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Introduction. Circulatory-respiratory death declaration is a common duty of physicians, but little is known about the amount of education and physician practice patterns in completing this examination. Methods. We conducted an online survey of physicians evaluating the rate of formal training and specific examination techniques used in the pronouncement of circulatory-respiratory death. Data, including level of practice, training received in formal death declaration, and examination components were collected. Results. Respondents were attending physicians (52.4%), residents (30.2%), fellows (10.7%), and interns (6.7%). The majority of respondents indicated they had received no formal training in death pronouncement, however, most reported self-perceived competence. When comparing examination components used by our cohort, 95 different examination combinations were used for death pronouncement. Conclusions. Formal training in death pronouncement is uncommon and clinical practice varies. Implementation of formal training and standardization of the examination are necessary to improve physician competence and reliability in death declarations.

Status myoclonus (SM) after cardiac arrest (CA) may signify devastating brain injury. We hypothesized that SM correlates with severe neurologic and systemic post-cardiac-arrest syndrome (PCAS). Charts of patients admitted with CA to Mayo Clinic Saint Marys Hospital between 2005 and 2019 were retrospectively reviewed. Data included the neurologic examination, ancillary neurologic tests, and systemic markers of PCAS. Nonsustained myoclonus was clinically differentiated from SM. The cerebral performance category score at discharge was assessed; poor outcome was a cerebral performance category score > 2 prior to withdrawal of life-sustaining therapies or death. Of 296 patients included, 276 (93.2%) had out-of-hospital arrest and 202 (68.5%) had a shockable rhythm; the mean time to return of spontaneous circulation was 32 ± 19 min. One hundred seventy-six (59.5%) patients had a poor outcome. One hundred one (34.1%) patients had myoclonus, and 74 (73.2%) had SM. Neurologic predictors of poor outcome were extensor or absent motor response to noxious stimulus (p = 0.02, odds ratio [OR] 3.8, confidence interval [CI] 1.2–12.4), SM (p = 0.01, OR 10.3, CI 1.5–205.4), and burst suppression on EEG (p = 0.01, OR 4.6, CI 1.4–17.4). Of 74 patients with SM, 73 (98.6%) had a poor outcome. A nonshockable rhythm (p

Coma trajectories are characterized by quick awakening or protracted awakening. Outcome is bookended by restored functionality or permanent cognitively and physically debilitated states. Given the stakes, prognostication cannot be easily questioned as a judgment call, and a scientific underpinning is elemental. Conventional wisdom in determining coma-outcome trajectories posits that (1) predictive models are better than personal experiences, (2) self-fulfilling prophesy is unchecked and driven by nihilism, with little regard for prior probability outcomes, and (3) recovery is impacted by patients' prior wishes and preexisting medical conditions-but also by what families are told about the patient's state and anticipated clinical course. Moreover, a predicted good outcome can be offset by a major subsequent complication, or a predicted poor outcome can be offset by aggressive care. This article examines some of these concepts, including how we decide on aggressiveness of care, how we judge quality of life, and the impact on outcome. Most patients who awaken quickly do well and can resume their pretrauma injury lives. In worse off, slow-to-awaken patients, outcomes are a mixed bag of limited innate resilience, depleted cognitive and physical reserves, and adjusted quality of life. Bias and noise are factors not easily measured in outcome prediction, but their influence on recovery trajectories raises some troubling issues.

BACKGROUND AND IMPORTANCE Progressive episodic spells of altered levels of consciousness, often advancing to include paroxysmal autonomic instability, may be indicative of a diencephalic dysfunction underlying spontaneous intracranial hypotension (SIH). A rare, and often indolent, etiology may be spinal cerebrospinal fluid (CSF) leak-an elusive diagnosis, especially in cases of CSF-venous fistula (CVF) that are often missed on routine computed tomography (CT) myelography and magnetic resonance imaging (MRI). CLINICAL PRESENTATION We report an unusual case of a 50-yr-old woman who presented with rapidly progressive cyclical, self-resolving episodes of altered mentation and decreased arousal later in the day. Scrutiny of serial brain MRIs led to a diagnosis of SIH, with severe downward diencephalic and brain stem displacement-resulting in cerebral aqueduct occlusion with obstructive hydrocephalus. Initial clinical improvement occurred with CSF diversion, but the patient quickly deteriorated-developing diencephalic spells, including extensor posturing and severely depressed levels of consciousness. Clinical improvement was seen with stopping CSF diversion and Trendelenburg-positioning. After intensive spinal imaging, dynamic CT myelography identified a left T10 nerve root diverticula and CSF-venous fistula. Surgical obliteration resulted in rapid, profound neurological improvement, and ultimately full neurological recovery by 1 yr. CONCLUSION In our patient, worsening episodes of confusion, postural headaches, and autonomic instability developed due to SIH, which induced profound downward displacement and compression of the diencephalon and brain stem, and accompanied by subsequent obstructive hydrocephalus. Diagnostic persistence identified the CVF, which had caused the complex multifold pathophysiology and clinical presentation. If suspicion remains high for CVF, persistent spinal imaging, particularly with dynamic myelography, may be crucial.

Heparin-induced thrombocytopenia (HIT) causes thrombosis and thrombocytopenia, usually due to prior heparin exposure, so-called classical HIT. However, in the autoimmune form, the signs and symptoms of HIT occur without prior heparin exposure. Development of cerebral venous sinus thrombosis (CVST) secondary to HIT is a rare occurrence, with relatively few reports in the literature. There is a need to better understand the clinical presentation and treatment paradigms in these rare cases. Therefore, we present the first systematic review of CVST occurring in classical and autoimmune HIT. Cases of HIT-induced CVST were identified through a systematic search of Pubmed from the date of inception to March 2021. Literature search revealed 21 cases of HIT and associated CVST with six cases (28.6%) of autoimmune HIT. Patients presented with signs and symptoms consistent with increased intracranial pressure, intracerebral hemorrhage (ICH), and/or focal neurologic deficits. Headache was the most common symptom with 12 patients (60.0%) presenting as such. 10 patients (47.6%) included in the study developed ICH. Non-heparin anticoagulants, especially direct thrombin inhibitors, were the first-line treatment for the majority of patients (55.6%). Intravenous immunoglobulin (IVIG) was used as treatment for select patients (16.7%) with autoimmune HIT. Few patients received surgical intervention for CVST (14.3%) or ICH (30.0%). Four patients had a full recovery, four patients had residual deficits, and seven patients ultimately expired. Symptoms of HIT-induced CVST are often related to CNS dysfunction. Non-heparin anticoagulants are important to treat CVST, even when patients have concomitant ICH, and may be supplemented with IVIG if treating autoimmune HIT. Rapid identification and treatment of HIT-induced CVST is imperative in order to prevent morbidity and mortality.

Neuromuscular respiratory failure can result from any disease that causes weakness of bulbar and/or respiratory muscles. Once compensatory mechanisms are overwhelmed, hypoxemic and hypercapnic respiratory failure ensues. The diagnosis of neuromuscular respiratory failure is primarily clinical, but arterial blood gases, bedside spirometry, and diaphragmatic ultrasonography can help in early assessment. Intensive care unit (ICU) admission is indicated for patients with severe bulbar weakness or rapidly progressing appendicular weakness. Intubation should be performed electively, particularly in patients with dysautonomia. Patients with an underlying treatable cause have the potential to regain functional independence with meticulous ICU care.

Purpose The optimal ventilatory settings in patients after cardiac arrest and their association with outcome remain unclear. The aim of this study was to describe the ventilatory settings applied in the first 72 h of mechanical ventilation in patients after out-of-hospital cardiac arrest and their association with 6-month outcomes. Methods Preplanned sub-analysis of the Target Temperature Management-2 trial. Clinical outcomes were mortality and functional status (assessed by the Modified Rankin Scale) 6 months after randomization. Results A total of 1848 patients were included (mean age 64 [Standard Deviation, SD = 14] years). At 6 months, 950 (51%) patients were alive and 898 (49%) were dead. Median tidal volume (V-T) was 7 (Interquartile range, IQR = 6.2-8.5) mL per Predicted Body Weight (PBW), positive end expiratory pressure (PEEP) was 7 (IQR = 5-9) cmH(2)0, plateau pressure was 20 cmH(2)0 (IQR = 17-23), driving pressure was 12 cmH(2)0 (IQR = 10-15), mechanical power 16.2 J/min (IQR = 12.1-21.8), ventilatory ratio was 1.27 (IQR = 1.04-1.6), and respiratory rate was 17 breaths/minute (IQR = 14-20). Median partial pressure of oxygen was 87 mmHg (IQR = 75-105), and partial pressure of carbon dioxide was 40.5 mmHg (IQR = 36-45.7). Respiratory rate, driving pressure, and mechanical power were independently associated with 6-month mortality (omnibus p-values for their non-linear trajectories: p < 0.0001, p = 0.026, and p = 0.029, respectively). Respiratory rate and driving pressure were also independently associated with poor neurological outcome (odds ratio, OR = 1.035, 95% confidence interval, CI = 1.003-1.068, p = 0.030, and OR = 1.005, 95% CI = 1.001-1.036, p = 0.048). A composite formula calculated as [(4*driving pressure) + respiratory rate] was independently associated with mortality and poor neurological outcome. Conclusions Protective ventilation strategies are commonly applied in patients after cardiac arrest. Ventilator settings in the first 72 h after hospital admission, in particular driving pressure and respiratory rate, may influence 6-month outcomes. Funding Agencies|Universita degli Studi di Genova; Swedish Research Council [Vetenskapsradet]; Swedish Heart-Lung Foundation; Stig and Ragna Gorthon Foundation; Knutsson Foundation; Laerdal Foundation; Hans-Gabriel and Alice Trolle-Wachtmeister Foundation for Medical Research; Region Skane; Swedish National Health Service

Metabolic derangements, when acute and severe, affect brain function. This presents mostly with a marked decline in the level of consciousness, resulting in impaired responsiveness, abnormal receptivity, impaired content, and loss of memory retention. The term metabolic encephalopathy has been used but is conjecture that can be challenged in the age of modern neuroimaging. We now recognize that many metabolic encephalopathies may involve structural lesions and at an early stage. Common clinical conundrums are the evaluation of the degree of brain injury and its recoverability. This review discusses the appropriate terminology for these conditions, the diagnostic approach, therapy recommendations, and prediction of recovery potential. In evaluating a presumed metabolic cause for encephalopathy, we must (1) search for and rule out structural injury to the brain despite an obvious explanatory metabolic derangement, (2) recognize that several confounding conditions often co-exist, and (3) acknowledge that resolution of brain dysfunction may be protracted despite normalization of laboratory values.

In this article, we commemorate the centenary of the discovery and clinical implementation of hyperosmolar therapy for the treatment of increased intracranial pressure (ICP). Following the pioneering work of anatomists Weed and McKibben in 1919, the use of hypertonic solutions was soon adopted into clinical practice, even though the preferred hypertonic agent, route of administration, and ideas regarding the physiological mechanism by which it reduced ICP diverged. These divergent conceptions and practices have continued to surround the use of hyperosmolar therapy into present times.

A clinical history leads to an examination, tests and a diagnosis. This time-honored sequence in medicine remains valid in critical illness, but in the heat of the moment there is a quickly appearing inevitable sketchiness. Intensivists should never be too unquestioning, too comfortable with incomplete information, or too unwilling to start over if information is muddled or contradictory. No scale in neurology looks at history. There is no tool or requirement to provide a standard system of communication. I review the essentials of history taking in a neurocritically ill patient. Examples of the value of a good medical history are shown but also the familiar biases when asking questions. There are obstacles, errors of commission and omission, and the importance of recognition of a clinical trajectory.

Diffuse subarachnoid hemorrhage is commonly attributed to the rupture of intracranial aneurysms or other vascular malformations. Non-aneurysmal hemorrhages often have a characteristic pattern or clear mechanism (e.g. trauma) with an often more benign clinical course. We report the case of a diffuse non-aneurysmal subarachnoid hemorrhage due to sudden gravitational changes encountered during complex airflight maneuvers, complicated by hydrocephalus and cerebral vasospasm. This case illustrates a rare phenomenon that may again be encountered in the future with the advent and advancement of civilian spaceflight.