Week 38: PEs, Ekos, TB, and Everything Else Pulm

This patient has PCP (Pneumocystis jiroveci pneumonia). This pneumonia is seen exclusively in immunocompromised patients. On chest X-ray, the classic “bat wing” appearance of perihilar infiltrates is seen. Additionally, an elevated serum lactate dehydrogenase is almost always present. The classic patient with PCP is HIV positive with AIDS and a CD4 count less than 200. However, the growing number of patients on chronic immunosuppression as transplant recipients or with autoimmune disease is increasing the number of persons at risk for this infection. Classically patients with PCP describe increasing fatigue, non-productive cough, dyspnea on exertion, pleuritic chest pain and fever. PCP is a fungal infection although it is treated with the antibacterial medicationtrimethoprim-sulfamethoxazole. In patients with HIV, they receive this medication prophylactically when their CD4 count is below 200. In addition to antibiotic therapy, a subset of patients requires steroids. Patients with a partial pressure of arterial oxygen < 70 mm Hg on room air or and A-a gradient of >35 mm Hg should receive prednisone as this improves mortality. With the initiation of antibiotic therapy, the death of fungal cells induces a significant inflammatory response in the lung which can worsen patient outcomes. The administration of steroids concomitantly with the antibiotics decreases this inflammatory response.

This patient has a health-care associated pneumonia (HCAP) requiring IV antibiotics and admission. HCAP is defined as infection occurring within 90 days of a 2-day or longer hospitalization; in a nursing home or long-term care residence; within 30 days of receiving intravenous antibacterial therapy, chemotherapy, or wound care or after a hospital or hemodialysis clinic visit. HCAP requires IV broad spectrum antibiotics because it may involve both the typical pathogens involved in community-acquired pneumonia (CAP) (Mycoplasma pneumonia, Haemophilus influenzae,Streptococcus pneumoniae and Chlamydia pneumoniae) as well as more resistant organisms (Acinetobacter species, Pseudomonas species, Staphylococcus aureus (including MRSA) Enterobacter species, Escherichia coli, Proteus species, Klebsiella species etc.). Treatment should be as follows (one antibiotic from each category):

Cavitary lesions of the lung have multiple causes, including both infectious and non-infectious etiologies. These include bacterial pneumonia, fungal disease, tuberculosis, malignancies and some pulmonary vascular disease. The bacteria most commonly associated with cavitations are anaerobes, aerobic gram-negative bacilli and Staph aureus. After arecent influenza infection, patients may develop a Staph aureus pneumonia. Of particular concern is community-associated methicillin-resistant Staph aureus (CA-MRSA) after influenza especially in a rapidly progressive pneumonia in younger, healthy patients. Staph pneumonias often have necrotizing features creating the cavitation and may also lead to the development of pneumatoceles.

Most patients evaluated for tuberculosis present with reactivation of an old infection. When an immunocompetent person is exposed to tuberculosis, the immune system effectively gains control over the infection in the lung. It remains quiet and often never re-activates during a person’s lifetime. Most patients are asymptomatic during primary infection and only develop symptoms during a re-activation. Approximately 8-10% of persons who do not take chemoprophylaxis after a primary infection (typically identified through a positive skin PPD test) will develop active tuberculosis. Cough is the most common symptom of pulmonary tuberculosis. Additionally, patients may develop fever (more common in the afternoon or evening), night sweats and hemoptysis. Due to the effects of cytokines (particularly tumor necrosis factor alpha), patient often lose weight. The classic X-ray finding on chest radiograph is a cavitary lesion in the upper lobe of the lung. However, tuberculosis can cause any abnormality on the X-ray including infiltrate in any portion of the lung. Lymphadenopathy is commonly seen in the hilum on X-ray.

Patients with lung abscess classically present with several weeks of cough, fever, pleuritic chest pain, weight loss, and night sweats. There may be cough productive of putrid sputum. Because the progression of lung abscess is indolent, tachycardia, tachypnea, or fever may be absent. The chest radiograph often shows an area of dense consolidation with an air-fluid level inside a thick-walled cavitary lesion. Those who abuse alcohol or have other conditions associated with the potential for aspiration are at greatest risk for lung abscess development.

Corticosteroids are used as adjunct therapy in HIV-positive patients with severe PCP (now known as Pneumocystis jiroveci pneumonia), defined by a room air arterial oxygen partial pressure (PaO₂) of less than 70 mm Hg or analveolar-arterial oxygen gradient that exceeds 35 mm Hg. When administered, steroids should be given before trimethoprim/sulfamethoxazole or pentamidine because microbial degradation and clearance caused by antibiotics may trigger a severe inflammatory response. Corticosteroid therapy can blunt this inflammatory response, improve oxygenation, and reduce the incidence of respiratory failure.

The patient has a high risk (previously referred to as massive) pulmonary embolism (PE). She is hypotensive with a blood pressure of < 90 mm Hg and thrombolysis is indicated. A high risk PE is defined as a PE which causes a systolic blood pressure < 90 mm Hg for more than 15 minutes. In patients with previously diagnosed hypertension, thrombolytics are indicated for a blood pressure < 100 mm Hg or a reduction of more than 60 mm Hg below the patient’s baseline. Some patients with a moderate risk (previously referred to as a submassive) PE may benefit from fibrinolysis as well, including those with moderate-to-severe respiratory distress, oxygen saturation < 95% or evidence of right heart strain (elevated troponin, elevated pro-BNP or right heart strain on echocardiogram). Fibrinolysis is achieved with alteplase, given intravenously as a 10 mg bolus followed by a 90 mg drip over 2 hours.

Enoxaparin IV (B) or heparin IV bolus and drip (C) are appropriate treatments for low or moderate risk pulmonary embolisms. However, this patient was hypotensive and should receive more aggressive treatment. Surgical embolectomy (D) is indicated for patients with high risk PE but contraindications to thrombolysis, floating thrombi in the right side of the heart or severe, refractory hypotension. Catheter-directed thrombectomy is another treatment strategy which is still under investigation.

Tachypnea is the most common vital sign abnormality seen in acute pulmonary embolism (PE). PE is a common, life-threatening disease caused by the occlusion of pulmonary arteries by blood clots. The majority of these clots originate in the deep venous system (more commonly in the legs than in the upper body). Patients can present with various symptoms including weakness, shortness of breath, malaise, syncope, dizziness or chest pain. In addition, PE can cause changes to all of the major vital signs. The most common presenting vital sign change, however, is tachypnea. Dyspnea at rest or with exertion is the most common presenting symptom.

Fever (A) can occur in PE although a temperature over 101.5°F is unlikely to be caused by a PE. While common in PE, Tachycardia (C) is not the most common vital sign abnormality, but is the most common EKG finding.​​ Hypoxia (B) is common in larger PE but is not frequently seen in smaller ones.

The initial treatment of community-acquired pneumonia (CAP) in an immunocompetent patient should be single coverage with a respiratory fluoroquinolone (such as moxifloxacin or levofloxacin) or combination coverage with a macrolide (such as azithromycin) or a tetracycline (such as doxycycline) and a second- or third- generation cephalosporin (such as ceftriaxone). That said, it is important to consider local resistance and prescribing patterns when making a specific antibiotic determination.

Patients with hospital-associated pneumonia (HAP) (A) should be treated with broader coverage (such as piperacillin/tazobactam or cefepime), including activity against methicillin-resistant Staph. aureus (vancomycin). A third-generation cephalosporin (C) alone is not considered adequate coverage for community-acquired pneumonia due to its poor activity against atypical organisms such as Mycoplasma pneumonia, Legionella pneumophila, and Chlamydia pneumoniae. Carbapenems (D) are broad-spectrum ß-lactams that are often used alone or in combination in the setting of known antibiotic resistance or allergy.

The chest radiograph demonstrates miliary tuberculosis (TB), or acute disseminated tuberculosis. The term miliary was first used to describe the pathologic lesions seen on radiography that appeared as small millet seeds. Miliary TB occurs when the host is unable to contain a recently acquired or a dormant TB infection. The condition was mostly seen in young children after primary infection but now is more common in the elderly and in persons infected with HIV. Spread of the mycobacteria occurs through the hematogenous route, which leads to the multisystem nature of miliary TB. Clinically, patients develop many of the similar signs and symptoms of active pulmonary TB—fever, weight loss, anorexia, and weakness. Hemoptysis is uncommon. The classic miliary pattern seen in the radiograph is present in approximately 50% of cases. Hyponatremia is sometimes seen from the development of SIADH. Mortality rates are higher than for other forms of TB, which is likely due to a delay in treatment.

Elevated LDH (A) commonly occurs in Pneumocystis jiroveci pneumonia. Also with Pneumocystis jiroveci pneumonia, steroids (C) should be administered prior to antibiotics when the PaO2 is <70 or the A-a gradient is >35. Trimethoprim-sulfamethoxazole (D) is the treatment for Pneumocystis jiroveci pneumonia. Treatment of miliary TB is the same as pulmonary TB.