**2. ICU infections**

### **2.1. Severe respiratory infections**

Pneumonia is one of the infections frequently requiring hospital admission and urgent antimicrobial treatment due to the risk of rapid evolution to respiratory and multiple organ failure, especially in immunocompromised patients, or when caused by MDRO. The diagnosis of severe pneumonia requires ICU admission given the need for assisted ventilation or oxygen therapy, in the presence of radiological changes, confirming the rapid progression, as well as the evolution towards sepsis [1, 2].

• antibiotic therapy, administration of antacids or H<sup>2</sup>

• administration of over 4 units of blood before the surgical intervention [5, 6].

cross-contamination but also the direct access of a massive bacterial inoculum.

presence of comorbidities (immune suppression or immunosuppressive treatments).

hospitalisation days accumulated until the onset of pneumonia.

tam or ertapenem (**Figure 1**).

The diagnosis of HAP should be rapidly reached, and the antibiotic treatment has to be promptly introduced, and any delay potentially aggravates the evolution and prognosis. The first antibiotic of choice depends on infection severity, patient's risk factors, and the number of

The empirical treatment of HAP or VAP occurring during the first five hospitalisation days in patients without risk factors for MDRO must include antibiotics active against not only aerobic Gram-negative bacilli (*Enterobacter* spp., *E. coli*, *Klebsiella* spp., *Proteus* spp., *Serratia* spp.), pathogens with respiratory tropism (*Haemophilus influenzae* and *Streptococcus pneumoniae*), but also methicillin-sensitive *S. aureus* (MSSA). Recommendations include therapeutic schemes based on ceftriaxone or a fluoroquinolone (ciprofloxacin or levofloxacin) or ampicillin-sulbac-

In the case of patients with HAP or VAP who are at risk for MDRO infection, regardless of the infection's severity, the antibiotic treatment must be directed against *P. aeruginosa*, *K. pneumoniae* (ESBL-producing strains), *Acinetobacter* spp. and MRSA. Antibiotic associations including antipseudomonal cephalosporins (ceftazidime), an antipseudomonal carbapenem (imipenem) or beta-lactam/beta-lactamase inhibitors (piperacillin-tazobactam), will be administered, in association with antipseudomonal fluoroquinolones (ciprofloxacin) or an

These factors disturb respiratory functions leading to obstructions, decreased pulmonary volume, decreased filtration of inhaled air, and decreased secretion clearance. The insertion of an endotracheal tube allows the direct access of pathogens into the lower airways or may cause lesions of the epithelial mucosa, which represent breaches. Additionally, inadequate hand hygiene of medical personnel, lack of adherence to universal precautions, errors in decontamination of equipment or in the practice of endotracheal aspiration may favour not only

This pneumonia is caused by a wide range of pathogens, and it may be plurietiological and is only rarely caused by viruses or fungi. The aetiological agents frequently involved in such infections are not only Gram-negative bacilli (*Pseudomonas aeruginosa, Klebsiella* spp., *Escherichia coli*) but also Gram-positive cocci such as *Staphylococcus aureus*. The frequency of MDRO is increasing and influences the treatment, as in the case of methicillin-resistant *Staphylococcus aureus* (MRSA), carbapenem-resistant *Pseudomonas*, fluoroquinolones, antipseudomonal penicillins and cephalosporins, extended-spectrum beta-lactamase-producing *Enterobacteriaceae* (ESBL), *Acinetobacter baumannii*, etc. The risk factors for MDRO infections are the use of antibiotics during the previous 90 days, the onset of pneumonia after 4 days of hospitalisation, circulation of such pathogens in the health care unit in question, as well as the

• thoracic or upper abdominal surgery,

nial traumas,

• emergency surgery,

blockers, barbituric therapy after cra-

http://dx.doi.org/10.5772/intechopen.79229

17

Infections and Multidrug-Resistant Pathogens in ICU Patients

Community-acquired pneumonia (CAP) is caused by bacteria in 85% of cases, the most frequently involved pathogens being *Streptococcus pneumoniae*, *Haemophilus influenzae* and *Moraxella catarrhalis*. Severe CAP cases may also be produced by other pathogens (influenza viruses, coronaviruses, Hanta virus, *Legionella*).

Pneumonia may trigger acute myocardial infarction in patients with heart diseases, while in splenectomised patients or with spleen dysfunction, *S. pneumoniae* may cause severe sepsis with lethal outcome within 12–24 h from onset, even under antibiotic therapy.

The treatment of CAP must cover both typical and atypical pathogens. Clinical studies have shown that monotherapy with respiratory fluoroquinolones or tigecycline is almost as effective as therapy with antibiotic associations (ceftriaxone plus doxycycline, azithromycin, or respiratory quinolones) [3].

On the other hand, presently ICUs are especially confronted with respiratory infections acquired during hospitalisation. According to 2012/506/EU European Parliament Decision, hospital-acquired pneumonia (HAP) occurs 48 h or more after admission and was not incubating at the time of admission, while ventilated-associated pneumonia (VAP) arises in 48 h after endotracheal intubation [4]. The microorganisms involved in the aetiology of these pneumonia cases originate in the oropharyngeal or upper airways colonisation flora or by direct inoculation of contaminated solutions, via an endotracheal catheter, or exogenous contamination of respiratory equipment caused by health care staff.

The hospital-acquired risk factors associated with this type of infection are:


**2. ICU infections**

16 Current Topics in Intensive Care Medicine

**2.1. Severe respiratory infections**

the evolution towards sepsis [1, 2].

respiratory quinolones) [3].

• long time sedation,

• post-trauma intubation,

• tracheostomy,

viruses, coronaviruses, Hanta virus, *Legionella*).

Pneumonia is one of the infections frequently requiring hospital admission and urgent antimicrobial treatment due to the risk of rapid evolution to respiratory and multiple organ failure, especially in immunocompromised patients, or when caused by MDRO. The diagnosis of severe pneumonia requires ICU admission given the need for assisted ventilation or oxygen therapy, in the presence of radiological changes, confirming the rapid progression, as well as

Community-acquired pneumonia (CAP) is caused by bacteria in 85% of cases, the most frequently involved pathogens being *Streptococcus pneumoniae*, *Haemophilus influenzae* and *Moraxella catarrhalis*. Severe CAP cases may also be produced by other pathogens (influenza

Pneumonia may trigger acute myocardial infarction in patients with heart diseases, while in splenectomised patients or with spleen dysfunction, *S. pneumoniae* may cause severe sepsis

The treatment of CAP must cover both typical and atypical pathogens. Clinical studies have shown that monotherapy with respiratory fluoroquinolones or tigecycline is almost as effective as therapy with antibiotic associations (ceftriaxone plus doxycycline, azithromycin, or

On the other hand, presently ICUs are especially confronted with respiratory infections acquired during hospitalisation. According to 2012/506/EU European Parliament Decision, hospital-acquired pneumonia (HAP) occurs 48 h or more after admission and was not incubating at the time of admission, while ventilated-associated pneumonia (VAP) arises in 48 h after endotracheal intubation [4]. The microorganisms involved in the aetiology of these pneumonia cases originate in the oropharyngeal or upper airways colonisation flora or by direct inoculation of contaminated solutions, via an endotracheal catheter, or exogenous con-

with lethal outcome within 12–24 h from onset, even under antibiotic therapy.

tamination of respiratory equipment caused by health care staff.

• general anaesthesia with endotracheal intubation,

• prolonged use of assisted ventilation,

The hospital-acquired risk factors associated with this type of infection are:

• other invasive procedures: bronchoscopy, nasogastric catheterisation,

• reintubation, change of ventilation circuits at intervals under 48 h,

• corticotherapy or other immunosuppressive treatments,

• administration of over 4 units of blood before the surgical intervention [5, 6].

These factors disturb respiratory functions leading to obstructions, decreased pulmonary volume, decreased filtration of inhaled air, and decreased secretion clearance. The insertion of an endotracheal tube allows the direct access of pathogens into the lower airways or may cause lesions of the epithelial mucosa, which represent breaches. Additionally, inadequate hand hygiene of medical personnel, lack of adherence to universal precautions, errors in decontamination of equipment or in the practice of endotracheal aspiration may favour not only cross-contamination but also the direct access of a massive bacterial inoculum.

This pneumonia is caused by a wide range of pathogens, and it may be plurietiological and is only rarely caused by viruses or fungi. The aetiological agents frequently involved in such infections are not only Gram-negative bacilli (*Pseudomonas aeruginosa, Klebsiella* spp., *Escherichia coli*) but also Gram-positive cocci such as *Staphylococcus aureus*. The frequency of MDRO is increasing and influences the treatment, as in the case of methicillin-resistant *Staphylococcus aureus* (MRSA), carbapenem-resistant *Pseudomonas*, fluoroquinolones, antipseudomonal penicillins and cephalosporins, extended-spectrum beta-lactamase-producing *Enterobacteriaceae* (ESBL), *Acinetobacter baumannii*, etc. The risk factors for MDRO infections are the use of antibiotics during the previous 90 days, the onset of pneumonia after 4 days of hospitalisation, circulation of such pathogens in the health care unit in question, as well as the presence of comorbidities (immune suppression or immunosuppressive treatments).

The diagnosis of HAP should be rapidly reached, and the antibiotic treatment has to be promptly introduced, and any delay potentially aggravates the evolution and prognosis. The first antibiotic of choice depends on infection severity, patient's risk factors, and the number of hospitalisation days accumulated until the onset of pneumonia.

The empirical treatment of HAP or VAP occurring during the first five hospitalisation days in patients without risk factors for MDRO must include antibiotics active against not only aerobic Gram-negative bacilli (*Enterobacter* spp., *E. coli*, *Klebsiella* spp., *Proteus* spp., *Serratia* spp.), pathogens with respiratory tropism (*Haemophilus influenzae* and *Streptococcus pneumoniae*), but also methicillin-sensitive *S. aureus* (MSSA). Recommendations include therapeutic schemes based on ceftriaxone or a fluoroquinolone (ciprofloxacin or levofloxacin) or ampicillin-sulbactam or ertapenem (**Figure 1**).

In the case of patients with HAP or VAP who are at risk for MDRO infection, regardless of the infection's severity, the antibiotic treatment must be directed against *P. aeruginosa*, *K. pneumoniae* (ESBL-producing strains), *Acinetobacter* spp. and MRSA. Antibiotic associations including antipseudomonal cephalosporins (ceftazidime), an antipseudomonal carbapenem (imipenem) or beta-lactam/beta-lactamase inhibitors (piperacillin-tazobactam), will be administered, in association with antipseudomonal fluoroquinolones (ciprofloxacin) or an

at least 48–72 h, a period during which the recommendation is to maintain the therapeutic scheme. If, after this interval of empirical treatment, the clinical status of the patient did not improve, the therapeutic scheme must be broadened, potential complications (pleurisy, pul-

Infections and Multidrug-Resistant Pathogens in ICU Patients

http://dx.doi.org/10.5772/intechopen.79229

19

The generalised septicaemic infection is an infection with an unpredictable outcome, high severity and increased mortality in the absence of adequate treatment. The correct choice of empirical antibiotic treatment depends on the intelligent use of clinical knowledge and epidemiological and microbiological data regarding the pathology in the area where the patient comes from. The lack of knowledge on the local resistance prevalence is a predictive factor for an incorrect treatment. The basic principle, which guides the treatment of the critical patient, is to rapidly initiate antibiotic treatment at correct doses, concordant with the pharmacokinetic and pharmacodynamic characters of the chosen drug and to adapt the treatment to the changes occurring in the clinical evolution and to the results of the antimicrobial sensitivity

Immediately after a patient with suspected sepsis is admitted, an attentive anamnesis and a thorough clinical examination are conducted in order to establish the entry and the location of the primary and secondary septic sites. The first emergency microbiological investigations are conducted (repeated blood cultures, cultures from secretions, lesions, urine, sputum, exudates, pleural fluid, etc.) together with evaluations of the renal, hepatic functions and state of

The practical approach includes the emergency admission of the patient into the ICU where prevention or correction of hypovolemia, functional and metabolic dysfunctions are attempted, concomitantly with the prompt initiation of antibiotic treatment according to the

The correct antibiotic treatment targets the resident microbial flora in the organ presumed to

The empirical treatment of sepsis consists of the association of bactericidal antibiotics with synergistic actions or monotherapy with an ultra-broad-spectrum antibiotic; antibiotics are administered intravenously in order to rapidly achieve an effective concentration in the infection site.

Empirical antibiotic therapy proved to be equally effective in beta-lactam-aminoglycoside associations, monotherapy with carbapenems, broad-spectrum penicillins/beta-lactamase inhibitors (ticarcillin/clavulanic acid, piperacillin/tazobactam) or third- and fourth-generation

The aetiology of sepsis varies with the age of the patient, and the empirical treatment must be adapted to the most probable aetiology, but correlated with age, weight and associated

monary abscess) and/or non-infectious causes must be sought.

consciousness, thus determining the severity of the case [8, 9].

**2.2. Bacteraemia and septicaemia**

*2.2.1. Generalised septicaemic infections*

tests as soon as these become available.

maximal probability criterion.

cephalosporins [10].

pathology.

be the source of the infectious process.

**Figure 1.** Antibiotic therapy in HAP.


**Table 1.** Empirical antibiotic treatment of HAP with MDRO.

aminoglycoside (tobramycin) and vancomycin or linezolid, to cover MRSA. If a *Legionella* infection is suspected, a macrolide (azithromycin) must also be associated [7] (**Table 1**).

The duration of the antibiotic treatment in HAP must be adjusted to the severity of the disease, the time required to obtain clinical improvement and the aetiological agent, but it has to exceed with at least 3 days the time to clinical improvement. The clinical response occurs after at least 48–72 h, a period during which the recommendation is to maintain the therapeutic scheme. If, after this interval of empirical treatment, the clinical status of the patient did not improve, the therapeutic scheme must be broadened, potential complications (pleurisy, pulmonary abscess) and/or non-infectious causes must be sought.
