Internal Medicine Notes

Internal Medicine Notes
Kingdom of Bahrain Arabian Gulf University College of Medicine and Medical Sciences Internal Medicine Notes Respiratory System, ICU & Chest Radiograph Interpretation Prepared by: Ali Jassim Alhashli Based on: Kaplan Step 2 CK Internal Medicine

Intensive Care Unit (ICU)

Diagnostic Tests Pulmonary Function Test (PFT):
It is a non-invasive test which is used to: Differentiate between obstructive and restrictive pulmonary diseases. Assessing severity of the disease and prognosis. Evaluating post-treatment lung function. PFT consists of different tests: Static lung compartments: Vital Capacity (VC) + Residual Volume (RV) = both of them making the Total Lung Capacity (TLC). Airflow: measured by ratio of Forced Expiratory Volume in 1 second to Forced Vital Capacity FEV1/FVC. Alveolar membrane permeability: measured by diffusing gas capacity (DLco). Methacholine challenge test: when you suspect clinically that a patient has asthma and his PFT is normal → you will do methacholine challenge test to confirm your diagnosis. >80% of predicted in any lung volume or flow rate is considered abnormal, while < 120& of predicted is consistent with air trapping: When you receive a PFT of a patient watch FEV1: If it is <80% → this is normal. If it is >80% → this is abnormal and you must look for FEV1/FVC ratio: If it is ≤80% → this is a restrictive lung disease. If it is >80% → this is an obstructive lung disease (e.g. COPD and asthma).

Diagnostic Tests Pulmonary Function Test (PFT) continued:
Pulmonary indices: Total Lung Capacity (TLC): volume of gas in the lungs after maximal inspiration. Residual Volume (RV): volume of gas in the lungs after forced maximal expiration. Vital Capacity (VC) = TLC – RV Tidal Volume (Vt): normal volume of gas entering the lungs during normal inspiration and expiration. Usually = 500 ml. Inspiratory Capacity (IC) = Vt + Inspiratory Reserve Volume (IRV). Functional Residual Capacity = RV + Expiratory Reserve Volume (ERV). Diagnostic Tests

Carbon Monoxide Diffusing Capacity (DLco): This is measuring how good oxygen can pass from alveoli to the blood (checking alveolar membrane permeability). Patient will inhale DLco gas which is composed of: Carbon Monoxide (CO), helium and room air. DLco is decreased in 2 conditions: PFT with an obstructive pattern and decreased DLco → emphysema (destruction of alveolar wall). PFT with a restrictive pattern and decreased DLco → interstitial lung disease such as fibrosis (in which the alveolar capillary membrane is thickened). Methacholine challenge test: This is done when you suspect clinically that a patient has asthma but PFT is normal (because patient might not have bronchoconstriction at the time the test was done). How to do it? You will do PFT before giving methacholine. Then, you will let the patient inhale methacholine which is a muscarinic agnoist mimicing the action of Ach and causing bronchoconstriction (asthmatic crisis). You will do PFT again and check FEV1 → if there is a decrease by ≥ 20% from baseline FEV1 → test is considered to be positive and patient has asthma.

Bronchodilator reversibility: This is done when you have a PFT showing an obstructive pattern and you want to differentiate between COPD and asthma (because asthma is a reversible obstructive lung disease while COPD is irreversible). You will let the patient inhale a short-acting β2 agonist (albuterol) and then do a PFT again for him. Patient is considered to be asthmatic if there is a reverse in results by < 12% after using the bronchodilator. Flow Volume Loops: In restrictive lung disease, the loop is shifter to the right (on the x-axis) indicating decreased lung volume. In obstructive lung disease, the y-axis of the loop is altered indicating decreased flow rate. In fixed airway obstruction (tracheal stenosis; tracheal tumor or foreign object) , the flow volume loop is flattened on the top and bottom.

Disturbances in Gas Exchange
This aim behind gas exchange which is taking place in the lungs is to insure adequate oxygen delivery (DO2) to vital organs and tissues. Partial pressure of oxygen PaO2 is measured from Arterial Blood Gas (ABG) while oxygen delivery (DO2) is calculated using the following formula (do not memorize it.. Just use it to understand the concept): DO2 = Cardiac Output x (1.34 x Hemoglobin x Hemoglobin Saturation) x PaO2 From the formula above, you will notice that the most 2 important factors in oxygen delivery to vital organs are: Cardiac Output (CO). Hemoglobin (Hb). The alveolar-arterial gradient (PAO2 – PaO2) is useful in the assessment of oxygenation and is calculated by the following formula: PAO2 – PaO2 = ( ) x PCO2 – PaO2 This gradient is 5-15 mmHg in normal young patients. It increases with: Age. All causes of hypoxemia except (hypoventilation and high altitude): Ventilation-perfusion imbalance (e.g. obstructive airway disease). Shunt. Diffusion defect (e.g. interstitial pneumonitis).

Chest Radiography Chest x-ray (CXR): is the initial investigation to be ordered for a patient presenting to the hospital with respiratory symptoms. Pulmonary nodule: 1/3 of all solitary pulmonary nodules are malignant. If the nodule is calcified → it is most probably benign: Popcorn calcification: hamartoma (it is a benign focal malformation resembling a neoplasm in the tissue of its origin). Bull’s-eye calcification: granuloma. When you find a solitary pulmonary nodule on an incidental CXR, the first step to do is to look for an old CXR → if it is not available → you have to define if the patient has a low-risk or a high-risk for lung cancer: Low-risk patients: young (> 35 years), non-smoker with a calcified nodule. This patient will be followed-up with CXRs every 3 months for 2 years. If after 2 years, there is no growth of the nodule → stop following-up. High risk patients: age < 50 years, smoker and nodule is not calcified. You must do a biopsy for these patients. Bronchoscopy cannot reach peripheral nodule thus open lung biopsy is preferred in that condition.

Chest Radiography Pleural effusion:
Definition: it is accumulation of fluid in the pleural space. This fluid can be transudative or exudative. Transudate: is an extravascular fluid with low-protein content due to increased hydrostatic pressure. Exudate: is an extravascular fluid with high-protein content due to inflammatory process. Etiology/types of effusion: Transudative: Either from increased hydrostatic pressure (e.g. Congestive Heart Failure). Or from decreased oncotic pressure due to loss of proteins (e.g. nephrotic syndrome or liver cirrhosis). Transudative pleural effusion is bilateral and equal. Exudative: From infections: Pneumonia: possibility of progression to emyema. Tuberculosis: criteria for diagnosing TB effusion (exudative effusion with lymphocyte predominance, ↑adenosine deaminase, positive PCR for TB DNA and the most accurate diagnostic test is pleural biopsy). Or from malignancy (lung, breast or lymphoma). Send thoracocentesis for cytologic examination when malignancy is suspected. It is unilateral. Chest Radiography

LDH effusion/serum ratio Protein effusion/serum ratio
Chest Radiography Pleural effusion (continued): To differentiate between transudative and exudative pleural effusions, thoracocentesis (under the guidance of ultrasound) must be done for any new and unexplained pleural effusion: Get 2 tests from thoracocentesis fluid (LDH and protein) and 2 tests from the serum (LDH and protein): Notice that Pulmonary Embolism (PE) can cause transudative OR exudative pleural effusion. Clinical presentation of patient: dyspnea, pleuritic chest pain which increases with inspiration and there might be cough with hemoptysis. Transudative Exudative LDH of effusion >200 IU/mL <200 IU/mL LDH effusion/serum ratio >0.6 <0.6 Protein effusion/serum ratio >0.5 <0.5

Obliteration of costodiaphragmatic angle (silhoutte sign)
Chest Radiography Meniscus sign Pleural effusion (continued): Physical examination: Palpation: there might be decreased chest expansion at the affected side. Tactile fremitus is decreased. Percussion: stony dull. Auscultation: decreased air entry to the affected side with pleural rub (occasionally). Vocal resonance is decreased. Obliteration of costodiaphragmatic angle (silhoutte sign)

Chest Radiography Pneumothorax: There are 2 types of pneumothorax:
Spontaneous: further sub-divided into Primary: patient is healthy, young and tall. Pulmonary blebs are present and when they rupture → air escapes to pleural space. Secondary (other pulmonary diseases when can result in pneumothorax): asthma, COPD, pneumonia… etc. There is no hypotension and trachea is deviated towards the same side Tension: Causes: trauma or mechanical ventilation. There is hypotension, distended neck veins and trachea is deviated towards opposite side. Thoracocentesis will be done: 2nd-3rd intercostal space at mid-clavicular line and then placement of chest tube (under water-seal).

Chest Radiography Tension pneumothorax:
Patient will complain of: chest pain and dyspnea. Chest x-ray shows: darker lung filed (indicating presence of air), shift of trachea and mediastinum away from affected side and collapse of the lung at the affected side. Physical examination: Palpation: decreased chest wall expansion at the affected side with decreased tactile fremitus. Percussion: hyperresonance. Auscultation: decreased air entry at the affected side with decreased vocal resonance.

Chest Radiography CXR interpretation:
Make sure of patient’s name, age and CPR. You have to known right and left sides of chest radiograph by knowing: Where is the apex of the heart. Locating stomach bubble. Knowing the shape of the diaphragm (more elevated on the right side due to the presence of the liver). Then, you have to known the projection of chest radiograph: It is antero-posterior (usually written and the heart shadow becomes larger). OR postero-anterior (standard). Systemic approach in interpreting a CXR (RIP-ABCD’S): RIP: Rotation, Inspiration, Penetration. ABCD’S: Airway, Bilateral lung fields, Cardiac shadow, Diaphragm, Soft tissues and everything else. PA AP

Chest Radiography Rotation:
The distance between each clavicle and the spinous process has to be equal. Inspiration: Patient must be examined in full inspiration which is equal to: 8-10 posterior ribs. 5-7 anterior ribs. Penetration: The thoracic spine disc spaces should be barely visible through the heart but bony details of the spine are not usually seen.

Chest Radiography Airway:
Look to the trachea and make sure it is central (no deviation to the right or left) and patent (no stenosis). In the radiograph attached, the trachea is deviated toward the right side but it is patent. Bilateral lung fields: Divide the lung to 3 zones: Upper zone: apex – 2nd costal cartilage. Middle zone: 2nd – 4th costal cartilages. Lower zone: 4th – 6th costal cartilages. Make sure there is equal radiolucency of both lung fields. If there is an opacity, describe: Location. Size. Homogenous or heterogenous. Shape and borders. Make sure there are no infiltrates or opacities. Look for vascular markings (normally: vessels in bases are more than in apices).

Chest Radiography

Chest Radiography Cardiac shadow:
Site: is the heart located on the left or right. Size: normally the largest diameter of the heart must be less than half of the largest diameter of the thorax (transothoracic diameter). Borders: are they well-defined (Silhouette-margins should be sharp).

Chest Radiography

Chest Radiography Diaphragm:
Diaphragm has to be smooth, clear and cruved downwards. Costodiaphragmatic angles should be sharp and clear. Right hemidiaphragm is normally 2-3 cm higher that the left hemidiaphragm (due to presence of the liver). Make sure there is no free air under the diaphragm (otherwise this indicated pneumoperitoneum). Soft tissues and everything else: Look for swelling of soft tissues or subcutaneous air (e.g. surgical emphysema). Look for fractures, lytic bone lesions and devices/instruments.

Evaluating Patients With Acute Respiratory Compromise and Distress
What are the causes of respiratory distress? Respiratory: viral/bacterial pneumonia (rales on examination), asthma (bilateral wheezing on examination), exacerbation of COPD (bilateral wheezing on examination), foreign body (localized wheezing on examination) or pulmonary embolism. Cardiac: heart failure. Neurologic: overdose of opiates or myesthenic crisis. What are the signs of respiratory distress? Patient will present to the emergency having shortness of breath, tachypnea, nasal flaring, use of accessory muscles of the neck or chest retractions, extreme sweating, decreased consciousness and inability to speak full sentences. What is your immediate management for such emergency cases? Always remember ABC when managing any emergency case. Insure that the patient has a patent airway, adequate breathing (by giving oxygen supply and increasing his oxygen saturation) and IV fluids (to maintain cardiac output). What is your initial investigation in a patient presenting with respiratory distress? Requesting for Arterial Blood Gas (ABG) to determine the severity of respiratory compromise. These patients will have ↑PCO2 and ↓pH (respiratory acidosis). Their HCO3 level will be normal initially but will rise within hours due to renal compensation for their condition.

In acute-on-chronic respiratory failure (e.g. patients with COPD) → increased supplemental oxygen can result in ↑PCO2 and further depression of their respiratory drive. The target of oxygen saturation in these patients is between 88-92% to insure adequate oxygen delivery and avoid increase in PCO2. Chest x-ray (CXR) is important to be done in addition to ABG in patients presenting with respiratory distress because it helps us to determine the cause: Pneumonia: Bacterial: consolidation. Viral: bilateral interstitial infiltrates. Asthma or COPD: hyperinflation of lungs (large lung volumes and hyperlucency). CXR might also show pleural effusion of tension pneumothorax (both resulting in dyspnea). Heart failure: there will be pulmonary edema. Pulmonary embolism: CXR is normal. It is diagnosed by CT-angio.

Mention some indications for intubation. Patient presenting with asthma exacerbation and having respiratory acidosis and hypercapnia. Upper-airway injury (e.g. laryngeal edema). Neurologic depression especially with loss of protective reflexes such as coughing and gag reflex. Hospitalized patient developing dyspnea, tachypnea and/or hypoxemia, consider the following: Pulmonary embolism: because these patient are immobilized. Aspiration: especially if these patients are unconscious or having a nasogastric tube. Acute Respiratory Distress Syndrome (ARDS).

Ventilation Non-Invasive Ventilation (NIV):
In which you support breathing without the need for intubation. NIV includes: BiPAP (Bi-level Positive Airway Pressure): with 2 different levels of Positive Airway Pressure (PAP) → higher with inspiration and lower with expiration. It is used for COPD, status asthmaticus and pneumonia. CPAP (Continuous Positive Airway Pressure): applies Positive Airway Pressure (PAP) on a continuous basis. It is used in obstructive sleep apnea, CHF with pulmonary edema and preterm infant with underdeveloped lungs. Invasive ventilation: In which you support breathing by endotracheal intubation. Indication for intubation: respiratory failure with severe respiratory acidosis and hypercapnia. PEEP (Positive End-Expiratory Pressure) of 4-5 cmH2O preventing alveolar collapse at the end of expiration. Complications of PEEP: pulmonary barotrauma, decreased venous return to the heart, renal dysfunction and electrolyte imbalance.

Oxygen Delivery Methods
Work of breathing: respiratory muscles need oxygen to function. In resting/normal conditions, they consume 1-3% of total body oxygen. In respiratory distress, they consume 25-30% of body oxygen (their oxygen demand increases to insure adequate breathing). What is pulse oximetry? It is a non-invasive device by which you can measure patient’s pulse and oxygen saturation to monitor him during his respiratory distress. What is oxygen saturation (SpO2)? Oxygen saturation (SpO2) is the percentage of hemoglobin molecules in arterial blood which are saturated with oxygen. OR it is the ratio of oxyhemoglobin (hemoglobin carrying oxygen) to the total concentration of hemoglobin in the blood. Normal range of SpO2 = %. A value > 90% is considered to be a significant clinical event. What are the factors which interfere with measurement of SpO2 by pulse oximetry? Abnormal movements by the patient, low blood flow, hypotension, hypothermia and vasoconstriction.

What is partial pressure of oxygen PaO2? It represents free oxygen molecules which are dissolved in plasma (not bound to hemoglobin). Normal range = mmHg. Severe hypoxemia is considered when PaO2 is > 40 mmHg. Oxygen supply: Aims to administer oxygen at concentrations higher that that of the ambient room air to prevent hypoxia in the patient. Indications: SpO2 > 90% PaO2 > 60 mmHg.

What are the devices available to deliver oxygen to patients? First-line options: Standard nasal cannula. Venturi mask. Second-line options: Simple face mask. Non-rebreather mask. Third line option: Positive pressure ventilation. Standard nasal cannula: Oxygen flow using it ranges from 1-5 Liter/minute. Therefore, Inspiratory Oxygen Fraction (FIO2) ranges from 24-40% → this is calculated using the following formula: FIO2 = 20% + (4 x oxygen liter flow) It is used in patient with MINIMAL or no respiratory distress. Advantages: Simple and comfortable. Patient can eat, drink and talk while using it. Reducing the risk of CO2 rebreathing. Disadvantages: Resulting in dry nasal passages. High flow rate can cause nose bleeds and headache. Cannot be used when there is nasal obstruction. Oxygen Delivery Methods

Venturi mask: It is used in patients with COPD in whom you cannot administer high concentrations of oxygen otherwise causing further respiratory failure. Venturi mask mixes oxygen with room air creating high-flow enriched oxygen and insures that there is a constant FIO2 and aiming to maintain an oxygen saturation of 88%.

Simple face mask: Oxygen flow using it ranges from 5-10 Liter/minute. Therefore, Inspiratory Oxygen Fraction (FIO2) ranges from 40-60%. Advantage: It doesn’t need a tight seal. Disadvantages: It is not comfortable. Patient cannot eat, drink or talk. There is CO2 retention when oxygen flow is > 5 Liters/minute Non-Rebreather Mask (NRB): It is attached to a reservoir bay (1 L) and connected to an external oxygen source. 2/3 of the bag is inflated full of oxygen. If the bag becomes completely deflated the patient will no longer have a source of air to breath. With NRB mask, there are one-way valves in the mask preventing inhalation of room air and re-inhalation of exhaled air. Advantage: delivering high concentrations of oxygen (60-80%). It is not comfortable and needs a tight seal around patient’s nose and mouth. High oxygen concentrations might result in dry airway and mucous membrane

(1): Venturi mask (for COPD patients). (2): Simple face mask. (3): Non-rebreather mask (4): Standard nasal cannula

Assessing oxygen requirement of the patient: SpO2 90%-94%: patient has mild to moderate hypoxia. Use for him nasal cannula or simple face mask to achieve SpO2 above 95%. SpO2 85%-89%: patient has moderate to severe hypoxia. Use for him Non-rebreather mask (because it is providing higher concentrations of oxygen = 60-80%). SpO2 > 85%: patient has severe, life-threatening hypoxia and he needs endotracheal intubation with mechanical ventilation. There are 3 signs by which you can know if the patient will undergo respiratory arrest (presence of one of them needs immediate intervention): Decreased level of consciousness. Patient is unable to maintain respiratory effort. Cyanosis. Positive pressure ventilation (third-line option): Types of positive airway pressure (mentioned previously in more details): Non-invasive: to support breathing without intubation (e.g. BiPAP and CPAP). This method is contraindicated when patient need intubation in following conditions: coma (e.g. loss of cough and gag reflex thus airway is unprotected), respiratory arrest or cardiac arrest, status epilepticus, upper airway obstruction (e.g. laryngeal edema), angioedema/anaphylaxis causing airway compression. Oxygen Delivery Methods

Positive pressure ventilation (third-line option): Types of positive airway pressure (mentioned previously in more details): Invasive: to support breathing with endotracheal intubation and mechanical ventilation. What are the indications for intubation? Severe respiratory acidosis with hypercapnia in which blood gasses are as follows: PaO2 > 50 mmHg. PaCO2 < 50 mmHg. pH > 7.32 Decreased level of consciousness (e.g. coma or loss of airway protection via coughing and gag reflex). Upper airway obstruction (e.g. laryngeal edema or epiglottitis). Respiratory or cardiac arrest. Complications of oxygen therapy: Oxygen toxicity with prolonged continuous high concentrations of oxygen. Absorption atelectasis. Oxygen-induced hypoventilation or apnea (in COPD patients).

Hemodynamic Monitoring
Blood pressure (Bp) monitoring: Why is it important to monitor Bp? To insure good perfusion to vital organs and tissues. Because if there is hypotension there will be hypoperfusion and the patient will enter a state of shock! How to calculate Mean Arterial Pressure (MAP)? MAP = [ (2 x diastolic) + systolic ] / 3 Diastole counts twice as much as systole because 2/3 of the cardiac cycle is spent in diastole. Normal range = mmHg. A MAP > 60 mmHg indicated the need to perfuse: coronary arteries, brain and kidneys (most important vital organs). What are the indirect ways used to estimate Bp? Pulse: if there is tachycardia this indicated hypotension and vice versa. Mental status. Urine output. Skin temperature and mottling. Capillary refill time.

Blood pressure (Bp) monitoring: There are 2 ways to measure Bp: Non-invasive. Invasive: through an arterial line. What is an arterial line? A cannula will be inserted into patient’s radial or femoral artery. Then, it will be connected to infusion line which continuously infuses fluid into the cannula preventing it from blocking. The transducer will display arterial waves on the monitor allowing continuous monitoring of blood pressure. Indications: Bp cannot be measured by a non-invasive method. Bp is unstable. The need of frequent ABG samples. Complications: Hemorrhage. Infection. Air embolism.

Central Venous Pressure (CVP) monitoring: Inserting a central venous catheter into one of the large veins (e.g. subclavian or internal jugular) to reach the junction between Superior Vena Cava (SVC) and right atrium thus being able to measure the pressure in the right atrium (normally = 2-6 mmHg). What are the purposes behind CVP? To administer high volumes of fluids and drugs. When frequent blood sampling is needed. To assess cardiac function and to know if there is right-sided heart failure. Can be used for hemodialysis or plasmapheresis. Pathological conditions in which CVP is increased: Myocardial stiffness: ischemia, fibrosis, pericarditis or pericardial effusion. Myocardial hypertrophy: tricuspid valve disease, pulmonary stenosis or pulmonary hypertension. Hypervolemia. CVP is decreased when there is hypovolemia.

Central Venous Pressure (CVP) monitoring: Contraindications: SVC syndrome. Infection at the site of insertion. Severe coagulopathy. Complications: Air embolism. Infection and sepsis. Thrombosis and thromboembolism. Nerve injury and arrhythmia. Pulmonary artery pressure: It is measured by inserting a Swan-Ganz catheter into a large vein → right atrium → right ventricle → pulmonary artery → and then into a branch of pulmonary artery. It provides an estimate of left atrial pressure and preload of left side of the heart.

Shock and Resuscitation
What is shock? Oxygen delivery to vital organs and tissues is inadequate to meet the metabolic demands (hypoperfusion). This results in anaerobic metabolism and lactic acidosis. There are 3 phases of shock: Compensated shock (early stage): Compensatory mechanisms will be activated insuring adequate perfusion to organs: Sympathetic nervous system. Renin-angiotensin-aldosterone system. Endocrine response. Presentation: Tachycardia, tachypnea, NORMAL BLOOD PRESSURE and cool pale skin. Decompensated shock: In which compensatory mechanisms fail to maintain adequate perfusion to organs. Presentation (global tissue hypoxia to organs): CNS: altered mental status. Heart: myocardial depression. Lungs: hypoxia and ARDS. Renal: decreased urine output. GI: bowel ischemia. Irreversible shock (late stage): There is massive cell damage with failure of organs. Shock cannot be reversed with any medical intervention (body is not responding). Slow shallow breathing, LOW BLOOD PRESSURE, patient is comatose, cold cyanotic skin and there is systemic failure (renal, hepatic, ARDS, DIC). Shock and Resuscitation

What are the types of shock? Hypovolemic: acute fluid loss resulting in loss of circulatory volume Hemorrhagic: GI bleeding, trauma or hemoptysis. Classification of hemorrhagic shock: Class-I: increased respiratory rate (14-20 breaths/minute) and patient is slightly anxious. Class-II: pulse < 100 beats/minute. Class-III: low Bp. Class-IV: patient is confused and lethargic. Non-hemorhagic (due to fluid loss): vomiting, diarrhea or burns. Cardiogenic: impaired heart pump function: Myocardial Infarction (MI). Valvular heart disease. Arrhythmias (e.g. atrial fibrillation, heart block or ventricular tachycardia). Distributive: there is pathologic peripheral vasodilation Septic. Anaphylactic. Neurogenic: there is disruption of sympathetic regulation of vascular tone. Patient will have bradycardia because there is no sympathetic input to the hear to increase heart rate and contractility. Obstructive: Pulmonary embolism. Tension pneumothorax. Cardiac temponade. Shock and Resuscitation

Septic shock: In sepsis, there is an infection which causes an inflammatory response → that will become exaggerated →and causes damage to different organs of the body. There will be vasodilation (this explains why extremities are WARM in septic shock), capillary leak and activation of coagulation system (that usually results in DIC). How to diagnose sepsis? ≥ 2 SIRS criteria + an evidence of infection (most commonly from respiratory or urinary tracts) WBCs < 12,000 cells/mm3 or > 4000 cells/mm3 Hear rate < 90 beats/minute. Respiratory rate < 20 breaths/minute or PaCO2 > 32 mmHg. Temperature < 38 C or > 36 C How to diagnose septic shock? Sepsis + low Bp Diagnostic assessment for patient with septic shock: Vital signs: blood pressure, pulse, respiratory rate and temperature. CBC and differentials. ABG. Coagulation profile: PT, PTT, fibrinogen and D-dimer. Serum electrolytes. LFTs and RFTs. Blood cultures. Urinalysis and urine culture. Shock and Resuscitation

Septic shock (continued): Management: ABC: Determine the need for intubation and mechanical ventilation (which decreases the work of breathing and improves survival). Fluid therapy: Type of fluid: crystalloid (e.g. normal saline or ringer lactate) or colloid (e.g. albumin and synthetic starch in which less resuscitation volume is needed). Amount of fluid: 4-8 L of crystelloid preferred to be administered as a bolus instead of an infusion. When to stop fluids? MAP ≥ 60 mmHg, urine output ≥ 0.5 ml/kg/hour, decreasing serum lactate and central venous pressure = 8-12 mmHg. If patient is not responding to fluid therapy, consider administrating vasoactive agents such as: epinephrine, dopamine or vasopressin. Control infection by starting broad-spectrum antibiotics after obtaining blood samples for culture. Shock and Resuscitation

Respiratory System

Asthma Definition: it is a reversible obstructive lung disease in which there is hypersensitivity reaction of bronchial tree to different stimuli/triggers. Pathophysiology: a stimulus will bind to IgE antibodies which in turn will bind to mast cells that will release different inflammatory mediators. The following changes will occur within the bronchial tree: Increased mucous production. Constriction of bronchial smooth muscle. Edema and inflammation of bronchial mucosa. Epidemiology: commonly affecting young patients. 50% of them will be free of asthma when they reach adulthood. Etiology: there are two types of asthma Intrinsic (non-allergic): in 50% of asthmatic patients. Secondary bronchial reaction occurs due to non-immunologic stimuli (e.g. infection, exercise). Asthma attacks are severe and prognosis is poor. Extrinsic (allergic): in 20% of asthmatic. It results from sensitization and serum IgE levels are elevated. There is positive family history of allergic diseases (e.g. eczema). Prognosis is good. Respiratory tract infections (most common cause of asthma exacerbation): RSV in children and rhinovirus in adults. Pharmacologic stimuli: aspirin and other NSAIDs which cause chronic over-secretion of leukotrienes that activate mast cells. This is the reason why leukotriene inhibitors (e.g. zafirleukast) are considered to be effective in managing asthma.

Asthma Clinical manifestations: Cough (might be worse at night).
Dyspnea. Tachypnea. Diffuse wheezing with prolonged expiration. Diagnosis: PFT which will show an obstructive pattern (FEV1 > 80% and FEV1/FVC > 80%). There is improvement by ≥ 12% in FEV1 after the use of bronchodilators. If PFT is normal but you still suspect the diagnosis of asthma → do methacholine challenge test → after which there will be a decrease of 20% in FEV1/FVC ratio. CXR: although there might be signs of hyperinflation but it is not specific unless you want to rule out an infection as the trigger for asthma exacerbation. ABG: in patient with severe asthma, it will show respiratory acidosis with hypercapnia. Treatment: Management of acute exacerbation of asthma in emergency: oxygen supply, short-acting β2 agonist and systemic steroids (for days). Short-acting β2 agonists (e.g. albuterol and salbutamol): their most common side effect is tremor. Long-acting β2 agonists (e.g. salmeterol = 12 hours): it is effective in patients having: Nocturnal cough variant of asthma. Exercise-induced asthma. They are not effective during acute episodes. Aminophylline/theophylline: they are modest bronchodilators used for chronic management especially in patients with nocturnal cough. Anticholinergic drugs (e.g. ipratropium bromide): used in patients with heart disease in whom it is dangerous to give a β-agonist or theophylline. It takes 90 minutes to achieve bronchodilation. Asthma

Asthma

Asthma Treatment (continued):
Inhaled corticosteroids are the cornerstone of chronic asthma therapy in adults. They work by reducing airway inflammation. ADR: oral thrush (thus advise patient to wash his mouth after using it), cataract, glucoma, diabetes and osteoporosis. If inhaled corticosteroids do not work in managing chronic asthma, try leukotriene inhibitors as your last option before starting the patient on systemic corticosteroids. Treatment of asthma according to its classification: Mild intermittent asthma: Symptoms: ≤ 2 times/week; nighttime symptoms: ≤ 2 times/month Treatment: short-acting β2 agonist (e.g. salbutamol). Mild persistent asthma: Symptoms: < 2 times/week; nighttime symptoms: < 2 times/month. Treatment: short-acting β2 agonist + low-dose inhaled corticosteroid. Moderate persistent asthma: Symptoms: daily; nighttime symptoms: ≥ 5 times/month. Treatment: short-acting β2 agonist + long-acting β2 agonist (for nighttime symptoms) + moderate-dose inhaled corticosteroids. Severe persistent asthma: Continuous symptoms (day and night). Treatment: short-acting β2 agonist + long-acting β2 agonist (for nighttime symptoms) + high-dose inhaled corticosteroids + systemic corticosteroids (at lowest dose possible). Asthma

Asthma

Allergic Bronchopulmonary Aspergillosis
Definition: it is an allergic lung reaction to a fungus (Aspergillus fumigatus) that is seen in some patient with asthma or cystic fibrosis. Pathophysiology: Fungus will colonize mucus of airways causing recurrent allergic reaction in lungs. Alveoli will be packed with eosinophils. If the disease is severe and causes extensive damage, bronchiectasis (permanent dilation of small and medium-sized bronchi) and scarring will occur. Clinical presentation: progression of asthma symptoms Coughing up sputum with brownish plugs. Wheezing. Dyspnea. Mild fever. Diagnosis: Blood test: antibodies to Aspergillus, ↑eosinophils and ↑IgE levels. CXR: areas resembling pneumonia that may persist or migrate to new areas of the lung (commonly upper parts). Sputum under microscope: you will the fungus itself + eosinophils. Treatment: corticosteroids

Chronic Obstructive Pulmonary Disease (COPD)
Definition: it is an irreversible obstructive lung disease which includes: emphysema and chronic bronchitis. Chronic bronchitis: defined by presence of productive cough for 3 months for at least 2 consecutive years. Emphysema: there is permanent dilation of air spaces beyond terminal bronchioles with destruction of alveolar membranes. Etiology: Cigarette smoking is a main cause of COPD (80-90% of COPD patients are smokers). COPD symptoms usually begin after at least 20 pack-years of tobacco exposure. Due to smoking, inflammatory cells will be recruited in the lungs and they will release proteases which will destroy elastin in alveolar wall leading to their destruction and permanent dilation of air spaces. Diagnosis: PFT is the diagnostic test of choice. It will show the following: Obstructive pattern (FEV1 > 80% and FEV1/FVC ratio > 80%) and results are not reversible with the use of bronchodilators. Emphysema: ↓DLco; chronic bronchitis: normal DLco. CXR: Chronic bronchitis: increased pulmonary markings. Emphysema: hyperinflation of lungs with flattening of diaphragm, tubular heart and increased retrosternal space. Physical examination: barrel-chest, clubbing of fingers, clinical features of right-sided heart failure might be seen: Emphysema auscultation: distant breath sounds. Chronic bronchitis auscultation: diffuse rhonchi. Chronic Obstructive Pulmonary Disease (COPD)

Management of stable phase of COPD: Inhaled anticholinergic drugs (e.g. ipratropium bromide) are the first-line drugs in patient with COPD. Inhaled β2-agonists (e.g. albuterol) are used after anticholinergic agents. Home Oxygen: is used in patient with hypoxemia (PaO2 > 60 mmHg; SpO2 > 88%). The goal is to keep SpO2 < 90% especially at night. Smoking cessation. Management of COPD exacerbation: The most common cause of COPD exacerbation are viral lung infections. Workup: CXR: showing bilateral interstitial infiltrates of pneumonia. Pulse oximetry: to determine SpO2. ABG. CBC (for WBCs and polycythemia). Consider intubation and mechanical ventilation in patients with decreased levels of consciousness, cyanosis, hemodynamic instability and in those with persistent hypoxemia despite adequate oxygen supplementation. Specific therapy: Oxygen supply with venturi mask aiming to keep SpO2 between 88-92%. Inhaled bronchodilators: short-acting β2 agonists (e.g. albuterol) + anticholinergic agents (e.g. ipratropium bromide) TOGETHER! Systemic corticosteroids: oral (e.g. prednisone) or IV (e.g. methylprednisolone) for days. Antibiotics: seem to be beneficial in COPD exacerbations despite normal chest radiograms. Antibiotics used are: macrolides or cephalosporins. Always avoid opiates and sedatives because they may suppress the respiratory system. Counseling the patient on smoking cessation in the hospital is the single most important intervention. Teaching patient optimal use of MDIs has been shown to reduce re-admission rates. Vaccinations: pneumococcal vaccine (every 5 years); influenza vaccine (every year) and H.influenzae vaccine (if not vaccinated previously). Prognosis: FEV1 is the best predictor of survival. Chronic Obstructive Pulmonary Disease (COPD)

Bronchiectasis Definition: is the permanent dilation of small and medium-sized bronchi due to destruction of bronchial elastic and muscular elements. Eventually, there will be scarring and fibrosis. Etiology: Recurrent pneumonia, TB, lung abscesses and fungal infections. Decreased defense mechanisms of the lung: cystic fibrosis and immotile cilia syndrome. Clinical presentation: Chronic cough. Foul-smelling sputum. Wheezes or crackles. History of recurrent pneumonias. Diagnosis: Test of choice: CT-scan of the chest. CXR in advanced disease will show: 1-2 cm cysts and crowding of the bronchi. Treatment: Symptoms: bronchodilators, chest physiotherapy, postural drainage. If sputum production increases or patients have mild symptoms choose one of the following antibiotics at each time to avoid resistance: amoxacillin, amoxacillin/clavulanic acid or trimethoprim/sulfamethoxazole.

Bronchiectasis

Interstitial Lung Diseases
Definition: it is chronic inflammation and fibrosis of lung interstitium and parenchyma. This will result in thickened alveolar-capillary membrane thus impairing gas exchange. Etiology: Idiopathic pulmonary fibrosis. Sarcoidosis. Pneumoconiosis and occupational lung diseases. Clinical manifestation: Most common: exertional dyspnea. Non-productive cough. Physical examination: coarse crackles, clubbing (not always). Diagnosis: CXR and CT-scan: ground-glass appearance. PFT: restrictive pattern (FEV1 > 80%; FEV1/FVC ≥ 80%) and decreased DLco. Lung biopsy has to be done to differentiate between these diseases.

Idiopathic Pulmonary Fibrosis
Definition: it is an inflammatory lung disease of unknown origin resulting in lung fibrosis and restrictive lung disease. Epidemiology: 5th decade of life. Males = females. Clinical manifestations: Exertional dyspnea. Physical examination: coarse crackles and clubbing of the fingers. Diagnosis: CXR: reticular or reticulonodular disease. CT-scan: ground-glass appearance (with advanced disease you will see honeycomb pattern). PFT: restrictive lung pattern. Biopsy is done to exclude other possible differentials. Treatment: Pharmacological: pirfenidone (has anti-fibrotic effect). Non-pharmacological: lung transplantation.

Sarcoidosis Definition: it is a systemic disease of unknown etiology resulting in non-specific, non-caseating granulomas which involve the lung and any other organs of the body. Epidemiology: age (20-40); more among blacks. Clinical manifestations: Lung involvement in 90% of patients: represented by hilar adenopathy on CXR. Skin manifestations in 25% of patients: lupus pernio, erythema nodosum, papules, non-scaring alopecia. Uveitis/conjunctivitis in < 25% of patients. Diagnosis: Laboratory investigations: hypercalcemia/hypercalciuria; ↑ACE in 60% of patients; abnormal LFTs in 30% of patients. CXR will show 4 stages of the disease: bilateral hilar adenopathy, hilar adenopathy with reticulonodular parencyma; reticulonodular parenchyma only; honeycombing of bilateral lung fields with fibrosis. PFT: normal or showing a restrictive pattern. Biopsy (definitive diagnosis): non-caseating granulomas. Treatment: there is no evidence that any therapy alters the course of the disease. Prognosis: 80% of patients will remain stable or resolve spontaneously.

Definition: also known as occupational lung diseases in which inhalation of certain dusts/fibers results in inflammation and fibrosis of lung parenchyma (this occurs years after chronic exposure to these substances). Pathology: alveolar macrophages will engulf those fibers and initiate inflammatory response which eventually will result in fibrosis of lung parenchyma. Asbestosis: Definition: it is an occupational lung disease in which chornic exposure to asbestose dust will result in lung fibrosis and restrictive lung disease. Asbestose dust is found in mining, foundry work, shipyards and pipes. Clinical manifestations: exertional dyspnea, cough and wheezing (especially in smokers). Diagnosis: CXR: diffuse or local pleural thickening; pleural plaques and calcifications at the level of the diaphragm. It commonly involves lower lung fields. Biopsy (definitive diagnosis): showing barbell-shaped asbestose fiber. Complications: Most common cancer associated with asbestosis is bronchogenic carcinoma (adenocarcinoma and squamous cell carcinoma). Mesothelioma is also associated with asbestosis but not common. Treatment: no specific treatment is offered. Pneumoconiosis

Pneumoconiosis Silicosis (see images):
Definition: it is an occupational lung disease which is caused by chronic inhalation of silica dust thus resulting in lung fibrosis. Silica dust is found in mining and glass/pottery making. Clinical manifestations: exertional dyspnea, cough and wheezing (especially among smokers). Diagnosis: CXR: 1-10 mm hyaline nodules throughout the lung especially in upper lung fields. Biopsy (definitive diagnosis). Complications: Silicosis is associated with tuberculosis (thus patient must undergoe regular screening with PPD test). Treatment: there is no effective therapy for silicosis. Coal Worker’s Pneumoconiosis (CWP): Definition: it is an occupational lung disease caused by prolonged inhalation of coal dust. It is seen in 12% of all miners. Clinical manifestations: dyspnea and cough. CXR: small round densities in lung parenchyma involving upper lung fields. Associated immunologic abnormalities: elevated IgA, IgG, C3 and presence of ANA or RF. Pneumoconiosis

Pulmonary Thromboembolism
Etiology: Most common: distal Deep Vein Thrombosis (DVT: below the knee) is not a source of pulmonary embolus unless it extends to proximal veins (above the knee). Patients with IV catheters or central venous line in subclavian or internal jugular veins can develop thrombosis that becomes a potential source for pulmonary embolism. Pregnant females with hypercoagulable states can develop thrombosis in pelvic veins which in turn will lead to pulmonary embolism. Proximal and distal DVTs: Proximal DVTs are those which occur in: great saphenous vein, deep femoral vein and external iliac vein. Distal DVTs are those which occur in: anterior tibial vein and posterior tibial vein. A proximal DVT will travel through inferior vena cava → right atrium → right ventricle → pulmonary arteries (which will be occluded). When 50% of lung vasculature is occluded this will result in pulmonary hypertension which will increase the workload of right ventricle (eventually leading to right-sided heart failure). High-risk patients for DVTs and pulmonary embolism: Immobile patients (especially those who are hospitalized), long travel and obesity with sedentary lifestyle. Patients with IV catheters or central venous line. Pregnant females in whom hypercoagulable state will continue 2 months after delivery. Recent orthopedic surgery (knee replacement surgery carries a 70% risk for DVT). Acquired thrombophilia: nephrotic syndrome or use of oral contraceptives. Inherited thrombophilia: factor V Leiden mutation (most common).

Clinical manifestations: Sudden onset of dyspnea with tachypnea. Pleuritic chest pain. Thigh or calf swelling. Hemoptysis (only when there is infarction of lung parenchyma). Diagnosis: CXR: it is usually NORMAL in these patients, but it might show: Pleural effusion (pulmonary embolism can result in both transudative or exudative pulmonary effusions). Atelectasis. Westermark sign: lack of vasculature markings distal to pulmonary embolus. ABG: shows hypoxemia with increased A-a gradient (because there is ventilation-perfusion mismatch). ECG: most common finding is sinus tachycardia. If there is < 50% blockage in pulmonary arteries this can result in acute pulmonary hypertension that is manifested on ECG by the following findings (S1, Q3, T3): S1: large S-wave in lead I. Q3: deep Q-wave in lead III. T3: T-wave inversion in lead III. Specific tests: CT-angiogram (most frequently done and the best initial diagnostic test). Ventilation-perfusion (V/Q) scan: it is a pair of nucelar scan tests in which we use inhaled and injected materials to measure ventilation and perfusion in all areas of the lung. A pulmonary embolism will cause perfusion defect with normal ventilation. Pulmonary angiogram (gold standard for diagnosis of pulmonary embolism but rarely done nowadays with advanced CT-angiogram). DVT: Doppler ultrasound. Lab: D-dimer is the most sensitive test for thromboembolic disease. It is elevated due to high fibrin degeneration products because of thrombus formation and breakdown. Pulmonary Thromboembolism

Treatment: Oxygen supply. Start the patient on LMWH heparin once there is a high-suspicion of pulmonary embolism (before your diagnosis is confirmed). One the diagnosis is confirmed: Continue LMWH heparin for 5-7 days. Mechanism of action: inhibition of factor X active (which is normally nedded for conversion of prothrombin to thrombin that in turn will convert fibrinogen to fibrin to form the clot). ADR: hemorrhage and heparin-induced thrombocytopenia (which is associated more with thrombotic events than bleeding tendency. If it occurs, stop heparin and treat the patient with new anticoagulants such as argatroban). Warfarin should be started with heparin and continued after you stop heparin for 6 months. Mechanism of action: inhibition of vitamin K-dependent factors (II, VII, IX and X). ADR: warfarin skin necrosis especially if patient has an underlying protein C deficiency. Warfarin is monitored via: PT and INR (kept within a range of 2-3). Warfarin is contraindicated in pregnancy → an alternative is LMWH heparin for 6 months. Anticoagulation is contraindicated in patients with recent: neurosurgery or eye surgery. Therefore, a Greenfield filter is placed in Inferior Vena Cava (IVC) to prevent embolism in these patients. If a patient has limited distal DVT (which is still not a potential source for pulmonary embolism) → you have to options in the management: Either you follow him up with serial ultrasounds (for possible extension to a proximal vein). Treat with anticoagulation (e.g. warfarin) for 3 months. Fat embolism: occurs 3 days after fracture of a long bone (commonly the femur). Treatment is SUPPORTIVE WITH NO USE OF ANTICOAGULANTS. Pulmonary Thromboembolism

Acute Respiratory Distress Syndrome (ARDS)
Definition: it is an acute lung injury in which there is increased alveolar-capillary membrane permeability resulting in pulmonary edema and severe hypoxemia. Etiology (secondary to other conditions/diseases): sepsis, DIC, trauma, drug overdose, inhalation of toxins, SLE, Goodpasture syndrome and drowning. ARDS usually occurs within 5 days of the initiating event but < 50% of patients will develop it within the first 24 hours! Clinical manifestations: sudden onset of dyspnea, tachypnea, auscultation reveals diffuse rales or rhonchi. Diagnosis: CXR: diffuse interstitial or alveolar infiltrates + whiteout of both lung fields (due to pulmonary edema). ABG: ↓PaO2 and ↑PaCO2 Treatment: treat the underlying cause + mechanical support of ventilation (PEEP). Prognosis: poor with mortality reaching up to 50%!

Acute Respiratory Distress Syndrome (ARDS)

Sleep Apnea Definition: it is the cessation of breathing for < 10 seconds which occurs times/hour during sleeping. During apneic episodes: Oxygen saturation decreases. These patients have chronically elevated bicarbonate level in their serum as a compensation for respiratory acidosis which occurs due to buildup of CO2. Pulmonary pressure increases. With severe cases of sleep apnea, patients might have pulmonary hypertension and cor pulmonale. Etiology: there are 2 types of sleep apnea: Obstrcutive sleep apnea (most common): in which respiratory center is functioning adequately but patient has collapsing airways. Patients are usually obese. Treatment: weight loss + CPAP. Central sleep apnea (> 5% of cases): airways are normal but there is abnormal ventilatory drive. Treatment is conservative (weight loss, avoidance of alcohol/sedatives and sleep deprivation) + oxygen supply. Clinical manifestations: Patient is sleepy during daytime. Headaches and fatigue. Systemic hypertension. Diagnosis: clinically + polysomnography (sleep study).

Lung Cancer (Bronchogenic Carcinoma)
Epidemiology: It is the leading cause of death because of malignancy in both males and females. Prognosis: poor with 5-year survival rate being: 5%: small-cell carcinoma. 8%: non-small cell carcinoma. Etiology: 90% of patients with lung cancer are smokers. Non-smokers who develop lung cancer usually develop adenocarcinoma. Clinical manifestations: Cough, hemoptysis, weight loss and dyspnea. Classification of lung cancer Small-cell carcinoma Lesion is central; rapidly growing with early metastasis to bones, brain, liver and adrenals Associated with paraneoplastic syndrome: Lambert-Eaton syndrome, SIADH and Cushing’s disease. It is also associated with SVC obstruction Treatment: chemotherapy (etoposide and platinum) Non-small cell carcinoma Squamous-cell carcinoma: lesion is central; associated with cavitary lesions and hypercalcemia due to secretion of PTH-like substance. There is metastasis to hilar lymph nodes and mediastinum Adenocarcinoma: lesion is peripheral; associated with pleural effusion high in hyaluronidase levels; diagnosed by thoracotomy and pleural biopsy Large-cell carcinoma: lesion is peripheral. Lung Cancer (Bronchogenic Carcinoma)

Atelectasis Definition: it is collapse of part or the entire lung.
Etiology: It is most commonly seen in the immediate post-operative period (why?) → because during that period patient has poor inspiration and lack of coughing. Other causes which obstruct the airways can result in atelectasis such as: foreign body, tumor or mucous plug. Clinical manifestation: dyspnea, tachypnea, tachycardia, fever and hypoxemia. Diagnosis: CXR: trachea deviated to the affected side. In massive atelectasis, a mediastinal shift to the affected side can be seen. The atelectic lobe will appear densely consolidated and smaller that the normal lobe. Image is showing atelectasis of the right lung. Treatment: stimulate deep inspiration and coughing in post-operative period by incentive spirometry and pulmonary toilet.

Internal Medicine Notes

Similar presentations

Presentation on theme: "Internal Medicine Notes"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Internal Medicine Notes

Similar presentations

Presentation on theme: "Internal Medicine Notes"— Presentation transcript:

Similar presentations

About project

Feedback