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Persons with uncomplicated influenza typically experience acute onset of respiratory symptoms (cough, rhinorrhea, congestion), myalgias, and headache with or without fever. During influenza season, clinicians should also consider influenza when there is only fever present or in patients who are afebrile and have respiratory symptoms [49]. Complications of influenza vary by age, underlying comorbidities or high-risk conditions such as pregnancy, and immune function; elderly and immunocompromised persons may not always manifest fever. Critically ill patients may be admitted with respiratory or multi-organ failure, exacerbation of an underlying condition such as chronic lung disease [50, 51], heart failure [52], or other extrapulmonary complications including stroke, encephalopathy, or encephalitis [30, 49, 53].
Influenza vaccination can reduce the risk of complications from influenza, including reducing illness severity and the risks of hospitalization, ICU admission, and death. The elderly, young children, pregnant women, and those with underlying medical conditions are most at risk for severe complications of influenza. A diagnosis of influenza should be considered in critically ill patients admitted with complications such as exacerbation of underlying chronic comorbidities, community-acquired pneumonia, and respiratory failure during influenza season. Influenza molecular assays are recommended for testing upper respiratory tract specimens in patients without signs of lower respiratory tract disease. However, because critically ill patients with lower respiratory tract disease may have cleared influenza virus in the upper respiratory tract, but have prolonged influenza viral replication in the lower respiratory tract, an endotracheal aspirate (preferentially) or bronchoalveolar lavage fluid specimen (if collected for other diagnostic purposes) should be tested by molecular assay. Antiviral treatment with standard-dose oseltamivir delivered orally or enterally by oro or naso-gastric tube is recommended as soon as possible for patients with suspected influenza without waiting for testing results. Corticosteroids should not be routinely administered for treatment of influenza and should only be given for other indications (e.g., exacerbation of asthma or chronic obstructive pulmonary disease, or septic shock), because of the risk for prolongation of influenza viral shedding and ventilator-associated pneumonia in critically ill influenza patients with respiratory failure. Future directions for treatment of influenza in critically ill patients include novel antiviral compounds, combination antiviral treatment with drugs with different mechanisms of action, immunomodulatory agents, and strategies for multi-modality, combination antiviral, and host-directed immunomodulatory therapies.
However, the nature of the disease has evolved over the last two decades, moving from a neonatal high mortality-risk disease towards less severe and much broader clinical presentations. Most cases manifest in the neonatal period, but increased later-onset presentations are recognized during childhood and adulthood. Familial cases with CCHS exist [22, 45, 46, 48, 53, 86, 95], due to parental transmission of somatic and germline mosaic mutations [6, 9, 72]. In the meantime, PHOX2B-mediated mechanisms have been extensively investigated and better understood in vitro [4, 5, 7, 8, 20, 24, 25, 68, 97], in vivo [27, 44, 70], and in CCHS patients [28, 33, 92,93,94, 99]. However, most pathogenic pathways are yet to be disclosed. In addition, a subset of patients with a CCHS phenotype has no mutation in PHOX2B. Recently, mutations of two new genes, MYO1H and LBX1, have been found in two consanguineous CCHS families [39, 88]. It is expected that other genes may account for the patients without any apparent causative PHOX2B mutation. Finally, although some molecules have shown effects on ventilation e.g. carbamazepine [81], desogestrel [89], CCHS currently has no curative treatment. Management is still supported by lifetime assisted ventilation and multi-disciplinary care. Research studies focus to target sensitive molecules for a putative pharmacologic treatment.
are commonly features of chronic or acute hypoventilation. In most cases, apnoeas and hypoventilation may occur at birth, or less frequently during childhood or adulthood. Less common are presentations including brief resolved unexplained events (BRUE), repeated oxygen desaturation, severe central sleep apnoeas, failure to wean from a ventilator after pneumonia, sleep hypoventilation more severe than expected for obstructive sleep apnoeas, acquired pulmonary hypertension, delayed recovery from anaesthesia or opioids, coma after sedatives, or near drowning [106]. Familial cases are diagnosed by genetic tests performed after an affected individual has been identified.
requires that the patient is cooperative, has a normal airway and needs ventilator support during sleep only (or has phrenic nerve pacing during the daytime). This is the first option in children and adults presenting with late-onset CCHS and requiring night time ventilation only. For patients who require daytime ventilatory support, mask ventilation should not be used alone, but may be considered in association with a respiratory pacing during wakefulness. There are infants with neonatal presentation of CCHS who have received mask ventilation without ever having had tracheotomy [71]. There is no available evidence comparing outcomes of children using tracheostomy ventilation and those with early mask ventilation. Mask ventilation needs a high degree of supervision by the carers during sleep, especially for infants and young children as there may be serious consequences of dislocation of the mask or obstruction of the upper airway.
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