Pneumonia in the ICU

© 2004 The Medicine Publishing Company Ltd383ANAESTHESIA AND INTENSIVE CARE MEDICINE 5:11

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the role of chloride in acid–base homeostasis. The primary determi-nants influencing SID clinically are the Na+ and Cl– concentrations. An increase in Cl– relative to Na+ decreases the SID and hence the pH. The pH increases when the concentration of these ions moves apart. Since Na+ control is more tightly regulated to control tonicity, Cl– is increasingly recognized as an important determinant of pH. For example, persistent vomiting often result in alkalosis. The traditional view is that this is due to H+ loss as HCl. In the Stewart hypothesis, plasma SID is increased because chloride (a strong ion) is lost without a corresponding strong cation. Increased SID forces a decrease in water dissociation and thus a decrease in plasma H+ concentration. The treatment of this disorder is chloride replacement with normal saline. The hyper chloraemic acidosis that arises following large volume saline infusions can be explained by the excess administration of chloride relative to sodium. Normal saline contains 150 mmol/litre of sodium and chloride compared with the normal plasma concentrations of 135 and 100 mmol/litre, respectively. The result is that SID is reduced, free water dissocia-tion increases and pH falls.

Practical acid–base interpretation

A practical method of determining acid–base status is given in Figure 4.

Acid–base interpretation

• Take a comprehensive history and examination

• Request a simultaneous blood gas and biochemical profile

• Assess the accuracy of the data

• Identify the primary disturbance

pH < 7.36 acidaemia

Respiratory acidosis: PaCO2 > 44 mm Hg (5.9 kPa)

Metabolic acidosis: HCO3– < 22 mmol/litre

Combined?

pH > 7.44 alkalaemia

Respiratory alkalosis PaCO3 < 36 mm Hg (4.8 kPa)

Metabolic alkalosis HCO3– > 26 mmol/litre

Combined?

• After identifying the primary or major abnormality (pCO2 for

respiratory and HCO3– for metabolic), estimate the expected

compensation of the other component. If the compensation is

not in the correct direction a mixed abnormality is present

• Assess any metabolic component from standard base excess

or deficit

• In a metabolic acidosis calculate the anion gap including K+

(normal 15 mmol/litre) and adjust for hypoalbuminaemic

patients

4

Community-acquired and nosocomial (hospital-acquired) pneu-monia are common conditions. Community-acquired pneumonia has an estimated incidence of 2–12 cases/1000 population/year. Most of these cases are managed outside hospital with about 20% requiring hospital admission. Of this group, about 10% develop severe pneumonia requiring treatment in an ICU. Nosocomial pneumonia is the second most common hospital-acquired infection and the most commonly acquired infection in the ICU. Nosocomial pneumonia usually affects mechanically ventilated patients and is described as ventilator-associated pneumonia. Death rates are increased in critically ill patients developing ventilator-associated pneumonia, with an estimated attributable mortality of 10–50%. Community-acquired pneumonia in hospital has been defined as symptoms and signs consistent with an acute lower respiratory tract infection associated with new shadowing on the chest radio-graph for which there is no other explanation (e.g. not pulmonary oedema or infarction). The illness is the primary reason for hospital admission. Nosocomial pneumonia is defined as pneumonia acquired after ahospital admission. It is divided into:• early onset (< 5 days after hospital admission or intubation)• late onset (≥ 5 days after hospital admission or intubation).

Community-acquired pneumonia

Severe community-acquired pneumonia is almost always a multi-system disease and at presentation patients will have, or will be rapidly developing, multiple organ failure. The importance of recognizing this aspect of the disease cannot be over-emphasized. Apparent stability on high-flow oxygen can rapidly change to respiratory, circulatory and renal failure. Progressive loss of tissue oxygenation needs to be anticipated, recognized and acted on to prevent progression to established organ failure. Assessing the severity of the disease in patients with community-acquired pneumonia is therefore an integral part of hospital man-agement in terms of initial presentation and monitoring response to treatment (Figure 1). Patients who have two or more core adverse prognostic features are at high risk of death and should be managed as having severe pneumonia. Patients who have one core adverse feature are at an increased risk of death. The presence of pre-exist-ing and/or additional adverse prognostic features can assist in deciding whether to treat such patients as having severe pneumo-nia. Patients who fulfil the criteria for severe community-acquired

Pneumonia in the ICUDavid Sinclair

David Sinclair is Consultant Physician at South Devon Healthcare Trust. rHe qualified from Birmingham University and has trained in respiratory

and intensive care medicine.

FURTHER READINGDriscoll P, Brown T, Gwinnut C, Wardle T. A simple guide to blood gas

analysis. London: BMJ Publishing Group, 1997.

tooley&stoker&barry&mac&hubble&sinclair.indd 383tooley&stoker&barry&mac&hubble&sinclair.indd 383 18/10/2004 13:16:0118/10/2004 13:16:01


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pneumonia on admission and who do not improve rapidly should be considered for transfer to an ICU. Independent indications for transfer to the ICU for respiratory and cardiovascular support are persisting hypoxia with PaO2 less than 8 kPa despite maximal oxygen administration, progressive hypercapnia, severe acidosis (pH < 7.26), persisting hypo tension or depressed conscious-ness. The mortality for patients with severe community-acquired pneumonia requiring ICU admission is high, ranging from 21.7 to 57.3% with an average of 36.5% in different studies.

MicrobiologyA small number of pathogens account for most infections, with Streptococcus pneumoniae being the most common pathogen in Europe and North America. In at least one-third of cases no pathogen can be isolated. The British Thoracic Society (BTS) recommends routineinvestigations for all patients with severe community-acquired pneumonia (Figure 2). Clinical overlap between different pathogens is great and no combination of symptoms and plain chest radiology reliably dif-ferentiates between the pathogens. Thus, the terms typical and atypical pneumonia, developed to differentiate differing pneumonic syndromes, are redundant and have no place in clinical practice.

Antimicrobial treatmentIf the specific pathogen has been identified then the choice of antimicrobial is straightforward. The optimal choice of antibiotics for the empirical treatment of severe community-acquired pneu-monia is less clear. In Europe, treatment must include effective treatment for S. pneumoniae, Legionella spp.,a Haemophilus spp. and Staphylococcus spp. Gram-negative bacteria are a rare cause of severe pneumonia but may be found in patients with pre-existing lung disease. The BTS guidelines recommend the com-bination of amoxicillin/clavulanate with clarithromycin and the optional addition of rifampicin. Alternative combinations for patients intolerant of the preferred combination include:

• substitution of cefuroxime, cefotaxime or ceftriaxone for amoxi-cillin/clavulanate; clarithromycin and rifampicin remain

• use of a single fluoroquinolone with Gram-positive cover(e.g. moxifloxacin or levofloxacin).

ICU managementThe BTS study of severe community-acquired pneumonia identified that most patients die of the complications of multiorgan failure rather than from respiratory failure alone. Of patients admitted to ICU with severe community-acquired pneumonia 32% developed acute renal failure, 55% developed septic shock, 25% developed CNS problems including vascular events and convulsions. Such patients are optimally managed by a team with experience of the complications of sepsis and commonly require invasive circulatory monitoring, aggressive fluid resuscitation, the use of vasopres-sors and inotropes and haemofiltration for renal replacement therapy. All patients with severe community-acquired pneumonia require high-flow oxygen therapy. Hypercapnia is a sign of ventilatory failure indicating the need for more intensive support. Depending on the clinical setting, more aggressive respiratory support can be provided by the application of continuous positive airway pressure (CPAP) or biphasic positive airway pressure (non-invasive ventila-tion, NIV) delivered via a face mask. Alternatively, a decision to proceed directly to tracheal intubation with mechanical ventilation may be made. It must be emphasized that unnecessary delay in intubation is associated with an excess mortality. Non-invasive respiratory support (CPAP or NIV) should be given only to patients with severe community-acquired pneumonia in designated and properly staffed critical-care areas. Enthusiasm for non-invasive support should not delay intubation. The optimal ventilatory strategy has not been established. How-ever, limiting tidal volume and airway pressure seems appropriate, given its success in the management of patients with the acute respiratory distress syndrome and considering that pneumonia is the most common cause of acute lung injury.

British Thoracic Society severity assessment used to determine the management of community-acquired pneumonia in hospital

Consider pre-existing adverse prognostic features• Age 50 years or over

• Any coexisting chronic illness

Consider core adverse prognostic features• New mental confusion

• Urea > 7 mmol/litre

• Respiratory rate 30/min or more

• Systolic blood pressure less than 90 mm Hg or diastolic blood

pressure 60 mm Hg or more

Consider additional adverse prognostic features• PaO2 < 8 kPa/SaO2 < 92% (any FiO2 )

• Chest radiograph shows bilateral or multilobar shadowing

1

British Thoracic Society routine investigations for patients with severe community-acquired pneumonia

• Blood cultures

• Sputum or lower respiratory tract sample for Gram stain,

routine culture and sensitivity tests

• Pleural fluid analysis, if present

• Pneumococcal antigen test on sputum, blood or urine

• Investigations for Legionella pneumonia including:

urine for Legionella antigen

sputum or lower respiratory tract samples for Legionella

culture and direct immunofluorescence

initial and follow-up serology for Legionella

• Respiratory samples for direct immunofluorescence to

respiratory viruses

• Chlamydia sp. and possibly Pneumocystis

• Initial and follow-up serology for Mycoplasma and Chlamydia

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Failure to improveLack of clinical response at 48–72 hours should prompt a review of the diagnosis and consideration of other conditions (e.g. car-diac failure, thromboembolic disease). The microbiological results should be reviewed and the complications of infection considered. Complications include the development of pulmonary abscess or necrosis, empyema, meningitis, endocarditis or nosocomial infection. Complications should be identified and treated. Man-agement includes surgical intervention, intercostal tube drainage and adjustment of antibiotic regimens. The possibility of immuno-suppression should be considered and the recent travel history reviewed. If a diagnosis of Pneumocystis carinii pneumonia is suspected it should be confirmed with bronchoalveolar lavage and consideration given, depending on the severity, to the use of adjunctive systemic steroids.

Ventilator-associated pneumonia

The division of patients with ventilator-associated pneumonia into early and late onset is important in terms of aetiology and treatment. Early onset commonly results from aspiration of endog-enous community-acquired pathogens, such as S. pneumoniae, Haemophilus spp. and Staphylococcus spp., with tracheal intuba-tion and impaired consciousness being the main risk factors. Late onset follows aspiration of oropharyngeal or gastric secretions containing potentially drug-resistant nosocomial pathogens such as methicillin-resistant Staphylococcus aureus (MRSA) and Gram-negative bacteria. Only late-onset ventilator-associated pneumonia is associated with an excess mortality.

Risk factors and preventive measuresRisk factors and preventive measures are given in Figure 3. Pre-ventive strategies, while simple and inexpensive, are not always easy to apply. In selective decontamination of the digestive tract, prolonged therapy with a mixture of oral non-absorbable antibiotics is combined with a short course of an intravenous broad-spectrum antibiotic to prevent colonization of the gastrointestinal tract with the resistant pathogens that cause ventilator-associated pneumo-nia. There is some evidence that selective decontamination of the digestive tract may improve outcome, particularly in patients following multiple trauma and burns, but there are concerns that

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Risk factors for ventilator-associated pneumonia

Risk factor Preventive measure

Antimicrobial therapy Minimize where possible

Intubation Non-invasive ventilation

Re-intubation Avoid re-intubation by non-

invasive ventilation

Nasotracheal intubation Prefer oral intubation

Supine body position Semi-recumbent body position

Pharmacological paralysis Avoidance of muscle relaxants

Daily change of ventilator

circuits

Change of ventilator circuit not

more than once per week

it could increase the risk of infection with MRSA. Therefore, it remains controversial and is not in widespread use.

Diagnostic strategiesClinical criteria for the diagnosis of suspected ventilator-associated pneumonia include a new and persistent infiltrate on the chest radiograph together with fever or hypothermia, leucocytosis or leucopenia, and purulent tracheobronchial secretions. Changes in oxygenation and signs of severe sepsis and/or septic shock may also occur. Many of these criteria are nonspecific and considerable diagnostic doubt is common. However, independent microbiologi-cal criteria using the bronchoscopic techniques of bronchoalveolar lavage and protected specimen brushing also have high rates of false-positive and false-negative results of up to 50%. Microbiologi-cal results obtained using these invasive techniques are similar to those from simple tracheobronchial aspiration. Isolation of pathogenic microorganisms in the respiratory tract without clinical signs of ventilator-associated pneumonia implies colonization and does not require therapy. Many studies regarding the optimal diagnostic strategy have been published, with conflicting results, and no clear framework has emerged. Current thinking suggests: • a low threshold for the diagnosis and empirical antimicrobial

treatment of ventilator-associated pneumonia• empirical treatment is guided by time of onset • selection of antimicrobial therapy is influenced by local patterns

of microbial resistance• regular surveillance and quantitative culture of tracheobronchial

aspirates from intubated patients can refine local empirical antimicrobial policies.

Recommendations for empirical antimicrobial treatment For patients with early-onset ventilator-associated pneumonia and no risk factors (Figure 3), core organisms such as commu-nity endogenous pathogens and non-resistant Gram-negative Enterobacteriaceae (GNEB) (including Escherichia coli, Klebsiella pneumoniae, Enterobacter spp., Serratia spp. and Proteus spp.)should be covered appropriately. For patients with late-onset ventilator-associated pneumonia and no risk factors, potentially drug-resistant microorganisms must also be taken into account. These include MRSA, GNEB, Pseudomonas aeruginosa and Acinetobacter spp. Although not an evidence-based strategy, most authorities recommend combination therapy. For patients with early or late onset and risk factors, treatment is identical to late-onset ventilator-associated pneumonia without risk factors, except when Legionella spp. are suspected. This gen-aeral framework for empirical initial antimicrobial treatment must be modified according to local requirements.

FURTHER READINGBaudouin S V. The pulmonary physician in critical care. 3: Critical care

management of community acquired pneumonia. Thorax 2002; x 57:267–71.

British Thoracic Society. Guidelines for the management of community

acquired pneumonia in adults. Thorax 2001; x 56 (suppl IV).

Ewig S, Bauer T, Torres A. The pulmonary physician in critical care.

4: Nosocomial pneumonia. Thorax 2002; x 57: 366–71.


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Pneumonia in the ICU