Cases reported "Reperfusion Injury"

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1/8. Skeletal muscle reperfusion injury: reversal by controlled limb reperfusion--a case report.

    Despite successful surgical revascularization of ischemic limbs, a local and systemic reperfusion injury may occur after normal blood reperfusion. Recent experimental and clinical application of controlled limb reperfusion in europe has demonstrated superior results, with lower morbidity and mortality. This new surgical technique includes modification of the reperfusate (calcium, pH, substrates, osmolarity, free radical scavenger) and the circumstances of initial reperfusion (time, temperature, pressure). This report describes the first application of controlled limb reperfusion after reperfusion injury. A 16-year-old boy underwent femoral access cardiopulmonary bypass for repeat cardiac repair with an ischemic time of 245 minutes. Postoperatively, severe ischemia/reperfusion syndrome developed with muscle contracture, immobility, and anesthesia of the right leg with a second ischemic time of about 6 hours. The systemic creatine phosphokinase level was 88,000 U/L; myoglobin was 27,000 ng/mL. He underwent controlled limb reperfusion by withdrawing blood from the aorta and mixing it with a crystalloid solution (calcium-reduced, hyperosmolar, hyperglycemic, alkalotic, glutamate- and aspartate-enriched, and containing a free radical scavenger) under controlled conditions (blood:crystalloid solution 6:1, for 30 minutes, reperfusion pressure < 50 mm Hg, and normothermia) before establishing normal blood reperfusion. Metabolic data from the central and femoral vein demonstrated a significant reduction of all previous elevated enzyme levels, avoidance of hyperkalemia, normalization of acidosis, and avoidance of systemic reperfusion injury with no multiorgan failure. limb salvage was accomplished and functional recovery almost complete. To the authors' knowledge, this is the first application of controlled limb reperfusion reported in north america. With this surgical technique we were able to prevent metabolic local and systemic reperfusion changes after prolonged ischemia and also reduced previous reperfusion changes. This report confirms former experimental data, and further clinical studies are warranted.
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2/8. Post-reperfusion rapidly progressive glomerulonephritis in post-transplant IgA nephropathy.

    Rapidly progressive glomerulonephritis (RPGN) is a rare occurrence in IgA nephropathy (IgAN) in renal transplant patients on immunosuppressive therapy. RPGN post ischemia-reperfusion has not been previously reported. We report a 62 year old male patient on azathioprine therapy, 9 years after left cadaveric renal transplantation due to end stage renal disease of unknown etiology, who presented with progressive deterioration in renal function and hematuria. Renal biopsy was consistent with IgAN. Duplex and CT scan demonstrated a decreased renal graft perfusion, due to severe atherosclerosis and stenosis of iliac arteries. The patient underwent left axilo-femoral bypass graft surgery with improvement in kidney graft perfusion and function. However, few weeks later, patient presented with pulmonary edema and advanced renal failure and he was initiated on hemodialysis. Repeated renal biopsy demonstrated crescentic GN. To the best of our knowledge, this is the first report of RPGN following reversal of ischemia and reperfusion. There was no evidence for atherembolic disease which is not uncommon after vascular surgery and it has been reported to be rarely associated to crescentic GN. Theoretical explanations for exacerbation of IgAN to crescentic GN, following successful reperfusion, could be enhancement of capillary damage, inflammation and oxidative stress. Putative mechanisms for these phenomena may be interaction of reperfusion-induced hyperfiltration, high intraglomerular capillary pressure, oxidative stress, increased polymorphonucler cells infiltration and inflammation; the presence of IgA immune deposits and azathioprine metabolites, both can also be associated to enhancement of oxidative stress.
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3/8. Case report: Aggressive blood pressure management for carotid endarterectomy hyperperfusion syndrome.

    PURPOSE: Cerebral hyperperfusion syndrome (CHS) is a rare but potentially devastating complication following cerebral revascularization. Management of CHS requires aggressive blood pressure control to prevent stroke and intracerebral hemorrhage. This case report documents a severe case of CHS, and outlines a successful outcome associated with aggressive blood pressure control. CLINICAL FEATURES: A 67-yr-old gentleman, nine days post left carotid endarterectomy, required tracheal intubation and intensive care unit admission following seizures and acute right-sided weakness. A computed tomography scan and magnetic resonance imaging revealed significant vasogenic edema in the left middle cerebral artery territory, without evidence of infarction. The history and radiographic findings suggested CHS. As such, a systolic blood pressure target was set at 90-140 mmHg. This blood pressure parameter was lower than typically targeted following acute ischemic or hemorrhagic stroke. Rapid clinical improvements were seen by day five, and tight blood pressure control was maintained throughout. Repeat computed tomography and magnetic resonance imaging revealed improved edema and no evidence of infarct or hemorrhage. CONCLUSION: Cerebral hyperperfusion syndrome is believed to occur following restoration of blood flow to a brain with impaired autoregulation due to chronic hypoperfusion. Massive brain edema and hemorrhage can result from higher pressures. Clinicians should be aware of this potential complication following cerebral revascularization procedures, and the importance of establishing blood pressure targets which are considerably lower than for other patients with similar clinical presentations.
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4/8. Normal perfusion pressure breakthrough complicating surgery for the vein of Galen malformation: report of three cases.

    Three cases are described of infants who developed malignant brain swelling (and in one case hemorrhage) after surgery for vein of galen malformations. The cause for the brain swelling was felt to be due to hyperperfusion, or the "normal perfusion pressure breakthrough" syndrome. Although well-described for cerebral parenchymal arteriovenous malformations, cases of this complication occurring in vein of galen malformations have not previously been reported. It is concluded from these cases that infants with large arteriovenous shunts, as attested by cardiac failure and cerebral atrophy, have an increased risk of developing this complication.
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5/8. Immediate haemodialysis and staged fasciotomy in the treatment of reperfusion injury.

    A 67-year-old man was admitted with traumatic arterial occlusion in his leg 24 h after an accident. A double-lumen catheter was inserted into the left iliac vein, after revascularization, and haemodialysis started using a new membrane dialyser to remove myoglobin effectively. Intramuscular pressure of the limb was measured and, when it was 35 mmHg, staged fasciotomy was performed. A modification of the procedure used to prevent myonephropathic metabolic syndrome and compartment syndrome is described.
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6/8. Postoperative compartment syndrome and the lithotomy position: a report of three cases and analysis of potential risk factors.

    There exists a definite association between the placement of patients in the modified lithotomy position and the development of postoperative compartment syndrome. It must be appreciated that this syndrome is potentially life-threatening and frequently results in long-term sequelae. We report three cases which illustrate the problem and analyze the multifactorial etiology of this condition and propose a strategy for its prophylaxis. The combination of direct pressure on the posterior compartment of the calf, elevation of the legs above heart level, a number of intraoperative variables, the preexistence of any lower limb arterial insufficiency, and in some cases, the use of intraoperative compression boots, may lead to a state of hypoperfusion in the anterior and posterior compartment musculature. Upon completion of the operation, removal from the lithotomy position, and correction of the etiological factors, a reperfusion occurs with the development of a capillary leak with subsequent tissue edema causing an increase in compartmental pressure which may result in neurovascular compromise. This is the compartment syndrome. Emphasis must be placed on the identification of high-risk patients, the prevention or rapid correction of any etiological factors, the early diagnosis of the problem, and an aggressive approach to its treatment.
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7/8. Massive pulmonary embolism: preliminary results of treatment with the Amplatz thrombectomy device.

    PURPOSE: To determine the feasibility of using the Amplatz thrombectomy device (ATD) to treat massive pulmonary embolism (PE). patients AND methods: Five patients (four men, one woman; mean age, 45.2 years) with massive PE underwent mechanical thrombectomy with the ATD, which creates a vortex that pulverizes and recirculates the clots within the pulmonary circulation. The patients were followed up for 7-18 months after thrombectomy. RESULTS: Marked improvement in pulmonary perfusion was observed in three patients at angiography and ventilation-perfusion scanning. No changes could be assessed in one patient who died shortly after the procedure. One patient developed hemoptysis during the procedure, most likely because of a reperfusion syndrome. A reduction in pulmonary artery pressure was observed in only one patient; the remaining patients had increased pressure. The four surviving patients were discharged within 8 days. CONCLUSION: Mechanical thrombectomy with the ATD provides rapid debulking of thrombus in some patients with massive PE and has the potential to improve treatment and outcomes of the most sick patients.
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8/8. Low cerebral blood flow and perfusion reserve induce hyperperfusion after surgical revascularization: case reports and analysis of cerebral hemodynamics.

    BACKGROUND: Hyperperfusion syndrome after surgical revascularization is a rare complication and there has not been any systematic study on factors that induce hyperperfusion after surgery. In this paper, we retrospectively analyzed the factors related to this syndrome. patients AND methods: We performed 46 cases of surgical revascularization including 33 cases of carotid endarterectomy (CEA) and 13 cases of superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis during the past 5 years. Among these, we encountered three cases of hyperperfusion syndrome despite well-controlled blood pressure postoperatively. To evaluate factors related to the occurrence of hyperperfusion syndrome, we examined four parameters: (1) regional cerebral blood flow (rCBF), (2) the increase in the ratio of the postoperative rCBF compared to the preoperative rCBF (increase ratio), (3) cerebral perfusion reserve presented by the increase of rCBF after acetazolamide administration (delta rCBF), and (4) the difference in mean blood pressure between the preoperative and postoperative state (delta BP). RESULTS: Preoperative rCBF was significantly lower in cases of hyperperfusion syndrome than the control cases (p < 0.01 Mann-Whitney U-test). Moreover delta rCBF was evidently lower in the hyperperfusion cases than the control (p < 0.05 Fisher's exact method). However, there was no significant difference in the delta BP between the hyperperfusion cases and the control cases. CONCLUSION: In cases of marked low perfusion (low rCBF) with poor perfusion reserve (low delta rCBF), hyperperfusion after surgical revascularization can occur even if blood pressure is adequately controlled.
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