Weaning failure due to isolated residual diaphragmatic paralysis after cervical spinal cord ischemia following aortic surgery- a case report.

BACKGROUND: Bilateral diaphragmatic dysfunction can lead to dyspnea and recurrent respiratory failure. In rare cases, it may result from high cervical spinal cord ischemia (SCI) due to anterior spinal artery syndrome (ASAS). We present a case of a patient experiencing persistent isolated diaphragmatic paralysis after SCI at level C3/C4 following thoracic endovascular aortic repair (TEVAR) for Kommerell's diverticulum. This is, to our knowledge, the first documented instance of a patient fully recovering from tetraplegia due to SCI while still exhibiting ongoing bilateral diaphragmatic paralysis. CASE PRESENTATION: The patient, a 67-year-old male, presented to the Vascular Surgery Department for surgical treatment of symptomatic Kommerell's diverticulum in an aberrant right subclavian artery. After successful surgery in two stages, the patient presented with respiratory insufficiency and flaccid tetraparesis consistent with anterior spinal artery syndrome with maintained sensibility of all extremities. A computerized tomography scan (CT) revealed a high-grade origin stenosis of the left vertebral artery, which was treated by angioplasty and balloon-expandable stenting. Consecutively, the tetraparesis immediately resolved, but weaning remained unsuccessful requiring tracheostomy. Abdominal ultrasound revealed a residual bilateral diaphragmatic paralysis. A repeated magnetic resonance imaging (MRI) 14 days after vertebral artery angioplasty confirmed SCI at level C3/C4. The patient was transferred to a pulmonary clinic with weaning center for further recovery. CONCLUSIONS: This novel case highlights the need to consider diaphragmatic paralysis due to SCI as a cause of respiratory failure in patients following aortic surgery. Diaphragmatic paralysis may remain as an isolated residual in these patients.

Spinal drain-related complications after complex endovascular aortic repair using a prophylactic automated volume-directed drainage protocol.

OBJECTIVE: A common measure to lower the risk for spinal cord ischemia (SCI) during complex endovascular aortic repair (cEVAR) is prophylactic cerebrospinal fluid drainage (CSFD). This method has caused controversy because of drain-related complications. Spinal drains are usually pressure directed. The objective of this study was to evaluate the risk of CSFD-related complications and SCI within the context of an automated volume-directed drain protocol. METHODS: This is a retrospective, single-center study of all cEVARs with CSFD at a tertiary vascular center between January 2014 and December 2020. Demographics, complications, and spinal drain data were recorded. All drainages were volume based using an automatic drainage system (LiquoGuard7; Möller Medical GmbH). Spinal drain complications were categorized as disabling and nondisabling according to the modified Rankin scale. The primary end point was any CSFD-related complication. RESULTS: A total of 448 cEVAR patients were identified, of whom 147 (32.8%) had prophylactic CSFD. The mean age was 69 years (63% male). The most common pathology (61%) was thoracoabdominal aortic aneurysm, and the most common procedure was branched EVAR (55.1%). Eighteen (12.2%) patients developed a CSFD-related complication, whereof three (2%) were disabling. Nineteen (13%) patients developed SCI: 12 (8.4%) paraparetic, 5 (3.4%) paraplegic, and 2 (1.4%) paresthesias. Of these, 13 (68%) had full reversal of symptoms, whereas 6 patients (4%) had residual symptoms and were deemed disabling. Drain-related complications were more common in patients with SCI (31.6%) compared with those without (9.4%, P = .014). In the latter group, only two patients (1.6%) developed a disabling drain-related complication. CONCLUSIONS: Selective use of prophylactic, automated volume-directed CSFD in patients at high risk for SCI was associated with a high incidence of complications and should be used with caution. Among those developing SCI, reversal was achieved frequently with increased CSFD volume, but at the price of more bleeding complications.

[Intensive care management of acute diseases of the aorta]. / Intensivmedizinisches Management akuter Aortenerkrankungen.

Acute aortic diseases represent a group of complex severe and often fatal medical conditions. Although they are significantly rarer than cardiac or thromboembolic events, they are an important differential diagnosis to be ruled out, e.g., in the clinical work-up of acute chest pain.Treatment, especially surgical interventions, depends on the progression, extent and size of the pathology and whenever possible should be performed in specialized centers with the appropriate experience.Intensive care monitoring is advisable as a range of peracute complications can occur even in initially stable patients. Depending on the clinical presentation and affected structures, a number of severe complications need to be anticipated by critical care physicians. Additionally, a notable symptom is severe and refractory hypertension, especially in the acute phase. This article provides a summary of the most frequent clinical pictures and corresponding treatment options. Furthermore, the principles of initial patient stabilization and treatment as well as the perioperative management of complex surgical procedures on the aorta are discussed.

Pseudoaneurysm of an intercostal artery: endovascular treatment with PK papyrus coronary stent to prevent spinal ischemia.

BACKGROUND: Endovascular treatment can be a fast and safe option in the case of acute, internal bleeding - but it requires special knowledge and technical skills. Interventionalists must consider the anatomy and potential complications. As in this case report, the anterior spinal artery, for example, can be a crucial vessel that must always be considered when embolizing intercostal or lumbar arteries. The risk of spinal ischemia has to be taken into account and should be minimized by choosing the appropriate treatment option. CASE PRESENTATION: We report about a 77 year old, male patient with upper gastrointestinal bleeding after esophagectomy and gastric conduit reconstruction. A CT scan identified a pseudoaneurysm of an intercostal artery penetrating the gastric conduit as the bleeding source. In the DSA, a direct connection between the intercostal artery and the anterior spinal artery appeared to be likely. Due to the associated risk of spinal ischemia, an embolization of the intercostal artery was not an option. We decided to implant a stentgraft that would stop the perfusion of the pseudoaneurysm, but preserve the perfusion of the intercostal artery. Due to the small diameter of the vessel, we could not implant our commonly used stentgrafts in this case. Therefore, we chose an uncommon solution and used a stentgraft that is designed primarily for coronary arteries. CONCLUSIONS: Whenever intercostal or lumbar arteries need to be embolized, a possible connection to the anterior spinal artery must be considered and interventionalists have to be aware of possible ischemic complications. In this case, a stentgraft designed primarily for coronary arteries offered a good endovascular treatment option for the pseudoaneurysm of an intercostal artery. The risk of spinal ischemia could be minimized by using this stentgraft.

Case Report: A Spinal Ischemic Lesion in a 24-Year-Old Patient With Fabry Disease.

Background: While cerebral lesions are common in Fabry disease (FD), spinal lesions have not been described, and their presence was suggested to be indicative of multiple sclerosis. Here, we present a FD patient with histopathological confirmed spinal ischemic stroke. Case presentation: A patient with genetically and biochemically diagnosed FD and characteristic manifestations (acroparesthesia, angiokeratomas, hypohidrosis, microalbuminuria, myocardial hypertrophy) presented with paraplegia, loss of all sensory modalities below Th9, and loss of bowel and bladder function. While cranial MRI was inconspicuous, spinal MRI showed a T2 hyperintense, non-contrast-enhancing lesion of the thoracic spinal cord. Lumbar puncture revealed mild pleocytosis, increased total protein and lactate levels, decreased glucose ratio, and negative oligoclonal bands. Rheumatic, neoplastic, and infectious disorders were excluded. The patient received intravenous and intrathecal methylprednisolone, plasmapheresis, intravenous immunoglobulins, and cyclophosphamide without clinical improvement. A biopsy of the thoracic lesion was performed. A histopathological examination revealed necrotic tissue consistent with spinal cord ischemia. Diagnostic work-up for stroke etiology clarification was not conspicuous. Two years onward, the patient suffered from a pontine infarction and a transient ischemic attack. Conclusion: The current case highlights the possible occurrence of spinal ischemic lesions in FD. Thus, the diagnosis of FD should not be prematurely discarded in the presence of spinal lesions.

Staged procedures for prevention of spinal cord ischemia in endovascular aortic surgery.

BACKGROUND: Spinal cord ischemia with development of paraplegia is the most relevant complication of thoracoabdominal aortic surgery caused by compromising the segmental arteries. To prevent this devastating complication in endovascular aortic surgery, staging procedures have been developed to reinforce collateral blood flood to the spinal cord. RESULTS: In patients with a medium to high risk for spinal cord ischemia, staged aortic repair is recommended. The classical staged repair is the two-step repair with delayed implantation of the aortic stent grafts. Additionally, more recent methods for short-term salvage of segmental artery perfusion by leaving an endoleak have been developed. Perfusion branches, delayed bridging stents as well as the open branch technique are among these methods. The latest option of staged repair is minimally invasive segmental artery embolization. CONCLUSION: Besides the nonsurgical options for monitoring and therapy of spinal cord ischemia, various staging procedures are available, which can be implemented depending on the patient and the aortic anatomy. Evidence that underlines staged repair for endovascular treatment of thoracoabdominal aortic pathologies is mostly based on retrospective studies.

Perioperative cerebrospinal fluid drainage for the prevention of spinal ischemia after endovascular aortic repair.

Endovascular treatment of thoracic and thoracoabdominal aortic diseases is accompanied by a risk of spinal ischemia in 1-19% of patients, depending on the entity and extent of the disease. The use of perioperative drainage of cerebrospinal fluid is one of the invasive measures to reduce the occurrence of this severe complication. This article reviews the incidence of spinal ischemia, its risk factors, the evidence for carrying out cerebrospinal fluid drainage and its modern use by means of an automated, pressure controlled system (LiquoGuard®7).

Controlled automated reperfusion of the whole body after 120 minutes of Cardiopulmonary resuscitation: first clinical report.

BACKGROUND: Cardiopulmonary resuscitation (CPR) is associated with a high mortality rate. Furthermore, the few survivors often have severe, persistent cerebral dysfunction. A potential cause for this unsatisfactory outcome after CPR is the combination of cardiac arrest (ischemia) and the inability to restore adequate hemodynamics during conventional CPR (reperfusion), resulting in ischemia/reperfusion injury of the whole body. Therefore we developed a concept counteracting this ischemia/reperfusion injury during the process of CPR. CASE PRESENTATION: We present data from a patient, in whom the concept of a novel controlled automated reperfusion of the whole body (CARL) was applied after 120 min of CPR under normothermic conditions. The patient survived without cerebral deficits and showed full recovery of all organs after prolonged cardiac arrest (CA) except for the spinal cord, where a defect at the level of the 11th thoracic vertebra caused partial loss of motoric function of the legs. CONCLUSION: This is the first reported clinical application of CARL after CA. The implementation of CARL resulted in unexpected survival and recovery after prolonged normothermic CA and CPR. In synopsis with the preclinical experience in pigs this case shows, that the new concept of CARL treating ischemia/reperfusion during the CPR may be an important element within the future treatment of CA. TRIAL REGISTRATION: Trial was retrospectively registered in the "German Clinical Trials Register" ( www.germanctr.de ) under No.: DRKS00005773 on July 28th, 2015.

Transcutaneous near-infrared spectroscopy for monitoring spinal cord ischemia: an experimental study in swine.

We aimed to assess the ability of near-infrared spectroscopy (NIRS) to detect spinal cord ischemia, and to evaluate changes in regional oxygen saturation (rSO2) following recovery of spinal cord circulation and cerebrospinal fluid drainage. Four 12-month-old female swine weighing 28.7-29.5 kg were acquired for this study. NIRS probes were placed along the midline of the upper (T6/7) and lower (T9/T10) thoracic vertebrae. The thoracic aorta was clamped distal of the left subclavian artery to induce spinal ischemia. Aortic cross-clamping was maintained for 30 min. Fifteen minutes after aortic de-clamping, the cerebrospinal fluid drainage catheter was opened to air, and cerebrospinal fluid drainage was initiated. Following aortic clamping, rSO2 in both upper and lower regions of the spinal cord decreased by 15 % within 5 min and by 20 % within 10 min (relative change). After aortic de-clamping, rSO2 values in both regions returned to baseline within 5 min. No changes in rSO2 in either the upper or lower vertebrae were observed following initiation of cerebrospinal fluid drainage. Histological analysis revealed that ischemic changes had occurred in all spinal levels. NIRS may be used to detect decreases in and recovery of spinal cord circulation following aortic clamping and de-clamping, whereas it may not reflect minor changes in spinal cord circulation due to cerebrospinal fluid drainage. Further clinical studies are required to investigate the potential for NIRS as an index of spinal cord circulation.

Vascular diseases of the spine.

Spinal vascular diseases are rare but potentially devastating diseases affecting the cord. This chapter gives an overview about their imaging features, differential diagnoses, the neurologic symptomatology, and the potential therapeutic approaches of these diseases, which might vary depending on the underlying pathologic condition.

Repeated early thrombolysis in cervical spinal cord ischemia.

Specific therapy of acute spinal ischemia is not established. We report the first case of an MRI-verified cervical spinal ischemia treated by thrombolysis and review the literature. A 72-year old woman with right-sided motor hemiparesis and trunk ataxia was treated by intravenous thrombolysis with full recovery. Three days later she developed again a severe right-sided sensorimotor hemiparesis and a second off-label intravenous thrombolysis was repeated. Magnetic resonance imaging revealed a right-sided posterior-lateral cervical spinal ischemia. Spinal ischemia may clinically present with a cerebral-stroke-like picture challenging diagnostic and therapeutic procedure. Systemic thrombolysis might be a treatment option in acute spinal ischemia. In addition, early repeated systemic thrombolysis may be considered in selected strokes.

An unusual cause of spinal cord ischemia after thoracic endovascular repair.

A 59-year-old left-handed man presented with chest pain and hypertension and was found to have an acute descending aortic dissection on imaging. After thoracic endovascular repair of the dissection, he developed left arm weakness and ischemia. Despite carotid-subclavian transposition, the patient was found to have persistent left triceps weakness as well as bilateral leg paresis. An urgent spinal drain was placed that improved his lower extremity deficit but did not greatly change his arm symptoms. Magnetic resonance imaging of the spine revealed previously undiagnosed severe multilevel spinal stenosis requiring operative decompression. To our knowledge, this is the first report of the contribution of cervical spinal stenosis to post-thoracic endovascular repair spinal ischemia.

Optic Nerve Sheath Diameter Measurement to Identify High-Risk Patients for Spinal Ischemia after Endovascular Thoracoabdominal Aortic Aneurysm Repair.

BACKGROUND & PURPOSE: Thoracic endovascular aortic repair (TEVAR) is associated with a reasonable risk of spinal ischemia. As cerebrospinal fluid pressure (CSFP) is correlated with the rate of paraplegia, a non-invasive method to estimate CSFP could help to estimate the patient's individual risk and guide the therapeutic approach. The quantification of the optic nerve sheath diameter (ONSD) using ocular sonography (OS) could be a suitable technique and was examined in the present study. METHODS: 28 patients with TEVAR were included. Five consecutive measurements of the ONSD were performed in each patient. The first before the intervention ("baseline"), the next immediately postinterventional at the intensive care unit (post1), measurements 3, 4 (post2, post3) on day 1 and 2 after the intervention and number 5 (post4) before discharge. Statistical analysis was done using the Wilcoxon-test. A p-value < 0.05 was considered statistically significant. RESULTS: A significant increase between baseline and post1-measurements (right eye: p = 0.006; left eye: p = 0.02) could be detected. A significant decrease was detected between post1 and post3 (right eye: p = 0.02; left eye: p < 0.01). A group of 5 patients had an additional increase of ONSD from post1 to post2, one of these patients developed a permanent paraplegia. Patients with spinal catheters had significantly lower ONSDs at nearly all time points. CONCLUSION: The present study is the first to prospectively examine and prove the possibility to monitor CSFP changes in patients with TEVAR associated transient spinal edema using OS. Systematic factors as artificial ventilation and body positioning did not have a significant effect.

The neuroprotective mechanism of puerarin in the treatment of acute spinal ischemia-reperfusion injury is linked to cyclin-dependent kinase 5.

Puerarin is shown to exert a variety of pharmacological effects including neuroprotective properties. However, mechanisms of the action are not fully understood. This study was designed to explore the mechanism of puerarin in treatment of acute spinal ischemia-reperfusion injury in rats. Acute spinal ischemia-reperfusion injury was conducted by aortic occlusion in twenty-eight male Sprague-Dawley rats, weighting 230-250 g. The animals were randomly divided into four groups. In the animals with puerarin treatment, 50 mg/kg of puerarin was injected intraperitoneally after reperfusion, and followed by the same dose of injection every 24h for 2 days. In the animals with roscovitine pre-treatment, 30 mg/kg roscovitine was intravenously administrated 60 min before spinal ischemia started. After spinal ischemia for 60 min followed by 48 h of reperfusion, the motor function, spinal infarction volume, apoptosis indices and the activities of Cdk5 and p25 were examined. Acute spinal ischemia-reperfusion resulted in an injury of the spines associated with motor deficit, elevation of Cdk5 and p25 activities, and increase in the spinal apoptosis number and spinal infarction volume. Puerarin improved motor function associated with the decreased apoptosis number, spinal infarction volume, and Cdk5 and p25 activities. The present study indicated that reduction of spinal injury was associated with inhibition of Cdk5 and p25, and that inhibition of Cdk5 and p25 was one of the neuroprotective mechanisms in the puerarin treatment of acute ischemia/reperfusion-induced spinal injury in rats.

Dexmedetomidine improves the histological and neurological outcomes 48 h after transient spinal ischemia in rats.

Dexmedetomidine, an α2 adrenoceptor agonist, provides neuroprotection against various cerebral ischemia models through its anti-apoptotic effects. Dexmedetomidine also improves paraplegia induced by intrathecal morphine after short-term spinal ischemia. However, there are no reports regarding dexmedetomidine׳s ability to provide neuroprotection solely against transient spinal ischemia. We investigated whether dexmedetomidine would provide spinal protection following transient spinal ischemia in rats. Adult male Sprague Dawley rats were randomly assigned to one of the following five groups: (1) intravenous infusion of 0.9% NaCl at the rate of 0.5 mL/h (control), (2) dexmedetomidine 0.1 µg/kg/h, (3) dexmedetomidine 1 µg/kg/h, (4) dexmedetomidine 10 µg/kg/h, or (5) intravenous infusion of 0.9% NaCl without spinal ischemia (sham). The rats received saline solution or dexmedetomidine from 30 min before spinal cord ischemia to 48 h after ischemia. Spinal cord ischemia was induced by intraaortic balloon occlusion combined with proximal arterial hypotension for 10 min. Ischemic injury was assessed by neurological deficit scores and the number of viable motor nerve cells in the anterior spinal cord at 48 h after reperfusion. Neurological deficit scores in the dexmedetomidine-treated rats were significantly lower than the scores in the control group at 24 and 48 h after ischemia (P<0.05). The number of viable motor nerve cells was significantly larger in the dexmedetomidine-treated rats than in the control rats (P<0.05), but the number of motor nerve cells in the dexmedetomidine group was significantly smaller than the sham group. Our results indicate that the continuous administration of dexmedetomidine improves neurological and histological outcomes 48 h after transient spinal ischemia in rats.

Influence of Tanshinone IIa on heat shock protein 70, Bcl-2 and Bax expression in rats with spinal ischemia/reperfusion injury.

Tanshinone IIa is an effective monomer component of Danshen, which is a traditional Chinese medicine for activating blood circulation to dissipate blood stasis. Tanshinone IIa can effectively improve brain tissue ischemia/hypoxia injury. The present study established a rat model of spinal cord ischemia/reperfusion injury and intraperitoneally injected Tanshinone IIa, 0.5 hour prior to model establishment. Results showed that Tanshinone IIa promoted heat shock protein 70 and Bcl-2 protein expression, but inhibited Bax protein expression in the injured spinal cord after ischemia/reperfusion injury. Furthermore, Nissl staining indicated a reduction in nerve cell apoptosis and fewer pathological lesions in the presence of Tanshinone IIa, compared with positive control Danshen injection.