D. P. Laporta MD presented to McGill Residents D. P. Laporta MD Departments of Adult Critical Care and Medicine, Sir MB Davis Jewish General Hospital McGill University presented to McGill Residents Critical Care (January 2000) Pulmonary (July July 2000

MASSIVE HEMOPTYSIS REFERENCES Bone: Pulmonary & Critical Care Medicine, 1998 ed., 1998 Mosby-Year Book, Inc. Ch R19 Massive Hemoptysis Ch M10 Pulmonary Hemorrhage Syndromes Jean Baptiste E «clinical Assessment and management of massive hemoptysis Crit Care Med 2000; 28: Dweik RA, Stoller JK. Role of bronchoscopy in massive hemoptysis, in : Flexible bronchoscopy in the 21st century. Clin. Chest Med. 1999; 20(1) March White R. Jr. Bronchial Artery Embolotherapy for Control of Acute Hemoptysis. Analysis of Outcome. Chest 1999; 115(4) April Fanburg BL et al, Case : A 17-Year-Old Girl with Massive Hemoptysis and Acute Oliguric Renal Failure. NEJM Weekly CPC. 1993; 329(27)

MASSIVE HEMOPTYSIS NATURAL HISTORY AND PROGNOSIS §MORTALITY Immediate : 7% of 113 patients who presented with massive hemoptysis died soon after onset. Etiology : TB 18.6%, CF 32%, Other 10% §DURATION If survive the initial episode, bleeding stops <3-6 days §RECURRENCE RATE 20-46% after bronchial embolization

MASSIVE HEMOPTYSIS Prognostic Features Associated with Death bleeding exceeding 1000 mL/24 h 600 mL of hemoptysis in <4 hours71%mortality 4-16 hous22% hours5% hemodynamic instability CXR evidence of aspiration bilateral bleeding sources inability to localize source of bleeding caused by a neoplasm inadequate pulmonary function debilitated states, and metastatic cancer MORTALITY 80 % if > 1L/24 h PLUS malignancy

OverestimateUnderestimate 400 ml = abN gas XC

Hemoptysis: is it real ? §GI §Factitious (Munchausen ’s) §Pseudo:drugs (RFP, clofazimine) §Serratia pneumonia §ENT

Bronchial Circulation §Come directly or indirectly from the aorta (T3-8) §Variability

Nonbronchial Nonbronchial systemic collateral arteries §in 45% of patients with hemoptysis §commonly: intercostal, subclavian, axillary & phrenics §uncommonly: IMA, thyrocervical, carotid, coronaries §Because of the many systemic arteries involved, routine arteriographic localization cannot be all-inclusive

MASSIVE HEMOPTYSIS ETIOLOGY (1) Infectious (bacterial, mycobacterial, viral, fungal, parasitic) Lung abscess Bronchiectasis (including cystic fibrosis) Mycetoma (e.g., aspergilloma) Infected BP Sequestration Septic emboli Infected aortic graft Neoplasm Malignant Bronchogenic Metastasis from pulmonary/extrapulmonary Benign (bronchial adenoma)

MASSIVE HEMOPTYSIS ETIOLOGY (2) Foreign body/trauma Aspirated foreign body Broncholith Tracheovascular fistula Trauma, Brachytherapy, Laser Cardiac/pulmonary vascular Pulmonary venous HTN Mitral stenosis, PVOD (Pulmonary embolus) Pulmonary artery Perforation (complicating Swan-Ganz catheter) Aneurysm/false (mycotic, Behcet’s, Hughes-Stovin) Arteriovenous malformations OWR, DieuLaFoye Fistulae (every vessel parring through the thorax)

MASSIVE HEMOPTYSIS ETIOLOGY (3) Alveolar hemorrhage Goodpasture's syndrome Systemic vasculitides/collagen vascular diseases…capillaritis Behcet's syndrome Essential mixed cryoglobulinemia, Henoch-Schonlein purpura Progressive systemic sclerosis Rheumatoid arthritis, Systemic lupus erythematosus, Mixed connective tissue disease Systemic necrotizing vasculitis, Wegener's granulomatosis Other Glomerulonephritis Immune complex associated glomerulonephritis Pauci-immune glomerulonephritis Familial Acute Leukemias

MASSIVE HEMOPTYSIS ETIOLOGY (4) Drug-induced Cocaine, D-penicillamine, Isocyanates, Nitrofurantoin, Trimellitic anhydride Anticoags, Thrombolytics, ASA

MASSIVE HEMOPTYSIS ETIOLOGY (4) Miscellaneous Idiopathic hemosiderosis Coagulation disorders Thrombotic thrombocytopenic purpura DIC Acquired coagulopathy (permissive) Endometriosis (Catamenial hemoptysis) Sarcoidosis Lymphangioleiomyomatosis Chronic Lung Disease –Emphysematous bullae –Pneumoconiosis

MASSIVE HEMOPTYSIS BEDSIDE ASSESSMENT OF THE PATIENT Clubbing, Simian crease, Cutaneous nodules/pustules + uveitis IVDU with septic thrombophlebitis, palpable purpura, malar rash Oral: ulcers, mucosal telangiectasias, Post-URI rhinitis, saddle nose Stridor/wheezing

MASSIVE HEMOPTYSIS MASSIVE HEMOPTYSIS Clinical History Young adult female... otherwise healthy with recurrent CHF & A fib with spontaneous pneumothorax + ILD menstruating

MASSIVE HEMOPTYSIS MASSIVE HEMOPTYSIS Clinical History Inflammatory Lung Diseases bronchiectasis abscess necrotizing pneumonia infected cavity/bulla (mycetoma)

MASSIVE HEMOPTYSIS MASSIVE HEMOPTYSIS Clinical History TUBERCULOSIS §more common in the presence of cavitary disease. §pathologic lesions l Rasmussen's aneurysms l bronchial artery erosions from tb airway inflammation or bronchiectasis; l secondary infections of prior tuberculous cavities (eg Aspergillus)

Specific clinical situations presenting with MASSIVE HEMOPTYSIS §Tracheostomy §Post-Partum §Southeast Asia, Middle East §South America §Lymphoma §Acute Leukemia §Cardiac Surgery

High-power magnification showing capillaritis, which is characterized by infiltration of the alveolar septae by neutrophils (arrow). Note the presence of scattered red cells in the parenchyma (H&E stain, original magnification × 400).

DIFFUSE ALVEOLAR HEMORRHAGE §Bloody BAL fluid §hemosiderin-laden macrophages §lack of infectious pathogens §...are sufficient to establish DAH.

Causes of MH Associated With a Normal Chest Radiograph

MANAGEMENT of MH 1. Make the right etiological DIAGNOSIS ! l Hx. Px, Sputum, Bloods, FOB, Imaging 2. Determine the SITE of bleeding l Hx, Px, CXR (?CT) l FOB : flexible, rigid observe mucosa etc., washings: culture incl TB, cytology 3. Airway control/pt stabilization surgical candidate ? 4. Specific Therapy

DOUBLE-LUMEN ETT IN MASSIVE HEMOPTYSIS §Requires expert §Small lumina : difficult insertion, easy obstruction §62 patients with MH 4/7 pts with DL-ETT : aspiration and death cause : loss of tube position and pulmonary aspiration during surgery. L bronchial ETI :0/12 deaths from L Fogarty- Tracheal ETI : aspiration

TIMING OF BRONCHOSCOPY The sicker, the earlier ! §site of bleeding visualized more commonly with early bronchoscopy (within 48 hours) §unlikely relevant in non-massive hemoptysis

Management of MH BRONCHIAL ARTERY EMBOLIZATION (1) §successful immediate control 64% to100%. §Technical inability to cannulate :13% §Recurrence of bleeding Immediate 20-40% Follow-up post BAE 1 year: 16 % 3 years : 23% §Complications : vessel perforation/intimal tears sequelae of bronchial artery occlusion (e.g., chest pain, fever, hemoptysis) inadvertent ectopic emboli. mesenteric occlusion vessels supplying the extremities ASA embolization §reduced withcoaxial microcatheter system :"superselective" ba catheterization/bae without occluding other branches

Management of MH BRONCHIAL ARTERY EMBOLIZATION (2) §most difficult : identify the vessel(s) responsible for bleeding. §injection in the descending aorta just below the left subclavian artery §may require a full-arch aortogram in some §LL bleeding w/no apparent bronchial supply: §UL bleeding: unilateral subclavian artery injection to exclude nonbronchial systemic collateral arteries. §formal bronchial arteriogram §blush,abnormal vessels, ensures that no communication to the anterior spinal artery

Intervention in MH: Medical or Surgical ? §Observational studies l no RCTs… selection bias l none used bae as part of medical therapy l wide range of mortality rates : surgical (1-50%) and medical (1.6-85%) l results are mixed …lower surgical mortality rates

Intervention in MH: Medical or Surgical ? §Current recommendations §Current recommendations : surgical resection preferred if: l BAE unavailable or failed l imminent survival threatened by transport to radiology (ABCs) l surgically operable patient with a localized (ie resectable) lesion as cause of MH which is deemed unlikely to be controlled by BAE: –Thoracic vascular injury/trauma – mycetoma +profuse collateral arterial supply, –hydatid cyst –bronchial adenoma –AVM

PA RUPTURE PA RUPTURE (1)  Epidemiology §Prevalence.06-.2% §Rebleed: 90 % within 3 days Mechanism: Pseudoaneurysm (Psan) §Mortality: all comers 45-65% if rebleed: 40-70% 26% if abnormal CXR is only manifest'n of PA rupture 65% if clinical hemorrhage (ie hemoptysis, hemothorax, parenchymal bleed - HHPB ) §CXR may be normal despite PA rupture ? Psan

PA RUPTURE PA RUPTURE (2) Contributory causes §technical errors (improper equipment, technique or judgment) §age > 60 §PA hypertension §anticoagulated §hypothermia §inhalational anesthetic agents §peri-CPB (especially intraop)