Nasalotherapy for treatment asthma and – Breathing chronic inflammatory diseases (página 2)

TREATMENT

The present document will omit the description of the multiple existing treatments, with their degree of effectiveness, faults and collateral effects, sufficiently known by medical personnel, in order to go on with the new proposal of treatment.

The proposed medication must combine and improve the favorable attributes of: oral bronchodilators, inhalators, and intranasal corticoids (5).

Such medication must have anti-inflammatory qualities on the airways and diminish the collateral effects of bronchodilators, corticosteroid and antiallergenic drugs (5).

It should also diminish the excessive dosage and use of inhalators, as well as the high costs and the limited action of the antileukotrienes.

In the search of a new treatment we must consider its effectiveness, diminution or elimination of collateral effects, long nonsynthomatic periods and diminution of costs.

Development of an oral medication would be the ideal, but it has been demonstrated that the most effective antiasthmatic therapies are those administered by nasal route.

The patients and they are the only approved therapy to reduce the inflammation of the airways of the asthmatic patient.

Inhaled corticosteroid can inhibit the eosinophils activation in the bronchial epithelium (6).

LOCAL ANESTHETICS

Local anesthetics have long been used as topical application on the nasal mucosa for a great number of otorrinolaringologic procedures (14).

Chemistry of the local anesthetics

Cocaine is the classic local anesthetic, and it is obtained from a plant, the other anesthetic agents are synthetic products.

Group 1. Ester type

Group 2. Amide type

Conformation of the molecule:

2. An aromatic lipophylic chain
3. An intermediate chain
4. An amino hydrophilic group

In ester type compounds as procaine, the aromatic lipophylic chain provides the P-amino benzoic acid.

In the agents amide type as lidocaine, the xylidine constitutes the aromatic lipophylic chain.

The aromatic lipophylic group makes the molecule easily soluble in lipids of cell membranes.

Procaine

Procaine, (P-aminobenzoil-dietil-amino-ethanol chlorhidrate), was the first synthetic local anesthetic.

It is probably the least toxic of all local anesthetics, with the fastest beginning of action and with the shortest duration. The liver destroys it quickly when it reaches the blood stream.

Great amounts of procaine may be given to animals of laboratory by intravenous injection without causing the death.

In usual doses that are used in general and special surgery, just like in odontolgy, procaine is almost free of disagreeable effects on respiratory and circulatory systems.

There have been injected up to 360 cc of the solution concentrated to 1% and up to 570 cc of the solution to the 0, 5% without annoying symptoms.

Infiltrating 0, 5 cc of the solution concentrated to 2% does not produce vasoconstriction or vasodilatation and it does not leave later effects on tissues.

Minimum lethal dose in milligrams by kilogram of corporal weight

750 milligrams/kg in rats, subcutaneous

425 mgs/kg in cobay, subcutaneous

53 mgs/Kg in rabbits, by intravenous route (p)

Lidocaine

Lidocaine is the local anesthetic of amide type, it is the local anesthetic with more use at present, and it has quite fast beginning of action, long lasting duration of action, with a power and toxicity 2 or 3 times greater than procaine.

There are solutions to 4% for topical use on tracheobronchial tree, nose, and orofarynx. Lidocaine has a great number of nonanesthesic uses, as antiarrhythmic in patients with ventricular arrhythmia, antiepileptic, and analgesic intravenous (o).

Absorption and metabolism of the local anesthetic

Local anesthetics do not penetrate the intact skin in important degree. Absorption of local anesthetic after its topical application on mucous membranes may be fast, and in some cases the concentration in blood may be similar to the concentration obtained by intravenous route.

Local anesthetics spread not only towards the inner of the epithelial cells but also towards the neighboring blood vessels. The sanguineous mass of local anesthetics is diluted mainly in its passage through the lung, which provides a cushioning base against the elevated concentration of the local anesthetic. It is excreted in small amounts by renal route without modification.

Most of it is metabolized in the blood or the liver to conjugated metabolites that are pharmacologically inactive and are excreted easily. These processes are made with relative speed of such way that half of the medication in the blood disappears generally in a lapse of 15 to 20 minutes (14).

Toxicity of the local anesthetics

Local anesthetics have the advantage that they are administered by the same health personnel, who are present, if any toxic phenomenon occurs.

The toxicity of the local anesthetic depends on the dose, the nature of the drug, the individual idiosyncrasy, the speed of absorption, and its elimination.

Respiratory depression is the most important toxic effect, and constitutes the habitual cause of death in procanic poisoning, also circulatory depression, effects on the central nervous system and on the cerebral cortex, cutaneous reactions of edematous or urticarial type and anaphylactic shock (15).

MECHANISM OF ACTION OF LOCAL ANESTHETICS

Within the mechanisms of action of local anesthetics, the properties mentioned will be only those that might have to do with their possible effect in the treatment of the bronchial asthma and inflammatory diseases of the respiratory system, which is the goal of the present document.

Local anesthetics have lipophylic properties because of their lipophylic aromatic chain.

Local anesthetic substitutes calcium ions (Ca++) not only in nervous membrane but also in any cell membrane (15)

THEORY ON THE MECHANISM OF ACTION OF THE LOCAL ANESTHETICS IN THE RELIEF OF BRONCHIAL ASTHMA AND CHRONIC DISEASES OF THE RESPIRATORY TRACT

Anti-inflammatory action

The antinflammatory action of the local anesthetics is made at level of the epithelium of the air way by the following mechanisms:

The stabilization of the cell membrane produced by the anesthetic’s aromatic lipophylic chain which adheres to membranes lipid portion.

This stabilization of the cell membranes of the epithelium blocks the citoquines and neuropeptides releasing.

The stabilization of the cell membranes of mast cells and eosinophyls by the same process blocking the histamine and leukotrienes releasing.

The occupation of the lipidic portion of the cell membrane blocks the action of the CAM (complex of attack of membrane of the complement), also blocking y the releasing of inflammatory mediators.

The stabilization of the membrane blocks the action of the IgE.

It also blocks the activation of the system of the complement by the displacement of the ions of Ca++,

Bronchodilatation

The local anesthetic's action is due to the autonomous system blockade producing a simpaticolitic and parasimpaticolitic effect.

The autonomous blockade produces relaxation of the bronchial smooth muscle.

The relaxation of the bronchial smooth muscle is also obtained by the displacement of the ions of Ca++ blocking the interaction of the actina and miosina which is necessary for muscular contraction.

Blocking glands secretion

Autonomic blockade caused by local anesthetic also blocks the cholinergic action on gland of the respiratory tract, and so it results in diminution of gland secretion

SCHEME OF TREATMENT AND PROCEDURES

USING PROCAINE

5.0 (five) milliliters of procaine 1% diluted in 50 (fifty) milliliters of distilled water

USING LIDOCAINE

3.0 (three) milliliters of lidocaine 1% without epinephrine diluted in 50(fifty) milliliters of distilled water.

Procedures

Instillation of 5 milliliters of the solution in each nasal window, till completing 50 milliliters.

You must use a disposable 10cc syringe without needle.

The solution must be allowed to leave normally but the patient is asked not to shake the nose.

So we can obtain a suitable perfusion and absorption of the medication by the nasal mucosa.

Respiratory exercises for clearing

Ask the patient to make long and deep inspirations and prolonged expirations

The therapist must press the patient thorax at the moment of the expiration, placing each hand on the costal grate side to side of the breastbone. This maneuver can be made by a patient relative at home two or three times per day.

This maneuver may cause intense cough in patients with abundant secretion, which contributes to a faster cleaning of the bronchial tree.

3 sessions of nasalotherapy with intervals of 3 days are performed to obtain an improvement of about 90%, but the patient improves his breathing since the first session.

When procaine is used, the total dose of procaine chlorhidrate provided to the patient is of 50 milligrams, most of which do not reach the blood stream because it remains in epithelium of the nasal mucosa or is expelled by the patient during the procedure.

When lidocaine is used, the total dose of lidocaine chlorhidrate is about 30 milligrams, with which occurs just like with procaine.

These doses are below the doses used in other procedures and very below the minimum lethal dose mentioned in the present document.

This treatment provides an improvement over 90 % in the great majority of the patients, with asymptomatic periods until by six months and more.

Materiales y métodos

Estudio no comparativo en 30 pacientes asmáticos manejados previamente con tratamiento convencional en el hospital san Rafael de Andes y en el hospital Gabriel Peláez M. del municipio de Jardín (Ant.Col)

Se administro 35 miligramos de lidocaína disuelta en 30 c.c. De agua destilada en forma tópica sobre la mucosa nasal, en tres sesiones, con intervalos entre sesión y sesión de 5 a 7 días, para un total de 105 miligramos de lidocaína por paciente

Signos-síntomas y patologías asociados

Referencias bibliográficas

1. Jacques Castro, Gemma. Asma en niños: que hay de nuevo, En: Hospital Practice, 2000; 6:153.
2. Dueñas Villamil, Rubén. EPOC. Nuevos avances en un viejo problema. En: Hospital Practice, 2000; 6:153.
3. ___________________. Asma en el adulto: manejo contemporáneo. En: Hospital Practice, 2000; 6:155.

   Terapéutica. Barcelona, Océano Grupo Editorial S.A. 9ª edición española, 1994, Págs. 717-723.

4. Berkow, Robert y Fletcher, Andrew, J. El Manual Merck de Diagnòstico y
5. Ibid. Pàgs 326-333.

   Understanding of asthma. Chest 1997; 111:2S-9S

6. Davies Robert J, Wang Jiahua, Abdelaziz Muntasir, et al. New Insigths into the
7. Grossman, jay. One air way, one disease. Chest 1997; 111: 11S-15S.

   Moderno S.A. 3ª edición, 1971, pàgs 37-52, 167-172.

8. Ganong, William F. Manual de Fisiología Mèdica. México D.F., El Manual
9. O'Byrne, Paul M. Leukotrienes in the pathogenesis of asthma. Chest 1997; 111: 27S-32S.
10. Huston DP. The biology of immune system. JAMA, 1997; 278: 1.804-1814
11. Costa JJ, Weller PF, Galli SJ. The cells of the allergic response. JAMA, 1997; 278: 1.815-1822
12. Nacleiro R, Solomon W. Rhinitis and inhalant allergens. JAMA 1997; 278: 1.842-1.848
13. Leff, Alan R. Future directions in asthma therapy: Is a cure possible? Chest; 111: 61S-68S.
14. Barnes, Petar J. Current therapies for asthma: Promises and limitations. Chest 1997; 111: 17S-23S-
15. Maldonado G. Dario, Bolívar G. Fabio, Caballero A. Andrés, et al. Recomendaciones para el diagnóstico y manejo del paciente con enfermedad pulmonar obstructiva crónica(EPOC). En: Revista Colombiana de Neumología, 1997; 9: S25-S27.
16. De Zubiria Salgado Alberto, Morales González Álvaro, Gama Rivera Maria Eugenia, et al. Asma, Diagnòstico y manejo. En: Revista Asociación Colombiana de Medicina Interna. Guillermo Vargas, Editor, 1996, 60 pàgs.
17. Paparella Michael M,Shumrick Donald A, Gluckman Jack L, Meyerhoff William L. Otorrinolaringología. Buenos Aires, Editorial Mèdica Panamericana. 3ª edición, 1994, pàgs. 3437-3437.
18. Miller, Ronald D. Anestesia. Barcelona, Ediciones Doyma S.A. edición española, 1988, pàgs 541-545, 555-558, 619-653
19. García Cubero a., Domínguez Lázaro A.R., Rodríguez Mosquera M. y col. Asma bronquial. Tribuna Mèdica 1989; 80: 147-160.
20. Brugman SM, Larsen GL, Henson PM et al. Increased lower airways responsiveness associated with sinusitis in a rabbit model. Am Rev. Respir Dis 1993; 147:314 320.G

The author:

Jaime Arango Hurtado

Medicine doctor

University of Antioquia 1984

Magíster in epidemiology

University of Antioquia 1994

The original of the present document has been registered, with the purpose of protecting its intellectual property legally.