Rabinstein, Alejandro A.

Objectives: Persistent cognitive impairment after critical illness is an important healthcare problem forecasted to worsen in the near future. However, the epidemiology is insufficiently explored. We aimed to determine potentially modifiable risk factors during ICU hospitalization that play a significant role in developing persistent cognitive impairment. Design: An observational case-control study. Settings: Mayo Clinic ICUs between July 1, 2004, and November 20, 2015. Patients: We conducted a study nested in a large cohort of 98,227 adult critically ill patients. Using previously validated computable phenotypes for dementia and cognitive impairment, we determined the onset of cognitive impairment relative to ICU hospitalization and associated risk factors. The primary endpoint of the study was new and persistent cognitive impairment documented between 3 and 24 months after ICU discharge. Interventions: Unadjusted and adjusted analyses were performed to identify potentially modifiable risk factors during ICU hospitalization. Measurements and Main Results: Among 21,923 unique patients identified as cognitively impaired (22% of the entire ICU cohort), 2,428 (2.5%) developed incident new and persistent cognitive dysfunction after the index ICU admission. Compared with age- and sex-matched ICU controls (2,401 pairs), cases had higher chronic illness burden (Charlson Comorbidity Index, 6.2 vs 5.1; p < 0.01), and were more likely to have multiple ICU stays (22% vs 14%; p < 0.01). After adjustment for baseline differences, new and persistent cognitive dysfunction was associated with higher frequency of acute brain failure in the ICU, a higher exposure to severe hypotension, hypoxemia, hyperthermia, fluctuations in serum glucose, and treatment with quinolones or vancomycin. Association with sepsis observed in univariate analysis did not persist after adjustment. Conclusions: Cognitive dysfunction is highly prevalent in ICU patients. Incident new and persistent cognitive impairment is less common but important, potentially preventable problem after critical illness. Chronic comorbidities and number of ICU stays increase the risk of post-ICU cognitive dysfunction irrespective of age. Modifiable ICU exposures were identified as potential targets for future prevention trials.

Endovascular therapy with mechanical thrombectomy is a formidable treatment for severe acute ischemic stroke caused by occlusion of a proximal intracranial artery. Its strong beneficial effect is explained by the high rates of very good and excellent reperfusion achieved with current endovascular techniques. However, there is a sizable proportion of patients who do not experience clinical improvement despite successful recanalization of the occluded artery and reperfusion of the ischemic territory. Factors such as baseline reserve, collateral flow, anesthesia and systemic factors have been identified as potential culprits for lack of improvement in the setting of timely and successful revascularization. Older age, baseline disability and perhaps radiological markers of chronic brain injury can affect the prognosis of patients treated with endovascular therapy. Collateral flow is a major determinant of outcome after endovascular therapy and it is manifested by the size of the core in relation to the volume of the salvageable tissue. Parenchymal and vascular imaging can help assess the quality of collateral flow, but the optimal radiological strategy for daily practice (i.e. the optimal combination of rapid availability and diagnostic precision) has not been established. A sizable body of observational evidence indicates that acute hypertension, hyperglycemia and fever are associated with worse outcomes after a stroke even after optimal reperfusion with endovascular therapy. Lastly, current randomized controlled trials in anesthesia for stroke demonstrate similar rates of good functional outcome between general anesthesia and conscious sedation suggesting equipoise exists.

Introduction: Elsberg syndrome (ES) is a rarely recognized cause of cauda equina syndrome and lower thoracic myelitis, mainly linked to reactivation, or occasionally primary, infection with herpes simplex virus type 2. West Nile virus neuroinvasive disease is rarely considered in the differential diagnosis of patients with ES. Case Report: A 63-year-old man with pancreatic cancer in remission and polymyalgia rheumatica on low-dose prednisone presented with a 10-day history of low-back pain and a viral-type illness with low-grade fever, nausea, and vomiting. Days later, he developed left leg monoparesis, neurogenic bladder, and bowel. Magnetic resonance imaging of the lumbar spine revealed a hyperintense signal abnormality within the central spinal cord and conus medullaris with mild swelling of the conus. Cells, proteins, and glucose in cerebrospinal fluid were 67/mm 3 , 70 mg/dL, and 58 mg/dL, respectively. Serology was positive for West Nile virus IgM. Nerve conduction studies and electromyography showed an acute motor neurogenic process affecting left lumbosacral segments. Conclusions: West Nile virus neuroinvasive disease is an uncommon condition that should be considered in patients with ES. Determining the etiology of ES in the acute setting may avoid unnecessary diagnostic investigations and treatments.

OBJECTIVEClinical trials forming the basis of current guidelines for the management of intracranial aneurysms have relied on patient-reported modified Rankin Scale (mRS) scores to assess functional outcome. The effect of patient demographics on perception of disability and, by extension, patient-reported mRS score, is not well understood.METHODSA consecutive series of patients with a previously treated or untreated unruptured intracranial aneurysm (UIA) prospectively underwent a structured interview with a trained nurse. At the conclusion of this interview, the patients were assigned an mRS score in accordance with their degree of disability. During the same visit, patients were also required to grade themselves on a paper sheet containing the mRS and corresponding information. Data on patient and aneurysm characteristics were also collected during the same visit. Agreement between patient- and nurse-reported mRS scores was assessed using Cohen’s kappa coefficient. The effect of patient demographics on the frequency of higher patient- than nurse-reported mRS scores was assessed using the Pearson’s chi-square and Fisher’s exact tests.RESULTSA total of 209 patients with a UIA were included in the study, 38 of whom (18.2%) had undergone previous treatment. The majority of patients were female (161/209, 77.0%), and the mean age of the cohort was 60.2 years (SD 13.7 years). Agreement between patient- and nurse-reported mRS scores occurred in 72.7% of cases (95% CI 66.3%–78.3%), with a kappa coefficient of 0.58 (95% CI 0.49–0.67). Patients younger than 75 years were more likely to report a higher mRS score than the nurse (19.4% vs 3.4%, p = 0.034). Among female patients, those without a college degree were more likely to report a higher mRS score than the nurse (22.5% vs 9.5%, p = 0.035).CONCLUSIONSThe results suggest that patient demographics may influence perception of disability. These findings should be considered when using patient-reported mRS scores to determine functional outcome.

Abstract While revascularization of the acutely or chronically occluded internal carotid artery has become commonplace with modern endovascular techniques, revascularization of an acutely occluded common carotid artery (CCA) is a controversial procedure with unique challenges. These challenges can be related to the lack of observable markers for identifying vessels during navigation or for identifying the exact location and extent of occlusion within the CCA, in addition to wide-ranging treatment risks. In this video, we illustrate the controversial revascularization of a 68-yr-old woman with an acute CCA occlusion who presented with fluctuating neurological symptoms. We believed treatment to be indicated by the lack of adequate collaterals on the intracranial CTA, and fluctuating symptoms in the absence of an intracranial major vessel occlusion, suggesting that the CCA occlusion was exerting important hemodynamic effects and at risk of causing a major stroke without revascularization, despite a low initial NIH stroke score. Though acute recanalization of patients with low NIH stroke score with stent-angioplasty is a controversial procedure, we believed it to be necessary in the case of our patient and believe it will likely be the focus of the next wave of large clinical trials dedicated to acute stroke.

Purpose of review There is an increasing realization in the critical care community that persistent cognitive impairment is a common and disabling complication after ICU care. In this review, we discuss the best available information on the magnitude of the problem, its possible mechanisms, risk factors, management strategies and prognosis. Recent findings Estimates of the incidence of persistent cognitive impairment after critical illness vary widely across studies but the most solid prospective information indicates that it may occur in 20–40% of patients discharged from the ICU. From the available evidence, it is difficult to discriminate between de novo cognitive impairment and exacerbation of preexistent cognitive decline. The pathogenesis is multifactorial but inflammatory mechanisms causing derangements of endothelial function and blood–brain barrier integrity might play an important role. Brain atrophy and white matter tract disruption can be structural correlates of the cognitive decline. Prolonged delirium in the ICU is the strongest risk factor for the development of subsequent persistent cognitive impairment. Management strategies are currently limited to those designed to prevent and improve delirium. Cognitive trajectories may vary but a substantial proportion of patients with cognitive impairment 3 months after ICU discharge are still cognitively impaired at 12 months. Summary Persistent cognitive impairment is a major complication of critical illness. Our knowledge of this problem remains incomplete. Collaborative research is indispensable to improve our understanding of this disabling sequel and to identify ways to prevent it.

Objectives: To evaluate the epidemiology of hyperammonemia unrelated to liver failure in the critical care setting. Design: Retrospective case series. Setting: Critically ill patients admitted to ICUs at Mayo Clinic, Rochester, MN (medical ICU, two mixed medical-surgical ICUs, coronary care unit, or the cardiosurgical ICU) between July 1, 2004, and October 31, 2015. Patients: Adult critically ill patients with hyperammonemia not related to acute or chronic liver failure. We excluded patients with diagnosis of moderate or severe liver disease, hyperbilirubinemia, and patients who denied the use of their medical records. Interventions: None. Measurements and Main Results: Of 3,908 ICU patients with hyperammonemia, 167 (4.5%) had no evidence of acute or chronic liver failure. One-hundred one patients (60.5%) were male with median age of 65.7 years (interquartile range, 50–74.5 yr) and median serum ammonia level of 68 µg/dL (interquartile range, 58–87 µg/dL). Acute encephalopathy was present in 119 patients (71%). Predisposing conditions included malnutrition 27 (16%), gastric bypass six (3.6%), total parenteral nutrition four (2.4%); exposure to valproic acid 17 (10%); status epilepticus 11 (6.6%), high tumour burden 19 (11.3%), and renal failure 82 (49.1%). Urea cycle defects were diagnosed in seven patients (4.1%). Hospital mortality was high (30%), and median ammonia level was higher among the nonsurvivors (74 vs 67 µg/dL; p = 0.05). Deaths were more likely in hyperammonemic patients who were older (p = 0.016), had greater illness severity (higher Acute Physiology and Chronic Health Evaluation III score, p < 0.01), malignancy (p < 0.01), and solid organ transplantation (p = 0.04), whereas seizure disorder was more common in survivors (p = 0.02). After adjustment, serum ammonia level was not associated with increased mortality. Conclusions: Hyperammonemia occurs in a substantial minority of critically ill patients without liver failure. These patients have a poor prognosis, although ammonia level per se is not independently associated with mortality. Serum ammonia should be measured when risk factors are present, such as nutritional deficiencies and protein refeeding, treatment with valproic acid, high tumour burden, and known or suspected urea cycle abnormalities.