Approach to Acute Respiratory Problems

1. Approach to Acute Respiratory Problems Royal Victoria Hospital Stéphane Beaudoin Respirology Resident PGY5

2. Objectives • To help residents develop an effective approach to the evaluation of dyspnea and hypoxia • To help residents become more familiar with the management of common acute respiratory emergencies • Acute severe asthma • Massive hemoptysis • Pneumothorax

3. Approach to Dyspnea: some Pearls • Dyspnea is a complex subjective sensation • Dyspnea ≠ tachypnea • Dyspnea ≠ hypoxemia • Dyspnea must be differentiated from • Pain • Fatigue • Weakness, deconditioning • Hence, a complaint of dyspnea must be qualified and quantified • Departure from baseline and progression in time • Specific impairments • Use of a standardized scale: MRC, NYHA

4. MRC Dyspnea Scale

5. Combined Approach to Dyspnea • Respiratory • Upper airways • Anaphylaxis / Foreign body / tumor • Vocal cord dysfunction • Lower airways • Anaphylaxis / Foreign body / tumor • Bronchospasm / exacerbation of obtructive lung disease / toxic inhalation / infection • Chest wall / Pleura • Effusion / tumor / PTx • Parenchyma • Infectious, inflammatory, neoplastic disorder / CHF • Vasculature • PE, chronic pulmonary HTN • Cardiovascular • CHF, arrhythmia, effusion/tamponade, valvvular dysfunction • Shock • Metabolic • Anemia / metabolic acidosis / intoxications • Other • Pregnancy • Pain, anxiety • Hyperventilation • Neuromuscular disorders

6. The 6 Causes of Hypoxemia • Low O2 content of inspired gas • High altitude • V/Q mismatch • Alveolar filling or airway obstruction or vascular anomalies • Shunt • Pulmonary (AVM, lobar / lung collapse) or extra-pulmonary (PFO) • Hypoventilation • Central, neuromuscular, myopathic, obesity, chronic lung disease • Low DLCO • Interstitial lung disease, Pulm HTN • Low Mixed Venous O2 sat % • Shock / low output state

7. V/Q mismatch and hypoxemia

8. The A-a Gradient • The efficiency of gas exchange can be assessed by comparing the measured arterial oxygen pressure (PaO2, via ABG) to the hypothesized ideal or maximal alveolar oxygen pressure • A-a gradient = PAO2- PaO2 • PAO2 = [FiO2 x (Patm- PH20)] – (PACO2 / RQ) • Under conditions of normal gas exchange (no V/Q anomalies / minimal shunt and normal DLCO), the difference between those is small • A normal A-a gradient in the face of hypoxemia narrows the differential to: • Low inspired O2 content • Hypoventilation • Limitations • Normal or expected A-a gradient varies with age: • A-a gradient = 2.5 + (0.21 x age) • FiO2, RQ, PH2O are imprecise in most clinical situations and the full equation is actually more complex • At high FiO2, the expected A-a gradient increases, but the exact magnitude is difficult to establish ( hence less reliable when high FiO2 used)

9. Approach to Hypoxemia • ABC’s, iv access, O2, monitoring • Airway difficulty assessment • Clinical assessment • Relevant history • Meticulous physical exam • CXR • ABG for pCO2 and A-a gradient

10. Acute Severe Asthma

11. Acute Severe Asthma • Predictors of a life-threatening attack • Prior ICU stay or intubation / ≥ 2 hospitalizations or > 3 ER visits in past year • Poor perception of symptoms by pt • Frequent use of relief bronchodilators • Low SES / Psychiatric illness, drug use • Cardiovascular or respiratory comorbidities • “All that wheezes is not asthma”! • DDx • CHF / bronchiolitis / toxic inhalation • Foreign body aspiration / tumor / anaphylaxis • PE, pneumonia, PTx • Vocal cord dysfunction • Hyperventilation • Flow rates are absolutely required for diagnosis and are the best method to follow the evolution of an attack

12. Acute Asthma • ABC’s, iv, O2, monitoring • Airway difficulty assessment • Clinical Assessment • Markers of severity • Silent chest • Pulsus paradoxus • Hypoxemia / hypercapnia (beware of normocapnea) • RR > 25-30 / HR >110 / inability to speak • FEV1 < 30% predicted • CXR is of low yield (done to exclude complications or alternative diagnoses) • Flow rates are absolutely required for diagnosis and are the best method to follow the evolution of an attack • ABG should be done if hypoxemia is present, in cases of severe distress, or if admission is contemplated

13. Acute Asthma: Management • Criteria for admission: • Presence of risk factors for life-threatening attack • Pre-therapy FEV1 < 25% • Post-therapy FEV1 < 40% • Hypoxemia / persistent markers of severe attack • Bronchodilator use more frequent than q 4hr • The “GBS” indicator… • A mild attack is defined by: • Mild symptoms • the absence of markers of severity • the normalization of flow rates post initial therapy • salbutamol use less than q 4h • A mild exacerbation can be treated with a four-fold increase in ICS dose or a course of oral steroids ( as part of a written action plan)

14. Acute Asthma: Management • Bronchodilators: MDI with spacer as effective as nebulized… • Salbutamol • MDI: 4-8 puffs q 20 min then q 1h • Neb: 2.5-5 mg q 20 min then q 1h • Ipratropium: provides an added bronchodilator effect acutely • MDI: 4-8 puffs q 20 min then q 1h • Neb: 500 mcg q 20 min then q1 h • Corticosteroids: dosing is controversial, but 40-60 mg likely sufficient • Route: po is equivalent to iv and is preferred unless pt is vomiting • Duration: 7-14 days, no taper • Need for higher iv doses in ICU pts is not clear • Magnesium sulfate • May provide a modest additional bronchodilation, but its impact on outcome is not clear • Most effective in severe airflow limitation, if response to bronchodilators is poor • Methylxanthines have no role in acute setting • The use of Heliox is controversial

15. Acute Asthma: Management • NIPPV • Very limited data; a cautious and supervised trial is reasonable • Intubation: • no clear decision rule; global clinical picture and progression should be used as guide • Can induce laryngospasm or worsened bronchospasm • Can cause marked hypotension • Ketamine is a good induction agent due to its bronchodilator effects • Ventilation strategies • Ensure adequate sedation (and paralysis if necessary) • The goal is normalization of gas exchange and reduction of the barotrauma risk • Low RR 6-10/ min / I:E ratio >2 / high inspiratory flow rates • Low Vt :max 8cc / kg • Cautious use of PEEPe: 50-80% of PEEPi (esp if spontaneous mode used)

16. The 5 Commandments of Asthma • Identify and address potential triggering factors • URTI, non-compliance, smoking, irritant exposure, allergies, NSAIDS, beta-blockers • Review and optimize puffer technique • Prescribe ICS to all pts • Educate pt about his illness • Vaccinate for Influenza at least

17. Massive Hemoptysis

18. A case • 62 F known for some “chronic lung disease” • Presented with ~ 180 cc of fresh hemoptysis over 1.5 day, in context of purulent secretions and worsened dyspnea (MRC 2→3)

19. Massive Hemoptysis

20. Massive Hemoptysis

21. Massive Hemoptysis • Definition is controversial: 100 cc/24h to 1,000 cc/24h • Rate of bleeding should also be considered • Consequences such as hypoxemia, need for admission / intubation should also be considered • Only 5-15% of all hemoptysis cases are considered massive • Mortality is significant • Up to 38% in recent studies • Significant epistaxis and UGI bleed must first be excluded • The importance of the little cup…

22. Massive Hemoptysis • Etiology: relative frequencies vary considerably based on center/population • Most common causes: • Bronchiectasis • TB • Mycetoma • Lung Malignancy • Diffuse alveolar hemorrhage (hemoptysis can be minimal) • Idiopathic • Others • Anatomic origin • Bronchial arteries → 90% • Non-bronchial arteries → 5 % • Pulmonary vessels → 5 %

23. Massive Hemoptysis • Management Goals: • Stabilize the respiratory and hemodynamic status • Identify the site of bleeding • Identify the cause of bleeding • Treat the underlying cause and / or perform active procedures to abort bleeding • In palliative situations: • Relieve anxiety, dyspnea, psychological distress • Green surgical towels and morphine iv

24. Massive Hemoptysis • ABC’s, iv access, O2, monitoring • ICU admission • Correct coagulopathy and hemodynamics • X-match and keep units in reserve • Focused Hx and physical exam • CXR / CT with angio protocol (aortogram) • Bronchoscopy: goal is localization of bleeding • Timing is controversial • Bronchoscopic interventions are temporizing at best

25. Massive Hemoptysis: Management • Supportive care is crucial • Bleeding side down (lateral decubitus) • Intubation required if resp failure is present or if very large amount of blood expectorated • Largest ETT possible • Seek help for selective intubation with either single or double-lumen tube (if bleeding side known) • Otherwise immediate bronchoscopy for localization and airway clearance • First line definitive procedure is Bronchial Artery Embolization • Surgery now reserved for refractory cases despite multiple embolizations, trauma, PA rupture, mycetoma

26. Bronchial Artery Embolization

27. Massive Hemoptysis: Special Case • 83 M 3 hrs post CABG x 3, MAZE, redo MVR, TV ring annuloplasty • Called for large amount of fresh blood coming from ETT • What is the cause? • What should be done?

28. Pneumothorax

29. 18 M with chest pain and mild dyspnea for 1 week

30. Review of Physiology • Under normal conditions, the tendancy of the lung to collapse and the tendancy of the chest wall to expand produce a negative pressure in the pleural space • This acts as a vacuum (or recoil pressure) that keeps the lung and the chest wall in close proximity and prevents lung collapse (due to principle of transmural pressure) • When the pleural space is disrupted and the pressure is allowed to equilibrate with atmospheric pressure, this recoil pressure is altered (or even eliminated) • The lung and the chest wall tend to return to their resting positions

31. Classification • Spontaneous Primary PTx: in a patient without apparent underlying pulmonary disease • Thought to be caused by the rupture of an air-containing space within or in vicinity to the visceral pleura, usually at the apex • Although patients have no apparent underlying lung disease, up to 80% have blebs or bullae on CT examination • Male sex, smoking, tall stature, and genetics are risk factors • Recurrence rate of 39% in ipsilateral lung and 15% in contralateral lung • Spontaneous Secondary PTx: in a patient with underlying pulmonary disease • Almost any lung condition can be associated with the development of a PTx • COPD is by far the most common etiology nowadays • Although the exact mechanism varies, the principles underlying the development of primary PTx are likely also playing a role (exacerbated by airway/parenchymal inflammation and architecture disruption) • Recurrence rates are usually higher and depend on the underlying etiology • Traumatic Pneumothorax (including iatrogenic)

32. Pneumothorax: Clinical Features • History: • Acute onset of pleuritic chest pain, usually at rest, +/- dyspnea • Symptoms can be out of proportion to the extent of lung collapse, especially in secondary pneumothorax where the reserve is limited • Trauma (even blunt) to exclude • Physical Exam: • Hypoxemia Severe hypoxemia due to shunting rare in primary PTx ≤25% • Major alterations in vitals usually only seen in tension PTx • Hyperexpanded hemithorax with ↑resonance, yet ↓excursion, ↓ vesicular sounds and fremitus • Contralateral tracheal deviation; s/c emphysema • Hamman sign: clicking/crunching sounds with heart beats influenced by position and respiration

33. Tension Pneumothorax • Tension PTx is a clinical diagnosis • Evidence of sudden deterioration in a patient known to have a PTx or highly suspected of having one should prompt initiation of therapy • severe hypoxemia, tachycardia, contralateral tracheal shift, ↑ JVP, shock • Radiologic signs are not specific • Caused by a one-way valve phenomenon producing a positive pleural pressure during most of the resp cycle • Main consequence is reduction of venous return/ cardiac output • Treatment consists of oxygen administration and immediate needle aspiration in 2nd ICS at mid-clavicular line and insertion of a chest tube

34. Radiological Diagnosis • A standard erect PA CXR is sufficient • Expiratory views are only marginally more sensitive and are not recommended for routine use • A sharply demarcated white pleural line without lung markings lateral to it is diagnostic • Mimickers: skin fold, tubings, ribs • Use of expiratory views /lateral decubitus views if unclear • A pleural effusion is present in up to15-25% of cases (usually an eosinophilic pleuritis in reaction to the presence of air; rarely hemorrhagic) • Supine patients • Deep sulcus sign / upper quadrant lucency / ↑sharpness of cardiac border or hemidiaphragm • CT scan recommended only if: • Diagnosis suspected despite normal CXR • To better define underlying disorder

35. Pneumothorax in a supine patient

36. Pneumothorax Size Estimation • Several quantification/measurement methods exist, and none is perfect • Most show good correlation, but poor agreement • Standard is measurement by CT volumetrics • Size estimation methods • Light Index % PTX = 1 – (lung diamater3/hemithorax diameter3) • Rhea Method % PTx determined by plotting the average of 3 interpleural distances on a nomogram • Collins Method % PTX = 4.2 + [4.7 x ( sum of interpleural distances)]

37. Pneumothorax Size Estimation • Measurement methods proposed by the BTS and ACCP to classify PTx as small/ large • ACCP: large defined as ≥ 3cm apex to cupola • BTS: large defined as > 2cm lung to chest wall at hilar level From MacDuff et al.Management of spontaneous pneumothorax: BritishThoracic Society pleural disease guideline 2010. Thorax 2010;65(Suppl 2):ii18eii31. figure 1

38. Management • Good quality evidence to guide clinical decision making is lacking • Data from available evidence difficult to compare due to the use of: • Different measurement methods • Different definitions/ decision thresholds • Guidelines produced by the BTS and the ACCP as well as recommendations from major textbooks differ in many apsects and are largely based on expert consensus • Nevertheless, there has been a shift towards more conservative initial treatment and reliance on patient’s status rather than PTx size • In general, treatment is more aggressive in secondary PTx cases

39. Management: Initial Therapy • All sources agree that asymptomatic patients with small PTx (primary or secondary) should be managed conservatively and observed • The exact observation period and the follow up schedule is not well-established ( the ACCP recommends 3-6hrs of observation and f/u CXR the next day) • Unless contraindicated, all patients should receive high concentration oxygen therapy • Can lead to a 4-fold increase in the reabsorption rate • Smoking cessation is of crucial importance

40. Question • How long does it take for a 25% PTx to resolve? • The reabsorption rate varies from 1.25-2.2% of a hemithorax volume per day • Hence it would take 12-13 d to resolve completely!

41. Management of Primary PTx • For large primary spontaneous PTx, opinions differ • ACCP: Drainage via pigtail or chest tube • Connected to either a water-seal system or a Heimlich valve • Reliable patients with good re-expansion can be discharged • BTS: Drainage only if symptomatic • Via needle aspiration (effective in ~ 60%) • Pigtail if aspiration fails or > 2.5L aspirated

42. Management of Secondary PTx • For asymptomatic patients with large PTX or symptomatic patients with PTx of any size, opinions again differ • ACCP: Drainage with chest tube (pigtail acceptable) • BTS: Drainage with pigtail (aspiration less effective) • For asymptomatic patients with small PTx, initial observation is recommended

43. 55 M post TTNA

44. 65 F with DAH, post IJ line…

45. Post-resolution Management • Return to normal activities allowed when free of symptoms • Return to contact sports/ heavy exercise upon complete resolution of PTx • Air travel recommendations (BTS guidelines) • No evidence that air travel precipitates recurrence • If no surgery is performed, patients may wish to wait one year given that most recurrences occur ≤ 1yr • If surgery is performed, travel is safe upon recovery • Waiting at least one week after CXR resolution is recommended (2 weeks if traumatic) • Diving recommendations (BTS guidelines) • Presence of blebs/bullae are a contra-indication • Previous spontaneous PTx is a contra-indication unless a bilateral surgical pleurectomy performed with normal lung Fx and CT post op

46. Summary • An affective approach to dyspnea / hypoxemia is the key to an accurate diagnosis • The management of asthma starts by the exclusion of alternative diagnoses, risk stratification, and early bronchodilator and corticosteroid therapy • The management of massive hemoptysis consists of patient stabilization, localization of the bleeding and identification of its cause, all leading to definitive interventions • The management of a pneumothorax depends on its type, its size and its clinical consequences • A tension PTx is a clinical diagnosis and required prompt intervention

47. Useful References • 2010 CTS Asthma Guidelines • 2010 GINA Asthma Guidelines • Analytic review: management of life-threatening asthma in adults. Mannam P, MD Siegel. Journal of intensive Care Medicine 2010. • Massive Hemoptysis: An update on the role of bronchoscopy in diagnosis and management. Sakr L, Dutau H. Respiration 2010. • 2010 BTS guidelines for Pneumothorax Evaluation & Management