Leech Therapy

Leeches are hermaphroditic ectoparasites of the class Hirudinea. There are several species of leech, but the most commonly used medicinal leech is Hirudo medicinalis. Leech therapy is indicated for relief of venous congestion in a failing flap. Improved tissue blood flow in leech-treated venous compromised flaps has been demonstrated (39). Leech therapy has also been used to treat a variety of other conditions including soft tissue swelling, periorbital hematoma, cauliflower ears, ecchymoses, and purpura fulminans (40). Leech therapy should be reserved for cases that are not amenable to surgical correction. The leeches are applied to the skin surface of the flap and

Testicular Vein Leech Therapy

allowed to feed until they fall off (15-120 min) (Fig. 4). The wound continues to ooze due to the action of several substances present in the leech saliva including hirudin, vasodilators, and hyaluronidase. Hirudin is the most potent natural inhibitor of thrombin known (41). The leech can ingest up to 8-10 ml blood, and the wound can continue to ooze another 50 ml blood from the bite site. Leech therapy is successful in 70-80% of cases (40).

The leech has a large posterior sucker for attachment and crawling and a smaller anterior sucker (the head) for feeding. The posterior end is sometimes mistaken for the head because it also leaves a bite mark. Placing a drop of blood at the desired site of attachment can facilitate application of the leech. Migration can occur so the leech must be closely supervised and the site should be encircled with surgical towels.

Complications associated with leech therapy include wound infection and bleeding requiring blood transfusion. Wound infection is most commonly caused by Aeromonas hydrophila, a facultative gram-negative rod that is part of the normal flora in the leech gut. Prophylactic antibiotics should be administered to cover this organism: Aeromonas hydrophila is sensitive to third-generation cephalosporins, ciprofloxacin, aminoglycosides, sulfa drugs, and tetracycline (41) (ceftriaxone is commonly used). The success of leech therapy drops to less than 30% in the presence of a clinically significant infection (40). Immunosuppression or arterial in sufficiency in the flap predisposes the patient to infection and are contraindications to leech therapy.


Skin flap delay is a technique to increase the vascular territory of a flap prior to its definitive transfer to a recipient site. The surviving length of a flap can be increased by at least 100%. Surgical flap delay involves incising the flap margins, extensive flap undermining at the donor site, or ligation of distal source vessels along the long axis of the flap. Pharmacological flap delay involves the use of medications to increase the vascular territory of a flap without surgical intervention. Surgical flap delay is the most effective method to augment flap circulation.

The principle behind surgical skin flap delay is interruption of the neurovascu-lar supply to the distal parts of a flap prior to definitive flap transfer. After a delay of up to 3 weeks, the flap is harvested and transferred to the recipient site. The technique is dependent upon the underlying vascular anatomy at the donor site. In areas of mobile skin such as the scalp and forehead, the neurovascular structures tend to course longitudinally in the subcutaneous plexus and can be interrupted by simply incising three sides of the flap without undermining (the flap edges are then resutured |

during the delay period). Limited undermining (below the subdermal plexus) may be necessary to interrupt the blood supply if the distal part of the flap is supplied by perforating vessels. The extent of safe undermining can be determined clinically by verifying that the capillary refill is as rapid in the undermined skin as that in the adja- >3

cent unoperated skin. A variety of incisions and extent of undermining is described in the older plastic surgery literature (42). o

The delay phenomenon describes the physiological events that result in clinical flap delay. The events are poorly understood and are frequently debated in the literature. There are several hypotheses regarding the mechanisms underlying the delay phenomenon including Reinisch's denervation supersensitivity-arteriovenous [AV] shunt mechanism (10), adrenergic spasm, and vascular collateral development. Reinisch's theory states that the sympathectomy created by surgical delay results in denervation supersensitivity that shuts down AV shunts, thus increasing nutrient blood flow to the distal parts of a flap. The adrenergic spasm hypothesis states that once the sympathetics are cut, the release of norepinephrine and subsequent vasoconstriction are significantly reduced during definitive flap transfer, resulting in improved flap survival (43). The development of vascular collaterals within the flap itself probably best accounts for the physiological events associated with flap delay. The angiosome concept helps to define the events during flap delay based on the dilation of vascular collaterals, especially at the choke vessel zone (44).

In nondelayed flaps, a source vessel can support the survival of its own vascular territory (angiosome) and an adjacent vascular territory or angiosome. The line of necrosis in nondelayed flaps generally corresponds to the choke vessel zone between the adjacent angiosome and the next angiosome along the axis of the flap. Delaying the flap interrupts the adjacent angiosome's neurovascular supply, resulting in dilation of the surrounding arterial choke vessels and increased capillary blood flow. In theory this allows easy through-flow for enhanced vascularity of the distal angiosome. This theory is supported by the histological findings of arterial vascular dilation and decreased vessel thickness, especially at the choke vessel zone, between 48 and 72 h after flap delay, not accompanied by vascular ingrowth or neovascularization (44). Venous valves direct blood flow in adjacent angiosomes away from the primary angiosome. The caliber of these vessels increases with flap delay; they become regurgitant and are bypassed by venous collateral vessels. The indications for surgical flap delay include the following:

To extend the expected survival of a flap by progressive division of source vessels along its vascular axis (a flap can be delayed several angiosomes beyond the source artery by progressive division of source vessels staged at time intervals of at least 5 days) (44) To define the survival length of an uncertain flap To improve the circulation of an established flap

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