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Mortality rates from pulmonary embolism (PE) remain significant, highlighting the need for alternative treatment strategies beyond traditional anticoagulation. Percutaneous interventions, including mechanical thrombectomy and catheter-directed thrombolysis, are emerging as promising options. Given the complex pathophysiology and unique risk profiles of these patients, meticulous multidisciplinary planning is essential. Anesthesiologists play a central role in coordinating care and managing perioperative risks to improve outcomes. This article provides insights into best safety practices and shares experiences from a leading quaternary center. It offers guidance for anesthesia providers to proactively engage in comprehensive risk stratification, participate in multidisciplinary discussions, and support robust contingency planning for managing PE patients undergoing percutaneous interventions in non-operating room anesthesia settings. [ABSTRACT FROM AUTHOR]

Pulmonary embolism (PE) embodies a large healthcare burden globally and is the third leading cause of morbidity and mortality worldwide. Submassive (intermediate-risk) PE accounts for 40% of this burden. However, the optimal treatment pathway for this population remains complex and ill-defined. Catheter-directed interventions (CDIs) have shown promise in directly impacting morbidity and mortality while demonstrating a favorable success rate, safety profile, and decreased length of stay (LOS) in the intensive care unit and hospital. This retrospective review included 22 patients (50% female) with submassive PE who underwent mechanical thrombectomy (MT). A total of 45% had a contraindication to thrombolytics, the mean pulmonary embolism severity index was 127, 36% had saddle PE, the average decrease in mean pulmonary artery pressure (PAP) was 7.2 mmHg following MT, the average LOS was 6.9 days, the 30-day mortality rate was 9%, the major adverse event (MAE) rate was 9%, and the readmission rate was 13.6%. A total of 82% had successful removal of thrombus during MT with no major bleeding complications, intracranial hemorrhage events, or device-related deaths. Acknowledging the limitation of our small sample size, our data indicate that MT in the intermediate-high-risk submassive pulmonary embolism (PE) cohort resulted in a decreased hospital length of stay (LOS) and in-hospital mortality compared to standard anticoagulation therapy alone. [ABSTRACT FROM AUTHOR]

Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant demyelinating neuropathy characterized by an increased susceptibility to peripheral nerve injury from trauma, compression, or shear forces. Patients with this condition are unique, necessitating distinct considerations for anesthesia and surgical teams. This review describes the etiology, prevalence, clinical presentation, and management of HNPP and presents contemporary evidence and recommendations for optimal care for HNPP patients in the perioperative period. While the incidence of HNPP is reported at 7–16:100,000, this figure may be an underestimation due to underdiagnosis, further complicating medicolegal issues. With the subtle nature of symptoms associated with HNPP, patients with this condition may remain unrecognized during the perioperative period, posing significant risks. Several aspects of caring for this population, including anesthetic choices, intraoperative positioning, and monitoring strategy, may deviate from standard practices. As such, a tailored approach to caring for this unique population, coupled with meticulous preoperative planning, is crucial and requires a multidisciplinary approach. [ABSTRACT FROM AUTHOR]

To evaluate the incidence of post-interventional contrast staining (PICS) in acute ischemic stroke (AIS) Chinese patients who were treated with endovascular thrombectomy (ET) and investigate potential association of PICS with functional outcome and intracerebral hemorrhage (ICH). This observational study was based on a single-center prospective registry study. AIS patients who underwent ET from January 2013 to February 2017 were recruited into this study. All patients had dual-energy CT (DECT) scan of the head at 12 to 24 hours post-ET. The primary outcome was the incidence of PICS. Secondary outcomes were total ICH, symptomatic ICH (sICH), 3-month functional outcome, and long-term functional outcome. One hundred and eighty patients were enrolled in this study. PICS was detected in 50 patients (28%) based on the post-interventional CT scan. We first used basic statistical analyses, showing that the incidence of both total ICH (60% vs. 25%, p<0.001) and sICH (18% vs. 8%, p=0.044) were higher in patients with PICS than those without, and fewer patients achieved no disability (mRS≤1) in the PICS group compared to the control group at both 3-month and long-term follow-up (p<0.01 each). However, multivariate regression analysis further revealed that PICS only increased total (adjusted odds ratio, 7.38; 95% confidence interval 1.66 to 32.9; p=0.009) but not sICH risk. Furthermore, the logistic regression analyses did not show statistical difference in good clinical outcomes or mortality between the two groups. PICS is a common phenomenon in Chinese AIS patients. It is associated with total ICH after ET, but it seems to have no effect on functional outcome and sICH. Further large-scale studies are warranted to validate these results. [ABSTRACT FROM AUTHOR]

Hypothermia is considered as a promising neuroprotective treatment for ischemic stroke but with many limitations. To expand its clinical relevance, this study evaluated the combination of physical (ice pad) and pharmacological [transient receptor potential vanilloid channel 1 (TRPV1) receptor agonist, dihydrocapsaicin (DHC)] approaches for faster cooling and stronger neuroprotection. A total of 144 male Sprague Dawley rats were randomized to 7 groups: sham (n=16), stroke only (n=24), stroke with physical hypothermia at 31°C for 3 h after the onset of reperfusion (n=24), high-dose DHC (HHC)(1.5 mg/kg, n=24), low-dose DHC (L-DHC)(0.5 mg/kg, n=32) with (n=8) or without (n=24) external body temperature control at ~38 °C (L-DHC, 38 °C), and combination therapy (L-DHC+ ice pad, n=24). Rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h. Infarct volume, neurological deficits and apoptotic cell death were determined at 24 h after reperfusion. Expression of pro- and anti-apoptotic proteins was evaluated by Western blot. ATP and reactive oxygen species (ROS) were detected by biochemical assays at 6 and 24 h after reperfusion. Combination therapy of L-DHC and ice pad significantly improved every measured outcome compared to monotherapies. Combination therapy achieved hypothermia faster by 28.6% than ice pad, 350% than L-DHC and 200% than H-DHC alone. Combination therapy reduced (p<0.05) neurological deficits by 63% vs. 26% with L-DHC. No effect was observed when using ice pad or H-DHC alone. L-DHC and ice pad combination improved brain oxidative metabolism by reducing (p<0.05) ROS at 6 and 24 h after reperfusion and increasing ATP levels by 42.9% compared to 25% elevation with L-DHC alone. Finally, combination therapy decreased apoptotic cell death by 48.5% vs. 24.9% with L-DHC, associated with increased anti-apoptotic protein and reduced pro-apoptotic protein levels (p<0.001). Our study has demonstrated that combining physical and pharmacological hypothermia is a promising therapeutic approach in ischemic stroke, and warrants further translational investigations. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated depressive or hibernation-like roles of phenothiazine neuroleptics [combined chlorpromazine and promethazine (C + P)] in brain activity. This ischemic stroke study aimed to establish neuroprotection by reducing oxidative stress and improving brain metabolism with post-ischemic C + P administration. Sprague-Dawley rats were subjected to transient (2 or 4 h) middle cerebral artery occlusion (MCAO) followed by 6 or 24 h reperfusion, or permanent (28 h) MCAO without reperfusion. At 2 h after ischemia onset, rats received either an intraperitoneal (IP) injection of saline or two doses of C + P. Body temperatures, brain infarct volumes, and neurological deficits were examined. Oxidative metabolism and stress were determined by levels of ATP, NADH, and reactive oxygen species (ROS). Protein kinase C-δ (PKC-δ) and Akt expression were determined by Western blotting. C + P administration induced a neuroprotection in both transient and permanent ischemia models evidenced by significant reduction in infarct volumes and neurological deficits post-stroke. C + P induced a dose-dependent reduction in body temperature as early as 5 min post-ischemia and lasted up to 12 h. However, reduction in body temperature either only slightly or did not enhance C + P-induced neuroprotection. C + P therapy improved brain metabolism as determined by increased ATP levels and NADH activity, as well as decreased ROS production. These therapeutic effects were associated with alterations in PKC-δ and Akt protein expression. C + P treatments conferred neuroprotection in severe stroke models by suppressing the damaging cascade of metabolic events, most likely independent of drug-induced hypothermia. These findings further prove the clinical potential for C + P treatment and may direct us closer towards the development of an efficacious neuroprotective therapy. [ABSTRACT FROM AUTHOR]

Along with thrombolytic therapy, which has a number of limitations, stroke outcome may be improved with neuroprotective therapies that disrupt ischemic cell death. Recent research has shown a neuroprotective role of ethanol administration during ischemic stroke, such as its ability to reduce infarct volume and neurologic deficit. In order to investigate this further, we assessed the hypothesis that ethanol's neuroprotective effect is through reduction of apoptosis and the modulation of the important apoptotic PKCδ and Akt signaling pathway. Ethanol (1.5 g/kg) was given by intraperitoneal injections to 54 Sprague-Dawley rats after 2 hours of middle cerebral artery (MCA) occlusion, followed by 3 or 24 hours of reperfusion. We measured apoptotic cell death, PKC-δ, and Akt mRNA and protein expressions in each of ischemic groups with or without ethanol treatment using ELISA, real-time PCR and Western blot analysis. Our results showed that cell death was significantly increased in rats following 2 hour MCA occlusion and 24 hour reperfusion. Subsequently, cell death was significantly reduced by an administration of ethanol. We further found that ethanol administration, prior to either 3 or 24 hours of reperfusion, significantly decreased the expression of PKC-δ while simultaneously increasing the expression Akt at both mRNA and protein levels at the two points. In conclusion, our study suggests that ethanol administration following ischemic stroke modulates the gene and protein profile in such a way that it increased expression of anti-apoptotic Akt and decreased the pro-apoptotic PKC-δ. This ultimately results in a decrease in neuronal apoptosis, thus conferring neuroprotection. [ABSTRACT FROM AUTHOR]

Background: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the best characterized genetic cause of vascular dementia and stroke and has been extensively reported in European and Asian populations. Objective: To report the pathological and genetic analysis of CADASIL in an African American man with a 15-base pair NOTCH3 duplication. Design: Case report. Setting: University hospital. Patient: A 78-year-old man with dementia, recurrent strokes, a family history of similar neurological disease, and white matter abnormalities seen on brain magnetic resonance imaging. Main Outcome Measures: Brain pathology and genetic analysis of NOTCH3. Results: The patient's brain showed widespread arteriopathy in large and small arteries. Using electron microscopy, granular osmiophilic material typical of CADASIL was identified abutting the plasma membrane of smooth muscle cells. Brain extracts contained elevated NOTCH3 protein levels. Sequencing of the NOTCH3 gene revealed a novel 15-base pair heterozygous duplication in exon 7, which is predicted to direct expression of a protein that contains 5 extra amino acids, including a cysteine residue. Conclusions: To our knowledge, this is the first reported pathological and genetic analysis of an African American patient with CADASIL. The mutation in NOTCH3 is the longest duplication within this gene yet reported. [ABSTRACT FROM AUTHOR]

Reperfusion strategies such as vascular thrombolysis and thrombectomy are the first-line treatments recommended for acute ischemic stroke. However, only half of these patients achieve functional independence after endovascular reperfusion of large vessel occlusions. Timely restoration of blood flow is crucial, but not all reperfusion results in benefit, a phenomenon termed futile reperfusion. Futile reperfusion occurs when brain tissue has already suffered irreversible damage before reperfusion or when other factors undermine the benefits of restored blood flow. These factors include reperfusion-not rescued injury, reperfusion-induced injury, and the no-reflow phenomenon. The success of reperfusion therapies also hinges on timing and tissue condition after stroke. Defining these time and tissue windows more precisely could refine stroke interventions, potentially expanding effective reperfusion opportunities tailored to individual patients, thereby reducing the incidence of futile reperfusion. This perspective article delves into the complexities of futile reperfusion and the critical roles of time and tissue windows in determining stroke outcomes.