Pre-admission ambient air pollution and blood soot particles predict hospitalisation outcomes in COVID-19 patients.

BACKGROUND: Air pollution exposure is one of the major risk factors for aggravation of respiratory diseases. We investigated whether exposure to air pollution and accumulated black carbon (BC) particles in blood were associated with coronavirus disease 2019 (COVID-19) disease severity, including the risk for intensive care unit (ICU) admission and duration of hospitalisation. METHODS: From May 2020 until March 2021, 328 hospitalised COVID-19 patients (29% at intensive care) were recruited from two hospitals in Belgium. Daily exposure levels (from 2016 to 2019) for particulate matter with aerodynamic diameter <2.5 µm and <10 µm (PM2.5 and PM10, respectively), nitrogen dioxide (NO2) and BC were modelled using a high-resolution spatiotemporal model. Blood BC particles (internal exposure to nano-sized particles) were quantified using pulsed laser illumination. Primary clinical parameters and outcomes included duration of hospitalisation and risk of ICU admission. RESULTS: Independent of potential confounders, an interquartile range (IQR) increase in exposure in the week before admission was associated with increased duration of hospitalisation (PM2.5 +4.13 (95% CI 0.74-7.53) days, PM10 +4.04 (95% CI 1.24-6.83) days and NO2 +4.54 (95% CI 1.53-7.54) days); similar effects were observed for long-term NO2 and BC exposure on hospitalisation duration. These effect sizes for an IQR increase in air pollution on hospitalisation duration were equivalent to the effect of a 10-year increase in age on hospitalisation duration. Furthermore, for an IQR higher blood BC load, the OR for ICU admission was 1.33 (95% CI 1.07-1.65). CONCLUSIONS: In hospitalised COVID-19 patients, higher pre-admission ambient air pollution and blood BC levels predicted adverse outcomes. Our findings imply that air pollution exposure influences COVID-19 severity and therefore the burden on medical care systems during the COVID-19 pandemic.

Prognosis and treatment of FOLFOX therapy related interstitial pneumonia: a plea for multimodal immune modulating therapy in the respiratory insufficient patient.

BACKGROUND: The FOLFOX regimen, i.e., folinic acid (FOL), fluorouracil (F) and oxaliplatin (OX), is a drug cocktail that is used to treat gastric and colorectal cancers. Despite the concomitant improvements in response rate, duration of response and patient survival, reports of serious toxic pulmonary side effects have progressively emerged. CASE PRESENTATION: We describe a patient who was treated with FOLFOX as an adjuvant to a rectosigmoidal resection of a rectosigmoidal carcinoma and who developed respiratory insufficiency requiring mechanical ventilation. Computed tomography (CT) imaging and open lung biopsy findings were compatible with interstitial pneumonia (IP). She received multimodal combination treatment (acetylcysteine, corticosteroids, immune globulins and cyclophosphamide) and survived. We performed a systematic literature search and reviewed all 45 reported cases of FOLFOX-related lung toxicity and/or pulmonary fibrosis for their clinical characteristics and their outcomes related to therapy. CONCLUSIONS: We found that for the 45 cases with available data, the median age was 70 years, and the male-female ratio was 3.5: 1. In the patients exhibiting only mild respiratory symptoms, discontinuation of the culprit drug (oxaliplatin) resulted in a 100% regression of the symptoms. However the prognosis of the respiratory insufficient patient proved to be grim: death occurred in 76.9% of the cases despite conventional treatment with corticosteroids. We therefore urge oncologists and critical care specialists not to limit their interventions to the discontinuation of chemotherapy, artificial ventilation, corticosteroids and glutathione replenishment and to consider the gradual introduction of additional immune-modulating agents whenever life-threatening respiratory symptoms in oxaliplatin-treated patients do not subside; all the more so considering the fact that our analysis showed that every patient who survived intubation and mechanical ventilation experienced a full clinical recovery.

Pre-admission air pollution exposure prolongs the duration of ventilation in intensive care patients.

PURPOSE: Air pollutant exposure constitutes a serious risk factor for the emergence or aggravation of (existing) pulmonary disease. The impact of pre-intensive care ambient air pollutant exposure on the duration of artificial ventilation was, however, not yet established. METHODS: The medical records of 2003 patients, admitted to the intensive care unit (ICU) of the Antwerp University Hospital (Flanders, Belgium), who were artificially ventilated on ICU admission or within 48 h after admission, for the duration of at least 48 h, were analyzed. For each patient's home address, daily air pollutant exposure [particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) and ≤ 10 µm (PM10), nitrogen dioxide (NO2) and black carbon (BC)] up to 10 days prior to hospital admission was modeled using a high-resolution spatial-temporal model. The association between duration of artificial ventilation and air pollution exposure during the last 10 days before ICU admission was assessed using distributed lag models with a negative binomial regression fit. RESULTS: Controlling for pre-specified confounders, an IQR increment in BC (1.2 µg/m3) up to 10 days before admission was associated with an estimated cumulative increase of 12.4% in ventilation duration (95% CI 4.7-20.7). Significant associations were also observed for PM2.5, PM10 and NO2, with cumulative estimates ranging from 7.8 to 8.0%. CONCLUSION: Short-term ambient air pollution exposure prior to ICU admission represents an unrecognized environmental risk factor for the duration of artificial ventilation in the ICU.

Emergence of colistin resistance during treatment of recurrent pneumonia caused by carbapenemase producing Klebsiella pneumoniae.

A 60-year-old woman received meropenem/colistin treatment for bilateral pneumonia caused by a ST15 carbapenemase producing Klebsiella pneumoniae. The patient recovered but re-infection with the same (ST15), but now colistin-resistant K. pneumoniae, occurred. The molecular mechanism of the emerged colistin resistance was identified as mgrB gene modification by insertion element (IS) IS903B.

Streptococcus pneumoniae meningoencephalitis with unusual and widespread white matter lesions.

Streptococcus pneumoniae is a common cause of bacterial meningitis, frequently leading to death or severe neurological impairment. We report an exceptional case of a 7-month-old child with meningoencephalitis caused by S. pneumoniae. Peculiar, widespread and unique signal abnormalities were found on magnetic resonance imaging (MRI) with extensive central nervous white matter injury as well as evidence of thrombosis of the lateral transverse sinus. These changes were observed very early in the course of the illness, presumably reflecting widespread cytotoxic edema, vasculitis and acute demyelination. These lesions occurred despite appropriate antibiotic and anti-inflammatory (glucocorticoid) therapy started very early in the course of the disease. Such diffuse white matter lesions in the early course of (pediatric) cases of S. pneumoniae meningoencephalitis have not been reported previously.

Tacrolimus-related polyneuropathy: case report and review of the literature.

Patients, in particular recipients of orthotopic liver transplants, receiving the immunosuppressant tacrolimus (FK-506), are at risk for developing central neurotoxic adverse events. We report the occurrence of a tacrolimus-induced peripheral neurotoxic event, i.e. pure motor axonal polyneuropathy of the lower limbs in a 44-year-old woman, 9 days after combined orthotopic liver and pancreas transplantation. She was treated for 5 days with intravenous immunoglobulins. Partial recovery followed over months to years. An overview of all 11 reported FK506-associated polyneuropathies is given.

Amniotic fluid embolism after surgical trauma: two case reports and review of the literature.

Amniotic fluid embolism (AFE) is a relatively rare condition usually occurring during or shortly after pregnancy and is catastrophic in most cases. The classical description is a sudden onset of dyspnoea, cyanosis and hypotension out of proportion to the blood loss, followed quickly by cardiorespiratory arrest. Up to 20% of patients will have seizures and up to 40% will have consumptive coagulopathy. If the patient survives the initial phase, a non-cardiogenic pulmonary oedema will follow in up to 70% of all cases. We report on two cases of severe and near fatal amniotic fluid embolism during pregnancy. Surgical trauma, caused by a blow in the stomach and a surgical intervention, was considered to be the aetiology.

Fomepizole as a therapeutic strategy in paediatric methanol poisoning. A case report and review of the literature.

UNLABELLED: Methanol poisoning is not frequently observed in children; however, without treatment, serious intoxication can be complicated by visual impairment, coma, metabolic acidosis, respiratory and circulatory insufficiency and death. Treatment in a paediatric intensive care is therefore compulsory. Methanol is metabolised in the liver by alcohol dehydrogenase to the toxic metabolites formaldehyde and formic acid. Classically, ethanol is given as a competitive inhibitor in order to avoid the formation of these compounds. We report on the use of fomepizole (4-methylpyrazole),a new and potent inhibitor of alcohol dehydrogenase, in a 3-year-old boy after the intake of a toxic amount of methanol. The course was uneventful and the use of fomepizole was not accompanied by any side-effects. An overview is given of all cases of paediatric poisoning in which fomepizole was used. CONCLUSION: Fomepizole seems to be a safe and valid alternative to ethanol in cases of paediatric methanol poisoning.