Delay of a flap is a technique for overcoming physiologic forces acting on the flap that limit flap survival. Flap delay enhances circulation to ensure flap survival after advancement, rotation, transposition, or transplantation (1). Delay may be accomplished via biochemical means, yet the most consistent and effective method is by surgical manipulation. Surgical delay may involve incision of the flap margins with partial flap elevation or strategic delay with division of specific pedicles to the flap (2,3). Flap delay improves perfusion of the flap through its undisturbed vascular pedicles. The empirical finding that if a flap is raised in two or more stages, the distant regions away from the vascular pedicle are more likely to survive than if the same flap had been raised in one operation is called the delay phenomenon.

At the beginning of the twenty-first century, the development of skin flaps and the transfer of skin was largely one of trial and error. Skin flaps were noted to survive to different lengths in different regions of the body in a poorly understood and unpredictable fashion. Staging the elevation and subsequent transfer of skin flaps from their donor sites to the desired location was known to improve flap survival. Creation of a tube of skin attached initially at both ends to its vascular pedicles and eventually divided from its base was described as early as 1845 by Dieffenbach as an advancement of the open flap method of nasal reconstruction of Tagliacozzi. Tubing a skin flap before transfer improved the survival length of the flap. Popularization of the tube pedicle, or surgical delay of the skin flap, was independently described by Aymard 1917, Filatov 1917, Ganzer 1917, and Gillies 1920 so the transfer of skin might be made more safe (4).

Early in the 1930s, Salmon investigated cutaneous vascular anatomy using injection studies and roentgenograms (5). This detailed work became the foundation for further anatomic discovery. Over the last two decades, Taylor and his colleagues have further developed cadaver vascular injection studies and have expanded the knowledge base of cutaneous and subcutaneous vascular anatomy (2,3,6,7,8,9,10,11). The concepts of angiosomes and choke vessels, as well as the anatomic changes that take place after surgical delay, have been developed from this work.

In 1984, Boyd et al. first described a surgical delay procedure of a TRAM flap that included bilateral ligation of the deep inferior epigastric vessels through an incision along the lower border of the projected flap (7). Expansion of this pioneering work led to a full description of the vascular territories (angiosomes) of the body by Taylor and Palmer in 1987 and set out the road map of arterial anatomy so that for the first time logical planning of incisions and flaps could be performed to create three-dimensional composite tissue territories (8). Specific application of the vascular anatomy of the TRAM flap based on the deep superior epigastric system and the case for a delay procedure were further documented by Moon and Taylor in 1988 (9).

Extensive research has been directed toward understanding the pathophysiology and biochemistry of the necrosis line of a skin flap. Hypotheses to explain the delay phenomenon can be organized into one of two basic premises: either delay improves flap vascularity or delay modifies a flap so that it can survive on less than its normal blood flow. The prime factor that produces these changes in the vascularity of a flap is believed to be ischemia (6,12,13). Diminution in blood supply to the flap creates an inflammatory and metabolic response. This response includes the development of an immediate hyperadrenergic state with the release of norepinephrine,
serotonin, and thromboxane from the tissues. The immediate vascular response of decreasing blood supply to a flap is vasoconstriction (14). Clearing of these vasoactive materials from the flap, along with transection of the sympathetic nerves accompanying the vascular supply, leads to the second phase of vascular response, which is a subsequent vasodilation (15). A biphasic flow response is seen where initial vasoconstriction is followed by vasodilation. The end organs of this kaleidoscope of vasoactive interactions are the vascular endothelium and smooth muscle cells within the blood vessels of the choke zones. The metabolic control of vessel lumen diameter and of vascular smooth muscle tone and proliferation has been linked to the behavior of the choke vessels (6). Bradykinin, glucagon, insulin, and prostaglandins PGE1 and PGE2 because endothelium-independent factors are also elements in this complex metabolic interaction.

The anatomic vascular change that takes place after a delay procedure has been documented to be an alteration in the caliber of existing vessels within the delayed flap and not an ingrowth of new vessels (2,3). In the animal model, surgical delay results in arterial rearrangement within the flap and venous dilation along the axis of the flap (13). Experimental work has shown that when a flap is delayed, the choke vessels that link two arterial territories together dilate. This improves perfusion beyond the choke zone and allows one adjacent vascular territory to be captured with safety by vessels of the flap base (2,3,16,17). Parallel changes occur in the venous network of the flap. Namely, vein caliber increases and the venous valves become regurgitant (3). This results in retrograde venous drainage toward the flap pedicle. In the delayed TRAM flap, venous drainage is directed toward the deep superior epigastric vein and away from the deep inferior epigastric venous system. The net effect of the physiologic changes that occur as a result of surgical delay is to improve perfusion of the conventional TRAM flap and thereby improve the reliability and safety of this flap.

Precise knowledge of arterial architecture is the basis for logical planning of flaps (10). The work of Salmon and subsequent investigators using cadaver injection radiographic studies have documented the vascular anatomy of the anterior chest and abdominal wall regions (5). The arteries and their branches all link together in a continuous network within and between the tissues. Arteries do not exist in isolation, and, as such, they do not supply discrete areas with strict geographic boundaries. Instead, arteries are linked in continuity with the perimeter of their three-dimensional anatomic territory by true anastomoses without change in caliber or by reduced-caliber choke arteries and arterioles (10). These composite segments of tissue that are supplied by a source artery supplying a block of muscle, nerve, and bone with overlying skin are called angiosomes (8).

It has been shown in animal models and clinically that when a flap is raised without a surgical delay, one adjacent anatomic vascular territory can be captured with safety (2,3). Furthermore, necrosis occurs in the region of the choke arterial connections in the watershed zone between the captured vascular territory and the territory beyond. Selective delay of flap vessels and manipulation of the necrosis line is shown in Figure 59.1. The anatomic effect of a delay is to dilate preexisting choke vessels between the territory of the delayed vessel and the next adjacent vascular territory. This enlargement of choke vessels that links these vascular territories together increases blood flow between adjacent territories and improves the survival length of a flap to a location beyond the second vascular territory. The conventional unipedicle TRAM flap that is based on the deep superior epigastric artery (DSEA), which bridges five angiosome territories (9), namely the DSEA angiosome itself followed by the ipsilateral deep inferior epigastric artery (DIEA) territory, is the first captured angiosome territory. This corresponds to Hartrampf zone I. The next territory extends farther into the second captured angiosome territory of the superficial inferior epigastric artery (SIEA), Hartrampf zone III. Across the midline is the contralateral DIEA territory, which also corresponds to a second captured angiosome and represents Hartrampf zone II. Beyond this are the vascular territories of the contralateral SIEA and deep circumflex iliac artery, which corresponds to Hartrampf zone IV (Fig. 59.2). Preoperative delay of the deep and superficial epigastric vessels on each side of the midline allows the capture of a second safe territory on the ipsilateral side, namely the ipsilateral SIEA territory and the contralateral DIEA territory (11). Anatomically, the delay renders the valves in the DIEA veins incompetent and regurgitant. Venous return from the skin is then directed toward the umbilicus and also across the midline. This essentially creates one combined vascular territory of the DSEA and DIEA. The preoperative delay of the vessels that radiate from the groin will enhance arterial flow into the flap from the DSEA by opening the choke vessels within the muscle and within the integument. This increase in nutrient blood flow from the DSEA within a surgically delayed TRAM flap has been quantitatively measured by laser Doppler flowmetry. In 1995, Codner et al. published a report confirming increased arterial inflow and decreased venous congestion within a surgically delayed TRAM flap (18). The clinical significance of this improved perfusion is improved viability and reliability of Hartrampf zones II and III areas of a delayed TRAM flap.