Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay

Case Study

The patient in the present case is E.B. – a 21-year old female who had arrived at the hospital with the following chief complaint: “I feel sick”. There was a set of symptoms displayed by the patient that came along with her main complaint. During the assessment, the patient was inquired about her other symptoms, their nature, the level of severity, their perceived causes, the factors that aggravated them, or made them go away, the treatments she might have applied, and the period for which she has been experiencing these symptoms.

According to the patient’s statement, she had suffered from a cough attack two weeks ago. She had believed that the cough was caused by flu which went away after a while; however, she started feeling worse again. The patient reported that she still had a fever, felt shaky, occasionally had a nonproductive cough, shortness of breath, heart skipping, and vomiting that started last night. She reported noticing no blood in the vomit, only food.

In addition to these symptoms, the patient mentioned an ongoing feeling of anxiety and a loss of sleep that she tied to her recent break up with her boyfriend. Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay. Also, the patient was inquired about such symptoms as the production of sputum during cough, headache, and dizziness – she denied all of them and said that she did not take any drugs. She mentioned that during her cough attack two weeks ago she took Tylenol because she believed this was the flu; and she did not take any cough medication at all.

The visual observations made during the physical exam revealed that the patient was sweating excessively, and her breath was heavy and interrupted; the overall behavior of the patient pointed to a high level of stress and nervousness; she appeared tense, restless, jittery, and impatient. She made several attempts to speed up the process of assessment and rush her treatment. Her responses to the assessment questions were short and brief.

The physical examination had to be focused on the systems connected to the patient’s major complaint and symptoms; these were her abdomen (due to vomiting and nausea), lungs, thyroid, and heart (heavy breath, elevated heartbeat, and heart skipping), skin, head, ears, nose, and eyes due to excessive sweating), and mouth and throat (because of coughing). The examination revealed tachycardia (150 beats per minute) with an irregular pulse, as well as systolic hypertension (160), accompanied by palpitations, anxiety, and tremor; also, the patient reported increased appetite and a loss of weight, hyper defecation, fever, fatigue, and insomnia – these symptoms are the signs of hyperthyroidism (Kravets, 2016; Ross et al., 2016).

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E.B seems to be affected by one of the complications that can occur in hyperthyroidism is thyrotoxicosis – a condition that leads to more serious health risks (Sayin, Ertek, & Cesur, 2014). Also, it can be suspected that E.B. is affected by Grave’s disease that is characterized by hyperthyroidism and a ropey isthmus that the patient also had (American Thyroid Association, 2017; De Groot, 2015).

Moreover, the patient’s symptoms (nausea, fever, cough, fast rate of breathing) also point to the potential of pneumonia acquired due to living in a dorm and being surrounded by other students; however, E.B. denied sputum production, dizziness, and headache – the other typical symptoms of this condition (Scott et al., 2013). Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay. To sum up, the differential diagnoses for this case are thyrotoxicosis, community-acquired pneumonia, and intoxication by drugs. The differentials identified for this case were elevated heartbeat, rapid breathing rate, suspected influenza, and dehydration. However, with the inclusion of the abnormal activity in the patient’s thyroid mentioned in the case study, the final diagnoses include community-acquired pneumonia and thyrotoxicosis.

References

American Thyroid Association. (2017). Grave’s disease. Web.

Kravets, I. (2016). Hyperthyroidism: Diagnosis and treatment. American Family Physician, 93(5), 363-370. Web.

Ross, S. D., Burch, H. B., Cooper, D. S., Greenlee,C., Laurberg, P., Maia, A. L.,… Walter, M. A. (2013). 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid, 26(10), 1343-1421. Web.

Sayin, I., Ertek, S., & Cesur, M. (2014). Complications of Hyperthyroidism. In Soto, G.D. (Ed.), Thyroid disorders – focus on hyperthyroidism (65-140). Hampshire, England: InTech. Web.

Scott, J. A., 2 Wonodi,C., Moisi, J.C., Deloria-Knoll, M., DeLuca, A. N., Karron, R. A., … Feikin, D. R. (2012).The definition of pneumonia, the assessment of severity, and clinical standardization in the pneumonia etiology research for child health study. Clinical Infectious Diseases, 54(2), 109–116. Web.

Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality worldwide. The clinical presentation of CAP varies, ranging from mild pneumonia characterized by fever and productive cough to severe pneumonia characterized by respiratory distress and sepsis. Because of the wide spectrum of associated clinical features, CAP is a part of the differential diagnosis of nearly all respiratory illnesses. Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay.

This topic provides a broad overview of the epidemiology, microbiology, pathogenesis, clinical features, diagnosis, and management of CAP in immunocompetent adults. Detailed discussions of each of these issues are presented separately; links to these discussions are provided within the text below.

DEFINITIONSPneumonia is frequently categorized based on site of acquisition.

●Community-acquired pneumonia (CAP) refers to an acute infection of the pulmonary parenchyma acquired outside of the hospital.

●Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma acquired in hospital settings and encompasses both hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP).

•HAP refers to pneumonia acquired ≥48 hours after hospital admission.

•VAP refers to pneumonia acquired ≥48 hours after endotracheal intubation.

Health care-associated pneumonia (HCAP; no longer used) referred to pneumonia acquired in health care facilities (eg, nursing homes, hemodialysis centers) or after recent hospitalization. The term HCAP was used to identify patients at risk for infection with multidrug-resistant pathogens. However, this categorization may have been overly sensitive, leading to increased, inappropriately broad antibiotic use and was thus retired. In general, patients previously classified as having HCAP should be treated similarly to those with CAP. (See “Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults”.)

EPIDEMIOLOGY

Incidence — CAP is one of the most common and morbid conditions encountered in clinical practice [1-3]. In the United States, CAP accounts for over 4.5 million outpatient and emergency room visits annually, corresponding to approximately 0.4 percent of all encounters [4]. CAP is the second most common cause of hospitalization and the most common infectious cause of death [5,6]. Approximately 650 adults are hospitalized with CAP every year per 100,000 population in the United States, corresponding to 1.5 million unique CAP hospitalizations each year [7]. Nearly 9 percent of patients hospitalized with CAP will be rehospitalized due to a new episode of CAP during the same year.

Risk factors

●Older age – The risk of CAP rises with age [7,8]. The annual incidence of hospitalization for CAP among adults ≥65 years old is approximately 2000 per 100,000 in the United States [7,9]. This figure is approximately three times higher than the general population and indicates that 2 percent of the older adult population will be hospitalized for CAP annually (figure 1).

●Chronic comorbidities – The comorbidity that places patients at highest risk for CAP hospitalization is chronic obstructive pulmonary disease (COPD), with an annual incidence of 5832 per 100,000 in the United States [7]. Other comorbidities associated with an increased incidence of CAP include other forms of chronic lung disease (eg, bronchiectasis, asthma), chronic heart disease (particularly congestive heart failure), stroke, diabetes mellitus, malnutrition, and immunocompromising conditions (figure 2) [7,10,11].

●Viral respiratory tract infection – Viral respiratory tract infections can lead to primary viral pneumonias and also predispose to secondary bacterial pneumonia. This is most pronounced for influenza virus infection. (See “Seasonal influenza in adults: Transmission, clinical manifestations, and complications”, section on ‘Pneumonia’.) Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay.

●Impaired airway protection – Conditions that increase risk of macroaspiration of stomach contents and/or microaspiration of upper airway secretions predispose to CAP, such as alteration in consciousness (eg, due to stroke, seizure, anesthesia, drug or alcohol use) or dysphagia due to esophageal lesions or dysmotility.

●Smoking and alcohol overuse – Smoking, alcohol overuse (eg, >80 g/day), and opioid use are key modifiable behavioral risk factors for CAP [7,10,12,13].

●Other lifestyle factors – Other factors that have been associated with an increased risk of CAP include crowded living conditions (eg, prisons, homeless shelters), residence in low-income settings, and exposure to environmental toxins (eg, solvents, paints, or gasoline) [7,10,11,14].

Combinations of risk factors, such as smoking, COPD, and congestive heart failure, are additive in terms of risk [15]. These risk factors and other predisposing conditions for the development of CAP are discussed separately. (See “Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults”, section on ‘Predisposing host conditions’.)

MICROBIOLOGY

Common causes — Streptococcus pneumoniae (pneumococcus) and respiratory viruses are the most frequently detected pathogens in patients with CAP [8,16]. However, in a large proportion of cases (up to 62 percent in some studies performed in hospital settings), no pathogen is detected despite extensive microbiologic evaluation [8,17,18].

The most commonly identified causes of CAP can be grouped into three categories:

●Typical bacteria

•S. pneumoniae (most common bacterial cause)

•Haemophilus influenzae

•Moraxella catarrhalis

•Staphylococcus aureus

•Group A streptococci

•Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella spp or Escherichia coli)

•Microaerophilic bacteria and anaerobes (associated with aspiration)

●Atypical bacteria (“atypical” refers to the intrinsic resistance of these organisms to beta-lactams and their inability to be visualized on Gram stain or cultured using traditional techniques) Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay.

•Legionella spp

•Mycoplasma pneumoniae

•Chlamydia pneumoniae

•Chlamydia psittaci

•Coxiella burnetii

●Respiratory viruses

•Influenza A and B viruses

•Rhinoviruses

•Parainfluenza viruses

•Adenoviruses

•Respiratory syncytial virus

•Human metapneumovirus

•Coronaviruses (eg, Middle East respiratory syndrome coronavirus)

•Human bocaviruses

The relative prevalence of these pathogens varies with geography, pneumococcal vaccination rates, host risk factors (eg, smoking), season, and pneumonia severity (table 1).

Certain epidemiologic exposures also raise the likelihood of infection with a particular pathogen (table 2). As examples, exposure to contaminated water is a risk factor for Legionella infection, exposure to birds raises the possibility of C. psittaci infection, travel or residence in the southwestern United States should raise suspicion for coccidioidomycosis, and poor dental hygiene may predispose patients with pneumonia caused by oral flora or anaerobes. In immunocompromised patients, the spectrum of possible pathogens also broadens to include fungi and parasites as well as less common bacterial and viral pathogens. (See “Epidemiology of pulmonary infections in immunocompromised patients” and “Approach to the immunocompromised patient with fever and pulmonary infiltrates”.)

While the list above details some of most common causes of CAP, >100 bacterial, viral, fungal, and parasitic causes have been reported. (See “Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults”, section on ‘Microbiology’.) Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay.

Important trends — Both the distribution of pathogens that cause CAP and our knowledge of these pathogens are evolving. Key observations that have changed our understanding of CAP and influenced our approach to management include:

●Decline in S. pneumoniae incidence – Although S. pneumoniae (pneumococcus) is the most commonly detected bacterial cause of CAP in most studies, the overall incidence of pneumococcal pneumonia is decreasing. This is in part due to widespread use of pneumococcal vaccination, which results in both a decline in the individual rates of pneumococcal pneumonia and herd immunity in the population. (See “Pneumococcal pneumonia in adults”, section on ‘Prevalence in community-acquired pneumonia’.)

Because pneumococcal vaccination rates vary regionally, the prevalence of S. pneumoniae infection also varies. As an example, S. pneumoniae is estimated to cause approximately 30 percent of cases of CAP in Europe but only 10 to 15 percent in the United States, where the population pneumococcal vaccination rate is higher [8].

●Increased recognition of respiratory viruses – Respiratory viruses have been detected in approximately one-third of cases of CAP in adults when using molecular methods [8]. The extent to which respiratory viruses serve as single pathogens, cofactors in the development of bacterial CAP, or triggers for dysregulated host immune response has not been established.

●Low overall rate of pathogen detection – Despite extensive evaluation using molecular diagnostics and other microbiologic testing methods, a causal pathogen can be identified in only half of cases of CAP. This finding highlights that our understanding of CAP pathogenesis is incomplete. As molecular diagnostics become more advanced and use broadens, our knowledge is expected to grow.

●Discovery of the lung microbiome – Historically, the lung has been considered sterile. However, culture-independent techniques (ie, high throughput 16S rRNA gene sequencing) have identified complex and diverse communities of microbes that reside within the alveoli [19-21]. This finding suggests that resident alveolar microbes play a role in the development of pneumonia, either by modulating the host immune response to infecting pathogens or through direct overgrowth of specific pathogens within the alveolar microbiome. (See ‘Pathogenesis’ below.)

Antimicrobial resistance — Knowledge of antimicrobial resistance patterns and risk factors for infection with antimicrobial-resistant pathogens help inform the selection of antibiotics for empiric CAP treatment (table 3).

●S. pneumoniae may be resistant to one or more antibiotics commonly used for the empiric treatment of CAP.

•Macrolide resistance rates vary regionally but are generally high (>25 percent) in the United States, Asia, and southern Europe. Resistance rates tend to be lower in northern Europe. (See “Resistance of Streptococcus pneumoniae to the macrolides, azalides, lincosamides, and ketolides”.)

•Estimates of doxycycline resistance are less certain and vary substantially worldwide. In the United States, rates tend to be less than 20 percent but may be rising. (See “Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole”.)

•Beta-lactam resistance rates also vary regionally but to a lesser extent than macrolide and doxycycline resistance. In the United States, <20 percent of isolates are resistant to penicillin and <1 percent to cephalosporins. (See “Resistance of Streptococcus pneumoniae to beta-lactam antibiotics”.)Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay.

•Fluoroquinolone resistance tends to be <2 percent in the United States but varies regionally and with specific risk factors such as recent antibiotic use or hospitalization. (See “Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole”.)

Because resistance rates vary even at local levels, clinicians should refer to local antibiograms to guide antibiotic selection when available. General epidemiologic data can be obtained through sources such as the Center for Disease Dynamics, Economics & Policy.

●Methicillin-resistant S. aureus (MRSA) is an uncommon cause of CAP. Risk factors for MRSA have two patterns: health care associated and community acquired. The strongest risk factors for MRSA pneumonia include known MRSA colonization or prior MRSA infection, particularly involving the respiratory tract. Gram-positive cocci on sputum Gram stain are also predictive of MRSA infection. Other factors that should raise suspicion for MRSA infection include recent antibiotic use (particularly receipt of intravenous antibiotics within the past three months), recent influenza-like illness, the presence of empyema, necrotizing/cavitary pneumonia, and immunosuppression (table 3).

In contrast with health care-associated MRSA, community-acquired MRSA (CA-MRSA) infections tend to occur in younger healthy persons [22]. Risk factors for CA-MRSA infection include a history of MRSA skin lesions, participation in contact sports, injection drug use, crowded living conditions, and men who have sex with men. (See “Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology”.)

CAP caused by CA-MRSA can be severe and is associated with necrotizing and/or cavitary pneumonia, empyema, gross hemoptysis, septic shock, and respiratory failure. These features may be attributable to infection with toxin-producing CA-MRSA strains. In the United States, these strains tend to be methicillin resistant and belong to the USA300 clone. (See “Virulence determinants of community-acquired methicillin-resistant Staphylococcus aureus”.)

●Pseudomonas is also an uncommon cause of CAP and tends to occur more frequently in patients with known colonization or prior infection with Pseudomonas spp, recent hospitalization or antibiotic use, underlying structural lung disease (eg, cystic fibrosis or advanced chronic obstructive pulmonary disease [bronchiectasis]), and immunosuppression. Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay. Antibiotic resistance is common among pseudomonal strains, and empiric therapy with more than one agent that targets Pseudomonas is warranted for at-risk patients with moderate to severe CAP (table 3). (See “Pseudomonas aeruginosa pneumonia” and ‘Inpatient antibiotic therapy’ below.)

PATHOGENESISTraditionally, CAP has been viewed as an infection of the lung parenchyma, primarily caused by bacterial or viral respiratory pathogens. In this model, respiratory pathogens are transmitted from person to person via droplets or, less commonly, via aerosol inhalation (eg, as with Legionella or Coxiella species). Following inhalation, the pathogen colonizes the nasopharynx and then reaches the lung alveoli via microaspiration. When the inoculum size is sufficient and/or host immune defenses are impaired, infection results. Replication of the pathogen, the production of virulence factors, and the host immune response lead to inflammation and damage of the lung parenchyma, resulting in pneumonia (figure 3).

With the identification of the lung microbiome, that model has changed [19-21]. While the pathogenesis of pneumonia may still involve the introduction of respiratory pathogens into the alveoli, the infecting pathogen likely has to compete with resident microbes to replicate. In addition, resident microbes may also influence or modulate the host immune response to the infecting pathogen. If this is correct, an altered alveolar microbiome (alveolar dysbiosis) may be a predisposing factor for the development of pneumonia.

In some cases, CAP might also arise from uncontrolled replication of microbes that normally reside in the alveoli. The alveolar microbiome is similar to oral flora and is primarily comprised of anaerobic bacteria (eg, Prevotella and Veillonella) and microaerophilic streptococci [19-21]. Hypothetically, exogenous insults such as a viral infection or smoke exposure might alter the composition of the alveolar microbiome and trigger overgrowth of certain microbes. Because organisms that compose the alveolar microbiome typically cannot be cultivated using standard cultures, this hypothesis might explain the low rate of pathogen detection among patients with CAP.

In any scenario, the host immune response to microbial replication within the alveoli plays an important role in determining disease severity. For some patients, a local inflammatory response within the lung predominates and may be sufficient for controlling infection. In others, a systemic response is necessary to control infection and to prevent spread or complications, such as bacteremia. In a minority, the systemic response can become dysregulated, leading to tissue injury, sepsis, acute respiratory distress syndrome, and/or multiorgan dysfunction. Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay.

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The pathogenesis of CAP is discussed in greater detail separately. (See “Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults”.)

CLINICAL PRESENTATIONThe clinical presentation of CAP varies widely, ranging from mild pneumonia characterized by fever, cough, and shortness of breath to severe pneumonia characterized by sepsis and respiratory distress. Symptom severity is directly related to the intensity of the local and systemic immune response in each patient.

●Pulmonary signs and symptoms – Cough (with or without sputum production), dyspnea, and pleuritic chest pain are among the most common symptoms associated with CAP. Signs of pneumonia on physical examination include tachypnea, increased work of breathing, and adventitious breath sounds, including rales/crackles and rhonchi. Tactile fremitus, egophony, and dullness to percussion also suggest pneumonia. These signs and symptoms result from the accumulation of white blood cells (WBCs), fluid, and proteins in the alveolar space. Hypoxemia can result from the subsequent impairment of alveolar gas exchange. On chest radiograph, accumulation of WBCs and fluid within the alveoli appears as pulmonary opacities (image 1A-B).

●Systemic signs and symptoms – The great majority of patients with CAP present with fever. Other systemic symptoms such as chills, fatigue, malaise, chest pain (which may be pleuritic), and anorexia are also common. Tachycardia, leukocytosis with a leftward shift, or leukopenia are also findings that are mediated by the systemic inflammatory response. Inflammatory markers, such as the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin may rise, though the latter is largely specific to bacterial infections. Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay. CAP is also the leading cause of sepsis; thus, the initial presentation may be characterized by hypotension, altered mental status, and other signs of organ dysfunction such as renal dysfunction, liver dysfunction, and/or thrombocytopenia [23].

Although certain signs and symptom such as fever, cough, tachycardia, and rales are common among patients with CAP, these features are ultimately nonspecific and are shared among many respiratory disorders (see ‘Differential diagnosis’ below). No individual symptom or constellation of symptoms is adequate for diagnosis without chest imaging. For example, the positive predictive value of the combination of fever, tachycardia, rales, and hypoxia (oxygen saturation <95 percent) among patients with respiratory complaints presenting to primary care was <60 percent when chest radiograph was used as a reference standard [24].

Signs and symptoms of pneumonia can also be subtle in patients with advanced age and/or impaired immune systems, and a higher degree of suspicion may be needed to make the diagnosis. As examples, older patients may present with mental status changes but lack fever or leukocytosis [25]. In immunocompromised patients, pulmonary infiltrates may not be detectable on chest radiographs but can be visualized with computed tomography.

The clinical and diagnostic features of CAP and sepsis are discussed in detail separately. (See “Diagnostic approach to community-acquired pneumonia in adults” and “Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis”, section on ‘Clinical presentation’.) Community-Acquired Pneumonia and Thyrotoxicosis Diagnostic Essay.