Citations

Abstract Background Soft tissue filler injections are frequently performed with a relatively low number of severe adverse events reported. While venous complications have been described, the majority of adverse events are generally associated with the arterial vascular system. Intra‐arterial product application can present with pain, skin discoloration, and potential tissue loss and/or injection related visual compromise. Aim We present the clinical case and the consecutive symptomology of a 39‐year‐old woman injected with calcium hydroxylapatite at the zygomatic arch with five perpendicular needle (27G 12mm) supraperiosteal bolus injections of 0.2 cc per site. Methods Immediately after the injections, weakness, nausea, vomiting, and loss of consciousness occurred. Additionally, left‐sided loss of sensation of her face, scalp, oral, and nasal mucosa occurred, with absence of left corneal reflex and ipsi‐lateral ear congestion. Subsequently, left‐sided masseteric atrophy and dysphagia occurred. Results One year after the injection procedure the sensory loss of her facial skin and scalp persisted, while the other symptoms improved. Medications involved in the symptomatic (not causal) partial recovery process were Dexamethasone, Vitamin B complex, Vinpocetine, Pentoxifyllin, and Thioctic acid. Conclusion The symptoms presented and the time‐related relationship to the injection procedure increases the likeliness of an association between the administration of the calcium hydroxylapatite product and a lesion of the trigeminal ganglion. The resulting symptoms can altogether be related to the functions of the ganglion. The connecting pathway between the injection site and the ganglion can be explained by the arterial vascular pathway.

Background: Data are limited on the need for and benefits of pump setting optimization with automated insulin delivery. We examined clinical management of a closed-loop control (CLC) system and its relationship to glycemic outcomes. Materials and Methods: We analyzed personal parameter adjustments in 168 participants in a 6-month multicenter trial of CLC with Control-IQ versus sensor-augmented pump (SAP) therapy. Preset parameters (BR = basal rates, CF = correction factors, CR = carbohydrate ratios) were optimized at randomization, 2 and 13 weeks, for safety issues, participant concerns, or initiation by participants' usual diabetes care team. Time in range (TIR 70–180 mg/dL) was compared in the week before and after parameter changes. Results: In 607 encounters for parameter changes, there were fewer adjustments for CLC than SAP (3.4 vs. 4.1/participant). Adjustments involved BR (CLC 69%, SAP 80%), CR (CLC 68%, SAP 50%), CF (CLC 44%, SAP 41%), and overnight parameters (CLC 62%, SAP 75%). TIR before and after adjustments was 71.2% and 71.3% for CLC and 61.0% and 62.9% for SAP. The highest baseline HbA 1c CLC subgroup had the largest TIR improvement (51.2% vs. 57.7%). When a CR was made more aggressive in the CLC group, postprandial time >180 mg/dL was 43.1% before the change and 36.0% after the change. The median postprandial time <70 mg/dL before making CR less aggressive was 1.8%, and after the change was 0.7%. Conclusions: No difference in TIR was detected with parameter changes overall, but they may have an effect in higher HbA 1c subgroups or following user-directed boluses, suggesting that changes may matter more in suboptimal control or during discrete periods of the day. Clinical Trials Registration number: NCT03563313.

Diabetic ketoacidosis is a life-threatening acute metabolic complication of uncontrolled diabetes. Severe cases of DKA (pH ≤ 7.00, bicarbonate level ≤ 10.0, anion gap > 12, positive ketones, and altered mental status) are commonly encountered in patients with type 1 diabetes and are thought to carry an ominous prognosis. There is not enough information on the clinical course of severely acidotic type 2 diabetes (pH ≤ 6.9) patients with DKA, possibly because this condition is rarely seen in developed countries. In this series, we present 18 patients with type 2 diabetes, DKA, and a pH ≤ 6.9 that presented to a tertiary university hospital over the past 11 years. The objective was to describe their clinical characteristics, the triggering cause, and emphasis on treatment, evolution, and outcomes. The majority of the patients were female (61%). Mean age was 40.66 years (23–59). The patients had been first diagnosed with type 2 diabetes on average 5.27 ± 3.12 years before admission. Glutamic acid decarboxylase (GAD65) antibodies were negative in all patients. The origin of DKA could be attributed to two main causes: treatment omission in 8 (44.4%) patients and infections in 7 (38.8%) patients. The most common symptoms described were general malaise, dyspnea, altered mental status, and abdominal pain. Mean serum glucose on admission was 613.8 ± 114.5 mg/dL. Mean venous pH was 6.84 ± 0.03 with an anion gap of 30.3 ± 2.9 and a venous HCO3level of 3.62 ± 1.35 mmol/L. All patients had acute renal failure on admission, with a mean serum creatinine of 1.57 ± 0.35 mg/dL compared to 0.55 ± 0.21 mg/dL at discharge. All patients received regular insulin infusion, aggressive fluid repletion, and 12 patients (66%) received bicarbonate infusion. Mean total insulin infusion dose was 181.7 ± 90.4 U (on average 0.14 ± 0.05 U/Kg/h). Mean time on infusion was 24.4 ± 12.6 hours. We recorded no mortality in this case series. Mean in-hospital stay was 5.0 ± 4.1 days. In conclusion, very severe DKA in type 2 diabetes is not uncommon in our population, shares many features with non-very-severe cases of DKA (bicarbonate therapy did not make a difference in mortality), and can be managed following standard published or institutional guidelines.