Patterns and predictors of serious surf-related injuries in Hawaii

Introduction Surfing is a popular leisure activity with inherent risk of injury that many participants fail to mitigate. There is a paucity of literature reporting severe surf-related trauma and associated risk factors. Methods A retrospective observational study of registry data from Honolulu’s main trauma center assessing surf-related injuries and risk factors for severe injury was performed between January 1, 2014 and December 31, 2018. Results Spine (35.1%), face (17.5%), and head (12.3%) injuries were the most common injuries identified in this cohort. A number of predictors for severe injury as well as serious spine injury were identified. Major risk factors for severe injury and serious spine injury included location of injury on Maui (Severe injury: OR 6.79, 95%CI 1.43–40.35, p = 0.0217; serious spine injury: OR 7.27, 95%CI 1.39–58.24, p = 0.0308) and being from one of the 48 contiguous states (severe injury: OR 3.33, 95%CI 1.10–10.98, p = 0.0388; serious spine injury: OR 2.95, 95%CI 1.08–8.46, p = 0.0379). Conclusion Understanding the nature of surf-related injuries and who is at risk can help to inform safety interventions that may prevent severe, sometimes irreversible injury. Efforts should be made to increase public awareness to the potential risk of surf-related activities.

AFM nanoindentation reveals decrease of elastic modulus of lipid bilayers near freezing point of water

Cell lipid membranes are the primary site of irreversible injury during freezing/thawing and cryopreservation of cells, but the underlying causes remain unknown. Here, we probe the effect of cooling from 20 °C to 0 °C on the structure and mechanical properties of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) bilayers using atomic force microscopy (AFM) imaging and AFM-based nanoindentation in a liquid environment. The Young’s modulus of elasticity (E) at each temperature for DPPC was obtained at different ionic strengths. Both at 20 mM and 150 mM NaCl, E of DPPC bilayers increases exponentially –as expected–as the temperature is lowered between 20 °C and 5 °C, but at 0 °C E drops from the values measured at 5 °C. Our results support the hypothesis that mechanical weakening of the bilayer at 0 °C is produced by structural changes at the lipid-fluid interface.

Abstract 11: Early Magnetic Resonance Imaging to Quantify Ischemic Brain Insult Early Following Cardiac Arrest in a Swine Model

Introduction: Hypoxic ischemic brain injury (HIBI) results from loss of oxygen or perfusion during cardiac arrest and is the most common cause of death/disability in patients surviving to admission. Diagnostic tests are crucial to identify irreversible injury thresholds for neuroprognostication. MRI DTI can detect cellular injury in response to HIBI, but imaging timing and severity of hypoxia vary widely. Hypothesis: We hypothesized that a model with fixed periods of ischemia followed by both standardized reperfusion and time to image acquisition would demonstrate a reliable gradient of injury. Such a model would allow neuroprotective strategies to be tested using early imaging biomarkers to quantify effects on cytoarchitecture. Methods: Eleven healthy swine (49 + 5 kg) under isoflurane anesthesia underwent control MRI with DTI at b2000/20 directions. Two animals each were then randomized to sham, 10, 15, 20, and one to 30-minutes of arrest. For reperfusion, extracorporeal membrane oxygenation (ECMO) catheters were placed in the distal aorta and right atrium, after which ventricular fibrillation was induced by a bipolar pacing catheter. Following the fixed period of ischemia, animals were reperfused at 2.8-3.5 L/min with unblended oxygenated blood. After 4 minutes they were defibrillated. Over two hours they were weaned from pump and decannulated with epinephrine and fluid boluses for hemodynamic support. Animals were re-imaged within two hours post-resuscitation using the same pre-arrest protocol. Whole brain ADC measurements were performed in the gray and white matter. Results: Baseline hemodynamic parameters: BP, Heart Rate, End-Tidal CO2, and SpO2 were similar between animals. When comparing pre- to post-arrest MRI, there was a strong linear correlation between percent gray matter ADC change (r=-0.87, p<0.001) and white matter ADC change (r=-0.79, p<0.001) with ischemia duration. Conclusion: MRI DTI changes observed following fixed periods of ischemia with ADC in gray and white matter correlated well with ischemia duration in the first few hours post arrest. These findings support the feasibility of MRI for measuring severity of insult in HIBI and an animal model that might serve as translational endpoint for neuroprotectant strategies.

Cerebrospinal Physiology

With its high metabolic rate and lack of substrate stores, the brain is dependent on a constant supply of oxygen and glucose. If blood flow stops, alterations in brain function occur within seconds and irreversible injury can occur within a few minutes. Many patients admitted to neurosciences intensive care units have acute strokes, are eligible for endovascular procedures, and may need other measures to preserve adequate cerebral blood flow. An understanding of the blood supply, venous drainage, and factors affecting cerebral perfusion is thus pivotal to the practice of neurologic critical care. This chapter reviews the anatomical and physiologic principles governing cerebral circulation and blood flow.

Effects of anesthesia on cerebral blood flow, metabolism, and neuroprotection

Administration of anesthetic agents fundamentally shifts the responsibility for maintenance of homeostasis from the patient and their intrinsic physiological regulatory mechanisms to the anesthesiologist. Continuous delivery of oxygen and nutrients to the brain is necessary to prevent irreversible injury and arises from a complex series of regulatory mechanisms that ensure uninterrupted cerebral blood flow. Our understanding of these regulatory mechanisms and the effects of anesthetics on them has been driven by the tireless work of pioneers in the field. It is of paramount importance that the anesthesiologist shares this understanding. Herein, we will review the physiological determinants of cerebral blood flow and how delivery of anesthesia impacts these processes.

Definition of pathogenetic variants of a hemophilic arthropathy by means of the functional assessment of microcirculation

Introduction. Better understanding of the pathogenesis of hemophilic arthropathy is crucial for prevention of irreversible injury to joints in patients with hemophilia. Research objective - to define a role of altered regulation of microcirculation in formation of joint injury in patients with hemophilia. Methods. The changes in knee and ankle joints in 82 patients with hemophilia were investigated by means of ultrasound and X-ray. Microcirculation was evaluated using computer infrared thermography and laser doppler flowmetry in joints of 44 patients and 46 healthy individuals. Results. Increased temperature and perfusion (M) are major risk factors of hemarthrosis development (RR=1.86 and RR=1.26) and are characteristic of joints with hemorrhages developing more often than 1 time per month. Increase in these indexes in joints without hemarthrosis in the anamnesis is a sign of a latent inflammation. Both decrease in the index of shunting (IS) and increase in a vibration amplitude of perfusion in the endothelial range (Amax E) are characteristic of joints with a recurrence of hemarthrosis more often than 3 times a month. Decrease in indexes of M and Amax E with concomitant increase in PSh demonstrate low risk of hemarthrosis. Conclusions. Changes of microcirculation in joints represent an important factor in the pathogenesis of hemophilic arthropathy development in the patients with variable risk of a recurrence of a hemarthrosis. Joint inflammation leads to endothelial dysfunction with poor vasospasm, to increase in Amax E and M that is a new diagnostic sign of a latent inflammation in joints. Decrease of PSh promotes recurrence of hemarthrosis because of strengthening of an imbuing of tissues of joint blood. Preservation of endothelium-mediated vasoconstriction, decrease in the neurogenic tone, increase in shunting of blood are characteristic features of hemophilic arthropathy in patients with infrequent recurrence of hemarthrosis.

Abstract 40: The Disappearing Core: Time to Re-think Irreversible Injury in This Era of Endovascular Therapy

Background and Purpose: Early and complete recanalization achieved in this new era of endovascular therapy (ET) can result in nearly imperceptible lesions on post-treatment MRI. In this context we have observed a pattern of lesion evolution on MRI that is atypical from that seen following IV tPA alone, including striking reversal of the ischemic core. We sought to determine the frequency of acute lesion reversal following ET, and its association with sustained reversal and clinical outcome. Methods: Patients were included in this study if: 1) ET for anterior territory ischemic stroke from Jan 2015 to July 2016, 2) baseline pre-ET and 24h MRI, and 3) consent for research. Two raters evaluated ADC maps for early “reversal” (defined visually as >50%) by comparing 24h to baseline. FLAIR MRI at 30d were later assessed for reversal from baseline, blinded to 24h scan. Early neurological improvement (ENI) was defined as decrease in NIHSS≥8 at 24h. Good clinical outcome defined as mRS≤2. Results: Twenty-two patients were included: median age 68.5 years, 73% women, median baseline NIHSS 19. Median time from last known well to recanalization 254 min. TICI 2b/3 in 91%. ADC reversal in 12 of 22 (55%) at 24h. Reversal at 30d was associated with 24hr (p=0.002) with two having no visually appreciable infarct at 30d. Baseline NIHSS did not differ for early reversal versus without (18.5 vs. 19.5), however NIHSS differed at discharge (1.5 vs. 8.5, p=0.003); early reversal is significantly associated with ENI (83% vs. 30%, p=0.027), but not with good clinical outcome at 30-90d (50% vs. 30%, p=0.415). Conclusions: In this new era of consistently effective ET, salvageable tissue includes not just penumbra but ischemic core, previously considered irreversibly injured. Despite lesion reversal and ENI, for some patients, independent outcome is not achieved, a finding that reinforces the need for adjunctive treatments to build upon the success of ET. Figure: Example of a patient with early ADC reversal.

Brain Multimodality Monitoring: A New Tool in Neurocritical Care of Comatose Patients

Neurocritical care patients are at risk of developing secondary brain injury from inflammation, ischemia, and edema that follows the primary insult. Recognizing clinical deterioration due to secondary injury is frequently challenging in comatose patients. Multimodality monitoring (MMM) encompasses various tools to monitor cerebral metabolism, perfusion, and oxygenation aimed at detecting these changes to help modify therapies before irreversible injury sets in. These tools include intracranial pressure (ICP) monitors, transcranial Doppler (TCD), Hemedex™ (thermal diffusion probe used to measure regional cerebral blood flow), microdialysis catheter (used to measure cerebral metabolism), Licox™ (probe used to measure regional brain tissue oxygen tension), and continuous electroencephalography. Although further research is needed to demonstrate their impact on improving clinical outcomes, their contribution to illuminate the black box of the brain in comatose patients is indisputable. In this review, we further elaborate on commonly used MMM parameters, tools used to measure them, and the indications for monitoring per current consensus guidelines.

Abstract 16939: Reversible Myocardial Ischemia Sufficient to Produce Transient Stunning Leads to Delayed Cardiac Troponin I Release That Reflects Focal Myocyte Apoptosis in the Absence of Pathological Infarction

Introduction: The release of cardiac troponin I (cTnI) after reversible ischemia is controversial. It has been hypothesized that elevations in serum cTnI in this scenario reflect selective release from an exchangeable pool rather than cellular necrosis since irreversible injury with sarcolemmal membrane disruption does not begin until ischemia exceeds 15 minutes following a total coronary occlusion. Objective: To determine whether cTnI release occurs after a brief coronary occlusion when the duration of ischemia is insufficient to induce myocyte necrosis. Methods: Closed-chest propofol-anesthetized swine (n=10) were subjected to a 10 minute LAD occlusion. Blood sampling was performed to measure serum cTnI concentrations before, during and after ischemia. Myocardial tissue was collected either 1 hour (n=5) or 24 hours (n=5) after reperfusion for pathological assessment of infarction (TTC) and apoptosis (TUNEL). Results: Regional LAD wall thickening was 60 ± 4% at baseline and became dyskinetic during coronary occlusion (-4 ± 2%, p<0.05). One hour after reperfusion, wall thickening improved but remained depressed relative to baseline, indicative of myocardial stunning (37 ± 4%, p<0.05). It returned to normal after 24 hours (59 ± 2%). Serum cTnI was 0.01 ± 0.01 ng/mL at baseline and remained unchanged at the end of ischemia. A slight increase in cTnI was observed 1 hour after reperfusion (0.06 ± 0.02 ng/mL, p<0.05 vs. baseline), followed by a marked elevation at 24 hours (1.02 ± 0.57 ng/mL, p<0.05 vs. baseline). TTC staining demonstrated no evidence of infarction. Heart tissue collected 1 hour after reperfusion demonstrated a regional increase in apoptotic myocytes (LAD: 17.7 ± 3.7 myocytes/cm 2 vs. Remote: 3.1 ± 2.0 myocytes/cm 2 , p<0.05). Myocyte apoptosis normalized 24 hours after reperfusion (LAD: 5.2 ± 2.3 myocytes/cm 2 vs. Remote: 3.6 ± 1.5 myocytes/cm 2 ) when serum cTnI remained elevated. Conclusion: A duration of reversible ischemia compatible with angina can lead to cTnI release that is similar in magnitude to that occurring with myocardial infarction. Rather than infarction or release from an exchangeable cTnI pool, the rise in serum cTnI is delayed and appears to reflect focal programmed myocyte death from apoptosis rather than myocardial necrosis.