Asystole in 2 Pediatric Patients During Dexmedetomidine Infusion

2021 ◽  
pp. 089719002110271
Author(s):  
Katrin Lichtsinn ◽  
Ila Sehgal ◽  
Alexandra Wilson

Introduction: Bradycardia is a known side effect of dexmedetomidine. Reports of sinus pauses or asystole, however, are rare. We present 2 cases of pediatric patients who developed asystole on a dexmedetomidine infusion. Summary of Cases: An 8-week-old male with RSV bronchiolitis and acute hypoxemic respiratory failure was started on dexmedetomidine for sedation at 0.2 mcg/kg/h with a maximum dose of 0.7mcg/kg/h. On Hospital day (HD) 4, on dexmedetomidine at 0.7 mcg/kg/h, he developed intermittent episodes of bradycardia with heart rates in the 60 s. Echocardiogram on HD 6 showed normal function. On HD 7, he began having periods of asystole lasting up to 6 seconds. Dexmedetomidine was discontinued, with the resolution of episodes of asystole after 6 hours. A 27-month-old male with a congenital left diaphragmatic hernia and pulmonary hypertension who had been weaned off sildenafil 6 months earlier underwent re-repair of left diaphragmatic hernia. Postoperatively he remained intubated and paralyzed. Dexmedetomidine was started at 0.3 mcg/kg/h for sedation, with a maximum dose of 1.2 mcg/kg/h. An echocardiogram on HD 3 showed good function with mild to moderate pulmonary hypertension. That evening, with dexmedetomidine at 1.1 mcg/kg/h, he developed a 15 second period of asystole requiring CPR. Dexmedetomidine was discontinued, and he was started on a midazolam infusion with no further episodes. Discussion: Both cases occurred in patients without cardiac conduction defects or on negative chronotropic or sympatholytic medications that have been associated with dexmedetomidine-induced asystole. We hypothesize that both episodes of asystole were due to increased patient-related vagal tone exacerbated by dexmedetomidine.

2018 ◽  
Vol 53 (5) ◽  
pp. 464-470 ◽  
Author(s):  
Deonne A. Dersch-Mills ◽  
Heidi L. Banasch ◽  
Kamran Yusuf ◽  
Alixe Howlett

Background: Continuous infusions of dexmedetomidine are increasingly used for sedation in critically ill pediatric patients. Emerging data suggest potential benefits when used for sedation in neonates, including reduced sedative requirements and earlier enteral feeds. Objective: To describe the use, adverse effects, and signs of withdrawal in a cohort of neonates receiving dexmedetomidine, the majority of whom were receiving concomitant opioids. Methods: This was a retrospective, descriptive review of 38 neonates receiving dexmedetomidine in a medical surgical neonatal intensive care unit, including data on duration of use, dose, adverse effects, weaning, and signs of withdrawal. Results: Dexmedetomidine was used for a median of 183 hours, at a median maximum dose of 0.5 µg/kg/h. Premature infants were started on dexmedetomidine at a later chronological age than term infants (41 vs 9 days, P = 0.004). Of 18 patients receiving an opioid infusion at the time of dexmedetomidine initiation, 67% had a dose reduction in opioids by 24 hours. The majority (89%) of neonates had at least 1 potentially related adverse effect during the dexmedetomidine infusion, though no discontinuations were needed as a result. In all, 80% of patients had their dexmedetomidine gradually weaned off, and 71% had at least 1 sign of withdrawal. Conclusions and Relevance: In this cohort, dexmedetomidine was often used in a postsurgical setting, with concomitant opioids, over prolonged periods. These factors appear to affect and likely confound the rates of adverse effects and withdrawal signs from dexmedetomidine. Clinicians considering the use of dexmedetomidine in a similar population can draw guidance from our data.


2021 ◽  
Vol 22 (15) ◽  
pp. 7923
Author(s):  
Santiago Alvarez-Argote ◽  
Caitlin C. O’Meara

Macrophages were first described as phagocytic immune cells responsible for maintaining tissue homeostasis by the removal of pathogens that disturb normal function. Historically, macrophages have been viewed as terminally differentiated monocyte-derived cells that originated through hematopoiesis and infiltrated multiple tissues in the presence of inflammation or during turnover in normal homeostasis. However, improved cell detection and fate-mapping strategies have elucidated the various lineages of tissue-resident macrophages, which can derive from embryonic origins independent of hematopoiesis and monocyte infiltration. The role of resident macrophages in organs such as the skin, liver, and the lungs have been well characterized, revealing functions well beyond a pure phagocytic and immunological role. In the heart, recent research has begun to decipher the functional roles of various tissue-resident macrophage populations through fate mapping and genetic depletion studies. Several of these studies have elucidated the novel and unexpected roles of cardiac-resident macrophages in homeostasis, including maintaining mitochondrial function, facilitating cardiac conduction, coronary development, and lymphangiogenesis, among others. Additionally, following cardiac injury, cardiac-resident macrophages adopt diverse functions such as the clearance of necrotic and apoptotic cells and debris, a reduction in the inflammatory monocyte infiltration, promotion of angiogenesis, amelioration of inflammation, and hypertrophy in the remaining myocardium, overall limiting damage extension. The present review discusses the origin, development, characterization, and function of cardiac macrophages in homeostasis, cardiac regeneration, and after cardiac injury or stress.


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