Background
Data on the prevalence of bacterial and viral co-infections among patients admitted to the ICU for acute respiratory failure related to SARS-CoV-2 pneumonia are lacking. We aimed to assess ...the rate of bacterial and viral co-infections, as well as to report the most common micro-organisms involved in patients admitted to the ICU for severe SARS-CoV-2 pneumonia.
Patients and methods
In this monocenter retrospective study, we reviewed all the respiratory microbiological investigations performed within the first 48 h of ICU admission of COVID-19 patients (RT-PCR positive for SARS-CoV-2) admitted for acute respiratory failure.
Results
From March 13th to April 16th 2020, a total of 92 adult patients (median age: 61 years, 1st–3rd quartiles 55–70; males:
n
= 73/92, 79%; baseline SOFA: 4 3–7 and SAPS II: 31 21–40; invasive mechanical ventilation:
n
= 83/92, 90%; ICU mortality:
n
= 45/92, 49%) were admitted to our 40-bed ICU for acute respiratory failure due to SARS-CoV-2 pneumonia. Among them, 26 (28%) were considered as co-infected with a pathogenic bacterium at ICU admission with no co-infection related to atypical bacteria or viruses. The distribution of the 32 bacteria isolated from culture and/or respiratory PCRs was as follows: methicillin-sensitive
Staphylococcus aureus
(
n
= 10/32, 31%),
Haemophilus influenzae
(
n
= 7/32, 22%),
Streptococcus pneumoniae
(
n
= 6/32, 19%), Enterobacteriaceae (
n
= 5/32, 16%),
Pseudomonas aeruginosa
(
n
= 2/32, 6%),
Moraxella catarrhalis
(
n
= 1/32, 3%) and
Acinetobacter baumannii
(
n
= 1/32, 3%). Among the 24 pathogenic bacteria isolated from culture, 2 (8%) and 5 (21%) were resistant to 3rd generation cephalosporin and to amoxicillin–clavulanate combination, respectively.
Conclusions
We report on a 28% rate of bacterial co-infection at ICU admission of patients with severe SARSCoV-2 pneumonia, mostly related to
Staphylococcus aureus, Haemophilus influenzae
,
Streptococcus pneumoniae
and Enterobacteriaceae. In French patients with confirmed severe SARSCoV-2 pneumonia requiring ICU admission, our results encourage the systematic administration of an empiric antibiotic monotherapy with a 3rd generation cephalosporin, with a prompt de-escalation as soon as possible. Further larger studies are needed to assess the real prevalence and the predictors of co-infection together with its prognostic impact on critically ill patients with severe SARS-CoV-2 pneumonia.
Zika Virus Associated with Meningoencephalitis Carteaux, Guillaume; Maquart, Marianne; Bedet, Alexandre ...
The New England journal of medicine,
2016-Apr-21, Volume:
374, Issue:
16
Journal Article
Looking for a sepsis source Contou, Damien; de Prost, Nicolas
Critical care (London, England),
01/2020, Volume:
24, Issue:
1
Journal Article
Peer reviewed
Open access
Authors, response Jan J. De Waele and Yasser Sakr To the editor, We agree with Drs. Contou and de Prost that in some patients with sepsis or septic shock, an infection diagnosis cannot be established ...in the first 24 h. In their study on patients admitted to 10 ICUs in France, indeed a septic shock diagnosis could not be confirmed in 26% of patients 2. In the majority of patients without confirmed septic shock, either no cause or another cause of the shock could be established, and only in less than 1 out of 3 patients, an infection cause was established later—most of these were pneumonia and urinary tract or abdominal infections. However, when only considering patients with a final diagnosis of septic shock, this diagnosis was in fact confirmed within 24 h in over 90% of the patients (374/411). The message here is that when an infection source cannot be identified within a 24-h timeframe, it is more likely that there is an alternative explanation for the shock and no infection is present. This does not mean however that the search for the infection source should not be continued. These data align with nicely the finding by Klein Klouwenberg et al. who demonstrated that in 1 out 6 patients in whom sepsis or septic shock was suspected in the emergency department, eventually no infection was documented 3. Clearly this demonstrates that we remain poor at diagnosing sepsis—read diagnosing infection—and that we should acknowledge that in many patients in whom we suspect infection, in fact there is none. However, using a systematic approach, we should try to maximize the chances of establishing a final diagnosis of septic shock 1.
Whether patients mainly die from refractory respiratory failure directly due to SARS-CoV-2 pneumonia or from sepsis as reported in non-COVID-19 ARDS patients 3 is unknown. ...the increased risk of ...pulmonary embolism extensively described among COVID-19 patients together with the SARS-CoV-2-associated myocardial injuries 4 may expose critically ill COVID-19 patients to death from a cardiac origin 5. Causes of death were categorized in four subgroups: (1) refractory respiratory failure, (2) shock with multiorgan failure, (3) cardiac death including proven pulmonary embolism (proximal thrombus on CT-pulmonary angiography with acute cor pulmonale on echocardiography and vasopressor requirement) and unexpected cardiac arrest (neither prior oxygen desaturation nor circulatory failure) and (4) neurological death (ischemic/hemorrhagic stroke with brain herniation). SEE PDF None of the patients dying from shock with multi-organ failure or from cardiac death died after a withholding (all the patients with unexpected cardiac arrest underwent cardiopulmonary resuscitation) or withdrawal procedure while all patients dying from a neurological cause died after a withdrawal procedure. In-hospital cardiac arrest in critically ill patients with covid-19: multicenter cohort study.
Hypercoagulability and endotheliopathy reported in patients with coronavirus disease 2019 (COVID-19) combined with strict and prolonged immobilization inherent to deep sedation and administration of ...neuromuscular blockers for Acute Respiratory Distress Syndrome (ARDS) may expose critically ill COVID-19 patients to an increased risk of venous thrombosis and pulmonary embolism (PE). We aimed to assess the rate and to describe the clinical features and the outcomes of ARDS COVID-19 patients diagnosed with PE during ICU stay. From March 13th to April 24th 2020, a total of 92 patients (median age: 61 years, 1st-3rd quartiles 55-70; males: n = 73/92, 79%; baseline SOFA: 4 3-7 and SAPS II: 31 21-40; invasive mechanical ventilation: n = 83/92, 90%; ICU mortality: n = 45/92, 49%) were admitted to our 41-bed COVID-19 ICU for ARDS due to COVID-19. Among them, 26 patients (n = 26/92, 28%) underwent a Computed Tomography Pulmonary Angiography which revealed PE in 16 (n = 16/26, 62%) of them, accounting for 17% (n = 16/92) of the whole cohort. PE was bilateral in 3 (19%) patients and unilateral in 13 (81%) patients. The most proximal thrombus was localized in main (n = 4, 25%), lobar (n = 2, 12%) or segmental (n = 10, 63%) pulmonary artery. Most of the thrombi (n = 13/16, 81%) were located in a parenchymatous condensation. Only three of the 16 patients (19%) had lower limb venous thrombosis on Doppler ultrasound. Three patients were treated with alteplase and anticoagulation (n = 3/16, 19%) while the 13 others (n = 13/16, 81%) were treated with anticoagulation alone. ICU mortality was higher in patients with PE compared to that of patients without PE (n = 11/16, 69% vs. n = 2/10, 20%; p = 0.04). The low rate of lower limb venous thrombosis together with the high rate of distal pulmonary thrombus argue for a local immuno-thrombotic process associated with the classic embolic process. Further larger studies are needed to assess the real prevalence and the risk factors of pulmonary embolism/thrombosis together with its prognostic impact on critically ill patients with COVID-19.
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