Step 3 Pulmonology I

• Even though it is not common, a new pleural effusion in a patient already on anti-tuberculosis treatment may occur and must be studied, because this can progress despite the clinical improvement of the patient.
• Thoracentesis is usually sufficient for diagnostic and therapeutic purposes.
• There is no need to change therapy, unless there is proof of a new infection or drug resistance.
• Some authors advocate the use of steroids in this setting, but this is not a universally accepted practice.

Cough induced by forced expiration is characteristic of airway hyperreactivity, and is usually suggestive of asthma; however, this presentation has also been described in some patients with COPD who can occasionally have an overlapping condition with asthma.

• Initial therapy for pulmonary embolism depends on the patient's hemodynamic stability.
• The majority of patients who present with pulmonary emboli are hemodynamically stable and can be managed with heparin anticoagulation.
• Fibrinolytic therapy is reserved for patients with hemodynamic instability.
• Due to its easier daily dosing schedule, most patients are treated with low molecular weight heparin, although an intravenous heparin infusion is a satisfactory treatment as well.

Intravenous heparin might be favored in patients with renal dysfunction or if there is high concern for bleeding risk as the drug has a relatively short half-life.

• Inferior vena cava filters should be considered in patients for whom anticoagulation is contraindicated, who have had complications of anticoagulation, or where anticoagulation has failed.
• Also in those with low cardiopulmonary reserve due to either prior pulmonary emboli or preexisting cardiopulmonary disease.

Hospital acquired pneumonia is defined as pneumonia that begins after 48 hours of admission in patients for whom there was no evidence of infection at the time of admission.

• Fever can be present in up to 14% of patients with pulmonary embolism and is usually low-grade.
• The clinical picture can be confusing for the possible presence of pneumonia given that patients may also have pulmonary opacities from infarction or atelectasis as well as an elevated WBC count secondary to the pulmonary embolism itself.

Patients with hypoxemia due to an acute asthma exacerbation should be immediately managed with oxygen inhalation, followed by administration of an inhaled beta-2 agonist, which is the mainstay of therapy.

• Patients have a right to make their own end of life decisions even if the treating physician does not agree.
• A patient's autonomy must always be upheld in end of-life decisions.

• The goal of treatment is to rapidly correct the airflow obstruction.
• This is most rapidly achieved by the administration of inhaled beta-2 adrenergic agonists, either by continuous nebulization or with the use of metered dose inhalers with a spacer.
• Systemic corticosteroids should also be administered early in the treatment of acute asthmatic exacerbation; however, their effect is usually not apparent in the first few hours.

• Some of the clues to a patient's clinical deterioration and poor outcome include a history of prior intubation, exhaustion or extreme fatigue, diaphoresis, change in consciousness (confusion and drowsiness), use of accessory muscles, presence of suprasternal retractions, depressed respiratory drive, marked tachycardia, pulsus paradoxus, PaC02 greater than 40 mmHg, and a peak expiratory flow rate less than 25% of the normal predicted.
• Any patient with the above signs and symptoms of impending respiratory failure should be immediately intubated to secure and protect the airways.

• These patients should have estimation of pretest probability with a standardized formula such as the modified Wells score for PE, which is elevated (more than 4).
• Patients with PE most often have a normal chest x-ray or mild, nonspecific changes such as pleural effusion or mild subsegmental atelectasis .
• Troponin can be elevated in the setting of large pulmonary emboli with resulting right heart strain and would not indicate acute cardiac ischemia.

• A CT pulmonary angiogram should be performed immediately to evaluate for PE.
• Ventilation/perfusion scintigraphy may be considered as an alternate test if the patient is unable to receive intravenous contrast agents (eg, renal insufficiency, contrast allergy).
• While results are pending, patients with signs of a clinically significant PE should receive oxygen and anticoagulation.

• Cardiac troponin levels are elevated in up to 30%-50% of patients with large pulmonary emboli, presumably due to acute right heart overload.
• However, in patients with pulmonary emboli, elevated cardiac troponin levels are associated with a higher risk of death.
• In PE, the elevated troponin levels generally resolve within 2 days, in contrast to the more prolonged elevations seen in patients with myocardial infarction.
• In addition, hypotension and hemodynamic instability in a patient with PE indicate a poor prognosis.

• Warfarin should be started after the patient has already begun heparin therapy, as it theoretically can have a pro-coagulant effect initially by causing a rapid decline in the endogenous anticoagulant protein C levels.
• Current guidelines recommend early initiation of warfarin (eg, same day as parenteral therapy is started) over delayed initiation and continuation of parenteral anticoagulation for a minimum of 5 days and until the International Normalized Ratio is 2 for at least 24 hours.

• A small amount of hemoptysis can be seen in the setting of pulmonary embolism (PE), particularly when there has been pulmonary infarction.
• In a clinically stable patient with low-grade hemoptysis, usual care, including anticoagulation, should continue as premature discontinuation of anticoagulation would increase the risk of recurrent PE.

• It is a common cause of a transudative pleural effusion in patients with cirrhosis and ascites and is usually located on the right.
• Although the exact mechanism is not completely understood, it may be caused by the passage of ascitic fluid through tiny diaphragmatic defects.

• Thoracentesis can remove the fluid, but the hepatic hydrothorax commonly recurs.
• Therefore, the primary therapy for patients with hepatic hydrothorax is similar to the treatment of ascites - sodium restriction and diuretics.
• Transjugular intrahepatic portosystemic shunt is second-line therapy.
• In addition, hepatic hydrothorax signals advanced liver disease and should prompt consideration for liver transplant.

• It is a well-known complication of IV drug abuse.
• This may result from septic thrombophlebitis and/or tricuspid endocarditis.
• Early tricuspid endocarditis is difficult to diagnose because heart murmurs are absent, but blood cultures are usually positive.

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• Initial management includes blood and sputum cultures with initiation of broad-spectrum antibiotics with anaerobic coverage (eg, clindamycin).
• Once the patient has been stabilized, a bedside swallowing assessment may be helpful.
• Definitive diagnosis is made with a videofluoroscopic swallowing study.
• Based on results, a multidisciplinary dysphagia rehabilitation program can be initiated, usually with input from the dietary service, nursing, and speech therapy.
• Specific interventions typically include thickened liquids and modified swallowing techniques.

• It is important to be aware of the limitations of a diagnostic study during the interpretation of results. For example, VQ scanning is less sensitive than a helical CT or pulmonary angiography for the diagnosis of pulmonary embolism.
• It is possible for a VQ scan to miss an embolus that can be detected by pulmonary angiography.

• ARDS is an inflammatory condition typically caused by infection (eg, sepsis, pneumonia), trauma (eg, fractures, pulmonary contusion), or other causes (eg, massive transfusion, pancreatitis).
• Lung injury causes release of proteins, inflammatory cytokines, and neutrophils into the alveolar space.
• This leads to leakage of bloody and proteinaceous fluid into the alveoli, alveolar collapse due to loss of surfactant, and diffuse alveolar damage.
• The end result is impaired gas exchange, decreased lung compliance (stiff lungs), and increased pulmonary arterial pressure (pulmonary hypertension) requiring invasive mechanical ventilation.

• The management of acute respiratory distress syndrome (ARDS) through mechanical ventilation involves the interplay of tidal volume, positive end-expiratory pressure (PEEP), and FiO2 .
• Tidal volumes and respiratory rate affect primarily ventilation; PEEP and FiO2 affect oxygenation.
• Low tidal volume ventilation (LTW) in ARDS allows permissive hypercapnia to maintain alveolar hypoventilation and prevents ventilator-associated lung injury.
• The initial tidal volume is set to 8 ml/kg predicted body weight (PBW) and decreased to 6 ml/kg PBW over the next 1-3 hours.

• The goals in ARDS are PaO2 of 55-80 mm Hg or oxygen saturation of 88%-95%.
• This is achieved by adjusting the FiO2 and PEEP.
• High PEEP improves oxygenation and prevents over -distension by opening collapsed alveoli and allowing more open alveoli to share the tidal volume.
• Low PEEP may not be adequate to open flooded alveoli and can contribute to lung injury by causing cyclical atelectasis.
• High PEEP is likely more advantageous in moderate-to-severe ARDS.

• Ongoing mechanical ventilation in acute respiratory distress syndrome (ARDS) is managed by adjusting the positive end-expiratory pressure level and fraction of inspired oxygen to the lowest level that allows a PaO2 to be maintained.
• Goals in ARDS are Pa02 of 55-80 mm Hg or oxygen saturation of 88%-95%.
• Permissive hypercapnia as a result of alveolar hypoventilation and low tidal volumes is safe for most patients, except those with elevated intracranial pressure or a seizure disorder.

• Aspiration pneumonitis is a chemical injury with inflammation of lung parenchyma due to the inhalation of foreign materials such as gastric contents (Mendelson's syndrome).
• Patients usually have a history of depressed level of consciousness and a witnessed vomiting or aspiration event.
• Respiratory distress occurs 2-5 hours after an aspiration event, and there are generally no features of infection.
• Treatment is supportive (without antibiotics).

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• Prerenal azotemia is associated with decreased fractional excretion of sodium; however, once ATN sets in, the fractional excretion of sodium increases (usually more than 2).
• Response to a fluid challenge is the gold standard in distinguishing prerenal azotemia (which responds to a fluid challenge with improved urine output) from ATN.

• Acute tubular necrosis should be suspected in patients with oliguria following a hypotensive episode.
• Muddy brown casts and high fractional excretion of sodium differentiate acute tubular necrosis from prerenal azotemia.

• In a patient with acute kidney injury (AKI), the goals of care include maintaining adequate renal perfusion (intravenous saline or vasopressors), avoiding nephrotoxic agents, and close monitoring of volume status and any acid-base and electrolyte disturbances.
• Excess saline infusion can worsen her clinical status by causing volume overload (pulmonary edema) and hyperchloremic metabolic acidosis (non-anion gap metabolic acidosis).

• Speech and swallowing evaluation, followed by diet modification, is performed in high-risk patients to prevent future episodes of aspiration.
• It is unclear whether percutaneous endoscopic gastrostomy tube placement prevents aspiration episodes or improves long-term survival of patients with swallowing difficulties.

• Increasing the PEEP can help prevent the atelectatic alveoli from collapsing during expiration.
• Many times there is no way of knowing if a patient has recruitable alveoli and the effect of PEEP is monitored by following the Pa02/Fi02 ratio.
• PEEP should be used with caution, especially in localized lung processes such as pneumonia, because the increased pressure can be distributed to the normal lung causing alveolar injury.
• PEEP can also worsen hypotension since it reduces preload.

• Anticoagulation with heparin or a low molecular weight heparin followed by oral warfarin is the treatment of choice for a patient with pulmonary embolism.
• An IVC filter is recommended in patients with complications of anticoagulation, contraindications to anticoagulation, or failure of anticoagulation.

• The most likely cause of endobronchial obstruction in this elderly male with an extensive smoking history is bronchogenic carcinoma.
• A carcinoid tumor is another cause of endobronchial obstruction, especially in younger and non-smoking patients.
• This causes stasis of secretions and recurrent pneumonias, even after successful treatment of previous episodes.

Causes of nonresolving pneumonia or pulmonary infiltrates are bronchoalveolar cell carcinoma, lymphoma, eosinophilic pneumonia, bronchiolitis obliterans organizing pneumonia (BOOP), systemic vasculitis, pulmonary alveolar proteinosis, and drugs (amiodarone).

Flexible bronchoscopy is a simple, invasive test that will definitely diagnose the cause of this patient's recurrent pneumonia, since it will enable the physician to visualize the actual endobronchial lesion, and take a tissue biopsy at the same time

RSI involves administering a rapidly acting sedative (eg, etomidate, propofol, midazolam) with a paralytic agent (eg, succinyl choline, rocuronium) to facilitate emergency intubation and prevent aspiration.

• Critically ill patients who are unstable with significant hypoxia require rapid-sequence intubation for ventilator support and/or airway protection.
• After initial stabilization of the airway, patients may be appropriately assessed for the underlying etiology.

• Findings on ECG indicating acute pulmonary hypertension and right ventricular (RV) strain include right bundle branch block, atrial arrhythmias, inferior Q waves, and ST -segment changes.
• The presence of RV strain indicates a possible increased overall mortality rate in hypotensive patients with massive PE.

• ECHO can identify signs of RV dysfunction, including increased RV size, decreased RV contractility, presence of RV thrombus, and tricuspid regurgitation.
• Massive PE causes pulmonary hypertension that dilates the tricuspid annulus and causes functional tricuspid regurgitation.

• Patients should always be told about mistakes in their care, as this forthrightness contributes to a strong patient-physician relationship.
• Some research has shown that when medical mistakes are made, patients and their families most care about receiving an explanation and an apology from the responsible physician(s) early in the process.
• Civil litigation is more often pursued when the patient and his family feel deceived or avoided.

• solitary pulmonary nodule (SPN), which is defined as a round opacity up to 3 cm in diameter surrounded by normal lung tissue.
• The first step is to compare previous x-rays or scans, as an SPN with stable size and appearance for the past 2 years has a low risk of malignancy and requires no further workup.
• X-ray findings favoring malignancy include size more than 3 cm or interval change in size, irregular border and ground glass appearance.
• Lesions that appear less likely to be malignant on CT can be followed with serial CT scans for 2 years to monitor for growth.