L6 Haemoptysis & Cyanosis Lecture Notes PDF

Medicine “Haemoptysis & Cyanosis” University Of Fallujah College Of Medicine Lecture : L6 Stage : 3rd Lecturer : Assistant Professor: Mohammed Ismael Dawood Department: Medicine Date: 31/10/2024 Basic Learning Objectives: 1. Clinical Definition of Haemopty...

Medicine “Haemoptysis & Cyanosis” University Of Fallujah College Of Medicine Lecture : L6 Stage : 3rd Lecturer : Assistant Professor: Mohammed Ismael Dawood Department: Medicine Date: 31/10/2024 Basic Learning Objectives: 1. Clinical Definition of Haemoptysis. 2. Differentiation between haemoptysis & hematemesis. 3. Simplified approach to haemoptysis. 4. Clinical definition of cyanosis. 5. Classification of cyanosis. 6. Clinical approach of cyanosis. Haemoptysis & Cyanosis Dr. Mohammed Ismael Dawood Assistant Professor of Medicine Haemopty sis 1. Is it true hemoptysis?  Coughing up any amount of blood is an alarming symptom, and nearly always brings the patient to the doctor.  A clear history should be taken to establish that it is true haemoptysis and not haematemesis, gum bleeding or Paramet nosebleed. Haemoptysis Haematemesis er History Respiratory disease GIT disease Blood Coughing out of blood Vomiting of blood Sputum Associated sputum Associated food particles Blood Frank Coffee ground or frank red or colour frothy PH Alkaline blood Acidic blood Pain Associated dyspnoea & Abdominal pain, Chronic DU 2. Is This massive Hemoptysis?  Massive hemoptysis, variably defined as (400 mL) within 24 h or 100−150 mL at one time, requires emergent care.  The approach would be: (Surgical) 1. Resuscitation: Intubate to protect the airways. 2. Bleeding cessation: Usually via pulmonary artery angiography& embolization (because most massive bleeds are arterial rather than venous). 3. Find the underlying cause. 3. Initial History & Examination:  Obtain a good history & perform detailed examination.  Focus on broad groups:  Infective: Fever, blood streaks mixed with purulent sputum.  Systemic symptoms: chronic cough, weight loss, night sweat (suggest TB or malignancy), chronic sputum production (bronchiectasis).  Autoimmune: Other autoimmune manifestations including renal impairment, sinusitis, Otitis media, rash, purpura, & neuropathies.  Cardiac aetiology: Congestive fluid overload, & murmur on examination.  Injuries: Chest trauma, Foreign body inhalation, Cocaine 1. NON-CARDIOPULMONARY: Epistaxis, Upper GI bleed, Coagulopathy. 2. CARDIAC: HF, Mitral stenosis. 3. PULMONARY: Airway—bronchitis (acute, chronic), bronchiectasis, malignancy, foreign body, trauma. Parenchyma:  malignancy—lung cancer, metastasis.  infections—necrotizing pneumonia (Staphylococcus, Pseudomonas), abscess, septic emboli, TB, fungal  alveolar hemorrhage—granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, anti-glomerular basement membrane disease, pulmonary capillaritis, connective tissue disease. vascular—pulmonary embolism, pulmonary hypertension, AVM, iatrogenic.  Many episodes of haemoptysis are unexplained, even after full 4. Do Initial investigations & CXR:  CBC, Renal Function, Liver Function, Coagulation Profile.  CXR: The cause of haemoptysis can be stratified based on CXR picture as follow:  Mass or nodule: Lung Cancer (single or multiple), Lung metastasis (Multiple), Infective as abscess(air fluid level), Aspergilloma (rounded mass in pulmonary cavity).  Consolidation or opacity: Infective as in TB, bacterial pneumonia, & fungal infection, Autoimmune diseases like Wegner granulomatosis, Goodpasture syndrome, SLE & scleroderma, Cardiac (mitral stenosis & pulmonary oedema).  Haemoptysis & Normal CXR: Consider one of the following: 1. First episode of hemoptysis with no risk factors for malignancy: observation and further evaluation & investigations if recurrent. 2. Patients with infective symptoms suggestive of bronchitis: Trial of antibiotic treatment & further investigations didn’t required unless haemoptysis persist. 3. Haemoptysis in chronic smoker or those with positive family history of lung cancer: HRCT scan & bronchoscope. 4. Persistent haemoptysis: Order HRCT scan & Cyanosi s  Bluish discoloration of the skin and/or mucous membranes are usually due to elevated quantity of reduced hemoglobin (>4 g/dL) in the capillary blood vessels.  Findings are most apparent in the lips, nail beds, ears, and malar eminences.  Cyanosis depends on absolute, not relative, quantity of desaturated hemoglobin, so may be less evident in patients with severe anemia, and more notable in patients with CENTRAL CYANOSIS:  Results from arterial desaturation or presence of an abnormal hemoglobin.  Usually evident when arterial saturation is ≤85%, or ≤75% in dark-skinned individuals.  Etiologies include: 1. Impaired pulmonary function: Poorly ventilated alveoli or impaired oxygen diffusion; most frequent in pneumonia, pulmonary edema, and chronic obstructive pulmonary disease (COPD); in COPD with cyanosis, secondary polycythemia is often present. 2. Anatomic vascular shunting: Shunting of desaturated venous blood into the arterial circulation may result from congenital heart disease or pulmonary atrioventricular (AV) fistula. 3. Decreased inspired O2: Cyanosis may develop in ascents to altitudes >4000 m (>13,000 ft). 4. Abnormal hemoglobins: Methemoglobinemia, sulfhemoglobinemia. PERIPHERAL CYANOSIS:  Occurs with normal arterial O2 saturation with increased extraction of O2 from capillary blood caused by decreased localized blood flow.  Contributors include:  vasoconstriction due to cold exposure.  decreased cardiac output (e.g., in shock).  heart failure.  peripheral vascular disease with arterial obstruction or vasospasm.  Local (e.g., thrombophlebitis) or central (e.g., constrictive pericarditis) venous hypertension intensifies cyanosis. Clinical Approach to cyanosis:  Inquire about duration (cyanosis since birth suggests congenital heart disease) and exposures (drugs or chemicals that result in abnormal hemoglobins).  Differentiate central from peripheral cyanosis by examining nailbeds, lips, and mucous membranes. Peripheral cyanosis is most intense in nailbeds and may resolve with gentle warming of extremities.  Check for clubbing, i.e., selective enlargement of the distal segments of fingers and toes, due to proliferation of connective tissue. Clubbing may be hereditary, idiopathic, or acquired in association with lung cancer, infective endocarditis, bronchiectasis, or hepatic cirrhosis. Combination of clubbing and cyanosis is frequent in congenital heart  Examine chest for evidence of pulmonary disease, pulmonary edema, or murmurs associated with congenital heart disease.  If cyanosis is localized to an extremity, evaluate for peripheral vascular obstruction.  Obtain arterial blood gas to measure systemic O2 saturation. Repeat while patient inhales 100% O2; if saturation fails to increase to >95%, intravascular shunting of blood bypassing the lungs is likely (e.g., right-to-left intracardiac shunts).  Evaluate for abnormal hemoglobins (e.g., spectroscopy, measurement of methemoglobin level).