viral pneumonia case study ppt

COVID-19 pneumonia and COVID-19 associated acute respiratory distress syndrome: diagnosis and management

VSEVOLOD ZVIRYK / SCIENCE PHOTO LIBRARY

Open access article

The Royal Pharmaceutical Society has made this article free to access in order to help healthcare professionals stay informed about an issue of national importance.

To learn more about coronavirus, please visit:  https://www.rpharms.com/coronavirus

After reading this article you should be able to:

• Understand the basic pathophysiology of COVID-19 pneumonia;
• Identify clinical symptoms that may suggest disease progression or require urgent medical attention;
• Describe evidenced-based and supportive therapies for management ;
• Appreciate the complexity of managing COVID-19 viral pneumonia and COVID-19 acute respiratory distress syndrome in the acute hospital setting and intensive care unit.

The COVID-19 pandemic has had a significant global impact. At the date of publication, around 203 million people across the world have tested positive for the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) since it was first identified in December 2019 ​[1]​ .

The most critically unwell patients require urgent admission to an intensive care unit (ICU), often because of severe type 1 respiratory failure with gross hypoxia, meaning that they require mechanical ventilation ​[2]​ . Severe respiratory complications, such as COVID-19 pneumonia and/or COVID-19 associated acute respiratory distress syndrome (CARDS), contribute to high ICU mortality rates and affect 15–30% of hospitalised COVID-19 patients ​[2]​ . At the peak of the pandemic, the ICU mortality rate for COVID-19 patients reached 58% ​[2]​ .

Fortunately, as knowledge has expanded and new evidence-based therapies have emerged, associated ICU mortality rates in the UK have fallen to around 37% at 28 days ​[3]​ . The number of COVID-19 ICU admissions has also decreased — mostly owing to the successful rollout of the UK COVID-19 vaccination programme ​[4]​ . However, the emergence of the more transmissible Delta variant , coupled with the recent easing of lockdown restrictions, has contributed to a third wave of COVID-19 infections in the UK ​[4,5]​ . This could potentially lead to an increase in the number of serious complications, such as severe COVID-19 pneumonia and CARDS.

It is therefore important that pharmacists can recognise the signs and symptoms of these diseases, and know how to appropriately manage patients presenting to community pharmacy and primary care.

This article provides an overview of COVID-19 pneumonia and CARDS, summarising the pathophysiology, diagnosis and evidenced-based management strategies.

Effects of COVID-19 on the respiratory system

Human SARS-CoV-2 is a single stranded RNA-enveloped virus, which causes COVID-19 infection. It is thought to have originated in animals owing to the high genetic similarity of the same virus found in bats and pangolins ​[2,6]​ . It is primarily a disease of the respiratory tract with entry into the human host via this route ​[2,7]​ .

SARS-CoV-2 causes damage to the alveolar epithelial lining, impeding oxygen (O 2 ) and carbon dioxide exchange ​[8]​ . Damage to the alveoli and a disrupted vascular endothelium, as a consequence of the inflammatory response, causes moderate to severe respiratory failure, requiring ICU admission, intubation and mechanical ventilation ​[7]​ .

COVID-19 pneumonia and acute respiratory distress syndrome

All patients admitted to ICU are at an increased risk of developing acute respiratory distress syndrome (ARDS). ARDS occurs frequently in the ICU and is characterised by fluid build up in the alveoli, resulting in an insufficient supply of oxygen from the lungs to the vital organs ​[8]​ . An ARDS-like pathophysiology has been observed in COVID-19 patients admitted to the ICU — CARDS ​[6]​ .   

The main components of CARDS are destruction of alveolar lining, endothelial damage and a high prevalence of thromboembolic events, including pulmonary embolism ​[8,9]​ .

The principal difference between CARDS and classic ARDS is the high coagulation burden associated with CARDS ​[10]​ . Although several unique pathophysiological features are also postulated in CARDS, such as intravascular thrombosis, endothelial dysfunction and excessive blood flow to collapsed lung tissue ​[2]​ . 

There is also sigificant overlap between CARDS and COVID-19 pneumonia, defined as SARS-CoV-2 infection confirmed by:

• A positive polymerase chain reaction (PCR) test;
• Pulse oximetry showing oxygen saturation (SpO 2 ) of <94% on room air;
• Ratio of arterial partial pressure of oxygen to fraction of inspired oxygen (PaO 2 /FiO 2 ) of <39.9kPa;
• A respiratory rate of >30 breaths/minute, or >50% lung infiltrates observed on radiological imaging ​[11]​ .

There is not a clear distinction between severe COVID-19 pneumonia and CARDS, which can confound diagnosis ​[10]​ . 

Diagnosis and investigation

SARS-CoV-2 infection is confirmed via a positive COVID-19 PCR test or lateral flow test . PCR tests are generally viewed as the ‘gold standard’ for COVID-19 diagnosis; however, lateral flow tests are cheaper, portable and provide rapid results. Studies to determine their level of sensitivity and specificity are ongoing ​[12]​ .

Similarly to community acquired pneumonia, COVID-19 pneumonia is diagnosed using a combination of chest X-ray (CXR), blood tests and clinical history ​[13]​ .

Radiological imaging

While no single feature of COVID-19 infection on the CXR is specific or diagnostic, viral pneumonia caused by SARS-CoV-2 presents as bilateral, peripheral, non-lobar ground glass opacities (hazy, grey areas) as shown in the Figure below .

CARDS is typically diagnosed by chest X-ray and regular CT-scans for in-depth assessment. In the ICU, pulmonary embolism is diagnosed by CT-pulmonary angiogram.

Wikimedia.org

Oxygen saturation

Oxygen saturation (SpO 2 ) is an important diagnostic tool for COVID-19 pneumonia, and measures the amount of haemoglobin-bound oxygen and free oxygen. The partial pressure of arterial O 2 (PaO 2 ) is measured by arterial blood gas  monitoring. In healthy individuals, SpO 2 is usually >95%. In patients with chronic lung disease or sleep apnoea, SpO 2 can range between 88–92% ​[14]​ .

In SARS-CoV-2 infection, patients have low SpO 2 levels. A phenomenon known as ‘silent hypoxia’ is reported, where patients present with minimal symptoms yet have significantly reduced pulse oximetry readings below 91%, particularly in the short term ​[2,15]​ .

Additional investigations

A pattern of characteristic abnormalities — such as a raised C-reactive protein (CRP), a low lymphocyte count and a raised ferritin level — have been identified in patients with severe disease and could stratify patients’ risk ​[2]​ .

Assessment and referral

Patients with COVID-19 typically present with a dry, persistent cough; temperature >38 o C and loss or change in sense of taste and smell (anosmia) ​[11,13]​ . A persistent high temperature, loss of appetite, confusion/delirium and reduced urine output are all causes for referral ​[13]​ . Patients with COVID-19 pneumonia/CARDs may also feel breathless and complain of tiredness, malaise, headache and a flu-like illness.  

In community and primary care, pharmacists should assess the severity of respiratory symptoms and determine the need for referral by asking the patient to describe their chest symptoms alongside the following questions:

• When do you experience breathlessness?
• Are you able to breathe comfortably when resting?
• Do you have difficulty finishing sentences without taking extra breaths?
• Do you avoid speaking because you are too breathless?
• Do you experience any chest tightness?
• How does your breathlessness affect your ability to carry out your usual daily activities? ​[16]​  

Pharmacists should refer patients immediately if patients are experiencing the following symptoms:

• Unable to breathe at a comfortable rate on moving or at rest;
• Rapid breathing, i.e. >30 breaths per minute;
• Unable to finish a sentence without taking extra breaths;
• May avoid speaking;
• Feeling ‘tight chested’;
• Unable to read or watch TV because they are too focused on breathing or feel too unwell;
• Coughing up blood;
• Blue lips ​[12]​ .

Patients with a consistent SpO 2 of 93–94% should contact their GP or NHS 111 as soon as possible; those with an SpO 2 of 92% or below should attend A&E or call 999 immediately ​[16]​ . Pharmacists should be aware of silent hypoxia, and variations in the measurement of  SpO 2 and overestimation in black African/Caribbean individuals ​[2,17]​ . For more information on how to assess and manage patients in community or primary care, see ‘ Community management of pneumonia and suspected COVID-19 ’.

Pharmacists should also be aware that selected patients are more likely to develop severe COVID-19 pneumonia, including frail people, older people, those with multiple comorbidities (including diabetes and cardiovascular disease), impaired immunity, male gender, obesity or a reduced ability to cough and clear secretions ​[12]​ .

Neither the symptoms described or the list of patients at risk of severe disease are exhaustive, and pharmacy professionals should refer to the NICE COVID-19 rapid guidelines ​[11]​ .  

Treatment of COVID-19 pneumonia and CARDs occurs mainly in secondary care, although milder cases of COVID-19 pneumonia have been managed in the community. Evidence around COVID-19 therapies is rapidly being updated; therefore, pharmacists must possess in-depth knowledge of treatment strategies ​[18]​ .

Up until June 2020, the mainstay of treatment for COVID-19 pneumonia and CARDS was symptomatic, supportive therapy, including oxygen and mechanical ventilation. More recently, evidence generated from the Randomised Evaluation of COVID-19 Therapy (RECOVERY) and Randomised, Embedded, Multi-factorial, Adaptive Platform Trial for Community-Acquired Pneumonia (REMAP-CAP) landmark trials are being used to guide therapy ​[19,20]​ . The adaptive (multi-domain) design of these studies allows interim results from domains to be shared as soon as they provide evidence of sufficient certainty to affect international treatment strategies ​[19,20]​ .

National guidance on the management of COVID-19 has also been published by the National Institute for Health and Care Excellence (NICE) and NHS England ​[13]​ . Although the NHS was overwhelmed with COVID-19 cases, patient enrolment in these vital studies continued as multidisciplinary teams recognised that evidence for novel therapy was essential.

Additional information about COVID-19 therapy trials can be found here .

Pharmacological therapies

The majority of pharmacological therapies, which have — to date — proven to be effective in the management of COVID-19, target the hyper-inflammatory processes that occur in moderate to severe COVID-19 disease ​[16,17]​ . Evidence shows that the following therapies can be given concomitantly, provided each is safe and appropriate for the patient at the time of presentation ​[11]​ .

Dexamethasone

Interim results from the RECOVERY trial support treatment with dexamethasone, a well-known, readily available and affordable corticosteroid ​[17]​ .

Dexamethasone has been shown to reduce mortality in ventilated patients by one-third, and by one-fifth in  hospitalised patients requiring oxygen therapy ​[17]​ . The absolute risk reduction in patients receiving dexamethasone was 3%, with a number needed to treat of 33 to save one life. However, no benefit was reported in patients who did not require oxygen treatment ​[19]​ .

The most effective dose of dexamethasone for the treatment of COVID-19 pneumonia remains under investigation — at present, patients are prescribed 6mg once daily for 10 days in line with the available evidence; however, there are studies investigating whether higher doses of dexamethasone (12mg once daily) are more effective ​[21]​ .

Prolonged steroid treatment causes immunosuppression, predisposing patients to risk of bacterial and fungal infections with resistant organisms. Pharmacists are central to upholding effective antimicrobial stewardship by reviewing the appropriateness of antimicrobials  prescribed, along with patient education on administration and adherence.

Steroid-induced hyperglycaemia can also occur and, in many cases, insulin therapy is required. Evidence shows that glucose control (aiming for blood glucose levels between 6–10mmol/L) for patients in intensive care leads to better outcomes. Pharmacist monitoring of blood glucose should occur throughout dexamethasone therapy ​[22]​ .

Treatment with remdesivir, an adenosine nucleotide prodrug — previously developed for the treatment of the Ebola virus — should be considered for adults with COVID-19 pneumonia, who are in hospital and receiving supplemental oxygen but who are not mechanically ventilated ​[23]​ .

A five-day course of intravenous remdesivir (200mg on day 1, then 100mg daily) reduces time to recovery by one-third but no mortality benefit has been reported ​[24]​ . Caution should be exercised in patients with severe liver or renal impairment ​[23]​ .

Tocilizumab

Interleukin-6 (IL-6) is an inflammatory cytokine that plays a key inflammatory role in COVID-19 pneumonia/CARDS ​[23]​ . The RECOVERY and REMAP-CAP trials found that tocilizumab, an IL-6 inhibitor, licensed in the treatment of rheumatoid arthritis, reduces mortality, time to ICU and hospital discharge and, in patients receiving oxygen, reduces the chance of progressing to mechanical ventilation ​[25]​ .

An 8mg/kg dose of tocilizumab by intravenous infusion is recommended for patients who require supplemental oxygen, have a CRP ≥75mg/L and are within 48 hours of advanced respiratory support ​[25]​ . Caution is advised in patients who have active bacterial or viral infection (other than SARS-COV-2) as these can be exacerbated by tocilizumab-induced immunosuppression ​[26]​ . Tocilizumab is reported to suppress CRP production for up to three months; therefore, caution is advised in using CRP to exclude sepsis in tocilizumab-treated patients ​[27]​ .

Therapies are assessed continually in COVID-19; therefore, a clear handover and medicines reconciliation upon transfer between care settings is essential ​[28]​ . A recently reported intervention is Regeneron, combination monoclonal antibody treatment , from the RECOVERY study, which provided clinical benefit in patients who had failed to mount an adequate immune response ​[29]​ .

Additional therapies

Patients admitted to ICU with COVID-19 pneumonia and CARDS require deep sedation and paralysis for prolonged periods ​[30]​ . There is a high risk of iatrogenic withdrawal upon sedation weaning and delirium. Pharmacists should collaborate with the multidisciplinary team to devise sedation weaning plans to reduce these risks ​[31]​ .

Oxygen is essential in the treatment of severe COVID-19 pneumonia/CARDs and is commonly started when SpO 2 is <94% on room air via nasal cannula ​[2]​ .

Advanced respiratory support, including high flow nasal oxygen [HFNO] or continuous positive airways pressure (CPAP), is considered when an SpO 2 ≥94% on 40% oxygen is unachievable ​[11]​ . If maximal non-invasive respiratory support fails to achieve adequate SpO 2 , then intubation and ventilation may be necessary ​[11]​ .

The Recovery-RS (Respiratory Support) trial is comparing the effectiveness of three ventilation methods in patients with COVID-19 (CPAP versus high flow nasal oxygen (HFNO) versus standard care) ​[32]​ . The results from RECOVERY-RS are important in identifying optimum ventilation methods.  

Thromboprophylaxis and anticoagulation

COVID-19 induces a hypercoagulable state, especially in severe disease, and it is essential that appropriate thromboprophylaxis and anticoagulation strategies are adhered to in hospitalised patients ​[2]​ .

Full dose anticoagulation is recommended in adults with COVID-19 infection receiving supplemental oxygen, but not in those receiving advanced respiratory support (HFNO, CPAP, non-invasive or mechanical ventilation).

In the ICU, the REMAP-CAP trial reported that treatment dose anticoagulation is futile, and is associated with a higher rate of bleeding events in critically ill patients ​[28]​ . Thromboprophylaxis with either standard or intermediate dose low molecular weight heparin (i.e standard prophylactic dose for those acutely unwell administered twice daily instead of once daily) is recommended. Trials are ongoing to establish the optimum dose of thromboprophylaxis in the ICU cohort ​[33]​ .

Follow up and monitoring

Persisting and long-lasting symptoms are reported after SARS-CoV-2 infection. The overarching term most commonly used is ‘long COVID’ ​[34]​ . The challenge after severe COVID-19 pnemonia and CARDs is that ICU admission can be prolonged, and symptoms of ‘ long COVID ’ are similar or overlap with post intensive care syndrome, which includes profound weakness and cognitive decline. This means a large number of patients are likely to require long-term rehabilitation ​[35]​ .

During extended admissions, ongoing medicines reconciliation and communication between care settings is vital. It is particularly important that details regarding inpatient corticosteroid and IL-6 inhibitor therapy is communicated to the patient’s care providers following discharge from ICU, to step down wards and primary care. The box summarises how pharmacists can facilitate this ​[28]​ .

Box: How pharmacists can support COVID-19 pneumonia and CARDs patients on discharge

Best practice recommendations for effective information sharing and integrated working:

• Ensure accuracy in prescribing between transfer of care. Caution should be taken when discontinuing unnecessary medications (e.g antipsychotics) on step down from ICU. Reconciliation of long term therapy is necessary to mitigate risks of unintentional discontinuation;
• Include details of prescribed therapy (e.g. dexamethasone and tocilizumab), as well as baseline and follow-up test results in clinical records/rehabilitation plans. These should be shared promptly between services during multidisciplinary meetings;
• Provide patients with a copy of their care plans or records to keep, including discharge letters, clinical records, rehabilitation plans and prescriptions;
• Advocate for one healthcare professional or team to provide care for the same patient as much as possible to ensure continuity of care;
• Provide medication counselling, and signpost patients to appropriate health and social care services after discharge from hospital.

The following is a case study to illustrate the typical presentation and ICU admission of a patient diagnosed with COVID-19 pneumonia. The case is fictional but has been based on several of the COVID-19 patients admitted to the ICU at King’s College Hospital.

Mrs AB is a female aged 44 years with a history of type 2 diabetes, hypertension and depression. Prior to experiencing COVID-19 pneumonia, she was fit, well and working full-time. Mrs AB felt unwell five days before hospital presentation, with aches and pains, intermittent fevers, headache and cough. She also reported loss of taste and smell. On presentation to the emergency department, her initial observations were:

A CXR reported bilateral infiltrates — characteristic of COVID-19 pneumonia — that was confirmed by a positive SARS-CoV-2 PCR test.

Mrs AB was admitted to a medical ward and received treatment with HFNO. She was prescribed dexamethasone 6mg daily for ten days and a five-day course of remdesivir (200mg on day 1, then 100mg daily thereafter) ​[24]​ .  

Around 24 hours after admission, her CRP was rising and oxygen requirements increasing. A CXR reported deterioration. Mrs AB was transferred to the ICU for intubation and ventilation, with a high clinical suspicion of a pulmonary embolism. Her oxygen requirements at intubation were 100%.

On ICU arrival, a CT pulmonary angiogram scan reported no evidence of pulmonary embolism. Mrs AB was prescribed an intermediate dose thromboprophylaxis for COVID-19. Her treatment with remdesivir was ceased on suspicion that a recent derangement in liver function was secondary to remdesivir.

Mrs AB remained in ICU for 69 days before being discharged to the ward.

Patient history from ICU:

• Rising inflammatory markers, CRP peaked at 467mg/L ferritin peak of 890ng/mL (normal level <200ng/mL in women);
• Challenging oxygenation, ongoing hypoxia — management included deep sedation with fentanyl, propofol and midazolam, paralysis and repositioning in the prone position;
• Secondary effects were low creatinine (owing to loss of muscle mass) and profound myopathy;
• Insulin infusion initiated to manage dexamethasone-induced hyperglycaemia, titrated as per local protocol (blood glucose peak = 20mmol/L).
• Tracheotomy on day 20;
• Development of multi-resistant gram-negative bacteraemia ( Klebsiella spp. ) and a positive Beta-D glucan result. Treated with meropenem, amikacin and anidulafungin;
• Upon weaning sedation, patient became extremely tachycardic and respiratory rate increased to 50–55 breaths per minute — secondary to iatrogenic withdrawal owing to rapid weaning of high doses of sedation;
• Gradual sedation weaning plan was devised, weaning midazolam and fentanyl infusions over 10–14 days, bridging on to intermittent diazepam and morphine.

In summary, COVID-19 pneumonia and CARDs are complex, multi-system disorders with a high risk of death. Patients that survive can have significant and lasting consequences. These are outlined in the earlier learning article ‘ Managing the long-term effects of COVID-19 ’. The clinical evidence in COVID-19 pneumonia and CARDS is continually updated. The authors of this article have done their utmost to provide an overview of the most up to date evidence, but acknowledge that the most recent evidence may not have been included at the time of publication.

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Author: Olivia Bailey, Associate Professor of Emergency Medicine, University of Iowa

Aaron Hultgren,Liliya Abrukin NYU School of Medicine and Bellevue Hospital Center

Editor: Alisa Hayes, Associate Professor of Clinical Emergency Medicine, University of Missouri - Columbia

Last updated: 2019. 

An 82-year-old male is brought in by his granddaughter from home for fever and productive cough that started earlier in the day. He has a past medical history of congestive heart failure and coronary artery disease. His vitals include a of temperature 38.5°C, heart rate of 110, blood pressure of 128/61, and an oxygen saturation of 92% on room air. You hear rales and rhonchi in the right mid-lung. How will you evaluate, treat, and disposition the patient?

Upon finishing this module, the student will be able to:

• Identify the common pathogens in pneumonia.
• Discuss diagnostic considerations for evaluating pneumonia.
• Describe the management and antibiotic treatment for pneumonia.
• Discuss discuss the disposition of patients with pneumonia.

Introduction

Pneumonia is a common infection and causes significant morbidity and mortality in the United States. In the US, it is the 8th leading cause of death, the most common cause of death from infection, and the 2nd most common cause of hospitalization in the United States. Physicians in the emergency department need to be able to diagnosis, appropriately treat, and disposition patients with pneumonia.

It is important to understand the different classifications of pneumonia.

Community -acquired pneumonia (CAP) is lung parenchyma infection in a non-hospitalized patient. 

Hospital -acquired pneumonia (HAP) or nosocomial pneumonia is a new lung parenchyma infection that occurs after 48 hours of hospitalization.

Ventilator -associated pneumonia (VAP) occurs in the subset of HAP patients that are mechanically ventilated.

Healthcare -associated pneumonia (HCAP) is no longer a classification that is utilized. Given the patient population of emergency medicine, the focus of this chapter will be on CAP.

Historically, pathogens have been divided into “typical” and “atypical.” Typical pathogens include Streptococcus pneumoniae (most common), Haemophilus influenzae, Staphylococcus aureus, Group A streptococci, Moraxella catarrhalis. Atypical pathogens include Mycoplasma pneumoniae, Chlamydophila pneumonia, Legionella species. Viruses such as influenza, parainfluenza, and respiratory syncytial virus can also cause pneumonia as can fungi.

Risk factors for pneumonia include increased age, chronic comorbidities such as COPD, viral upper respiratory infections, smoking,  heavy alcohol use, difficulty protecting the airway or other lifestyle factors such as crowded living conditions.

Signs and Symptoms

Patients with pneumonia may present with signs and symptoms such as fever, chills, cough, pleuritic pain, sputum production, chest pain, shortness of breath, anorexia or malaise. Elderly patients may present with fatigue, confusion or delirium. There can be a range of vital sign abnormalities depending on severity, including tachypnea, tachycardia, hypoxia and hypotension. Patients may present in septic shock as a result of pneumonia. 

Initial Actions and Primary Survey

All patients should have a set of vital signs including temperature, pulse, blood pressure, pulse oximetry, and respiratory rate. The “ABCs” approach focuses on stabilizing airway, breathing, and circulation. Acutely ill patients will need peripheral access, monitoring, and supplemental oxygen, as well as early antibiotics and pressors if the present in septic shock. Patients in respiratory distress may require supplemental oxygen, noninvasive positive pressure ventilation, or endotracheal intubation.

Airway - Evaluate the airway for stridor, edema, or upper airway obstruction.

• Reposition patient airway.
• Place patient on nasal cannula and/or a non-rebreather. (use both for preoxygenation if preparing to intubate). 
• Perform airway maneuvers/adjuncts such as head tilt/chin lift, jaw thrust, or nasal trumpet insertion.

Breathing – Assess for adequate ventilation. Look for tachypnea, increased work of breathing, and signs of respiratory distress such as nasal flaring, retractions, or tripoding. Imminent or impending respiratory failure may require endotracheal intubation with rapid sequence intubation (RSI).

• Actions may include:
• Supplemental oxygen (nasal cannula or non-breather)
• Non-invasive ventilations (BIPAP)
• Invasive ventilation (with rapid sequence endotracheal intubation)

Circulation – Assess perfusion of vital organs and identify signs of cardiovascular compromise from pneumonia causing sepsis or septic shock.

• Place 2 large-bore peripheral IVs
• Saline bolus of 30cc/kg
• Early broad-spectrum antibiotics
• Severe sepsis and septic shock patients may require central line placement and vasopressor support.

Disability – Assess patient’s mental status. Pneumonia may cause respiratory compromise resulting in hypoxia, hypercarbia, or respiratory failure leading to somnolence, confusion, and altered mental status. Poor mentation and inadequate protection of the airway may require intubation. Patients who cannot protect their airway should not be placed on non-invasive ventilation. Consider aspiration pneumonia in patients with decreased mental status or conditions that may lead to dysphagia.

Presentation

Classically the “typical” CAP caused by Streptococcus pneumoniae is described as presenting with the sudden onset of fever, productive cough, and pleuritic chest pain. Atypical CAP may have a more protracted course beginning with upper respiratory symptoms, slowly worsening cough, malaise and fatigue. These classic presentations of typical and atypical pneumonias are not considered to be sensitive or specific for identifying pneumonia in prospective studies.

“Classic” Presentations:

Typical Pneumonias

• Streptococcus pneumoniae – bloody or rust-colored sputum, single episode of shaking chills
• Haemophilus influenzae – fever, muscle pain, fatigue, history of COPD, smoker
• Klebsiella pneumoniae – currant jelly sputum, bulging minor fissure, often right upper lobe. Alcoholics, diabetics, and COPD patients are at risk.

 Atypical Pneumonias

• Mycoplasma pneumoniae – “walking pneumonia;” upper respiratory symptoms, gradually worsening over weeks or even months, bullous myringitis may be present
• Chlamydophila pneumoniae – pharyngitis, laryngitis and sinusitis, associated with outbreaks in close-contact settings (dorms, prisons), staccato cough
• Legionella – respiratory and gastrointestinal symptoms, relative bradycardia
• Pseudomonas aeruginosa risks factors: immunocompromised, cystic fibrosis

Aspiration Pneumonia 

• This occurs when there is aspiration of colonized oropharyngeal material. It should be differentiated from aspiration pneumonitis which is a chemical injury from inhalation of gastric contents due to regurgitation that can occur with drug overdose, seizures, cerebrovascular accident, or use of anesthesia. Patients at risk for aspiration include patients with dysphagia due to neurologic disorder, nursing home residents, and patients who abuse alcohol. 
• Immunocompromised Patients represent a special subset of pneumonia given the increased susceptibility to a spectrum of potential pathogens. Patients comprising this population include those with solid organ transplants, cystic fibrosis, HIV/AIDS, hematopoietic cell transplants, pregnant women, and patients with other immune defects.
• General considerations include obtaining a thorough past medical history, as well as asking about medications such as chemotherapy, immunomodulating agents, and chronic steroid use. Leukopenia and CD4 count may guide evaluation and treatment considerations. 
• Pneumocystis jirovecii (previously classified as Pneumocystis carinii) is typically found in immunocompromised patients, such as those with HIV/AIDS. Symptoms include dyspnea, nonproductive cough, and fever. Chest x-ray usually shows bilateral infiltrates, but may also present with lobar consolidation. Treatment is trimethoprim-sulfamethoxazole (TMP-SMX) and adjunctive corticosteroids in severe disease. 
• Tuberculosis is another important consideration in immunocompromised patients as well as patients with a history of prior tuberculosis infection, night sweats, weight loss, or exposure from shelters, prisons, or recent travel to endemic areas.

Physical Examination

A full physical exam is important to both evaluate for alternative diagnoses as well as clues related to a particular pneumonia. The physical exam starts with initial vitals and inspection of the patient for respiratory distress. Patients sitting upright or in the “tripod position” with nasal flaring, chest retractions, and abdominal breathing exhibit an increased work of breathing and may have impending respiratory failure. Review of vital signs may show tachypnea, tachycardia, hypotension, hypoxia, and fever. Examination of the chest involves a four-step process: inspection, palpation, percussion, and auscultation of the chest. The positive predictive value of abnormal breath sounds in acute respiratory illness is 55%, further illustrating the difficulty in diagnosing pneumonia with the physical exam. There are no individual or combination of clinical findings that rule in the diagnosis of pneumonia (Metlay et al. 1999).

Examiners should look for other causes of dyspnea with their associated presentations, such as congestive heart failure, pericardial effusions, pleural effusions, pulmonary embolus, and neoplasms. Lastly it is important to evaluate the head, ears, eyes, nose, and throat as many of these patients may initially had an upper respiratory infection that developed into a bacterial pneumonia and concomitant bacterial infections.

Diagnostic Testing

Figure 1 (Above): Right middle lobe pneumonia on chest x-ray. Image Used with Permission by James Heilman, MD

Chest radiography is the main diagnostic modality to evaluate for pneumonia in the ED setting, although it is not always confirmatory. Absence of abnormal vital signs or abnormalities on chest examination reduces the likelihood of pneumonia and the need for further diagnostic studies (Metlay et al. 1999). Factors that predict pneumonia on chest x-ray include temperature >37.8 OC, tachycardia, absence of asthma, rales, and locally decreased breath sounds on auscultation. Pulmonary infiltrates on chest x-ray confirm the clinical diagnosis.

Lobar consolidation is typical of Streptococcus pneumoniae or Klebsiella pneumoniae while multi-lobar infiltrates are more consistent with Staphylococcus aureus and Pseudomonas aeruginosa. Atypical infections such as Mycoplasma pneumoniae, Chlamydophila, and Legionella may reveal patchy infiltrates on radiography. Despite these patterns on chest radiography, it is important to note that typical pathogens can present with diffuse infiltrates and atypical pathogens with discrete consolidations. Radiographic evidence of pneumonia may not be evident on initial chest radiography in patients with early aspiration pneumonias or severe dehydration; however, infiltrates may present on later imaging. Posteroanterior and lateral chest radiographs are recommended in patients that are able to stand and are stable enough to travel to radiology.

Bedside ultrasound is a reliable, noninvasive diagnostic tool for the detection of pneumonia in children, adolescents and adults, with a sensitivity of 86%, a specificity of 89% and a LR 7.8 (95% CI, 5.0-12.4) (Shah et al. 2013). Emergency physicians with advanced sonography skills may be able to identify consolidation. However, ultrasound is operator dependent and therefore its use is only as good as its user. Ultrasound can be very useful in identifying or guiding drainage of pleural effusions related to pneumonia.

Computer Tomography of the chest is more sensitive than plain films of the chest and may be used with patients with an equivocal chest x-ray or when other etiologies for the patient’s presentation are suspected such as pulmonary embolism or mass.

An EKG should be ordered on patients with pneumonia, especially those with tachycardia, chest pain, hypotension or who are ill appearing. Patients with congestive heart failure, cardiovascular disease, and severe sepsis/septic shock may develop cardiac ischemia and infarction secondary to a severe pneumonia.

Blood cultures should be obtained in any patient ill enough to require ICU admission or mechanical ventilation, all patients with suspected sepsis, as well patients with CAP that are at increased risk for bacteremia and resistant organisms.

These risk factors for CAP patients include:

• Cavitary lesions
• Chronic severe liver disease
• Pleural effusion
• Alcohol abuse

Sputum induction for gram stain and culture should not be routinely performed in the emergency department as it poses an infection risk to both providers and other patients and is unlikely to change ED management.

Antimicrobial treatment options for pneumonia may change depending on a number of factors, including local sensitivities and institutional availability. Refer to institutional antimicrobial stewardship guidelines for determining antibiotic regimens.

Outpatient Treatment:

• Previously healthy and no antibiotics in past 3 months
• Macrolide or doxycycline
• Comorbidities like chronic heart, lung, liver, or renal disease, diabetes, alcoholism, immunosuppression, cancer, asplenia or antibiotics in past 3 months
• Respiratory fluoroquinolone OR
• Beta-lactam PLUS a macrolide

Inpatient, non-ICU Treatment:

• Anti-pneumococcal beta-lactam PLUS a macrolide

Inpatient, ICU Treatment:

• Anti-pneumococcal beta-lactam PLUS azithromycin OR
• Anti-pneumococcal beta-lactam PLUS respiratory fluoroquinolone OR
• For penicillin-allergic patients, respiratory fluoroquinolone PLUS aztreonam

If Pseudomonas aeruginosa is a consideration:

• Piperacillin-tazobactam, cefepime, imipenem, or meropenem PLUS ciprofloxacin or levofloxacin

If community-acquired MRSA is a consideration (empyema, recent influenza, IV drug use, abscess, severe pneumonia):

• Add vancomycin or linezolid

Table 1: Antibiotics for Treatment of Pneumonia

Aspiration Pneumonia:

• Ampicillin-sulbactam or amoxicillin-clavulanate
• If poor dentition: imipenem, meropenem, or piperacillin-tazobactam

Disposition

Clinical judgment is essential to determine the disposition of the patient with CAP as patients may be treated as an outpatient, placed in an observation unit, or treated as an inpatient on a floor or ICU. Patients with the inability to tolerate oral antibiotic treatment, hypoxia, sepsis, or respiratory distress will require admission. Patients with pneumonia with severe sepsis or septic shock will need critical care management. Risk stratification instruments may aid emergency clinicians on patient disposition for community-acquired pneumonia. Review the prediction rules listed below via the links.

Pneumonia Severity Index (PSI): https://www.mdcalc.com/psi-port-score-pneumonia-severity-index-cap

CURB-65: https://www.mdcalc.com/curb-65-score-pneumonia-severity

Pearls and Pitfalls

• Management of pneumonia should start with an ABC approach and stabilization of the patient with an acute pneumonia.
• Identify appropriate antibiotics. Familiarize yourself with your local antibiogram and institutional stewardship guidelines.
• Chest radiography continues to be the mainstay for diagnosis of pneumonia; however, ultrasound and CT scan may be helpful in certain situations.
• Disposition of patients with pneumonia should be based on clinical judgment along with risk stratification instruments.
• Patients with a new oxygen requirement or who are unable to take oral antibiotics will generally require admission.

Case Study Resolution

Your patient’s oxygen saturation improved with 2L oxygen via nasal cannula. An IV fluid bolus is ordered. Chest X-ray confirms pneumonia. Treatment with ceftriaxone and azithromycin is started. You suspect the patient would benefit from hospitalization, and this is supported by the PSI score you calculated. Patient is admitted to the floor for further care.

Corbo J, Friedman B, Bijur P, Gallagher EJ. Limited usefulness of initial blood cultures in community acquired pneumonia. Emerg Med J. 2004; Jul;21(4):446-448. PMID: 15208227

Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with community acquired pneumonia. N Engl Med. 1997; 336: 243-250. PMID: 8995086

Halm EA, Teirstein AS. Clinical Practice. Management of community-acquired pneumonia. N Engl J Med. 2002 Dec 19;347(25): 2039-2045. PMID: 12490686

Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Disease Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007; 44 Suppl 2:S27. PMID: 17278083

Marik PE. Aspiration Pneumonitis and Aspiration Pneumonia. N Engl J Med. 2001; 344: 665-671. PMID: 11228282

Metlay JP, Kappor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA 1997: 278(17): 1440-1445. PMID: 9356004

Plouffe JF, Martin DR. Pneumonia in the emergency department. Emergency medicine Clinics of North America. 2008 May;26(2):389-411. PMID: 18406980

Slaven EM, Santanilla JI, DeBlieux PM. Healthcare-associated pneumonia in the emergency department. Semin Respir Crit Care Med. 2009 Feb;30(1):46-51. PMID: 19199186

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Article Contents

Case presentation, acknowledgments.

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Scenario 1: A Patient with Mild Community-Acquired Pneumonia—Introduction to Clinical Trial Design Issues

• Article contents
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David N. Gilbert, Scenario 1: A Patient with Mild Community-Acquired Pneumonia—Introduction to Clinical Trial Design Issues, Clinical Infectious Diseases , Volume 47, Issue Supplement_3, December 2008, Pages S121–S122, https://doi.org/10.1086/591391

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A prototypical patient is presented to introduce important design issues for clinical trials of antibacterials in the treatment of community-acquired pneumonia.

Of the 4 million or more patients in the United States treated annually for community-acquired pneumonia (CAP), ∼80% are cared for on an outpatient basis [ 1 , 2 ]. Admittedly, the patient population is heterogeneous. However, 2 subgroups constitute a significant percentage of the total.

The first subgroup consists of young, otherwise-healthy individuals who are nonsmokers aged <40 years. “Atypical” pathogens, such as Mycoplasma pneumoniae or Chlamydia pneumoniae , are identified frequently as the etiologic organism. Streptococcus pneumoniae may be the etiologic organism, especially during or after viral tracheobronchitis.

In contrast, individuals in the second group are older. Often, they have used tobacco products for years and meet clinical criteria for chronic bronchitis and/or emphysema.

To focus on clinical trial design issues pertinent to the population of patients with mild pneumonia, a typical clinical-trial candidate patient is described below.

Present illness. A 35-year-old male resident of Boston, Massachusetts, presents with fever and cough. He was well until 3 days earlier, when he suffered the onset of nasal stuffiness, mild sore throat, and a cough productive of small amounts of clear sputum. Today, he decided to seek physician assistance because of an increase in temperature to 38.3°C and spasms of coughing that produce purulent secretions. On one occasion, he noted a few flecks of bright-red blood in his sputum.

Other pertinent history. It is March. He lives in a home in the city with his wife and 3 children, aged 7, 9, and 11 years. The children are fully immunized. The 11-year-old child is recovering from a “nagging” cough that has persisted for 10–14 days.

The family has a pet parakeet who is 5 years old and appears to be well. The patient has not traveled outside the city in the past year. He is an office manager.

The patient smokes 1 pack/day and has done so since the age of 15 years. Several times a month, especially during the winter, on arising from sleep, he produces ∼1 tablespoon of purulent sputum.

Medical history. The patient has no history of familial illness, hospitalizations, or trauma. There are no drug allergies or intolerance. The only medication he takes is acetaminophen occasionally, for headaches. He drinks beer or wine in moderation.

Physical examination. His body temperature is 38.9°C (100°F), his pulse is 110 beats/min and regular, and his respiratory rate is 18 breaths/min. His oxygen saturation is 93% while breathing room air. There is mild erythema of the mucosa of the nose and posterior oropharynx. Inspiratory “rales” are heard at the right lung base.

Laboratory and radiographic findings. His hemoglobin level is 12.5 g/dL, with a hematocrit of 36%. His WBC count is 13,500 cells/µL, with 82% polymorphonuclear cells, 11% band forms, and 7% lymphocytes. His platelet count is 180,000 cells/µL. The results of a multichemistry screen are unremarkable.

Chest radiography documents bilateral lower lobe infiltrates that are more pronounced on the right side. There are no pleural effusions.

Management questions. A validated prediction rule forecasts that this patient's risk of death from his CAP is <1% [ 3 ]. Therefore, he is a candidate for outpatient therapy.

What is the likely microbiological diagnosis? On the basis of the cough of 2 weeks' duration in the patient's 11-year-old child, the pneumonia could be due to M. pneumoniae or another atypical pathogen. However, this illness could represent pneumococcal pneumonia superimposed on a viral upper respiratory tract infection.

Clinical trial design questions. These are the hard questions and illustrate some of the many reasons for this workshop: Is the patient of sufficient reliability to participate in an outpatient clinical trial of antibacterials for mild CAP? Is it ethical or, from a practical standpoint, feasible to conduct a placebo-controlled trial? If an active comparator drug is used, how does one generate a valid and defensible margin of noninferiority?

What are valid, reproducible, and quantifiable clinical end points (outcomes)?

It would help greatly if the etiology of the pneumonia could be determined for the majority of the enrolled patients. What are the current diagnostic tools that can be applied and thereby “enrich” the patient population?

Multiple precautions are necessary to avoid bias in the interpretation of the results of clinical trials. For example, what are acceptable methods in the “blinding” of treatment arms?

How can investigators reliably and with reasonable sensitivity detect adverse drug effects?

The articles that follow address these questions and more. Participants in this workshop uniformly agreed that the interaction of US Food and Drug Administration regulations, industry sponsors, and Infectious Diseases Society of America academics represents an opportunity to modernize future clinical trials for CAP.

Supplement sponsorship. This article was published as part of a supplement entitled “Workshop on Issues in the Design and Conduct of Clinical Trials of Antibacterial Drugs for the Treatment of Community-Acquired Pneumonia,” sponsored by the US Food and Drug Administration and the Infectious Diseases Society of America.

Potential conflicts of interest. D.N.G. serves on the speakers' bureau of Abbott Laboratories, Bayer, GlaxoSmithKline, Lilly, Merck, Pfizer, Roche, Schering-Plough, and Wyeth; and has received consulting fees from Advanced Life Sciences and Pacific Beach Bioscience.

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Pediatric Pneumonia Clinical Presentation

• Author: Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA; Chief Editor: Russell W Steele, MD  more...
• Sections Pediatric Pneumonia
• Practice Essentials
• Pathophysiology
• Epidemiology
• Patient Education
• Physical Examination
• Patients With Recurrent Pneumonias
• Approach Considerations
• Complete Blood Cell Count
• Sputum Gram Stain and Culture
• Blood Culture
• Inflammatory Markers
• Polymerase Chain Reaction
• Skin Testing
• Gastric Aspirates
• Cold Agglutinin Testing
• Urine Latex Agglutination Testing
• Direct Antigen Detection
• Imaging Studies
• Bronchoscopy
• Bronchoscopic Alveolar Lavage
• Protected Brush Tracheal Aspirate Sampling
• Lung Aspiration
• Lung Puncture
• Thoracentesis
• Hospitalization
• Hemodynamic Support
• Respiratory Management
• Pharmacologic Therapy
• Management of Pleural Effusions
• Long-term Monitoring
• Medication Summary
• Penicillins
• Cephalosporins
• Glycopeptides
• Macrolide Antibiotics
• Aminoglycosides
• Antituberculosis Agents
• Antiviral Agents
• Questions & Answers
• Media Gallery

Newborns with pneumonia rarely cough; more commonly they present with poor feeding and irritability, as well as tachypnea, retractions, grunting, and hypoxemia. Grunting in a newborn suggests a lower respiratory tract disease and is due to vocal cord approximation as they try to provide increased positive end-expiratory pressure (PEEP) and to keep their lower airways open.

After the first month of life, cough is the most common presenting symptom of pneumonia. Infants may have a history of antecedent upper respiratory symptoms. Grunting may be less common in older infants; however, tachypnea, retractions, and hypoxemia are common and may be accompanied by a persistent cough, congestion, fever, irritability, and decreased feeding. Any maternal history of Chlamydia trachomatis infection should be determined.

Infants with bacterial pneumonia are often febrile.  But those with viral pneumonia or pneumonia caused by atypical organisms may have a low-grade fever or may be afebrile. The child's caretakers may complain that the child is wheezing or has noisy breathing. Toddlers and preschoolers most often present with fever, cough (productive or nonproductive), tachypnea, and congestion. They may have some vomiting, particularly post-tussive emesis. A history of antecedent upper respiratory tract illness is common.

Older children and adolescents may also present with fever, cough (productive or nonproductive), congestion, chest pain, dehydration , and lethargy. In addition to the symptoms reported in younger children, adolescents may have other constitutional symptoms, such as headache, pleuritic chest pain, and vague abdominal pain. Vomiting, diarrhea, pharyngitis, and otalgia/otitis are other common symptoms.

Travel history is important because it may reveal an exposure risk to a pathogen more common to a specific geographic area (eg, dimorphic fungi). Any exposure to tuberculosis (TB) should always be determined. In addition, possible exposure to birds (psittacosis), bird droppings (histoplasmosis), bats (histoplasmosis), or other animals (zoonoses, including Q fever, tularemia, and plague) should be considered.

In children with evidence for recurrent sinopulmonary infections, a careful history to determine the underlying cause is needed. The recurrent nature of the infections may serve to  unveil an innate or acquired immune deficiency, an anatomic defect, or another genetic disease (eg, cystic fibrosis, ciliary dyskinesia).

Tuberculosis

A history of TB exposure to possible sources should be obtained in every patient who presents with signs and symptoms of pneumonia (eg, immigrants from Africa, certain parts of Asia, and Eastern Europe; contacts with persons in the penal or detention system; close contact with known individuals with TB). Children with TB usually do not present with symptoms until 1-6 months after primary infection. These may include fever, night sweats, chills, cough (which may include hemoptysis), and weight loss.

The signs and symptoms of pneumonia are often nonspecific and vary widely based on the patient’s age and the infectious organisms involved. Tachypnea is the most sensitive finding in patients with diagnosed pneumonia.

Initial evaluation

Early in the physical examination, identifying and treating respiratory distress, hypoxemia, and hypercarbia are important. Visual inspection of the degree of respiratory effort and accessory muscle use should be performed to determine both the presence and severity of respiratory distress. The examiner should simply observe the patient's respiratory effort and count the respirations for a full minute. In infants, observation should include an attempt at feeding, unless the baby has extreme tachypnea.

Pulmonary findings in all age groups may include accessory respiratory muscle recruitment, such as nasal flaring and retractions at subcostal, intercostal, or suprasternal sites. Signs such as grunting, flaring, severe tachypnea, and retractions should prompt the clinician to provide immediate respiratory support. Retractions result from an effort to increase intra-thoracic pressure in order to compensate for decreased compliance.

An emergency department (ED)-based study conducted in the United States found that respiratory rate alone and subjective clinical impression of tachypnea did not discriminate children with and without radiographic pneumonia. [ 26 ]

The World Health Organization (WHO) clinical criteria for pneumonia have also been reported to demonstrate poor sensitivity (34.3%) in diagnosing radiographic pneumonia in children presenting to the pediatric ED. [ 27 ] However, children with tachypnea as defined by WHO respiratory rate thresholds were more likely to have pneumonia than were children without tachypnea. The WHO thresholds are as follows:

Children younger than 2 months: Greater than or equal to 60 breaths/min

Children aged 2-12 months: Greater than or equal to 50 breaths/min

Children aged 1-5 years: Greater than or equal to 40 breaths/min

Airway secretions may vary substantially in quality and quantity but are most often profuse and progress from serosanguineous to a more purulent appearance. White, yellow, green, or hemorrhagic colors and creamy or chunky textures are not infrequent. If aspiration of meconium, blood, or other proinflammatory fluid is suspected, other colors and textures reflective of the aspirated material may be observed.

Infants may have external staining or discoloration of skin, hair, and nails with meconium, blood, or other materials when they are present in the amniotic fluid. The oral, nasal and, especially, tracheal presence of such substances is particularly suggestive of aspiration.

An assessment of oxygen saturation by pulse oximetry should be performed early in the evaluation of all children with respiratory symptoms. Cyanosis may be present in severe cases. When appropriate and available, capnography may be useful in the evaluation of children with potential respiratory compromise.

Cyanosis of central tissues, such as the trunk, implies a deoxyhemoglobin concentration of approximately 5 g/dL or more. This is consistent with severe derangement of gas exchange from severe pulmonary dysfunction as in pneumonia. However, congenital structural heart disease, hemoglobinopathy, polycythemia , and pulmonary hypertension (with or without other associated parenchymal lung disease) must also be considered.

Chest pain may be observed with inflammation of or near the pleura. Abdominal pain or tenderness is often seen in children with lower lobe pneumonia. The presence and degree of fever depends on the microorganism involved, but high temperature (38.4°C) within 72 hours after admission and the presence of pleural effusion have both been reported to be significantly associated with bacterial pneumonia. [ 8 ]

Pneumonia may occur as a part of an alternate generalized etiology. Therefore, signs and symptoms suggestive of other disease processes, such as rashes and pharyngitis, should be sought during the examination.

Auscultation

Auscultation is perhaps the most important portion of the examination of the child with respiratory symptoms. The examination is often very difficult in infants and young children for several reasons. Babies and young children often cry during the physical examination, making auscultation difficult. The best opportunity for success lies in prewarming hands and instruments and the use of a pacifier to calm the infant. The opportunity to listen to a sleeping infant should never be lost.

Older infants and toddlers may cry because they are ill or uncomfortable. But, most often, they may experience stranger anxiety. For these children, it is best to spend a few minutes with the parents in the child's presence. If the child sees that the parent trusts the examining physician, then he or she may be more willing to let the examiner approach. A small toy may help to gain the child's trust.

Any part of the examination using instruments should be deferred as long as possible, because the child may find the medical equipment threatening. Occasionally, if the child is allowed to hold the stethoscope for a few minutes, he or she becomes less frightened. Even under the best of circumstances, examining a toddler is difficult. If the child is asleep when the physician begins the evaluation, auscultation should be performed early.

Children with respiratory symptoms may have a concomitant upper respiratory tract infection with copious upper airway secretions. This creates another potential problem: the transmission of upper airway sounds. In many cases, the sounds created by upper airway secretions can almost obscure true breath sounds and lead to erroneous diagnoses. If the origin of sounds heard through the stethoscope is unclear, the examiner should listen to the lung fields and then hold the stethoscope near the child's nose. If the sound patterns from both locations are approximately the same, the likely source of the abnormal breath sounds is the upper airway.

Even when the infant or young child is quiet and has a clear upper airway, the child's normal physiology may make the examination difficult. The minute ventilation is the product of the respiratory rate an

Occasionally, a patient has pneumonia that continues to manifest clinically (persistent or unresponsive pneumonia), radiographically (eg, 8 weeks after antibiotic treatment), or both despite adequate medical management. Studies have documented that the usual pathogens (eg, pneumococcus, non-typeable H influenza , Moraxella catarrhalis ) may be the causative agents.

Other patients may present with a history of recurrent pneumonias, defined as more than 1 episode per year or more than 3 episodes in a lifetime, and again the organisms responsible are the aforementioned common pathogens.

These patients merit special mention because they require a more extensive workup by a specialist. One useful way to categorize these patients is based on radiographic findings with and without symptoms. This method places these children in 1 of 3 categories that help to narrow the differential diagnoses (see Table below).

A careful history and examination are helpful to further narrow the differential diagnosis. However, more testing is often needed to confirm most of such diagnoses and is generally outside the scope of a primary care provider.

Table. Categorizing Patients Based on Symptoms, to Assist in Differential Diagnosis of Patients With Recurrent Pneumonias (Open Table in a new window)

UNICEF, Save the Children, and Every Breath Counts. Every child’s right to survive: a 2020 agenda to end pneumonia deaths. UNICEF. Available at https://www.unicef.org/reports/every-childs-right-survive-pneumonia-2020 . 2020 Jan; Accessed: June 4, 2020.

Rudan I, Boschi-Pinto C, Biloglav Z, Mulholland K, Campbell H. Epidemiology and etiology of childhood pneumonia. Bull World Health Organ . 2008 May. 86 (5):408-16. [QxMD MEDLINE Link] .

Shah VP, Tunik MG, Tsung JW. Prospective evaluation of point-of-care ultrasonography for the diagnosis of pneumonia in children and young adults. JAMA Pediatr . 2013 Feb. 167 (2):119-25. [QxMD MEDLINE Link] .

Metinko AP. Neonatal pulmonary host defense mechanisms. Polin RA, Fox WW, eds. Fetal and Neonatal Physiology . 3rd ed. Philadelphia, Pa: WB Saunders Co; 2004. 1620-73.

Barnett ED, Klein JO. Bacterial infections of the respiratory tract. Remington JS, Klein JO, eds. Infectious Diseases of the Fetus and Newborn Infant . 6th ed. Philadelphia, Pa: Elsevier Saunders Co; 2006. 297-317.

Bone RC, Grodzin CJ, Balk RA. Sepsis: a new hypothesis for pathogenesis of the disease process. Chest . 1997 Jul. 112(1):235-43. [QxMD MEDLINE Link] .

Li F, Zhang Y, Shi P, Cao L, Su L, Fu P, et al. Mycoplasma pneumoniae and Adenovirus Coinfection Cause Pediatric Severe Community-Acquired Pneumonia. Microbiol Spectr . 2022 Apr 27. 10 (2):e0002622. [QxMD MEDLINE Link] .

Michelow IC, Olsen K, Lozano J, et al. Epidemiology and clinical characteristics of community-acquired pneumonia in hospitalized children. Pediatrics . 2004 Apr. 113(4):701-7. [QxMD MEDLINE Link] .

Stoll BJ, Hansen NI, Higgins RD, et al. Very low birth weight preterm infants with early onset neonatal sepsis: the predominance of gram-negative infections continues in the National Institute of Child Health and Human Development Neonatal Research Network, 2002-2003. Pediatr Infect Dis J . 2005 Jul. 24(7):635-9. [QxMD MEDLINE Link] .

Mishaan AM, Mason EO Jr, Martinez-Aguilar G, et al. Emergence of a predominant clone of community-acquired Staphylococcus aureus among children in Houston, Texas. Pediatr Infect Dis J . 2005 Mar. 24(3):201-6. [QxMD MEDLINE Link] .

Kotecha S, Hodge R, Schaber JA, Miralles R, Silverman M, Grant WD. Pulmonary Ureaplasma urealyticum is associated with the development of acute lung inflammation and chronic lung disease in preterm infants. Pediatr Res . 2004 Jan. 55(1):61-8. [QxMD MEDLINE Link] .

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• (Left) Gram stain demonstrating gram-positive cocci in pairs and chains and (right) culture positive for Streptococcus pneumoniae.
• A breakdown of test results and recommended treatment for pneumonia with effusion. Gm = Gram; neg = negative; pos = positive; VATS = video-assisted thoracic surgery
• (A) Anteroposterior radiograph from a child with presumptive viral pneumonia. (B) Lateral radiograph of the same child with presumptive viral pneumonia.
• Radiograph from a patient with bacterial pneumonia (same patient as in the preceding image) a few days later. This radiograph reveals progression of pneumonia into the right middle lobe and the development of a large parapneumonic pleural effusion.
• Right lower lobe consolidation in a patient with bacterial pneumonia.
• (A) Anteroposterior radiograph from a child with a left lower lobe infiltrate. (B) Lateral radiograph of the same child with a left lower lobe infiltrate.
• Anteroposterior radiograph from a child with a round pneumonia.
• Table. Categorizing Patients Based on Symptoms, to Assist in Differential Diagnosis of Patients With Recurrent Pneumonias

Contributor Information and Disclosures

Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA Professor of Emergency Medicine and Clinical Pediatrics, Weill Cornell Medical College; Attending Physician, Departments of Emergency Medicine and Pediatrics, Lincoln Medical and Mental Health Center; Adjunct Professor of Emergency Medicine, Adjunct Professor of Pediatrics, St George's University School of Medicine, Grenada Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA is a member of the following medical societies: American Academy of Pediatrics , American Academy of Urgent Care Medicine, American College of Emergency Physicians , American Heart Association , American Medical Association , Association of Clinical Research Professionals , Public Responsibility in Medicine and Research , Society for Academic Emergency Medicine , Society for Simulation in Healthcare Disclosure: Nothing to disclose.

Marie-Micheline Lominy, MD Attending Physician, Lincoln Medical Center; Physician in Pediatric Adolescent Medicine, Boston Children's Health Physicians Marie-Micheline Lominy, MD is a member of the following medical societies: American Academy of Pediatrics , Haitian Medical Association Abroad, Haiti Red Cross Society Disclosure: Nothing to disclose.

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics , American Association of Immunologists , American Pediatric Society , American Society for Microbiology , Infectious Diseases Society of America , Louisiana State Medical Society , Pediatric Infectious Diseases Society , Society for Pediatric Research , Southern Medical Association Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha , American Academy of Pediatrics , American Society for Microbiology , Infectious Diseases Society of America , Pediatric Infectious Diseases Society , Phi Beta Kappa Disclosure: Received research grant from: Pfizer;GlaxoSmithKline;AstraZeneca;Merck;American Academy of Pediatrics, Novavax, Regeneron, Diassess, Actelion<br/>Received income in an amount equal to or greater than $250 from: Sanofi Pasteur.

Nicholas John Bennett, MBBCh, PhD, FAAP, MA(Cantab) Nicholas John Bennett, MBBCh, PhD, FAAP, MA(Cantab) is a member of the following medical societies: Alpha Omega Alpha , American Academy of Pediatrics Disclosure: Nothing to disclose.

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics , Association of Pediatric Program Directors , Infectious Diseases Society of America , and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Brent R King  , MD, MMM Clive Nancy and Pierce Runnells Distinguished Professor of Emergency Medicine; Professor of Pediatrics, University of Texas Health Science Center at Houston; Chair, Department of Emergency Medicine, Chief of Emergency Services, Memorial Hermann Hospital and LBJ Hospital

Jeff L Myers, MD, PhD Chief, Pediatric and Congenital Cardiac Surgery, Department of Surgery, Massachusetts General Hospital; Associate Professor of Surgery, Harvard Medical School

Mark I Neuman, MD, MPH Assistant Professor of Pediatrics, Harvard Medical School; Attending Physician, Division of Emergency Medicine, Children's Hospital Boston

Mark I Neuman, MD, MPH is a member of the following medical societies: Society for Pediatric Research

José Rafael Romero, MD Director of Pediatric Infectious Diseases Fellowship Program, Associate Professor, Department of Pediatrics, Combined Division of Pediatric Infectious Diseases, Creighton University/University of Nebraska Medical Center

José Rafael Romero, MD is a member of the following medical societies: American Academy of Pediatrics , American Society for Microbiology , Infectious Diseases Society of America , New York Academy of Sciences , and Pediatric Infectious Diseases Society

Manika Suryadevara, MD Fellow in Pediatric Infectious Diseases, Department of Pediatrics, State University of New York Upstate Medical University

Isabel Virella-Lowell, MD Department of Pediatrics, Division of Pulmonary Diseases, Pediatric Pulmonology, Allergy and Immunology

Garry Wilkes, MBBS, FACEM Director of Emergency Medicine, Calvary Hospital, Canberra, ACT; Adjunct Associate Professor, Edith Cowan University, Western Australia

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

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• Viral Pneumonia
• Chlamydial Pneumonias
• Aspiration Pneumonitis and Pneumonia
• Hospital-Acquired Pneumonia (Nosocomial Pneumonia) and Ventilator-Associated Pneumonia
• Pneumocystis jiroveci Pneumonia (PJP)
• Fungal Pneumonia
• Aspiration Pneumonia Imaging
• Europe Approves Exblifep for UTIs and Pneumonia
• Dehydration May Stall Pneumonia Recovery in Kids
• Specific Antipsychotics Linked to Increased Pneumonia Risk

• Drug Interaction Checker
• Pill Identifier
• Calculators

Learn about the nursing care management of patients with pneumonia .

Table of Contents

• What is Pneumonia? 

Community-Acquired Pneumonia

Hospital-Acquired Pneumonia

Pneumonia in the Immunocompromised Host

Aspiration pneumonia, pathophysiology, epidemiology.

• Clinical Manifestations 

Complications

Assessment and diagnostic findings, medical management, nursing assessment, nursing care planning & goals, nursing priorities, nursing interventions, discharge and home care guidelines, documentation guidelines, what is pneumonia.

Respiratory diseases are rampant today because it is easier spread in crowded areas. Pneumonia is one of the most common respiratory problems and it affects all stages of life.

• Pneumonia is an inflammation of the lung parenchyma caused by various microorganisms, including bacteria, mycobacteria, fungi , and viruses.
• Pneumonitis is a more general term that describes the inflammatory process in the lung tissue that may predispose and place the patient at risk for microbial invasion.

Classification

Pneumonia is classified into four: community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP), pneumonia in the immunocompromised host, and aspiration pneumonia .

• CAP occurs either in the community setting or within the first 48 hours after hospitalization .
• The causative agents for CAP that needs hospitalization include streptococcus   pneumoniae , H. influenza , Legionella , and Pseudomonas aeruginosa .
• Only in 50% of the cases does the specific etiologic agent become identified.
• Streptococcus pneumoniae is the most common cause of CAP in people younger than 60 years of age.
• Viruses are the most common cause of pneumonia in infants and children.
• HAP is also called nosocomial pneumonia and is defined as the onset of pneumonia symptoms more than 48 hours after admission in patients with no evidence of infection at the time of admission.
• HAP is the most lethal nosocomial infection and the leading cause of death in patients with such infections.
• Common microorganisms that are responsible for HAP include Enterobacter species , Escherichia coli , influenza , Klebsiella species , Proteus , Serratia marcescens , S. aureus , and S. pneumonia .
• The usual presentation of HAP is a new pulmonary infiltrate on chest x-ray combined with evidence of infection.
• Pneumonia in immunocompromised hosts includes Pneumocystis pneumonia, fungal pneumonias and Mycobacterium tuberculosis .
• Patients who are immunocompromised commonly develop pneumonia from organisms of low virulence .
• Pneumonia in immunocompromised hosts may be caused by the organisms also observe in HAP and CAP.
• Aspiration pneumonia refers to the pulmonary consequences resulting from entry of endogenous or exogenous substances into the lower airway.
• The most common form of aspiration pneumonia is a bacterial infection from aspiration of bacteria that normally reside in the upper airways.
• Aspiration pneumonia may occur in the community or hospital setting.
• Common pathogens are S. pneumonia , H.influenza , and S. aureus .

Having an idea about the disease process helps the patient understand the treatment regimen and its importance, increasing patient compliance .

• Pneumonia arises from normal flora present in patients whose resistance has been altered or from aspiration of flora present in the oropharynx.
• An inflammatory reaction may occur in the alveoli, producing exudates that interfere with the diffusion of oxygen and carbon dioxide.
• White blood cells also migrate into the alveoli and fill the normally air-filled spaces .
• Due to secretions and mucosal edema , there are areas of the lung that are not adequately ventilated and cause partial occlusion of the alveoli or bronchi .
• Hypoventilation may follow, causing ventilation -perfusion mismatch.
• Venous blood entering the pulmonary circulation passes through the under ventilated areas and travels to the left side of the heart deoxygenated.
• The mixing of oxygenated and poorly oxygenated blood can result to arterial hypoxemia .

Pneumonia has affected a lot of people, especially those who have a weak immune system. Learning statistics on pneumonia could give you an idea about how many has fallen victim to this respiratory disease.

• Pneumonia and influenza account for nearly 60,000 deaths annually .
• Pneumonia also ranks as the eighth leading cause of death in the United States.
• It is estimated that more than 915, 000 episodes of CAP occur in adults 65 years old and above in the United States.
• HAP accounts for 15% of hospital-acquired infections and is the leading cause of death in patients with such infections.
• The estimated incidence of HAP 4 to 7 episodes per 1000 hospitalizations.

Each type of pneumonia is caused by different and several factors.

• Streptococcus pneumoniae . This is the leading cause of CAP in people younger than 60 years of age without comorbidity and in those 60 years and older with comorbidity.
• H aemophilus influenzae.   This causes a type of CAP that frequently affects elderly people and those with comorbid illnesses.
• Mycoplasma pneumoniae. 
• Staphylococcus aureus . Staphylococcus pneumonia occurs through inhalation of the organism.
• Impaired host defenses. When the defenses of the body are down, several pathogens may invade the body.
• Comorbid conditions. There are several conditions that lower the immune system, causing bacteria to pool in the lungs and eventually result in pneumonia.
• Supine positioning . When the patient stays in a prolonged supine position, fluid in the lungs pools down and stays stagnant, making it a breeding place for bacteria.
• Prolonged hospitalization. The risk for hospital infections or nosocomial infections increases the longer the patient stays in the hospital.

Clinical Manifestations

Pneumonia varies in its signs and symptoms depending on its type but it is not impossible to diagnose a specific pneumonia through its clinical manifestations.

• Rapidly rising fever . Since there is inflammation of the lung parenchyma, fever develops as part of the signs of an infection.
• Pleuritic chest pain . Deep breathing and coughing aggravate the pain in the chest.
• Rapid and bounding pulse. A rapid heartbeat occurs because the body compensates for the low concentration of oxygen in the body.
• Tachypnea. There is fast breathing because the body tries to compensate for the low oxygen concentration in the body.
• Purulent sputum. The sputum becomes purulent because of the infection in the lung parenchyma which produced sputum-filled with pus.

It is better to prevent the occurrence of pneumonia instead of treating the disease itself. Here are several ways that can help prevent pneumonia.

• Pneumococcal vaccine. This vaccine can prevent pneumonia in healthy patients with an efficiency of 65% to 85%.
• Staff education. To help prevent HAP, the CDC (2004) encouraged staff education and involvement in infection prevention .
• Infection and microbiologic surveillance. It is important to carefully observe the infection so that there could be an appropriate application of prevention techniques.
• Modifying host risk for infection . The infection should never be allowed to descend on any host, so the risk must be decreased before it can affect one.

Pneumonia has several complications if left untreated or the interventions are inappropriate. These are the following complications that may develop in patients with pneumonia.

• Shock and respiratory failure. These complications are encountered chiefly in patients who have received no specific treatment and inadequate or delayed treatment.
• Pleural effusion . In pleural effusion , the fluid is sent to the laboratory for analysis, and there are three stages: uncomplicated, complicated, and thoracic empyema.

Assessment and diagnosis of pneumonia must be accurate since there are a lot of respiratory problems that have similar manifestations. The following are assessments and diagnostic tests that could determine pneumonia.

• History taking . The diagnosis of pneumonia is made through history taking, particularly a recent respiratory tract infection.
• Physical examination. Mainly, the number of breaths per minute and breath sounds is assessed during physical examination.
• Chest x-ray.  Identifies structural distribution (e.g., lobar, bronchial); may also reveal multiple abscesses/infiltrates, empyema (staphylococcus); scattered or localized infiltration (bacterial); or diffuse/extensive nodular infiltrates (more often viral). In mycoplasmal pneumonia, chest x-ray may be clear.
• Fiberoptic bronchoscopy .  May be both diagnostic (qualitative cultures) and therapeutic (re-expansion of lung segment).
• ABGs / pulse oximetry .  Abnormalities may be present, depending on extent of lung involvement and underlying lung disease.
• Gram stain/cultures.  Sputum collection; needle aspiration of empyema, pleural, and transtracheal or transthoracic fluids; lung biopsies and blood cultures may be done to recover causative organism. More than one type of organism may be present; common bacteria include Diplococcus pneumoniae, Staphylococcus aureus, a-hemolytic streptococcus, Haemophilus influenzae; cytomegalovirus (CMV). Note: Sputum cultures may not identify all offending organisms. Blood cultures may show transient bacteremia.
• CBC.  Leukocytosis usually present, although a low white blood cell (WBC) count may be present in viral infection, immunosuppressed conditions such as AIDS , and overwhelming bacterial pneumonia. Erythrocyte sedimentation rate (ESR) is elevated.
• Serologic studies, e.g., viral or Legionella titers, cold agglutinins.  Assist in differential diagnosis of specific organism.
• Pulmonary function studies.  Volumes may be decreased ( congestion and alveolar collapse); airway pressure may be increased and compliance decreased. Shunting is present ( hypoxemia ).
• Electrolytes .   Sodium and chloride levels may be low.
• Bilirubin.  May be increased.
• Percutaneous aspiration /open biopsy of lung tissues.  May reveal typical intranuclear and cytoplasmic inclusions (CMV), characteristic giant cells ( rubeola ).

The management of pneumonia centers is a step-by-step process that zeroes on the treatment of the infection through identification of the causative agent.

• Blood culture . Blood culture is performed for identification of the causal pathogen and prompt administration of antibiotics in patients in whom CAP is strongly suspected.
• Administration of macrolides . Macrolides are recommended for people with drug-resistant S. pneumoniae .
• Hydration is an important part of the regimen because fever and tachypnea may result in insensible fluid losses.
• Administration of antipyretics . Antipyretics are used to treat fever and headache.
• Administration of antitussives . Antitussives are used for treatment of the associated cough .
• Bed rest. Complete rest is prescribed until signs of infection are diminished.
• Oxygen administration. Oxygen can be given if hypoxemia develops.
• Pulse oximetry. Pulse oximetry is used to determine the need for oxygen and to evaluate the effectiveness of the therapy.
• Aggressive respiratory measures. Other measures include administration of high concentrations of oxygen, endotracheal intubation, and mechanical ventilation .

Nursing Management

Nurses are expected to perform both dependent and independent functions for the patient to aid him or her towards the restoration of their well-being.

SEE ALSO: 11 Pneumonia Nursing Care Plans for a comprehensive nursing care plan and management guide

Nursing assessment is critical in detecting pneumonia. Here are some tips for your nursing assessment for pneumonia.

• Assess respiratory symptoms. Symptoms of fever, chills, or night sweats in a patient should be reported immediately to the nurse as these can be signs of bacterial pneumonia.
• Assess clinical manifestations. Respiratory assessment should further identify clinical manifestations such as pleuritic pain , bradycardia, tachypnea , and fatigue , use of accessory muscles for breathing, coughing, and purulent sputum.
• Physical assessment. Assess the changes in temperature and pulse; amount, odor, and color of secretions; frequency and severity of cough ; degree of tachypnea or shortness of breath ; and changes in the chest x-ray findings.
• Assessment in elderly patients. Assess elderly patients for altered mental status , dehydration , unusual behavior, excessive fatigue , and concomitant heart failure .

Through the data collected during assessment, the following nursing diagnoses are made:

• Ineffective airway clearance related to copious tracheobronchial secretions.
• Activity intolerance related to impaired respiratory function.
• Risk for deficient fluid volume related to fever and a rapid respiratory rate.

Planning is essential to establish the interventions that are appropriate for the patient’s condition.

• Improve airway patency .
• Rest to conserve energy.
• Maintenance of proper fluid volume.
• Maintenance of adequate nutrition .
• Understanding of treatment protocol and preventive measures.
• Absence of complications.
• Maintain/improve respiratory function.
• Prevent complications.
• Support recuperative process.
• Provide information about disease process, prognosis, and treatment.

These nursing interventions , if implemented appropriately, would result in the achievement of the goals of the management of pneumonia.

To improve airway patency:

• Removal of secretions. Secretions should be removed because retained secretions interfere with gas exchange and may slow recovery.
• Adequate hydration of 2 to 3 liters per day thins and loosens pulmonary secretions.
• Humidification may loosen secretions and improve ventilation.
• Coughing exercises. An effective, directed cough can also improve airway patency.
• Chest physiotherapy. Chest physiotherapy is important because it loosens and mobilizes secretions.

To promote rest and conserve energy:

• Encourage avoidance of overexertion and possible exacerbation of symptoms.
• Semi-Fowler’s position. The patient should assume a comfortable position to promote rest and breathing and should change positions frequently to enhance secretion clearance and pulmonary ventilation and perfusion.

To promote fluid intake:

• Fluid intake. Increase in fluid intake to at least 2L per day to replace insensible fluid losses.

To maintain nutrition:

• Fluids with electrolytes. This may help provide fluid, calories, and electrolytes.
• Nutrition-enriched beverages. Nutritionally enhanced drinks and shakes can also help restore proper nutrition.

To promote patient’s knowledge:

• Instruct patient and family about the cause of pneumonia, management of symptoms, signs, and symptoms, and the need for follow-up.
• Instruct patient about the factors that may have contributed to the development of the disease.

Expected patient outcomes include the following:

• Demonstrates improved airway patency.
• Rests and conserves energy by limiting activities and remaining in bed while symptomatic and then slowly increasing activities.
• Maintains adequate hydration.
• Consumes adequate dietary intake.
• States explanation for management strategies.
• Complies with management strategies.
• Exhibits no complications.
• Complies with treatment protocol and prevention strategies.

Patient education is crucial regardless of the setting because self-care is essential in achieving a patient’s well-being.

• Oral antibiotics. Teach the patient about the proper administration, potential side effects, and symptoms to report.
• Breathing exercises. Teach the patient breathing exercises to promote secretion clearance and volume expansion.
• Follow-up check up. Strict compliance to follow-up checkups is important to check the latest chest x-ray result or physical examination findings.
• Smoking cessation. Smoking should be stopped because it inhibits tracheobronchial ciliary action and irritates the mucous cells of the bronchi.  

Documentation of data must be accurate and up-to-date to avoid unnecessary legal situations that might occur.

• Document breath sounds, presence and character of secretions, use of accessory muscles for breathing.
• Document character of cough and sputum.
• Document respiratory rate, pulse oximetry/O2 saturation, and vital signs.
• Document plan of care and who is involved in planning .
• Document client’s response to interventions, teaching, and actions performed.
• Document if there is use of respiratory devices or airway adjuncts.
• Document response to medications administered.
• Document modifications to plan of care.

See also: Respiratory System NCLEX Practice Questions and Reviewer (220 Questions)

13 thoughts on “Pneumonia”

This is very helpful. Thank you very much. I learned a lot for my upcoming exam next week. May God bless you.

Very useful keep on updating us with such strong information ,may you be blessed 🙏

Wow thanks so much love the website

Hi Marianne, The article is super good. I really appreciate it. Thanks a lot!!!

Thank you I like the explanation and am glad to you

very much thanks to nurseslabs.com

Thanks very much for Nurseslabs

You’re very welcome for the Nurseslabs resources! I’m thrilled to hear that you found the information on pneumonia helpful. Can you share any personal tips or experiences in managing pneumonia cases that have helped you in your nursing studies or clinical practice? Sharing practical insights can be incredibly beneficial for fellow students and aspiring nurses. 🩺💬📚

This is very helpful.Thank you so much.

You wrote : Pneumonia is the most common cause of CAP Did you mean the other way around? thanks

Hi, thanks, this has been updated.

Thank you so much Nurseslabs! 🙏🙏

Thank you faith!

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Pediatric Community-Acquired Pneumonia: Diagnosis and Management in the Emergency Department

*NEW* Quick Search this issue!

A significant challenge in the management of pediatric community-acquired pneumonia is identifying children who are more likely to have bacterial pneumonia and will benefit from antibiotic therapy while avoiding unnecessary testing and treatment in children who have viral pneumonia. This issue offers guidance for obtaining historical information and interpreting physical examination findings, discusses the utility of various diagnostic studies, and provides recommendations for the treatment of community-acquired pneumonia and associated complications. You will learn:

Common viral and bacterial etiologies of community-acquired pneumonia, key historical information and physical examination findings that can help differentiate viral and bacterial causes of pneumonia, when diagnostic studies are indicated, and which studies are recommended, which patients should receive antibiotics, and which should be discharged home with return precautions and appropriate follow-up, recommendations for outpatient and inpatient empiric antibiotic regimens, appropriate management of complications, including pleural effusion/empyema, case presentations, introduction, critical appraisal of the literature.

• Differentiation of Viral Causes From Bacterial Causes
• Viral Etiologies
• Streptococcus pneumoniae
• Staphylococcus aureus and Streptococcus pyogenes
• Mycoplasma pneumoniae
• Less Common Bacterial Causes
• Bronchiolitis
• Recurrent Viral-Induced Wheeze and Asthma
• Congenital Heart Disease
• Foreign-Body Aspiration
• Metabolic Disorders
• Primary Care Providers
• Emergency Medical Services
• Initial Stabilization
• History of Present Illness
• Past Medical History
• Immunization Status
• Family History
• Temperature
• Respiratory Rate
• Pulse Oximetry
• Other Physical Examination Findings
• Complete Blood Cell Count
• Erythrocyte Sedimentation Rate
• C-Reactive Protein
• Procalcitonin
• Combination Testing
• Chemistries
• Blood Culture
• Sputum Culture
• Other Microbiological Assays
• Patients With Asthma
• Computed Tomography
• Antipyretics
• Intravenous Fluids
• Albuterol and Corticosteroids
• Antibiotics
• Management of Parapneumonic Effusion and Empyema
• Patients With Bronchopulmonary Dysplasia
• Patients With Neuromuscular Disease
• Patients Who Are Immunodeficient
• Transcriptomics
• Scoring Systems/Risk Models
• Disposition

Risk Management Pitfalls in the Management of Pediatric Patients with Community-Acquired Pneumonia

• Time- and Cost-Effective Strategies
• Case Conclusions
• Clinical Pathway for Management of Pediatric Patients With Community-Acquired Pneumonia
• Table 1. Variables Used to Distinguish Viral From Bacterial Pneumonia
• Table 2. Empiric Outpatient Therapy for Children With Community-Acquired Pneumonia 1
• Table 3. Empiric Antibiotic Therapy for Children Hospitalized With Community-Acquired Pneumonia 1
• Figure 1. Pleural Effusion on Chest X-Ray
• Figure 2. Pneumatocele on Chest X-Ray
• Figure 3. Round Pneumonia on Chest X-Ray
• Figure 4. Point-of-Care Ultrasound for Identification of Pneumonia

Worldwide, pneumonia is the most common cause of death in children aged < 5 years. Distinguishing viral from bacterial causes of pneumonia is paramount to providing effective treatment but remains a significant challenge. For patients who can be managed with outpatient treatment, the utility of laboratory tests and radiographic studies, as well as the need for empiric antibiotics, remains questionable. This issue reviews viral and bacterial etiologies of community-acquired pneumonia in pediatric patients, offers guidance for obtaining historical information and interpreting physical examination findings, discusses the utility of various diagnostic techniques, and provides recommendations for the treatment of previously healthy and medically fragile children.

A previously healthy 4-year-old girl is brought to the ED for fever and abdominal pain that started 10 hours ago. The girl’s temperature is 39.4°C (103°F). On physical examination, she is ill-appearing, and she states that her belly really hurts. Her abdominal pain appears to be severe, and she is upset, so your abdominal examination is limited. There is no respiratory distress, and her lungs are clear to auscultation. You place an IV and give her morphine for pain. The girl’s peripheral WBC count is 26,000 cells/mcL, with 82% neutrophils. You perform an ultrasound, but the appendix cannot be visualized. You recall that pneumonia can present as abdominal pain and wonder if that could be the case for this patient. Should you order a CT scan of the abdomen or start with a chest x-ray?

A previously healthy 8-year-old girl is referred to the ED for fever ranging from 38.9°C-39.4°C (102°F-103°F) and cough for 8 days. She was started on amoxicillin-clavulanate 2 days prior but has not improved. On physical examination, she is alert, nontoxic, and not in respiratory distress. Chest auscultation reveals decreased breath sounds and questionable rales in the left lower lobe. The high fever and localized chest findings prompt you to obtain a chest x-ray that shows a large left-sided pleural effusion . As you look at the film, you begin to wonder… Should you order a CT scan? What is the utility of ultrasound in this patient? Is a chest tube indicated and, if so, what labs would be useful to run on the pleural fluid? What is the most appropriate antibiotic coverage for this patient?

Your next patient is a 2-year-old boy who was brought in for fever and difficulty breathing. His temperature is 39.4°C (103°F). He appears nontoxic but is in moderate respiratory distress. His pulse oximetry is 92% on ambient air, and his respiratory rate is 56 breaths/min. His past medical history includes a prior hospitalization for pneumonia. His immunizations are up-to-date. Chest auscultation reveals bilateral wheezes and localized rales in the left lower lobe. The resident working with you orders an albuterol nebulization but is concerned that the patient has pneumonia, given the fever and focal rales. You consider starting antibiotics and transferring the patient to the nearest children’s hospital. Is it common for children to have repeat episodes of pneumonia? Are there other questions on review of systems that might be helpful in this patient?

Worldwide, pneumonia is the leading cause of death in children aged < 5 years. 1 In the United States, there are an estimated 1.5 million cases 2 and 150,000 hospitalizations 3 annually for pneumonia. Community-acquired pneumonia (CAP) is defined as “the presence of signs and symptoms of pneumonia in a previously healthy child caused by an infection that has been acquired outside of the hospital.” 4

The challenge for the emergency clinician is identifying the children who are more likely to have bacterial CAP and will benefit from antibiotic therapy while avoiding unnecessary testing and treatment in the majority of children who will have viral etiologies. Children aged < 5 years bear the highest burden of disease; in this population, viral etiologies predominate. 1,4,5 Bacterial causes increase in incidence with age. 5 Differentiating viral from bacterial pneumonia on the basis of radiological and laboratory findings is difficult. Studies have shown that chest x-ray (CXR) cannot reliably differentiate viral from bacterial pneumonia. 6,7 For this reason, expert guidelines recommend against the routine use of both CXR and antibiotics for the majority of young children with the diagnosis of CAP. 1,4 In spite of this, it is common for young children to receive CXRs, blood work, and antibiotics for respiratory distress. Additionally, it can be difficult to differentiate CAP from other causes of respiratory distress, such as bronchiolitis and asthma. Finally, certain populations have a higher risk for bacterial pneumonia and complications, and deserve special consideration.

This issue of Pediatric Emergency Medicine Practice provides guidance on obtaining appropriate historical information, interpreting physical examination findings, and using laboratory testing and imaging judiciously in order to accurately differentiate between the various causes of pneumonia in children. Recommendations for antibiotic choice and indications for admission are also provided.

A literature search was performed used the following terms: neonatal pneumonia , pneumonia NOT bronchiolitis , and pediatric pneumonia AND community acquired , bacterial , diagnosis , physical exam , viral , atypical , fungal , diagnostic imaging , x-ray , ultrasound , inflammatory markers , CRP , procalcitonin , CBC , PCR , viral testing , computerized tomography scan , antibiotics , mycoplasma , atelectasis , medically complex , medically fragile , and aspiration . Available studies included observational studies, cross-sectional studies, randomized controlled trials, meta-analyses, Cochrane Database of Systematic Reviews analyses, and review articles. Multiple guidelines exist, most notably the Finnish, British Thoracic Society (BTS), World Health Organization (WHO), and Infectious Diseases Society of America (IDSA) guidelines. Of the thousands of articles that resulted, a total of 143 articles were selected, representing the most pertinent and current literature available.

There are several limitations associated with the available literature. Varying definitions of pneumonia exist in the literature and guidelines, making consensus difficult and limiting comparative analyses. In addition, despite a large body of literature, more prospective studies are needed, particularly of emerging diagnostic studies (such as ultrasound). Most notably, no definitive, agreed-upon gold standard for diagnosis exists; some studies use radiographs only, while some use laboratory findings plus radiographs, and some are based on the overall clinical picture. Limitations also exist in the available tests for pneumonia. Viral detection does not necessarily mean causation, and similarly, upper respiratory cultures and associated laboratory markers do not distinguish active infection from colonization. Furthermore, agreed-upon gold standards of diagnosis (such as blood cultures) are rarely positive except in complicated pneumonias, while sputum cultures, considered to be accurate in diagnosis, are difficult to obtain in young children. These deficits in knowledge in the literature of the specific viral, bacterial, and atypical causes of CAP limit the ability to provide narrow and definitive treatment.

2. “The 4-year-old boy had asthma, fever, wheezing, and rales on exam. His chest CXR was read by the radiologist as left lower lobe infiltrate versus atelectasis. I sent him home on amoxi-cillin, and he came back 2 days later with persistent cough, wheeze, and rales. His fever had resolved. Repeat CXR showed resolution of the infiltrate.”

Wheezing is typically a viral process and neither the presence of rales nor findings on CXR reliably differentiate viral from bacterial pneumonia. Furthermore, radiographic lobar pneumonia does not typically resolve in 2 days, suggesting, in this case, that the initial CXR finding was atelectasis rather than infiltrate. In a young child with asthma, fever, wheezing, and suspected CAP, consider a viral process first. Treat the asthma exacerbation with bronchodilators and corticosteroids. If there is concern for bacterial CAP, consider CXR or treat empirically with amoxicillin, but do not forget to give the patient corticosteroids.

3. “I gave my patient ceftriaxone for lobar pneumonia.”

Rates of resistant pneumococcus have declined since the introduction of PCV. Current recommendations for uncomplicated lobar pneumonia are to give amoxicillin or ampicillin. Indications for ceftriaxone include incomplete vaccination status and areas in which resistance is common.

6. “The 8-year-old girl with fever for 8 days and cough had lobar consolidation with significant pleural effusion, so I obtained a chest CT.”

Given the inherent risk of ionizing radiation associated with CT, lung ultrasound should be the initial modality used to assess findings concerning for empyema demonstrated on CXR in pediatric patients in the emergency setting. If the patient is not in significant distress, a CT scan in the ED can often be avoided.

Tables and Figures

Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of patients. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study is included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the author, are  highlighted .

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Publication Information

Jonathan Cooper-Sood, MD; Rebecca Wallihan, MD; James Naprawa, MD

Peer Reviewed By

Michael Gottlieb, MD; Dante Pappano, MD, MPH

Publication Date

April 1, 2019

Pub Med ID: 30908905

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A systematic review of the clinical features of pneumonia in children aged 5-9 years: Implications for guidelines and research

Priya m kevat.

1 Murdoch Children’s Research Institute, Melbourne, Victoria, Australia

2 University of Melbourne, Melbourne, Victoria, Australia

3 Royal Children’s Hospital Melbourne, Melbourne, Victoria, Australia

Melinda Morpeth

Hamish graham, associated data.

Childhood pneumonia presents a large global burden, though most data and guidelines focus on children less than 5 years old. Less information is available about the clinical presentation of pneumonia in children 5-9 years of age. Appropriate diagnostic and treatment algorithms may differ from those applied to younger children. This systematic literature review aimed to identify clinical features of pneumonia in children aged 5-9 years, with a focus on delineation from other age groups and comparison with existing WHO guidance for pneumonia in children less than 5 years old.

We searched MEDLINE, EMBASE and PubMed databases for publications that described clinical features of pneumonia in children 5-9 years old, from any country with no date restriction in English. The quality of included studies was evaluated using a modified Effective Public Health Project Practice (EPHPP) tool. Data relating to research context, study type, clinical features of pneumonia and comparisons with children less than 5 years old were extracted. For each clinical feature of pneumonia, we described mean percentage (95% confidence interval) of participants with this finding in terms of aetiology (all cause vs Mycoplasma pneumoniae ), and method of diagnosis (radiological vs clinical).

We included 15 publications, eight addressing all-cause pneumonia and seven addressing Mycoplasma pneumoniae . Cough and fever were common in children aged 5-9 years with pneumonia. Tachypnoea was documented in around half of patients. Dyspnoea/difficulty breathing and chest indrawing were present in approximately half of all-cause pneumonia cases, with no data on indrawing in the outpatient setting. Chest and abdominal pain were documented in around one third of cases of all-cause pneumonia, based on limited numbers. In addition to markers of pneumonia severity used in children <5 years, pallor has been identified as being associated with poorer outcomes alongside comorbidities and nutritional status.

Conclusions

Quality research exploring clinical features of pneumonia, treatment and outcomes in children aged 5-9 years using consistent inclusion criteria, definitions of features and age ranges are urgently needed to better inform practice and guidelines. Based on limited data fever and cough are common in this age group, but tachypnoea cannot be relied on for diagnosis. While waiting for better evidence, broader attention to features such as chest and abdominal pain, the role of chest radiographs for diagnosis in the absence of symptoms such as tachypnoea, and risk factors which may influence patient disposition (chest indrawing, pallor, nutritional status) warrant consideration by clinicians.

Protocol registration

PROSPERO: CRD42020213837.

Childhood pneumonia is responsible for a large mortality burden globally however most guidelines for low resource settings are focused on pneumonia in children less than 5 years old [ 1 , 2 ]. Focus on young children has been justified by the fact that more than 90% of childhood pneumonia deaths occur in young children less than 5 years of age [ 3 ]. Yet pneumonia is also important for older children. Global Burden of Disease estimates suggest that pneumonia accounts for around 7% of deaths in children aged 5-9 years [ 3 ].

While children aged 5-9 years are generally regarded as at lower risk for pneumonia and pneumonia death, the risk may still be substantial in certain contexts or patient cohorts (for example, children with chronic health conditions or disability). Appropriate diagnostic and treatment algorithms may differ from those applied to younger children and this group has not been addressed in previous guidelines.

The aim of this review was to describe the available evidence for clinical features of pneumonia in children aged 5-9 years in community, primary care, or hospital settings, with a focus on delineation from other age groups and comparison with existing WHO guidance for pneumonia in young children.

The protocol for this study was registered on PROSPERO, the international prospective register of systematic reviews (registration number CRD42020213837). We searched MEDLINE via Ovid, EMBASE via Ovid and PubMed in August 2020 using key search terms including synonyms for pneumonia, ages 5-9 years, and clinical findings or diagnosis (example in Appendix S1 in the Online Supplementary Document ). No date restriction was applied. We did not restrict by location of study but for practical reasons we restricted the search to studies available in English language.

We included studies that contained original data on the clinical features of pneumonia among children aged 5-9 years, published in English language. We excluded case reports, small case series (<10 participants), conference abstracts, or those in which data relating to children aged 5-9 years was not meaningfully disaggregated.

PK completed initial title and abstract screening. Full-text screening was completed by three reviewers (PK, MM, AG), with each article screened by two of these reviewers (PK, MM, AG) and any conflicts resolved by the majority opinion from the third remaining reviewer (PK, MM, AG). Reference lists of included articles were searched to identify additional relevant studies missed from the search.

We extracted data from included studies with a standardised data extraction tool. Information extracted included: year of publication, study details, inclusion and exclusion criteria, pneumonia diagnostic/case definition criteria, aetiological agent(s), participant characteristics (including socioeconomic status), presence of comorbid conditions, respiratory and extra-pulmonary clinical features, chest radiograph findings, treatment received, and outcomes, with comparison to the under 5 years age group wherever possible. Data extraction was completed by two reviewers (PK, MM), with data from each article extracted by one of these reviewers (PK, MM) and the extracted information checked by the second reviewer (PK, MM). Any conflicts were resolved by the majority opinion from a third reviewer (AG).

We separated data from studies describing pneumonia of any aetiology (all-cause pneumonia) and studies describing pneumonia attributed to Mycoplasma pneumoniae , given that several studies addressed Mycoplasma pneumoniae specifically. For each clinical feature, we described the number and percentage of patients who were documented to have the feature in each study. Using aggregated data of all studies which included each clinical feature we calculated the mean percentage and 95% confidence interval according to the cause of pneumonia (all-cause and attributable to Mycoplasma pneumoniae ) and the method of diagnosis (radiological or clinical). If studies stipulated their inclusion criteria as a clinical diagnosis with or without radiological diagnosis, they were included in the studies based on clinical diagnosis for analysis (as we were unable to identify which participants had a radiograph performed). Due to the relatively weak quality of the studies identified and the variable nature of the data from the studies we did not perform any additional statistical analysis, to avoid over-interpretation of the data available.

We used the EPHPP tool to evaluate the risk of bias in included studies [ 4 ]. This tool was modified to assess the study designs included (Table S1 in the Online Supplementary Document ). Application of the EPHPP tool required separate evaluation and consensus between two reviewers (PK, MM).

The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement was followed, with a checklist completed (Table S2 in the Online Supplementary Document ) [ 5 ].

A total of 2641 references were retrieved, and an additional four relevant publications were identified through reference list screening ( Figure 1 ). After duplicates were removed, 1776 references were screened, and 301 proceeded to full-text review. Two articles were excluded as the full text was unavailable, after authors were contacted twice to request them. Fifteen studies were included in qualitative synthesis after inclusion and exclusion criteria were applied.

Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow diagram.

Study descriptions

Studies had variable methods to identify patients with pneumonia. Seven of the 15 studies included children with radiologically confirmed pneumonia (two of these requiring clinical features in addition) and eight of the 15 studies were based on clinical diagnosis with or without a radiograph. The heterogeny in diagnostic methods was significant. For example, one study based on radiological diagnosis only included patients with obvious chest indrawing. Furthermore, of those based on clinical diagnosis, three studies included children with or without a radiograph being performed, three required clinician diagnosis alone, and two studies were of Mycoplasma pneumoniae positive patients that described clinical features and/or chest radiograph changes consistent with pneumonia. Eight studies addressed all-cause pneumonia ( Table 1 ) whilst seven discussed pneumonia attributable to Mycoplasma pneumonia e, based on a variety of diagnostic assays ( Table 2 ). Three out of the 15 studies, Macpherson et al [ 12 ], Salih et al [ 13 ] and Forgie et al [ 11 ], were from low or lower-middle income settings. Twelve studies described inpatients only, one study by Harris et al [ 9 ] was of outpatients, and two studies by Korppi et al [ 8 ] and Othman et al [ 19 ] included a combination of inpatients and outpatients.

Clinical features described in children aged 5-9 y diagnosed with pneumonia of any aetiology (all-cause pneumonia)

CAP – community acquired pneumonia, RCT – randomised controlled trial, WCC – white cell count, PFTs – pulmonary function tests, ALRI – acute lower respiratory infection, CXR – chest x-ray, y – year, mo – months

*Values significant with P  < 0.05 when the <2 years group was compared to the ≥2 years group (combined data for 2-4 years and ≥5 years).

†Corrected percentage value due to error in calculated percentage within study.

‡Tachypnoea was defined by age-specific WHO criteria: respiratory rate >50 breaths/min in infants <12 months old, >40 breaths/min in children aged 1-5 years and >30 breaths/min in children aged ≥6 years.

§Conventional therapy = amoxicillin/clavulanate if ≤5 years of age and erythromycin if >5 y of age.

‖Abnormal respiratory rate was defined as >24 breaths/min for patients ≤2 year of age and >20 breaths/min for patients >2 year of age.

¶Fever was defined as ≥100.5°F oral or ≥101°F rectal, or history in the last 24 h.

**Absolute numbers and percentages are extrapolated data.

†† P values not calculated in this study.

‡‡Weight <80% of median value using National Center for Health Statistics reference values (United States Department of Health, Education and Welfare, 1976).

Clinical features described in children aged 5-9 y diagnosed with pneumonia attributable to Mycoplasma pneumoniae

ICD-10 - International Classification of Diseases 10th edition, CXR – chest x-ray, PCR – polymerase chain reaction, CAP – community acquired pneumonia, LRTI – lower respiratory tract infection, ICU – intensive care unit, VATS – video-assisted thorascopic surgery, y – years, d – days

*Pneumonia pattern characterised by WHO Standardization of Interpretation of Chest Radiographs for the diagnosis of community acquired pneumonia in children.

†Study text states that “one-half of the children had lobar pneumonia in both groups”, however study Figure 3 suggests a higher number (between 40 and 60 patients with lobar pneumonia for each of the ≤5 years and >5 years groups).

‡Data for a symptom/sign was included if able to be disaggregated from combined data.

§ P values relate to comparison of <5 years group with 5 to <10 years and 10-14 years groups.

‖Tachypnoea was defined as a respiratory rate >99 th percentile for age.

¶Includes any type of rash, urticaria and Stevens-Johnson Syndrome.

**112/134 total patients had CXRs, fraction of children aged 7-15 years who had CXRs not specified.

††Absolute numbers and percentages not described.

Three of the eight studies that explored all-cause pneumonia included patients with comorbid conditions, three specifically excluded those with comorbidities, and two did not specify information about comorbidities. A significant proportion of participants aged 5-9 years in study by Macpherson et al had comorbid disease including malaria (28.77%), asthma (10.91%), neurological disorders (10.77%), severe malnutrition (9.48%) or HIV (8.32%) [ 12 ]. Meanwhile, 46% of children aged 5-14 years in study by Salih et al were underweight [ 13 ], and a variety of underlying chronic comorbid conditions were described by Udomittipong et al but not disaggregated by age [ 10 ]. Within the group of studies addressing Mycoplasma pneumoniae , four included those with chronic conditions or comorbidities, two excluded children with these and one did not specify information about comorbidities. Chronic pulmonary disease and asthma were most frequently described as pre-existing underlying disease [ 17 , 19 , 20 ].

Most studies were of weak quality when assessed with the EPHPP tool ( Table 1 and Table 2 ). The exceptions were Macpherson et al [ 12 ] and Harris et al [ 9 ], which were assessed as moderate quality. There were seven retrospective observational studies, six studies with prospective recruitment of participants, one randomized controlled trial (RCT) and one descriptive study based on interview and questionnaire data. Describing clinical features of pneumonia was a primary objective in thirteen of the studies; two were not conducted with this as a primary aim but included clinical features of pneumonia in a description of participants. Many studies (8/15) did not specify or utilise a standardised data collection method. Although all studies included participants aged 5-9 years, study populations also included older and younger children. Three studies provided data disaggregated for the 5-9 age range exactly; the remaining twelve studies overlapped with the target population with a sufficiently close age range to be representative. In some studies, there was a paucity of disaggregated data relating to clinical features in children 5-9 years old. There were also differing definitions and terms for some clinical features between studies. Most importantly, the definition of fast breathing varied from >20 breaths per minute [ 9 ], to >40 breaths per minute [ 8 ], to a respiratory rate >99 th percentile for age [ 20 ].

Study outcomes

Aggregated data regarding the proportion of older children with specific respiratory symptoms and extra-pulmonary clinical features is summarised in Table 3 .

Overall data regarding proportion of children with specific clinical features in included studies

*Includes dyspnoea/difficulty breathing/gasping/breathlessness, combined data from 4-6 and ≥7-14 age groups from Gao et al included [ 14 ].

†Includes flaring/nasal flaring.

‡Includes indrawing/recession/chest wall indrawing/chest recession/chest retraction, Forgie et al excluded from analysis as study selected for patients with indrawing [ 11 ].

§Includes all utilised definitions of tachypnoea and abnormal respiratory rate, data pertaining to respiratory rate of ≥40 breaths per minute rather than ≥50 breaths per minute included from Juvén et al [ 7 ].

‖Includes crepitations/rales/crackles/pulmonary crackles at onset, data included if able to be disaggregated from other abnormal breath sounds, combined data from 4-6 and ≥7-14 age groups from Gao et al included [ 14 ].

¶Includes wheeze/wheezes/wheezing/auscultation – wheezing, data included if able to be disaggregated from other abnormal breath sounds, fraction and percentage of children with auscultation finding rather than reported symptom included from Sondergaard et al [ 20 ].

**Includes all utilised definitions of fever, data pertaining to fever >37.5°C rather than fever >39.5°C included from Korppi et al [ 8 ].

††includes any pallor present

‡‡Includes inability to drink/poor appetite/refusal to eat/cannot eat or drink/feeding difficulties.

§§Data included if able to be disaggregated from other gastrointestinal symptoms.

‖‖Data included if able to be disaggregated from pain at other sites.

¶¶Includes chest pain/thoracic pain.

***Includes any type of rash, urticaria and Stevens-Johnson Syndrome.

Cough was the most common clinical feature, documented in around 90% of patients in both all-cause and Mycoplasma cohorts, whether diagnosed clinically or radiologically. Fever was also common in both cohorts but more common in Mycoplasma (91.7%, 95% confidence interval (CI) = 91.2-92.3) compared to all-cause pneumonia (74.8%, 95% CI = 73.6-76.0).

Tachypnoea was identified in around half of patients overall but less frequently in the Mycoplasma cohort (all-cause pneumonia 55.4%, 95% CI = 53.6-57.2 and Mycoplasma pneumoniae 40.1%, 95% CI = 37.9-42.3). The study of outpatients by Harris et al had the highest prevalence of tachypnoea but the lowest threshold for defining tachypnoea (>20 breaths per minute for children older than 2 years) [ 9 ]. The percentage of patients with tachypnoea was lower for patients with a radiological diagnosis (all-cause pneumonia 48.0%, 95% CI = 42.9-53.1 and Mycoplasma pneumoniae 8.5%, 95% CI = 7.7-9.2) compared to a clinical diagnosis (all-cause pneumonia 77.0% comprising 1 study with 937/1216 patients and Mycoplasma pneumoniae 50.1%, 95% CI = 48.5-51.7). Of note, less than 10% of patients with a radiological diagnosis of Mycoplasma pneumoniae had documented tachypnoea.

Dyspnoea/difficulty breathing was documented in 29.1% (95% CI = 28.2-30.8) of all-cause pneumonia patients and 23.1% (95% CI = 22.4-23.8) of Mycoplasma pneumoniae patients. In the all-cause pneumonia cohort, the proportion of patients with dyspnoea was higher in the clinical diagnosis group (43.0%, 95% CI = 42.3-43.7) compared to the radiological (14.9%, 95% CI = 13.7-16.1). Chest indrawing was observed in approximately half of all-cause pneumonia cases, all of which were based on clinical diagnosis. There was only one small study of Mycoplasma pneumoniae patients which documented chest-indrawing in 30.0% (14/46) of patients [ 19 ]. Crackles or crepitations were variably described between studies but documented in around one half of patients overall. Wheeze or rhonchi were described in around one quarter of patients.

Chest and abdominal pain were each included in two studies of all-cause pneumonia (radiological diagnosis) and both were documented in around one third of patients. Abdominal pain was included in one small study of Mycoplasma pneumoniae patients (radiological diagnosis) and was found in 17% (11/66) of patients [ 15 ]. Headache, nausea and vomiting also occurred in around one third of patients in the all-cause pneumonia cohort, though these are non-specific symptoms that may occur in a range of illnesses. Skin manifestations were described in one study addressing Mycoplasma pneumoniae with data disaggregated by age and, in this study, were found in 25% (21/88) children [ 20 ].

With respect to chest radiograph findings in all studies, one study by Gao et al selected for patients with segmental/lobar Mycoplasma pneumoniae and additionally reported on the presence of pleural effusions (4%-5%) [ 14 ]. Aside from this, only a small number of study participants overall in the 5-9 year age range had disaggregated chest radiograph findings reported ( Table 4 ). Lobar changes were documented in around half of patients who had chest radiographs but any further conclusions are limited by the variable inclusion and diagnostic criteria and limited data.

Chest radiograph findings document in studies in children 5-9 y with pneumonia

*Data included if able to be disaggregated from other chest x-ray findings and both numerator and denominator clearly stated.

†Includes lobar consolidation/lobal consolidation/lobar infiltration and segmental/lobar pneumonia, Gao et al excluded from analysis as selected for patients with segmental/lobar pneumonia [ 14 ].

‡Includes interstitial changes/interstitial pattern.

§Includes pleural effusion/empyema, combined data from 4-6 y and ≥7-14 y groups from Gao et al included [ 14 ], data for pleural effusion rather than single case of empyema included from Sondergaard et al [ 20 ].

Outcome data for children aged 5-9 years with pneumonia were available from a single study of inpatients in Kenya, which was also the largest study in the review [ 12 ]. Macpherson et al described risk factors associated with mortality in children aged 5-14 years admitted to hospital with pneumonia [ 12 ]. Outcome information was available for 1825/1832 (99.5%) patients, of whom 145 (7.9%) died. Inpatient case fatality was higher in children aged 10-14 years compared to the 5-9 year age group (14.05% vs 6.43%, P  < 0.001). For children aged 5-10 years, risk factors for death demonstrated in multi-variate analysis included the presence of severe pallor (OR = 9.89, 95% CI = 4.68 to 20.93, P  < 0.001), mild/moderate pallor (OR = 2.85, 95% CI = 1.35-6, P  < 0.006), reduced consciousness (OR = 6.27, 95% CI = 2.8-14.08, P  < 0.001), central cyanosis (OR = 6.35, 95% CI = 1.33-30.25, P  < 0.02), a weight for age Z-score of≤-3 SD (OR = 2.99, 95% CI = 1.61-5.55, P  < 0.001) and comorbid HIV (OR = 2.49, 95% CI = 1.18-5.28, P  < 0.017). A respiratory rate >30 breaths per minute and inability to drink were associated with poor outcome, though did not reach statistical significance. Sex, presence of grunting, crackles, chest wall indrawing and comorbid malaria were not associated with mortality and wheeze was found to be relatively protective (not statistically significant). Additional analysis demonstrated that the combination of clinical characteristics used by WHO to define severe pneumonia in children less than 5 years old was poor in discriminating those at risk of death (sensitivity: 0.56, specificity: 0.68 and AUC: 0.62) in this study.

Regarding pneumonia severity and the need for inpatient treatment in children aged 5-9 years, there is little additional data to draw upon beyond the study by Macpherson et al [ 12 ]. Studies involving outpatients either did not describe chest indrawing or did not disaggregate data by age in combination with admission status [ 8 , 9 , 19 ]. Whilst lethargy was documented frequently, reduced consciousness as a specific sign was only described in the study by Macpherson et al [ 12 ].

Comparison with clinical features of pneumonia in younger children was made in six out of eight all-cause pneumonia studies and all seven Mycoplasma pneumoniae studies ( Table 1 and Table 2 ). In all studies which included chest and abdominal pain and compared frequency between older and younger children, they were found to be more common in older children [ 6 - 8 ]. Crocker et al found that abdominal pain was a reported symptom in all 12 cases in which pleural effusion or empyema were detected in children aged 3-16 years [ 6 ]. Comparison of chest auscultation findings between age groups demonstrated no clear trends, with some studies finding crackles and wheeze to be more common in younger children but other studies reporting greater frequency in older children [ 7 , 9 , 13 ]. Similarly, one study found that normal breath sounds were more common in children older than 5 years and another found that it was less common [ 7 , 11 ]. Inconsistent use of terms for auscultation findings between studies limited comparison. In a study of 127 children with Mycoplasma pneumoniae , Ma et al found that children less than 5 years of age were more likely to have a severe illness course, including intensive care unit admission, supplemental oxygen requirement and need for video-assisted thoracoscopic surgery (VATS) [ 15 ]. Vomiting also occurred more often in younger children with Mycoplasma pneumoniae [ 15 , 19 ]. Segmental or lobar consolidation on chest radiograph was a more common finding in older children for both all-cause pneumonia and Mycoplasma pneumoniae groups [ 13 , 16 , 18 ].

Comparative analysis of clinical features between those with and without comorbidities was not possible as data was not disaggregated for subgroups of participants with comorbidities in the 5-9 year age range in studies that included such participants.

There is a paucity of quality evidence describing clinical features of pneumonia in children aged 5-9 years. This review explored findings from 15 studies, eight addressing pneumonia of all causes and seven addressing pneumonia attributable to Mycoplasma pneumoniae . The lack of evidence highlights the urgent need for research to understand clinical features, treatment approaches and outcomes for children 5-9 years of age with pneumonia, which remains one of the highest causes of death in this age group globally [ 3 ]. However, the evidence that does exist indicates that applying existing WHO definitions of pneumonia for children under 5 years of age, to this older age group, is likely to lower the diagnostic yield.

Current WHO guidelines for children under 5 years old distinguish simple cough from pneumonia based on the presence or absence of tachypnoea. Among studies in this review, tachypnoea lacked standard definitions and this complicates interpretation of findings. However approximately only half of patients in the all-cause pneumonia cohort were documented to have tachypnoea, and this was lower for Mycoplasma pneumoniae patients, notably those diagnosed radiologically. Higher proportions of children with pneumonia in clinically diagnosed groups may represent later diagnosis. Alternatively, it may reflect greater emphasis on accurate measurement and recording of respiratory rate in clinicians using clinical diagnosis. The data on clinical diagnosis regarding tachypnoea in the all-cause pneumonia cohort is based on the Kenyan study, which is a cohort of sick children in a high burden setting. Yet, even amongst these patients around 1 in 4 did not have tachypnoea (respiratory rate >30 breaths per minute) documented on admission [ 12 ]. The measurement of respiratory rate is a skill which is often not performed well or documented correctly; the evidence indicates that it cannot be relied upon to identify pneumonia among older children with cough [ 21 ].

If tachypnoea cannot be relied on to diagnose pneumonia in older children, then addition of other symptoms to aid diagnostic approaches should be considered. Although the study numbers are small, chest pain and abdominal pain were relatively common in children aged5-9 years with all-cause pneumonia, whether due to their ability to report symptoms, or to the likelihood that researchers sought to identify these symptoms in older children. Chest radiographs may also have a greater role in diagnosing children with pneumonia in this age group, particularly in the setting of persistent cough and fever without other signs to confirm pneumonia (or alternative diagnoses). It should be noted, the data on chest radiograph findings in pneumonia in this age group is limited and there is insufficient data supporting the use of radiographs to distinguish pneumonia aetiology (eg, Mycoplasma from all-cause).

Symptoms used to define severe pneumonia in children <5 years of age, such as reduced conscious state, central cyanosis and/or hypoxia (oxygen saturation <90%) and inability to eat or drink [ 1 , 2 ], still have relevance in older children in low and lower-middle income settings in terms of their risk of mortality and therefore the severity of pneumonia. Similarly, nutritional status and underlying chronic conditions (including HIV) are associated with mortality in older children and should be part of any risk stratification approach used by clinicians to determine the need for admission and treatment [ 1 , 2 ]. Pallor, whether mild, moderate or severe, was identified as being associated with a higher risk of mortality in children 5-9 years old and should also be part of a clinician’s consideration of risk and patient disposition [ 12 ]. This is consistent with recent evidence suggesting that pallor is an important marker of serious disease in younger age groups [ 22 - 24 ]. The sign of chest indrawing has been an important and evolving marker of pneumonia severity and therefore need for admission in guidelines for children under 5 years old [ 25 ]. This review identified no data on the management of chest indrawing in children aged 5-9 years in the outpatient setting. Given chest compliance reduces with age [ 25 ], it is reasonable to suspect that chest indrawing may indicate greater severity in older children, as its presence may suggest generation of greater intrathoracic pressures to maintain ventilation. The Kenyan study in this review examined risk of death in older children with pneumonia and found no association between chest indrawing and mortality [ 12 ]. This finding, among others described above, is based on a single study in one context and should be interpreted with caution. Of note no radiological studies of all-cause pneumonia documented the presence or absence of chest indrawing in patients, despite its potential importance in guiding treatment.

Our review identified several studies relating to Mycoplasma pneumoniae in children 5-9 years of age mostly from high income countries, from which data has been reported separately to not unduly influence data on all-cause pneumonia, and to consider differences in clinical features. While Mycoplasma pneumoniae is important in pneumonia in older children, the emphasis on this organism in this review may represent bias on the part of researchers in considering it above other aetiologies. There is a clear need for more data on other potential aetiologies (eg, influenza), but particularly those relevant in the global context, such as HIV and tuberculosis.

Based on the available evidence for Mycoplasma pneumoniae , there are no respiratory clinical features that can distinguish it from pneumonia of other aetiologies in children aged 5-9 years. This is consistent with other studies that demonstrated no clinical or radiological features to identify Mycoplasma pneumoniae and guide therapeutic decisions [ 26 , 27 ]. Considering Mycoplasma pneumoniae as an aetiology and treating this possibility is therefore important, including in HIV positive children among whom it has also been shown to be common [ 28 ]. Skin symptoms may be useful in distinguishing Mycoplasma pneumoniae as a potential aetiological agent in pneumonia in older children, however there may be bias in seeking and reporting on these symptoms in studies focused on Mycoplasma pneumoniae and disaggregated supportive evidence was available from only one study in this review [ 20 ]. Separately, a review by Schalock and Dinulos [ 29 ] specifically addressing Mycoplasma pneumoniae -induced cutaneous disease in paediatric and adult populations and a study by Sauteur et al [ 30 ] in paediatric patients aged 3-18 years described skin manifestations as a feature of Mycoplasma pneumoniae , such as exanthematous skin eruptions, urticaria, erythema nodosum, Mycoplasma pneumoniae -induced rash and mucositis (MIRM) and Stevens-Johnson Syndrome. A key limitation in determining aetiology is that available diagnostic tests for Mycoplasma pneumoniae may not distinguish infection from carriage [ 31 ].

Implications for WHO pneumonia guidelines

The relatively weak quality of studies and limited evidence in this review should be kept in mind when interpreting the findings. Evidence related to risk factors for death, for example, is derived from a single study of moderate quality. Different definitions (eg, for tachypnoea), different nomenclatures (eg, crepitations) and absence of documentation of key signs (eg, chest indrawing) should be noted. Nonetheless, there are some implications to be considered for WHO guidelines while further research is conducted and evidence is generated.

Cough and fever are common clinical features in pneumonia in children aged 5-9 years. However, tachypnoea, used to define pneumonia according to WHO criteria in children <5 years of age, may not be present in older children with pneumonia. Inclusion of chest pain and abdominal pain in diagnostic approaches for older children might expand recognition of pneumonia in this age group, especially if other signs are absent. Furthermore, chest radiographs may have greater importance for diagnosis. Clear definitions of tachypnoea are required for both clinical application and to standardise future research.

Symptoms reflecting severity of pneumonia in children <5 years of age (eg, reduced conscious state, hypoxia and inability to drink) have relevance in older children in low resource settings with respect to risk of mortality, and therefore severity of pneumonia. Separate to these markers of severe disease, other patient factors such as poor nutritional status, comorbid chronic conditions and pallor are associated with poor outcomes. As a result, they should be part of the clinician’s consideration of risk of a poor outcome for children aged 5-9 years with pneumonia, and inform decision making on patient disposition.

There is minimal data on chest indrawing in children aged 5-9 years, particularly its management in outpatient settings, to guide management recommendations. Without further evidence, it may be safest to recommend admission if chest indrawing is present.

Although there are differences in the proportions of patients with clinical features between the all-cause pneumonia and Mycoplasma cohorts, these cannot be used to distinguish pneumonia of different aetiologies in children aged 5-9 years on an individual level. Guidelines should account for causative agents other than pneumococcus and antibiotic recommendations should be altered accordingly. The addition of an antibiotic to cover for Mycoplasma pneumoniae (eg, macrolide) when treating pneumonia in this age group should be strongly considered, particularly in severe cases, in children with malnutrition and/or other co-morbidities, and when deterioration occurs on alternate therapy. Skin symptoms may be useful in distinguishing Mycoplasma pneumoniae as a potential aetiological agent in pneumonia in children aged 5-9 years, though there is limited evidence available and large potential for bias.

Limitations

This review was conducted with a rigorous systematic approach, broad search strategy to capture relevant publications and methods to minimise risk of bias. It was limited by the databases that were searched, restriction of publications to the English language and unavailability of two full-text articles. Overall, the key limitation is the breadth and depth of existing research pertaining to pneumonia in children aged 5-9 years that is available to inform decision making.

Further studies exploring clinical features of pneumonia in children aged 5-9 years are warranted to strengthen evidence and understanding of the presentation of pneumonia in this age group. Studies using consistent definitions of clinical features and age ranges would enable aggregation of data and comparison between studies and settings. A wider range of studies in outpatient and inpatient settings, which identify clinical features associated with pneumonia severity and help to define critical values of concern for key signs, eg, tachypnoea, would better identify children at risk of poor outcomes. Conversely, understanding the prevalence of features such as chest indrawing in outpatient settings would aid in guiding safe management of children in the community.

Studies describing pneumonia aetiology and associated clinical features in children aged 5-9 years are needed to better inform antimicrobial choices, or clinical scenarios in which particular antimicrobial choices should be prioritised.

Studies should also explore the presentation of pneumonia in children aged 5-9 years with comorbid chronic conditions, given that this group is likely to be at higher risk of recurrent and more severe pneumonia.

CONCLUSIONS

There is a lack of evidence describing clinical features of pneumonia in children aged 5-9 years highlighting an urgent need for further research to guide best practice. Despite the quality and quantity of data, there are some findings which should be considered in relation to whether existing WHO definitions of pneumonia in children less than 5 years of age can be applied to older children. Based on limited data fever and cough are common in this age group, but tachypnoea cannot be relied on for diagnosis. While waiting for better evidence, broader attention to features such as chest and abdominal pain, the role of chest radiographs for diagnosis in the absence of symptoms such as tachypnoea, and risk factors which may influence patient disposition (chest indrawing, pallor, nutritional status) warrants consideration by clinicians.

Additional material

Acknowledgments.

Full list of ARI Review group : Trevor Duke, Hamish Graham, Steve Graham, Amy Gray, Amanda Gwee, Claire von Mollendorf, Kim Mulholland, Fiona Russell (leadership group, MCRI/University of Melbourne); Maeve Hume-Nixon, Saniya Kazi, Priya Kevat, Eleanor Neal, Cattram Nguyen, Alicia Quach, Rita Reyburn, Kathleen Ryan, Patrick Walker, Chris Wilkes (lead researchers, MCRI); Poh Chua (research librarian, RCH); Yasir Bin Nisar, Jonathon Simon, Wilson Were (WHO).

Acknowledgements: We would like to acknowledge librarian, Poh Chua, at the Royal Children’s Hospital Melbourne, who assisted with formulating and conducting our literature search.

Disclaimer: The authors alone are responsible for the views expressed in this publication and they do not necessarily represent the views, decisions or policies of the World Health Organization.

Funding: Funding was provided by the World Health Organization (WHO).

Authorship contributions: HG, AG and members of the ARI Review group conceived the study and initiated the study design. PK and AG led the conduct of searches. Data extraction was led by MM and PK with input from AG. Data analysis was conducted by PK, AG, and MM. The manuscript was drafted by PK, with input from AG, MM and HG. All authors contributed to revisions and approved the final manuscript.

Competing interests: The authors completed the ICMJE Unified Competing Interest Form (available upon request from the corresponding author), and declare no conflicts of interest.

Ep 130 Community Acquired Pneumonia: Emergency Management

While community acquired pneumonia (CAP) is ‘bread and butter’ emergency medicine, and the diagnosis is often a ‘slam dunk’, it turns out that up one third of the time, we are wrong about the diagnosis; that x-rays are not perfect; that blood work is seldom helpful; that not all antibiotics are created equal and that deciding who can go home and who needs to go to the ICU isn’t always so clear cut. With this in mind we are taking a deep dive into CAP with Dr. Leeor Sommer and Dr. Andrew Morris , from diagnosis to disposition so that we can better achieve our EM goals of stabilizing sick patients, getting the right diagnosis, initiating the best treatment with the information at hand, prognosticating/appropriately deciding on disposition of patients, and being healthcare and antimicrobial stewards…

Podcast: Play in new window | Download (Duration: 1:30:46 — 83.2MB)

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Podcast production, sound design & editing by Anton Helman; Script writing assistance by Andrew Cameron & Anton Helman.

Written Summary and blog post by Alexander Hartt and Anton Helman September, 2019

Cite this podcast as: Helman, A., Sommer, L., Morris, A. Episode 130 – Community Acquired Pneumonia – Emergency Management. Emergency Medicine Cases. September, 2019. https://emergencymedicinecases.com/community-acquired-pneumonia .  Accessed [date]

Sources of the high misdiagnosis rate of CAP in the ED

Some of the reasons why we misdiagnose CAP up to 1/3 of the time in the ED include pressure to make early treatment and disposition decisions (because of time-to-antibiotic “rules” in some jurisdictions), the expectation to have a definitive diagnosis when consulting services for admission, because the classic constellation of symptoms (cough, shortness of breath and fever) is often absent, there are many pneumonia mimics (CHF and PE being the most critical to identify and treat in the ED), early anchoring bias , there is overlap in clinical presentation of viral URI and pneumonia, blood tests may be misleading, CXR has poor accuracy, and there is no single historical or physical exam finding that has high enough likelihood ratio to shift pretest probability significantly.

To aid diagnostic accuracy and avoid over prescribing antibiotics, force yourself to consider the diagnosic criteria for CAP: fever, respiratory symptoms and imaging evidence of an infiltrate. Pay close attention to respiratory rate and oxygen saturation – the vast majority of patients with CAP will have an elevated respiratory rate and abnormal O2 sat, but don’t be fooled by the marathon runner – they can maintain perfectly normal vitals with their CAP.

Likelihood ratios for physical findings in CAP

The highest positive likelihood ratios of clinical findings for CAP from a 2019 meta-analysis are RR≥20 (3.47), fever (3.21) and HR>100 (2.79).

Normal vital signs combined with a normal pulmonary examination had a summary estimate -LR = 0.10 in a 2018 metaanalysis.

Normal vital signs alone have a -LR = 0.18 for CAP.

Pitfall : Using diagnosis of “acute bronchitis” in patients with viral respiratory illness, as it is a non-specific term that sets expectations by patients to be treated with antibiotics for a viral illness.

Blood tests for diagnosis and prognosis of CAP are promising statistically but usually not pragmatically useful

WBC > 10,400 per mm 3 has +LR = 3.4, -LR = 0.52 for CAP, but normal values do not rule out pneumonia and WBC is not included in any of the prognostic decision tools. WBC in the extremes (<4, >20) may be of prognostic significance.

CRP of >200mg/L hav been found to have a +LR>5, while <75mg/L have been found to have a -LR<0.2, however, most patients will have values between these extremes, in which case there is little diagnostic or prognostic utility.

Procalcitonin may be a significantly better predictor for blood culture positivity in CAP than WBC count, C-reactive protein, and other clinical parameters, may reduce antibiotic exposure, and has been used to help guide cessation of antibiotic treatment, however procalcitonin does not appear to pragmatically change antibiotic exposure, LOS or mortality in the ED setting. Our experts recommend not ordering procalcitonin in the ED.

Hypoglycemia (blood glucose < 70 mg per dL or 3.89 mmol per L) at presentation is associated with increased 30-day mortality even after adjustment for other variables, including comorbid illness and Pneumonia Severity Index (PSI) score.

Lactate has been shown to be a better predictor of 28-day mortality, hospitalization and ICU admission than CURB-65 in ED CAP patients.

Chest x-ray indications, accuracy, false negatives and false positives for community acquired pneumonia

Indications for chest x-ray in patients with acute respiratory illness for CAP :

• At least one abnormal vital sign (Fever, tachycardia, RR>20)
• Two of: decreased breath sounds, crackles, absence of asthma

Common conditions that may lead to false negative chest x-ray in CAP

• Volume depletion
• Neutropenia
• Early disease (first 12 hours)

Subtle chest x-ray findings that are often missed in CAP

• Silhouetting of heart border
• Small pleural effusion
• Retrocardiac infiltrate

Pitfall: Assuming that a non-apical lung infiltrate cannot be acute pulmonary tuberculosis

Indications for CT chest in suspected community acquired pneumonia

• Clinical course is not as expected (long duration, worsening despite appropriate CAP treatment)
• Recurrent infections
• An x-ray with atypical findings
• Neutropenic patients
• Profound immunocompromised state

While CT chest may be more accurate than chest x-ray at visualizing the upper lobes/lingula, showing interstitial edema of atypical pathogens, further characterizing necrotizing infection, multilobar disease, empyema, and pleural involvement, it is rarely indicated in the ED for suspected CAP.

POCUS perfomed by experienced operators is more accurate than chest x-ray for community acquired pneumonia, but is limited by the time it takes to perform

A 2014 meta-analysis concluded that, in the hands of experienced operators , ultrasound examination has a sensitivity and specificity as high as 94% and 96% , respectively. Ultrasound examination may offer an ideal alternative diagnostic modality in pediatric patients and critically ill patients in whom it is difficult to obtain a 2-view chest x-ray. However, for patients who are stable enough to go to the radiology department to get a 2 view chest x-ray, the time required to complete a thorough lung POCUS exam may be a limiting factor.

Indications for blood cultures in suspected community acquired pneumonia

• Severe CAP requiring ICU admission
• Evidence of sepsis
• Cirrhosis, asplenia or neutropenia
• Cavitary lesions or empyema on chest x-ray

Indications for sputum gram stain and cultures in suspected community acquired pneumonia

Patients with CAP are able to produce a valid sputum sample only 70% of the time. The sensitivity of sputum Gram stain ranges from 15% to 69% and specificity ranges from 11% to 100%. Many elderly patients with CAP are not able to produce an adequate specimen.

Consider sputum gram stain and cultures in the ED for patients with:

• Intubated patients with CAP
• History of alcohol abuse, liver disease, lung disease, leukopenia, cavitary infiltrates, asplenia, pleural effusion, and recent travel

Urine Legionella and Pneumococcus are rarely indicated in the ED

A 2009 retrospective analysis of Legionella CAP found 6 factors to be independent predictors:

• Fever (OR 1.67, p < 0.0001)
• Absence of sputum production (OR 3.67, p < 0.0001)
• Low serum Na (OR 0.89, p = 0.011)
• Elevated lactate (OR 1.003, p = 0.007)
• Elevated CRP (OR 1.006, p < 0.0001)
• Thrombocytopenia (OR 0.991, p < 0.0001)

Legionella may occur any time of year, but more illness is found in the summer and early fall.

Urine antigen testing in a 2009 meta-analysis showed a pooled sensitivity of 74% and specificity of 99% based on poor quality evidence.

In low prevalence areas, urine Legionella testing is not recommended in the ED by our experts as it is not cost effective.

Testing for Pneumococcal urine antigen in the ED is not recommended by our experts because empiric therapy will cover strep pneumococcus.

Antibiotic recommendations for community acquired pneumonia in Ontario

Consult your local biogram for recommendations in your area

• No risk factors for MRSA or pseudomonas, hemodynamically stable, non-ICU: amoxicillin or doxycycline (if penicillin allergy) or amoxicillin-clavulanic acid (if poor oral hygiene or non-ICU inpatient admission anticipated)
• No risk factors for MRSA or pseudomonas and are hemodynamically unstable, or have ICU admission planned, or are unable to tolerate oral antibiotics: IV ceftriaxone
• MRSA risk factors: add vancomycin or l inezolid
• Pseudomonas risk factors: piperacillin-tazobactam or miropenem

The vast majority of pneumonias are caused by only 2 bacteria: Streptococcus pneumonia and Haemophilus influenzae . All strep pneumonia and most H flu are susceptible to penecillin or amoxicillin. Therefore,the first line antibiotic for CAP patients without risk factors for MRSA or pseudomonas and who are hemodynamically stable, based on a Cochrane review is amoxicillin 1g po bid.

For patients with true penicillin allergy doxycycline 100mg po bid is the recommended first line antibiotic for these with CAP. It has good atypical coverage and a low risk for C. diff.

Amoxacillin-clavulinic acid (Clavulin) does not appear to confer added coverage against strep pneumo (as the mechanism for resistance is not via beta-lactamase), however it can be considered as an alternative to amoxicillin or doxycycline in patients with poor oral hygiene and for non-ICU inpatients.

There is no consensus in the literature around adding azithromycin for atypical coverage. A 2014 JAMA article suggests that time to clinical stability favours the addition of azithromycin but there is no benefit for patient oriented outcomes. Likewise, the often mentioned anti-inflammatory properties of azithromycin does not confer benefit for patient oriented outcomes. In high prevalence Legionella regions, in patients with predictors (listed above) it is not unreasonable prescribe azithromycin in the ED.

Fluoroquinolones should not be first or even second line therapy. Serious adverse reactions include:

• Tendinopathy
• Multiple drug interactions
• Partial treatment of tuberculosis leading to diagnostic delay
• Increased risk of aortic dissection

Update 2022: A meta-analysis of six randomized controlled trials involving 834 patients comparing doxycycline to macrolides and fluoroquinolones for the treatment of non-severe community acquired pneumonia in adults found similar efficacy and adverse event rates, with lower length of hospitalization and lower cost of antimicrobial agent in the doxycycline group compared to levofloxacin group. Abstract

Oral antibiotics are as effective as IV antibiotics for most community acquired pneumonia

Oral antibiotics are recommended over IV antibiotics in the vast majority of ED patients with CAP or suspected CAP. There are at least 9 RCTs that show no clinical benefit for IV antibiotics over oral antibiotics for CAP. The bioavailablility of almost all antibiotics commonly used for CAP are comparable whether IV or po. In addition, IV antibiotics have a higher rate of side effects, and take longer time to administer in the ED.

IV antibiotics such as Cefriaxone are indicated in CAP patients who:

• Are hemodynamically unstable
• Have ICU admission planned
• Are unable to tolerate PO

MRSA is on the decline but should still be considered for at risk patients

Empiric therapy with vancomycin or linezolid for MRSA was recommended in 2011 IDSA guidelines for MRSA for hospitalized patients with severe community-acquired pneumonia defined by one of the following:

• A requirement for admission to the ICU
• Necrotizing or cavitary infiltrates

However, the prevalence of MRSA since 2011 has been declining with two 2016 studies finding a prevalence of only 0.7-3%.

MRSA nasal screening is of little value considering the low prevalence of MRSA CAP and the poor positive predictive value of the test. A meta-analysis of 22 studies with 5243 patients found that nasal screening had a pooled sensitivity of 70.9%, specificity of 90.3%, positive predictive value (PPV) of 44.8%, and negative predictive value (NPV) of 96.5% for MRSA pneumonia.

Indications for extended antibiotic coverage for Pseudomonas in community acquired pneumonia

Consider broadening antibiotic coverage to cover Pseudomonas with piperacillin-tazobactam, meropenem or ciprofloxacin in the setting of:

• Bronchiectasis
• Tracheostomy
• Septic shock
• Broad spectrum antibiotics for >7 days in the last month
• Hospitalization for >1 day in last 3 months
• Immunocompromised (chemo, chronic steroids)
• Nursing home resident with poor functional status

It is unnecessary to provide antimicrobial coverage for anaerobes in patients suspected of aspiration pneumonia in the ED

Even in the setting of true aspiration pneumonia, the organisms involved are usually susceptible to beta-lactams (ceftriaxone). There is no need to add metronidazole or clindamycin.

Five-7 days duration of antibiotic treatment for uncomplicated community acquired pneumonia is sufficient

For uncomplicated CAP, 5-7 days of antibiotics is sufficient. More complex cases involving immunocompromised patients and those with structural lung disease will likely benefit from longer therapy. A metaanalysis of studies comparing treatment durations of 7 days or less with durations of 8 days or more showed no differences in outcomes and prospective studies have shown that 5 days of therapy are as effective as 10 days and 3 days are as effective as 8.

Treatment failure is defined by lack of defervenscence within 4-5 days and lack of subjective patient improvement within 72hrs

Our experts define treatment failure by a lack of defervescence within 4-5 days and lack of subjective patient improvement within 72hrs. Radiographic improvement can take weeks so is unreliable.

Adjunctive steroids may be of benefit in patients with severe community acquired pneumonia

Steroids are thought to curb the inflammatory response in CAP, reduce the frequency of acute respiratory distress syndrome, and decrease the length of illness. A systematic review and metaanalysis suggested that steroids reduce the need for mechanical ventilation and rate of acute respiratory distress syndrome by 5% with an NNT=20, however there are other high quality studies not reviewed in the metaanalysis that show no benefit. The SCCM/ESICM guidelines and expert consensus seems to favour steroids being reserved for those with severe CAP and those taking steroids chronically.

Initial steroid dosing options in the ED include:

• Dexamethasone 10mg IV
• Methylprednisolone 40mg IV
• Hydrocortisone 50mg IV

Learn more about steroid treatment in Journal Jam 17- Steroids for CAP and COVID Pneumonia

Update 2022: A meta-analysis of 16 RCTs including 3,842 hospitalized patients with community acquired pneumonia found no difference in all cause, in hospital mortality with corticosteroid therapy (RR 0.85, 95% CI 0.67 – 1.07), but was associated with a reduction in progression to mechanical ventilation (RR 0.51, 95% CI 0.33 – 0.77). Steroid use was also associated with subsequent readmission (RR 1.20, 95% CI 1.05 – 1.38). Abstract

Resuscitation of the patient with community acquired pneumonia and septic shock

Fluid choice and volume: Based on the SALT-ED and SMART trials, most experts agree that Ringer’s Lactate is the fluid of choice in septic shock patients. While massive fluid resucitation may worsen hypoxemia respiratory failure and precipitate need for intubation, under-resuscitation may worsen end-organ damage. Aiming for a MAP≥65 is a reasonable goal in addition to physical signs of end organ perfusion such as urine output and normal sensorium.

Norepinephrine indications and timing : Based on the CENSER trial it is reasonable to start peripheral norepinephrine as soon as the MAP <65 and/or there are signs of poor organ perfusion; the trial suggests that early norepinephrine in addition to fluid resuscitation results in less cardiogenic pulmonary edema, and possibly lower mortality.

The role of NIPPV in severe CAP: While NNPV theoretically theoretically prevents CAP patients from clearing secretions and mucus plugging, it may be used for limited periods of time as a bridge to intubation, and may be especially helpful in those with concurrent COPD exacerbation, where the evidence is clear for clinical benefit.

Learn more about COPD and pneumonia in Episode 24: COPD & Pneumonia

The role of High-Flow Nasal Cannula (HFNC) in severe CAP: The FLORALI trial suggested that HFNC may improve 90 day survival as well as subjective dyspnea and respiratory discomfort at 1-hr compared to non-rebreather and BiPAP in severely hypoxic CAP patients. It also showed that HFNC is non-inferior to non-rebreather facemask and BiPAP for reducing the need for intubation. HFNC is thought to reduce the work of breathing prior to respiratory exhaustion.

Pneumonia Severity Index (PSI) is the risk stratification tool of choice for community acquired pneumonia

PSI is more sensitive than SMART-COP and much more sensitive than CURB-65 for determining which patients will require ICU admission, while offering equal sensitivity for mortality for CAP overall. Despite CURB-65 having a higher specificity for CAP than PSI, our experts recommend PSI as the risk stratification tool of choice.

Problems with PSI

• PSI may underestimate the severity of pneumonia in an otherwise young healthy patients
• PSI does not include psychosocial conditions or cognitive impairments that may preclude discharge from the ED
• Any patient over 50 years of age is automatically classified as risk class 2 which may exaggerate their risk

Note that all CAP risk stratification tools rely on blood work so they do not apply to those well enough to not get lab testing.

Validated IDSA/ATS criteria for ICU admission

Patients with 3 or more criteria may benefit from ICU admission:

• Respiratory rate >29 breaths/min
• Hypotension requiring volume resuscitation
• PaO2/FiO2 < 250 (patients requiring >3 liters oxygen)
• Temperature < 36C
• Multilobar infiltrates
• BUN >20 mg/dL
• WBC <4,000/mm3
• Platelets <100,000/mm3

In addition, multilobar pneumonia is an independent risk factor for increased mortality in CAP.

Discharge criteria for outpatient care in patients with community acquired pneumonia

Some experts recommend a CURB-65 score of zero as criteria for outpatient care, however CURB-65 was validated as mortality prediction tool, and was not designed to determine disposition. Our experts recommend the following minimal criteria for outpatient care of CAP:

• Normal mental status
• Able to tolerate oral intake
• Psychosocial support

Oxygen saturations less than 92% are associated with major adverse events in outpatients with CAP.

Update Oct 2019: Diagnosis and Treatment of Adults with Community-acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of America Plus an excellent summary of the guidelines on emDocs

Take home points for emergency management of community acquired pneumonia

• We often misdiagnose CAP. To help us be better diagnosticians think about the diagnostic criteria (fever, respiratory symptoms and imaging evidence of infiltrate) and pay close attention to respiratory rate and oxygen saturation– the vast majority of patients with CAP will have an elevated respiratory rate and abnormal O2 sat, but don’t be fooled by the marathon runner – they can maintain perfectly normal vitals with their CAP.
• Not all cough is CAP. Think about the differential so that you do not overdiagnose CAP and you do not miss other important diagnoses.
• Not all patients in the ED with cough require a chest x-ray. Indications for chest x-ray include: At least one abnormal vital sign (fever, tachycardia, RR>20) and 2 of decreased breath sounds, crackles or absence of asthma. If you do get a chest x-ray remember that they can be normal or near normal early on the clinical course and in severely dehydrated or immunocompromised patients. Consider the differential diagnosis when you see an infiltrate – don’t just assume CAP.
• Procalcitonin has little, if any, role in the ED but may be useful for the inpatient team in predicting prognosis and duration of therapy. While WBC is usually unrevealing, extremes of WBC can help risk stratify your patients.
• For the septic CAP consider high flow nasal oxygen and/or NIPPV as a bridge to intubation; fluid resuscitation requires a delicate balance of considerations – don’t just slam in a few litres of crystalloid, but at the same time be sure not to under-resuscitate. Start peripheral norepinephrine early in CAP patients with septic shock – as soon as the MAP<65.
• For antibiotic choices, consult your local biogram. In Ontario, the recommended first-line outpatient therapy for CAP is currently amoxicillin 1g po bid. The recommended first-line inpatient non-ICU therapy for CAP is now amoxicillin-clavulanate 875mg/125mg po bid or ceftriaxone 1g iv q24h. Consideration for adding azithromycin empirically should only be given during the months of June through October to cover Legionella, MRSA only for those at risk (the prevalence is declining) and coverage for pseudomomas only in at risk patients. Oral antibiotics and as effective as IV antibiotics for the majority of patients with CAP.
• Recommended duration of therapy for most CAP is 5-7 days. Know the exceptions.
• PSI is the risk stratification tool of choice. Low-risk patients suitable for discharge from the ED should be defined by a PSI ≤ 70 and an oxygen saturation of at least 92% on room air. Use a PSI >130 as criteria for ICU admission.

Expand to view reference list

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Other FOAMEd resources on Community Acquired Pnuemonia

https://emcrit.org/ibcc/pneumonia/

Community Acquired Pneumonia – (LITFL CCC, Chris Nickson)

Evidence-based treatment for severe community-acquired pneumonia (PulmCrit)

Radiologic – Ultrasonic – Pathologic correlation for pneumonia (PulmCrit)

Antibiotics

Which patients with pneumonia need MRSA coverage? (PulmCrit)

Update in community acquired pneumonia: Macrolide resistance (Anand Swaminathan, Rebel EM)

Six reasons to avoid fluoroquinolones in the critically ill (PulmCrit)

Modes of noninvasive support

Pneumonia, BiPAP, secretions, and HFNC: Lessions learned from FLORALI trial (PulmCrit)

Mastering the dark arts of BiPAP & HFNC (PulmCrit)

Metabolic therapies

Steroid for community-acquired pneumonia (PulmCCM, Jon-Emile Kenny)

Corticosteroids for pneumonia: Ready for primetime? (emDocs, Brit Long)

Metabolic resuscitation for severe pneumonia? (PulmCrit)

POCUS for pneumonia

Pneumonia: Five minute sono (Jacob Avila)

Pneumonia US library (LITFL, James Rippey)

Drs. Helman, Sommer and Morris have no conflicts of interest to declare

About the Author: Anton Helman

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my name is Felix. I am working as an ED physician in Germany and enjoy listening to your podcast. Please keep up that fantastic work! Relating to your current episode of CAP I would like to mention two points. 1- I am very glad that you provide good evidence for treating patients orally. However in our healthcare system we are often kind of forced to go for iv antibiotics for inpatients. The health insurance declines paying the hospital bill if the patient did not receive iv medication postulating the stay was not necessary. 2- You were quite sceptic about the use of CRP/leucocyte count/pct because high values do exist in viral infections as well. However I think if someone has markedly elevated levels it still means that there is some important inflammation going on. So in an ill appearing patient with high inflammatory markers I would then treat with antibiotics because of the possible (threatening) bacteremia and take the risk of unnecessary treatment and possible adverse events of the drug in case of a viral cause.

I hope you can follow my reasoning although I am lacking some fluency in English… Thanks again for you great podcasts – I am looking forward to the next episode. Felix

In uncertainty a CAT scan of the chest is more accurate . Further PCR is developing rapidity of diagnosis eg TB and there are faster tests for drug sensitivity emerging .

Was not totally clear when, if ever, it is indicated to give fluoroquinolones (levofloxacin, moxifloxacin) PO for CAP in the outpatient setting. Is it only recommended if there are contraindications to amoxicillin or doxycycline? It appears where I work (California) that we are more apt to give Levofloxacin to elderly with CAP. Perhaps there is a belief that it’s better.than amoxicillin. Thanks.

For outpatient Amoxicillin is first line and if allergy to Penicillin then Doxycycline regardless of age. FDA has warned that fluoroquinolones are associated with Aortic Dissection, so probably best to avoid them in the elderly, especially if history of hypertension or AAA. While fluoroquinolones are in the newest guidelines as a choice for “severe” CAP, the evidence is weak that they are any better than first line agents for outpatient CAP. For severe CAP, ceftriaxone +/- azithro (for at risk patients) is a better choice.

The question :What distinguishes bronchitis from pneumonia was not answered . Looking Sick A lot of coughing with phlegm Aches and Pains Increased respiratory rate above 20 low po2 at 94 and below higher fever 39.0C and in severer cases tachcardia PR 110 or greater hypotension BP pressure systolic 90 or less respiratory rate 24 and over and Po2 on air by pulse Oximeter 92 and below Would be alerting .

Hi thanks for the excellent podcast. In the U.K. we use CURB score not only to help decide whether to admire but also use for treatment guidance. You didn’t mention Mycoplasma pneumonia – when to suspect and what treatment to add.

HI I am an Advanced Nurse Practitioner working in a Rual Access Hospital without on site supervision. I love these keeps me up to date and is fast and easy reads. Thank you so much for keeping it free. Karla

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