Opioid-related xylazine toxicity manifesting as myonecrosis, rhabdomyolysis, multifocal ischemic cerebral infarcts, and cerebral edema.

This article provides a report of a case of organ dysfunction, myonecrosis, rhabdomyolysis, multifocal ischemic cerebral infarcts, and cerebral edema after a patient's use of xylazine and fentanyl. Within the US opioid epidemic, xylazine is emerging as a troubling national sub-story. The prevalence of xylazine within illicitly manufactured opioids and the proportion of opioid-involved overdose deaths with detected xylazine are rising dramatically, the latter increasing 276% between 2019 and 2022. A 27-year-old woman with opioid use disorder, active intravenous drug use, and prior bacteremia presented to our institution's emergency department (ED) with left lower extremity pain and associated weakness, new acute bilateral hearing loss, multiple electrolyte derangements, and cerebral infarcts followed by cerebral edema, leading to an emergent sub-occipital decompressive craniectomy and placement of an external ventricular drain. A definitive mechanism was not determined; however, we hypothesized that xylazine toxicity played a role in her clinical presentation, which could have future clinical implications, including the possibility to incorporate xylazine as part of toxicology screens.

Association of Autonomic Storming with Urinary Catheter Removal in NMDA Receptor Encephalitis: A Case Report.

We present a case of a 47-year-old female who presented with altered mental status and was found to have severe anti-NMDA receptor encephalitis. Her intensive care unit course was complicated by paroxysmal sympathetic storming. She also had urinary retention for which a catheter was placed early in her admission, but attempts at removal were associated with worsening storming. Her average Clinical Features Scale score was 5.9 when the catheter was not in place compared to 3.6 with the catheter in place. This is the first case report to our knowledge demonstrating an association between urinary catheter removal and autonomic storming in anti-NMDA receptor encephalitis.

Cerebral Microdialysis in Neurocritical Care.

PURPOSE OF REVIEW: A major goal in neurocritical care is to monitor for and prevent secondary brain injuries. However, injuries occurring at the cellular and molecular levels evade detection by conventional hemodynamic monitoring and the neurological exam. Cerebral microdialysis (CMD) is an invasive means of providing nearly continuous measurements of cerebral metabolism and is a promising tool that can detect signs of cellular distress before systemic manifestations of intracranial catastrophe. RECENT FINDINGS: In this review, we describe the technique of CMD and the common biomarkers used to monitor cerebral energy metabolism. We examine the published evidence on how CMD data reflect secondary injuries and improve understanding of the pathophysiology of traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage. We also discuss some of the caveats of the technique, including how CMD probe position affect the sensitivity of capturing energy failures, and how abnormal levels of cerebral glucose and lactate can reflect different states of cerebral energy metabolism. In order to best incorporate cerebral metabolic monitoring into the management of neurocritical care patients, neurointensivists must be familiar with the nuances in the limitations as well as the interpretations of data obtained from cerebral microdialysis.

Cerebral Microdialysis.

A variety of neuromonitoring techniques are available to aid in the care of neurocritically ill patients. However, traditional monitors lack the ability to measure brain biochemistry and may provide inadequate warning of potentially reversible deleterious conditions. Cerebral microdialysis (CMD) is a safe, novel method of monitoring regional brain biochemistry. Analysis of CMD analytes as part of a multimodal approach may help inform clinical decision making, guide medical treatments, and aid in prognostication of patient outcome. Its use is most frequently documented in traumatic brain injury and subarachnoid hemorrhage. Incorporating CMD into clinical practice is a multidisciplinary effort.

Variability in Diagnosis and Treatment of Ventilator-Associated Pneumonia in Neurocritical Care Patients.

BACKGROUND: Clinical approach to ventilator-associated pneumonia (VAP) in the neurocritical care unit (NCCU) varies widely among physicians despite training and validated criteria. METHODS: Prospective observational study of all mechanically ventilated patients with suspected VAP over 18 months in an academic NCCU. Patients meeting VAP criteria by a surveillance program (SurvVAP) were compared to treated patients who did not meet surveillance criteria (ClinVAPonly). We identified appropriate/potentially inappropriate antibiotic treatment and factors associated with excessive antibiotic days (EAD). RESULTS: Of 622 ventilated patients, 83 cases were treated as VAP. Of these, 26 (31.3 %) had VAP by CDC criteria (SurvVAP) (VAP rate = 7.3 cases/1,000 ventilator days). Clinical features significantly more prevalent in SurvVAP cases (vs. ClinVAPonly) were change in sputum character, tachypnea, oxygen desaturation, persistent infiltrate on chest X-ray and higher clinical pulmonary infection score, but not positive sputum culture. Treatment with pneumonia-targeted antibiotics for >8 days was significantly more common in ClinVAPonly versus SurvVAP patients (73.7 vs. 30.8 %, p < 0.001) even after excluding patients with other infections (p = 0.001). Based on current guidelines, the ClinVAPonly group contributed 225 EAD, including 38 vancomycin days, 70 piperacillin-tazobactam days and 85 cephalosporin days with cost figure over four times that of EAD in SurvVAP group. No pre-specified factors were associated with continued VAP treatment beyond 8 days. CONCLUSIONS: Incongruency between clinically and surveillance-defined VAP is common in acute neurological disease although outcomes did not differ between groups. Clinician behaviors rather than clinical factors may contribute to prolonged prescribing.

Management of intracerebral pressure in the neurosciences critical care unit.

Management of intracranial pressure in neurocritical care remains a potentially valuable target for improvements in therapy and patient outcomes. Surrogate markers of increased intracranial pressure, invasive monitors, and standard therapy, as well as promising new approaches to improve cerebral compliance are discussed, and a current review of the literature addressing this metric in neuroscience critical care is provided.

Use of Transcranial Doppler (TCD) ultrasound in the Neurocritical Care Unit.

Transcranial Doppler (TCD) is a portable device that uses a handheld 2-MHz transducer. It is most commonly used in subarachnoid hemorrhage where cerebral blood flow velocities in major intracranial blood vessels are measured to detect vasospasm in the first 2 to 3 weeks. TCD is used to detect vasospasm in traumatic brain injury and post-tumor resection, measurement of cerebral autoregulation and cerebrovascular reactivity, diagnosis of acute arterial occlusions in stroke, screening for patent foramen ovale and monitoring of emboli. It can be used to detect abnormally high intracranial pressure and for confirmation of total cerebral circulatory arrest in brain death.

Brain code and coma recovery: aggressive management of cerebral herniation.

Cerebral herniation occurs due to lateral or vertical shifts in brain tissue as a complication of an intra- or extra-axial nervous system pathology. Midline shift of midline brain structures has been independently associated with poor outcome in a variety of neurologic injuries. Herniation may present as a subacute phenomenon constituting mild and progressive alteration of consciousness or as a hyperacute scenario wherein there is rapid decompensation of intracranial compliance. If left uncontrolled, cerebral herniation will lead to destruction of arousal mechanisms and result in a comatose state. A protocol-based approach for the management of herniation has the potential to minimize or reverse these shifts and in conjunction with clinical examination, radiologic data and neuromonitoring techniques offer the option of preventing a second catastrophe. In this article, the authors discuss the mechanisms that lead to coma in brain-herniating patients and the treatment choices that have been successfully used in this patient population.

Early prognostication in acute brain damage: where is the evidence?

PURPOSE OF REVIEW: Early prognostication in acute brain damage remains a challenge in the realm of critical care. There remains controversy over the most optimal methods that can be utilized to predict outcome. The utility of recently reported prognostic biomarkers and clinical methods will be reviewed. RECENT FINDINGS: Recent guidelines touch upon prognostication techniques as part of management recommendations. In addition to novel laboratory values, there have been few reports on the use of clinical parameters, diagnostic imaging techniques, and electrophysiological techniques to assist in prognostication. SUMMARY: Although encouraging, newer markers are not capable of providing accurate estimates on outcomes in acute injuries of the central nervous system. Traditional markers of prognostication may not be applicable in the light of newer and effective therapies (i.e. hypothermia). Substantial research in the field of outcome determination is in progress, but these studies need to be interpreted with caution.

The prevention and regression of atherosclerotic plaques: emerging treatments.

Occlusive vascular diseases, such as sudden coronary syndromes, stroke, and peripheral arterial disease, are a huge burden on the health care systems of developed and developing countries. Tremendous advances have been made over the last few decades in the diagnosis and treatment of atherosclerotic diseases. Intravascular ultrasound has been able to provide detailed information of plaque anatomy and has been used in several studies to assess outcomes. The presence of atherosclerosis disrupts the normal protective mechanism provided by the endothelium and this mechanism has been implicated in the pathophysiology of coronary artery disease and stroke. Efforts are being put into the prevention of atherosclerosis, which has been shown to begin in childhood. This paper reviews the pathophysiology of atherosclerosis and discusses the current options available for the prevention and reversal of plaque formation.

Metabolic, renal, and nutritional consequences of bariatric surgery: implications for the clinician.

Management of obesity-associated comorbidities costs about $60 billion/year, about 5% of total US healthcare expenditure. Bariatric surgery is the only proven effective weight loss therapy for severely obese patients with a BMI > or =35 kg/m2. Bariatric surgery produces long-term weight loss, improves quality of life, and reduces the number of sick days and medication costs. Surgery has a profound effect on the metabolic milieu and nutritional status from the first few days after surgery, even before significant weight loss has been achieved. Metabolic effects of bariatric surgery reduce obesity-related comorbidities like type 2 diabetes, hypertension, metabolic syndrome, and cardiovascular disease risk. Improvement in renal function is seen, but adverse effects like oxalate nephropathy can lead to chronic kidney disease or end-stage renal disease (CKD/ESRD). Surgery can also lead to micronutrient deficiencies, making dietary supplementation necessary. Reduction in insulin resistance and hypertension after surgery makes medication adjustment imperative. Improvement in comorbidities and nutritional deficiencies after bariatric surgery has important clinical implications.

Neuropsychological deficits associated with Complex Regional Pain Syndrome.

We sought to elucidate the existence of neuropsychological subtypes in Complex Regional Pain Syndrome (CRPS). One hundred thirty seven patients with CRPS were administered tests that assess executive control, naming/lexical retrieval, and declarative memory. A 2-step cluster analysis that does not require any a priori specification regarding the number of clusters, classified patients into three groups. Group 1 obtained scores that were in the average range on all tests (n = 48; normal CRSP group). Group 2 (n = 58; dysexecutive CRSP group) presented with mild impairment or statistically low average test performance on working memory/verbal fluency tests. Group 3 (n = 31; global CRSP group) produced scores in the statistically low average/borderline range on all tests with particularly reduced scores on naming/declarative memory tests. Between-group analyses found that the CRPS group 1 obtained higher scores than CRPS groups 2 and 3 on all tests. However, groups 2 and 3 were equally impaired on executive tests. CRPS group 3 was impaired on tests of naming/memory tests compared to the other groups. Significant neuropsychological deficits are present in 65% of patients, with many patients presenting with elements of a dysexecutive syndrome and some patients presenting with global cognitive impairment.