New-Onset Pediatric Diabetes Complicated By Diabetic Ketoacidosis and Invasive Rhinocerebral Mucormycosis With Internal Carotid Artery Occlusion.

BACKGROUND: Diabetic ketoacidosis (DKA) has increased in prevalence in the emergency department (ED) in recent years. The complications of DKA are life threatening and necessitate rapid identification and management. Pediatric complications include cerebral edema, venous thrombosis, acute kidney injury, and severe infections including necrotizing fasciitis and mucormycosis. Rhinocerebral mucormycosis carries a high mortality rate and requires early treatment with antifungals and surgical debridement. CASE REPORT: A 16-year-old boy with no significant past medical history presented to the ED with new-onset DKA complicated by hypothermia, hyperosmolar hyperglycemic state, cerebral edema, and multifactorial shock. During a complicated pediatric intensive care unit admission, he was found to have fatal invasive rhinocerebral mucormycosis, causing internal carotid artery occlusion with evidence of both direct and hematogenous spread into his brain. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Early identification of shock and appropriate management with intravenous fluids, vasopressors, and reversal of the underlying process is key in hypotensive children. In pediatric DKA, the emergency physician must consider cerebral edema, appropriate fluid resuscitation, and identify the likely precipitants leading to the onset of DKA. Thorough workup for potential precipitants should be initiated in the ED, searching for etiologies including infection, intoxication, insulin deficiency, inflammation, and ischemia. We must remember that pediatric patients, especially those with new DKA, are susceptible to life-threatening infection, including mucormycosis. Mucormycosis is a rare diagnosis, and management includes antifungal therapies and involvement of otorhinolaryngology.

Utility of Hypertonic Saline and Diazepam in COVID-19-Related Hydroxychloroquine Toxicity.

BACKGROUND: Hydroxychloroquine (HCQ) poisoning is a life-threatening but treatable toxic ingestion. The scale of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (COVID-19) and the controversial suggestion that HCQ is a treatment option have led to a significant increase in HCQ use. HCQ poisoning should be at the top-of-mind for emergency providers in cases of toxic ingestion. Treatment for HCQ poisoning includes sodium bicarbonate, epinephrine, and aggressive electrolyte repletion. We highlight the use of hypertonic saline and diazepam. CASE REPORT: We describe the case of a 37-year-old man who presented to the emergency department after the ingestion of approximately 16 g of HCQ tablets (initial serum concentration 4270 ng/mL). He was treated with an epinephrine infusion, hypertonic sodium chloride, high-dose diazepam, sodium bicarbonate, and aggressive potassium repletion. Persistent altered mental status necessitated intubation, and he was managed in the medical intensive care unit until his QRS widening and QTc prolongation resolved. After his mental status improved and it was confirmed that his ingestion was not with the intent to self-harm, he was discharged home with outpatient follow-up. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: For patients presenting with HCQ overdose and an unknown initial serum potassium level, high-dose diazepam and hypertonic sodium chloride should be started immediately for the patient with widened QRS. The choice of hypertonic sodium chloride instead of sodium bicarbonate is to avoid exacerbating underlying hypokalemia which may in turn potentiate unstable dysrhythmia. In addition, early intubation should be a priority in vomiting patients because both HCQ toxicity and high-dose diazepam cause profound sedation.

Platelet-Rich Plasma for the Treatment of Low Back Pain: a Comprehensive Review.

PURPOSE OF REVIEW: Back pain is a growing problem worldwide, incurring enormous economic costs and disability. Current treatment modalities often provide adequate relief but fail to address underlying conditions. Regenerative cellular modalities aim to restore anatomical function in degenerative conditions which may cause low back pain. Platelet-rich plasma (PRP) consists of an increased concentration of autologous platelets suspended in a small amount of plasma. PRP can be administered via injection or topically and is prepared using various techniques. RECENT FINDINGS: While a unifying mechanism of action is not well understood, biochemical and cellular changes involved in inflammation and mechanical structure have been detected in both in vitro and in vivo studies. At a higher level, PRP injection research utilizing animal models and patient data have provided insights into pain relief, chondroprotection, and factors that impact the therapy's efficacy. Recently, a small number of studies have promoted PRP injection as a relatively safe means of treating patients with degenerative disc disease who have failed other means of managing their lower back pain. PRP injections for sacroiliac joint-related pain are not an accepted or common treatment modality; the evidence for their efficacy remains to be seen outside of small RCTs and case reports. A small number of prospective trials have suggested there may be some benefit to using PRP injection in the treatment of pain or functional decline caused by facet joint arthropathy. These commonly used modalities require further study to improve quality of evidence and to investigate the safety and efficacy of PRP injections for various common causes of chronic low back.

Altered sleep composition after traumatic brain injury does not affect declarative sleep-dependent memory consolidation.

Individuals with a history of traumatic brain injury (TBI) often report sleep disturbances, which may be caused by changes in sleep architecture or reduced sleep quality (greater time awake after sleep onset, poorer sleep efficiency, and sleep stage proportion alterations). Sleep is beneficial for memory formation, and herein we examine whether altered sleep physiology following TBI has deleterious effects on sleep-dependent declarative memory consolidation. Participants learned a list of word pairs in the morning or evening, and recall was assessed 12-h later, following an interval awake or with overnight sleep. Young adult participants (18-22 years) were assigned to one of four experimental groups: TBI Sleep (n = 14), TBI Wake (n = 12), non-TBI Sleep (n = 15), non-TBI Wake (n = 15). Each TBI participant was >1 year post-injury. Sleep physiology was measured with polysomnography. Memory consolidation was assessed by comparing change in word-pair recall over 12-h intersession intervals. The TBI group spent a significantly greater proportion of the night in SWS than the non-TBI group at the expense of NREM1. The TBI group also had marginally lower EEG delta power during SWS in the central region. Intersession changes in recall were greater for intervals with sleep than without sleep in both groups. However, despite abnormal sleep stage proportions for individuals with a TBI history, there was no difference in the intersession change in recall following sleep for the TBI and non-TBI groups. In both Sleep groups combined, there was a positive correlation between Intersession Change and the proportion of the night in NREM2 + SWS. Overall, sleep composition is altered following TBI but such deficits do not yield insufficiencies in sleep-dependent memory consolidation.