Cardiopulm I 2024 Pulmonary Risk Factors and Disease PDF

Pulmonary Risk Factors and Disease  Objectiv By the end ofes this lecture you should be able to: Name at least 3 interventions focused on secretion management in CF Identify at least 4 different asthma triggers Identify a...

Pulmonary Risk Factors and Disease  Objectiv By the end ofes this lecture you should be able to: Name at least 3 interventions focused on secretion management in CF Identify at least 4 different asthma triggers Identify at least 4 different things PTs should advocate in caring for people with asthma Distinguish between  (1) Pulmonary Disease Restrictive vs. Obstructive OBSTRUCTIVE: Bronchopulmonary Dysplasia (sounds familiar) Cystic Fibrosis Asthma Bronchitis → Bronchiectasis Emphysema  (2) Obstructive Pulmonary Disease Respiratory tract diseases that produce an obstruction to air flow (especially out) which can ultimately affect the mechanical function and gas exchange of the lungs  (3) Risk Factors Risk Factors include: Age: (Prematurity, Elderly) Premature babies lack surfactant Immunocompromise Environmental Factors Smoking Genetics Restricted Thoracic Movement  Smoking What does it produce to the lungs? - Produces a low level chronic inflammation in the lungs This results in what cells? - increased phagocytes, neutrophils, and alveolar macrophages all contribute to the breakdown of elastin in the alveoli  Hypoxia Hypoxia is inadequate oxygenation It can result from: Pulmonary Disease with impaired diffusion V-Q mismatching:shunting Inadequate O2 transport Inadequate tissue oxygenation Sickle cell or anemia  Ventilation Ventilation is defined as movement of gases in and out of the lungs (↓ = hypo- ) (↑ = hyper- )  Hypoventila tion Causes: Respiratory center depression Neural conduction interference Respiratory muscle disease Restriction of the thorax Restriction of lung excursion  Hyperventilation Anxiety Lesion of CNS Medications/ Hormones Increased Metabolism Hypoxia/ CO2 retention (short term) Acidosis Hypotension Pain  (1) Bronchopulmonary Dysplasia (BPD) BPD: Chronic lung disease of early infancy Presentation: O2 dependency beyond 1 mos., and vent support Infants at risk include those with: Prematurity (2) BRONCHOPULMONARY DYSPLASIA Occurs in some with Resp Dist Synd infants who require what type of intervention? - WHO REQUIRE PROLONGED VENTILATION AKA Pulmonary Fibroplasia and ventilator lung  (3) BRONCHOPULMONARY DYSPLASIA Occurs more in LBW babies who rec’d high flow O2 for 5 d or longer Does severe BPD correlate with developmental delays in infants? – YES, many infants recover and improve over time however severe  (4) BPD: Stage 1: Hyaline Pathology membrane disease caused by decreased surfactant Stage 2: Tissue granulation, obliterating bronchitis Stage 3: Emphysematous changes (distended terminal airways and open alveoli)(hyperinflation) Emphysema: lungs are overstreched and full of air Stage 4: Subepithelial fibrosis, right ventricular  (5) BPD: Pathogenesis Barotrauma (injury caused by pressure) O2 Toxicity (cellular tissue damage occurs from excessive oxygen levels in the blood) Pulmonary interstitial edema Patent Ductus Arteriosus (PDA)  BPD: Clinical Features(6) Infants will present with: Tachypnea Cyanosis Bronchiolitis or PNA May require a tracheostomy  (1) Cystic Fibrosis History 1938 Andersen: Cystic Fibrosis of the Pancreas Classified as an exocrine gland dysfunction “Baby is salty to kiss” 1989 Chromosome 7 located  (2) Incidence Most common inherited life shortening illness of Caucasians 1/2000 live births Autosomal recessive trait 5% of population is a heterozygote carrier  (3) Normal Pancreatic Function Pancreas secretes enzymes which aid in what? - in the digestion of fats and proteins Normal mucous bathes and protects internal surfaces, transports chemicals between organs through small ducts Flows easily, carrying bacteria, dirt  (4) Cystic Fibrosis Pathology Abnormal Gene- affects the transmembrane conductance regulator (CFTR) protein CFTR is present in the respiratory tissue, GI tracts, as well as the sweat glands, and reproductive system CFTR changes the cell permeability to NaCl, causing an electrolyte abnormality Accumulation of hyper viscous secretions leads to progressive obstruction of mucous secreting exocrine glands, preventing delivery to target organs Organs most affected: lungs, pancreas, reproductive system,  (5) Cystic Fibrosis Impairments 1) Dysfunctional Cl channel epithelial function causes abnormal concentrations of Na and Cl 2) Blocked exocrine gland function 3) Increased susceptibility to chronic endobronchial colonization  Pancreatic Dysfunction Viscous secretions begin to obstruct pancreas in utero with periductal inflammation and fibrosis Maldigestion of protein = greasy, bulky, foul smelling stools  Pulmonary Dysfunction Obstruction of small airways Air trapping and atelectasis Progressive airway obstruction Decreased gas exchange Opportunistic bacteria, inflammation, bronchiectasis, and irreversible airway damage  (6) Presentation Patients are likely to present with: Persistent Cough, Recurrent Pneumonia, Excessive Appetite/Poor Weight Gain, Salty Skin/Sweat, Bulky, Foul-Smelling Stools, Infertility, Nasal Polyps, Chronic Wheeze, Glucose Intolerance, Tachypnea, Cyanosis/Digital Clubbing, Pneumothorax:Exertional Dyspnea, does not mean necessarily that Pneumothorax, Hemoptysis, Right the whole lung, but it can be partial If a pt has severe pneumothorax, check for tracheal deviation  (7) Associated Medical Complications ↑ Incidence of DM, Intestinal Obstruction, Hepatobiliary involvement, Recurrent Pancreatitis Obstruction of the vas deferens (98% infertility in males, ↓ fertility in females) Sinusitis (Persistent HA) Pneumothorax 2º rupture of bronchiectatic cysts or subpleural blebs, Clubbing (look at fingernails), Anorexia, Malnutrition  Lifesp Persons arean living into their 3rd and 4th decades of life.  Genetic Counseling Controversial Screening for prospective parents to determine presence of gene Genetic testing of the fetus to determine presence of the disease  (8)Medical Tests for Diagnosis Sweat Test: Quantitative pilocarpine iontophoresis. Measures Cl levels in sweat. > 60 mEq/L Nasal PD: Potential difference of electrical charge across the mucous membrane of the nose. Nl –5 to –30 mV, CF –40 to –80 mV Stool Analysis: Find malabsorption ↑ fat in stool (>7% is abnl with CF see 20%  (8) Sputum Cultures May be positive for: Strep Pseudomonas Burkholderia Cepacia (nosocomial) Haemophilus Influenza Klebsiella  (9a) CXR Findings are negative early in the disease process Later, X-rays demonstrate streaky, white bands across the lung fields PNA, bronchiectasis, atelectasis, pneumothorax  (9b) CF CXR Strea ky White bands YOU PUT THEM IN ALL POSTURAL CONDITIONS FOR DRAINAGE  (10) PFT Tests will Pulmonary Function reveal the following problems Obstructive Components will see: Air trapping, Increased RV and FRC, Increased PaCO2 Restrictive Components will see: Restricted air flow, Decreased TLC, VC  (11a) CPT Assessment Auscultation - Rales/sonorous wheezes Increased A/P diameter (Barrel Chest) Chronic, productive cough Will the pt utilize accessory  CF does not trandelenbu Leads to GU (11b) CPT Mod trandelenbu Treatment Postural Drainage What’s wrong w/this picture? →→ FET (forced expiration technique) (huffing) as effective as 2-3 CPT treatments/day ACB (Active cycle breathing) uses FET in conjunction with thoracic exp. exercises AD (Autogenic draining)(uses segmental breathing)  Airwa (11c) CPT clearanc able to c effectiv Treatment Intrapulmonary Percussive Ventilator (IPV) machine that delivers small bursts of air to help clear mucous  to breath more deeply PEP (positive expiratory pressure) demonstrated to improve exercise tolerance and secretion clearance when paired with FET  (12) CF PEP/Flutter Person breathes through a mask or hand held device Air flows in freely but exhale encounters resistance (+ vibration c flutter device) This keeps airways open allowing air to get behind mucous facilitating clearance  (13) CF PEP/Aerobika Aerobika Another oscillating positive expiratory pressure device Instruct pt to keep cheeks taut Dial allows control of resistance  (14) CF If cheeksPEP/Aerobika taut oscillation translates better to deeper structures  (15) CPT Treatment PEP (positive expiratory pressure)/flutter Inflatable therapy vest Trunk Mobility/Postural Education Exercise encouragement Mucolytics  (16) CF PT Any PT program should advocate regular exercise, the benefits of which include:  ↑ sputum clearance  ↑ aerobic fitness  psychological benefits  (17) CF Nutrition Balanced diet - high calorie Enzyme supplementation for fat and protein digestion May require supplemental nutrition at night by NG or IV (hydration essential for adequate expectoration of secretions)  (18) CF Abx Pharmacology Nebulizers Mucous thinners CFTR Modulation Therapies  CF Pharmacology, Abx Abx to address acute infections Prophylactic use of antibiotics Controversial Tolerance to antibiotics  CF Pharmacology Mucolytics ↓ sputum thickness facilitating clearance of secretions Nebulizers deliver medications in the form of a mist  CF New Drugs, CFTR Modulators First drug: Kalydeco, a CFTR potentiator, approved Jan 2012, counters mutation present in 4% CF cases, cost: ≈$300,000 yr Second drug: Orkambi, a combination drug which incorporates Kalydeco, approved 2015 for CF pts 12 and older, cost: NYT ≈$300,000 Article: F.D.A. Approves New Cystic Fibrosis Drug yr By Andrew Pollack Published: January 31, 2012  CF New Drugs, CFTR Modulators In 2019, huge breakthrough: Trikafta, a highly effective CFTR modulator Approved for patients with CF who have at least one F508del mutation in the CFTR gene, estimated to represent 90% of the CF population Reduces mucus→infections→scarring Taken as 3 tablets/day  (1) Lung Pioneer: Transplant Toronto group 1987, double lung transplant Does it need to be done unilaterally or bilaterally? - Must be done bilaterally Approach is bilateral sub mammary incisions for anterolateral approach (2) Lung Transplant Criteria Severe pulmonary disease with marked hypoxemia Increase in the frequency of hospitalizations Increased antibiotic resistance No other significant vital organ disease History of medical compliance Acceptable psychological profile Complicated by fact many recipients are adolescents May tend to skip follow up rx in order to fit in better with pee  (3) Lung Transplant Will implanted lugs have more or less mucous? - Implanted lungs won’t have CFTR defect so there will be less mucous Will CF keep on affecting other systems post transplant? - BUT CF process is ongoing in all other affected systems 2015 study using Canadian CF Registry found 67% of recipients living >5 yrs with half of that # living >10 yrs Stephenson, A.L., Tom, M., Berthiaume, Y. et al, A contemporary survival analysis of individuals with  (4) Lung Transplant P/O Immunological suppression post op Risk of rejection Pts may be colonized with infectious agents (esp in sinuses) that can infect new lungs Unique challenges (only organ transplant that comes into contact with the outside world)  CF Research Attempts to normalize electrolyte transport of the epithelium Delivery of CFTR to epithelial cells by modified adenovirus Gene Therapy  CF Resources Cystic Fibrosis Foundation: http://www.cff.org/ Excellent website packed with information  (1) ASTHMA Greek: “To Pant.” Normal airways are dynamic, they dilate to move ↑ air as during exercise and constrict to protect airways as during exposure to irritating gases = airways less dynamic  (2) Asthma Episodic in nature Acute episodes alternate with symptom free periods Chronic inflammatory disease Airways narrow in response to a stimulus  (3a) ASTHMA: Acute Attack Sxs: ↑ mucosal edema, ↑ secretions, hyperactive airways (bronchospasm) Loud audible wheezes, rales and rhonchi Can be a life threatening event Asthma  (3b) ASTHMA: Acute Attack Acute episodes can be triggered by: Allergens Infection Environmental Stress (esp cold) Emotional Stress EXERCISE  (4a) Exercise Induced Bronchospasm Caused by loss of heat and water from the lungs during exercise due to hyperventilation of dry cool air It is estimated that 80% to 90% of people with asthma have EIB Many patients only have bronchospasm with exercise  (4b) Exercise and EIB Asthma (exercise induced broncospasm) is defined as transitory constriction of the lower airways following strenuous exercise EIB is found in ≈ 80% of asthmatics EIB is also found in > 15% of Olympic athletes  (4c) Managing EIB Whether the EIB is a component of chronic asthma or only emerges with elite level physical activity - Management options are similar: – Pre-exercise warm up – Avoidance of environmental triggers Good (including cold) a diar – Pharmacology (adherence) don’t cause – Diet: sodium restriction and hydration, fish oil supplements (anti- inflammatory), Vitamin C (thought to ↓ oxidative damage but evidence is weak) Preventing SOB is better than  (5a) Asthma Meds Quick relief (rescue) medications Short acting beta agonists – Commonly albuterol Anticholinergics (Ipratropium) (blocks acetylcholine, more often rx for COPD than asthma) Oral corticosteroids (for severe attacks (prednisone) )  (6a) Asthma Meds Long term asthma control medications Inhaled corticosteroids Long acting beta agonists (LABAs)   beta antagonist (open airways) Theophylline (taken in pill form) Leukotriene modifiers (↓ immune response)  Asthma Meds Many patients are prescribed both maintenance and rescue inhalers Need to rinse and spit after LABAs every uses Inhaled steroids Beta Agonists  Asthma Meds Some patients can control symptoms with just short acting meds If the person doesn’t have their inhaler with them it doesn’t do any good  (6b) Asthma Meds (Broncodilators) are delivered via Metered Dose Inhalers (MDIs).  (7) Role of PT As a therapist you should advocate: warm up and cool down chest wall stretching pacing of activities energy conservation proper hydration avoidance of triggers (smoke, dust mites, pollution, pets (dander), mold, cold) Make sure coaches and exercise trainers when a pt/child is  Role of PT Reinforce the use of prescribed medications Emphasize importance of continued use of meds even when patient is feeling well to avoid the consequences of noncompliance Remember economic factors can  (8) Asthma Is As Asthma does Can people outgrow asthma? - Many people “outgrow” asthma; they are only symptomatic when young Does it disappear? - Asthma goes into remission, does not just disappear, unwise to consider it “gone” At the very least think of those with a h/o asthma as people with a prior history of bronchospastic  Bronchial It’s like an ablatio reduce the activit Thermoplasty Using bronchoscope, lungs are heated to 149 degrees F 3 stage procedure (3 weeks in between) Costs $20,000 Sig ↓ in ER visits and lost work Some insurances now covering NYT Article by Anahad O’Connor 9/4/12  (1) Bronchitis Hypertrophy of the mucous glands and increase in goblet cells Loss of ciliary action Thickening of bronchial wall Obstruction, inflammation,↑secretions Thick, tenacious, mucopurulent secretions Bronchitis  (2) Chronic Bronchitis Early stage: 10 -100ml of sputum expectorated in the AM Later stage: Prolonged phase of expiration Coarse rales, rhonchi, and wheezes  (2a) Chronic Bronchitis Sxs: Chronic productive cough with morning expectoration Color of Sputum: clear, mucoid, may be purulent Recurrent chest infections Overweight, cyanotic (clubbing) (CO2 retention) LE edema, R sided failure  (5) Bronchitis Purulent Sputum: separates into 3 layersSigns upon standing 1. Upper: frothy, white or greenish/brown 2. Middle: thin mucoid 3. Lower: thick plugs Clubbing Bronchial Breath Sounds  (3) Role of PT As a therapist: Advocate for smoking cessation, infection prevention and proper hydration (making mucous easier to expel) You can provide education about airway clearance techniques  (4a) Bronchiectasis Permanent abnormal dilation and distortion of bronchi (a) caused by destruction of the elastic and muscular components of the bronchial walls Describes an anatomic abnormality NOT a single disease  (4b) Bronchiectasis (b) Commonly caused by: Necrotizing infections of the trachea and bronchial tubes – Necrotizing PNA (remember, recurrent infections are typically seen in chronic bronchitis and CF) – TB – Pertussis Decreased incidence with vaccinations for pertussis, and use of antibiotics (Pertussis is resurgent, new guidelines  (4c) Bronchiectasis Other causes: Chronic gastroesophageal reflux with aspiration Foreign body aspiration Lung diseases that upset the pressure balance that keeps the lungs open – Sarcoidosis – Interstitial Fibrosis – TB Smoke or other inhalation injury Bronchiectasis What BS likely heard on auscultation? BRONCHOWHATSIS? DO NO T CO NF US E BR ON CHI (4d) Bronchiectasis: Clinical Features Patients will present with: Cough, copious mucopurulent sputum, fetid breath, recurrent pulmonary infections Frequently seen in conjunction with: Cystic Fibrosis Immotile Cilia Syndrome Kartagener’s Syndrome [which consists of bronchiectasis, sinusitis, situs inversus (heart on the right  (5) Bronchitis Purulent Sputum: separates into 3 layersSigns upon standing 1. Upper: frothy, white or greenish/brown 2. Middle: thin mucoid 3. Lower: thick plugs Clubbing Bronchial Breath Sounds  (1) Emphysema Anatomical changes in the lungs characterized by hyperinflation especially at the alveolar level Break down of capillary wall Blebs can cause what? - Blebs (balloon like stretched out alveoli) when stressed can cause a  (2) Emphysema What causes alveolar destruction? What rarely causes it? Cigarette smoking or other irritants ↑ macrophages and neutrophils in the lung leading to alveolar destruction Rarely, caused solely by inherited deficiency of Alpha-1 antitrypsin (protects elastic prop of lung) Result: Alveoli lose elastic recoil, air is trapped, gas exchange is impeded Alveolar Changes DLCO = is going to be low % Alveolar Destruction  Pathogene sis Cigarette smoking Leads to a disruption of the elastic fiber network Lungs have ↑ compliance coupled with ↓ elasticity Leads to air trapping Remember we rely on elastic recoil to drive normal, unforced exhalation Does Smoking Cause COPD? – sorta; 1/5 people  ?????????????????????? Do all smokers develop COPD? No, only about 20% Does all COPD come from smoking? Sort of 85% to 90% of emphysematics have a history of smoking  Clinical Picture DOE → Dyspnea at rest It’s Cough but have scant production not cou (mucus plugs) cou COM Thin (cachectic), eating effortful Tachypneic with prolonged exhalation (what is the normal ratio of in:out 1:1, 1:2, 2:1?) Use accessory muscles for ventilation Typical posture braced on knees Barrel Chest  (3) Diagnosis Commonly remembered as pink puffer Polycythemia: ↑ production of RBCs, why? = don’t have enough O2 so the body compensates it  (4) COPD X- ray flattening of See hyperinflation, diaphragm becomes less acute Hyperinfla trapping = diaphtagm down = c costophte F c t t a  (5) PFT Obstructive Components will see: Air trapping, Increased RV and disproportionate reduction in the FEV1 as compared to the FVC (FEV1/FVC ratio on a PFT) are the Pas hallmarks of obstructive lung Faili disease  FEV1/FVC Tell tale result for obstructive dz Obstructive  ABG Associated With COPD The pCO2 rises because of the retention of CO2 This drives the pH down (lower #s are more acid) The HCO3 (bicarbonate produced by the kidneys) also rises to attempt to balance the pH Typically resulting in: Respiratory acidosis with partial metabolic  (6) Emphysema Pharmacology Lots of overlap with asthma meds (remember, asthma and COPD can coexist) Beta-2 selective agonists frequently prescribed (both short and long acting) Inhaled corticosteroids frequently prescribed Anticholinergics: (Spiriva, Atrovent) bind competitively at acetylcholine receptor sites, long lasting (Pts frequently c/o dry mouth) Mucolytics like Mucomyst thin secretions to aid with expectoration, pulmonary toileting  GOLD Global Initiative for Chronic Obstructive Lung Disease (GOLD) http://www.goldcopd.org/ Resource for patients and caregivers  GOL Recommendations for D treatment  (7) Role of PT As a therapist: Advocate smoking cessation Teach energy conservation Teach breath control, PLB DO NOT ASK THESE PATIENTS TO TAKE DEEP BREATHS  bc they only trap air Teach controlled huffing, active cycle of breathing, forced expiration technique  Smoking Cessation During the first year, lung function improved in patients who quit smoking and declined in those who continued. Subsequently, the rate of decline in those who continued was twice that of those who quit. Function declined in those who relapsed and improved in those who quit regardless of when the change occurred. Based on data from Scanlon PD et al: Smoking cessation and lung function in mild-to-moderate chronic obstructive pulmonary disease; the Lung Health Study. American Journal of Respiratory and Critical Care Medicine 161:381–390, 2000.  REMEMBE R:A DISEASE IN COPD IS NOT ITSELF IT IS A DESCRIPTIVE DIAGNOSIS A BLANKET TERM WHICH CAN BE USED TO REFER TO CHRONIC BRONCHITIS OR EMPHYSEMA ALONE OR IN COMBINATION  Venn Diagram Review Proof that someone out there understands how you feel  Obstructive Pulmonary Disease Bronchopulmonary Dysplasia Cystic Fibrosis Asthma Bronchitis → Bronchiectasis  Objectiv esbe able to: You should now Name at least 3 interventions focused on secretion management in CF – CPT, exercise, drainage, meds, an machines for resistance Identify at least 4 different asthma triggers – smoking, exercise, cold, stress Identify at least 4 different things PTs caring for people with asthma should  Lab Related The rest of the slides introduce topics that will be covered more fully in the lab sessions  Chest Physical Therapy Postural drainage/Bronchial drainage Percussion and vibration Breathing exercises (you’re already an expert) Coughing/huffing (you’re already an expert)  Goals of CPT Prevent accumulation of secretions ↑ mobilization/drainage of secretions ↑ relaxation/avoid muscle splinting Maximize chest wall mobility Regain efficient breathing pattern  Goals of CPT Instruct in use of respiratory muscles Develop respiratory endurance ↑ cardiopulmonary exercise tolerance Prevent atelectasis = do deep breathing If you cannot breath, you cannot Maximize coughfunction effectiveness  Exclusion/Discharge Criteria Unstable Unable (OMS, sepsis, etc.) Inappropriate (either too bad or too good)  Postural Drainage Middl sidelin Align segmental bronchi with quart Lower gravity Bacte speci Collect secretions centrally Cough/expectorate to remove secretions Can supplement with P & V  Positions Choose where to focus based on chart review and auscultation No trandelenburg  Postural Drainage RML has the most limited access Take extra care with RML positioning  Trendelenburg Trendelenburg Reverse Trendelenburg  Trendelenburg Use with caution Postural Drainage (Trendelenburg?)  Trendelenburg Not endorsed by Cystic Fibrosis Foundation Implicated in fostering/exacerbating GERD Still depicted in many reference manuals Through the Lifespan  Postural Drainage Contraindications ICP > 20 mmHg Unstabilized head/neck injury Active hemorrhage Hemoptysis Empyema Bronchopleural fistula Pulmonary edema assoc with CHF  Postural Drainage Contraindications Large pleural effusions PE  put on them on blood thinners and no putting their head down Confused/anxious patients Rib fracture Surgical wound Post op where joint compression contraindicated  Contraindications Trendelenburg Neuro dx: Cerebral aneurysm, ICF drain, coma, recent CVA, uncontrolled sz ↑ ICP contraindicated Uncontrolled HTN Distended abdomen  ascitis Post esophageal procedures  esophageal verisces Cardiovascularly unstable: Acute MI, pulmonary HTN,  Contraindications Trendelenburg Aneurysm, esp AAA Continuous tube feedings Unstable fluid balance: CHF, during HD, ascites Recent hemoptysis related to lung CA Uncontrolled airway, aspiration risk  Contraindications Trendelenburg Even if Trendelenburg is not directly contraindicated USE WITH CAUTION Implicated in worsening of GERD Implicated in increasing risk of aspiration  NEURO pts  Percussi on Loosens secretions Use cupped hand Should sound hollow Percuss only over ribs Percuss for at least one minute Also called tapotement or clapping Percussi on Clapping not Slapping Percussi on  Contraindicati ons Pneumothorax Platelets < 50,000 Cardiovascularly unstable pt Over rib fx or lesion Osteoporosis, CA mets, prolonged steroid use Over sx incisions/sternotomy Over recent graft, burn or wound Bony instability and weightbearing status  Contraindicati ons When blood too thin (↑ INR(>5), etc.) Hemoptysis Undrained empyema Subcutaneous emphysema PE Flail chest Awaiting R/O for MI Acute TB Severe pain Recent spinal fusion Vibrati on Gentler than percussion Uses flat hand Always go “down and in” (meaning from outer branches of tracheobronchial tree towards central main stem bronchi) COORDINATE WITH EXHALE Vibrati on  Contraindicati ons Pneumothorax Platelets < 50,000 Cardiovascularly unstable pt Over rib fx or lesion, CA mets Over sx incisions/sternotomy Over recent graft, burn or wound Osteoporosis, prolonged steroid use (relative)  Contraindicati ons When blood too thin (↑ INR, etc.) Hemoptysis Undrained empyema Subcutaneous emphysema PE Flail chest Awaiting R/O for MI Acute TB Severe pain Recent spinal fusion