[Tissue expansion--a revolutionary technique in the reconstructive surgery].
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Biomedical subjects
Publications and source records attributed to J B Wieslander.
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In a blind randomized study, two groups of six rabbits were treated with either the fibrinolytic inhibitor tranexamic acid, 14 mg/kg bw, or isotonic saline solution (control group) given intraaortically as single bolus injections 5 min prior to arteriotomy and intimectomy of central ear arteries. Arteriotomic bleeding times, accumulations of 32P-labeled platelets, patency, and sizes of thrombus deposits 2 hr after reperfusion were recorded. Fixed vessels were observed by scanning electron microscopy. Bleeding times were similar in the two groups. The patency rate in the tranexamic acid group was 2/12, i.e., a significant reduction (P less than 0.05) from 7/12 in the control group. Thrombus deposits in occluded vessels contained large amounts of fibrin and red cells. Platelet accumulations in occluded vessels were significantly lower in the tranexamic acid group than in the control group, which indicates that the ratio of fibrin to platelets was increased in thrombi formed during antifibrinolytic treatment. This study has demonstrated the importance of normal fibrinolytic capacity in limiting thrombus formation following microarterial trauma. It is suggested that the use of antifibrinolytic agents in microvascular surgery should be restricted.
The effects of dextran 40 on platelet function and thrombus formation have been studied in vivo in arteries of the rabbit ear. Intra-aortic infusions of 32P-labelled platelets were followed by infusions of 1.7 g dextran 40 in 17 ml saline/kg b w. Treated and untreated groups were studied using as trauma either end-to-end anastomosis or arteriotomy (7 mm)/intimectomy (5 mm). After restoring blood flow, bleeding times at the sites of anastomosis and arteriotomy/intimectomy were recorded. Accumulations of labelled platelets were followed in vivo for 2 hours, after which patencies were determined and amounts of red thrombotic material evaluated. In a separate series of measurements, haematocrit levels after dextran infusion were studied. Nearly all vessels in the end-to-end anastomosis groups were patent. In the arteriotomy/intimectomy groups, there was a significant increase in patency following dextran infusion. Dextran infusion did not alter platelet accumulation following end-to-end anastomosis, but following arteriotomy/intimectomy median values were somewhat reduced. Its antithrombotic effects must therefore arise mainly at stages of thrombus formation subsequent to platelet deposition.
The efficacy of topical prostacyclin as an antithrombotic agent was tested in a model of microvascular trauma. Preliminary measurements were made to determine a suitable dosage. Twenty-seven central arteries of rabbit ears were then prepared and 32P-labelled platelets infused intraaortically. Arteriotomy (7 mm) was followed by intimectomy (5 mm). Fifteen vessels in a control group were irrigated with Ringer's lactate and 12 vessels in an experimental group were treated with prostacyclin (10 ng/ml) in normal saline. Bleeding times at the sites of arteriotomy intimectomy, in vivo accumulations of isotope-labelled platelets, amounts of red thrombotic material, and patency were recorded. Patency was lower following prostacyclin treatment (1/12 as against 5/15) but not significantly so, and there were no statistically significant differences in other parameters. Prostacyclin treatment decreased vessel wall tone, interfering with blood-flow and promoting thrombus formation.
About 10 h after administering acetylsalicylic acid (ASA) orally in doses of 4 mg and 20 micrograms/kg b.w., the central arteries of rabbit ears were subjected to severe vascular trauma (arteriotomy/intimectomy). Bleeding times from the trauma regions at reperfusion were measured and the activities from accumulating 32P-labelled homologous platelets recorded until 2 h after reperfusion when patencies were determined. In other studies, the effects of ASA on ex vivo platelet aggregation (aggregometry), thromboxane production, euglobulin clot lysis time and bleeding time following arterial puncture were investigated. Relative to controls, the following parameters were changed: patency was increased, as were the bleeding times following arterial puncture and thromboxane production was reduced. The median values of platelet accumulation were lower, but the changes were not statistically significant. Aggregometry showed decreased rates of platelet aggregability following treatment with ASA 4 mg/kg.
To illustrate how the technique of tissue expansion may be adapted for different types of reconstruction, the following cases are described: a 10-year-old girl with a circumferential naevus from shoulder (at the back) and umbilicus (at the front) to the knees; a 3-year-old boy with a severe injury to the left arm; a 36-year-old man with an amputation injury of the left hip; and an 18-year-old girl with scars from a complicated fracture of the left lower leg. In all cases function and/or appearance were considerably improved.
More than 100 patients (38 in the head and neck) have been treated by the insertion of tissue expanders since the technique was introduced six years ago. Our methods have been refined as we have learned more, and these improvements are described. Morbidity is high when untrained surgeons start to use the technique. The most important decision is the planning of the expander and filling port pockets, but above all the location of the incision(s): Incisions must be kept small and away from the defect, the pocket, and the future flap. Intraoperative filling of the expander reduces the need for drains by preventing haematoma and seroma formation, and reduces the formation of expander envelope folds. The optimal location of the valve is a "quiet" area above or lateral to (or both) the expander, and at least 7 cm away. Mathematical formulas are useless in predicting available flap length, as elasticity and contractility depend on individual factors. A good estimation of flap length is twice the height of the expander above the skin surface or the distance over the dome of the expander minus the corresponding measurement of its base. Overexpansion by 30-50% makes the procedure more predictable.
The effect of isovolemic hemodilution using dextran-60 on arterial blood flow in the rabbit ear was investigated. The animals were anesthetized and an electromagnetic flow probe was applied around the central artery of the ear. Isovolemic hemodilution was performed during a 15 min exchange period. Two degrees of hemodilution were investigated [8.5 and 17 ml dextran-60/kg body weight (b.w.)] and compared with a nontreated control group. The two levels of hemodilution induced reductions in hematocrit to 29 and 21%, respectively, from the control level of about 40%. In all groups, blood pressure maintained constant levels throughout each experiment, which lasted 240 min. In the controls, ear artery blood flow was unchanged or decreased slightly during the experiment. The lower level of hemodilution caused a slight increase of blood flow after 4 h. In the group treated with 17 ml/kg b.w. dextran, blood flow gradually increased after 90 min following hemodilution. After 240 min, flow rates had increased to two- or threefold the initial rate in this group. Although other possibilities exist, the increased blood flow following hemodilution may be interpreted as reflecting a decreased resistance to flow in the tissue due to the decreased viscosity of the blood.
To investigate if low-dose acetylsalicylic acid (ASA), 4 mg/kg b.w., infused peroperatively or 10 hours preoperatively has antithrombotic effects, the central arteries of rabbit ears were prepared and 32P-labeled platelets injected. Arteriotomy and intimectomy were performed and blood flow was restored. Bleeding times at the sites of arteriotomy/intimectomy, in vivo accumulations of isotope-labeled platelets, amounts of red thrombotic material, and patency were recorded. Bleeding times following arterial puncture and the effect of ASA on thromboxane production were studied separately. Ten hours after ASA administration, bleeding times were shortened at the sites of arteriotomy/intimectomy but were prolonged following arterial puncture. Platelet accumulations were lower in patent vessels in this group than in an untreated control group. Peroperative ASA treatment increased but treatment 10 hours prior to blood flow restoration did not significantly affect the number of occlusions. Thromboxane production in ASA-treated rabbits is largely inhibited even 14 hours after administration.
Twenty-four arteries of rabbit ears, divided into two groups of 12 vessels each, were prepared and 32P-labelled platelets were infused. Arteriotomy/intimectomy was performed after 1 hr and in vivo platelet accumulation recorded for 2 hr. Group A comprised untreated control animals and group B was treated with 1 g hydroxyethyl starch (HES), MW 450,000 in 17 ml saline/kg b.w. (Plasma-steril). Vessel bleeding-times were normal, patency was improved, and intraluminal thrombotic material was reduced after HES treatment. Initial in vivo platelet accumulation was rapid and reached similar levels in both groups. However, the platelet accumulation curves decreased more frequently following HES than in the control group. HES does not prevent platelet accumulation at trauma sites, but reduces the sizes of the thrombi formed and may enhance disaggregation/fibrinolysis.
The antithrombotic effect of heparin used as a wash-out solution in small arteries has been evaluated following severe vessel trauma (arteriotomy/intimectomy). Twenty-three central arteries of rabbit ears were prepared and platelets labeled with phosphorus-32 injected intraaortically. The arteries were positioned in double vascular clamps and opened by arteriotomy, and intimectomy was performed. After reestablishing blood flow, arteriotomic bleeding times, platelet accumulation in vivo, patency, and the amounts of intraluminal red thrombotic material were recorded. The rabbits were divided into two groups. In group A (12 vessels) the vessel interior was flushed with 2 ml of saline or Ringer's lactate solution. Group B (11 vessels) was similar except that the vessels were flushed with 2 ml of heparin, 100 IU/ml, in Ringer's lactate solution. In the control group (A) the bleeding time was 5 +/- 2 min, while in group B bleeding was so profuse that extra sutures had to be used in 6 of the vessels. Although significantly fewer platelets accumulated in heparin-treated animals, the patency frequencies and amounts of thrombotic material observed in both groups were similar. The final volume of thrombus formed is thus not always proportional to the degree of platelet accumulation. Washout of small traumatized arteries with heparin is thus not beneficial.
Twenty microarterial end-to-end anastomoses were performed on the central arteries of the ears in 12 rabbits divided into two groups: Group A (10 anastomoses) served as control and Group B (10 anastomoses) was treated with 4 mg ASA per kg b.w. given as a single intraaortical dose 5 min prior to infusion of 32P-labelled platelets. Two hours later blood-flow was reestablished after end-to-end anastomoses. Anastomotic bleeding-times, qualitative and quantitative differences in platelet accumulation and patency were registered. In addition, platelet aggregability and thromboxane production were studied in 3 rabbits. The bleeding-times (median and quartiles) in group A were 3(+0)-2 min and in group B 3(+2)-0 min. In vivo accumulation of 32P-labelled platelets was somewhat increased initially (p less than 0.05) in the ASA group. Poor patency was registered in two vessels, one in each group, all other vessels having good patency. Aspirin peroperatively in low doses (4 mg/kg) did not markedly affect bleeding-times or patency rates in microarterial anastomoses, but platelet accumulation in vivo was initially increased. The radioactivity values decreased with time in all aspirin cases but only in 50% of the control group vessels, suggesting efficient platelet disaggregation/fibrinolysis. This might favour the view that PGI2 production in the endothelium recovers more rapidly than the pro-aggregatory mechanisms affected by ASA. ASA-treatment led to almost complete inhibition of thromboxane production for at least four hours, but, despite this, a moderate decrease in platelet aggregability occurred only when collagen was used as stimulant.
A 29-year-old woman sustained a severe combined forehead-scalp avulsion injury (20 X 17 cm) in an automobile accident 4 years ago. The skull was covered with split skin-grafts. The defect was successfully removed by the use of simultaneous and repeated tissue expansion of the normal occipital area and the remains of the forehead. The case illustrates the possibility of using large expander volumes (1,700 cc) in the head area and the fact that even narrow skin bridges (2.0 cm above the left eyebrow) can be expanded. The expander shape can be chosen to create a desired flap size and form. Finally, hair thickness and growth can be quite acceptable even after huge expansions of the scalp.
Seven patients with a bone tumor were operated on with local excision and a free vascularized fibular graft. Four of the patients received both chemotherapy and radiotherapy. The blood flow in the grafts was evaluated by scintigraphy within 1 week after the operation. The median follow-up time was 4 (1-5) years. All but one graft-host junction healed primarily. There were 5 graft fractures in 3 patients. Four of the fractures occurred in 2 patients who received preoperative and postoperative chemotherapy and radiotherapy. Three of these fractures healed without surgery. Resorption of the grafts was never seen, whereas hypertrophy was observed in 6 patients. None of the patients had any permanent morbidity at the donor site. One patient had tumor recurrence and died after 2 years. Our findings indicate that a vascularized bone graft is also a useful alternative for reconstruction of large bone defects in patients receiving both chemotherapy and radiotherapy.
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In 36 rabbits, small catheters were introduced into the central artery of one ear and into the saphenous arteries of both legs. Saline, metrizamide 170 mg I/ml, iohexol 137 mg I/ml and iopentol 137 mg I/ml, all solutions isotonic with blood, were tested. Perfusion with the test-solutions was performed with 2 ml x 3 at intervals of 5 min. In the case of iopentol, a dose-response study was performed, 1 ml x 3 and 4 ml x 3 being also tested. The solutions were administered under gentle pressure and at room temperature. Blood reflow was always observed between injections. All perfusates caused endothelial damage. Minor trauma led to endothelial cell contraction. More severe trauma increased the degree and numbers of contracted endothelial cells, frequently resulting in patches of denudation, sometimes the location for thrombus formation. In the control group only few effects on the endothelium were noted. Metrizamide caused more intimal damage at all times studied than either iohexol or iopentol. The immediate effects of saline and iopentol were quite identical, but at 2 h and 24 h iopentol caused much less intimal damage than saline.
Twenty-four arteries of rabbit ears, divided into three groups of eight, were prepared and 32P-platelets injected. Arteriotomy (7 mm) and intimectomy (5 mm) were performed and in vivo platelet accumulation followed for 2 hours. Group A comprised untreated control animals, group B was treated with 17 ml saline/kg bw, and group C with 1 g dextran and 17 ml saline/kg bw (Macrodex). Significant differences in platelet accumulation were observed only between the control and Macrodex groups at 105 and 120 minutes. In the control and saline groups four of eight vessels showed poor or no patency. All Macrodex vessels showed good patency. Control and saline vessels had large amounts of red thrombotic material, except for three saline cases with small amounts. After Macrodex treatment five of eight vessels were apparently clean, while the other three showed only small amounts of red thrombotic material. Dextran seems not to influence platelet function but rather to inhibit fibrin stabilization and probably increases fibrinolysis. Vascular patency was only endangered by the formation of solid fibrin-containing red thrombi.
Microarterial anastomoses were performed on the central arteries of the ears in rabbits. An untreated control group was compared with two groups treated with saline solution and dextran 70 in saline solution respectively. Anastomotic bleeding times were prolonged in both treated groups. In vivo accumulation of 32phosphorous labelled platelets infused prior to any treatment was measured at the anastomotic sites for two hours after anastomosis. Treatment with saline solution resulted in prolonged periods of platelet accumulation--desaggregation processes and abnormally high levels in 50 per cent of the rabbits. Treatment with dextran resulted in increased quantitative accumulation of platelets at all times compared with the control groups. In some rabbits treated with dextran, platelet accumulation patterns indicated microembolization due to increased platelet thrombus fragility. Despite increased platelet accumulation in the dextran groups all vessels showed good patency and only small amounts of thrombosis material compared with the control and saline solution groups. Poor patency was registered only in one instance in the control group and two instances in the saline solution group. Using ex vivo platelet aggregometry, saline solution slightly decreased and dextran slightly increased platelet aggregability. The conclusion is that dextran does not act as an antiplatelet agent but minimizes formation of dangerous solid fibrin platelet thrombi due to a defective fragile fibrin structure adn perhaps increased fibrinolysis.