WHY INCISIONS (SUPERFICIAL WOUNDS) IN HIJAMAH?

Let us take a much closer look at the physiology of making incisions in the treatment of Hijamah (Wet Cupping Therapy).

Pathophysiology of wound healing

1. Pathophysiology of wound healing and factors affecting it.

2. Introduction

A wound is a disruption of the normal structure and function of the skin and underlying soft tissue. Acute wounds in normal, healthy individuals heal through an orderly sequence of physiological events that include haemostasis, inflammation, epithelialization, fibroplasia, and maturation. When this process is altered, a chronic wound may develop and is more likely to occur in patients with underlying disorders such as peripheral artery disease, diabetes, venous insufficiency, nutritional deficiencies, and other disease states.

3. Wound mechanism

 Wounds are generally classified as acute or chronic. Chronic wounds are generally associated with physiological impairments that slow or prevent wound healing. Wounds may be caused by a variety of mechanisms including acute injury to the skin (abrasion, puncture, crush,Incisions), surgery and other etiologies that cause initially intact skin to break down (eg,ischemia, pressure).

4. Surgical wounds.

Surgical wounds are a controlled form of trauma created in the operating room environment.

Classified according to the degree of bacterial load or contamination of the surgical wound. The categories, clean, clean-contaminated, contaminated, and dirty are used to predict the risk of surgical wound infection which can impact wound healing. The majority of clean and clean-contaminated wounds are closed primarily at the completion of the surgery. Contaminated and dirty wounds (eg,  faecal contamination, debridement for wound infection) are typically packed open.

5. Phases of wound healing

 Wound healing occurs as a cellular response to tissue injury and involves activation of keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets. The process involves organized cell migration and recruitment of endothelial cells for angiogenesis. Many growth factors and cytokines released by these cell types coordinate and maintain wound healing.

6.  Acute wounds transition through the stages of wound healing as a linear pathway, with clear start- and endpoints.

Chronic wounds are arrested in one of these stages, usually the inflammatory stage, and cannot progress further.

7. Haemostasis

 Immediately after injury to the skin, small vessels within the wound constrict to provide at least a measure of haemostasis for 5 to 10minutes. Platelets aggregate in severed vessels and trigger the clotting cascade and release essential growth factors and cytokines that are important for the initiation and progression of wound healing (eg, platelet-derived growth factor, transforming growth factor- ).β The fibrin matrix that results stabilizes the wound and provides a provisional scaffold for the wound healing process.

8. Inflammation

 The lag phase because wound strength does not begin to return immediately.

 The inflammatory phase is completed within 3 days, except in the presence of infection or other causes of wound chronicity. Key components of this phase are increased vascular permeability, and cellular recruitment. The presence of necrotic tissue, foreign material and bacteria result in the abnormal production of metallo proteases which alter the balance of inflammation and impair the function of the cytokines

. The healing progression of chronic wounds usually becomes arrested in this inflammatory stage

9. Epithelialization

Also called migration refers to basal cell proliferation and epithelial migration occurring in the fibrin bridgework inside a clot. it continues until individual cells are surrounded by cells of similar type. In a clean surgical wound, the epithelial cells migrate downward to meet deep in the dermis. Migration ceases when the layer is rejuvenated; this is normally completed within 48 hours of surgery.  The superficial layer of epithelium creates a barrier to bacteria and other foreign bodies. However, it is very thin, easily traumatized, and gives little tensile strength.

10. Fibroplasia

 Fibroplasia consists of fibroblast proliferation, accumulation of ground substance, and collagen production. Fibroblasts are transformed from local mesenchymal cells, are usually present in the wound within 24 hours, and predominate by the 10th postoperative day. They attach to the fibrin matrix of the clot, multiply, and produce glycoprotein and mucopolysaccharides, which make up ground substance.

 Fibroblasts produce contractile proteins. These contractile cells, which are designated myofibroblasts, are present in the wound by the 5thday and have characteristics of smooth muscle cells with the ability to contract. Myofibroblastic cells are lost via apoptosis as repair resolves to form a scar. In pathological fibrosis, myofibroblasts persist and are responsible for fibrosis via increased matrix synthesis and for contraction. The exuberant scarring may impede normal organ function or, in the case of skin, result in keloid.

This is why in hijamah whilst administering the incisions they should NOT be deeper than 1mm. Otherwise tissue scaring may occur such as keloids.

 Fibroblasts also synthesize collagen, the primary structural protein of the body. Collagen production begins on the 2nd post operative day, when it is secreted as an amorphous gel devoid of strength.

 Maximum collagen production does not begin until day 5 and continues for at least 6 weeks. The developing collagen matrix stimulates angiogenesis. Granulation tissue is the result of the combined production of collagen and growth of capillaries.

11. Maturation

 Key elements of maturation include collagen cross-linking, collagen remodelling, and wound contraction.

 FIVE types of collagen have been identified;

Types I and III predominate in the skin and aponeurotic layers.

The tensile strength of the wound is directly proportional to the amount of collagen. As disorganized collagen is degraded and reformed, covalent cross-links are formed that enhance tensile strength.

 Maximum strength depends upon the interconnection of collagen subunits.

12. Impaired wound healing

 There is usually not a single primary factor that contributes to impaired wound healing. There are multiple, smaller contributing issues that can disrupt the process. As examples,-local tissue ischemia and neuropathy can impair chemotaxis during the haemostasis and inflammatory stages.-Tissue necrosis and infection alter the balance of inflammation and compete for oxygen.-Uncontrolled periwound edema and wound instability disrupt myofibroblast activity, and collagen deposition and cross-linking.

13. Risk factors for non-healing chronic wounds affect a substantial proportion of the population and contribute to a significant burden in the hospital setting. Certain patients are at risk for development of a non-healing wound such as:

 Impaired arterial or venous circulation,

 Immuno compromised states

 The elderly

 Diabetes

 And any patient with Neuropathy or Spinal cord injury.

CONCLUSION

The most common non healing wounds affecting the lower extremities are associated with Peripheral Artery Disease, Diabetes and Chronic Venous Syndromes.

After haemostasis has been achieved, acute wounds normally heal in an orderly and efficient manner characterized by four distinct, but over lapping, phases:

 Inflammation,

 Epithelialization,

 Fibroplasia, and

 Maturation

Many disease states alter the process of wound healing. The most common of which are diabetes, thrombosis  and chronic venous ailments which occlude blood vessels.

However by administering Hijamah,,not only will these diseases be cured but will remove blood stasis from any occluded blood vessels in the path of the treatment.

Note some ailments such as diabetes can be treated by Hijamah but cannot be entirely cured by it alone. Other modes of treatments should be employed.