An approach to common sleep presentations in infants and toddlers.

BACKGROUND: Healthy sleep is vital for optimal child development, yet over 30% of Australian parents report having children with disrupted sleep affecting all family members. These sleep difficulties might co-exist with sleep breathing disorders, contributing to morbidity and reduced quality of life. OBJECTIVE: This article aims to provide general practitioners (GPs) with an evidence-based, biopsychosocial approach to managing common sleep problems in infants and preschool-aged children. DISCUSSION: Strategies and techniques are outlined to aid GPs in promoting healthy sleep during infancy, educating parents on typical sleep patterns and supporting families in managing problematic sleep patterns in toddlers. Emphasis is placed on a tailored approach to developing a healthy sleep environment to meet the child's needs and parental values. Valuable resources and indications for specialist consultation are included.

Optimising sleep in adolescents: The challenges.

BACKGROUND: Adolescence is a stage of significant transition as children develop into young adults. Optimal sleep is crucial during this period to ensure physical, emotional and mental wellbeing. However, it is well recognised that insufficient quality and quantity of sleep is common among adolescents worldwide. OBJECTIVE: This article aims to provide general practitioners with an overview of the key issues encountered in adolescent patients relating to sleep and summarises approaches to assessment and evidence-based management of sleep problems in this population. DISCUSSION: This review highlights the physiological changes that affect sleep during adolescence and how other factors, including unhealthy sleep behaviours, influence these. It discusses the importance of healthy sleep and the consequences of sleep disturbance in adolescents. Management strategies are outlined, focusing on the key common issues that affect sleep in the teenage years, and guidance on when to consider co-management with specialist care is provided.

Reduced forced expiratory flow but not increased exhaled nitric oxide or airway responsiveness to methacholine characterises paediatric sickle cell airway disease.

BACKGROUND: Asthma and airway hyper-responsiveness are reportedly more common in children with sickle cell disease (SCD). AIM: To determine airway responsiveness, airway inflammation and clinical features of asthma in SCD. METHODS: A prospective, single-centre study of 50 SCD children without overt pulmonary vascular disease and 50 controls. Exhaled nitric oxide (FeNO) and total serum IgE were measured and spirometry and methacholine challenge were performed. The methacholine dose-response slope (DRS) was calculated. RESULTS: Doctor diagnosis of asthma was made in 7 (14%) SCD versus 12 (24%) control subjects (p=0.203). FeNO levels were similar in SCD and controls (p=0.250), and were higher in those with atopy and an asthma diagnosis (OR 4.33, 95% CI 1.7 to 11.1; p<0.05). zFEV1 (p=0.002) and zFEV1/FVC (p=0.003) but not zFVC (p=0.098) were lower in SCD versus controls. DRS was higher in those with asthma (p=0.006) but not in SCD versus controls (p=0.403). DRS correlated with FeNO and blood eosinophil count in controls but not SCD. In SCD, DRS was higher in those admitted to hospital with respiratory symptoms (n=27) versus those never admitted (n=23) (p=0.046). DRS was similar in those with at least one acute chest syndrome episode (n=12) versus those with none (n=35) (p=0.247). CONCLUSIONS: SCD children have airflow obstruction despite having minimal evidence of pulmonary vascular disease. Airflow obstruction is not associated with increased methacholine sensitivity or eosinophilic inflammation, at least as judged by FeNO. Airflow obstruction in SCD does not appear to be related to childhood eosinophilic asthma, but its pathophysiology remains ill understood.

The impact of sickle cell disease on exercise capacity in children.

BACKGROUND: Little is known about pulmonary vascular complications in children with sickle cell disease (SCD). We hypothesized that transfer factor (diffusing capacity of the lung for carbon monoxide [D(LCO)] ) may be used as a surrogate for the size of the pulmonary vascular bed and that pulmonary vascular abnormalities in children with SCD may limit exercise capacity. METHODS: Fifty stable patients with SCD aged 10 to 18 years and 50 healthy control subjects matched for race and age were recruited. Incremental ergometer cardiopulmonary exercise testing was performed using respiratory mass spectrometry for exhaled gas analysis. A rebreathing maneuver was used to measure functional residual capacity, effective pulmonary blood fl ow (Qpeff), and D(LCO), and helium dilution was used to calculate minute ventilation, oxygen consumption, and CO 2 production. RESULTS: In the 89 evaluable subjects, there were no ventilatory differences between SCD and control subjects. Qpeff was consistently 15% to 20% greater in subjects with SCD than control subjects at all stages, but D(LCO) corrected for both surface area and hemoglobin was only about 7% to 10% greater in subjects with SCD at all stages. As a result, the D(LCO)/Qpeff ratio was considerably lower in SCD at all stages. Arteriovenous oxygen content difference was about one-third less in SCD at all stages. CONCLUSIONS: Contrary to our hypothesis, failure to maintain a sufficient Qpeff to compensate for anemia led to exercise limitation. The ratio of pulmonary capillary blood volume to fl ow is reduced throughout, implying subtle pulmonary vascular disease; however, this was not a factor limiting exercise.

Paediatric sickle cell disease: pulmonary hypertension but normal vascular resistance.

BACKGROUND: Adults with sickle cell disease (SCD) and pulmonary hypertension have high mortality but death in SCD children with pulmonary hypertension is rare. The authors hypothesised that pulmonary hypertension in SCD children may be secondary to anaemia-induced high cardiac output rather than pulmonary vascular disease. METHODS: Two independent, validated techniques were used to estimate pulmonary vascular resistance (PVR) in 50 SCD children and 50 matched controls. Tricuspid regurgitant jet velocity (TRV) and right ventricular outflow tract velocity time integral were measured using Doppler echocardiography; PVR was calculated from their ratio. Acetylene rebreathing technique using respiratory mass spectrometry was also performed to calculate pulmonary blood flow and stroke index, an estimate of PVR. RESULTS: TRV was higher in SCD children compared with controls (2.28 vs 2.14 m/s, p=0.02). Fifteen of 34 (44%) children with haemoglobin of the SS genotype (HbSS) versus 1/16 (6%) children with haemoglobin of the SC genotype (HbSC) had pulmonary hypertension (TRV≥2.5 m/s) (p=0.009). Right ventricular stroke volume was higher (p<0.05) and Doppler PVR lower (1.20 (0.19) vs 1.31 (0.20) Wood units, p=0.04) in SCD children with pulmonary hypertension compared with controls. Qpeff and stroke index were higher in SCD children compared with controls (p<0.001 for both) and correlated with anaemia (p<0.001) and TRV (p=0.03). There was no correlation between TRV and history of asthma or acute chest syndrome. CONCLUSIONS: Pulmonary hypertension due to raised cardiac output is common in HbSS SCD children and is associated with normal PVR. PVR should be measured before therapy with agents such as sildenafil or bosentan is contemplated.