proved that continuous epidural anesthesia produces a positive effect on lung function parameters in postoperative period (5-8 ) and even can be recommended as a method of treatment of some chronic lung diseases (9). More recently, studies demonstrated the effectiveness of cervical epidural block for the treatment of SA .(10-11). The opinion about absolute effectiveness of EB in asthmatic patients are not unanimous. Some investigators described an asthmatic attack that have been provoked by epidural anesthesia(12-13). It was hypothesized that etiology of bronchospasm may have been related to sympathetic nervous blockade allowing unopposed parasympathetically mediated bronchoconstriction (13). The aim of this report was to evaluate the bronchodilating effect of EB accomplished at middle thoracic level and impact of EB on catecholamine response in BA patients.

Materials and Methods

During the period of 1974-1978 yr. 53 patients with BA were treated in ICU of Hospital 25 in Sanct-Petersburg (male-20, female-33 , age ranged from 24 to 81y, median range 43,6). 25 patients had moderate form of BA, 28 patients - severe form of BA, and 15 patients had been admitted to ICU in SA. The duration of SA was 24 hours ( 3 patients) , 24-72 hours ( 10 patients) and more than 72 hours ( 2 patients). 48 patients had intrinsic form and 5 patients had extrinsic form of BA. In 51 patients BA was combined with chronic bronchitis and 41 patients had concomitant ischemic heart disease. The basic therapy in all study patients was generally accepted and included sympathomimetics, methylxantines, b-2 agonists and glucocorticoids (20 patients).

Epidural space catheterized at middle thoracic level (T 7/8) and 8-10 ml of 2% Lidocain were injected into the catheter 3 times a day for a period 3-5 days. Thus, each patient received 10-15 EB.

Pulmonary function parameters were measured before EB and at the 7th and 14th days after EB: forced vital capacity (FVC), residual volume (RV), functional residual capacity (FRC), total lung capacity (TLC), forced expired volume in one second (FEV 1), resistance to airflow (R) , alveolar ventilation (VA), functional dead space (VD), alveolar capillary diffusion (DL). The plasma level of epinephrine (E), norepinephrine (NE) were examined before EB and after 30 and 60 min after EB. Frequency data were analyzed with Student test.

The distinctive positive effect ( ceasing or essential decreasing asthmatic attacks in frequency ) was observed in 44 ( 83%) patients, in 9 (17%) patients EB did not produce any reliable effect. 13 (86.6%) patients with SA were successfully treated with the course of EB and 2 (3.7%) patients died as a result of severe SA. During and after EB until the time of discharge from the hospital patients received methylxantines, beta2-agonists, mucolytic agents and, if previously being on steroids, the same dose of glucocorticoids.

At the examination before EB the BA patients were characterized with gross functional lung tests abnormalities. There were augmentation of bronchial resistance ( R 3.8 folds greater than normal values and FEV1 2.8 folds less than normal indices) and reallocation of lung volumes ( FRC 1.7 folds greater and RV 2.3 folds greater than in control group). Clinical improvement was attended with significant (P< 0.05) decrease of R (from 9.28+/-1.70 cmH2O/L/s to 5.23+/-0.72 cmH2O/L/s) and augmentation of FEV1 (from 6.0 +/- 0.4 L to 4.3+/-0.3 L) ( tab. 1).

There were no statistically significant impact of EB on TLC, VA, VD and DL parameters.

Table 1. Impact of epidural blockades on pulmonary function parameters. Mean +/- SD

Parameters -- Control group (n=45) -- Before EB (n=25) -- 7th day post EB (n=25)

FVC (L) --------------4.31+/-0.10 -------------------------2.2 +/- 0.3------------------------- 3.3 +/-0.3 **

RV (L)--------------- 2.13+/- 0.06------------------------- 5.0 +/- 0.3 -------------------------3.6 +/- 0.4 **

FRC (L) -------------3.48+/- 0.09------------------------- 6.0 +/- 0.4 -------------------------4.3 +/- 0.3 **

FEV1 (L/s )-------- 2.85+/- 0.07------------------------- 1.02 +/- 0.1*---------------------- 1.7 +/- 0.1 **

R (cmH2O/L/s)-- 2.39+/- 0.10-------------------------- 9.28 +/-1.70 *--------------------- 5.23 +/-0.72 **

Student test: * p< 0.05 in comparison with control group; ** p< 0.05 in comparison with "before EB" group

At the examination of lung functional parameters on the 14th day after ending the course of EB the values that reflected bronchial resistance, lung volumes and lung ventilation were stable and did not significantly changed from data received at the 7th day of the post EB period.

Bolus of 8-10 ml of 2% Lidocain injected into epidural space produced skin hypalgesia in the zone supplied with innervation from D4.2 +/-0.9 to L 1.1+/-1.8 segments of spinal cord. Thus 10.7+/-2.1 segments of spinal cord were involved in sensory block. This clinical observation was confirmed with radiologic investigation where the distribution of equivalent volumes of radiopaque solutions along the epidural space was studied. Thus , 8-10 ml of anesthetic combined with radiopaque solution injected into epidural space extended in cranial direction on 5.6+/-0.8 and in caudal direction on 4.8+/-0.15 vertebrae bodies.

The neuroendocrine background of BA patients was characterized by significant (p< 0.05 ) decrease in NE plasma level. The level of plasma E were close to normal values. EB induced significant (p< 0.05) increase in plasma E level ( from 1.62 +/- mg/L to 3.01 +/- 0.41 mg/L) and no significant decrease in plasma NE concentration ( tab. 2)

Table 2.- Adrenergic response to epidural blockades in patients with bronchial asthma ( Mean+/-SD ).

Indices-------- control group --- before EB--- 30 min after EB--- 1 hour after EB

Epinephrine mg/L-- 1.32 +/- 0.25 --------1.62 +/- 0.26 -------3.01 +/- 0.41* --------------2.3 +/- 0.86

Norepinephrine mg/L 4.91 +/- 0.50----- 1.93 +/- 0.46 **--- 1.43 +/- 0.73---------------- 1.01 +/- 0.91

Epinephrine/

Norepinephrine---- 0.26------------------ 0.83 -------------------2.10--------------------------- 2.27

Student test:* p<0.05 in comparison with " before EB" indices; **p< 0.01 in comparison with controls

The influence of epidural anesthesia (EA) on cateholamines release was examined in multiple studies but mainly in response to surgery (14 -17). Thus, these data being mainly contradictory; hardly may be extrapolated to BA patients. It was found that EB with sensory analgesia level as high as C8 did not significantly decrease the plasma concentration of E in unstressed volunteers. The plasma concentration of NE significantly decreased only when the level of sensory analgesia was approximately C8 (18).

The results of our study suggest that injection into the epidural space of a local anesthetic solution decreases bronchial resistance and stops the asthmatic attack resistant to bronchodilating therapy. However the true mechanisms of efficacy of EB in BA patients are still remains poorly delineated. We suppose that preganglionic blockade of sympathetic nerve fibers leads to decrease of NE plasma concentration and probably to some compensatory increase of suprarenal chromaffin substance activity with corresponding augmentation of E in plasma of asthmatic patients. This results indicate that EB accomplished at middle thoracic level in patients with BA affects the adrenergic system favorably influencing epinephrine/norepinephrine relationship that can play a beneficial role in cases of resistant bronchoconstriction.

References

1. Bromage PR: Spinal Epidural Analgesia. Edinburg,1954

2. Filippov SV: Dlitelnaja periduralnaja blokada pri lechenii tjazhielyh form bronchial, noi astmy. Vestnik Chiryrgii 12:53-55,1973

3. Schelkynov VS: Dlitel, naia peridural, naia anestesia. Vestnik Chirurgii 5:87-92,1967

4. Zhidkov CP, Degt,iareva Zia: Vli, ianie peridural, hoi blokady na functiu vneshnego apparata dychania i vegetativnyiu nervnyiu sistemy bol, nych bronchial, noi astmoi. Anestesiologia i Reanimatologia 6:52-54,1977

5. Mayrin SA: Dlitel, naia peridural, naia anestesia kak metod obesbolivania v posleoperationnom periode. Experimental, naia chirurgia Anestesiologia 3:54-57,1967

6. Myneyuki M, Ueda J,Urabe N, Fakeshita H, Janamoto A: Postoperative pain relief and respiratory function in man. Anesthesiology 29:304-313, 1968

7. Bromage PR: Spirometry in assessment of analgesia after abdominal surgery. Brit Med J: 3: 589-593, 1955

8. Isaac M: A critical evaluation of ventilatory function after epidural analgesia.

Indian J Anesth 16: 304-312, 1968

9. Lund PC: Clinical application of epidural blocks. Int Anesth Clin 1: 567-574,1963

10. Noda J, Ohama J, Suzuki S: The effectiveness of cervical epidural block for the treatment of status asthmaticus. Masui 43(8): 1251-1255, 1994

11. Kon H, Aoki M, Yamamoto S, Ikeda M, Namiki A, Ohmichi M: A case of successfully managed acute asthmatic attack by cervical epidural block during mechanical ventilation. Kokyu To Junkan 38(10): 1041-1044, 1990

12. Eldor J, Frankel DZ, Barav E, Nyska M: Acute bronchospasm during epidural anesthesia in asthmatic patients. J Asthma 26(1): 15-16, 1989

13. Wang CY, Ong GS: Severe bronchospasm during epidural anaesthesia.

Anaesthesia 48(6): 514-515, 1993

14. Tsuji H, Shirasaka C: Inhibition of adrenergic response to upper abdominal surgery with

prolonged epidural blockade. Jpn J Surg 12:5 344-348, 1982

15. Shibata K, Taki Y, Futagami A, Yamamoto K, Kobayashi T, Murakami S: Effects of upper

thoracic epidural anesthesia on hemodynamics and oxygen supply-demand relationship in

hypovolemic dogs. Masui 40:12 1777-1782, 1991

16. Smeets HJ, Kievit J, Dulfer FT, van Kleef JW: Endocrine-metabolic response to abdominal aortic surgery: a randomized trial of general anesthesia versus general plus epidural anesthesia. World J Surg 17:5 601-606, 1993

17. Norman JG, Fink GW: The effects of epidural anesthesia on the neuroendocrine response to major surgical stress: a randomized prospective trial. Am Surg 63:1 75-80, 1997

18. Stevens RA, Artuso JD, Kao TC, Bray JG, Spitzer L, Louwsman DL: Changes in human plasma cateholamine concentrations during epidural anesthesia depend on the level of block Anesthesiology 74:6 1029-1034, 1991

All the data from this study were originally published in 1977 in «Vestnik Chirurgii» (4) (Russian Federation)