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Hypoxia and hyperoxia are both worrisome issues potentially affecting SCUBA divers, but validated methods to monitor these two conditions underwater are still lacking. In this experiment, a volunteer SCUBA diver was equipped with a pulse oximeter to detect peripheral oxygen saturation (SpO2) and a device to monitor the oxygen reserve index (ORi™). ORi™ values were compared with arterial blood oxygen saturation (SaO2) and the partial pressure of oxygen (PaO2) obtained from the cannulated right radial artery at three steps: at rest out of water; at -15 m underwater after pedaling on a submerged bike; after resurfacing. SpO2 and ORi™ mirrored the changes in SaO2 and PaO2, confirming the expected hyperoxia at depth. To confirm the potential usefulness of an integrated SpO2 and ORi™ device, further studies are needed on a broader sample with different underwater conditions and diving techniques.

OBJECTIVE: To study the long-term anatomic and physiologic effects of nocturnal normobaric hyperoxia (NNBH) in a patient with treatment-resistant diabetic macular edema (DME).
METHODS: A 64-year-old diabetic man with bilateral DME requiring regular anti-VEGF treatments in both eyes was started on 5 LPM (40% FiO2) NNBH treatment 6-h per night. Visual acuity, OCT measurements of retinal thickness and volume, as well as the number of injections given in each eye were retrospectively examined one year prior and prospectively after initiation of NNBH, as well as before and after a planned 1-month discontinuation of NNBH.
RESULTS: The patient received 12 anti-VEGF injections in the year prior to beginning NNBH treatment (4 OD; 8 OS) and did not require any injections after commencing NNBH treatment. Visual acuity improved and stabilized to 20/20 and macular edema rapidly resolved in both eyes following initiation of NNBH. After a planned 1-month NNBH vacation, DME recurred but quickly resolved once NNBH treatment was restarted.
CONCLUSIONS: This model case demonstrates that a 6-h NNBH regimen can be successful in treating DME and improving vision, without the need for intravitreal injections. NNBH is a more acceptable treatment regimen compared to 24-h continuous oxygen delivery and may provide a less invasive alternate method for treating DME in patients with diabetes. Further study is warranted.

UNASSIGNED: Management of hypoxemia in patients with severe COVID-19 respiratory failure is based on the guideline recommendations for specific SpO2 targets. However, limited data exist on systemic O2 utilization. The objective of this study was to examine systemic O2 utilization in a case series of patients with this disease.
UNASSIGNED: Between March 24, and April 9, 2020, 8 patients intubated for severe COVID-19 respiratory failure had near-simultaneous drawing of arterial blood gas (ABG), central venous blood gas (cVBG), and central venous oxygen saturation (ScvO2) at a mean of 6.1 days into hospitalization. Three patients were managed with indirect cardiac output (CO) monitoring by FloTrac sensor and Vigileo monitor (Edwards Lifesciences, Irvine, CA). The oxygen extraction index (OEI; SaO2-ScvO2/SaO2) and oxygen extraction fraction (OEF; CaO2-CvO2/CaO2 ≥ 100) were calculated. Values for hyperoxia (ScvO2 ≥ 90%), normoxia (ScvO2 71-89%), and hypoxia (ScvO2 ≤ 70%) were based on the literature. Mean values were calculated.
UNASSIGNED: The mean partial pressure of oxygen (PaO2) was 102 with a mean fraction of inspired O2 (FiO2) of 44%. One patient was hyperoxic with a reduced OEI (17%). Five patients were normoxic, but 2 had a reduced OEF (mean 15.9%). Two patients were hypoxic but had increased systemic O2 utilization based on OEF or OEI.
UNASSIGNED: In select patients with severe COVID-19 respiratory failure, O2 delivery (DO2) was found to exceed O2 utilization. SpO2 targets based on systemic O2 utilization may help in reducing oxygen toxicity, especially in the absence of anaerobic metabolism. Further data are needed on the prevalence of systemic O2 utilization in COVID-19.
UNASSIGNED: Garg RK, Kimbrough T, Lodhi W, DaSilva I. Systemic Oxygen Utilization in Severe COVID-19 Respiratory Failure: A Case Series. Indian J Crit Care Med 2021;25(2):215-218.

Pneumocephalus is defined as the presence of air inside the cranial vault. Benign and tension pneumocephalus are different ends of the same disease spectrum. Tension pneumocephalus leads to the formation of a pressure gradient, requiring emergent surgical decompression to prevent herniation of the intracranial structures. In this report, we present a rare case of tension pneumocephalus with essentially benign radiological findings secondary to a ruptured cholesteatoma. The patient was a 64-year-old woman with a history of end-stage renal disease on hemodialysis and hypertension. She presented to the emergency department (ED) with acute-onset weakness and decreased mentation. Physical exam findings were consistent with a cerebrovascular accident (CVA). CT scan and CT angiogram (CTA) were unremarkable for ischemia or hemorrhage but showed signs of free intracranial air, consistent with the diagnosis of pneumocephalus. After the activation of the code stroke, neurosurgery and neurology were consulted. Worsening respiratory status led to a decision to proceed with emergent intubation, but it was held based on the family\'s decision to proceed with comfort measures. The patient\'s status declined further within minutes and she died. Afterward, the case was discussed with the radiologist, who interpreted the cause as a cholesteatoma that had eroded through the temporal bone.

Hyperoxic myopia is a phenomenon reported in individuals who have prolonged exposure to an increased partial pressure of oxygen (PO2) and subsequently have a myopic (nearsighted) change in their vision. To date, there are numerous accounts of hyperoxic myopia in dry hyperbaric oxygen treatment patients; however, there have been only three confirmed cases reported in wet divers. This case series adds four confirmed cases of hyperoxic myopia in wet divers using 1.35 atmospheres (ATM) PO2 at the Navy Experimental Diving Unit (NEDU). The four divers involved were the first author\'s patients at NEDU. Conditions for two divers were confirmed via record review, whereas the other two divers were diagnosed by the first author. All subjects were interviewed to correlate subjective data with objective findings. Each subject completed five consecutive six-hour hyperoxic (PO2 of 1.35 ATM) dives with 18-hour surface intervals. Each individual was within the U. S. Navy Dive Manual\'s standards for general health. Visual acuity was measured prior to diving. Within three to four days after diving, the individuals reported blurry vision with an associated myopic refraction shift. Each diver had spontaneous resolution of his myopia over the next two to three weeks, with no significant residual symptoms. The divers in this case series were exposed to an increased PO2 (1.35 ATM for 30 hours over five days), a lesser exposure than that in other reports of hyperoxic myopia in wet divers diagnosed with hyperoxic myopia (1.3-1.6 ATM for 45-85 hours in 12-18 days). Furthermore, this pulse of exposure was more concentrated than typically seen with traditional hyperbaric oxygen therapy. Hyperoxic myopia continues to be a risk for those conducting intensive diving with a PO2 between 1.3-1.6 ATM. Additional investigation is warranted to better define risk factors and PO2 limits regarding ocular oxygen toxicity.

The greatest danger faced by divers who use oxygen-enriched gas mixtures is central nervous system oxygen toxicity (CNS-OT). CNS-OT is characterised by convulsions resembling grand-mal epileptic seizures, which may terminate in drowning and death. Elevated arterial levels of carbon dioxide (CO₂) (hypercapnia) represent a major risk factor for CNS-OT when breathing hyperoxic gas mixtures. To reduce the risk of a diver being involved in a CNS-OT incident due to hypercapnia, candidates for combat diving are examined at our institute using a routine physiological training procedure, in which they are tested for CO₂ detection and retention. We present the case of a candidate for combat diving, who unexpectedly exhibited signs typical of CNS-OT while breathing pure oxygen under normobaric conditions with > 3 kPa inspired CO₂. Severe headache and nausea, as well as facial muscle twitching, appeared during one of these routine tests. Subsequent medical examination including neurological tests, magnetic resonance imaging and an electroencephalogram were unremarkable. To the best of our knowledge, an event such as this has never previously been published in the medical literature. We present a discussion of the case, and a review of the relevant literature regarding CO₂ as a risk factor for the development of CNS-OT.

Methemoglobinemia is an increase in the methemoglobin levels in the blood. Infants are more susceptible to develop secondary methemoglobinemia because of the limited activity of methemoglobin reductase B enzyme. We report a case of life-threatening methemoglobinemia secondary to ingestion of Ferula asafoetida herbal remedy in an infant who presented with cyanosis and severe respiratory distress. The patient had two brothers who had a glucose-6-phosphate dehydrogenase deficiency and the patient\'s deficiency status was unknown, and thus, methylene blue was not initiated whereas ascorbic acid was unavailable. Accordingly, the patient was successfully treated with hyperoxia. Based on this case, the authors suggest that the use of F. asafoetida as an herbal remedy should be avoided in infants, and pediatricians should be aware of such toxicity and inform parents appropriately.

While oxygen administration has been in clinical practice, the focus has generally been on avoidance of hypoxemia. More recently, renewed emphasis has been placed on the potential deleterious effects of hyperoxia. The aim of this study is to investigate the incidence of intraoperative inadvertent hyperoxia among neonate, which was defined at three different thresholds: normoxia (PaO2 60-100 mmHg), hyperoxia (PaO2 101-199 mmHg), and severe hyperoxia (PaO2 ≥ 200 mmHg). This study included 65 patients with 174 eligible arterial blood gas (ABG) samples, who were less than 60 weeks post-menstrual age and required a non-cardiac surgical procedure. Among the 65 patients, 62 (96%) patients experienced either hyperoxia or severe hyperoxia during general anesthesia on at least one ABG. Among the 174 ABG readings, only 28 (16%) had PaO2 levels within our defined normoxia range. The incidence of hyperoxia in neonate under general anesthesia is high. Although it is unknown if brief exposure during anesthesia is associated with similar outcomes, educational initiatives seem warranted to increase awareness of these clinical concerns, as there seems to be limited clinical benefit from such care.

Hyperbaric oxygen exposure is a recent hazzard for higher animals that originated as humans began underwater construction, exploration, and sports. Exposure can lead to abnormal brain EEG, convulsions, and death, the time to onset of each stage of pathology decreasing with increase in oxygen pressure. We provide evidence that hyperoxia, through oxidative phosphorylation, increases the energy state ([ATP]/[ADP][Pi]) of cells critical to providing glucose to cells behind the blood brain barrier (BBB). Brain cells without an absolute dependence on glucose metabolism; i.e. those having sufficient ATP synthesis using lactate and glutamate as oxidizable substrates, are not themselves very adversely affected by hyperoxia. The increased energy state and decrease in free [AMP], however, suppress glucose transport through the blood brain barrier (BBB) and into cells behind the BBB. Glucose has to pass in sequence through three steps of transport by facilitated diffusion and transporter activity for each step is regulated in part by AMP dependent protein kinase. The physiological role of this regulation is to increase glucose transport in response to hypoxia and/or systemic hypoglycemia. Hyperoxia, however, through unphysiological decrease in free [AMP] suppresses 1) glucose transport through the BBB (endothelial GLUT1 transporters) into cerebrospinal fluid (CSF); 2) glucose transport from CSF into cells behind the BBB (GLUT3 transporters) and (GLUT4 transporters). Cumulative suppression of glucose transport results in local regions of hypoglycemia and induces hypoglycemic failure. It is suggested that failure is initiated at axons and synapses with insufficient mitochondria to meet their energy requirements.