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Internal Med MKSAP Pulmonary/Critical Care
Terms in this set (49)
Manage moderate chronic obstructive pulmonary disease.
* In patients with moderate chronic obstructive pulmonary disease, therapy with a long-acting β2-agonist or a long-acting anticholinergic agent improves quality of life and pulmonary function compared with therapy with short-acting bronchodilators alone.
This patient has stage II chronic obstructive pulmonary disease (COPD) as defined by the guidelines of the Global Initiative for Obstructive Lung Disease (GOLD). GOLD stage II disease is defined by a postbronchodilator FEV1/FVC ratio less than 70% and an FEV1 less than 80% but more than 50% of predicted with or without chronic symptoms. In patients with GOLD stage II disease, maintenance treatment with one or more long-acting bronchodilators such as a long-acting β2-agonist (salmeterol or formoterol) is recommended, along with as-needed albuterol. Pulmonary rehabilitation can be considered in addition to medical treatment in symptomatic patients. Starting or adding a long-acting anticholinergic agent would also be appropriate.
Inhaled corticosteroids, oral corticosteroids, theophylline, and montelukast would be inappropriate for this patient. Theophylline's narrow therapeutic window and poor bronchodilator effect make it a poor choice. Oral corticosteroids are not recommended routinely in COPD because of their systemic side effects. Montelukast is used as a third-line agent in asthma but has not been shown to be efficacious in COPD. The GOLD guidelines recommend consideration of inhaled corticosteroids in patients whose lung function is less than 50% and who experience recurrent exacerbations. When inhaled corticosteroids are combined with a long-acting β2-agonist in such patients, the rate of decline in quality of life and health status is significantly reduced and the frequency of acute exacerbations is reduced by 25%; lung function is also improved and dyspnea alleviated.
Evaluate a low-risk patient with a very small pulmonary nodule.
* In a patient at low risk for malignancy no follow-up is required for an incidentally noted pulmonary nodule 4 mm or smaller.
Studies of chest CT screening have shown that 25% to 50% of patients have one or more pulmonary nodules detected on the initial CT scan. Even in patients at relatively high risk for lung cancer, the likelihood that a small nodule is malignant is low (<1%). For example, the risk of malignancy is about 0.2% for nodules smaller than 3 mm and 0.9% for nodules 4 to 7 mm. The Fleischner Society recommendations include no follow-up for low-risk patients with nodules 4 mm or smaller and follow-up CT at 12 months for patients with such nodules who are at risk for lung cancer.
Diagnose intensive care unit-acquired weakness
* Patients with intensive care unit-acquired weakness have diffuse, flaccid weakness and often present with difficulty with ventilator weaning.
Patients with intensive care unit (ICU)-acquired weakness have diffuse weakness and decreased muscle tone. The disorder may be first recognized in patients with unexplained difficulty weaning from the ventilator. ICU-acquired weakness is a term used to encompass critical-illness poly-neuropathy and critical-illness myopathy. Treatment with paralytic agents and systemic corticosteroids, as well as sepsis and immobilization, increase the risk of developing ICU-acquired weakness. Treatment is supportive, including discontinuation or reduction of corticosteroids, aggressive management of existing disorders, and physical rehabilitation.
Evaluate vocal cord dysfunction
* Laryngoscopy during an exacerbation of vocal cord dysfunction shows adduction of the vocal cords during inspiration.
This patient likely has vocal cord dysfunction (VCD). Patients with VCD can have throat or neck discomfort, wheezing, stridor, and anxiety. The disorder can be difficult to differentiate from asthma; however, affected patients do not respond to the usual asthma therapy. Diagnosing VCD is made more difficult by the fact that many of these patients also have asthma. The chest radiograph in this patient showed decreased lung volumes, which is in contrast to hyperinflation that would be expected in acute asthma. Oxygen saturation is typically normal in patients with VCD.
Laryngoscopy, especially when done while the patient is symptomatic, can reveal characteristic adduction of the vocal cords during inspiration. Another test that helps make the diagnosis is flow volume loops, in which the inspiratory and expiratory flow rates are recorded while a patient is asked to take a deep breath and then to exhale. In patients with VCD, the inspiratory limb of the flow volume loop is "flattened" owing to narrowing of the extrathoracic airway (at the level of the vocal cords) during inspiration.
Recognize a typical presentation of a carcinoid tumor.
* Carcinoid tumors are neuroendocrine tumors with an indolent growth pattern that often present with endobronchial obstruction.
A carcinoid tumor is the most likely tumor in a young person who has never smoked and who has evidence of endobronchial obstruction. Bronchial carcinoid is a slow growing tumor that originally was classified as an adenoma but has been reclassified as a malignant neoplasm because of its ability to metastasize. Most bronchial carcinoid tumors are located in proximal airways and cause symptoms by either obstructing an airway or bleeding. Common presenting symptoms include cough or wheeze, hemoptysis, and recurrent pneumonia in the same pulmonary lobe. The carcinoid syndrome is caused by systemic release of vasoactive substances such as serotonin, and the most typical features include cutaneous flushing and diarrhea. Bronchial carcinoids are not commonly associated with the carcinoid syndrome because of their relatively small amount of serotonin production.
Evaluate a tuberculous pleural effusion
* A patient with tuberculous pleural effusion typically presents with a lymphocyte-predominant exudative effusion; however, within the first 1 to 2 weeks, neutrophils can predominate as the cellular response evolves from neutrophils to lymphocytes.
The patient likely has a tuberculous pleural effusion based on the subacute (3-week) duration of symptoms and the characteristics of the pleural effusion. Because of the patient's age and the presentation with an isolated pleural effusion, primary tuberculosis is most likely. A tuberculous effusion is typically exudative by both protein (pleural fluid to serum protein ratio greater than 0.5) and lactate dehydrogenase (LDH) criteria (pleural fluid to serum LDH ratio greater than 0.6 and pleural fluid to serum upper limits of normal LDH ratio greater than 0.67). The cellular response in the pleural fluid is classically lymphocytic (greater than 80% mature lymphocytes). However, it can be neutrophilic within the first 2 weeks, after which it typically evolves into the classic lymphocyte-predominant exudate. Whereas pleural fluid cultures for Mycobacterium are positive in less than one third of cases, the combination of pleural biopsy for histologic evaluation and culture is typically positive in more than two thirds of cases.
Manage a patient with an exacerbation of asthma
* The response to inhaled bronchodilators is more predictive of the clinical course in a patient with asthma than initial physical examination and findings.
This patient presented with signs of a severe asthma exacerbation. Decreased breath sounds, accessory muscle use, sternocleidomastoid or suprasternal retractions, inability to speak in full sentences, and paradoxical pulse greater than 15 mm Hg are associated with severe airflow obstruction, although the absence of these findings does not necessarily exclude the presence of a high-risk exacerbation. However, the initial physical examination and findings are less predictive of the clinical course in a patient with asthma than the response to bronchodilators. This patient has responded well to bronchodilators, with improved ability to speak and reduced accessory muscle use. Wheezing may become more prominent in the early stages of recovery owing to improved airflow through narrowed airways. According to the newest National Asthma Education and Prevention Program's guidelines, admission to the intensive care unit is recommended for symptomatic patients with even mild carbon dioxide retention (PCO2 greater than 42 mm Hg) or severely decreased lung function despite aggressive bronchodilator treatment (persistent FEV1 or peak expiratory flow less than 40% of predicted). This patient does not meet the criteria for admission to the intensive care unit or intubation and mechanical ventilation at this time. The best disposition for this patient would be admission to the hospital ward; his FEV1 has not improved enough to warrant discharge.
Diagnose malignant hyperthermia.
* Malignant hyperthermia is an inherited skeletal muscle disorder characterized by a hypermetabolic state precipitated by exposure to volatile inhalational anesthetics and the depolarizing muscle relaxants.
This patient most likely has malignant hyperthermia, which is an inherited skeletal muscle disorder characterized by a hypermetabolic state precipitated by exposure to volatile inhalational anesthetics (halothane, isoflurane, enflurane, desflurane, sevoflurane) and the depolarizing muscle relaxants succinylcholine and decamethonium. It usually occurs on exposure to the drug but can occur several hours after the initial exposure and can develop in patients who were previously exposed to the drug without effect. Increased intracellular calcium leads to sustained muscle contractions, with skeletal muscle rigidity and masseter muscle spasm, tachycardia, hypercarbia, hypertension, hyperthermia, tachypnea, and cardiac arrhythmias. Rhabdomyolysis and acute renal failure can develop. Malignant hyperthermia should be suspected in patients with a family history of problems during anesthesia.
Malignant hyperthermia is life-threatening unless treated promptly and aggressively. Supportive measures include hydration and decreasing the fever. Dantrolene, a skeletal muscle relaxant, is given as a bolus of 1 mg/kg intravenously and then 2 mg/kg every 5 to 10 minutes until the symptoms resolve. Response to dantrolene is not diagnostic of the disorder but is supportive if signs and symptoms resolve quickly. For those patients with a known history, pretreatment with dantrolene before the anesthetic agent is administered prevents the development of symptoms.
Neuroleptic malignant syndrome
The neuroleptic malignant syndrome is a life-threatening disorder caused by an idiosyncratic reaction to neuroleptic tranquilizers (dopamine D2-receptor antagonists) and some antipsychotic drugs. The most common offending neuroleptic agents are haloperidol and fluphenazine. The syndrome occurs with all drugs that cause central dopamine receptor blockade, usually soon after starting a new drug or with dose escalation. It has been reported in patients with Parkinson disease who abruptly discontinue levodopa or anticholinergic therapy. Most patients with the syndrome develop muscle rigidity, hyperthermia, cognitive changes, autonomic instability, diaphoresis, sialorrhea, seizures, arrhythmias, and rhabdomyolysis within 2 weeks after initiating the drug.
the serotonin syndrome presents with high fever, muscle rigidity, and cognitive changes. Findings unique to the serotonin syndrome are shivering, hyperreflexia, myoclonus, and ataxia. The serotonin syndrome is caused by the use of selective serotonin reuptake inhibitors, a category of drug that this patient has not been exposed to.
Diagnose cryptogenic organizing pneumonia.
* Cryptogenic organizing pneumonia most often presents with subacute disease progression and bilateral opacities on chest radiograph.
This nonsmoker without any exposure history has acute to subacute development of nonspecific systemic and respiratory symptoms with a dominant alveolar (opacification) process on chest radiograph. The tempo of the disease process is the key to differentiating cryptogenic organizing pneumonia (COP) from other interstitial lung diseases. COP (formerly called idiopathic bronchiolitis obliterans organizing pneumonia) is often acute or subacute, with symptom onset occurring within 2 months of presentation in three fourths of patients. The presentation is so suggestive of an acute or subacute lower respiratory tract infection that patients have almost always been treated with and failed to respond to one or more courses of antibiotics before diagnosis.
Idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia (NSIP), or lymphocytic interstitial pneumonia (LIP) typically follows a prolonged course with evidence of respiratory symptoms and radiographic findings that progress slowly over months or years. Radiographic findings in COP are also distinct from those in IPF, NSIP, and LIP. A dominant alveolar opacification process is typically present in patients with COP. The opacities are almost always bilateral with varied distribution. One of the key radiographic features of COP is the tendency for COP opacities to "migrate" or involve different areas of the lung on serial examinations. Although the radiographic findings of IPF, NSIP, and LIP are varied, they all have a dominant interstitial (reticular) pattern with or without opacities. LIP (which is very rare) is one of the few interstitial lung diseases that can present with cystic changes on high-resolution CT.
Treat stable acute pulmonary embolism.
* Acute pulmonary embolism can be treated initially with subcutaneous unfractionated heparin, low-molecular-weight heparins, or fondaparinux without the need for dosage adjustment.
This patient has had an acute pulmonary embolism 1 day post partum. The patient has no evidence of active bleeding, and there is no increased risk for bleeding from anticoagulation. Subcutaneous administration of unfractionated heparin, low-molecular-weight heparins, and fondaparinux are all safe and effective for the treatment of acute pulmonary embolism. A recent clinical trial showed that high-dose subcutaneous unfractionated heparin, administered without dose adjustment guided by the activated partial thromboplastin time, was as safe and effective as low-molecular-weight heparin administered in the same fashion.
indications for IVC filter
There are four generally accepted indications for placement of an inferior vena cava filter: (1) absolute contraindication to anticoagulation (for example, active bleeding); (2) recurrent pulmonary embolism despite adequate anticoagulation therapy; (3) bleeding complication of anticoagulation therapy; and (4) hemodynamic or respiratory compromise severe enough that a subsequent pulmonary embolism might be lethal. This patient has no indication for an inferior vena cava filter.
Indications for Oxygen in COPD
* In a patient with severe chronic obstructive pulmonary disease, at-rest oxygen saturation less than or equal to 88% is an indication for long-term continuous oxygen therapy.
The long-term administration of oxygen for more than 15 hours per day to patients with chronic obstructive pulmonary disease (COPD) increases survival, and may also improve hemodynamics, hematologic characteristics, exercise capacity, lung mechanics, and mental status. Indications for continuous long-term oxygen therapy for patients with COPD include:
* PO2 less than or equal to 55 mm Hg or oxygen saturation less than or equal to 88%
* Po2 less than or equal to 59 mm Hg or oxygen saturation less than or equal to 89% if there is evidence of cor pulmonale, right heart failure, or erythrocytosis (hematocrit greater than 55%).
This patient's resting oxygen saturation is 86% and his PO2 is 55 mm Hg, and, therefore, continuous long-term oxygen therapy is indicated.
Chronic hypoxemia leading to the development of cor pulmonale portends a poor prognosis. Nocturnal oxygen therapy is better than no oxygen therapy at all, but continuous therapy is better than nocturnal therapy in severely hypoxemic patients with erythrocytosis, elevated pulmonary artery pressures, and respiratory acidosis. No study has shown a survival benefit when oxygen is prescribed for exercise-induced oxygen desaturation or when used as needed for symptoms of breathlessness.
Recognize prophylaxis for high-altitude pulmonary edema
* Nifedipine is used both to prevent and to treat high-altitude pulmonary edema.
High-altitude pulmonary edema (HAPE) is a form of noncardiogenic pulmonary edema due to leakage of fluid and hemorrhage into the alveolar spaces. The most effective preventive measure for HAPE is an appropriately gradual ascent to altitude (not greater than 300 to 500 m [984 to 1640 ft] daily above an altitude of 2000 m [6562 ft], with scheduled rest days every 3 or 4 days). Nifedipine is used to prevent and to treat HAPE.
* The most common causes of chylothorax are cancer and trauma; other causes are pulmonary tuberculosis, chronic mediastinal infections, sarcoidosis, lymphangioleiomyomatosis, and radiation fibrosis.
Chylothorax is drainage of lymphatic fluid into the pleural space secondary to disruption or blockage of the thoracic duct or one of its lymphatic tributaries. Malignancy is the most common cause of chylothorax, but trauma is the second most common cause. Chylothorax can present about 2 to 10 days after penetrating or non-penetrating trauma to the chest. The pleural fluid in chylothorax is usually milky but may also be serous or serosanguineous in malnourished patients with little fat intake. The pleural fluid triglyceride concentration in a chylothorax is typically greater than 110 mg/dL (1.24 mmol/L) and occurs in association with a low pleural fluid cholesterol concentration. If the triglyceride level is less than 50 mg/dL (0.56 mmol/L), chylothorax is unlikely. When the pleural fluid triglyceride concentration is between 50 and 110 mg/dL (0.56 and 1.24 mmol/L), a lipoprotein analysis should be done and the presence of chylomicrons would confirm the diagnosis in such cases.
* Thymomas may be associated with a paraneoplastic syndrome such as myasthenia gravis.
Up to 75% of patients with myasthenia gravis have thymic abnormalities, such as hyperplasia or tumor. Therefore, evaluation of patients with suspected myasthenia gravis should include CT scan of the chest. The CT image shows an anterior mediastinal mass, and the diagnosis of myasthenia gravis is supported by the findings of ptosis and the elevated acetylcholine receptor binding antibody (AChR-Ab). Myasthenia gravis is characterized by weakness with a predilection for various muscles, particularly the ocular, bulbar, proximal extremities, neck, and respiratory muscles. Symptoms of this condition are traditionally worsened by fatigue, exertion, a rise in body temperature, stress, and intercurrent infections. Approximately 30% to 50% of patients with thymoma have myasthenia gravis, and the tumors are most likely to be located in the anterior mediastinum.
Recognize indications for methacholine challenge testing in cases of suspected asthma
* Methacholine challenge testing is most useful in evaluating patients with suspected asthma who have episodic symptoms and normal baseline spirometry.
This patient's history is consistent with, but not typical of, asthma. This presentation is sometimes referred to as cough-variant asthma. Asthma is often an episodic disease, with normal examination findings and spirometry between episodes. In such cases, a bronchial challenge test, such as with methacholine, can induce bronchoconstriction even when the patient is asymptomatic and spirometry is normal. Methacholine challenge testing is done by giving the patient increasing concentrations of methacholine by nebulization and performing spirometry after each dose until there is a greater than 20% decrease in FEV1 from baseline. The methacholine dose that leads to a 20% decrease in the FEV1 is known as the provocative concentration 20 (PC20) and is calculated from a dose-response curve. In general, a PC20 of less than 4 mg/mL is consistent with asthma. A PC20 between 4 and 16 mg/mL suggests some bronchial hyperreactivity and is less specific for asthma. A PC20 above 16 mg/mL is considered normal. The sensitivity of a positive methacholine challenge test in asthma is in the range of 85% to 95%.
Manage a pulmonary nodule that is negative on CT enhancement study.
* A nodule that is nonenhancing on dynamic CT contrast study is likely benign, and observation is appropriate.
The attenuation coefficient of a pulmonary nodule is a measure of its density and is expressed in Hounsfield units. Enhancement after contrast reflects nodule vascularity and is an indicator of malignancy or active inflammation. A nodule that shows less than 15 Hounsfield units of enhancement on dynamic contrast study is highly likely to be benign; a multicenter study showed a 97% negative predictive value at a cutoff of 15 Hounsfield units.
Reevaluation of the nodule at 3 months would be appropriate given the low likelihood that this is a malignant nodule.
Diagnose acute eosinophilic pneumonia
* Acute eosinophilic pneumonia may present as hypoxemic respiratory failure after 1 to 2 weeks of low-grade fever and systemic symptoms.
This patient's dramatic presentation is typical of acute eosinophilic pneumonia, which must be differentiated from other causes of idiopathic acute respiratory distress syndrome. Treatment of respiratory failure due to acute eosinophilic pneumonia with intravenous corticosteroids is efficacious, with clinical improvement over 12 to 24 hours. If a patient does not respond to corticosteroid therapy, another diagnosis should be considered. Acute eosinophilic pneumonia is idiopathic, but it has been associated with inhaled environmental antigens. Recently, initiation of cigarette smoking has been linked to acute eosinophilic pneumonia in a Japanese population and in military recruits.
Manage a patient with a malignant pleural effusion and lung entrapment.
* The development of severe, anterior chest pain during therapeutic thoracentesis is virtually diagnostic of an unexpandable lung with the development of significant negative intrapleural pressure.
The development of severe, anterior chest pain during therapeutic thoracentesis is virtually diagnostic of an unexpandable lung with the development of significant negative intrapleural pressure. The anterior chest pain is quickly relieved by allowing air entry into the pleural space through the thoracentesis needle or catheter. In this situation, the patient is best managed with an indwelling catheter. The patient and his family are instructed to drain the pleural fluid when breathlessness ensues and to discontinue drainage immediately when anterior chest pain develops.
This patient has two distinct pathophysiologic causes of his pleural effusion: (1) fluid produced by the malignant involvement of the pleura primarily due to increased levels of vascular endothelial growth factor and (2) an unexpandable lung due to tumor involvement of the visceral pleura. Therefore, an indwelling catheter removes the "malignant fluid," and when this volume of fluid has been removed, further fluid removal (due to the unexpandable lung) results in a significant decrease in pleural pressure causing anterior chest pain.
Diagnose cyanide toxicity from sodium nitroprusside therapy.
* Sodium nitroprusside when used in high doses or over a period of days can produce toxic blood concentrations of cyanide.
Cyanide may cause toxicity through parenteral administration, smoke inhalation, oral ingestion, or dermal absorption. Sodium nitroprusside, when used in high doses or over a period of days, can produce toxic blood concentrations of cyanide. In most patients, cyanide release from sodium nitroprusside is slow enough that the body's innate detoxification mechanisms can eliminate the cyanide before it interferes with cellular respiration. However, patients with low thiosulfate reserves (for example, malnourished or postoperative patients) are at increased risk for developing symptoms, even with therapeutic dosing.
A severe anion gap metabolic acidosis, combined with a reduced arterial-venous oxygen gradient (less than 10 mm Hg due to venous hyperoxia), suggests the diagnosis of cyanide toxicity. Apnea may result in a combined metabolic and respiratory acidosis. The treatment of cyanide poisoning is empiric because laboratory confirmation can take hours or days. Treatment includes administration of both sodium thiosulfate and hydroxocobalamin.
Treat α1-antitrypsin deficiency.
* Intravenous augmentation therapy with an α1-antitrypsin (AAT) is the most direct and efficient means of elevating AAT levels in plasma and lung interstitium.
α1-Antitrypsin (AAT) deficiency is associated with early-onset pulmonary emphysema, liver disease, and, rarely, skin disease. In suitable candidates, intravenous infusion of pooled human AAT is the most direct and efficient method of elevating AAT levels in plasma and lung interstitium. Augmentation therapy is most effective in patients with an FEV1 35% to 60% of predicted and an FEV1/FVC ratio 30% to 65%. The selection criteria include:
High-risk phenotype (Pi
Z [protease inhibitor Z])
* Plasma AAT levels below 50 to 80 mg/dL (0.5-0.8 g/L)
* Nonsmoker or ex-smoker
* Likely adherence to the protocol
* Airflow obstruction with spirometry
* Age at least 18 years
Estimated mean annual cost for patients receiving therapy is $40,000. Efficacy data are derived from observational (not randomized, controlled) trials that suggest that therapy retards the rate of FEV1 decline.
* A pulmonary presentation including pneumothorax and abnormal chest imaging often showing cysts/nodules is the primary event leading to the diagnosis of lymphangioleiomyomatosis in most patients.
This patient presents with subacute respiratory complaints and high-resolution CT findings of diffuse cysts in the clinical context of a young woman with a spontaneous pneumothorax who is otherwise healthy and has never smoked. The diagnosis is most likely lymphangioleiomyomatosis (LAM), a rare disease that accounts for less than 1% of all cases of interstitial lung diseases and occurs nearly exclusively in women in their childbearing years. The histopathologic feature of pulmonary LAM is proliferation of atypical smooth muscle-like cells associated with cystic changes. LAM may occur in patients with multiorgan hamartomas and a diagnosis of the autosomal dominant neurocutaneous syndrome called tuberous sclerosis complex. LAM also may present as a sporadic form in which renal and lymphatic hamartomas occur without diagnostic criteria for the tuberous sclerosis complex. The sporadic form of LAM presents with pulmonary complications and occurs only in women. Spontaneous pneumothorax is the initial cause for presentation in 36% of cases. Physical examination is often normal. Crackles and digital clubbing are usually absent.
Many young women with LAM are initially thought to have emphysema. However, patients with LAM are much younger than those with emphysema and present with respiratory complications 86% of the time, which include pneumothorax, as in this case, and chylothorax. Although the HRCT appearance of emphysema may mimic LAM, the cystic air spaces that occur in LAM are more uniform in appearance and distribution. Testing for α1-antitrypsin deficiency may be appropriate to exclude emphysema in young, nonsmoking patients.
Manage systemic sclerosis-associated interstitial lung disease.
* Pulmonary disease occurs in 70% of patients with systemic sclerosis and is the primary cause of mortality.
Approximately 50% of patients with systemic sclerosis who have pulmonary manifestations develop severe pulmonary involvement within the first 3 years of disease onset. In this patient, the high-resolution CT (HRCT) findings show minimal lung involvement (less than or equal to 20%) and are not diagnostic of active alveolitis; therefore, therapy is not indicated at this time. Follow-up and HRCT imaging and pulmonary function testing can determine whether this patient will benefit from systemic cytotoxic therapy. Pulmonary disease occurs in 70% of patients with systemic sclerosis and is the primary cause of death: 15% of affected patients develop severe restrictive pulmonary disease, with an associated 10-year mortality rate of 50%. Pulmonary fibrosis is more common in diffuse cutaneous systemic sclerosis than in limited cutaneous disease.
A recent study of interstitial lung disease in patients with systemic sclerosis showed that patients with extensive, but not moderate, alveolitis benefit from treatment with cyclophosphamide. FVC less than 70% of predicted was predictive of response to therapy. Goh and colleagues showed that clinicians' visual assessment of extent of lung disease on HRCT of less than 20% was highly predictive of survival at 120 months.
Manage a parapneumonic pleural effusion
* Immediate pleural space drainage, with or without fibrinolytic therapy, is indicated in a patient with acute bacterial pneumonia and a parapneumonic effusion with septations.
Pleural infections often resolve with antibiotic therapy alone, but fibrinous organization and lung entrapment require invasive treatment in about 10% of parapneumonic effusions. Effusions at risk for loculation are called complicated parapneumonic effusions. Because clinical prediction is unreliable, thoracentesis should be done to assess the need for invasive treatment provided that the effusion can be clearly visualized on ultrasonography. This patient with presumed underlying chronic obstructive pulmonary disease had typical symptoms of an acute bacterial pneumonia with development of a parapneumonic effusion with septations, low pleural fluid pH, low glucose, and elevated lactate dehydrogenase level. All of these factors suggest that the patient will have a poor outcome without immediate pleural space drainage with either thoracostomy tube placement or a radiologically guided small-bore catheter. The evidence for use of fibrinolytic agents is still unclear, but in this situation, pleural space drainage is imperative and, with the ultrasonographic findings, a trial of a fibrinolytic agent is warranted before performing video-assisted thoracoscopic surgery (VATS). Intrapleural administration of fibrinolytic agents does not cause systemic thrombolysis. Early VATS or thoracotomy is the generally preferred approach for patients who are candidates for surgery and who have persistent sepsis and loculation.
Provide nutritional support to a malnourished patient in the intensive care unit
* Patients in the intensive care unit require 25 to 30 nonprotein kcal/kg/d and 1.0 to 1.5 protein kcal/kg/d to meet the energy expenditures associated with critical illness.
Reliable changes in albumin require at least 2 to 3 weeks of nutritional supplementation. Since albumin is formed in the liver, diseases of the liver cause the hepatocytes to lose the ability to synthesize albumin. Prealbumin is another protein status indicator. Prealbumin's short half-life of 2 days and small serum pool allow small changes in nutritional status to be identified in a short time frame. Low prealbumin levels result from either inadequate nutrition or inflammatory stress. Prealbumin levels less than 5 mg/dL (50 mg/L) indicate severe protein and calorie malnutrition. Prealbumin should be used as an indicator of nutritional improvement and as a measure of how well nutritional interventions are working. Prealbumin can be measured once or twice per week and used as a sensitive monitor of nutritional progress.
Diagnose connective tissue disease-related lymphocytic interstitial pneumonia
* Lymphocytic interstitial pneumonia is detected at open lung biopsy in approximately one third of patients with Sjögren syndrome.
The diagnostic open lung biopsy specimen in this patient with Sjögren syndrome shows the histopathologic features of lymphocytic interstitial pneumonia (LIP), a rare form of interstitial lung disease (ILD) that may occur in one third of patients with ILD and Sjögren syndrome. Affected patients may develop ILD with known connective tissue disease, or ILD may be the presenting finding in a patient with undiagnosed connective tissue disease.
Evaluate a patient with non-small cell lung cancer.
* Positron emission tomography (PET) scanning (or PET-CT if available) is helpful in the preoperative evaluation of patients with known or suspected non-small cell lung cancer.
Positron emission tomographic (PET) scanning has been shown to be cost effective in the preoperative management of patients with non-small cell lung cancer. Randomized studies evaluating the addition of PET to the standard workup found that the procedure identifies advanced disease and precludes unnecessary thoracotomy in approximately 1 in 5 patients. PET-CT has been shown to have higher sensitivity and specificity for assessing lung cancer stage than CT and PET done separately. PET-CT may not be widely available but will likely completely replace PET alone. Current guidelines identify low-risk patients for surgery based upon preoperative spirometry.
Manage ventilator settings in a patient with the acute respiratory distress syndrome.
* A lung-protective ventilator strategy employing low tidal volumes reduces mortality in patients with the acute respiratory distress syndrome.
The patient has developed the acute respiratory distress syndrome (ARDS) complicating aspiration pneumonia. A lung-protective ventilator strategy should be used to reduce the risk of ventilator-induced lung injury by minimizing alveolar overdistention. A randomized controlled trial in patients with acute lung injury compared ventilation with tidal volumes of 6 mL/kg and 12 mL/kg ideal body weight and found an absolute mortality reduction of 8% in the low-tidal-volume group.
The cause of the patient's bilateral infiltrates is ARDS rather than poorly responding pneumonia. His fever curve and right lower lobe infiltrate have improved, and he has minimal secretions. A change in antibiotic therapy is not indicated.
Recognize and treat hypothermia.
* In patients with severe hypothermia (temperature less than 30.0 °C [86.0 °F]), active internal rewarming measures using warmed intravenous fluids, warm and humid oxygen, peritoneal lavage, and extracorporeal rewarming should be considered.
Manage severe chronic obstructive pulmonary disease.
* Treatment of GOLD stage III chronic obstructive pulmonary disease includes short-acting bronchodilators as needed and regular treatment with one or more long-acting bronchodilators with an inhaled corticosteroid and pulmonary rehabilitation.
This patient has severe (GOLD stage III) chronic obstructive pulmonary disease (COPD) defined as FEV1/FVC <70% and FEV1 30% to 50% of predicted with or without chronic symptoms (cough, sputum production). Treatment for this patient includes support for his smoking cessation, short-acting bronchodilators as needed, and regular treatment with one or more long-acting bronchodilators, as well as an inhaled corticosteroid, along with pulmonary rehabilitation.
Diagnose exercise-induced asthma.
* Exercise-induced asthma is confirmed by exercise challenge testing (to greater than 85% of maximal predicted heart rate) with postexercise spirometry showing a 15% or greater fall in FEV1.
Exercise-induced asthma (EIA) occurs in nearly 90% of patients with asthma who exercise at sufficient intensity and is more common with exercise in cold, dry air. Exercise challenge testing (to greater than 85% of maximal predicted heart rate) with postexercise spirometry confirms the diagnosis. An exercise challenge test has a high specificity for the diagnosis when the fall in FEV1 after exercise is 15% or greater. Airway obstruction after exercise peaks in 5 to 15 minutes and resolves in 20 to 30 minutes. Prophylaxis with short-acting inhaled β-agonists, such as albuterol, 5 to 10 minutes before exercise, prevents EIA in more than 80% of patients. With appropriate management, patients with EIA need not limit their involvement in sports.
Chronic symptoms (cough, sputum production)
FEV1 ≥80% of predicted
FEV1 50% to 80% of predicted
FEV1 30% to 50% of predicted
IV. Very Severe
FEV1 ≤30% of predicted or ≤50% of predicted plus chronic respiratory failure
Recognize the diagnostic value of pleural fluid amylase value and amylase isoenzymes in the diagnosis of a pleural effusion.
* An elevated pleural fluid amylase level suggests that the cause of the pleural effusion is pancreatic disease, esophageal perforation, or malignancy.
A pleural fluid amylase concentration greater than the upper limits of normal for serum amylase or a pleural fluid to serum amylase ratio greater than 1.0 suggests the following diagnoses: pancreatic disease (either acute pancreatitis or pancreaticopleural fistula), malignancy (most commonly adenocarcinoma of the lung), and esophageal perforation. Finding salivary isoamylase in pleural fluid virtually excludes acute pancreatitis and pancreaticopleural fistula.
Recognize the neuroleptic malignant syndrome.
* The neuroleptic malignant syndrome can result from administration of neuroleptic agents and abrupt withdrawal of antiparkinsonian medications.
The neuroleptic malignant syndrome can result from administration of neuroleptic agents, such as haloperidol. Acute and abrupt withdrawal of antiparkinsonian medications may also precipitate the syndrome and may be the cause for this patient's symptoms. The pathogenesis of this syndrome results from dopamine D2 receptor antagonism. Muscular rigidity and altered mental status occur early, followed by hyperthermia, hypertension, tremors, fever, dysphagia, diaphoresis, myoclonus, and autonomic dysfunction. Criteria for the diagnosis of neuroleptic malignant syndrome are based on clinical features, although elevations in serum potassium, creatine kinase, and lactate dehydrogenase levels and a metabolic acidosis are common. The mortality rate is 10% to 20%, although the rate is generally higher in patients who develop severe muscle necrosis and rhabdomyolysis.
Manage progressive idiopathic pulmonary fibrosis.
* Lung transplantation in eligible patients is the only therapy known to improve survival in patients with idiopathic pulmonary fibrosis.
Lung transplantation is the only therapy that improves survival in patients with idiopathic pulmonary fibrosis (IPF), and referral to a transplant center should be considered for all eligible patients with the disorder. Patients referred for transplantation should be free of significant other organ dysfunction, be younger than 65 years, have acceptable nutritional status, and have a satisfactory psychosocial profile and support system.
IPF is a relentlessly progressive form of interstitial lung disease, with a median survival from diagnosis of 3 to 4 years. No medical therapy has shown survival benefit in randomized, placebo-controlled clinical trials. Current options to manage patients with IPF include (1) referral of eligible patients for transplantation, (2) referral of interested patients for clinical research trials, (3) observation with supportive care and no medical therapy, and (4) a trial of corticosteroid therapy with or without a cytotoxic agent in an educated patient aware of the risks of unproven therapy.
Manage chronic obstructive pulmonary disease exacerbation with noninvasive positive-pressure ventilation.
* Noninvasive positive-pressure ventilation should be initiated early in the course of moderate or severe exacerbations of chronic obstructive pulmonary disease unless there is a specific contraindication to use of non-invasive ventilation.
The patient is having a moderate to severe exacerbation of chronic obstructive pulmonary disease (COPD) and should be placed on noninvasive positive-pressure ventilation (NPPV). A landmark study found that NPPV reduced the need for intubation, the length of hospital stay, and the mortality rate in such patients. Suitable candidates for NPPV include patients with moderate to severe dyspnea, use of accessory respiratory muscles, respiration rate greater than 25/min, and pH less than 7.35 with PCO2 greater than 45 mm Hg. Contraindications to NPPV include impending respiratory arrest, cardiovascular instability, altered mental status, high aspiration risk, production of copious secretions, and extreme obesity, as well as surgery, trauma, or deformity of the face or upper airway.
Diagnose allergic bronchopulmonary aspergillosis.
* The characteristic features of allergic bronchopulmonary aspergillosis include moderate to severe persistent asthma, bronchiectasis and chest radiographic abnormalities, elevated serum IgE level, eosinophilia, and a positive skin test to Aspergillus fumigatus.
Allergic bronchopulmonary aspergillosis (ABPA) is a rare (occurring in 1% to 2% of patients with asthma), but important, complication in patients with asthma. These patients develop humoral and cell-mediated immune responses to Aspergillus fumigatus in their airways, leading to persistent inflammation, airway damage with development of central bronchiectasis, and eventually pulmonary fibrosis. Features of the disorder include moderate to severe persistent asthma, expectoration of brown sputum that contains Aspergillus organisms, bronchiectasis and radiologic abnormalities (infiltrate, mucous plugging), elevated levels of serum total IgE (typically greater than 0.1 mg/dL [1.0 mg/L]), a positive skin test to A. fumigatus, and eosinophilia. Treatment often requires the use of systemic corticosteroids. A skin test to determine the presence of allergic response to Aspergillus is an important first step in evaluating patients with ABPA because essentially all patients with ABPA have a positive skin test. However, many patients with a positive skin test do not have ABPA, and therefore, the positive predictive value of the skin test is low. A negative skin prick test followed by negative intradermal skin test virtually excludes the diagnosis of ABPA, provided that the tests were done using optimal extracts and technique. If the skin test is positive, the next diagnostic step is measurement of serum total IgE. ABPA is excluded if the serum total IgE concentration is less than 0.1 mg/dL (1.0 mg/L). If skin testing for Aspergillus is not available, measuring serum total IgE may be an efficient way to pursue the diagnosis.
Smoking cessation options
* A high-dose nicotine patch in combination with another antismoking therapy, such as nicotine replacement therapy (gum and/or spray), is the most effective therapy for smoking cessation.
This patient has already used a nicotine patch unsuccessfully. However, using the high-dose patch again but in combination with another therapy, such as nicotine replacement with gum or spray, gives the best long-term cessation rate.
Bupropion has been shown to be effective in smoking cessation and is generally well tolerated. However, seizures occur in approximately 0.1% of patients who take the drug, and the risk appears to be higher in patients with a preexisting seizure disorder, anorexia nervosa, or bulimia. This patient has a history of seizure disorder, and, therefore, bupropion is contraindicated.
Varenicline can be used for smoking cessation, and the patient should try to stop smoking 1 week after starting varenicline. The common side effects are nausea and abnormal dreams. The U.S. Food and Drug Administration (FDA) has issued information regarding post-marketing reports of suicidal thoughts and erratic/aggressive behavior in patients who have taken varenicline. Many cases suggest new-onset depression, suicidal ideation, and emotional/behavioral changes within days to weeks after treatment initiation. It is not clear whether these effects are related to the drug itself or to the effects of smoking cessation. In this patient with a history of major depression and suicidal ideation, varenicline would not be indicated. In 2008, the FDA reported that it is increasingly likely that varenicline is associated with serious neuropsychiatric symptoms. There are also reports of patients experiencing drowsiness that affects their ability to drive or operate heavy machinery.
Manage chronic thromboembolic pulmonary hypertension.
* The definitive therapy for chronic thromboembolic pulmonary hypertension is pulmonary thromboendarterectomy.
This patient has echocardiographic evidence of pulmonary hypertension and evidence on ventilation/perfusion scanning of regional perfusion defects suggestive of chronic thromboembolic pulmonary hypertension (CTEPH). Pulmonary angiography is typically performed next and can confirm the diagnosis and determine whether the large-vessel obstruction is amenable to surgical therapy. The definitive therapy is pulmonary thromboendarterectomy, which is performed only in centers with special expertise in the preoperative evaluation, surgery, and postoperative therapy for these patients.
CTEPH is a progressive disease that causes significant mortality if not evaluated and treated in a timely manner. Although CTEPH is a complication of acute pulmonary embolism, the disease is due to a combination of organized intra-arterial scarring and a secondary small-vessel reaction. Acute anticoagulation with heparin followed by chronic warfarin therapy or thrombolysis would do little to reverse the disease. Bosentan may have a role in the treatment of patients with CTEPH in whom surgery is not possible.
Recognize a paraneoplastic syndrome associated with small cell carcinoma.
* The ANNA-1 antibody is the most common antibody present in a sensory neuropathy due to small cell lung carcinoma.
Paraneoplastic neurologic disorders are associated with systemic malignancy but are not related to direct tumor involvement or to other toxic or metabolic, infectious, or vascular complications of cancer. Paraneoplastic sensory neuropathy is commonly associated with lung carcinoma (particularly small cell carcinoma) but may develop in patients with other malignancies. The neurologic syndrome precedes the diagnosis of cancer in most patients. Paraneoplastic sensory neuropathy manifests with progressive paresthesias, profound sensory ataxia, and multimodality sensory loss. Such patients usually have limited-stage small cell lung carcinoma at presentation.
Refer a patient with severe chronic obstructive pulmonary disease for lung transplantation.
* Patients who have emphysema, an FEV1 not greater than 20% of predicted, and homogeneous disease on high-resolution CT or DLCO not greater than 20% should be considered for lung transplantation.
Patients with homogenous emphysema, an FEV1 not greater than 20% of predicted, and DLCO not greater than 20% of predicted have a median survival of 3 years and should be considered for lung transplantation. This patient is a candidate for transplantation. Functional capacity and quality of life are improved after lung transplantation, but the effect on overall survival is mixed.
The National Emphysema Therapeutic Trial of lung volume reduction surgery reported mixed results on patient outcomes. For patients with very reduced lung function (FEV1 less than 20%), low DLCO (less than 20%), and diffuse disease, the mortality rate was greater with surgery than with medical therapy. However, in patients with predominant upper lobe emphysema and low baseline exercise tolerance, functional capacity and survival improved. Patients with homogeneous emphysema, FEV1 less than 20% of predicted, and DLCO less than 20% of predicted have high mortality rates with lung volume reduction surgery.
Manage drug-induced organizing pneumonia.
* Organizing pneumonia is a nonspecific reparative reaction that can occur in infections, connective tissue diseases, drug reactions, and radiation-induced lung injury.
This patient has organizing pneumonia, which is likely caused by treatment with pegylated interferon alfa. Organizing pneumonia is a nonspecific reparative reaction that can occur in infections, connective tissue diseases, drug reactions, and radiation-induced lung injury. The presentation and radiographic findings depend on the cause of the organizing pneumonia. Organizing pneumonia presenting without an identifiable cause is termed cryptogenic organizing pneumonia (COP, formerly called idiopathic bronchiolitis obliterans organizing pneumonia). Patients with COP often present with such systemic symptoms as fever and weight loss. The typical radiographic presentation of COP is bilateral migratory patchy alveolar infiltrates. Organizing pneumonia can present radiographically as a distinct nodule or nodules indistinguishable from malignancy. Focal organizing pneumonia is typically positron emission tomographic (PET) scan-positive, and, therefore, PET does not differentiate focal organizing pneumonia from malignancy.
Recognize and treat organophosphate poisoning.
* Pralidoxime (2-PAM) reactivates acetylcholinesterase and can reverse the muscle weakness, paralysis, and respiratory depression of organophosphate toxicity.
This patient likely has organophosphate poisoning. Organophosphates are a diverse group of chemicals used in both domestic and industrial settings that include insecticides, nerve gases (soman, sarin, tabun, VX), ophthalmic agents (echothiophate, isoflurophate), and antihelmintics (trichlorfon). Exposure to organophosphate insecticides may occur by dermal, gastrointestinal, inhalational, and intravenous routes. Organophosphate insecticides inhibit both cholinesterase and pseudocholinesterase activities. The inhibition of cholinesterase activity leads to accumulation of acetylcholine at synapses, causing overstimulation and disruption of neurotransmission in both the central and peripheral nervous systems. Signs and symptoms of organophosphate poisoning include muscarinic effects, nicotinic effects, and central nervous system effects peripherally at muscarinic receptors and nicotinic receptors. Muscarinic manifestations include excessive salivation, diarrhea, vomiting, hypersalivation, respiratory distress with bronchorrhea and bronchospasm, abdominal pain, depressed level of consciousness, and muscle fasciculations. The muscarinic signs of organophosphate poisoning can be recalled with the help of the mnemonic DUMBELS—Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, Emesis, Lacrimation, Salivation. Nicotinic manifestations include increased muscle weakness, skeletal muscle fasciculations, and respiratory failure secondary to diaphragmatic paralysis. Central nervous system effects include altered mental status and seizures. Organophosphate insecticide poisoning is a serious condition that requires rapid diagnosis and treatment.
Amyl nitrite, sodium nitrite, and sodium thiosulfate are used to treat cyanide toxicity and are ineffective in the treatment of organophosphate poisoning. The most common early clinical manifestations of cyanide poisoning include headache and confusion, coma, tachypnea, tachycardia, and skin flushing. Excessive salivation, wheezing, and bronchorrhea do not occur. An anion-gap metabolic acidosis typically occurs as well as a low arterial-venous oxygen gradient as a result of hyperoxygenation of the venous blood.
Diagnose the reactive airways dysfunction syndrome.
* The reactive airways dysfunction syndrome follows a single, accidental inhalation of high levels of a nonspecific respiratory irritant in patients who typically do not have a history of asthma; the diagnosis is confirmed by a positive methacholine challenge test.
Many chemicals are irritants to the respiratory tract, affecting both the upper and lower airways. Asthma occurring after an acute, high-level exposure to an irritant is called the reactive airways dysfunction syndrome (RADS). Respiratory tract irritants reported to cause RADS include chlorine and its derivatives (hydrochloric acid, chlorine dioxide, phosgene), acids, ammonia, bromine, bleaches, isocyanates, formaldehyde, pyrolysis products contained in smoke, and aromatic hydrocarbons in sealants. RADS follows a single, accidental inhalation of high levels of a nonspecific respiratory irritant in patients who typically do not have a history of asthma. Within minutes of exposure, the patient develops cough, wheezing, dyspnea, and chest tightness. Symptoms persist even after the exposure has stopped and may last for years. The diagnosis is based on history and confirmed by a positive methacholine challenge test. Methacholine challenge testing can be done safely in patients with asthma provided that appropriate guidelines are followed and that the FEV1 is greater than 70% of predicted. Pharmacologic management is similar to that of other forms of asthma. Avoidance of nonspecific asthma triggers is often helpful.
Recognize and manage the propofol infusion syndrome.
* The propofol infusion syndrome in adults occurs primarily in patients with acute neurologic or acute inflammatory diseases complicated by severe infection or sepsis and who are receiving catecholamines or corticosteroids in addition to propofol.
This patient has the propofol infusion syndrome, and the drug should be discontinued and replaced by fentanyl and midazolam. The propofol infusion syndrome is a rare and often fatal syndrome originally described in critically ill children undergoing long-term propofol infusion at high doses. The syndrome has recently been reported in adults, mostly in patients with acute neurologic illnesses or acute inflammatory diseases complicated by severe infections or even sepsis and who are receiving catecholamines and/or corticosteroids in addition to propofol. The main features of the syndrome consist of cardiac failure, rhabdomyolysis, severe metabolic acidosis, and renal failure associated with hyperkalemia. Central nervous system activation with production of catecholamines and corticosteroids, and systemic inflammation with cytokine production are priming factors for cardiac and peripheral muscle dysfunction. High-dose propofol, but also supportive treatments with catecholamines and corticosteroids act as triggering factors.
Monitor respiratory status of a patient with neuromuscular weakness.
* Patients with neuromuscular weakness and tenuous respiratory status should be monitored with serial measurement of vital capacity.
In patients with neuromuscular weakness and tenuous respiratory status, serial measurement of vital capacity is an effective method to anticipate the need for mechanical ventilatory support before the onset of respiratory arrest. Patients with vital capacity under 15 to 20 mL/kg, who are unable to generate more than 30 cm H2O of negative inspiratory force, or with declining values are at high risk of ventilatory failure requiring invasive mechanical ventilation. Patients with bulbar dysfunction may not be able to accurately perform bedside spirometry and are at increased risk of rapid deterioration due to acute aspiration events.
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