Reperfusion injury

As reperfusion injury, a disease process is known which is the restored blood flow after a more or less prolonged hypoperfusion (ischemia) of a limb triggered ( eg as a result of the tourniquet syndrome ) or an organ. The term Reperfusionsparadox called the apparent contradiction that the re-circulation can lead to additional damage.

Occurrence

Reperfusion injury occur in different medical fields there and have each an independent clinical significance.

In transplantation medicine of reperfusion injury caused by reperfusion of the graft. In his episode of rejection, organ failure and damage to the organism as a whole can be caused by toxic reactions.

In cardiology, the reperfusion injury occurs in the treatment of acute myocardial infarction, for example by PTCA, thrombolysis or stent implantation.

In vascular surgery, it comes after revascularization of a closure of an arterial flow area to a reperfusion injury, the extent of which depends not only on the duration of the closure, but especially of its localization.

In traumatology mainly come before reperfusion damage after injury of big arteries of extremities.

The cause of ischemia may be an acute arterial occlusion ( embolism), vascular injury in the context of trauma or prolonged compression of the feeding artery from the outside ( setting, tourniquet ).

Disease

Clinically, there is a general tissue damage in the affected body part and to acidosis (acidosis ) of the whole organism. This leads to local heat, redness and swelling of the affected portion, the leg or arm to the development of a compartment syndrome with extensive rhabdomyolysis. Generalized symptoms of mild acceleration of spontaneous breathing ( tachypnea ) to drop in blood pressure, cardiac arrhythmia due to hyperkalemia, clotting disorders, kidney failure or even cardiovascular arrest may be enough. The severity of reperfusion injury is directly related to the duration of ischemia and the extent of the ischemic region of the body. The hardest of reperfusion injury after long standing acute Leriche syndrome ( occlusion of the lower abdominal aorta - abdominal aorta - " riding " by a thrombus in the bifurcation into the pelvic arteries ).

Pathophysiology

The pathophysiological sequence leading to reperfusion injury, were as follows:

The lack of oxygen during ischemia leads within minutes to an almost complete degradation of ATP, the universal energy source of the cell, resulting in an increase of hypoxanthine. At the same time it is due to the function stops the ATP-gated ion transporter to potassium efflux and calcium influx. This and the increase of hypoxanthine lead to a conversion of the enzyme xanthine dehydrogenase to xanthine oxidase, which oxidizes hypoxanthine in the presence of oxygen at again successful reperfusion to xanthine. In this conversion, the production of free oxygen radicals such as superoxide, hydrogen peroxide or hydroxyl radicals that can damage cell membranes and thus contribute to progression of the damage by the preceding ischemia damage by lipid peroxidation.

In addition to these direct cell-damaging effects of oxygen radicals in the rain especially neutrophils and beyond the training of adhesion molecules. The result is an enhanced binding of white blood cells to the endothelium of small blood vessels and the migration of these white blood cells into the surrounding tissue. There especially excited neutrophils in turn can turn large amounts of oxygen radicals and partly self- aggressive acting neurotransmitters, such as the platelet- activating factor (PAF ) or leukotriene release. This new white blood cells are stimulated, which accumulate in the damaged tissue.

By this reaction chain entertaining vicious circle can develop themselves with constantly new oxygen radical formation and stimulation of white blood cells. The release of cell-damaging granules and the formation of aggressive oxygen metabolic intermediates causes further tissue damage, a massive increase in the permeability of the endothelium and a further increase of the edema. In addition to the increasing tissue pressure, which can pose a significant obstacle to the re- flow with blood, increasing the flow path through the tissue in addition to a deterioration of acidified by hypoperfusion metabolism and thus to an increase of tissue damage.

In addition to selectins, which mainly mediate the first contact of the white blood cells to the vascular endothelium, is presented VCAM -1 (vascular cell adhesion molecule 1 ) and especially ICAM -1 ( intercellular adhesion molecule 1 ) out as the most important adhesion molecules, which for the migration of white blood cells by the vascular endothelium are necessary.

If the blood flow to the tissue to be restored, so new oxygen for oxidative reactions are available, the conversion of hypoxanthine to xanthine, which massively oxygen free radicals are formed which further damage the tissue begins.

Treatment

Preventing this process can be with today's medical means not, but by cooling down the affected tissue prior to reperfusion, the activity of the enzymes can be reduced. This leads to a slower production of dangerous oxygen radicals and can thus reduce tissue damage. Since the reperfusion injury usually occurs during surgery to correct the ischemia, can be counteracted by the anesthesiologist immediately by hyperventilation of metabolic acidosis (Development of respiratory alkalosis). In more severe cases, the acidosis must be " buffered" in addition with sodium bicarbonate. In addition, where appropriate circuit supportive drugs ( catecholamines ) and diuretics are used.

Swell

• Brigitte Marian: illness, disease causation and images. Facultas University Press; 1 edition (October 2007). ISBN 3-7089-0183-5
• Local heat shock - A conditioning method for reducing the inflammatory response and to improve microvascular perfusion in transferred osteomyokutanen cloth; Dissertation by Thilo John Shepherd (2006)

• Pathophysiology
• Cardiovascular physiology
• Vascular Surgery