Adult and Pediatric Respiratory Emergency

1. Adult and Pediatric Respiratory Emergency Christopher Martella, DO FACOEP

2. Adult and Pediatric Respiratory Emergency • Discuss the differential diagnosis of Adult and Pediatric Respiratory Emergencies • Pathophysicology • Epidemiology • History • Physical findings • Treatments

3. Adult and Pediatric Respiratory Emergencies • DDX in Adults • HEENTAngiodema Anaphylaxis Pharyngeal infections Deep neck infections Foreign body Neck trauma Chest wall Rib fractures Flail chest Pulmonary COPD exacerbation Asthma exacerbation Pulmonary embolism Pneumothorax Pulmonary infection ARDS Pulmonary contusion or other lung injury Hemorrhage Cardiac ACS ADHF Flash pulmonary edema High output failure Cardiomyopathy Arrhythmia Valvular dysfunction Cardiac tamponade Neurological Stroke Neuromuscular disease • Toxic/metabolic Organophosphate poisoning Salicylatepoisioning CO poisoning Toxic ingestion Diabetic ketoacidosis Sepsis Anemia Acute chest syndrome Miscellaneous Hyperventilation Anxiety Pneumomediastinum Lung tumor Pleural effusion Intra-abdominal process Ascites Pregnancy Massive obesity

4. Adult and Pediatric Respiratory Emergencies • DDX in children • Respiratory tract Infection Epiglottitis Retropharyngeal abscess Peritonsillar abscess Croup Tracheitis Bronchiolitis Pneumonia Asthma Anaphylaxis Foreign body Upper airway Lower airway Esophageal • Biologic or chemical weapons • Chest wall/thoracic Chest wall deformity (eg, thoracic dystrophy, flail chest) Air leak (eg, tension pneumothorax) Mass lesion (eg, pulmonary sequestration, malignancy) • Cardiovascular Heart failure Cyanotic heart disease Pericarditis Cardiac tamponade Myocarditis • Nervous system Depressed ventilation (from ingestion, injury, or infection) Hypotonia (poor pharyngeal tone, ineffective respiratory effort) Loss of airway protective reflexes (aspiration) • Gastrointestinal Splinting from abdominal pain Abdominal distention Aspiration as the result of gastroesophageal reflux • Metabolic/endocrine Acidosis (eg, diabetic ketoacidosis, severe dehydration, sepsis) Hyperthyroidism Hypothyroidism • Hematologic Decreased oxygen carrying capacity (eg, severe anemia, methemoglobinemia) • Trauma Blunt or penetrating (eg, pneumothorax, pulmonary contusion) Inhalational injury (eg, airway burn, smoke inhalation)

5. Asthma History • Time of onset • Current medications • Recent use of beta 2 agonists • Risk factors for severe disease is ED visits, hospitalizations, ICU admits intubations, repeated courses of oral glucocorticoids, hx of intubation and food allergy

6. Asthma Physical findings Use of accessory muscles Brief fragmented speech Inability to lie supine Diaphoresis Agitation Cyanosis, depressed mental status, inability to maintain respiratory effort Pulmonary Index in pediatrics patients I to E ratio Pulus paradoxus

11. Asthma Clinical finding Hypoxia -nearly all asthma patients have hypoxia as a result of V/Q mismatch. Beta 2 agonist may worsen this mismatch by causing pulmonary vasodilation in areas of the lung that are poorly ventilated Marked hypoxia PO2<60 SaO2<90 Infrequent but potential cause of complications and death. Recommendations for continuous Pulse ox monitoring for patients with PEFR <40 % of baseline Hypercapnia (ABG) Asthma patients are usually tachynic therefore normal or high PaCO2 could be an ominous sign Chest x-ray rarely helpful unless patient with fever suspected PTX Labs not helpful

12. Asthma Treatment for Adult patient • Oxygen to maintain SaO2 >92% • Inhaled beta agonist Albuterol 2.5-5.0 mg neb x 3 q 20 minutes then 1-4 hours as needed or MDI w/ spacer 4 puffs q 10 min or 8 puffs q 20 min for up to 4 hours then 1-4 hours as needed • Critically ill patients continuous neb 10-15 mg over one hour • IV hydration NSS bolus to replace insensible losses Nebs vs MDI essentially no difference and MDI maybe better

13. Asthma Ipratopium 500mcg neb q 20 minutes for three doses, then as needed or 8 puffs via MDI q 20 min then as needed for up to 3 hours. Usually reserved for severe obstruction failing to improve despite beta agonists

14. Asthma Systemic glucocorticoids Speeds rate of recovery with patients with persistent wheezing despite intensive bronchodilator therapy likely secondary to airway flow obstruction due to airway inflammation and intraluminal mucous plugging Current guidelines encourage early systemic glucocorticoids for all patients who have a moderate (PEFR of < 70%) or severe exacerbation ( PEFR<40%)

15. Asthma Systemic glucocorticoids Optimal dose unknown Corticosteroids: give methylprednisolone 60-125 mg IV or prednisone 40-60 mg po; alternatives include: dexamethasone 6-10 mg IV or hydrocortisone 150-200 mg IV; steroids may be given IM or orally if IV access is unavailable PO absorbed rapidly with similar bioavailability to IV IV dosing can be used for vomiting or severely ill patients IM as effective as PO Duration rough guide 10-14 days for severe attacks Tapering is not necessary

16. Asthma • Magnesium • IV MGSO4 has a bronchodilator activity possibly due to inhibition of calcium influx into airway smooth muscle cells • Routine use does not seem to confer significant benefit beyond beta agonists and systemic glucocorticoids, MgSO4 is suggested for patients who have life-threatening exacerbations • Dose 2 gm over 20 minutes

17. Asthma • Nonstandard therapies • Helium-oxygen • Leukotriene receptor antagonist • BiPAP • Terbutaline 0.25 mg SC q 20 minx 3 doses • Epinephrine 0.2-0.5 ml 1 :1000 SC Ineffective therapies Methylxanthines Inhaled glucocorticoids Empiric antibiotics

18. Asthma Treatment in Peds Similar approach to adults Levalbureol vs Racemic albuterol Dosing Parental beta 2-agonist Epinephrine and Terbutaline

20. Asthma • Parental beta 2-agonist Epinephrine and Terbutaline May be superior to inhaled beta 2-agonists for children with severe exacerbations and poor inspiratory flow or anxious young children who are uncooperative with or have suboptimal response to initial aerosolized therapy. The intramuscular route may provide for more rapid drug absorption, although direct comparisons are lacking. In this setting, terbutaline may be expected to produce fewer adverse effects than epinephrine.

21. CHF Heart failure (HF) is a common clinical syndrome representing the end-stage of a number of different cardiac diseases. It can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. There are two mechanisms by which reduced cardiac output and HF occur: Systolic dysfunction Diastolic dysfunction.

22. CHF The New York Heart Association's classification: Class I describes a patient who is not limited with normal physical activity by symptoms. Class II occurs when ordinary physical activity results in fatigue, dyspnea, or other symptoms. Class III is characterized by a marked limitation in normal physical activity. Class IV is defined by symptoms at rest or with any physical activity.

23. CHF • Frequency • United States • More than 3 million people have congestive heart failure (CHF), and more than 400,000 new patients present yearly. The prevalence rate of CHF is 1-2%. • Mortality/Morbidity • Approximately 30-40% of patients with congestive heart failure (CHF) are hospitalized every year. • CHF is the leading diagnosis-related group (DRG) among hospitalized patients older than 65 years. • 5-year mortality rate after diagnosis was reported in 1971 as 60% in men and 45% in women. In 1991, data from the Framingham heart study showed the 5-year mortality rate for CHF essentially remaining unchanged, with a median survival of 3.2 years for males and 5.4 years for females. • The most common cause of death is progressive heart failure, but sudden death may account for up to 45% of all deaths. Patients with coexisting insulin-dependent diabetes mellitus have a significantly increased mortality rate.

24. CHF • Race • Blacks are 1.5 times more likely to die of CHF than whites are. Nevertheless, black patients appear to have similar or lower in-hospital mortality rates than white patients. • Sex • Prevalence is greater in males than in females in patients aged 40-75 years. • No sex predilection is noted among patients older than 75 years. • Age • Prevalence of CHF increases with increasing age and affects about 10% of the population older than 75 years.

25. CHF • Causes • The most common cause of heart failure is coronary artery disease, • Other disease processes include • hypertension, • valvular heart disease • congenital heart disease • myocarditis and infectious endocarditis. • CHF is often precipitated by cardiac ischemia or dysrhythmias, cardiac or extracardiac infection, pulmonary embolus, physical or environmental stresses, changes or noncompliance with medical therapy, dietary indiscretion, or iatrogenic volume overload. • One also must consider systemic processes such as pregnancy and hyperthyroidism as precipitants of CHF.

26. CHF • History • Anxiety • Dyspnea at rest • Dyspnea upon exertion: This has been found to be the most sensitive symptom reported, yet the specificity for dyspnea is less than 60%. • Orthopnea and paroxysmal nocturnal dyspnea the sensitivity for orthopnea and PND is only 20-30% but specificity 74-80%. • Cough: Cough that produces pink, frothy sputum is highly suggestive of congestive heart failure (CHF). • Edema • Nonspecific symptoms • Weakness • Lightheadedness • Abdominal pain • Malaise • Wheezing • Nausea

27. CHF • Physical Findings for the vet with Acute decompensated heart failure (ADHF) • Displaced Apical Pulse most sensitive and specific of all physical findings of Systolic HF. Apical impulse laterally displaced past midclavicular line • Peripheral edema, jugular venous distention, and tachycardia are highly predictive of congestive heart failure (CHF). specificity of physical examination reported at 90% • Tachypnea, using accessory muscles of respiration, has been observed. • Hypertension may be present. • Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle [LV] function) may be observed. • The skin may be diaphoretic or cold, gray, and cyanotic. • Jugular venous distention (JVD) is frequently present. • Wheezing or rales may be heard on lung auscultation. • Cardiac auscultation may reveal aortic or mitral valvular abnormalities (S3 or S4). • Lower extremity edema may also be noted, especially in the subacute process.

28. CHF Work up Labs Chem 7, CBC, Cardiac enzymes, BNP ABG levels may be of benefit in evaluation of hypoxemia, ventilation/perfusion (V/Q) mismatch, hypercapnia, and acidosis. ECG nonspecific tool but may be useful in diagnosing concomitant cardiac ischemia, prior myocardial infarction (MI), cardiac dysrhythmias, chronic hypertension, and other causes of left ventricular hypertrophy ECHO Emergency transthoracic echocardiography may help identify regional wall motion abnormalities as well as globally depressed or myopathic left ventricular function. ECHO may help reveal cardiac tamponade, pericardial constriction, and pulmonary embolus. ECHO is also useful in revealing valvular heart disease, such as mitral or aortic stenosis or regurgitation.

29. CHF Work up CXR Chest radiography is the most useful tool diagnostic tool. A recent study showed that 1 out 5 patients admitted to the hospital with CHF lacked signs of congestion on chest radiograph. • Cardiomegaly may be observed with a cardiothoracic ratio greater than 50%. Pleural effusions may be present bilaterally or if they are unilateral more commonly observed on the right. • Early CHF may manifest as cephalization of pulmonary vessels, generally reflecting a pulmonary capillary wedge pressure (PCWP) of 12-18 mm Hg. As the interstitial fluid accumulates, more advanced CHF may be demonstrated by Kerley B lines (PCWP is 18-25 mm Hg). • Pulmonary edema is observed as perihilar infiltrates often in the classic butterfly pattern, reflecting a PCWP of more than 25 mm Hg. • Several limitations to chest radiography are observed when attempting to diagnose CHF. Classic radiographic progression is often not found, and as much as a 12-hour radiographic lag from onset of symptoms may occur. In addition, radiographic findings frequently persist for several days despite clinical recovery.

36. CHF • Treatment depends on • Acuity of presentation • Volume status • Systemic perfusion • As always in Every ER lecture ABC’s • Noninvasive positive pressure Ventilation • Endotracheal intubation

37. CHF Treatment Acute Decompensated Heart Failure HOSPITALIZATION — Hospital admission is recommended for patients with ADHF with the following clinical conditions: • Hypotension • Worsening renal function • Altered mentation • Dyspnea at rest • Also consider hospitalization for: Worsened congestion, even if without dyspnea; typically reflected by a weight gain of ≥5kg Signs and symptoms of pulmonary or systemic congestion, even in the absence of weight gain Major electrolyte disturbance Associated comorbid conditions such as pneumonia, pulmonary embolus, diabetic ketoacidosis, or symptoms suggestive of TIA or stroke Repeated ICD firings Previously undiagnosed HF with signs and symptoms of systemic or pulmonary congestion High BNP levels Poor compliance or ability to manage symptoms as an outpatient

38. CHF • Acute Pulmonary edema with normal or elevated BP • Sublingual NTG 0.4 mg q minute until reduction of BP or improvement of symptoms. IV NTG gtt can be used with rapid titration to 200ug/min or higher • IV Nitroprusside or Nesirtidemay can be used as an alternative • Diuretics IV Furosemide (40mg ) or bumetanide(1-3 mg) Ethacrynic acid (50mg) for sulfa allergy • Morphine 2-5 mg IV venodialtor • Contraindication to Vasodilators Right Ventricular MI, AS, Hypertrophic Cadiomyopathy • Goal of therapy in HCM with Pulmonary edema is to decreasing outflow gradient by slowing the hear in the ICU

39. CHF • Decompensated HF • Stable vitals, adequate oxygenation with symptoms i.e. SOB, DOE, JVD orthopnea and S3 • Usually do well with Diuresis, O2 and BP control

40. CHF Beta-blockers, particularly carvedilol, have been shown to improve symptoms in patients with moderate-to-severe heart failure. However, the role of beta-blockers in the acute setting is currently unclear; limit use until hemodynamic studies indicate that further deterioration is not possible.  Digoxin has no place in the treatment of acute HF Potassium sparring diuretics such as Spironolactone are generally reserved for class III or IV HF, aggressive use could result in hypokalemia Nitroprusside Cardiac steal syndrome Angiotensin-Coverting Enzyme Inhibitor

41. CHF • Drugs to aviod • Calcium channel blockers may result pulm edema and cardigenic shock secondary to negative inotropic effects • NSAIDS inhibits effects of ACEI and diuretics • Antiarrhythmics HFf patients are sensitive to pro-arrhythic and cardiodepressent effects

42. CHF • Pediatric • Most common cause is Congenital Heart Disease and dx in first 4 weeks of life • Masquerades or co-exists with pneumonia or sepsis • Symptoms poor feeding, weak cry, grunting and nasal flaring, diaphoresis, lethargy, poor weight gain, Murmur

43. CHF/Peds DDX of CHF based upon age Age Spectrum 1 min anemia, acidosis, hypoxia, hypoglycemia, 1 hour hypocalcemia, sepsis 1 day PDA 1 week hypoplastic L verntricle 2 weeks Coarctation 1 month VSD 3 months SVT 1 year Myocarditis, Cardiomyopathy, severe anemia 10 year Rheumatic fever

44. Pulmonary Embolus DEFINITIONS — PE refers to obstruction of the pulmonary artery or one of its branches by material (eg, thrombus, tumor, air, or fat) that originated elsewhere in the body Classification Acute or Chronic Submassive or Massive which is defined as causes hypotension, defined as a systolic blood pressure <90 mmHg or a drop in systolic blood pressure of ≥40 mmHg from baseline for a period >15 minutes NATURAL HISTORY — Untreated PE is associated with a mortality rate of approximately 30 percent. Recurrent embolism is the most common cause of death.

45. Pulmonary Embolus PROGNOSIS RV dysfunction — RV dysfunction due to PE predicts increased PE-related mortality Brain natriuretic peptides (BNP)  — An elevated BNP or N-terminal pro-brain natriuretic peptide (NT-proBNP) predicts RV dysfunction and mortality, according to three meta-analyses RV thrombus have a higher 14-day mortality

46. Pulmonary Embolus PATHOPHYSIOLOGY — Most PE arise from thrombi in the deep venous system of the lower extremities. However, they may also originate in the right heart or the pelvic, renal, or upper extremity veins. It is estimated that 50 to 80 percent of iliac, femoral, and popliteal vein thrombi Fortunately, most calf vein thrombi resolve spontaneously and only 20 to 30 percent extend into the proximal veins if untreated

47. Pulmonary Embolus SYMPTOMS / SIGNS Dyspnea most common symptoms were at rest or with exertion (73 percent), Pleuritic pain (44 percent) cough (34 percent) >2-pillow orthopnea (28 percent) Calf or thigh pain (44 percent) Calf or thigh swelling (41 percent) Wheezing (21 percent) Tachypnea (54 percent) Tachycardia (24 percent), Rales (18 percent), Recreased breath sounds (17 percent), Accentuated pulmonic component of the second heart sound (15 percent)

48. Pulmonary Embolus • Laboratory — Routine laboratory findings are nonspecific. They include leukocytosis, an increased ESR, and an elevated serum LDH or AST (SGOT) with a normal serum bilirubin. • Arterial blood gas (ABG) measurements and pulse oximetry have a limited role in diagnosing PE • The typical arterial blood gas findings are not always seen • Hypoxemia can be minimal or absent. A PaO2 between 85 and 105 mmHg exists in approximately 18 percent of patients with PE. • Up to 6 percent may have a normal alveolar-arterial gradient for oxygen. Troponins, BNP, ECG, CXR V/Q Lower Extremity Ultrasound

49. Pulmonary Embolus • D-dimer — D-dimer is a degradation product of cross-linked fibrin. It can be detected in serum using a variety of different assays: • Enzyme-linked immunosorbent assay (ELISA) (results in >8 hrs) • Quantitative rapid ELISA (results in 30 min) • Semi-quantitative rapid ELISA (results in 10 min) • Qualitative rapid ELISA (results in 10 min) • Quantitative latex agglutination assay (results in 10 to 15 min) • Semi-quantitative latex agglutination assay (results in 5 min) • Erythrocyte agglutination assay (SimpliRED) (results in 2 min) Angiography — Pulmonary angiography is the definitive diagnostic technique or "gold standard" in the diagnosis of acute PE. It is performed by injecting contrast into a pulmonary artery branch after percutaneous catheterization, usually via the femoral vein. A filling defect or abrupt cutoff of a small vessel is indicative of an embolus. A negative pulmonary angiogram excludes clinically relevant PE. Spiral CT  98 percent of patients with PE were detected by CT-PA The frequency of negative CT-PA among patients without PE was more consistent, around 90 percent

50. Pulmonary Embolus • Wells criteria • PE is unlikely (score ≤4) or likely (score >4). The modified Wells Criteria include the following : • Clinical symptoms of DVT (3 points) • Other diagnoses less likely than PE (3 points) • Heart rate >100 (1.5 points) • Immobilization ≥3 days or surgery in previous four weeks (1.5 points) • Previous DVT/PE (1.5 points) • Hemoptysis (1 point) • Malignancy (1 point)