LAST MINUTE EMERGENCY MEDICINE - PART 8 docx

OBSTRUCTIVE/RESTRICTIVE LUNG DISEASE 421 TAB LE 17-2 2 INDICATIONS FOR HOSPITALIZATION OF COPD Marked increase in symptoms, such as sudden development of resting dyspnea Severe background COPD Onset of new physical signs (cyanosis, peripheral edema) Failure of exacerbation to respond to medical management Significant comorbidities New arrhythmia Diagnostic uncertainty Older age Insufficient home support Adapted by the author from the Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, 2005 update, http://www.goldcopd.org. TAB LE 17-2 3 CLINICAL SIG NS OF CYSTIC F IBROSIS Respiratory Chronic productive cough Recurrent pneumonia Persistent chest radiograph abnormalities Airway obstruction Clubbing Sinusitis Nasal polyps GI Meconium ileus Distal intestinal obstruction Rectal prolapse Pancreatic insufficiency Pancreatitis Biliary cirrhosis Failure to thrive Other Male infertility Osteoporosis Adapted with permission from Ratjen, 2003. 422 CHAPTER 17 / THORACIC-RESPIRATORY DISORDERS PHYSICAL AND CHEMICAL IRRITANTS Pneumoconiosis Definition: Pneumoconiosis is a general term for fibrotic lung disease caused by dust inhalation. Specific inhalants include asbestosis, silicosis, and coal worker’s pneumoconiosis. Etiology: Exposure to inert dusts, such as coal, asbestos, talc, aluminum powder, or silica causes pulmonary fibrosis. Clinical Presentation: Patients with exposure are often asymptomatic for decades despite CXR findings. When the disease is advanced, patients experience dyspnea consistent with restrictive lung disease and have fine crackles on examination. Patients with asbestos exposure are at higher risk of lung cancer, especially if they smoke. Diagnosis: CXR shows diffuse nodular infiltrates. Pleural thickening and plaques are common in asbestosis. Treatment: There is no specific treatment for pneumoconiosis. Patients should receive influenza and pneumococcal vaccines, be encouraged to stop smoking, and have supplemental oxygen if they have resting hypoxemia or exercise induced oxygen desaturation. Inhalational Injury Definition: Inhalational injury results from breathing fumes, usually smoke. The inhalation may cause thermal burns, chemical irritation, and other toxic effects. Inhalation injury is the main cause of death in burn patients. Etiology: Thermal injury typically occurs above the vocal cords, except in the case of steam inhalation, which causes burns below the cords. Small particles can reach the terminal bronchioles, where they cause inflammation and bronchospasm. Toxic effects from inhaled gases such as carbon monoxide and cyanide may lead to tissue asphyxia. Clinical Presentation: Patients present with shortness of breath. Physical signs include carbonaceous sputum, singed nasal hairs, hoarseness, and wheezing. Diagnosis: The diagnosis is usually suggested by history. An ABG should be drawn to measure carboxyhe- moglobin. CXR may initially be normal but shows pulmonary edema after 24 hours. Bronchoscopy may be necessary to evaluate the full extent of the pulmonary damage. Treatment: Humidified oxygen should be administered. Indications for intubation are listed in Table 17-24. PULMONARY EMBOLISM 423 TAB LE 17-2 4 INDICATIONS FOR INTUBATING PATIENTS WITH INHALATIONAL INJURY Carbonaceous sputum Hoarse voice Full thickness burns of the face or perioral region Circumferential neck burns Altered mental status Hypoxia Supraglottic edema Adapted from Schwartz and Balakrishnan, 2004. TAB LE 17-2 5 RISK FACTORS FOR PULMONARY E MBOLI Vessel wall trauma: Surgery within the last 3 mo Hypertension Stasis: Immobilization Stroke Obesity Long-distance travel Bedrest >48 h Indwelling venous catheter Hypercoagulability: Heavy cigarette smoking (a pack per day) Adenocarcinoma Pregnancy Oral contraceptives/hormone replacement therapy Family history/genetic: factor V Leiden mutation, factor VIII mutation, lupus anticoagulant, hyperhomocysteinemia, many others PULMONARY EMBOLISM Pulmonary Embolism/Infarct Definition: Pulmonary embolism (PE) is a disease in which emboli, usually blood clots from the lower extremities, block the pulmonary vasculature and may cause symptoms ranging from mild dyspnea to car- diovascular collapse. 424 CHAPTER 17 / THORACIC-RESPIRATORY DISORDERS Etiology: Most PEs result from thrombi originating in the ileofemoral veins. Upper extremity, right heart, renal, and pelvic thrombi are less common. Most infrapopliteal thrombi do not cause PEs, but approximately 20% of these calf thrombi will migrate proximally. PEs are usually multiple and in the lower lobes of the lung. Larger emboli will lodge at the bifurcation of the main pulmonary artery and cause cardiovascular collapse, while smaller ones will travel to the peripheral pulmonary vasculature, leading to pulmonary infarcts and pleuritic chest pain. Risk factors for PE are listed in Table 17-25; however, approximately half of patients with PE will not have any known risk factors. Other nonthrombotic emboli include air, amniotic fluid, bone marrow, talc from IV drug use, and septic emboli. Clinical Presentation: No finding is reliably sensitive or specific for PE, and one-third of patients thought to be at high risk based on symptoms do not have the disease. Symptoms do, however, help determine the risk of PE. In the PIOPED study, 97% of patients had either dyspnea, tachypnea, or chest pain. Though most PEs originate in the legs, the majority of patients with PE do not have leg symptoms. Fevers higher than 103 ◦ F are rare. Diagnosis: An ABG, ECG, CXR, CBC, troponin, and brain natriuretic peptide (BNP) only serve to rule out other diseases. They are not helpful ruling in the diagnosis of PE. Rare findings on CXR include Hampton hump, a wedge-shaped density at the lung periphery caused by pulmonary infarction, and Westermark sign, enlarged proximal pulmonary arteries with peripheral oligemia. An ECG may show right heart strain (right bundle branch block, T-wave inversion in V1-V4, an S wave in lead I, and both a Q wave and inverted T wave in lead III). The classic ECG finding of S1Q3T3 is neither pathognomonic, sensitive, nor specific. The most common ECG finding is nonspecific ST-segment and T-wave abnormalities. D-dimer D-dimer negative D-dimer positive Low prestest probability: no PE No leg symptoms: perform chest CT angiogram Leg symptoms: perform ultrasound Ultrasound negative Low prestest probability: no PE Moderate/ high prestest probability: continue work-up Ultrasound Positive: treat for PE Chest CT negative Low prestest probability: no PE Moderate/ high prestest probability: continue work-up Chest CT positive: treat for PE Moderate/ high prestest probability: continue work-up –FIGURE17-2— Diagnostic approach for pulmonary embolism. PULMONARY EMBOLISM 425 TAB LE 17-2 6 MODIFIED WELLS CRITERIA FOR PULMONARY EMBOLISM RISK STRATIFICATION Criteria: Points: Symptoms of DVT 3 Other diagnosis less likely than PE 3 Heart rate >100 bpm 1.5 Immobilization/surgery in preceding month 1.5 Previous DVT/PE 1.5 Hemoptysis 1 Malignancy 1 Probability: Points: High >6 Moderate 2–6 Low >2 Data from Wells PS, Anderson DR, Rodger M, et al. Excluding Pulmonary Embolism at the Bedside Without Imaging. Ann Intern Med 2001;135:98–107. Many diagnostic algorithms have been suggested for PE (Figure 17-2). Patients are first assigned a pretest probability based on certain findings (see Table 17-26). D-dimer may be used to risk stratify the patient; nega- tive predictive values depend on the assay, but may be greater than 99%. If the D-dimer is elevated, imaging is indicated. Chest CT has replaced ventilation/perfusion (V/Q) scan as the study of choice, since almost three- quarters of V/Q scans are nondiagnostic. Chest CT quality depends on the scanner generation and experience of the reader. Lower-extremity ultrasound may be helpful if leg symptoms are present. Pulmonary angiogram, the gold standard, is indicated if other studies are nondiagnostic and a strong suspicion for PE remains. Treatment: Treatment of PE is outlined in Table 17-27. During the diagnostic evaluation, consider em- pirically initiating heparin therapy before the diagnosis is confirmed. TABLE 17-27 TREATMENT OF PULMONARY EMBOLISM Stable patients Oral anticoagulation with INR 2–3 Bridging heparin therapy until therapeutic INR: equal efficacy for unfractionated and low molecular weight heparin If known cause of PE, anticoagulation for 6 mo after cause resolves If idiopathic PE, consider indefinite anticoagulation Unstable patients Thrombolysis is recommended, but no mortality benefit over heparin alone Embolectomy, either percutaneous or surgical, for patients with contraindications to thrombolysis 426 CHAPTER 17 / THORACIC-RESPIRATORY DISORDERS PULMONARY INFECTIONS Lung Abscess Definition: A lung abscess is a suppurative, necrotic area of the lung parenchyma. Etiology: Lung abscesses are usually due to aspiration, but may also occur due to superinfection of lung infarcts or neoplasms. They aretypically caused by anaerobes, though aerobic bacteria may causeabscesses in immunosuppressed patients. Risk factors include impaired ability to protect the airways, such as alcoholism or stroke, and gingival disease. Clinical Presentation: Patients have indolent courses characterized by weeks of cough, fever, pleuritic chest pain, weight loss, and night sweats. Diagnosis: A CXR may show an area of consolidation with a cavitary lesion containing an air-fluid level. Multiple abscesses are uncommon. Treatment: Patients can be treated with antibiotics such as clindamycin, possibly in combination with a second-generation cephalosporin. Abscess drainage occurs spontaneously through the bronchial tree. Failure to recover on antibiotics mandates percutaneous drainage or thoracotomy. Pneumonia Definition: Pneumonia isaninfectionofthe lungs and can generally be visualized on CXR. It is considered community-acquired if the patient has not been hospitalized in the past 3 months, has not received IV antibiotics recently or chemotherapy, is not on dialysis, and does not reside in a nursing home. Etiology: Streptococcus pneumoniae is the most common cause of community-acquired pneumonia. Atyp- ical agents are the second most common cause including M. pneumoniae, C. pneumoniae, and Legionella. These agents cannot be differentiated from typical causes based on CXR findings or symptoms. H. influenzae, Staph. aureus, and gram-negative bacilli are other causes. Anaerobes were previously thought to be the most common etiologic agents of aspiration pneumonia, and may still be in alcoholics, but recent studies indicate that Strep. pneumoniae, Staph. aureus, and H. influenzae are common causes of aspiration pneumonia in pa- tients with dysphagia, such as nursing home residents and stroke patients. Viruses, predominantly influenza virus, cause up to 15% of pneumonia, with parainfluenza and adenoviruses occurring less commonly. Clinical Presentation: Patients present with fever and respiratory symptoms such as cough (>90%), dys- pnea (66%), and pleuritic chest pain (60%). Vital sign abnormalities include fever, tachypnea, hypotension, tachycardia, and hypoxia. Physical examination may reveal crackles on auscultation. Diagnosis: CXR confirms the diagnosis and is the only test that needs to be done in outpatients. Infiltrates may remain on CXR for 2 months. Further testing is indicated in hospitalized patients. A blood chem- istry panel and ABG help risk-stratify patients using the the patient outcomes research team (PORT) score (see Table 17-28). A CBC may also be helpful, as leukocytosis greater than 15,000 cell/µL makes bacterial infection more likely than viral, and anemia is suggestive of mycoplasma. Blood cultures are currently rec- ommended prior to the initiation of antibiotics, though they are positive in only 10% of cases and rarely change antibiotic therapy. Gram stain and culture of sputum are controversial and useless if done after antibiotic administration. If done, an appropriate specimen must contain multiple polymorphonuclear leukocytes and few epithelial cells. Urinary antigen tests are available for Legionella and Strep. pneumonia. PULMONARY INFECTIONS 427 The CDC recommends HIV testing in patients aged 15–54. CT scans may be used to detect interstitial disease, empyema, cavitation, multifocal disease, and adenopathy. Thoracentesis should be performed if effusions are present. Treatment: PORT (Tables 17-28 and 17-29) published a scoring system that can reduce hospital admissions by allowing for better selection of patients with lower mortality risk who may be safely discharged. It is important to note that this prediction rule was validated as a mortality prediction rule, not as a decision TAB LE 17-2 8 PNEUMONIA PREDICTION RULE (PORT SCORE) PATI ENT CHARACTERISTIC POINTS Age: Men Age in years Women Age in years – 10 Nursing home resident +10 Coexisting illness: Neoplastic disease +30 Liver disease +20 CHF +10 Cerebrovascular disease +10 Renal disease +10 Physical examination findings: Altered mental status +20 Respirations >30/min +20 Systolic BP <90 mm Hg +20 Temperature <95 ◦ F(35 ◦ C) or ≥104 ◦ F (40 ◦ C) +15 Pulse ≥125 bpm +10 Laboratory and radiology findings: Arterial pH <7. 35 +30 Blood urea nitrogen ≥30 mg/dL +20 Sodium <130 mmol/L +20 Glucose >250 mg/dL +10 Hematocrit <30% +10 PaO 2 <60 mm Hg or sat <90% +10 Bilateral pleural effusions +10 Total points Sum of above Adapted with permission from Fine MJ, Auble TE, Yealy DM, et al. A Prediction Rule to Identify Low-Risk Patients with Community Acquired Pneumonia. N Engl J Med 1997;336:243–50. TAB LE 17-2 9 PNEUMONIA SEVERITY INDEX FROM PORT SCORE CLASS PORT SCORE MORTALITY (%) SUGGESTED THERAPY Class I <51 0.1 Oral antibiotics at home Class II 51–70 0.6 Oral antibiotics at home—if vomiting or unreliable, then short stay Class III 71–90 0.9 Oral antibiotics at home—if vomiting or unreliable, then short stay Class IV 91–130 9.5 Inpatient + IV antibiotics Class V >130 26.7 Inpatient + IV antibiotics Data from Fine MJ, Auble TE, Yealy DM, et al. A Prediction Rule to Identify Low-Risk Patients with Community Acquired Pneumonia. N Engl J Med 1997;336:243–250. TAB LE 17-3 0 EMPIRIC THERAPY FOR COMMUNITY-ACQUIRED PNEUMONIA PATI ENT CHARACTERISTICS ANTIBIOTIC TREATMENT OUTPATI ENT Previously healthy: No recent antibiotics Macrolide ∗ or doxycycline Recent antibiotic therapy Respiratory FQ † alone, or AM ‡ plus high-dose amoxicillin, or AM plus high-dose amoxicillin-clavulanate Comorbidities (COPD, DM, CHF, renal insufficiency, cancer): No recent antibiotics AM or respiratory FQ Recent antibiotic therapy AM plus beta-lactam § , or respiratory FQ alone Aspiration Amoxicillin-clavulanate or clindamycin Influenza with bacterial superinfection Beta-lactam or respiratory FQ INPATIENT FLOOR No recent antibiotics AM plus beta-lactam, or respiratory FQ alone Recent antibiotic therapy AM plus beta-lactam, or respiratory FQ alone depending on nature of recent antibiotics ICU Not at risk for Pseudomonas  Beta-lactam plus AM or respiratory FQ At risk for Pseudomonas Antipseudomonal beta-lactam ¶ plus ciprofloxacin, or antipseudomonal beta-lactam plus aminoglycoside plus respiratory FQ or macrolide Adapted from the Guidelines of the Infectious Diseases Society of America, 2003. ∗ Macrolide: erythromycin, azithromycin, clarithromycin. † Respiratory flouroquinolone: moxifloxacin, gatifloxacin, levofloxacin, gemifloxacin. ‡ Advanced macrolide: azithromycin, clarithromycin. § High-dose amoxicillin, high-dose amoxicillin-clavulanate, cefpodoxime, cefprozil, or cefuroxime.  Risk factors for Pseudomonas include severe structural lung disease, recent antibiotics, recent stay in the hospital. ¶ Piperacillin-tazobactam, imipenem, meropenem, cefepime. PULMONARY INFECTIONS 429 tool for admission. Strict interpretation could allow for hypoxic patients to be inappropriately treated as outpatients. No prediction rule can replace clinical judgment. Once disposition has been decided, empiric antibiotics should be initiated to cover both typical and atypical organisms, taking into consideration recent antibiotic use and risk factors (see Table 17-30). Pnuemococcal vaccine should be given every 5 years to patients who are older than 65, functionally or anatomically asplenic, and with chronic cardiac or pulmonary disease. Influenza vaccine should be given annually to patients older than 50 or with chronic diseases. Pulmonary Tuberculosis Tuberculosis (TB) is one of thetop ten diseases responsible for all-age mortality worldwide.With the presence of HIV, TB is an infectionto consider in immunosuppressed patients. Although TBusually attacks the lungs, it can affect almost any part of the body. Primary TB is usually a self-limited infection and may be asymptomatic. Reactivation TB usually occurs in the upper lobes of lungs. TABLE 17-31. PULMONARY TUBERCULOSIS. TABLE 17-32. SIDE EFFECTS OF COM MON ANTITUBERCULOSIS DRUGS. 430 CHAPTER 17 / THORACIC-RESPIRATORY DISORDERS TAB LE 17-3 1 PULMONARY TUBERCULOSIS LATENT TUBERCULOSIS REACTIVATION TUBERCULOSIS EPI DEMIOLOGY 1/3 world population infected with TB Prevalence currently at an all-time low in the USA after a peak in 1992 5% of latent TB activates within 2 yrs 5% of latent TB activates after 2 yrs 10% of HIV patients with latent TB develop active TB every year 80% of active TB is pulmonary tuberculosis; most of the remainder is lymphatic DIAGNOSIS Mantoux test: purified protein derivative (PPD) injected into volar surface of forearm, measured 48–72 h after injection Sputum acid-fast stain reveals acid fast bacilli, “red snappers” Sputum culture is the gold standard Area of induration (not erythema) for test to be considered Risk group: positive Low pretest probability— general population 15 mm Moderate pretest probability—health care workers, homeless, immigrants 10 mm High pretest probability—TB exposure, chest radiograph positive, or im- munosuppressed 5mm BCG vaccination status should not be considered when interpreting test results Anergy testing (e.g., with Candida) is no longer recommended [...]... 2003;361: 681 – 689 Rodrigo GJ, Rodrigo C, Hall JB Acute Asthma in Adults Chest 2004;125:1 081 –1102 Sack JL, Brock CD Identifying Acute Epiglottitis in Adults Postgrad Med 2002;112 :81 86 Schwartz LR, Balakrishnan C Thermal Burns In Tintinalli JE (ed.) Emergency Medicine 6th ed New York: McGrawHill, 2004, p 1221 Shores CG, Hackeling TA, Triana RJ Complications of Airway Devices In Tintinalli JE (ed.) Emergency Medicine. .. Table 1 8- 1 2) CARDIOVASCULAR DRUGS 453 — Digoxin-induced bidirectional ventricular tachycardia The EKG demonstrates the alternating QRS axis characteristic of bidirectional ventricular tachycardia and is nearly pathogenic for cardioactive steroid poisoning The 89 -year-old patient’s serum digoxin concentration was 4.0 ng/ml (Courtesy of Ruben Olmedo, MD, Mount Sinai School of Medicine. ) – F IGU R E 1 8- 3 ... metabolization process forms N-acetyl- p-benzoquinoneimine (NAPQI) Glutathione will convert NAPQI to other nontoxic APAP conjugates; however, glutathione stores are depleted during an overdose NAPQI is toxic to the liver and causes hepatic necrosis 440 CHAPTER 18 / TOXICOLOGIC EMERGENCIES – F I G U R E 1 8 - 1 — The Acetaminophen Rumack-Matthew nomogram for determining the risk of acetaminophen-induced hepatoxicity... (ed.) Emergency Medicine 6th ed New York: McGraw-Hill, 2004, p 85 4 El Oakley RTM, Wright JE Postoperative Mediastinitis: Classification and Management Ann Thorac Surg 1996;61:1030–1036 Ernst A, Feller-Kopman D, Becker HD, et al Central Airway Obstruction Am J Respir Crit Care Med 2004;169:12 78 1297 Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma 1997 NIH Publication No 98 0451... >50 nearly diagnostic of toxic alcohol poisoning The osmolar gap may diminish and an anion gap acidosis worsens as toxic alcohols are metabolized to their toxic organic acids (see Tables 1 8- 7 and 1 8- 8 ) TA B L E 1 8 - 7 TOXIC ALCOHOLS PATHOPHYSIOLOGY Ethanol r Breakdown of ethanol by ADH and Aldehyde DH leads to excess NADH r Excess NADH leads to ketoacidosis and impaired gluconeogenesis Isopropanol... TA B L E 1 8 - 6 SELECTED TOXIN AND ANTIDOTES INGESTION ANTIDOTE Acetaminophen N-acetylcysteine Ethylene glycol Ethanol or 4-methyl pyrazole Methanol Ethanol or 4-methyl pyrazole Anticholinergics Physostigmine Organophosphates Atropine, Pralidoxime (2-PAM) Warfarin Vitamin K Digoxin Fab fragments Beta blockers Glucagon Lead BAL, EDTA, DMSA Mercury BAL, penicillamine Arsenic BAL, DMSA, D-penicillamine... Emergencies 8th ed New York: McGraw-Hill, 2006, page 59, Figure 5-1 3 TA B L E 1 8 - 1 2 INDICATIONS FOR DIGIBIND INDICATIONS FOR DIGIBIND IN DIGOXIN TOXICITY K+ >5 mEq/L Cardiovascular collapse Co-ingestion of other drugs (beta blocker, calcium channel blocker) Ingestion of >10 mg acutely with cardiac compromise Digoxin levels >6 ng/mL with cardiac compromise Antihypertensives A N G I OT E N S I N - CO N... Ethambutol Red-green color blindness, peripheral neuropathy Streptomycin Ototoxic, nephrotoxic 432 CHAPTER 17 / THORACIC-RESPIRATORY DISORDERS TUMORS Breast, pulmonary and chest wall tumors may be diagnosed in the ED Table 1 7-3 3 summarizes relevant information for the emergency physician TA B L E 17 - 3 3 THORACIC–RESPIRATORY TUMORS TYPES OF TUMORS CLINICAL PRESENTATION DIAGNOSIS TREATMENT Small-cell carcinoma... Emergency Medicine 6th ed New York: McGraw-Hill, 2004, p 1501 Small PM, Fujiwara PI Management of Tuberculosis in the United States NEJM 2001;343: 189 –200 Snow V, Mottur-Pilson C, Gonzales R Principles of Appropriate Antibiotic Use for Treatment of Acute Bronchitis in Adults Ann Intern Med 2001;134:5 18 520 Vaughan DJ Pneumomediastinum February 9, 2005 www.emedicine.com Wise CW Major Causes of Musculoskeletal... indicate the need for N-acetylcysteine therapy With permission from Flomenbaum Neal E, Goldfrank Lewis R, et al Goldfrank’s Toxicologic Emergencies 8th ed New York: McGraw-Hill, 2006, page 527, Figure 34–2 Clinical Toxicity: There are four stages of toxicity: r Stage 1 (30 minutes–24 hours)—asymptomatic or mild symptoms with nausea, vomiting, malaise, anorexia r Stage 2 (24– 48 hours)—clinical and laboratory . sensitive, nor specific. The most common ECG finding is nonspecific ST-segment and T-wave abnormalities. D-dimer D-dimer negative D-dimer positive Low prestest probability: no PE No leg symptoms:. 2003;361: 681 – 689 . Rodrigo GJ, Rodrigo C, Hall JB. Acute Asthma in Adults. Chest 2004;125:1 081 –1102. Sack JL, Brock CD. Identifying Acute Epiglottitis in Adults. Postgrad Med 2002;112 :81 86 . Schwartz. JE (ed.). Emergency Medicine. 6th ed. New York: McGraw- Hill, 2004, p. 1221. Shores CG, Hackeling TA, Triana RJ. Complications of Airway Devices. In Tintinalli JE (ed.). Emergency Medicine. 6th