Brachial plexus injury and upper rib fracture after median sternotomy in cardiac surgery.

OBJECTIVES: Sternal retractors utilized during open-heart surgeries through median sternotomy can cause upper rib fractures which sometimes further leads to brachial plexus injury. We aimed to investigate the incidence of brachial plexus injury and upper rib fractures in open-heart surgeries and how these injuries are associated with each other. METHODS: We investigated 1050 cases during the past five years. The incidence of brachial plexus injury and upper rib fractures after median sternotomy was assessed in all patients and the patients who sustained were evaluated for the affected side, the level of paralysis. RESULTS: Ten cases (0.95%) exhibited brachial plexus injury after median sternotomy. Nine cases developed paralysis on left upper extremity. In all ten cases, sensory and motor nerve impairment were exhibited in the lower plexus. Rib fractures were observed in 35.0% of cases after median sternotomy and the usage of asymmetric sternal retractors to harvest left internal thoracic artery (LITA) significantly affected the side of fracture. CONCLUSION: Sternal retractors utilized during open-heart surgeries through median sternotomy may cause rib fractures and brachial plexus injury, so operators should be aware of these complications.

Endovascular Therapy for Isolated Brachiocephalic Pseudoaneurysm.

In this study, we present a successful endovascular therapy using a small-diameter stent graft for a 73-year-old man who developed asymptomatic pseudoaneurysm of the brachiocephalic artery. An 8F sheath was placed in the brachial artery, and a stiff guidewire was advanced to the descending aorta. The stent graft was delivered to the brachiocephalic artery via the brachial approach. After the initial dilatation, the stent graft was post-dilated to maximum diameter. Final digital subtraction angiography confirmed no endoleak. We believed that endovascular for a brachiocephalic pseudoaneurysm using a small-diameter stent graft might be a minimally invasive and simple method useful in clinical practice.

Complete post-operative resolution of "temporary" end-stage kidney disease secondary to aortic dissection without static renal artery obstruction: a case study.

BACKGROUND: Acute kidney injury (AKI), which may progress to end-stage kidney disease (ESKD), is a potential complication of aortic dissection. Notably, in all reported ESKD cases secondary to aortic dissection, imaging evidence of static obstruction of the renal arteries always shows either renal artery stenosis or extension of the dissection into the renal arteries. CASE PRESENTATION: We present the case of a 58-year-old man with hypertension who was diagnosed with a Stanford type B aortic dissection and treated with medications alone because there were no obvious findings indicative of dissection involving the renal arteries. He had AKI, which unexpectedly progressed to ESKD, without any radiological evidence of direct involvement of the renal arteries. Thus, we failed to attribute the ESKD to the dissection and hesitated to perform any surgical intervention. Nevertheless, the patient's hormonal levels, fractional excretion values, ankle brachial indices, and Doppler resistive indices seemed to indirectly suggest kidney malperfusion and implied renal artery hypo-perfusion. However, abdominal computed tomography imaging only revealed progressive thrombotic obstruction of the false lumen and compression of the true lumen in the descending thoracic aorta, despite the absence of anatomical blockage of renal artery perfusion. Later, signs of peripheral malperfusion, such as intermittent claudication, necessitated surgical intervention; a graft replacement of the aorta was performed. Post-operatively, the patient completely recovered after 3 months of haemodialysis, and the markers that had pre-operatively suggested decreased renal bloodstream normalised with recovery of kidney function. CONCLUSIONS: To the best of our knowledge, this is the first report of severe AKI, secondary to aortic dissection, without direct renal artery obstruction, which progressed to "temporary" ESKD and was resolved following surgery. This case suggests that only coarctation above the renal artery branches following an aortic dissection can progress AKI to ESKD, despite the absence of radiological evidence confirming an obvious anatomical blockage. Further, indirect markers suggestive of decreased renal blood flow, such as ankle brachial indices, renal artery resistive indices, urinary excretion fractions, and hormonal changes, are useful for evaluating concomitant AKI and may indicate the need for surgical intervention after a Stanford type B aortic dissection.

[Treatment of Mediastinitis after Open Heart Surgery Using Negative Pressure Wound Therapy with Irrigation].

Mediastinitis occurs after open heart surgery in a small number of cases. When it occurs, early diagnosis and treatment are important. A 69-year-old male patient suffered from mediastinitis after total aortic arch replacement. He has cured completely by negative pressure wound therapy (NPWT) with irrigation method. The vacuum-assisted closure( VAC) method is very useful for wound repair and has recently been used to treat mediastinitis. However, the use of VAC alone does not always result in complete cure. NPWT with irrigation is a very useful infection control method. Performing NPWT before VAC might contribute to improving the outcomes of mediastinitis treatment. However, it is difficult to decide when to switch from NPWT with irrigation to VAC.

Surgical treatment of papillary fibroelastoma in the aortic valve: a case report.

With the exception of myxomas, primary tumors of the heart are very rare. We present here our experience with papillary fibroelastoma in the aortic valve. We could not preserve the aortic valve because of the wide attachment of the tumor to the valve and aortic regurgitation.

Intrathecal injection of hepatocyte growth factor gene-modified marrow stromal cells attenuates neurologic injury induced by transient spinal cord ischemia in rabbits.

BACKGROUND: Our previous studies showed that transfer of hepatocyte growth factor (HGF) gene or transplantation of marrow stromal cells (MSCs) remarkably attenuated neurologic injuries after spinal cord ischemia. We sought to investigate a novel neuroprotective strategy of transplantation of human HGF gene-modified MSCs on ischemic spinal cords. METHODS: Human HGF gene was transferred into MSCs in vitro. The HGF gene-modified MSCs were transplanted by means of intrathecal injection. Two days later, spinal cord ischemia was induced by occlusion of the infrarenal aorta with a balloon catheter for 40 or 50 min. Hind-limb motor function was assessed during a 14-day recovery period with Tarlov criteria, and then histologic examination was performed. RESULTS: Human HGF was detected in the cerebrospinal fluid from 2 to 16 days after transplantation of HGF gene-modified MSCs. Compared with the controls, transplantation of HGF gene-modified MSCs or MSCs alone significantly improved the Tarlov scores 1, 2, 7, and 14 days after spinal cord ischemia of 40 or 50 min (P < 0.01, respectively) and increased the number of intact motor neurons in the lumbar spinal cord (P < 0.01, respectively). When the ischemic period was extended to 50 min, the Tarlov scores and the number of intact motor neurons of rabbits transplanted with HGF gene-modified MSCs were markedly higher than those of the rabbits transplanted with MSCs only (P < 0.05, respectively). CONCLUSIONS: Transplantation of HGF gene-modified MSCs induces powerful neuroprotection on spinal cords against ischemia-reperfusion injury and is more therapeutically efficient than transplantation of MSCs only.

Congenital systemic and coronary-to-pulmonary artery fistulas.

Congenital systemic-to-pulmonary artery fistulas are very rare, with the exception of congenital heart disease and pulmonary sequestration. We describe the first reported case of left internal mammary and bronchial artery to pulmonary artery fistulas associated with bilateral coronary arteries to pulmonary artery fistulas.

Interleukin-1 receptor antagonist attenuates the severity of spinal cord ischemic injury in rabbits.

OBJECTIVE: Thoracic and thoracoabdominal aortic surgery is sometimes complicated by subacute or delayed paraplegia. Pro-inflammatory cytokine interleukin-1 (IL-1) beta has been implicated in extensive inflammation and progressive neurodegeneration after ischemia. Using a rabbit model, we investigated the neuroprotective effects of IL-1 receptor antagonist (IL-1ra) in a temporal fashion. METHODS: Spinal cord ischemia was induced by aortic cross-clamping in New Zealand White rabbits. The animals were assigned to three groups. Group C (n = 20) received saline (0.2-mL) and Group I (n = 20) received IL-1ra (200-microg/0.2-mL) intrathecally just after reperfusion. Group S (n = 3) underwent sham operation without aortic occlusion. We assessed the neuroprotective effects of IL-1ra by evaluating neurological function, histopathological changes, and in-situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL staining). We also measured the levels of Nitric Oxide (NO) and S100beta in cerebrospinal fluid (CSF). Each evaluation was performed sequentially within 120 hours after reperfusion. RESULTS: Group C showed progressive deterioration of motor function which became statistically significant from 48 hours after the onset of reperfusion (P < .05, P < .01, P < .001, P < .001 at 48, 72, 96, and 120 hours, respectively). Compared to Group C, a higher number of viable neurons was observed with less severe spinal cord injury in Group I (P < .01, .05 and .05 at 24, 72, and 120 hours, respectively). TUNEL-positive neurons were also significantly reduced by the administration of IL-1ra (P <.01 and .05 at 24, and 120 hours, respectively). The difference between Group C and Group I with regard to NO was significant at 72 and 120 hours (P < .05), while that in terms of S100beta was significant only at 24 hours (P < .05). CONCLUSIONS: Administration of IL-1ra attenuates spinal cord ischemic-reperfusion injury as evidenced by reducing both neuronal necrosis and apoptosis.

Effect of prophylactically administered edaravone during antegrade cerebral perfusion in a canine model of old cerebral infarction.

OBJECTIVE: Reactive free radical species are thought to be involved in postoperative neurologic dysfunction after antegrade selective cerebral perfusion in brains with old infarction. We assessed the brain protective effect of prophylactically administered edaravone, a free radical scavenger, for antegrade selective cerebral perfusion in brains with or without old infarction in a canine model. METHODS: A canine model of old cerebral infarction was created by injecting cylindric silicone embolus into the middle cerebral artery. Animals showing obvious neurologic deficits and surviving 4 weeks or longer were included in the model. Deep hypothermia with antegrade selective cerebral perfusion was performed in both intact (non-edaravone, group A; edaravone-treated, group B) and infarcted animals (non-edaravone, group C; edaravone-treated, group D). Serum concentrations of malondialdehyde, hexanoyl-lysine, glutamate, and venous-arterial lactate difference were measured, and central conduction time and amplitude of somatosensory evoked potentials were assessed during the operation. RESULTS: Compared with the intact groups, serum concentrations of malondialdehyde and hexanoyl-lysine in group C significantly increased at the end of antegrade selective cerebral perfusion, whereas that of glutamate did so in the rewarming phase. Increases in all these biochemical parameters were suppressed in group D. In group C, the venous-arterial lactate difference was significantly greater in the rewarming phase at 28 degrees C compared with intact groups. A significant prolongation of postoperative central conduction time and decrease in neuronal activity were detected in group C, both of which recovered in group D. CONCLUSION: Prophylactic administration of edaravone exerted a significant protective effect against postoperative neurologic dysfunction after antegrade selective cerebral perfusion in a canine model with old cerebral infarction.