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Massive Hemoptysis. 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.
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Massive Hemoptysis D. P. Laporta MDDepartments of Adult Critical Care and Medicine, Sir MB Davis Jewish General HospitalMcGill Universitypresented to McGill ResidentsCritical Care (January 2000)Pulmonary (July July 2000
MASSIVEHEMOPTYSISREFERENCES • 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; 28:1642-7 • 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 52-1993: A 17-Year-Old Girl with Massive Hemoptysis and Acute Oliguric Renal Failure. NEJM Weekly CPC. 1993; 329(27)
MASSIVEHEMOPTYSIS NATURAL HISTORY AND PROGNOSIS • MORTALITY Immediate : 7% of 113 patients who presented with massivehemoptysis 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
MASSIVEHEMOPTYSIS Prognostic Features Associated with Death Magnitude of Bleed • bleeding exceeding 1000 mL/24 h 600 mL of hemoptysis in <4 hours 71%mortality 4-16 hous 22% 16-48 hours 5% • 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 + Underlying Etiology
Overestimate Underestimate 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
Nonbronchialsystemiccollateral 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
MASSIVEHEMOPTYSIS 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)
MASSIVEHEMOPTYSIS ETIOLOGY (2) Foreign body/traumaAspirated foreign bodyBroncholithTracheovascular fistulaTrauma, Brachytherapy, Laser Cardiac/pulmonary vascularPulmonary 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)
MASSIVEHEMOPTYSIS ETIOLOGY (3) Alveolar hemorrhage Goodpasture's syndrome Systemic vasculitides/collagen vascular diseases…capillaritisBehcet's syndromeEssential mixed cryoglobulinemia, Henoch-Schonlein purpuraProgressive systemic sclerosisRheumatoid arthritis, Systemic lupus erythematosus, Mixed connective tissue disease Systemic necrotizing vasculitis, Wegener's granulomatosis Other Glomerulonephritis Immune complex associated glomerulonephritisPauci-immune glomerulonephritis Familial Acute Leukemias
MASSIVEHEMOPTYSIS ETIOLOGY (4) Drug-induced Cocaine, D-penicillamine, Isocyanates, Nitrofurantoin, Trimellitic anhydride Anticoags, Thrombolytics, ASA
MASSIVEHEMOPTYSIS 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
MASSIVEHEMOPTYSISBEDSIDE 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
MASSIVEHEMOPTYSISClinical History Young adult female ... • otherwise healthy • with recurrent CHF & A fib • with spontaneous pneumothorax + ILD • menstruating
MASSIVEHEMOPTYSISClinical History Inflammatory Lung Diseases • bronchiectasis • abscess • necrotizing pneumonia • infected cavity/bulla (mycetoma)
MASSIVEHEMOPTYSISClinical HistoryTUBERCULOSIS • more common in the presence of cavitary disease. • pathologic lesions • Rasmussen's aneurysms • bronchial artery erosions from tb airway inflammation or bronchiectasis; • 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.
MANAGEMENT of MH 1. Make the right etiological DIAGNOSIS ! • Hx. Px, Sputum, Bloods, FOB, Imaging 2. Determine the SITE of bleeding • Hx, Px, CXR (?CT) • 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
TIMINGOF 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 MHBRONCHIAL 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 MHBRONCHIAL 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 • no RCTs… selection bias • none used bae as part of medical therapy • wide range of mortality rates : • surgical (1-50%) and medical (1.6-85%) • results are mixed …lower surgical mortality rates
Intervention in MH: Medical or Surgical ? • Current recommendations: surgical resection preferred if: • BAE unavailable or failed • imminent survival threatened by transport to radiology (ABCs) • 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 (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 (2) Contributory causes • technical errors (improper equipment, technique or judgment) • age > 60 • PA hypertension • anticoagulated • hypothermia • inhalational anesthetic agents • peri-CPB (especially intraop)