Chest Book 2024 PDF

2024 58th Class CHEST BOOK ‫علم ينتفع به‬ BY : Ahmed ibrahim Take a breath  INDEX to chest Topics Chest Page Pulmonary Embolism...

2024 58th Class CHEST BOOK ‫علم ينتفع به‬ BY : Ahmed ibrahim Take a breath  INDEX to chest Topics Chest Page Pulmonary Embolism 1 Acute Dyspnea 25 Acute Respiratory Distress 32 Asthma Exacerbations 42 Pulmonary Embolism  CHEST Pulmonary embolism Definition obstruction of part of, or the entire pulmonary vascular tree, usually caused by thrombus from a distant site. Pathophysiology 1) Deep venous system of the lower limbs & pelvis: 75%. 2) Leg thrombi embolize, with a higher incidence in above than below knee clots: 20% 3) Paradoxical emboli: Should be considered as the cause for a stroke in the young. 4) Septic emboli: in endocarditis, in association with intraventricular septal defects/arteriovenous (AV) shunts or central venous access. ts/arteriovenous (AV) shunts or central venous access. A.I 1 Pulmonary Embolism Lecture 1 Hemodynamic effect of PE 1. Size of the clot 2. which area of the pulmonary vascular tree it subsequently obstructs, 3. pre-existing state of the myocardium.  lodge at the bifurcation of the main pulmonary arteries,  Large Clot causing Haemodynamic compromise.  Travel more distally, infarcting the lung:  multiple, bilateral & affect the lower lobes where  Small Clot blood flow is greatest.. Pathophysiological Response  The mean pulmonary arterial pressure (PAP):  does not ↑ until ≥ 50% of the vascular bed is occluded.   The RV: start to fail as the PAP > 40 mmHg acutely. CVS effect  This sequence is more in patient with cardiopulmonary disease.  V/Q mismatch.  Bronchospasm.  Respiratory Effect  Alveolar collapse.  Pulmonary edema.  Systemic hypoxemia.  Uncommon. Pulmonary Infarction  Is peripheral than central. "‫"علم ينتفع به‬ A.I 2 Pulmonary Embolism Lecture 1  Days to weeks by fibrinolysis.  Resolution  Provided no recurrence Etiology 1 Activation of Clotting Cascade Venous stasis. Injury to the vessel wall, ↑↑ blood coagulability predisposing to thrombus formation. 2 Venous Stasis ↑↑ by immobility and dehydration. In addition, coagulation factors may be altered in various disease states, e.g., in the acute phase response, malignancy, and autoimmune disease. "‫"علم ينتفع به‬ A.I 3 Pulmonary Embolism Lecture 1 Risk factor for venous thromboemolism 1 Major Risk Factor  Major abdominal / pelvic surgery   Orthopedic surgery especially lower limb Surgery  Post operative intensive care)  Pregnancy (Higher incidence with multiple births)  Obstetrics  CS  Pre-eclampsia. . Pelvic/ abdominal  Malignancy  2. Metastatic / advanced  Fracture  Lower limb problems  VV  Hospitalization Limited mobility  Institutional care  Long haul flight  Previous Proven VTE 2 Minor Risk Factor 1. Congenital heart disease 2. Congestive heart failure (CCF)  3. Hypertension CVS 4. Central venous access 5. Superficial venous thrombosis "‫"علم ينتفع به‬ A.I 4 Pulmonary Embolism Lecture 1 1. OCP especially 3rd generation (higher estrogen level)  Estrogens 2. Hormonal replacement therapy. 1. Occult malignancy. 6. Dialysis. 2. Neurogenic disability. 7. Myeloproliferative 3. Thrombotic disorders. disorders.  Miscellaneous 4. Obesity. 8. Inflammatory bowel disease 5. Nephrotic syndrome. (IBD). 9. Behcet disease. Categories of PE Acute massive PE A large clot may lodge at the bifurcation of the main pulmonary arteries. PE associated with pulmonary infarction. Sub massive PE: PE without pulmonary infarction (the most common type). Chronic thromboembolic disease: Repeated small showers of emboli over months to years results in severe pulmonary hypertension. "‫"علم ينتفع به‬ A.I 5 Pulmonary Embolism Lecture 1 Clinical picture of PE 1 Acute PE 1) Isolated dyspnea (25%): Sudden onset of dyspnea without circulatory collapse. 2) Pulmonary infarction with pleuritic chest pain ± hemoptysis (60%) 3) Circulatory collapse in a previously well patient (10%): Hypotension ± loss of consciousness (Syncope) → Usually due to massive PE. 4) Collapse (Hypotension) in patient with poor reserve (10%): May be due to small PE, often in the elderly with limited cardio-respiratory reserve. 1 Chronic PE Typically presents with more insidious onset of dyspnea over the course of weeks to months, due to recurrent small PE. Clinical manifestation of DVT: 1. Unilateral swelling with duskiness of the leg. 2. Pain over calf muscles on dorsi-flexion. (Homan's sign). 3. There may be palpable tender cord in femoral triangle. "‫"علم ينتفع به‬ A.I 6 Pulmonary Embolism Lecture 1 Examination of patient with PE May be normal. RR : The most common physical finding is unexplained tachypnea (RR > 20/min) in 70% of patients. HR : Tachycardia (pulse >100/min). AF. General Bp : hypotension ( shock state). examination Temperature : low grade fever There may be central cyanosis, elevated jugular venous pulse, Signs of DVT (common, in around 25%). There may be shallow breathing & reduced chest movement (due to pleural pain), Manifestations of respiratory distress with accessory muscle use, Chest examination pleural rub, or signs of pleural effusion Pulmonary hypertension (Loud P2 and splitting of the second heart Cardiac sound), with a gallop rhythm (acute right ventricular strain ). examination "‫"علم ينتفع به‬ A.I 7 Pulmonary Embolism Lecture 1 Risk stratifaction Risk stratification of patients with acute PE is mandatory for determining the appropriate diagnostic and therapeutic strategies. Risk Assessment based on the presence of Haemodynamic instability to identify those at high risk of early mortality. CRITERIA FOR High-risk pulmonary embolism: Definition of Haemodynamic instability, which delineates acute high-risk pulmonary embolism (one of the following clinical manifestations at presentation) Cardiac arrest Obstructive shock Persistent hypotension  Need for  Systolic BP < 90 mmHg or  Systolic BP < 90 mmHg cardiopulmonary  vasopressors required to  or systolic BP drop ≥40 resuscitation achieve a BP ≥90 mmHg mmHg, lasting longer than 15 despite adequate filling min and not caused by new- status onset arrhythmia, hypovolaemia, or sepsis And End-organ hypoperfusion 1. altered mental status 2. cold, clammy skin 3. oliguria/anuria 4. increased serum lactate "‫"علم ينتفع به‬ A.I 8 Pulmonary Embolism Lecture 1 Step by step risk stratification In Acute Pulmonary Embolism High risk PE Identification of patients at a of early mortality requiring a Step 1 Hemodynamic rapid diagnosis, monitored unit and prompt reperfusion instability treatment Low risk PE: can be safely treated as outpatients by estimation of 30- PESI/SPESI ≤ 2 day mortality based on clinical parameters (e.g., original Step 2 &Absence of RVD and sPESI) and treated by anticoagulation only. Intermediate-risk PE: Intermediate- high risk: RVD & elevated Monitored unit and rescue reperfusion. troponin or Step 3 Intermediate- low risk plasma lactate Ward unit & anticoagulation only Indicator of risk Hemodynamic Clinical RV dysfunction on Elevated cardiac instability paraemters of PE TTE or troponin levels severity and/or CTPA Early mortality risk comorbidity : PESI Class lll- V or Spesi > 1 High + + + + Intermediate - + + + High Intermediate Intermediate - + One (or none) positive low Low - - - Assesment optional : if assessed negative "‫"علم ينتفع به‬ A.I 9 Pulmonary Embolism Lecture 1 Wells criteria and modified Wells criteria: Clinical feature SCORE According to wells criteria Clinical symptoms of DVT (Leg 3 High >6 swelling, pain with palpation) 2-6 Moderate 3 Other diagnosis less likely than PE Low 100 Immobilization (>3 days) or 1.5 surgery in the previous 4 weeks According to modified wells criteria Previous DVT / PE 1.5 PE likely >4 Hemoptysis 1 Malignancy 1 PE unlikely ≤4 PESI Clinical feature SCORE Class total Age Class 1 = very low risk 125 History of chronic lung disease 10 HR ≥ 110 20 SBP < 100 mmHg 30 RR ≥ 30 / min 20 Temp < 36 C 20 Altered mental status? (Disoriented, lethargy, stupor or 60 coma SaO2 on room air 20 "‫"علم ينتفع به‬ A.I 10 Pulmonary Embolism Lecture 1 SPESI Clinical feature SCORE 1 Age > 80 1 Risk class Cancer Low risk 0 1 High risk ≥1 Chronic cardiopulmonary disease 1 Pulse ≥ 100 bpm SBP < 100 mmHg 1 Arterial SaO2 < 90% with or 1 without O2 Active cancer (diagnosed within last 12 m) or on active treatment Pulmonary Embolism Rule-Out Criteria (PERC): Use: Used in patients with low probability of PE: Wells score < 2 or Modified Well’s score ≤ 4. To determine whether or not diagnostic further imaging / lab work is indicated. Criteria: 1) Age < 50 year 2) Pulse < 100 beat per minute 3) SaO2 > 95 % on room air 4) NO hemoptysis 5) NO exogenous estrogen use. 6) NO prior venous thromboembolism 7) NO surgery or trauma requiring hospitalization within the past 4 weeks. 8) NO unilateral leg swelling. "‫"علم ينتفع به‬ A.I 11 Pulmonary Embolism Lecture 1 Investigations 1 ECG Non-specific changes may be present in many cases. Most common finding is sinus tachycardia. The classic S1Q3T3 pattern is un-common (in 10-20%). AF, RBBB, anterior T wave inversion (right ventricular strain) are common. Electrocardiogram of a patient with pulmonary embolism showing sinus tachycardia S1,Q3,T3 and RBBB. 2 CXR Small effusions are present in 40% (80% are exudates, 20% transudates). Focal infiltrates Segmental collapse Raised hemidiaphragm can also occur. Hampton’s hump (wedge shaped opacity pleural based with apex towards hilum). Westermark’s sign: a focus of lung oligemia distal to pulmonary embolus represented radiologically by hypertranslucency. "‫"علم ينتفع به‬ A.I 12 Pulmonary Embolism Lecture 1 Elevated right copula of diaphragm Hampton’s hump: Westermark’s sign Hampton’s hump: Acute pulmonary embolism Infarct Peripheral wedge-shaped areas of Hyper attenuation Linear bands Not specific "‫"علم ينتفع به‬ A.I 13 Pulmonary Embolism Lecture 1 3 ABGS Normal → especially in the young and healthy. Show hypoxia and hypocapnia → due to hyperventilation, Show increased A–a gradient → are more commoner. 4 D-Dimer  Positive D-dimer test > 500 ng/mL  Age adjusted D-dimer cut-off values: Value (Age X10 ug/L, in patients aged >50 years) can be used as an alternative to the fixed cut-off value.  It is a good negative test → can excluding PE. Use  A positive result → needs further investigation. NB  The sensitivity ranges from 87% to 99%, depending on the assay used. 5 Laboratory Biomakers cardiac troponin I or T: Markers of 30 - 60% with acute PE, have elevated cardiac troponin I or T. myocardial Heart-type fatty acid-binding protein (HFABP): injury an early and sensitive marker of myocardial injury Markers of BNP or NT-pro BNP: right Elevated BNP or NT-pro BNP concentrations reflect the severity of ventricular RVD and haemodynamic compromise in acute PE. dysfunction plasma Lactate: Others Elevated arterial plasma Lactate levels ≥2 mmol/L predict PE-related complications.. "‫"علم ينتفع به‬ A.I 14 Pulmonary Embolism Lecture 1 6 CTPA It is the gold standard investigation and is recommended as the initial imaging technique in suspected non-massive  PE. Uses It has a sensitivity of >95%. Filling defect or abrupt cut-off of the vessel. Absent, decreased or delayed filling of lung zone.  Findings Pleural based wedge shaped opacity (pulmonary infarction). Filling defect lesion Plural wedge opacity Peripheral wedge shaped areas of hyperattenuation Linear bands Not specific "‫"علم ينتفع به‬ A.I 15 Pulmonary Embolism Lecture 1 Acute PE polo mint sign: peripheral intraluminal filling defect forming acute angles with the vessel wall Railway track sign CHRONIC PE Peripheral, cresent shaped interluminal defect forms obtuse angles with the veseel wall 7 Isotope lung scanning (V/Q scan): Mostly now superseded by CTPA. May be useful as a first-line imaging investigation in patients with a normal CXR and with no concurrent cardiopulmonary disease. 8 Leg CUS Around 70% of patients with a proven PE have a proximal DVT leg imaging can be used as an alternative to lung imaging in those with clinical DVT. "‫"علم ينتفع به‬ A.I 16  Pulmonary Embolism Lecture 1 9 CT Venography It can be combined with CTPA to image the pelvic leg veins simultaneously. 10 ECHO The transesophageal route → is more sensitive, enabling visualization of intrapulmonary and intracardiac clot. Graphic Representation of Transthoracic Echocardiographic Parameters In The Assessment of Right Ventricular Pressure Overload 11 ]] Transthoracic US May show peripheral infarcts with peripheral PEs. "‫"علم ينتفع به‬ A.I 17 Pulmonary Embolism Lecture 1 Prophylaxis against PTE Non pharmacologic (During surgical operations): Pharmacologic agents: Graded compression stockings. Low molecular weight heparin. Intermittent pneumatic compression Oral anticoagulant : boots. (warfarin), new oral anticoagulant Vena cava filters (e.g Greenfield (dabigatran , apixaban, filter). rivaroxaban). Anti-platlet (acetyl salicylic acid ). NB Recommendations for IVC filters IVC filters should be considered in patients with acute PE and absolute contraindications to anticoagulation Patients who survived from recent massive PE (a second PE may be fatal) Recurrent VTE despite adequate anticoagulation Post-pulmonary thromboendarterectomy in PHT. Routine use of IVC filters is not recommended. "‫"علم ينتفع به‬ A.I 18 Pulmonary Embolism Lecture 1 Treatment of Acute PE Route infusion or SC every 4 hours 80 IU/kg given as an Loading dose intravenous bolus. Maintenance dose. 18 IU/kg/h Unfractionated Adjust infusion rate until the Heparin activated partial When to stop thromboplastin time (APPT) = 1.5-2.5 that of the control (45-75 seconds bleeding & heparin induced Risk of thrombocytopenia is high 1- only by subcutaneous injection. eg. Heparin Route Enoxaparin is more safe and easier to Efficacy administer. Low molecular weight Can be used in outpatient cases. Uses heparin ‘or fondaparinux (anti- bleeding & heparin induced factor Xa) thrombocytopenia is lower than Risk of unfractionated type "‫"علم ينتفع به‬ A.I 19 Pulmonary Embolism Lecture 1 Adjust the dose of prothrombin time and activity (international normalized ratio INR) to be Warfarin (VKA ): between 2 and 3 that of the control, initially measured every 1-2 days. NOACs are recommended as the first choice for anticoagulation treatment in preference to a VKA. 2- Eg : Oral anti Dabigatran (antithrombin). coagulant Rivaroxaban (anti-factor Xa). New oral Apixaban (anti-factor Xa). anticoagulant : Edoxaban (anti-factor Xa). No need for routine monitoring with the use of fixed dose and has rapid onset of action but expensive. Dabigatran Rivaroxaban APixaban Edoxaban Factor lla Factor Xa Factor Xa Target Factor Xa (antithrombin) 12-17 5-9 12 Half life 6- 10 (Hour) Time to peak 1-5 2-4 1- 3 1-2 (hour) "‫"علم ينتفع به‬ A.I 20 Pulmonary Embolism Lecture 1 Dosing in nonvascular 150 mg BID 20 mg OD 5 mg BID 60 mg OD AF 15 mg BID for 21 I0 mg BID for 60 mg OD after 150 mg BID after 5- ID Dosing in VTE day 7days 5 days of days of parenteral treatment parenteral Followed by 20 mg Followed by 5mg anticoagulation OD BID anticoagulation Renal clearance as 80 33 27 -50 unchanged drug % Drug interaction P-gp 3A4/P-gp 3A4/P-gp 3A4/P-gp pathway Length of anticoagulation : Temporary provoking risk factor: 3 months Lifelong anticoagulation is recommended for: patients presenting with recurrent VTE (with at least one previous episode of PE or DVT). extended anticoagulation A reduced dose of apixaban (2.5 mg b.i.d.) or rivaroxaban (10 mg o.d.) should be considered after the first 6 months of treatment 3- Reperfusion Treatment 1. systemic Thrombolysis 2. Surgical Embolectomy 3. Catheter Directed Thrombolysis and Half-Dose Thrombolysis 4. Balloon Pulmonary Angioplasty "‫"علم ينتفع به‬ A.I 21 Pulmonary Embolism Lecture 1 Systemic thrombolysis  High Risk PE (systolic BP 180 mmHg Advanced liver disease Infective endocarditis Active peptic ulcer "‫"علم ينتفع به‬ A.I 22 Pulmonary Embolism Lecture 1 Catheter directed thrombolysis Ultrasound-assisted Catheter-directed high frequency ultrasound : thrombolysis: can enable the thrombolytic agent to better penetrate the embolus. Rheolytic embolectomy injects pressurized saline through the catheter's distal tip : while macerated thrombus is aspirated through a catheter port Rotational A rotating device at the catheter tip can be used to embolectomy: fragment the thrombus: while fragmented clot is continuously aspirated. Suction embolectomy Thrombus can be manually aspirated: through a large-lumen catheter using an aspiration syringe and a hemostatic valve. Thrombus Mechanical disruption of the thrombus can be achieved by fragmentation: : 1. manually rotating a standard pigtail 2. or balloon angioplasty catheter into the thrombus; small fragments move distally 3. and thereby result in reduced pulmonary vascular resistance Surgical pulmonary embolectomy for patients with high-risk PE: in whom recommended thrombolysis is contraindicated or has failed. "‫"علم ينتفع به‬ A.I 23 Pulmonary Embolism Lecture 1 Concolusion Take a breath "‫"علم ينتفع به‬ A.I 24 Acute Dyspnea  CHEST Acute dyspnea Definition Difficult breathing. Difficult or labored breathing. Undue awareness of breathing. Need to breathe more. Uncomfortable or unpleasant breathing. Types Acute Chronic develops over hours to days occurs for more than four to eight weeks Dyspnea as an emergency Exacerbation of chronic dyspnea Within minutes or hours (acute) Acute worsening of chronic breathlessness 1) Acute attack of asthma that may be caused by a new problem or a 2) Tension pneumothorax worsening of the underlying disease : 3) Pulmonary oedema 1) Asthma 4) Pulmonary embolism (acute massive) 2) COPD 5) Pneumonia 3) Heart failure 6) Laryngeal oedema. Sizable foreign body aspiration A.I 25 Acute Dyspnea Lecture 2 Causes pulmonary disease may be the primary manifestation of lung disease myocardial ischemia or dysfunction Anemia: impair oxygen delivery, increased cardiac outpu neuromuscular disorders obesity Deconditioning: altered or utilization of oxygen, sedentary existence⭢ ⬇⬇ fitness ⭢⬇⬇ maximal cardiac output, ⭢ ⬇⬇ capillary density in the muscles, ⭢and ⬇⬇ mitochondrial capacity to sustain aerobic metabolis DD of acute dyspnea HEENT “head, eyes, ears, nose, and throat“ Toxic / metabolic 1. Angioedema 1. Organophosphate poisoning 2. Salicylate poisoning 2. Anaphylaxis 3. CO poisoning 3. Pharyngeal infections 4. Toxic ingestion 4. Deep neck infections 5. Diabetic ketoacidosis 6. Sepsis 5. Foreign body 7. Anemia 6. Neck trauma 8. Acute chest syndrome Chest wall Neurologic 1. Rib fractures Stroke 2. Flail chest Neuromuscular disease "‫"علم ينتفع به‬ A.I 26 Acute Dyspnea Lecture 2 Pulmonary Cardiac 1. COPD exacerbation 1. ACS “Acute coronary syndrome” 2. ADHF “Acute decompensated heart 2. Asthma exacerbation failure” 3. Pulmonary embolism 3. Flash pulmonary edema 4. Pneumothorax 4. High output failure 5. Cardiomyopathy 5. Pulmonary infection 6. Arrhythmia 6. ARDS 7. Valvular dysfunction 7. Pulmonary contusion or other lung injury 8. Cardiac tamponade 8. Hemorrhage Miscellanous 1. Hyperventilation 1. Intra-abdominal process 2. Anxiety 2. Ascites 3. Pneumomediastinum 3. Pregnancy 4. Lung tumor 4. Massive obesity 5. Pleural effusion "‫"علم ينتفع به‬ A.I 27 Acute Dyspnea Lecture 2 Assessment "‫"علم ينتفع به‬ A.I 28 Acute Dyspnea Lecture 2 Intial steps Optimize arterial oxygenation. (ABC) Determine the need for emergency airway management and ventilatory support. Identify whether a life-threatening condition exists, such as: 1. Acute coronary syndrome 7. Pericardial tamponade 2. Acute heart failure 8. Pulmonary embolism (PE) 3. Arrhythmia 9. Pneumonia or other infection 4. Angioedema and anaphylaxis 10. Poisoning (e.g, carbon monoxide) 5. Asthma exacerbation 11. Trauma (e.g, pneumothorax, hemothorax) 6. COPD exacerbation 1 History Pre-existing medical conditions such as Asthma, COPD, Prior DVT or PE, or ischemic heart disease Family history of hypercoagulable disorders Prolonged bed rest prior to acute onset dyspnoea Acute pulmonary embolism. may indicate Left ventricular failure associated with chest Orthopnea “defined as dyspnea on lying flat that pain, points to aortic dissection, pulmonary relieved by sitting embolism or acute coronary syndrome. Fever, cough, and sputum indicates: An infectious cause. Anxiety precedes dyspnoea it could be: Panic attack or pychogenic dyspnea Urticaria with anaphylaxis; and wheezing with acute bronchospasm "‫"علم ينتفع به‬ A.I 29 Acute Dyspnea Lecture 2 Hemoptysis is associated with a number of PE, Severe valvular conditions, including disease (eg, mitral stenosis), 2 Physical examination Stridor Stridor is a sign of airway obstruction. Inspiratory stridor Expiratory stridor or mixed insp. & expiratory stridor  Obstruction above vocal  Obstruction below vocal cords cords  eg, Croup, bacterial tracheitis,  eg FB, Epiglottitis, FB. Angioedema. Wheezes Wheezing represents bronchoconstriction, bronchospasm, or obstruction below level of trachea & is found with: Asthma, Anaphylaxis, A foreign body in a mainstem bronchus, ADHF, or a fixed lesion such as a tumor. Crackles Found in presence of interalveolar fluid, as seen with pneumonia or ADHF. Diminshed Caused by processes that prevent air from entering the lungs, Breath sound Such as severe COPD, severe Asthma, Pneumothorax, Tension pneumothorax, Pleural effusion, Hemothorax, and others. dysrhythmia A response to the underlying disease (eg, tachycardia in the setting of PE) OR The cause of dyspnea itself (eg, atrial fibrillation). "‫"علم ينتفع به‬ A.I 30 Acute Dyspnea Lecture 2 Heart A murmur may be physiologic or represent ADHF murmurs 1. Aetiological treatment: the corner stone of treatment. 2. Palliative treatment: aiming to ameliorate the sensation of dyspnea A. Fitness training and rehabilitation program B. Oxygen C. Continuous positive airway pressure (CPAP). D. Minor tranqulizers cautiously Take a breath "‫"علم ينتفع به‬ A.I 31 Acute Respiratory Distress  CHEST Acute respiratory Distress Definition A Form of acute lung injury characterized by non cardiogenic pulmonary edema and refractory hypoxemia that is produced by : neutrophil-mediated cytotoxicity to lung cells (alveolar epithelium and capillary endothelium) as a result of a wide variety of insults to the lung, either directly or indirectly. Epidimiology 10% of admissions to ICU ARDS accounts for 23% of ventilated patients mortality up to 45% Pathophysiology Tissue damage → release of inflammatory mediators (interleukin-1) → inflammatory reaction → migration of neutrophils into alveoli → injury to alveolar capillaries and endothelial cells (diffuse alveolar damage, DAD) A.I 32  ARDS Lecture 3 Berlin Criteria of ARDS Within one week of a known predisposing factor (e.g., sepsis, pneumonia) or Acute onset new or worsening respiratory symptoms. On Chest Imaging (X-ray or CT): Bilateral Similar appearance to pulmonary edema opacitixes not fully explained by effusions, lobar/lung collapse, or nodules”. Respiratory “not fully explained by cardiac failure or fluid overload” with objective Failure assessment (e.g., echocardiography) ARDS severity divides to : Category PaO2/FIO2 Mild 200 - 300 Hypoxemia Moderate 100-200 measured with a PEEP ≥ 5 cm H2O Severe ≤ 100. NB One of the major limitations of the Berlin Definition is that: its requirement for invasive or non-invasive ventilation cannot be met in settings where mechanical ventilation is no t available. High-flow nasal oxygen (HFNO) is a type of non-invasive advanced respiratory support that allows the delivery of high-flow and humidified air through a nasal cannula HFNO is a novel system of respiratory support, which allows delivery of oxygenation at variable concentrations, reduces the work of breathing, provides CPAP, and assists in CO2 removal. "‫"علم ينتفع به‬ A.I 33  ARDS Lecture 3 New global definition of ARDS By expanding the definition of ARDS and the use of pulse oximetry (SpO2/FIO2 ) and ultrasound to help diagnose and stage ARDS, and High-Flow Nasal Oxygen HFNO to treat it, we will be able to help many more patients who are in resource limited settings It includes: Intubation High flow nasal oxygen (HFNO) more than or equal to 30L/min (is no longer or Requirement) NIV/CPAP more than or equal to 5 cmH2O end expiratory pressure PaO2/FiO2 less than or equal to 300 mmHg Hypoxemia or level SpO2/FiO2 with pulse oximetry less than or equal to 315 mmHg with SpO2 less than or equal to 97% Bilateral chest can be confirmed by chest x-ray, CT Scan or USG (Ultrasonography) by a opacities well-trained operator New Criteria New definition Classification Criteria Mild Moderate Severe Time to installation Up to 7 days Pulmonary edema Not explained by cardiogenic edema or intravascular volume overload Bilateral infiltrate on chest x ray or CT Radiological Or lung ultrasound ( by a trained professional) features (not explained by 203- 300 with NIV/CPAP 101 – 200 com ≤ 100 com Hypoxemia PEEP ≥ 5 PEEP ≥5 PaO2/FIO2 Or HFNO > 30 L / min Hypoxemia ≤ 315 with sPO2 ≤ 97 % SpO2 / FIO2 "‫"علم ينتفع به‬ A.I 34  ARDS Lecture 3 Causes of ARDS 1 Direct Causes (Pulmonary) Infectious Non Infectious 1) Thoracic trauma: Lung contusion. Blast injury. 2) Near-drowning. 3) Toxic gas inhalation: Phosgene. 1) Pneumocystis carinii pneumonia. Smoke inhalation. 2) Influenza pneumonia 4) Pulmonary embolism: Air embolism. Fat embolism. Amniotic fluid embolism. 5) Aspiration of gastric contents (Mendelson's syndrome). 6) Drugs. 2 Indirect Causes (Extra-Pulmonary) 1) Sepsis (particularly Gram-negative septicaemia). 2) Multiple trauma. 3) Acute pancreatitis. 4) Severe burns. 5) Multiple blood transfusions. 6) Disseminated intravascular coagulation. 7) Cardiopulmonary bypass. 8) Anaphylaxis. "‫"علم ينتفع به‬ A.I 35  ARDS Lecture 3 Clinical features of ARDS 1 Symptoms Generally ARDS develops more rapidly (hours) after direct insults to the lung, than after indirect insults (24-48 h). Progressive dyspnea and non productive cough several hours or days after a predisposing condition. 2 Signs Acute dyspnea Tachypnea and tachycardia Cyanosis Scattered inspiratory crepitations may be heard on auscultation Fever, cough, and chest pain may also be present. Jugular pressure is not elevated. Investigations of ARDS 1 Lab Arterial blood gases analysis: marked hypoxemia PaO2/FiO2 < 300 CBC: leukocytosis in sepsis or pneumonia Lipase: elevated in pancreatitis Blood cultures: to identify bacteremia "‫"علم ينتفع به‬ A.I 36  ARDS Lecture 3 2 Radiology Chest x-ray is usually sufficient for diagnosis shows fluffy opacities either throughout the lung predominantly peripherally Chest X-ray Air bronchograms are common Kerley's lines, pleural effusions and dilatation of upper zone vessels are rare Additional Investigations Echocardiography No valvular lesion with pulmonary capillary wedge pressure < 18mmHg ECG tachycardia. Non cardiogenic (ARDS) Typical images of chest CT of ARDS patients. Three patterns of ARDS on CT images. a, b Focal, c, d diffuse, e, f patchy pulmonary edema "‫"علم ينتفع به‬ A.I 37  ARDS Lecture 3 NB Radiological differentiation of cardiogenic (high-pressure) and non cardiogenic (ARDS) pulmonary edema High-pressure Acute lung injury pulmonary edema (non cardiogenic) (cardiogenic) Cardiac size Enlarged Normal Upper lobe vessels Dilated Normal Kerley's lines. Present Absent Lung shadowing Central, hazy Peripheral, patchy Air bronchograms Unusual Frequent High-pressure pulmonary edema (cardiogenic) "‫"علم ينتفع به‬ A.I 38  ARDS Lecture 3 Treatment of ARDS The chief treatment strategy is supportive care. 1 Respiratory Support Mechanical Ventilation A lung-protective ventilatory strategy is advocated to reduce lung injury Mechanical Ventilation Protocol: From 4 to 8 mL/kg of ideal body weight Tidal volume (TV) (IBW), Respiratory rate (RR) up to 35 bpm, Inspiratory-to-expiratory time (I/E) ratio less than 1 The protocol allows for a low or a high PEEP strategy (PEEP, 5- 20cmH2O) relative to FiO2 Either strategy tolerates a PEEP of up to 24 cm H2O in patients requiring 100% FiO2 Goals : SpO2 88% to 95% PaO2 55 mmHg to 80 mmHg PH goal 7.30 to 7.45 NB  Prone positioning is recommend for >12 hours per day in patients with severe ARDS on mechanical ventilation.-  The improvement of oxygenation during prone ventilation is multifactorial, but occurs mainly by reducing lung compression and improving lung perfusion "‫"علم ينتفع به‬ A.I 39 ARDS Lecture 3 Venovenous extracorporeal membrane oxygenation (ECMO) Now is recommended for select patients with severe ARDS. ECMO : is the use of prolonged cardiopulmonary bypass to treat severe respiratory failure in newborns, children and adults.- The basic principle : is to pump some of the patient’s own blood through an artificial membrane or hollow fiber oxygenator to rest the lungs and give them a chance to heal. 2 Non respiratory Support Indications : Nosocomial infection of the injured lung(mortality rate approaching 90%.) Antibiotics: Anti-Biotics use : based on clinical suspicion or cultures The most common organisms implicated in nosocomial pneumonia are Gram negative, particularly pseudomonas aeruginosa Patients are mechanically ventilated, guarded against fluid overload with Fluid balance diuretics, and given nutritional support until improvement is observed. Steroids Therapy: should be considered in all patients with attention to the cause of ARDS e.g., COVID-19, community-acquired pneumonia) and concomitant conditions (e.g., sepsis) to determine dose and duration. Drug therapy: Neuromuscular blockade (NMB) is recommended in early treatment of patients with severe ARDS. Pulmonary vasodilators to reduce right ventricular after load e.g. intravenous prostaglandin E1 and inhaled nitric oxide. "‫"علم ينتفع به‬ A.I 40 ARDS Lecture 3 Exogenous surfactant therapy.- Drug therapy Anti-inflammatory therapy: pentoxifylline Outcome of ARDS There are reports of 30% to 40% mortality up until the 1990s, but over the past 20 years, while mortality rates are now around 9 % to 20%, it is much higher in older patients The primary cause of death in patients with ARDS was sepsis or multiorgan failure. ARDS has significant morbidity as these patients remain in the hospital for extended periods and have significant weight loss, poor muscle function, and functional impairment. Many of the patients who survive ARDS appear to regain useful lung function others may developed pulmonary fibrosis. Take a breath "‫"علم ينتفع به‬ A.I 41  Asthma Exacerbation  CHEST Asthma Exacerbations Definition 1. Associated with Airway hyperresponsiveness leads to Recurrent episodes of Wheezing, Breathlessness, Chest tightness, & Coughing. Particularly at night or in the early morning. 2. These episodes → Reversible either spontaneously or with treatment. 3. Many cells and cellular elements play a role. Pathophysiology Antigen (allergen) & antibody (IgE) reactions on the surface of mast cells → disruption of the cells → release of the preformed mediators. OR Parasympathetic stimulation → bronchoconstriction → ↑ in mucous secretions. A.I 42  Asthma Lecture 4 Clinical Picture 1 Symptoms  Wheezes   Cough ( chronic – worse at night) Recurrent attacks of  Difficulity in breathing and chest tightness (Dyspnea )  after exercise, upper respiratory tract infections, or Symptoms occur or allergen exposure  worsen  at night, disturbing the patients sleep.  Family Hx of  Asthma or atopic disease 2 Signs   No signs are detected or minimal signs (Normal ) In between attacks  Harsh vesicular breath sounds with prolonged expiration During attacks  Audible wheezes and rhonchi on auscultation  There may be silent chest in severe cases.  Characterized by → Variability, periodicity, and  The course of asthma unpredictability; exacerbations vary from brief to sever ones. "‫"علم ينتفع به‬ A.I 43  Asthma Lecture 4 Levels of Asthma Partially Controlled Characteristic Controlled (Any measure during any Uncontrolled (All of the following) week)  Day time symptoms None (≤ 2 /week) ≥2 /week ≥3 features of Need for reliever / rescue partly controlled  treatment asthma present in any week  Limitation of activities None Any Noctornal  Symptoms/ awakenin Lung function Normal < 80% predicted or personal best (if known) (PEF or FEV1)  Exacerbaions None ≥ 1 /year 1 in any week Asthma attacks Respiratory arrest Mild Moderate Severe imminent (near fatal asthma) Walking Talking At rest Infant-softer Infant stops shorter cry; feeding Breathless difficulty feeding Can lie down Prefers sitting Hunched forward Talks in Sentences Phrases Words Drowsy or Alertness May be agitated Usually agitated Usually agitated confused "‫"علم ينتفع به‬ A.I 44  Asthma Lecture 4 Respiratory Increased Increased Ofter > 30/min - Rate Accessory Pardoxical muscles & Usually thoraco- suprasternal abdominal Reactions movement Moderate, often only Loud Usually loud Absence of Wheeze end expiratory wheeze Absence Pulsus Absent May be present Often present suggests paradoxus < 10 mmHg 10-25 mmHg > 25 mmHg (adult) respiratory 20-40 mmHg (child muscle fatigue PEF after < 60% predicted or initial personal best (< bronchodilator Over 80% Approx. 60-80% 100 L/min adults) % predicted or - or % personal response lasts < 2 best hrs < 60 mmHg PaO2 (or air Normal > 60 mmHg Possible cyanosis Test not usually and/or necessary > 45 mmHg - PaCO2 < 45 mmHg < 45 mmHg Possible respiratory failure SaO2% (on air) > 95% 91-95% < 90% - Hypercapnea (hypoventilation) develops more readily in young children than in adults and adolescents "‫"علم ينتفع به‬ A.I 45  Asthma Lecture 4 NB Normal rates of breathing in awake children Age Normal rate < 60/min < 2 months < 50/min 2-12 months < 40/min 1-5 years < 30/min 6-8 years Acute severe asthma 1 Definition Progression of an attack of bronchospasm to the point where the patient is breathless at rest 2 Symptoms 1) Difficult speech: Patient unable to complete sentences in one breath 2) Anxiety and diaphoresis 3) Respiratory distress at rest. Near fatal asthma Definition It is progressive acute severe asthma with imminent respiratory arrest: Clinical picture Same as acute severe asthma + 1) Patient is drawsing, fatigued. 4) Paradoxical thoraco-abdominal movements. 2) Head sagging. 5) Bradycardia. 3) Central cyanosis. 6) Blood gases hypoxaemia and hypercapnea "‫"علم ينتفع به‬ A.I 46  Asthma Lecture 4 Criteria for Diagnosis of Acute Severe Asthma Signs: Use of accessory muscles of respiration. Respiratory rate > 30/min. - Pulse > 120/mL Pulsus paradoxus inspiratory fall of systolic blood pressure > 10 mmHg. Cyanosis (in very severe attacks). Chest auscultation: Inspiratory and expiratory wheeze There may be silent chest i.e; inaudible wheezes which become audible later on with improvement of the attack. By investigations : Blood gases: In acute severe attacks → ↓PaO2 “arterial oxygen tension” wih normal PaCO2. ↑ PaCO2 is → indication of mechanical ventilation 1 Oxygen therapy Oxygen should be administered by nasal cannula or face mask. 2 Bronchodilators  Administered by nebulizer (Salbutamol solution) may be repeated every Short-acting 2- 10-20 min for one houre till patient improve. agonist (SABA): NB, large volume spacers designed for conventional MDI, may be used, if no available nebulizer. "‫"علم ينتفع به‬ A.I 47  Asthma Lecture 4 Ipratropeum  a combination of neublized 2-agonists and anticholenergic ipratropneium bromide bromide may produce better bronchodilator effect than either drug alone Loading dose:  half the patient's body weight in kg x 10 in I.V. infusion over 30 min (e.g. for a 60 kg patient dose = 10 x 30 = 300 mg aminophylline). Theophylline Maintenance dose:  0.5 mg/kg/hour I.V.  Parenteral hydrocortisone in a dose up to 4 mg/kg which may be Corticosteroids: repeated.  Effective within 4-6 hours. 3 Hydration plenty of oral and I.V fluids 4 Mechanical ventilation Indication of mechanical ventilation: 1) Patients who are drowsy or comatosed. 2) Patients who are exhausted with respiratory muscle fatigue. 3) Paradoxical thoracoabdominal movement. 4) Presence of cyanosis and hypercapnia. 5) Previous history of mechanical ventilation in intensive care "‫"علم ينتفع به‬ A.I 48 Asthma Lecture 4 Primary Care Patient present with acute or subacute asthma exacerbation Is it asthma Asecss the Factors for asthma related death ? pateint Sevrity of exacerbation ? consider worst feature Mild /Moderate Severe Life threatening Talking in phrases Talks in words,sits hunched forwards, agitated Prefer sitting to lying RR : > 30/min RR : ↑↑ Acc.muscle in use Drowsy, confused Acc.muscle not used or silent chest Pulse : >120 bpm Pulse : 100-120 bpm O2 sat: < 90 % O2 sat: 90-95 % PEF < 50 % PEF > 50 % Urgent Start treatment Transfer to acute care facility SABA 4-10 puffs by pMDI + spacer, repeat every 20 minutes for 1 hour While waiting: Worsening Prednisolone: adults 40-50 mg, Give SABA, ipratropium Children 1-2 mg/kg, max. 40mg bromide, O2 systemic Controlled oxygen (if available): target corticosteroid saturation 93-95% (children: 94-98%) Improving Worsening CONTINUE TREATMENT with SABA AS NEEDED ASSESS RESPONSE AT 1 HOUR (or earlier) Improving ASSESS FOR DISCHARGE ARRANGE AT DISCHARGE 1. symptoms improved, not needing 1) Reliever: continue as needed. SABA 2) Controller: start, or step up. 2. PEF improving, and > 60-80% of 3) Check inhaler technique, personal best or predicted adherence 3. Oxygen saturation > 94% room air 4) Prednisolone: continue, usually Resources at home adequate for 5-7 days (3-5 days for children) 5) Follow up: within 2-7 days (1-2 days for children) "‫"علم ينتفع به‬ A.I 49 Asthma Lecture 4 Follow up Review symptoms and signs: Is the exacerbation resolving? Should prednisone be continued? Reliever: reduce to as-needed. Controller: continue higher dose for short term (1-2 weeks) or long term (3 months), depending on background to exacerbation. Risk factors: check and correct modifiable risk factors that may have contributed to exacerbation, including inhaler technique and adherence. Refer if > 1-2 exacerbations in a year. Action plan: Is it understood? Was it used appropriately? Does it need modification? Take a breath "‫"علم ينتفع به‬ A.I 50