Heridas Fetales Crecimiento y Factores

Es útil revisar algunos conceptos referentes a las heridas fetales y a los factores de crecimiento que empiezan a tener aplicación clínica en úlceras de difícil tratamiento.

Heridas Fetales

En el período fetal, la cicatrización es diferente y se caracteriza por falta de inflamación y de polimorfonucleares, presencia de monocitos y ausencia de contracción y epitelización, en lesiones expuestas al líquido amniótico (103).

Lo más interesante es la inexistencia de cicatriz final, la poca acumulación de colágeno (104, 105) Y los altos niveles de glicosaminoglicanes y ácido hialurónico (106); lo anterior hace pensar más en una estructura en regeneración que en un proceso de reparación.

Las razones para que esto ocurra no son claras, aunque podría ser responsable el medio ambiente fetal con recuentos leucocitarios y niveles de tensión de oxígeno y de factor estabilizante de la fibrina más bajos que en la época posnatal (107, 108). El contacto con el líquido amniótico no parece ser importante (109).

Factores de crecimiento

Son polipéptidos que promueven la proliferación celular actuando sobre receptores externos y que desencadenan cambios intracitoplásmicos que preparan la célula para iniciar la síntesis de ADN Y el proceso mitótico. También facilitan la migración de leucocitos y fibroblastos (110).

Se ha logrado aislar los factores derivados de las plaquetas, y su utilidad en el tratamiento de heridas de evolución tórpida se ha comprobado a través de varios estudios recientes (111-113). Igualmente, se ha demostrado el beneficio de las aplicaciones tópicas del factor de crecimiento epidérmico para acelerar la cicatrización de quemaduras y de áreas donantes de injertos de espesor parcial (114-116).

Miscelanea

La cicatrización es más rápida en ambientes cálidos (300 C) que en fríos (200 C) lo que puede explicarse por la vasoconstricción asociada a estos últimos.

La falta de sensibilidad en el área lesionada suprime este efecto (8), no afecta la contracción ni la epitelización y facilita las ulceraciones por incrementar la colagenólisis ya que la isquemia asociada a presión prolongada disminuye la llegada de alfa-dos macroglobulina del suero que inhibe las colagenasas (117).

Igualmente se ha demostrado un aumento entre el 30 y el 45% de la epitelización y una mayor producción de colágeno si se colocan vendajes oclusivos, quizá por el incremento local de la temperatura (118).

El mecanismo de producción de la herida es un factor interesante en la determinación de la velocidad de los procesos reparativos.

Se observa mayor rapidez cuando no hay infección ni tejido necrótico local, como ocurre en las incisiones quirúrgicas efectuadas con el bisturí convencional.

La utilización de criocirugía, cauterios, ácidos, cáusticos, agentes hemostáticos y láser, retarda en grado variable la cicatrización, puesto que los tejidos desvitalizados deben ser desbridados por la reacción celular antes de iniciar la fibroplasia (119).

Aunque los estudios iniciales con este último demostraron que se favorecía la adherencia de injertos de piel, las investigaciones posteriores comprobaron que se retarda la epitelización y se disminuye la ganancia de fuerza tensil (120).

Hasta el momento no se ha demostrado que el uso de estos instrumentos posea una ventaja real en términos de disminución del tiempo quirúrgico, menor hemorragia o mejor cicatriz, excepto en pacientes con coagulopatías o cuando se realizan procedimientos en áreas excesivamente vascularizadas (121).

El láser de bióxido de carbono no ocluye vasos de calibre mayor de 2 mm y el de argón produce una destrucción tisular biológicamente inaceptable en los bordes de la incisión:

Solamente el de neodimio (Nd: YAG) ofrece algunas ventajas puesto que suprime la producción de colágeno en fibroblastos cultivados y en la piel normal, por lo que podría llegar a ser de utilidad en el tratamiento de queloides (122). Por su parte, los de baja energía, como helioneón (He-Ne) o galio (Ga-As) parecen estimular la fibroplasia in vitro (122). 

La aplicación tópica de miel disminuye el edema perilesional, ejerce actividad bactericida, favorece la neovascularización y ayuda al desbridamiento (123). El uso local de factores derivados de plaquetas autólogas estimula la formación de tejido de granulación y acelera la epitelización en algunas ulceraciones crónicas de las extremidades (124).

Es interesante anotar que el envejecimiento fisiológico retarda y prolonga todas las fases reparativas (53, 125) puesto que las mitosis celulares son más escasas, la ganancia de fuerza tensil más lenta y la síntesis de sustancias necesarias para la cicatrización, más pobre. Lea También: Cicatrización y Terapia Inmunosupresora

Abstract

Wound healing is a complex biological process involving several stages wich may be altered by numerous drugs and common diseases. 

This article updates current knowledge regarding the different alterations that might be associated with malnourishment and vitamin deficiencies and the nature of the problems observed after radiotherapy. Finally, it reviews some information regarding fetal wound healing and the growth factors that have became available for the treatment of chronic non-healing wounds. 

Referencias

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12. Alvarez O M, Gilbreath R L: Effeel ef dielary thiamine on intermoleeular collagen cross-linking during wound repair: A meehanical and biochemical assessmenl. J Trauma 1982; 22: 20
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18. Miller T A: Tbe healing of parlial-thickness skin injuries. In: Hunt T K: Wound healing and wound in fections: Tbeory and surgical praclice. Applelon-Century-Crofts, New York, 1980
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22. Perrins D J D: Hyperbaric oxygen and skin coverage. HBO Rev 1983; 4: 179 25. Slack W 1, Tbomas D A, Perrins D: Hyperbaric oxygenation in chronic osteomyelilis. Lancel 1: 1093-965.
    

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32. O’Hare R P, Fallon A, Bradley J F, Burns J, McGee J O D: lsolation of collagen stimulating factor s from healing wounds. J Clin Pathol 1983; 36: 707
33. Ahonen J, Jiborn H, Zeberfeldt B: Hormone intluence on wound healing. In: Hunt T K: Wound healing and wound infeetion: Theory and surgical practice. Appleton-Century-Crofts, New York, 1980
    

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39. Titscher R. Wrba H: Stimulation of immune response in lung cancer patients by vitamin A therapy. Oncology 1977; 34: 234
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41. AlIen H 1.., Wase A, Bear W T: Indomethacin and aspirin: Effect of nonsteroidal anti-inflammatory agents on the rate of fracture repair in the ra!. Acta Orthop Scand 1980; 51: 595
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45. Kulick A, Michael 1, Smith S, Hadler K: Oral ibuprofen: Evaluation of its effeet on peritendinous adhesions and the breaking of a tenorrhaphy. J Hand Surg 1986; 11A: 110
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    Otras Fuentes

56. Moynahan E J: Penicillamin in the treat· ment of morphea and keloids in children. Postgr Med J 1974 Aug (Suppl); 39
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59. Scher K S, Scon-Conner C E H: Detrimental effect of a cephalosporin on early fascial healing. Surg Forum 1986; 37: 116
60. Zimmerman A, Truss F: The effect of antibiotic drugs on wound healing. Urol Res 1974; 2: 73
61. Scher K S, Scott-Conner C E H, Montany P F: Effect of cephalosporins on fascial healing after celiotomy. Am J Surg 1988; 155: 361
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    Lecturas Recomendadas

67. Tran D T, Miller S H, Buck D et al: Potentiation of infection by epinephrine. Plast Reconstr Surg 1985; 76: 933
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72. Brinckerhoff C E, McMillan R M, Dayer J M, Harris E D: Inhibition by retinoic acid of collagenase production in rheumatoid synovial cells. N Engl J Med 1980; 303: 432
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    Otras Lecturas Recomendadas

78. Goodson W H I1I, Radolf J, Hunt T K: Wound healing and diabetes. In: Hunt T K: Wound healing and wound infection: Theory and surgical practice. New York, Appleton-Century-Crofts, 1980
79. Seifter E, Rettura G, Padawer J et al: Impaired wound healing in streptozocin diabetes. Prevention by supplemental vitamin A. Ano Surg 1981; 194: 42
80. Mosely L H, Finseth F, Goody M: Nicoline and its effecl on wound healing. Plast Reconslr Surg 1978; 61: 570
81. Lawrence W T, Murphey R C, Robson M C el al: Tbe delrimenlal effecl of cigarette smoking on flap survival: Ann experimental sludy in the ra!. Bril J Plasl Surg 1984; 37: 216
82. Benvenisle K, Thut P: Tbe effect of chronic alchoholism on wound healing. Proc Soc Exp Biol Med 1981; 166: 568
83. Buknall T E: Tbe effect of local infeclion upon wound healing: An experimental study. Brit J Surg 1980; 67: 851
84. Robson M C, Slenberg B D, Heggers J P: Wound healing a1terations caused by infeclion. Clin Plast Surg 1990; 17: 485
85. Colin J F, Elliol P, Ellis H: The effect of uremia upon wound healing: An experimenlal study. Brit J Surg 1979; 66: 793
86. Grinell F, Billingham R E, Burgess L: Distribution of fibronectin during wound healing in vivo. J Invest Dermatol 1981; 76: 181
87. Repesh L A, Fitzgerald T J, Furchl L T: Fibronectin involvement in granulation tissue and wound healing in rabbits. J Histochem Cytochem 1982; 30: 351
88. Hulsey T K, O’Neill J A, NebblettWR, Meng H C: Experimental wound healing in essenlial fatty acid deficiency. J Pedialr Surg 1980; 15: 505
    

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89. Uitto J, Tan E M L, Ryhanen L: Inhibition of collagen accumulation in fibrotic processes: Review of pharmacological agents and new approaches with amino acids and their analogues. J Invest DermaloI1982; 79: 113
90. Bayer 1, Ellis H: Jaundice and wound healing: Ano experimental study. Bril J Surg 1976; 63: 392
91. Amstrong C P, Dixon J M, Duffy S W et al: Wound healing in obslructive jaundice. Bril J Surg 1984; 71: 267
92. Askew A R, Bates G J, Balderson G: Jaundice and the effect of sodium taurocholate taken orally upon abdominal wound healing. Surg Gynecol Obstet 1984; 159: 207
93. Viljoen D L, Bloch C, Beighton P: Plaslic surgery in pseudoxanthoma elas- ‘ ticum: Experience in nine patients. Plast Reconslr Surg 1990; 85, 233
94. Levenson S M, Gruber C A, Rettura G et al: Supplemental vitamin A prevents the acute radiation-induced defect in wound healing. Ann Surg 1984; 200: 494
95. Mustoe T A, Purdy J, Gramates P et al: Reversal of impaired wound healing in irradiated rats by plateletderived growth factor-BB. Am J Surg 1989; 158: 345
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97. Rowlatt U: Intrauterine wound healing in a 20-week human fetus. Virchows Arch [A] 1979; 381: 353
98. Robinson B W, Goss A N: Instrauterine healing of fetal rat cheek wounds. Cleft Palate J 1981; 18: 251
99. Hallock G G, Rice D C, McClore H M: In utero Iip repair in the rhesus monkey. Plast Reconstr Surg 1987; 80: 855
    

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100. Krummel T M, Nelson J M, Diegelmann R F et al: Fetal response to injury in the rabbit. J Pediatr Surg 1987; 7: 640
101. Playfair J H L, Wolfendale M R, Key H E M: The leukocytes of peripheral blood in the human fetus. Bril J. Haematol 1963; 9: 336
102. Chignier E, Baguet J, Dessapl B et al: Skin healing and fibrin stabilizing factor levels in the rabbit fetus. J Surg Res 1981; 31: 415
103. Sullivan W G: In utero cleft Iip repair in the mouse without an incision. Plast Reconstr Surg 1989; 84: 723
104. McGralh M H: Peptide growth factors and wound healing. Clin Plast Surg 1990; 17: 421
105. Doucette M M, Fylling C P, Knighton D R: Prevention of lower extremity amputation due to nonhealing wounds in a high-risk population: Use of plalelet derived wound healing formula and a defined wound care protocol. Arch Phys Med Rehabil 1989; 70: 780
106. Knighton D R, Ciresi K F, Fiegel V D et al: Slimulation of repair in chronic nonhealing cutaneous ulcers: A prospeclively randomized blinded trial using platelet-derived wound healing formula. Surg Gynecol Obstet 1990; 170: 56
107. Fylling C P, Knighton D R, Gordinier R: Tbe use of a comprehensive wound care protocol including topical growth factor lherapy in treatment of diabelic plantar ulcers. In: Ward J: Diabetic neuropathy, Wiley, Chicherter, U. K., 1990
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111. Basson M D, Bumey R F: Defective wound healing in patients with paraplegia and quadriplegia. Surg Gynecol Obstet 1980; 155: 9
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SOCIEDAD COLOMBIANA DE CIRUGÍA
XVII Congreso Nacional
“Avances en Cirugía”
” HOTEL TEQUENDAMA “
14, 15, 16 Y 17 de agosto de 1991

Conferencistas invitados

• Doctor Luis Eduardo Cortés – Estados Unidos
• Doctor Lemuel Herrera – Estados Unidos
• Doctor Enrique Moreno – España
• Doctor Raúl Praderi – Uruguay
• Doctor Aurelio Rodríguez – Estados Unidos

Habrá presentación de “Trabajos Libres”. Quienes deseen participar en ellos, deberán enviar el respectivo resumen a la sede de la SOCIEDAD antes del 15 de junio de 1991.
Igualmente se realizarán “Almuerzos de Trabajo” con temas de interés para los asistentes.
Informes e inscripción de trabajos: Calle 100 ND 14 – 63, Of. ND 502 – Tel: 257-4560 y Telefax 257-4501. Bogotá, D.E., Colombia.

Doctor Alberto Kurzer Schan Jefe de la Secc. de Cirugía Plástica, Maxilofacial y de la Mano, U. de Antioquia, Hosp. Univ. San Vicente de Paúl  Medellín, Colombia.