Surgery was once regarded as the treatment of choice in operable patients with massive hemoptysis. Bronchial artery embolization (BAE) is an excellent nonsurgical alternative; it is proven to be very effective and lacks the mortality and morbidity encountered in surgical interventions. Nevertheless, surgery is recommended in patients with massive hemoptysis caused by thoracic vascular injury, arteriovenous malformation, leaking thoracic aneurysm with bronchial communication, hydatid cyst, and other conditions in which BAE would be inadequate. MEDICAL MANAGEMENT: Conservative medical therapy may suffice in certain conditions, like bronchiectasis, coagulopathies, Goodpasture's syndrome, and acute bronchopulmonary infections. Preparation for other interventions (endobronchial tamponade, BAE, or surgery in eligible candidates) should be undertaken if the bleeding fails to respond to conservative measures. Supportive therapy should be applied vigorously to all patients with massive hemoptysis.

Mortality remains very high among septic patients despite the advanced treatments rendered in intensive care units. The development of septic shock is multifactorial. Tissue damage and organ dysfunction may be caused not only by the microorganisms but also by the inflammatory mediators released in response to the infection. Cytokines (tumor necrosis factor, interleukin-1, interleukin-6, interleukin-8, high-mobility group box-1 protein, macrophage migratory inhibitory factor) and noncytokines (nitric oxide, platelet-activating factor, complements, and eicosonoids) may inflict tissue injury and contribute to multiple organ dysfunction and cell death (or apoptosis). Gram-negative bacteria are the most common organisms identified in septic patients. The pathological effects of gram-negative bacteria are conveyed through lipopolysaccharide derived from the bacterial cell membrane. Lipopolysaccharide activates the nuclear factor kappa B, which triggers the release of inflammatory mediators. Protein components from gram-positive bacteria, fungi, or viruses may evoke the activation of nuclear factor kappa B in a similar fashion as lipopolysaccharide. Endogenous anti-inflammatory mediators are released in response to the infection and act to control the overwhelming systemic inflammatory response. The fragile balance between negative and positive feedback on the inflammatory mediators is the key factor that modulates the cellular damage and influences the clinical outcome.

The impact of chikungunya virus (CHIKV) infection on diabetic patients (DPs) has not been described. We aimed to compare clinical features of CHIKV infection in DPs and nondiabetic patients (NDPs), and to evaluate its effects on glycemic control among DPs. We recorded clinical information and, in DPs, glycemic control. Forty-six DPs and 53 NDPs aged ≥ 20 years living in Haiti, with acute CHIKV infection, were studied. Diabetes duration was 7.1 ± 6.1 years. The most common acute CHIKV clinical manifestations were arthralgia (100.0% DPs and 98.1% NDPs, P = 1.000) and fever (86.9% DPs and 90.5% NDPs, P = 0.750). In DPs as compared with NDPs, arthralgia was more intense (mean pain score of 6.0/10 ± 2.2 versus 5.1/10 ± 2.0, P = 0.04) and took longer to improve (8.2 ± 3.0 versus 3.5 ± 2.5 days, P < 0.0001). Severe arthralgia was more prevalent (58.7% versus 20.8%, P = 0.0002), as was myalgia (80.4% versus 50.9%, P = 0.003), and fever lasted longer (5.1 ± 1.8 versus 3.7 ± 1.7 days, P = 0.0002). Among DPs, median fasting capillary glucose before versus after disease onset was 132.5 and 167.5 mg/dL (P < 0.001), corresponding to a median increase of 26.8% (interquartile range: 14.4–50.1%). Antidiabetic medication was titrated up in 41.3%. In summary, among DPs, CHIKV infection has a significant negative impact on glycemic control and, compared with NDPs, results in greater morbidity. Close clinical and glycemic observation is recommended in DPs with CHIKV infection.

Context: Iodine deficiency is the leading cause of preventable neurodevelopmental delay in children worldwide and a possible public health concern in Haiti. Objective: To determine the prevalence of iodine deficiency in Haitian young children and its influence by environmental factors. Design: Cross-sectional study, March through June 2015. Setting: Community churches in 3 geographical regions in Haiti. Participants: 299 healthy Haitian children aged 9 months to 6 years; one-third each enrolled in a coastal, mountainous, and urban region. Main Outcome Measures: Urinary iodide, serum thyrotropin (TSH), goiter assessment, and urinary perchlorate and thiocyanate. Results: Mean age was 3.3±1.6 years, with 51% female, median family income USD 30/week, and 16% malnutrition. Median urinary iodide levels were normal in coastal (145 μg/L, interquartile range [IQR] 97 to 241) and urban regions (187 μg/L, IQR 92 to 316), but revealed mild iodine deficiency in a mountainous region (89 μg/L, IQR 56 to 129), P &lt; 0.0001. Grade 1 goiters were palpated in 2 children, but TSH values were normal. Urinary thiocyanate and perchlorate concentrations were not elevated. Predictors of higher urinary iodide included higher urinary thiocyanate and perchlorate, breastfeeding, and not living in a mountainous region. Conclusions: Areas of mild iodine deficiency persist in Haiti’s mountainous regions. Exposure to two well-understood environmental thyroid function disruptors is limited.