Regulation of Blood Flow to the Skin

Flap physiology

Regulation of blood flow to the skin

 Cutaneous flaps are regulated at the level of the microcirculation - this is where thermoregulation of blood flow occurs.  primary regulator of blood flow is arteriolar network controlled by systemic and local mechanism 

Systemic control

1. Neural regulation  The most important system of cutaneous circulatory control.  acts through sympathetic adrenergic fibres.  Vasoconstriction is induced by alpha-adrenergic receptors  vasodilation by beta-adrenergic receptors.  act together to maintain the basal tone of vascular smooth muscle at the arteriovenous anastomoses, arterioles and arteries.  as alpha-adrenergic predominate, increased sympathetic tone leads to vasoconstriction & decreased tone vasodilatation  cholinergic fibres give rise to bradykinin release which contributes to vasodilation.  Serotonin receptors are located mostly at AV anastamoses and cause vasoconstriction.

2. Humoral regulation  adrenaline & noradrenaline have direct action on alpha-adrenergic receptors leading to vasoconstriction  serotonin, PGF2, thromboxane A2 constrict  bradykinin, histamine, PGE2, prostacyclin, leukotriene dilate  important to realize that the effects of local injury to the artery can completely override basal vascular tone, and can cause vascular spasm even in the absence of sympathetic innervation.

Local control (autoregulation)

1. Metabolic factors  primarily as vasodilators and include hypercapnea, hypoxia, acidosis and hyperkalaemia.  These factors are not as significant in the skin as in the muscle which has higher metabolic requirements. 2. Physical factors  myogenic reflex, which triggers vasoconstriction in response to distention of isolated cutaneous vessels and thereby maintains capillary flow at a constant level independent of arterial pressure.  Local hypothermia (which acts directly on vascular smooth muscle causing vasoconstriction)  increased blood viscosity (haematocrit >40 - 45%) may also decrease flow. (The effect of haematocrit was looked at by Kim and colleagues who found that normovolaemic anaemia with an Hct = 19% had no significant effect on the survival of pedicled musculocutaneous flaps.)

These same concepts of cutaneous blood flow can be applied to muscles but with the following differences: 1. Arteriovenous shunts are believed to be absent in muscle. 2. Muscle has a much higher capillary density than skin (1000-2000/mm2 vs 16-55/mm2 in skin). 3. The metabolic demand of muscle is far greater than that of skin and thus autoregulation plays a more important role. 4. Epinephrine causes vasodilatation, in direct contrast to the vasoconstriction seen in skin. 5. As regards local control, metabolic autoregulation is limited but still more than that in skin, and blood flow is minimally changed in response to temperature fluctuations. 6. Myogenic tone is very important in muscle blood flow regulation but has little effect on cutaneous vessels, whereas sympathetic vasoconstrictors are the predominant means of regulating cutaneous blood flow.

Pathophysiology and haemodynamics of flap transfer

 Primary changes include the insult of ischaemia and the loss of sympathetic innervation.  The following are the circulatory changes that take place in a pedicled flap after partial interruption of its blood supply during elevation and transfer:

10 - 24 hours  reduction in arterial blood supply  progressively decreasing circulatory efficiency for the first 6 hours; plateau at 6 - 12 hours  increase in circulatory efficiency beginning at 12 hours  marked congestion and oedema during the 1st 24 hours  marked dilatation of arterioles and capillaries

1 - 3 days  increasing isotope appearance  improvement in pulse amplitude  little or no improvement in circulation (NOT efficiency) during the 1st 48 hours  increase in number and caliber of longitudinal anastomoses  increase in the number of small vessels in the flap

3 - 7 days  progressive increase in circulatory efficiency until a plateau at 7 days  vascular anastomoses between flap and recipient bed present at 2 -3 days, becoming functionally significant at 5 - 7 days  increase in size and number of functioning vessels  re-orientation of vessels along the long axis of the flap

1 week  circulatory function well established between flap and recipient bed  pulsatile blood flow approaches pre-operative levels

7 - 14 days  no further significant increase in vascularization  arterial pattern becomes normal  isotope clearance indicates circulatory efficiency surpassing normal values at 10 - 21 days, returning to normal after three weeks

2 weeks  progressive regression of the vascular system  continuous maturation of the anastomoses between pedicled flap and recipient site

3 weeks  vascular pattern approximates pre-operative state  flap achieves 90% of its final circulation  vital staining occurs simultaneously with the recipient limb  fully developed vascular connections between pedicle and recipient site

4 weeks  all vessels decreased in diameter  few remaining normally formed vessels

Timing of flap division

 Most flaps can be safely divided between 10 days and 3 weeks.  But depends on : regional anatomical differences; flap viability; ?infection/haematoma