Coexisting Cerebral Salt Wasting Syndrome and Central Diabetes Insipidus in a Patient with Posterior Cerebrovascular Infarction: A Case Report

<b><i>Background:</i></b> Disorders of sodium balance are common in critically ill neurologic patients. However, the coexisting of cerebral salt wasting syndrome (CSW) and central diabetes insipidus (CDI) in such patients is rare. Early recognition of such conditions is challenging, thus making the prognosis ominous. <b><i>Case Presentation:</i></b> A 50-year-old male patient presented with acute posterior cerebrovascular infarction complicated by several attacks of disturbed sodium homeostasis. The first attack manifested as hypernatremia (up to 161 mmol/L) and polyuria with high urine sodium (188 mmol/L) could only be explained by CSW on top of CDI. Especially the patient was not receiving any hyperosmolar or sodium-containing fluids. Serum sodium was corrected by desmopressin acetate. Later, the patient developed 2 attacks of hyponatremia (down to 119 mmol/L) diagnosed as CSW that was treated with fludrocortisone. Finally, he developed hypernatremia (up to 165 mmol/L) diagnosed as CDI and was treated with desmopressin acetate. <b><i>Conclusion:</i></b> Sodium hemostasis disorders require full consideration of serum electrolytes, intravascular volume state, and urine electrolytes in view of the clinical condition. Early diagnosis and administration of the proper treatment are the cornerstones of successful management.

A143 ACUTE ESOPHAGEAL NECROSIS: A COMPLICATION OF DIABETIC KETOACIDOSIS

Background Acute esophageal necrosis (AEN) is a rare entity associated with diabetic ketoacidosis (DKA). The pathogenesis is thought to be linked to low volume state, microvascular disease, impaired gastric and esophageal motility increasing acid reflex, all rendering the esophagus prone to injury. Aims We report a case of AEN as a complication of DKA in a patient without any overt gastrointestinal bleeding (GIB), along with a literature review. Methods Keywords “esophageal necrosis” and “diabetic ketoacidosis” were used in MEDLINE and BASE to retrieve English articles reporting cases of AEN in DKA. Results A 63 year old male with history of hypertension, dyslipidemia and non-insulin dependent diabetes mellitus presented to Emergency with 5 day history of severe epigastric pain, dysphagia to solids and liquids, nausea and vomiting (without any overt GIB). Most recent HbA1c was 8.4%. His diabetes was managed with metformin and semaglutide. Bloodwork revealed a hemoglobin of 165g/L and leukocytes of 17.9x109/L. Chemistries showed an anion gap of 25 with bicarbonate of 5mmol/L. Venous blood gas showed acidemia (pH=7.02). B-hydroxybutyrate level was 10.2mmol/L. Urinalysis was negative for leukocytes or nitrites. An abdominal CT ruled out bowel obstruction or intra-abdominal infection/abscess as the source of his discomfort but demonstrated circumferential wall thickening of the distal esophagus. No other triggers were found for this patient’s DKA except perhaps a recently started ketogenic diet. After resolution of DKA, he continued to experience severe epigastric pain, reflux symptoms, and dysphagia. An esophagogastroduodenoscopy (EGD) was performed, which showed AEN with circumferential black, necrotic inflammatory changes in the mid to distal esophagus. Erosions were seen in the body and antrum of the stomach, and multiple clean based ulcers were seen in the duodenum. Patient was started on an insulin regimen prior to discharge. Review of literature shows a total of 13 cases of AEN in DKA, with only one case where the patient did not present with any clinical bleeding. Risk factors for AEN include, hypertension, diabetes mellitus, malignancy, male gender, older age, chronic kidney disease, alcohol abuse and cardiovascular disease. While no medications have been linked to AEN, our patient was recently started on semiglutide, which has been implicated in impaired gastric emptying and increased GERD symptoms. This may further explain why the patient developed AEN. Conclusions AEN is a rare entity, especially in the context of DKA. Usually patients present with overt GIB; however, on occasion dysphagia, nausea, and vomiting can be the predominant symptoms. Hence, the threshold to perform EGD in patients with DKA should be low, given their low volume state and potentially impaired gastrointestinal motility due to microvascular disease or medications, putting them at higher risk for AEN. Funding Agencies None

TIME TO LUNG VOLUME STABILITY AFTER PRESSURE CHANGE DURING HIGH-FREQUENCY OSCILLATORY VENTILATION

ABSTRACTObjectivesClinicians have little guidance on the time needed before assessing the effect of a mean airway pressure (PAW) change during high-frequency oscillatory ventilation (HFOV). We aimed to determine 1) time to stable lung volume after a PAW change during HFOV and, 2) the relationship between time to volume stability and the volume state of the lung.MethodsContinuous lung volume measurements (respiratory inductive plethysmography) after 1-2 cmH2O PAW changes made every 10 minutes during an open lung strategy (n=13 infants) were analysed with a bi-exponential model. Time to stable lung volume (extrapolated to maximum 3600s) was calculated if the model R2 was >0.6.Results196 PAW changes were made, with no volume change in 33 (17%) occurrences. 125 volume signals met modelling criteria for inclusion; median (IQR) R2 0.96 (0.91, 0.98). The time to stable lung volume was 1131 (718, 1959)s (PAW increases) and 647 (439, 1309)s (PAW decreases), with only 17 (14%) occurring within 10 minutes and time to stability being longer when the lung was atelectatic.ConclusionsDuring HFOV, the time to stable lung volume after a PAW change is variable, often requires more than 10 minutes and is dependent on the preceding volume state.Impact StatementIn infants without preterm respiratory distress syndrome the time to achieve lung volume stability after a PAW change during HFOV is usually greater than 10 minutes.The volume state of the lung at the time of PAW change influences the time required to achieve a stable new lung volume; being shorter when the lung is well recruited and longer when the lung is already atelectatic.Clinicians should be aware that it may require least 10 minutes before assessing the clinical response to a change in PAW during HFOV

Working Memory

Working memory refers to how we keep track of what we are doing moment to moment throughout our waking lives. It allows us to remember what we have just done, focus on what we are doing now, to solve problems, be creative, think about what we will be doing in the next few seconds, and continually to update in our mind changes around us throughout the day. This book brings together in one volume, state-of-the-science chapters written by some of the most productive and well-known working memory researchers worldwide. Chapters cover leading-edge research on working memory, using behavioural experimental techniques, neuroimaging, computational modelling, development across the healthy human lifespan, and studies of neurodegenerative disease and focal brain damage. A unique feature of the book is that each chapter starts with answers to a set of common questions for all authors. This allows readers very rapidly to compare key differences in theoretical assumptions and approaches to working memory across chapters, and to understand the theoretical context before going on to read each chapter in detail. All authors also have been asked to consider evidence that is not consistent with their theoretical assumptions. It is very common for authors to ignore contradictory evidence. This approach has led to new interpretations and new hypotheses for future research to greatly enhance our understanding of this crucial human ability.

Three-dimensional Multi-site Random Access Photostimulation (3D-MAP)

Optical control of neural ensemble activity has been crucial for understanding brain function and disease, yet no technology can achieve optogenetic control of very large numbers of neurons at extremely fast rates over a large volume. State-of-the-art multiphoton holographic optogenetics requires high power illumination that only address relatively small populations of neurons in parallel. Conversely, one-photon holographic techniques can stimulate more neurons but with a trade-off between resolution and addressable volume. We introduce a new one-photon light sculpting technique, termed Three-Dimensional Multi-site random Access Photostimulation (3D-MAP), that simultaneously overcomes all these limitations by dynamically modulating light in both the spatial and angular domain at multi-kHz rates. Electrophysiological measurements confirm that 3D-MAP achieves high spatial precision in vitro and in vivo. Using 3D-MAP, we then interrogate neural circuits with 3D multi-site illumination with high resolution over a large volume of intact brain that existing techniques cannot achieve.

Effect of volume status on the estimation of mean systemic filling pressure

Various methods for indirect assessment of mean systemic filling pressure (MSFP) produce controversial results compared with MSFP at zero blood flow. We recently reported that the difference between MSFP at zero flow measured by right atrial balloon occlusion (MSFPRAO) and MSFP estimated using inspiratory holds depends on the volume status. We now compare three indirect estimates of MSFP with MSFPRAO in euvolemia, bleeding, and hypervolemia in a model of anesthetized pigs ( n = 9) with intact circulation. MSFP was estimated using instantaneous beat-to-beat venous return during tidal ventilation (MSFPinst_VR), right atrial pressure-flow data pairs at flow nadir during inspiratory holds (MSFPnadir_hold), and a dynamic model analog adapted to pigs (MSFPa). MSFPRAO was underestimated by MSFPnadir_hold and MSFPa in all volume states. Volume status modified the difference between MSFPRAO and all indirect methods (method × volume state interaction, P ≤ 0.020). All methods tracked changes in MSFPRAO concordantly, with the lowest bias seen for MSFPa [bias (confidence interval): −0.4 (−0.7 to −0.0) mmHg]. We conclude that indirect estimates of MSFP are unreliable in this experimental setup. NEW & NOTEWORTHY For indirect estimations of MSFP using inspiratory hold maneuvers, instantaneous beat-to-beat venous return, or a dynamic model analog, the accuracy was affected by the underlying volume state. All methods investigated tracked changes in MSFPRAO concordantly.

Effect of PEEP, blood volume, and inspiratory hold maneuvers on venous return

According to Guyton's model of circulation, mean systemic filling pressure (MSFP), right atrial pressure (RAP), and resistance to venous return (RVR) determine venous return. MSFP has been estimated from inspiratory hold-induced changes in RAP and blood flow. We studied the effect of positive end-expiratory pressure (PEEP) and blood volume on venous return and MSFP in pigs. MSFP was measured by balloon occlusion of the right atrium (MSFPRAO), and the MSFP obtained via extrapolation of pressure-flow relationships with airway occlusion (MSFPinsp_hold) was extrapolated from RAP/pulmonary artery flow (QPA) relationships during inspiratory holds at PEEP 5 and 10 cmH2O, after bleeding, and in hypervolemia. MSFPRAO increased with PEEP [PEEP 5, 12.9 (SD 2.5) mmHg; PEEP 10, 14.0 (SD 2.6) mmHg, P = 0.002] without change in QPA [2.75 (SD 0.43) vs. 2.56 (SD 0.45) l/min, P = 0.094]. MSFPRAO decreased after bleeding and increased in hypervolemia [10.8 (SD 2.2) and 16.4 (SD 3.0) mmHg, respectively, P < 0.001], with parallel changes in QPA. Neither PEEP nor volume state altered RVR ( P = 0.489). MSFPinsp_hold overestimated MSFPRAO [16.5 (SD 5.8) vs. 13.6 (SD 3.2) mmHg, P = 0.001; mean difference 3.0 (SD 5.1) mmHg]. Inspiratory holds shifted the RAP/QPA relationship rightward in euvolemia because inferior vena cava flow (QIVC) recovered early after an inspiratory hold nadir. The QIVC nadir was lowest after bleeding [36% (SD 24%) of preinspiratory hold at 15 cmH2O inspiratory pressure], and the QIVC recovery was most complete at the lowest inspiratory pressures independent of volume state [range from 80% (SD 7%) after bleeding to 103% (SD 8%) at PEEP 10 cmH2O of QIVC before inspiratory hold]. The QIVC recovery thus defends venous return, possibly via hepatosplanchnic vascular waterfall.

An Unusual Case of Asystole Occurring during Deep Brain Stimulation Surgery

Background. Symptomatic bradycardia and hypotension in neurosurgery can produce severe consequences if not managed appropriately. The literature is scarce regarding its occurrence during deep brain stimulation (DBS) surgery.Case Presentation. A 67-year-old female presented for left DBS lead placement for essential tremors. During lead implantation, heart rate and blood pressure dropped rapidly; the patient became unresponsive and asystolic. Chest compressions were initiated and epinephrine was given. Within 30 seconds, the patient became hemodynamically stable and conscious. A head CT demonstrated no acute findings. After deliberation, a decision was made to complete the procedure. Assuming the etiology of the episode was the Bezold-Jarisch reflex (BJR), appropriate accommodations were made. The procedure was completed uneventfully.Conclusion. The episode was consistent with a manifestation of the BJR. The patient had a history of neurocardiogenic syncope and a relatively low-volume state, factors prone to the BJR. Overall, lead implantation can still occur safely if preventive measures are employed.