Case Report: Congenital tuberculosis in a premature infant requiring extracorporeal membrane oxygenation.

Congenital tuberculosis is a rare infectious disease with less than 500 cases documented worldwide. Mortality is significant, ranging from 34 to 53%, and death without treatment is inevitable. Patients exhibit nonspecific symptoms such as fever, cough, respiratory distress, feeding intolerance, and irritability which can make appropriate diagnosis challenging in Peng et al. (2011) Pediatr Pulmonol 46(12), 1215-1224. Tuberculosis prevalence is particularly high in developing countries where access to resources can be limited in World Health Organization (2019) Global tuberculosis report 2019, Geneva. We present a 2.4-kg premature male infant with acute respiratory distress syndrome secondary to congenital tuberculosis caused by Mycobacterium bovis and tuberculosis-immune reconstitution inflammatory syndrome who was successfully supported with veno-arterial extracorporeal membrane oxygenation.

High-Frequency Jet Ventilation in Infants With Congenital Heart Disease.

BACKGROUND: High-frequency jet ventilation (HFJV) is primarily used in neonates but may also have a role in the treatment of infants with congenital heart disease and severe respiratory failure. We hypothesized that HFJV would result in improved gas exchange in these infants. METHODS: We retrospectively reviewed the records of all pediatric patients with complex congenital heart disease treated HFJV in our pediatric cardiac ICU between 2014 and 2018. Patients in whom HFJV was started while on extracorporeal membrane oxygenation (ECMO) were excluded. We extracted data on demographics, pulmonary mechanics, gas exchange, the subsequent need for ECMO, use of inhaled nitric oxide, and outcomes. RESULTS: We included 27 subjects (median [interquartile range {IQR}] weight 4.4 [3.3-5.4] kg; median [IQR] age 2.5 [0.3-5.4] months), 22 (82%) of whom had cyanotic heart disease. Thirteen subjects (48%) survived and 6 (22%) required ECMO. HFJV was started after a median (IQR) of 8.4 (2.1-26.3) d of conventional mechanical ventilation. The subjects spent a median (IQR) of 1.2 (0.5-2.8) d on HFJV. The median (IQR) pre-HFJV blood gas results (n = 25) were pH 7.22 (7.17-7.31), [Formula: see text] 69 (51-77) mm Hg, and [Formula: see text] 51 (41-76) mm Hg. Median (IQR) initial HFJV settings were peak inspiratory pressure of 45 (36-50) cm H2O, breathing frequency of 360 (360-380) breaths/min, and inspiratory time of 0.02 (0.02-0.03) s. Compared with conventional mechanical ventilation, at 4-6 h after HFJV initiation, there were significant improvements in the median pH (7.22 vs 7.34; P = .001) and [Formula: see text] (69 vs 50 mm Hg; P = .001), respectively, but no difference in median [Formula: see text] (51 vs 53 mm Hg; P = .97). CONCLUSIONS: HFJV was associated with a decrease in [Formula: see text] and an increase in pH in infants with congenital heart disease who remained on HFJV 4 to 6 h after initiation.

Pannexin 1 channels control the hemodynamic response to hypoxia by regulating O2-sensitive extracellular ATP in blood.

Pannexin 1 (Panx1) channels export ATP and may contribute to increased concentration of the vasodilator ATP in plasma during hypoxia in vivo. We hypothesized that Panx1 channels and associated ATP export contribute to hypoxic vasodilation, a mechanism that facilitates the matching of oxygen delivery to metabolic demand of tissue. Male and female mice devoid of Panx1 (Panx1-/-) and wild-type controls (WT) were anesthetized, mechanically ventilated, and instrumented with a carotid artery catheter or femoral artery flow transducer for hemodynamic and plasma ATP monitoring during inhalation of 21% (normoxia) or 10% oxygen (hypoxia). ATP export from WT vs. Panx1-/-erythrocytes (RBC) was determined ex vivo via tonometer experimentation across progressive deoxygenation. Mean arterial pressure (MAP) was similar in Panx1-/- (n = 6) and WT (n = 6) mice in normoxia, but the decrease in MAP in hypoxia seen in WT was attenuated in Panx1-/- mice (-16 ± 9% vs. -2 ± 8%; P < 0.05). Hindlimb blood flow (HBF) was significantly lower in Panx1-/- (n = 6) vs. WT (n = 6) basally, and increased in WT but not Panx1-/- mice during hypoxia (8 ± 6% vs. -10 ± 13%; P < 0.05). Estimation of hindlimb vascular conductance using data from the MAP and HBF experiments showed an average response of 28% for WT vs. -9% for Panx1-/- mice. Mean venous plasma ATP during hypoxia was 57% lower in Panx1-/- (n = 6) vs. WT mice (n = 6; P < 0.05). Mean hypoxia-induced ATP export from RBCs from Panx1-/- mice (n = 8) was 82% lower than that from WT (n = 8; P < 0.05). Panx1 channels participate in hemodynamic responses consistent with hypoxic vasodilation by regulating hypoxia-sensitive extracellular ATP levels in blood.NEW & NOTEWORTHY Export of vasodilator ATP from red blood cells requires pannexin 1. Blood plasma ATP elevations in response to hypoxia in mice require pannexin 1. Hemodynamic responses to hypoxia are accompanied by increased plasma ATP in mice in vivo and require pannexin 1.

Effects of repleting organic phosphates in banked erythrocytes on plasma metabolites and vasoactive mediators after red cell exchange transfusion in sickle cell disease.

BACKGROUND: Red blood cell (RBC) exchange (RCE) transfusion therapy is indicated for certain patients with sickle cell disease (SCD). Although beneficial, this therapy is costly and inconvenient to patients, who may require it monthly or more often. Identification of blood and plasma biomarkers that could improve or help individualise RCE therapy is of interest. Here we examined relevant blood and plasma metabolites and biomarkers of vasoactivity and RBC fragility in a pilot study of SCD patients undergoing RCE using either standard RBC units or RBC units treated with a US Food and Drug Administration (FDA)-approved additive solution containing phosphate, inosine, pyruvate, and adenine ("PIPA"). MATERIALS AND METHODS: In this prospective, single-blind, cross-over pilot clinical trial, patients were randomised to receive either standard RBC exchange or PIPA-treated RBC exchange transfusion with each RCE session over a 6-month treatment period. Pre- and post-transfusion blood samples were obtained and analysed for RBC O2 affinity, ATP, purine metabolites, RBC microparticles, and cell free haemoglobin. RESULTS: Red blood cell O2 affinity was maintained after PIPA-RCE in contrast to standard RCE, after which P50 fell (net O2 affinity rose). Plasma ATP did not change significantly after RCE using either of the RBC unit types. Exchange transfusion with PIPA-treated RBC units led to modest increases in plasma inosine and hypoxanthine. Plasma cell free haemoglobin fell after either standard or PIPA-treated RBC exchange transfusion (novel findings), and to a similar extent. RBC-derived microparticles in the plasma fell significantly and similarly after both standard and PIPA-treated RCE transfusion. DISCUSSION: In summary, treatment of RBCs with PIPA prior to RCE elicited favourable or neutral changes in key metabolic and vascular biomarkers. Further study of its efficacy and safety is recommended and could ultimately serve to improve outcomes in chronically transfused SCD patients.

Visual Diagnosis: An Adolescent Male With Severe Facial Swelling and Scalp Infection.

Scalp eruptions are common in infants, children, and adolescents and the etiology can be broad. Allergic contact dermatitis can result after multiple non eventful uses of a hair care product, including shampoo, relaxers, and coloring agents. Symptoms of allergic contact dermatitis include intense pruritus with weeping, pain, and stinging sensations. Signs on physical examination include swelling with scaly erythematous plaques as well as bullae with vesicles and pustules in severe cases. The forehead, eyelids, and postauricular areas also are subject to swelling. Definitive diagnosis of allergic dermatitis involves patch testing to determine the specific allergen. Education about avoidance of the allergen and recommendations for allergen-free products are the most important aspects of managing patients with allergic contact dermatitis. Treatment depends on the severity and extent of involvement. First-line treatment is topical corticosteroids, followed by topical calcineurin inhibitors. For more extensive dermatitis, systemic corticosteroids are beneficial.