Citations

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.

Objective: To assess the long-term outcomes of patients hospitalized with severe West Nile neuroinvasive disease. Design: Retrospective cohort. Setting: Patients admitted to a referral center (Saint Mary’s Hospital, Mayo Clinic). Participants: Twenty-six patients with West Nile neuroinvasive disease were identified by retrospective search of electronic database of Saint Mary’s Hospital from January 1999 to November 2016. Interventions: Retrospective electronic medical records review and prospective telephone follow-up. Measurements and Main Results: Functional disability and cognitive outcomes were evaluated with the modified Rankin Scale and the Telephone Interview for Cognitive Status scores. Data on the time that the patient returned home after the hospitalization for West Nile neuroinvasive disease and the time of return to work were also collected. We identified 26 patients (81% males), 59 ± 17 years old. After a median hospital stay of 14.5 days (3–126), four patients died and 90% of survivors had a modified Rankin Scale of 3–5. Two additional patients died, and 80% of survivors had a modified Rankin Scale of 0–2 after a median follow-up of 73 months (1–144). Seven patients had cognitive impairment, which was severe in two of them. The combination of encephalitis and acute flaccid paralysis at presentation was associated with lower likelihood of returning home within 1 month after discharge (p < 0.01). Patients who required mechanical ventilation were more likely to have a modified Rankin Scale of 3–5 at last follow-up (p = 0.03), less likely to return home within 1 month of discharge (p < 0.01), less likely to return to their jobs (p < 0.01), and showed a trend toward having cognitive impairment (p = 0.05). Conclusions: Despite having poor outcomes at discharge, most West Nile neuroinvasive disease survivors with severe early disability can recover functional independence in the long term, justifying aggressive support during the acute phase and extensive rehabilitation efforts.

Spontaneous intracranial hypotension (SIH) is an uncommon headache etiology, typically attributable to an unprovoked occult spinal CSF leak. Although frequently benign, serious complications may occur, including cerebral venous thrombosis (CVT). The objective of this study was to examine a highly complicated case of CVT attributable to SIH as a lens for understanding the heterogeneous literature on this rare complication, and to provide useful, evidence-based, preliminary clinical recommendations. A 43-year-old man presented with 1 week of headache, dizziness, and nausea, which precipitously evolved to hemiplegia. CT venography confirmed CVT, and therapeutic heparin was initiated. He suffered a generalized seizure due to left parietal hemorrhage, which subsequently expanded. He developed signs of mass effect and herniation, heparin was discontinued, and he was taken to the operating room for clot evacuation and external ventricular drain placement. Intraoperatively, the dura was deflated, suggesting underlying SIH. Ventral T-1 CSF leak was identified, which failed multiple epidural blood patches and required primary repair. The patient ultimately made a complete recovery. Systematic review identified 29 publications describing 36 cases of SIH-associated CVT. Among 31 patients for whom long-term neurological outcome was reported, 25 (81%) recovered completely. Underlying coagulopathy/risk factors were identified in 11 patients (31%). CVT is a rare and potentially lethal sequela occurring in 2% of SIH cases. Awareness of the condition is poor, risking morbid complications. Evaluation and treatment should be directed toward identification and treatment of occult CSF leaks. Encouragingly, good neurological outcomes can be achieved through vigilant multidisciplinary neurosurgical and neurocritical care.