Physiologic and biochemical rationale for treating COVID-19 patients with hyperbaric oxygen.

The SARS-Cov-2 (COVID-19) pandemic remains a major worldwide public health issue. Initially, improved supportive and anti-inflammatory intervention, often employing known drugs or technologies, provided measurable improvement in management. We have recently seen advances in specific therapeutic interventions and in vaccines. Nevertheless, it will be months before most of the world's population can be vaccinated to achieve herd immunity. In the interim, hyperbaric oxygen (HBO2) treatment offers several potentially beneficial therapeutic effects. Three small published series, one with a propensity-score-matched control group, have demonstrated safety and initial efficacy. Additional anecdotal reports are consistent with these publications. HBO2 delivers oxygen in extreme conditions of hypoxemia and tissue hypoxia, even in the presence of lung pathology. It provides anti-inflammatory and anti-proinflammatory effects likely to ameliorate the overexuberant immune response common to COVID-19. Unlike steroids, it exerts these effects without immune suppression. One study suggests HBO2 may reduce the hypercoagulability seen in COVID patients. Also, hyperbaric oxygen offers a likely successful intervention to address the oxygen debt expected to arise from a prolonged period of hypoxemia and tissue hypoxia. To date, 11 studies designed to investigate the impact of HBO2 on patients infected with SARS-Cov-2 have been posted on clinicaltrials.gov. This paper describes the promising physiologic and biochemical effects of hyperbaric oxygen in COVID-19 and potentially in other disorders with similar pathologic mechanisms.

ARTERIAL INSUFFICIENCIES: Hyperbaric Oxygen Therapy for Selected Problem Wounds.

The use of hyperbaric oxygen (HBO2) for the treatment of selected problem wounds has focused almost entirely on the diabetic foot ulcer (DFU) in recent years. The prevalence of DFUs in today's patient population and the reimbursement available for the treatment of DFUs have given it priority status in discussions about problem wounds, but there are sound fundamental reasons why additional oxygen may have benefits in the treatment of non-DFU wounds.

The effect of the prone maximal restraint position with and without weight force on cardiac output and other hemodynamic measures.

BACKGROUND: The prone maximal restraint (PMR) position has been used by law enforcement and emergency care personnel to restrain acutely combative or agitated individual. The position places the subject prone with wrists handcuffed behind the back and secured to the ankles. Prior work has indicated a reduction in inferior vena cava (IVC) diameter associated with this position when weight force is applied to the back. It is therefore possible that this position can negatively impact hemodynamic stability. OBJECTIVES: We sought to measure the impact of PMR with and without weight force on measures of cardiac function including vital signs, oxygenation, stroke volume (SV), IVC diameter, cardiac output (CO) and cardiac index (CI). METHODS: We conducted a randomized prospective cross-over experimental study of 25 healthy male volunteers (22-43 years of age) placed in 5 different body positions: supine (SU), prone (PR), prone maximal restraint with no weight force (PMR-0), prone maximal restraint with 50 lbs added to the subject's back (PMR-50), and prone maximal restraint with 100 lbs added to the subject's back (PMR-100) for 3 min. Heart rate (HR), blood pressure (BP), and oxygenation saturation (O2 sat) were monitored. In addition, echocardiography was performed to measure left ventricular outflow tract diameter (LVOTD), and SV, CO, and CI were then calculated. Data were analyzed using repeated measures ANOVA with pair-wise comparisons when appropriate to evaluate changes with each variable with respective positioning. RESULTS: Despite a small decrease in SV between SU and PMR positions, there were no statistically significant differences in CO between the 5 different positions. There were also no differences in CI between positions other than a small decrease when comparing SU and PMR-50 only (mean difference -0.39 L/stroke, p = 0.005). There was no evidence of hemodynamic compromise in any of the PMR positions when evaluating HR, MAP or O2 sat. CONCLUSIONS: PMR with and without weight force did not result in any changes in CO or other evidence of cardiovascular or hemodynamic compromise.

Severe sodium channel blockade and cardiovascular collapse due to a massive lamotrigine overdose.

BACKGROUND: Cardiac arrest due to lamotrigine (LTG) has been reported after co-ingestion with bupropion, but severe sodium channel blockade in the absence of other toxins has not been described. We report a case of cardiac arrest and status epilepticus following a massive LTG overdose. CASE REPORT: A 48 year-old female was brought to the ED with seizure-like activity subsequent to ingesting 7.5 g of LTG. Vital signs were HR 131, BP 107/68, T 99.4°F, RR 16. She was intubated in the ED for a low GCS. Initial ECG demonstrated a narrow-complex normal sinus rhythm, and her labs were unremarkable. Three hours after intubation she developed status epilepticus, and a pulseless wide-complex tachycardia. She was aggressively resuscitated during which time pulses were periodically reestablished, but lost each time seizures recurred. She was not stabilized until the convulsions were terminated with vecuronium. Her post-resuscitation ECG demonstrated a junctional tachycardia with a 3 mm R-wave in aVR. The LTG level was 74.7 mcg/ml (therapeutic: 3-14 mcg/ml). Comprehensive LC-MS/MS drug screen was negative for all screened compounds. DISCUSSION: This is the first report of cardiovascular collapse due to LTG with the highest drug concentration to date. CONCLUSION: The degree of neurologic and cardiovascular toxicity seen in this case are novel and illustrate the potential for severe sodium channel blockade after massive LTG poisonings. Drug levels are not clinically relevant in the acute setting due to the time delay in obtaining results, and recurrent seizure activity may be the only clinical finding that precedes severe cardiac toxicity.

Limited communication and management of emergency department hyperglycemia in hospitalized patients.

BACKGROUND: Hyperglycemia is often overlooked and unaddressed in hospitalized patients, and early and intensive management may improve outcomes. OBJECTIVE: To evaluate communication and early management of emergency department (ED) hyperglycemia. METHODS: This was a retrospective cohort study of patients with an initial serum glucose >or=140 mg/dL at an urban, academic institution. We randomly selected cases from a consecutive sample of ED visits with at least 1 serum glucose result during a 1-year period. We recorded clinical data and compared the content of inpatient and ED-written discharge instructions. RESULTS: Of the 27,688 initial ED glucose results during the study period, 3517 (13%) were 140-199 mg/dL, and 2304 (8%) values were >or=200 mg/dL. In our sample of 385 patients, 293 (76%) patients were hospitalized. Inpatient or ED discharge instructions informed 36 (10%) patients of their hyperglycemia and 23 (6%) of a plan for further evaluation and management. There was no difference between inpatient and ED instructions for either of these variables (P = 0.73 and 0.16, respectively). Overall, 107 (55%) patients with glucose values 140-199 mg/dL and 31 (16%) patients with glucose >or=200 mg/dL had no prior diabetes diagnosis. Only 61 (16%) received insulin in the ED for their hyperglycemia, and hyperglycemia was charted as a diagnosis in 36 (9%) cases. CONCLUSIONS: Most ED patients with even mild hyperglycemia were hospitalized. Recognition, communication, and management of ED hyperglycemia were suboptimal and represent a missed opportunity to identify undiagnosed diabetes and to initiate early glycemic control for hospitalized patients.