61 research outputs found

    A rigid barrier between the heart and sternum protects the heart and lungs against rupture during negative pressure wound therapy

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    <p>Abstract</p> <p>Objectives</p> <p>Right ventricular heart rupture is a devastating complication associated with negative pressure wound therapy (NPWT) in cardiac surgery. The use of a rigid barrier has been suggested to offer protection against this lethal complication, by preventing the heart from being drawn up and damaged by the sharp edges of the sternum. The aim of the present study was to investigate whether a rigid barrier protects the heart and lungs against injury during NPWT.</p> <p>Methods</p> <p>Sixteen pigs underwent median sternotomy followed by NPWT at -120 mmHg for 24 hours, in the absence (eight pigs) or presence (eight pigs) of a rigid plastic disc between the heart and the sternal edges. The macroscopic appearance of the heart and lungs was inspected after 12 and 24 hours of NPWT.</p> <p>Results</p> <p>After 24 hours of NPWT at -120 mmHg the area of epicardial petechial bleeding was 11.90 ± 1.10 cm<sup>2 </sup>when no protective disc was used, and 1.15 ± 0.19 cm<sup>2 </sup>when using the disc (p < 0.001). Heart rupture was observed in three of the eight animals treated with NPWT without the disc. Lung rupture was observed in two of the animals, and lung contusion and emphysema were seen in all animals treated with NPWT without the rigid disc. No injury to the heart or lungs was observed in the group of animals treated with NPWT using the rigid disc.</p> <p>Conclusion</p> <p>Inserting a rigid barrier between the heart and the sternum edges offers protection against heart rupture and lung injury during NPWT.</p

    Tremendous bleeding complication after vacuum-assisted sternal closure

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    Vacuum-assisted closure (VAC) of complex infected wounds has recently gained popularity among various surgical specialties. The system is based on the application of negative pressure by controlled suction to the wound surface. The effectiveness of the VAC System on microcirculation and the promotion of granulation tissue proliferation are proved. No contraindications for the use in deep sternal wounds in cardiac surgery are described. In our case report we illustrate a scenario were a patient developed severe bleeding from the ascending aorta by penetration of wire fragments in the vessel. We conclude that all free particles in the sternum have to be removed completely before negative pressure is used

    Major bleeding during negative pressure wound/V.A.C.® - therapy for postsurgical deep sternal wound infection - a critical appraisal

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    Negative-pressure wound therapy, commercially known as vacuum-assisted closure (V.A.C.®) therapy, has become one of the most popular (and efficacious) interim (prior to flap reconstruction) or definite methods of managing deep sternal wound infection. Complications such as profuse bleeding, which may occur during negative-pressure therapy but not necessarily due to it, are often attributed to a single factor and reported as such. However, despite the wealth of clinical experience internationally available, information regarding certain simple considerations is still lacking. Garnering information on all the factors that could possibly influence the outcome has become more difficult due to a (fortunate) decrease in the incidence of deep sternal wound infection. If more insight is to be gained from fewer clinical cases, then various potentially confounding factors should be fully disclosed before complications can be attributed to the technique itself or improvements to negative-pressure wound therapy for deep sternal wound infection can be accepted as evidence-based and the guidelines for its use adapted. The authors propose the adoption of a simple checklist in such cases

    Effects on heart pumping function when using foam and gauze for negative pressure wound therapy of sternotomy wounds

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    <p>Abstract</p> <p>Background</p> <p>Negative pressure wound therapy (NPWT) has remarkable effects on the healing of poststernotomy mediastinitis. Foam is presently the material of choice for NPWT in this indication. There is now increasing interest in using gauze, as this has proven successful in the treatment of peripheral wounds. It is important to determine the effects of NPWT using gauze on heart pumping function before it can be used for deep sternotomy wounds. The aim was to examine the effects of NPWT when using gauze and foam on the heart pumping function during the treatment of a sternotomy wound.</p> <p>Methods</p> <p>Eight pigs underwent median sternotomy followed by NPWT at -40, -70, -120 and -160 mmHg, using foam or gauze. The heart frequency, cardiac output, mean systemic arterial pressure, mean pulmonary artery pressure, central venous pressure and left atrial pressure were recorded.</p> <p>Results</p> <p>Cardiac output was not affected by NPWT using gauze or foam. Heart frequency decreased during NPWT when using foam, but not gauze. Treatment with foam also lowered the central venous pressure and the left atrial pressure, while gauze had no such effects. Mean systemic arterial pressure, mean pulmonary artery pressure and systemic vascular resistance were not affected by NPWT. Similar haemodynamic effects were observed at all levels of negative pressure studied.</p> <p>Conclusions</p> <p>NPWT using foam results in decreased heart frequency and lower right and left atrial filling pressures. The use of gauze in NPWT did not affect the haemodynamic parameters studied. Gauze may thus provide an alternative to foam for NPWT of sternotomy wounds.</p

    Pressure transduction and fluid evacuation during conventional negative pressure wound therapy of the open abdomen and NPWT using a protective disc over the intestines

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    <p>Abstract</p> <p>Background</p> <p>Negative pressure wound therapy (NPWT) has gained acceptance among surgeons, for the treatment of open abdomen, since very high closure rates have been reported with this method, compared to other kinds of wound management for the open abdomen. However, the method has occasionally been associated with increased development of fistulae. We have previously shown that NPWT induces ischemia in the underlying small intestines close to the vacuum source, and that a protective disc placed between the intestines and the vacuum source prevents the induction of ischemia. In this study we compare pressure transduction and fluid evacuation of the open abdomen with conventional NPWT and NPWT with a protective disc.</p> <p>Methods</p> <p>Six pigs underwent midline incision and the application of conventional NPWT and NPWT with a protective disc between the intestines and the vacuum source. The pressure transduction was measured centrally beneath the dressing, and at the anterior abdominal wall, before and after the application of topical negative pressures of -50, -70 and -120 mmHg. The drainage of fluid from the abdomen was measured, with and without the protective disc.</p> <p>Results</p> <p>Abdominal drainage was significantly better (p < 0. 001) using NPWT with the protective disc at -120 mmHg (439 ± 25 ml vs. 239 ± 31 ml), at -70 mmHg (341 ± 27 ml vs. 166 ± 9 ml) and at -50 mmHg (350 ± 50 ml vs. 151 ± 21 ml) than with conventional NPWT. The pressure transduction was more even at all pressure levels using NPWT with the protective disc than with conventional NPWT.</p> <p>Conclusions</p> <p>The drainage of the open abdomen was significantly more effective when using NWPT with the protective disc than with conventional NWPT. This is believed to be due to the more even and effective pressure transduction in the open abdomen using a protective disc in combination with NPWT.</p

    No hypoperfusion is produced in the epicardium during application of myocardial topical negative pressure in a porcine model

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    ABSTRACT: BACKGROUND: Topical negative pressure (TNP), commonly used in wound therapy, has been shown to increase blood flow and stimulate angiogenesis in skeletal muscle. We have previously shown that a myocardial TNP of -50 mmHg significantly increases microvascular blood flow in the myocardium. When TPN is used in wound therapy (on skeletal and subcutaneous tissue) a zone of relative hypoperfusion is seen close to the wound edge. Hypoperfusion induced by TNP is thought to depend on tissue density, distance from the negative pressure source, and the amount negative pressure applied. When applying TNP to the myocardium, a significant, long-standing zone of hypoperfusion could theoretically cause ischemia, and negative effects on the myocardium. The current study was designed to elucidate whether hypoperfusion was produced during myocardial TNP. METHODS: Six pigs underwent median sternotomy. Laser Doppler probes were inserted horizontally into the heart muscle in the LAD area, at depths of approximately, 1-2 mm. The microvascular blood flow was measured before and after the application of a TNP. Analyses were performed before left anterior descending artery (LAD) occlusion (normal myocardium) and after 20 minutes of LAD occlusion (ischemic myocardium). RESULTS: A TNP of -50 mmHg induced a significant increase in microvascular blood flow in normal myocardium (**p = 0.01), while -125 mmHg did not significantly alter the microvascular blood flow. In ischemic myocardium a TNP of -50 mmHg induced a significant increase in microvascular blood flow (*p = 0.04), while -125 mmHg did not significantly alter the microvascular blood flow. CONCLUSION: No hypoperfusion could be observed in the epicardium in neither normal nor ischemic myocardium during myocardial TNP

    Up-regulation of endothelin type B receptors in the human internal mammary artery in culture is dependent on protein kinase C and mitogen-activated kinase signaling pathways

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    <p>Abstract</p> <p>Background</p> <p>Up-regulation of vascular endothelin type B (ET<sub>B</sub>) receptors is implicated in the pathogenesis of cardiovascular disease. Culture of intact arteries has been shown to induce similar receptor alterations and has therefore been suggested as a suitable method for, <it>ex vivo</it>, in detail delineation of the regulation of endothelin receptors. We hypothesize that mitogen-activated kinases (MAPK) and protein kinase C (PKC) are involved in the regulation of endothelin ET<sub>B </sub>receptors in human internal mammary arteries.</p> <p>Methods</p> <p>Human internal mammary arteries were obtained during coronary artery bypass graft surgery and were studied before and after 24 hours of organ culture, using <it>in vitro </it>pharmacology, real time PCR and Western blot techniques. Sarafotoxin 6c and endothelin-1 were used to examine the endothelin ET<sub>A </sub>and ET<sub>B </sub>receptor effects, respectively. The involvement of PKC and MAPK in the endothelin receptor regulation was examined by culture in the presence of antagonists.</p> <p>Results</p> <p>The endohtelin-1-induced contraction (after endothelin ET<sub>B </sub>receptor desensitization) and the endothelin ET<sub>A </sub>receptor mRNA expression levels were not altered by culture. The sarafotoxin 6c contraction, endothelin ET<sub>B </sub>receptor protein and mRNA expression levels were increased after organ culture. This increase was antagonized by; (1) PKC inhibitors (10 μM bisindolylmaleimide I and 10 μM Ro-32-0432), and (2) inhibitors of the p38, extracellular signal related kinases 1 and 2 (ERK1/2) and C-jun terminal kinase (JNK) MAPK pathways (10 μM SB203580, 10 μM PD98059 and 10 μM SP600125, respectively).</p> <p>Conclusion</p> <p>In conclusion, PKC and MAPK seem to be involved in the up-regulation of endothelin ET<sub>B </sub>receptor expression in human internal mammary arteries. Inhibiting these intracellular signal transduction pathways may provide a future therapeutic target for hindering the development of vascular endothelin ET<sub>B </sub>receptor changes in cardiovascular disease.</p

    Wound contraction and macro-deformation during negative pressure therapy of sternotomy wounds

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    <p>Abstract</p> <p>Background</p> <p>Negative pressure wound therapy (NPWT) is believed to initiate granulation tissue formation via macro-deformation of the wound edge. However, only few studies have been performed to evaluate this hypothesis. The present study was performed to investigate the effects of NPWT on wound contraction and wound edge tissue deformation.</p> <p>Methods</p> <p>Six pigs underwent median sternotomy followed by magnetic resonance imaging in the transverse plane through the thorax and sternotomy wound during NPWT at 0, -75, -125 and -175 mmHg. The lateral width of the wound and anterior-posterior thickness of the wound edge was measured in the images.</p> <p>Results</p> <p>The sternotomy wound decreased in size following NPWT. The lateral width of the wound, at the level of the sternum bone, decreased from 39 ± 7 mm to 30 ± 6 mm at -125 mmHg (p = 0.0027). The greatest decrease in wound width occurred when switching from 0 to -75 mmHg. The level of negative pressure did not affect wound contraction (sternum bone: 32 ± 6 mm at -75 mmHg and 29 ± 6 mm at -175 mmHg, p = 0.0897). The decrease in lateral wound width during NPWT was greater in subcutaneous tissue (14 ± 2 mm) than in sternum bone (9 ± 2 mm), resulting in a ratio of 1.7 ± 0.3 (p = 0.0423), suggesting macro-deformation of the tissue. The anterior-posterior thicknesses of the soft tissue, at 0.5 and 2.5 cm laterally from the wound edge, were not affected by negative pressure.</p> <p>Conclusions</p> <p>NPWT contracts the wound and causes macro-deformation of the wound edge tissue. This shearing force in the tissue and at the wound-foam interface may be one of the mechanisms by which negative pressure delivery promotes granulation tissue formation and wound healing.</p

    Increased expression of vascular endothelin type B and angiotensin type 1 receptors in patients with ischemic heart disease

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    <p>Abstract</p> <p>Background</p> <p>Endothelin-1 and angiotensin II are strong vasoconstrictors. Patients with ischemic heart disease have elevated plasma levels of endothelin-1 and angiotensin II and show increased vascular tone. The aim of the present study was to examine the endothelin and angiotensin II receptor expression in subcutaneous arteries from patients with different degrees of ischemic heart disease.</p> <p>Methods</p> <p>Subcutaneous arteries were obtained, by biopsy from the abdomen, from patients undergoing coronary artery bypass graft (CABG) surgery because of ischemic heart disease (n = 15), patients with angina pectoris without established myocardial infarction (n = 15) and matched cardiovascular healthy controls (n = 15). Endothelin type A (ET<sub>A</sub>) and type B (ET<sub>B</sub>), and angiotensin type 1 (AT<sub>1</sub>) and type 2 (AT<sub>2</sub>) receptors expression and function were examined using immunohistochemistry, Western blot and <it>in vitro </it>pharmacology.</p> <p>Results</p> <p>ET<sub>A </sub>and, to a lesser extent, ET<sub>B </sub>receptor staining was observed in the healthy vascular smooth muscle cells. The level of ET<sub>B </sub>receptor expression was higher in patients undergoing CABG surgery (250% ± 23%; P < 0.05) and in the patients with angina pectoris (199% ± 6%; P < 0.05), than in the healthy controls (100% ± 28%). The data was confirmed by Western blotting. Arteries from CABG patients showed increased vasoconstriction upon administration of the selective ET<sub>B </sub>receptor agonist sarafotoxin S6c, compared to healthy controls (P < 0.05). No such difference was found for the ET<sub>A </sub>receptors. AT<sub>1 </sub>and, to a lesser extent, AT<sub>2 </sub>receptor immunostaining was seen in the vascular smooth muscle cells. The level of AT<sub>1 </sub>receptor expression was higher in both the angina pectoris (128% ± 25%; P < 0.05) and in the CABG patients (203% ± 41%; P < 0.05), as compared to the healthy controls (100% ± 25%). The increased AT<sub>1 </sub>receptor expression was confirmed by Western blotting. Myograph experiment did however not show any change in vasoconstriction to angiotensin II in CABG patients compared to healthy controls (P = n.s).</p> <p>Conclusion</p> <p>The results demonstrate, for the first time, upregulation of ET<sub>B </sub>and AT<sub>1 </sub>receptors in vascular smooth muscle cells in ischemic heart disease. These receptors may play a role in the pathophysiology of ischemic heart disease and could provide important targets for pharmaceutical interventions.</p
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