L2- COPD, smoke inhalation, EVALI

characterization of COPD

• persistent respiratory sx

• airflow obstruction

• hx of significant exposure to noxious particles or gases

• largely irreversible and progressive

COPD- epidemiology

predisposing factors

• inhaled pollutants

  • cigarette smoke

  • biomass fuel for cooking and heating

  • occupation al dusts and chemical

• alpha 1 antitrypsin def

main patterns of COPD

1) chronic bromchitis

• a mucus problem

• blue bloaters

2) emphysema

• structural problem

• pink puffers

chronic bronchitis: pathogenesis

• repeated noxious environmental exposure → chronic inflammation and irritation of bronchioles→ increase mucus gland size and volume + ciliary damage→ bronchial endothelial thickening + excessive mucus production and retention → airway obstruction + chronic cough and phlegm production

chronic bronchitis: physiologic consequences

1) airway obstruction disrupts ventilation

• decrease tidal vol due to

  • increase resistance to air flow in and out

  • air trapping leads to hyperinflation and reduced capacity for inhalation

2) damage to the mucociiary defenses

• reduces clearance of pathogens

  • increase risk of pulmonary infections (ex. pneumonia)

emphysema: pathogenesis

• resident alveolar macrophages phagocytes pathogens adn irritants and release protease

  • proteases destroy pathogens and break down collagen and elastin→ structural issue

• chronic irritant exposure leads to increase protease production/activity and decreased antiprotease activity

• results in destruction of capillaries and alveolar wal with air space enlargement (dilation)

alpha 1 antitrypsin

• protease inhibitor

• synthesized by hepatocytes

alpha 1 antitrypsin deficiency

• genetic disorder

• deficiency at AATT= protease > antiprotease

• results in increased risk of emphysema, even with limited exposure to air pollutants

in which pts might you suspect alpha 1 antitrypsin deficiency

• young pt with no smoke exposure

physiologic consequences- emphysema

alveolar wall and capillary destruction

• septal destruction reduces alveolar surface area→ decreased area for gas exchange→ increased dead space

• elastin destruction impairs ability to recoil→ air trapping→ decreased tidal volume

clinical presentation- chronic COPD

• productive cough (bronichitis)

• sputum production

• SOB (emphysema)

clinical presentation: acute exacerbation COPD

• increased cough

  • freq and severity

• increased sputum

  • vol or change in character

• increased SOB

general physical exam- COPD

± cachexia

vital signs- COPD

± hypoxemia and tachypnea

pulmonary exam findings- chronic bronchitis

• noisy lungs- rales, rhonchi, wheezing

• signs of RHF

  • cyanosis

  • peripheral edema

physical exam findings- emphysema

• lung sounds are absent or distant

• hyperresonance to percussion

• barrel chest

dx criteria- COPD

1) respiratory sx consistent with COPD

• chronic cough

• sputum production

• dyspnea

2) persistent airflow limitation

• post- bronchodilator FEV1/FVC <70%

• obstructive pattern

3) no alternative explanation fro sx and airflow obstruction

DDx- COPD

1) asthma

• complete or near complete reversibility of airflow obstruction

2) CHF

• dyspnea

• dilated heart

3) bronchiectasis

• recurrent pneumonia

• hemoptysis

• Digital clubbing

• characteristics imaging abnormalities

initial assessment- COPD

1) spirometry

2) assess fro severity

• GOLD ABE

3) CBC with differntial

4) CXR

5) test fro alpha 1 antitrypsin deficiency

what conforms obstructive pattern

• FEV1/FVC <70%

• FEV1 is disproportionately reduced relative to FVC

GOLD ABE spirometry

• pre and post bronchodilator spirometry

• COPD is irreversible

  • remains <0.7 with bronchodilator

• use FEV1 to assess COPD severity

• degree of airflow obstruction is prognostic factor

GOLD ABE- sx severity

• subjectively how severe is pt airflow obstruction

• mMRC

• CAAT

GOLD ABE assessment

CBC results- COPD

• secondary polycythemia (erythrocytosis)- physiologic adaptation to chronic hypoxemia, more. ommon in chronic bronchitis

• anemia

  • likely anemia of chronic disease

• leukocytosis, neutrophilia, elevated eosinophils

  • eosinophil count- used to guide therapy

  • start ICS if eos >300 cells

most reliable radiographic findings of COPD

1) hyperinflation

2) flattening of the diaphragms

additional radiographic findings of COPD

• increase in the retrosternal clear space

• hyperlucency of lungs

• prominent pulm arteries

• may contain bullae

radiographic findings- chronic bronchitis

• increased pulm vasculature

• right heart enlargement

• increased AP diameter

radiographic findings- emphysema

• decreased pulm vasculature

• hyperinflation, flattened diaphragms

• hyperlucency

• bullae/blebs

• increased AP diameter

stable COPD management

1) non pharm tx

2) oxygen therapy if needed

3) pharm management

• rescue therapy fro EVERYONE- short acting bronchodilator (SABA + SAMA). + therapy based on ABE placement

non pharm tx- COPD

• stop smoking

• vaccinations

• avoid precipitating environmental exposures

• pulm rehabilitation

• physical activity

• adequate sleep/healthy diet

oxygen therapy

• supplemental O2 via nasal cannula 1-3L/minute

• pts with

  • resting O2 saturation <88% OR

  • ABG with PaO2 <55mmHg OR

  • cor pulmonae

• titrate to O2 sat of 92%

why do you not want to shoot for 100% oxygen therapy

• pts with COPD have chronic hypercapnia→ central chemoreceptors become “numb” to hypercapnia → rely on relative hypoxia to maintain respiratory drive

• must find balance btwn providing adequate oxygenation and maintaining respiratory respiratory drive

  • too much O2= loss of respiratory drive

pharmacological tx- COPD

aim to reduce obstruction of airflow→ improve sx

1) inhaled bronchodilators

• provide sx relief and reduce exacerbation risk

• do not improve mortality

2) corticosteroids

• reduce exacerbations + treat exacerbations

3) human alpha 1 antitrypsin

• replacement therapy- if applicable

anticholinergics MOA

prevent Ach from binding to muscarinic receptors on smooth muscle leading to less bronchoconstriction and decrease secretions

anticholinergics- SE

• dry mouth

• thirst

• blurred vision

• urinary retention

• difficulty swallowing

SAMAs

anticholinergic

• iprtropium bromide

LAMAs

anticholinergic

• tiotropium

• aclidnium

• umeclidinium

• glycopyrrolate

beta 2 agonist- MOA

• bind to B2 adrenergic receptors

beta 2 agonist - SE

• beta 1 cross reactivity

  • CNS stimulation

  • tremor

  • tachycardia

  • restlessness

  • hypokalemia

SABAs

B2 agonist

• albuterol

LABAs

beta 2 agonist

• formoterol

• salmeterol

• indacaterol

• arformoterol

• vilanterol

• oldaterol

steroids for COPD- ICS

• helps reduce exacerbations

• recommend if blood eos >300

steroids fro COPD- oral corticosteroids

• only used to tx exacerbations of COPD

  • long term use not recommended

side effects of oral corticosteroid use

• osteoporosis

• weight gain

• cataracts

• glucose intolerance

• increased risk of infection

• adrenal suppression

initial pharmacological tx- COPD

• rescue inhaler (albuterol ± ipratropium) + ABE category

initial pharm tx- COPD group A

• minimum sx, ,low risk of exacerbation

• long acting bronchodilator

  • LAMA preferred (due to decrease mucus prod)

initial pharm tx- COPD group B

• more sx, low risk of exacerbation

• LABA + LAMA

initial pharm tx- COPD group E

• high sx, high risk of exacerbation

• LABA + LAMA ± ICS

COPD exacerbation

• episodic acute worsening of cardinal sx of COPD over <14 days

• often caused by airway infection or pollution

characteristic of COPD exacerbation

• increased cough

  • frequency and severity

• increased sputum

  • volume or change in character

• increased dyspnea

COPD exacerbation management

• oxygen therapy- titrate to resting O2 sat 88-92%

• nebulized SABA/SAMA fro bronchodilation

  • duoneb (albuterol and ipratropium)

• systemic corticosteroids for airway inflammation

  • ex. prednisone burst

  • IV solumedrol

• empiric abx fro 5 days

  • if requiring hospitalization or if >2 or 3 cardinal sx present

COPD exacerbation abx- no RF

• macrolide (azythromycin) OR

• 2nd/3rd cephalosporin (cefpodoxime)

COPD exacerbation abx- with RF

• amoxicillin- clavulanate OR

• respiratory FQ (levofloxacin)

smoke inhalation assessment

1) thermal injury to upper airway (UA)

2) injury to lower airways ad lung parenchyma

3) impaired tissue oxygenation

UA- smoke inhalation

• thermal injury to UA

• often results in upper airway obstruction

• cause:

  • inhalation of superheated gases → immediate injury results in erythema, ulcerationsm and edema

UA smoke inhalation- S/Sx

skin:

• soot in the mouth/nose

• burns on the face/neck

ENT/pulm

• mucosal edema

• impaired ability to clear oral secretions

• inspiratory stridor

• black sputum

UA smoke inhalation- exam

• fiberoptic laryngoscope or bronchoscope

UA smoke inhalation- tx

• airway management

  • endotracheal intubation for most pts

    • low threshold fro intubation

  • tracheostomy is necessary

• high humidity face mask with supplemental O2

• suctioning (if applicable)

• elevation of the heas 30 degrees

  • promotes secretion clearing

• topical epinepherine

  • can be used to resuce edema of the oropharyngeal mucous membrane

lower airway smoke inhalation

• injury to the lower airways and lung parenchyma

• thermal burns are usually limited to UA

• causes:

  • inhalation of chemicals in the smoke

    • toxic gases and products of combustion

    • aldehydes and organic acids

LA smoke inhalation- early exam findings

• dyspnea, tachypnea, tachycardia

• wheezing, rhonchi

LA smoke inhalation- 1-2 days exam findings

• can develop pulmonary alveolar edema

LA smoke inhalation- 2-3 days exam findings

• sloughing of bronchiolar mucosa

  • leads to atelectasis, airway obstructio, worsening hypoxemia

LA smoke inhalation- 5-7 days exam findings

bacterial colonization and pneumonia

LA smoke inhalation tx

• protect airway- likely will need endotracheal intubation

• suctioning of debris and secretions

• supplemental O2

  • humidification of inspired gases

• bronchodilators

• chest PT to help clear secretions

NOT recommended tx for LA smoke inhalation

• corticosteroids

  • ineffective and possibly harmful

• prophylactic abx

smoke inhalation- impaired tissue oxygenation

• carbon monoxide and cyanide poisoning should be suspected in all pts

• diffusion and perfusion are interrupted

CO poisoning source

• fire related smoke = MC cause

• poorly functioning or improperly vented heating systems

• car exhaust

CO poisoning- patho

1) impaired O2 delivery

• CO has 240x greater affinity for binding hemoglobin than O2

• carboxyhemoglobin = CO bound to heme

2) impaired O2 utilization

• impairment of oxidative phosphorylation at the mitochondrial level

• injury to myocytes

3) reactive O2 species

• superoxide generation and oxidative stress

CO poisoning- Sx

mild-moderate

• headache

• nausea

• dizziness

• drowsiness

• vomiting

severe

• seizures, syncope, coma

• cardiac: angina, dyspnea, cardiac dysrhythmia, hypotension

CO poisoning physical exam

• bright red retinal vessels on fundoscopy

• cherry-red skin/lips

  • classic but uncommon

CO poisoning workup

• serum carboxyhemoglobin levels increase

  • do not correlate with severity!

• ABG

  • falsely elevated PO2

  • lactic acidosis from cellular hypoxia and cytochrome oxidase inhibition

• CBC, CMP, UA, CXR

• troponin

  • MI is common among moderately to severe CO poisoning pt

• masimo pulse CO-oximeter

  • regular pulse oximters and ABG cannot differentiate oxyhemoglobin vs carboxyhemoglobin

goal of CO poisoning tx

• remove from CP source and provide high flow O2

  • high flow → competitive binding of heme by O2

tx for mild CO poisoning

• 100% O2 via nonrebreather

• continue until COHb <10%

tx for severe CO poisoning

• hyperbaric O2chamber (if available)

• goal= reduce neurological sequelae

cyanide

• mitochondrial toxin that is among most rapidly lethal poisons

• hydrogen cyanide

  • colorless gas with odor of bitter almonds

hydrogen cyanide poisoning source

• in industrialized countries, the most common cause= domestic fires

• other sources include industrial, medical, diet, and cyanide salt ingestion

cyanide poisoning patho

• disrupts the aerobic metabolism in mitochondria via inhibiting cytochrome oxidase

• despite ample oxygen, cells cannot utilize bc of poisoned electron transport chain

• leads to anaerobic metabolism

• damaging to systemic tissues, especially cardiovascular system and brain (bc lactic acid)

cyanide poisoning sx and physical exam

• similar to CO poisoning

• may detect bitter almond odor

cyanide poisoning labs

• venous O2 (SpO2) increase

  • tissues failed to uptake arterial O2

• ABG

  • increased anion gap acidosis

• increased serum lactate

• cyanide levels- unreliable adn untimely

cyanide poisoning- tx

• hydroxocobalamin

  • injectable form of B12

  • causes red discoloration of skin and body fluids fro 2-3 days

EVALI

• e-cigarette or vaping product associated lung injury

EVALI contributing factors

• diacetyl

• THC/adulteration of THC

• adulteration of delivery devices

• vitamin E acetate

  • strongly linked

EVALI clinical presentation

• respiratory sx

  • cough, SOB, CP

• constitutional sx

  • fever, weight loss, chills

• GI sx

  • n/v/d

• continued sx

  • fatigue, dyspnea, decreased exercse capacity may linger

• tachycardia

• tachypnea

• hypoxemia

EVALI- workup

• no specific labs

• could see leukocytosis, elevated CRP and ESR

• imaging- may look similar to pneumonia

  • CXR→ bilateral opacities

  • chest CT→ nonspecific

EVALI - dx

• dx of exclusion

• reported use of e-cig or vapign product in last 3 months

• pulmonary infiltrates on chest imaging

• negative infectious workup

• no alternative plausible dx

EVALI- dispossition

• admit if sus and have following:

  • O2 sat <95 on RA

  • are in respiratory distress

  • or have comorbidities

EVALI- tx

• stop vaping

• systemic steroids

• empiric abx

  • cover for PNA

• supplemental O2