PULMONARY (10%) Flashcards
RSV (RESPIRATORY SYNCYTIAL VIRUS)
Bronchiolitis = inflammation of the small airways of the lungs
Acute Bronchiolitis = Lower respiratory tract infection of the SMALL AIRWAYS
Bronchiolitis = most often caused by RSV infection
- mostly affects young children, affecting almost every child at some point in their life
Bronchiolitis = usually occurs in children < 2 y/o
RSV named because it causes the cells lining the respiratory tract to merge, causing a large multinucleated cell = SYNCYTIA
RSV = PNEUMOVIRIDAE FAMILY / PARAMYXOVIRUS FAMILY
RSV TRANSMISSION = RESPIRATORY DROPLETS
- person sneezes or coughs –> sends thousands of droplets into the environment, 6 feet away (like influenza)
- droplets can then land in mouth / noses of people nearby and get inhaled into the lungs
- RSV can also survive on surfaces (fomites) for a few hours, so can become infected after touching object and then eyes / nose / mouth
RSV is the most common cause of lower respiratory tract infections in children worldwide
Virtually all children contract it by the age of three
It’s the leading cause of pneumonia and bronchiolitis in infants. It may play a major role in the pathogenesis of asthma bronchiolitis
PATHOPHYSIOLOGY
1) RSV passes epithelial cell lining of nasopharynx –> some local damage
2) RSV makes it way down respiratory tree - down trachea –> main bronchi –> bronchioles
Bronchioles = primary target of RSV
RSV = enveloped linear negative sense strand of RNA
- once virus enters its virus into a respiratory epithelial cell, must be transcribed into positive sense mRNA via RNA polymerase
- then translated into protein –> invades other cells, creating multinucleated syncytia out of some cells, and destroying others
NK cells are attracted to destroy viral-infected cells. Immune cells release chemokines –> inflammatory reaction that causes epithelial cells to SECRETE MORE MUCUS, and makes the blood vessels of the airway more leaky
Children already have narrower airways than adults
More immune cells enter damaged airways, creating Inflammation and Swelling which narrows the airway, and narrow airways become filled with mucus / fluid –> airways become even smaller
Since children already have narrower airways to begin with = explains the disproportionate response to RSV
Dead cells and mucus can create a plug in bronchioles and trap air. Over time, the air diffuses out into the bloodstream and the bronchiole collapses (atelectasis)
Sometimes the mucus/dead cell plug creates a one-way valve, allowing air to enter but not leave, so bronchiole airway becomes overinflated (air trapping)
Proliferation / necrosis of bronchiolar epithelium produces obstruction from sloughed epithelium, increased mucus plugging, and submucosal edema –> leads to peripheral airway narrowing + obstruction
Can have both atelectasis and air-trapping occur at different bronchioles
- both make it difficult to bring in O2 and release CO2 –> HYPOXEMIA
Syncytia formation (fusion of epithelial cells into a large giant cell) is a hallmark feature of respiratory syncitial virus (RSV), a virus responsible for most cases of childhood pneumonia infections.
CAUSES OF BRONCHIOLITIS
⦁ MC cause = ** RSV **
⦁ other viruses = Adenovirus, Human Bocavirus, Human Metapneumovirus
⦁ Bacteria: Mycoplasma pneumoniae
- can have multiple pathogens at once causing bronchiolitis
SIGNS / SYMPTOMS OF BRONCHIOLITIS (RSV) - initially = similar to common cold ⦁ congestion ⦁ rhinorrhea ⦁ pharyngitis / sore throat ⦁ cough ⦁ low-grade fever ⦁ decreased appetite
- if infection becomes more severe ⦁ dyspnea ⦁ wheezing ⦁ fever ⦁ hypoxia ⦁ nasal flaring / subcostal or intercostal retractions ⦁ nail-bed cyanosis
HYPOXIA (increase HR + RR to get blood / oxygen to lungs / tissues faster)
⦁ tachycardia
⦁ tachypnea
- may require hospitalization
may have APNEA = short periods of time where infant stops breathing altogether
Infants with bronchiolitis may present with fussiness, low grade fever, coryza, congestion, and apnea.
Symptoms resolve in 5-7 days (unless develop pneumonia)
** ACUTE OTITIS MEDIA = MC co-infection of RSV bronchiolitis **
** ASTHMA = MC complication later in life **
DIAGNOSIS
⦁ clinical
- based on time of year / circulation of RSV, age, and symptoms
⦁ nasopharyngeal swab (for viral antigens)
⦁ CXR - diffuse infiltrates**
RISK FACTORS FOR RSV
⦁ not breastfed
⦁ born premature
⦁ disorders where can’t easily clear own airways
TREATMENT
Indications for hospitalization include moderate tachypnea with feeding difficulties, visible retractions, and oxygen desaturation
⦁ supplemental oxygen (humidified)
⦁ fluids to prevent dehydration
⦁ nebulized albuterol or duoneb (albuterol + ipratropium bromide)
⦁ nebulized racemic epi (if albuterol not effective)
⦁ antipyretics
⦁ Ribavarin (antiviral) = used for RSV + Hep C
⦁ Steroids (controversial) - only if hx of RAD (reactive airway disease)
OXYGEN = the only treatment shown to improve bronchiolitis
a trial of bronchodilators can be attempted in children with severe disease, and then continued if the child clinically improves.
PREVENTATIVE
⦁ Palivizumab = monthly injections for those born premature / have pulmonary or cardiac conditions - targets the RSV F (fusion) protein
- monoclonal antibody
- cannot be given if RSV is already contracted
- typically reserved for high-risk infants / children (babies born at 29 weeks or less and are < 1 year)
ACUTE BRONCHIOLITIS
Bronchiolitis = inflammation of the small airways of the lungs
Acute Bronchiolitis = Lower respiratory tract infection of the SMALL AIRWAYS
Bronchiolitis = most often caused by RSV infection
- mostly affects young children, affecting almost every child at some point in their life
Bronchiolitis = usually occurs in children < 2 y/o
PATHOPHYSIOLOGY
Children already have narrower airways than adults
More immune cells enter damaged airways, creating Inflammation and Swelling which narrows the airway, and narrow airways become filled with mucus / fluid –> airways become even smaller
Since children already have narrower airways to begin with = explains the disproportionate response to RSV
Dead cells and mucus can create a plug in bronchioles and trap air. Over time, the air diffuses out into the bloodstream and the bronchiole collapses (atelectasis)
Sometimes the mucus/dead cell plug creates a one-way valve, allowing air to enter but not leave, so bronchiole airway becomes overinflated (air trapping)
Proliferation / necrosis of bronchiolar epithelium produces obstruction from sloughed epithelium, increased mucus plugging, and submucosal edema –> leads to peripheral airway narrowing + obstruction
CAUSES OF BRONCHIOLITIS
⦁ MC cause = ** RSV ** (50-70%)
⦁ other viruses = Adenovirus, Human Bocavirus, Human Metapneumovirus, Influenza, Parainfluenza
⦁ Bacteria: Mycoplasma pneumoniae
- can have multiple pathogens at once causing bronchiolitis
RISK FACTORS FOR BRONCHIOLITIS ⦁ Infants < 2 y/o = MC affected ⦁ Infants < 6 months especially ⦁ exposure to cigarettes ⦁ not breastfed ⦁ born premature (< 37 weeks) ⦁ crowded conditions ⦁ disorders where can't easily clear own airways ⦁ MC in fall + spring
COMPLICATIONS
⦁ ** otitis media (strep pneumo) = MC acute co-infection
⦁ ** asthma = MC complication later in life
SYMPTOMS
⦁ fever
⦁ URI symptoms x 1-2 days (rhinorrhea / congestion / cough / pharyngitis) —> respiratory distress symptoms of…
⦁ wheezing ⦁ tachypnea ⦁ nasal flaring ⦁ cyanosis ⦁ subcostal / intercostal retractions ⦁ decreased appetite
DIAGNOSIS
⦁ Nasopharyngeal swab: RSV / monoclonal antibody testing
⦁ CXR = hyperinflation, peribronchial cuffing, etc.
⦁ ** pulse ox ** = single best predictor of disease in children
- ** if pulse ox < 96% = admit to hospital **
Hospitalization and administration of ribavirin if:
1) O2 < 95%
2) age < 3 months
3) respiratory rate > 70
4) atelectasis on CXR
TREATMENT
o supportive if mild
⦁ ** humidified oxygen = mainstay of treatment **
⦁ IV fluids
⦁ antipyretics: Tylenol / ibuprofen (motrin)
⦁ B2 agonists - nebulized albuterol or duoneb
o medications
⦁ B2 agonists - nebulized albuterol**
⦁ nebulized racemic epi (if albuterol not effective)
⦁ steroids = NOT indicated unless hx of underlying reactive airway disease
⦁ Ribavarin (antiviral) = given if severe lung or heart disease, or immunocompromised patient
o prevention
⦁ Palivizumab = prophylaxis in high-risk groups
⦁ hand-washing!
CROUP
(LARYNGOTRACHEOBRONCHITIS)
(LARYNGOTRACHEITIS)
- inflammation/swelling around larynx / trachea
Croup is just inflammation / swelling around the vocal chords / trachea, croup is NOT the actual virus
Croup = a respiratory infection that is usually caused by a virus. It leads to swelling inside the wind pipe, which interferes with normal breathing and produces the classic symptoms of “barking” cough, stridor, and a hoarse voice. Fever and runny nose may also be present. Often it starts or is worse at night.
** MC due to PARAINFLUENZA VIRUS **
- patient will have had a viral infection (or maybe bacterial infection) that causes swelling / inflammation to occur in the upper airway –> obstructs breathing
CAUSES ⦁ ** MC = PARAINFLUENZA VIRUS ** ⦁ adenovirus ⦁ RSV ⦁ influenza A/B ⦁ mycoplasma pneumonia etc
Usually report patient having had cold symptoms prior to development of this cough
- causes irritation, coughing, hoarseness, difficulty breathing
** MC in 6 months - 3 years
SIGNS / SYMPTOMS
⦁ ** BARKING COUGH ** (seal-like cough)
⦁ mild fever (from viral infxn…or bacterial infxn)
⦁ hoarseness of voice
⦁ ** loud high-pitched INSPIRATORY STRIDOR **
- symptoms = usually SUDDEN and at NIGHT
1) “BARKING COUGH” - harsh + seal-like
2) STRIDOR - both inspiratory + expiratory - worsened by crying or agitating the child
3) HOARSENESS from laryngitis
4) DYSPNEA - worse at night
- may have upper respiratory infection symptoms either preceding or at the same time, may have fever
Severe croup can result in pulsus paradoxus secondary to upper airway obstruction.
PULSUS PARADOXUS is seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and CROUP
DIAGNOSIS
⦁ clinical - don’t need xray, but can do one
⦁ need to r/o epiglottitis + foreign body aspiration
⦁ PA NECK XRAY = ** STEEPLE SIGN **
- narrowing of trachea in subglottic region = 50%
TREATMENT o Mild = no stridor at rest, no respiratory distress ⦁ cool, humidified air ⦁ antipyretics ⦁ hydration ⦁ Dexamethasone (oral or IM) 0.6mg/kg single dose ⦁ supplemental O2 if < 92% - patients can be discharged home
o Moderate = Stridor at rest with mild/mod retractions
⦁ steroids - oral or IM dexamethasone- single dose
- or nebulized budesonide (not oral!)
⦁ racemic epi (nebulized) - only with signs of distress (stridor at rest)
- observe for 3-4 hrs after, may be discharged home if improvement is seen
oral budesonide has not been shown to be effective in croup
o Severe = Stridor at rest + marked retractions
⦁ Dexamethasone (oral or IM) +
⦁ Nebulized racemic Epi +
⦁ hospitalization
nebulized albuterol will NOT help - only helps dilate LOWER AIRWAY, not upper airway
- IM steroids has shown no increased benefit to oral steroids - either one can be used
Most cases can be managed on an outpatient basis and will resolve within 3-7 days.
ex: Patient will present as → a 2-year-old boy who is brought to you by his father who is concerned about a “barking cough,” mild fever, and a hoarse voice. He reports that he had a runny nose last week that has since resolved. Physical exam reveals an inspiratory stridor
PERTUSSIS = WHOOPING COUGH
- HIGHLY CONTAGIOUS secondary infection to BORDATELLA PERTUSSIS = gram negative coccobacilli
- therefore looks like a short pink rod on gram stain
Transmission = through respiratory droplets - sneeze or cough
- rarely seen now due to widespread vaccination
- gram negative coccobacillus
- MC seen in children < 2
Causes violent coughing spells “paroxysms” - that make it difficult to breathe
** 100 day cough ** in adults
Swollen airways cause the inspiratory “whooping” sound
Bordatella pertussis bacteria releases toxins that help the bacteria anchor to the epithelial layer
- One of the toxins paralyzes the cilia - cannot sweep back and forth anymore
Cilia sweep away mucus and any bacteria attached to the mucus. Paralyzed cilia prevents clearing of the bacteria, allowing Bordatella pertussis to remain attached to epithelia
Mucus starts to build up due to cilia paralysis –> violent cough to try and clear the mucus
Pertussis toxin causes increase in lymphocyte level in the blood –> specifically the population of T-cells floating around. Pertussis toxin causes T cells to divide, causing them to leave the spleen / thymus and enter circulation, as well as prevents them from leaving circulation to enter tissues
Pertussis toxin also makes tissues more sensitive to histamine, so airway swells up –> harder to breathe –> “whooping” sound upon inspiration
Another toxin - Adenylate cyclase - prevents phagocytosis of bacteria
3 Exotoxin mechanisms
1) Pertussis toxin inactivates Gi via ADP-ribosylation. Loss of Gi-mediated AC inhibition leads to an overactive AC.
2) Adenylate cyclase itself is also produced by B. pertussis. AC converts ATP into cyclic AMP (cAMP), a second messenger in many cellular pathways. cAMP production causes edema of the respiratory mucosa.
- increase of conversion from ATP to cAMP –> prevents phagocytic function. Lymphocytes cannot leave bloodstream –> lymphocytosis *****
- increased cAMP –> increased insulin in body –> Hypoglycemia **
3) Tracheal cytotoxin damages ciliated cells lining the respiratory tract, which can prevent clearance of the organism.
CLINICAL MANIFESTATIONS
- 7-10 day incubation period
- Catarrhal phase –> Paroxysmal phase –> Convalescent phase
1) CATARRHAL PHASE
- upper respiratory symptoms x 1-2 weeks
- nasal congestion / cough / low grade fever / rhinorrhea / sneezing / lacrimation / etc.
- very contagious*** during this phase - presence of a lot of bacteria in respiratory tract
- multiplication of bacteria that starts to damage the airway
2) PAROXYSMAL PHASE
- lasts 1-6 weeks
- severe paroxysmal coughing fits with INSPIRATORY WHOOPING SOUND after cough fits
- whooping sound comes from air sliding past glottis that is still partially closed from being swollen
- immune system is killing and clearing bordatella pertussis bacteria in this phase, but still have enough airway damage to have continued symptoms
- post-coughing emesis may be present during paroxysmal phase = “cough so hard they vomit”
- can also end up with a collapsed lung, broken ribs, or petechiae on face / eyes from burst capillaries
Infants may show gasping, cyanosis, apnea. Decreased O2 levels can lead to seizures, encephalopathy, or even death
- Increased risk of pneumonia due to other bacteria that take advantage of damaged airway
Paroxysms of coughing can occur spontaneously, or can be provoked by YAWNING, laughing stretching, laughing, yelling, or exercise.
- coughing often lasts 2-4 weeks, scattered rhonchi
- may develop subconjunctival hemorrhage from increased pressure with coughing fits
3) CONVALESCENT PHASE = 2-3 weeks
- cough slowly improves
- paroxysms + whooping sound fade
- airway heals
DIAGNOSIS
- best to diagnose Pertussis during the catarrhal phase
PCR of NASOPHARYNGEAL SWAB = gold standard (polymerase chain rxn - identifies DNA of bacteria)
- can also do culture or pertussis antigen serology
- culture = grown in Bordet Gengou Agar (Bordet-ella!) or Regan-Lowe medium
- elevated lymphocytes (normal = 15-40% of total WBC)
PERTUSSIS VACCINE = best way to prevent the infection, or lessen symptoms if infection does occur
vaccine is > 90% effective in preventing pertussis
- can be given in 3rd trimester of pregnancy
- over time, decreased levels of antibody = why it is important to continue getting boosters (ex: elderly)
- booster = Tdap
LABS
- Lymphocytosis = 60-80% lymphocytes on differential (normal = 15-40%)
- WBC count may be as high as 50,000 (normal = 4,500 - 11,000)
TREATMENT
1) mainstay of treatment = SUPPORTIVE THERAPY - oxygen, nebulizers, mechanical ventilation as needed
2) Antibiotics used to decrease contagiousness - however, abx only shortens the duration of infection if given in the first 7 days of symptom onset (catarrhal or early paroxysmal phase), and most patients don’t present yet with symptoms indicative of pertussis
⦁ ERYTHROMYCIN, or AZITHROMYCIN. Macrolides = treatment of choice
- Macrolides may increase risk of infantile pyloric stenosis in infants < 1 month
⦁ Bactrim = 2nd line if allergic to macrolides
COMPLICATIONS OF PERTUSSIS
- *Pneumonia
- encephalopathy
- otitis media
- sinusitis
- seizures
Increased mortality in infants due to apnea and cerebral hypoxia associated with coughing fits
Pertussis = now more common in adolescents and adults than in children. A cough lasting longer than 2 weeks accompanied by paroxysms of coughing, inspiratory whoop, or posttussive emesis should raise suspicion for pertussis.
pertussis should be suspected in an adult with a cough lasting >2 weeks
EPIGLOTTITIS
TRUE EMERGENCY!!!!
- Inflammation of the epiglottis => can interfere with breathing
- MC CAUSE = HIB (haemophilus influenza B)*
- gram negative rod
- has been a decrease in incidence due to vaccination
- other causes ⦁ strep pneumo* ⦁ staph aureus ⦁ GABHS ⦁ strep agelectiae ⦁ strep pyogenes ⦁ M. cat
Non-HIB seen more commonly in adults (esp crack, cocaine use)
MC in children 3 months - 6 years*
Males = 2X more common
DM = risk factor
generally sudden in onset (acute)
SYMPTOMS
⦁ DROOLING
⦁ MUFFLED, HOT POTATO VOICE*
3 D’s = DYSPHAGIA, DROOLING, DISTRESS
⦁ fever
⦁ odynophagia (difficulty / painful swallowing)
⦁ inspiratory stridor (also with croup)
⦁ dyspnea
⦁ hoarseness
often in TRIPOD POSITION - leaning forward
Patients sit with neck hyperextended and chin protruding (sniffing dog position)
DO NOT EXAMINE THE PATIENT - could cause spasm
BE PREPARED TO INTUBATE - do not give IV ABX prior to intubation, as this could also cause spasm
DIAGNOSIS
⦁ ** LARYNGOSCOPY ** = definitive diagnosis - provides direct visualization, however, could induce bronchospasm!
⦁ LATERAL NECK XRAY - STAT - THUMBPRINT SIGN
TREATMENT
Secure airway - call anesthesiology and prepare to establish airway, transfer to OR to perform exam
- tracheostomy if necessary to maintain airway
⦁ maintain airway + supportive management = place child in comfortable position and keep them calm.
Admit for observation ==> humidified O2, IV antibiotics (ceftriaxone + clindamycin), and IV corticosteroids
⦁ Dexamethasone to decrease airway edema, and be prepared to intubate
⦁ IV ABX = Ceftriaxone (most likely HIB) or Vanco for anti-staph - call ID specialist for regional coverage/most likely etiology
EX:
Your patient is a 45 year old male that is not immunized. He presents with a fever of 102, dysphagia, drooling, and shortness of breath. Lungs are clear. O2 Sat 100%. Pulse 102. RR-24. Soft tissue neck reveals a thumb sign. All of the following are acceptable management plans except:
A Give a Racemic Epinephrine aerosol treatment and discharge the patient home on steroids = NO
B Begin Vancomycin and Ceftriaxone
C Intubate the patient in the operation room
D Consult anesthesia or ENT
Question 36 Explanation:
In the treatment of epiglottitis racemic epinephrine can help momentarily, but ultimately the patient needs to be intubated and admitted to the hospital. Airway protection is the mainstay of treatment. The patient usually needs to be intubated for 2-3 days prior to weaning attempts. The role of steroids is controversial. Vancomycin helps with anti-staph coverage and Ceftriaxone covers the most common organism haemophilus influenza type B. Anesthesia and/ or ENT should be consulted for airway management.
Patient will present as → a 3-year-old who is brought into the emergency room by her parents. The child has had a high fever, sore throat, and stridor. She has a muffled voice and is sitting up on the stretcher drooling while leaning forward with her neck extended. The patients parents are adamantly against vaccinations, claiming that they are a “government conspiracy.” You order a lateral neck x-ray, which shows a swollen epiglottis.
PULMONARY EMBOLISM
- occurs when an embolus (type of blockage - either blood, fat, air, amniotic fluid, bacteria, tumors) suddenly gets lodged inside a pulmonary artery
FAT BAT = fat, air, thrombus, bacteria, amniotic fluid, tumors
- also can occur from changing central venous lines - to prevent infection, but can cause clot to dislodge
- depending on which pulmonary artery or arteries are affected by the embolus, this can decrease the amount of oxygenated blood that gets to the body
Most people who die from PE die from subsequent PEs, not their first one
PATHOPHYSIOLOGY
1) network of veins bring blood from the body back to the heart via SVC and IVC
2) superficial veins drain into deep veins, which rely on the skeletal muscle pump compress veins and propel blood in legs to move blood forward, one-way valves prevent backflow
3) SVC / IVC –> RA –> RV –> Pulmonary arteries –> lungs
- the pulmonary arteries split at the
* ** PULMONARY SADDLE *** –> R + L lungs
- R + L pulmonary arteries branch further into smaller and smaller arteries –> arterioles –> capillaries
4) The capillaries form networks around alveoli = where gas exchange occurs in lungs
5) an embolus at any of these arteries blocks blood from flowing to lung tissue downstream, and also blocks blood from picking up enough oxygen
6) If no blood flowing past an alveoli ==> alveoli are being ventilated with fresh air, but are not getting perfused with blood - getting oxygen to the alveoli, but no blood to pick up that oxygen
= ** VENTILATION PERFUSION MISMATCH **
= V / Q MISMATCH
- the body needs oxygen to function, and can therefore only tolerate a small amount of V/Q mismatch before the lungs are no longer able to meet the needs of the body
V/Q mismatch depends on the NUMBER, SIZE, + LOCATION of the PE
V/Q mismatch essentially tells us the amount of lung tissue that is being denied blood flow
⦁ *** MC CAUSE OF PE = DVT *** o Virchow's Triad ⦁ venous stasis ⦁ hypercoagulability ⦁ damage to vessel endothelium
MC location for DVT = left iliofemoral vein
- then popliteal veins, then calf veins
Air emboli are associated with scuba divers who ascend quickly from deep depths. Also trauma, surgery, being on a ventilator, and scuba diving
Patients who are pregnant can present with an amniotic fluid embolism which is a type of pulmonary embolism that can lead to DIC
Fat emboli are associated with long bone fractures and liposuction; they usually present with the classic triad of hypoxemia, neurologic abnormalities, and petechial rash.
RISK FACTORS FOR PE ⦁ smoking ⦁ cancer ⦁ pregnancy ⦁ OCP ⦁ surgery ⦁ infection ⦁ immobilization - long plane / car rides / bed-ridden ⦁ obesity
patients who undergo c-section are 3-5x more likely to develop a DVT than a patient with a vaginal delivery.
SIGNS / SYMPTOMS OF PE
- small PE may not cause any symptoms
- large PE can cause sudden / severe symptoms like
⦁ SOB / dyspnea = MC symptom
⦁ chest pain
⦁ fatigue
⦁ hemoptysis
⦁ tachycardia
⦁ tachypnea = * MC sign */ hyperventilation
⦁ hypoxia
⦁ pleuritic chest pain - pain worsens when breathing
⦁ sudden death if PE at pulmonary saddle (blocking blood flow access to both lungs = no oxygen supply whatsoever)
- may hear crackles (rales)
- JVD
- Homan’s sign = indicative of DVT = pain with dorsiflexion
Classic presentation = post-op patient with sudden tachypnea, tachycardia, with cough or hemoptysis
⦁ hyperventilation (attempt to get more oxygen, despite that fact that problem is blood flow)
==> rapid release of CO2 ==> RESPIRATORY ALKALOSIS (elevated blood pH)
If someone has a PE = important to check for ASD (atrial septal defect) - as clot can travel to brain
If multiple PEs occur over time = can lead to
** PULMONARY HYPERTENSION ** and ** RIGHT VENTRICULAR FAILURE ** as more pressure is required to move blood past obstructed arteries
If massive PE: syncope, hypotension, PEA
** Factor V Leiden = MC predisposing condition **
DIAGNOSIS
⦁ best initial test = Helical CT scan
⦁ ** CT pulmonary Angiography ** = gold standard test = dye injected into vessels to identify blockages
⦁ V/Q scan = reveals areas of the lungs that are ventilated but are not being perfused with blood - use if patient in renal failure, contrast allergy, or pregnant
⦁ EKG = tachycardia + S1Q3T3 (rare)
- shows ST segment changes
⦁ CXR = ** Westermark sign ** = avascular markings or ** Hampton’s Hump ** = triangular or rounded pleural-based infiltrate usually located adjacent to the hilum
- normal CXR = MC finding in PE
LABS
⦁ D-dimer = helps to rule out PE = plasmin breaks down fibrin into d-dimer
- only get this test if likelihood of PE is LOW
⦁ ABG will show respiratory alkalosis secondary to hyperventilation
TREATMENT
- some small clots resolve on their own
- larger clots typically need intervention
⦁ 1) LMWH (SQ) or IV heparin anticoagulant
LMWH - Lovenox / Enoxaparin potentiates antithrombin III
- SQ injection. Compliant, low-risk patients can be discharged home during bridging therapy
- duration of action = about 12 hours
- don’t need to monitor PTT
- antidote = protamine sulfate, but not as effective as with UFH
- lower risk of HIT
- CI = renal failure (Cr > 2.0) - because LMWH is excreted by kidneys… and thrombocytopenia
IV UFH potentiates antithrombin III + inhibits thrombin / other coagulation factors
- continuous IV drip - requires hospitalization for bridging therapy
- duration of action = 1 hour after IV drip discontinued
- must monitor PTT to 1.5 - 2.5x normal value
- antidote = protamine sulfate
- risk of HIT
- INR between 2.0 - 3.0 = considered therapeutic; when reached INR of 2-3 = add LMWH or Coumadin
- discharged on PO Coumadin (Warfarin) x 3-6 months after
- warfarin = inhibits vitamin K dependent coagulation factors (2, 7, 9, 10 = extrinsic pathway)
- should be overlapped with heparin for at least 5 days
- Adjust the warfarin dose to maintain a target INR of 2-3 for at least 24 hours
⦁ thrombolytics (Altepase) = only if hemodynamically unstable = give if acute PE + Hypotension
definite CI = CVA or internal bleed within 3 months
relative CI = uncontrolled HTN, surgery / trauma within 6 weeks
⦁ pulmonary thrombectomy - surgically remove clot = reserved for patients with CI to thrombolytics or ineffective thrombolytics
PREVENTION
⦁ anticoagulant therapy (warfarin / heparin) - inhibit clotting cascade
⦁ IVC filter = helpful in patients at high risk of recurrence who are unable to tolerate anticoagulants
⦁ compression stockings
⦁ frequent calf exercises
⦁ early ambulation
WELL’S CRITERIA FOR PULMONARY EMBOLISM
1) clinical signs/symptoms of DVT = 3 points
2) PE = most likely diagnosis = 3 points
3) tachycardia = 1.5 points
4) immobility > 3 days = 1.5 points
5) previous hx of DVT or PE = 1.5 points
6) hemoptysis = 1 point
7) malignancy = 1 point
CLINICAL SIGNS / SYMPTOMS OF DVT o swelling of leg o redness / discoloration o pain / tenderness of leg o increased warmth
> 6 = high probability of PE
2-6 = moderate probability
< 2 = low probability
PERC CRITERIA = Pulmonary Embolism Rule out Criteria
⦁ Age < 50 ⦁ Pulse < 100 ⦁ O2 > 95% ⦁ No prior PE ⦁ no recent trauma or surgery ⦁ no hemoptysis ⦁ no use of exogenous estrogen ⦁ no unilateral leg swelling
if any are positive = cannot rule out PE
PNEUMOTHORAX
Pneumothorax = Air within the pleural pace
ANATOMY
- lungs are surrounded by visceral pleura
- then pleural space
- then parietal pleura
Within the pleural space = normally have lubricating fluid that reduces friction as the lungs expand and contract
2 forces that create a slight vacuum within the pleural space = 1) muscle tension from the diaphragm and chest wall as they expand outward = balanced with 2) elastic recoil of the lungs that are pulled inward
==> This creates a negative water pressure within the pleural space (-5) compared to pressure of 0 in both lungs + thoracic cavity
In pneumothorax, air gets between the visceral and parietal pleura
PATHOPHYSIOLOGY
⦁ Pneumothorax forms when the seal of the pleural space gets punctured and air moves in
⦁ this makes the pressure in the pleural space = 0
⦁ since the negative pleural pressure is lost ==> the 2 opposing forces no longer pull on one another ==>
⦁ lungs pull inward and collapse
COLLAPSED LUNG
- limited ability to exchange air –> decreased amount of oxygen available for the rest of the body
- -> build up of CO2 in the body because of decreased ability to release air
TYPES OF PNEUMOTHORAX
1) PRIMARY SPONTANEOUS PNEUMOTHORAX
⦁ no underlying lung disease
⦁ occurs in “tall thin young males” - usually in 20s
⦁ positive family hx
⦁ can happen from smoking, diving, high altitude flying, or holding breath
MC cause of primary spontaneous pneumothorax = Rupture of subpleural apical blebs due to high negative intrapleural pressures
- air leaks from alveoli –> creates air bullae on lung
- if bullae breaks, air can fill pleural space
2) SECONDARY SPONTANEOUS PNEUMOTHORAX ⦁ with an underlying lung disease - asthma - COPD - emphysema - lung cancer - CF** - HIV related - pneumocystis - TB - Marfan's syndrome / Ehlers Danlos**
Patients with Marfan syndrome are prone to recurrent pneumothoraces.
3) TRAUMATIC PNEUMOTHORAX
⦁ trauma or chest injury
- *rib fracture / stab wound / GSW rips through parietal pleura, allowing air to enter from outside directly into pleural space
4) IATROGENIC PNEUMOTHORAX
⦁ “medically caused” - medical interventions that went wrong, such as chronic mechanical ventilation (can cause barotrauma to lungs), or some sort of procedure
- CPR, thoracentesis, ventilation, subclavian line placement, rapid pre-oxygenation rate
An overly rapid pre-oxygenation rate prior to intubation can cause a pneumothorax
After placing a central venous catheter (CVC), a chest radiograph should be obtained immediately to ensure adequate line placement and to assess for complications before the line is used
Pneumothorax formation may occur during the supraclavicular approach of a brachial plexus block
5) TENSION PNEUMOTHORAX (MC after trauma** or infection)
⦁ essentially the same as any other pneumothorax, however, what makes it tension is that air in the pleural space cannot exit AT ALL
- a one-way valve is created, allowing air to flow into pleural space, however, flap of tissue only allows air in + prevents air from getting out –> continues to expand
- over time, so much air in pleural space can start compressing the heart and other lung, and starts shifting large structures such as the trachea (tracheal deviation) + mediastinal shift
- can prevent heart from filling up properly –> reduced cardiac output
- can prevent other lung from expanding properly –> reduced oxygen
⦁ most serious type –> goes into severe respiratory distress, to where patient can die
⦁ medical emergency = don’t have time to diagnose via cxr, like others - falling O2 sats, hypotension, tracheal deviation
CATAMENIAL PNEUMOTHORAX = occurs during menstruation (ectopic endometrial tissue in pleura)
SYMPTOMS OF PNEUMOTHORAX
⦁ dyspnea / SOB
⦁ pleuritic chest pain (pain while breathing)
⦁ decreased breath sounds on affected side
⦁ unequal respiratory expansion
⦁ ** HYPERRESONANCE ** on percussion
⦁ Decreased tactile fremitus
⦁ Decreased egophany
⦁ JVD (jugular veins distended) = tension
⦁ hypotension + tachypnea + tachycardia = tension
JVD = due to increased pressure on the collapsed lung, blood backs up on right side of heart (cannot send as much blood to lungs) –> backs up right side of heart –> JVD
(pressure in pulmonary artery = really high!)
Hyperresonance = indicates that too much AIR is present in the lungs (pneumothorax / asthma / emphysema)
Dullness to percussion = indicates abnormal lung density / consolidation (atelectasis, tumor, plural effusion, pneumonia, fibrous tissue, hemothorax)
Egophony is an increased resonance of voice sounds heard when auscultating the lungs, often caused by lung consolidation and fibrosis - due to enhanced transmission of high-frequency sound across fluid / tissue.
- normal lungs (filled with air), do not readily transmit sounds, while consolidated lung tissue more readily transmits sounds
- Egophany = decreased with air (pneumothorax
- increased with fluid / excess tissue (consolidation) = pneumonia / pleural effusion
- *** Although in pleural effusion = egophony is only heard above the effusion in an upright patient
increased Tactile fremitus = indicates denser tissue / consolidation
decreased tactile fremitus = air or fluid in pleural space(pneumothorax, effusion)
Tactile fremitus increases in intensity whenever the density of lung tissue increases, such as consolidation or fibrosis
- causes of increased tactile fremitus include: Pneumonia, Lung tumor or mass, Pulmonary fibrosis, Atelectasis.
Tactile fremitus will decrease when a lung space is occupied with an increase of fluid or air (pleural effusion, pneumothorax and emphysema)
DIAGNOSIS
⦁ CXR = INITIAL test for all pneumothoraces except tension (emergency!)
- absent vascular markings due to air
- air (black)
- may see outline of collapsed lung
- may see hyperexpanded diaphragm
- tracheal deviation to other side = tension
- mediastinal shift (heart pushed to other side) = tension
⦁ CT = ** still considered gold standard **
- but xray more commonly used in practice because it is cheaper, faster, and has less radiation exposure
TREATMENT
⦁ if “small “ pneumothorax and not tension = can be managed with just oxygen
- small = < 2-3 cm or <15-20% of diameter between visceral and parietal pleura
= OBSERVE x at least 6 hrs, then repeat CXR to affirm no progression
- f/u in 24-48 hours
- often spontaneously resolves within 10 days
- Tx = ** HIGH FLOW OXYGEN ** (10L/min) - shown to increase air resorption 3-4x faster than 1.25% every day
- If patients remain stable for 4-6 hours, they can be released with follow-up in several days. Patients should be instructed to immediately seek medical attention should they become short of breath.
For otherwise healthy, young patients with a small primary spontaneous pneumothorax (<3 cm between the lung and the chest wall on chest X-ray), observation alone may be appropriate. The intrinsic resorption rate is approximately 1-2% a day and is accelerated with the administration of 100% oxygen. Many physicians observe these patients for 6 hours and then repeat the chest X-ray. If the repeat chest X-ray shows no increase in the size of the pneumothorax, the patient can be discharged with follow-up in 24 hours. Air travel and underwater diving (which cause changes in atmospheric pressure) must be avoided until the pneumothorax completely resolves.
⦁ Chest tube (thoracostomy) if large pneumothorax or if severe symptoms
- 4th-5th or 5th-6th ICS - mid axillary line
⦁ Needle Decompression (14G) = if TENSION PMX* - followed by chest tube
- 2nd ICS (between 2nd + 3rd rib) at the midclavicular line
- hear gush of air
RECURRENT PNEUMOTHORACES
ex: tall thin young males who have had recurrent primary spontaneous pneumothoraces can have PLEURODESIS done = via Video-assisted thoracoscopic surgery or Thoracotomy
Pleurodesis = a procedure that scars the lung tissue so that it adheres to the parietal pleura, providing a sturdier barrier in that portion of the lung wall and obliterating the pleural space
lung tissue is scarred either via an irritant (talc powder) or through mechanical abrasion, in order for it to adhere tightly to the parietal pleura, thereby eliminating the pleural space.
SPONTANEOUS PNEUMOTHORAX
Patient will be a young, tall, thin, man
PE will show decreased breath sounds, decreased fremitus, hyperresonance to percussion
CXR will show the absence of lung markings along lung periphery
Treatment is:
< 20% in a healthy patient: observation with oxygen administration
> 20%: chest tube thoracostomy
ON TEST
- if not a tension pneumothorax = get an xray first
- if tension pneumothorax = needle decompression first
PLEURAL EFFUSION
PLEURAL EFFUSION
- The abnormal accumulation of fluid in the pleural space
- generally the entrance + exit of fluid into pleural space is about equal
- fluid accumulation occurs when there is either an increase in entry fluid or decrease in exit fluid
- there are capillaries in visceral and parietal pleura through which interstitial fluid leaks out and into pleural space; lymphatic vessels then drain the pleural fluid in an equal balance
** MC cause of pleural effusions overall = CHF **
MOST COMMON CAUSES OF PLEURAL EFFUSION ⦁ heart failure (MC transudative) ⦁ bacterial pneumonia (exudative) ⦁ PE (exudative) ⦁ Malignancy (MC exudative) ⦁ viral infections (not as common as bacterial) (exudative) ⦁ cardiac surgery (exudative) ⦁ pancreatitis (exudative)
- can be either TRANSUDATIVE issue = too much fluid leaks out of capillaries either due to INCREASE IN HYDROSTATIC PRESSURE or DECREASE IN ONCOTIC PRESSURE
- or can be EXUDATIVE issue = too much fluid leaks out of capillaries due to INFLAMMATION of pulmonary capillaries –> damage makes them more leaky - creates larger spaces in capillary membrane for fluid to leak out
TRANSUDATIVE PLEURAL EFFUSION (increased fluid)
o TRANSUDATIVE EFFUSIONS ⦁ heart failure (CHF) ⦁ cirrhosis ⦁ nephrotic syndrome ⦁ atelectasis
⦁ CHF
- increased in hydrostatic pressure = the force that blood exerts on the walls of the vessels (blood pressure - pushing force) - due to increased volume
- Heart failure: heart can’t effectively pump blood to body, so blood backs up into the lungs –> increased hydrostatic pressure in pulmonary vessels, which forces fluid out of pulmonary capillaries and into the pleural space
⦁ Cirrhosis
⦁ Nephrotic Syndrome
- decrease in oncotic pressure = if there is a decrease in solute concentration in pulmonary vessels, fluid will leak into pleural space with higher oncotic pressure, as solutes cannot cross capillary walls
- Cirrhosis = not making enough proteins –> low oncotic pressure in vessels
- Nephrotic syndrome = proteins lost in urine –> low oncotic pressure in vessels
- Mechanism of Transudative Effusions
⦁ increased hydrostatic pressure (CHF)
⦁ decreased oncotic pressure (albumin - cirrhosis or nephrotic syndrome)
⦁ increased negative intrapleural pressure (atelectasis)
⦁ ascites
o Transudative fluid = clear
EXUDATIVE PLEURAL EFFUSION (increased fluid)
- inflammation of capillaries –> larger spaces in capillary membrane, allowing fluid, immune cells and large proteins + enzymes (LDH) to leak out of capillaries and into pleural space
⦁ infection (pneumonia) = MC exudative
⦁ malignancy
⦁ trauma
⦁ inflammatory conditions (SLE, RA, sjogrens - autoimmune conditions)
o Exudative fluid = cloudy (full of immune cells)
o EXUDATIVE EFFUSIONS
⦁ malignancy
⦁ inflammatory processes (trauma, autoimmune, infection)
- Mechanism = increased vascular permeability due to infection or inflammation
LYMPHATIC PLEURAL EFFUSION (decreased drainage)
- chylothorax = lymphatic fluid accumulates in the pleural space due to an disruption in the thoracic duct - prevents drainage
⦁ damage to thoracic duct during surgery
⦁ tumors in mediastinum that compress thoracic duct
o Lymphatic fluid = filled with fat looks like milk
- high in triglycerides
MEDICATIONS THAT CAN LEAD TO PLEURAL EFFUSION ⦁ Methotrexate ⦁ Amiodarone ⦁ Phenytoin ⦁ Nitrofurantoin ⦁ Beta blockers
BETty sold her FUR coat for METH/AM/PHEtamines
- beta blockers
- nitroFURantoin
- METHotrexate
- AMiodarone
- PHEnytoin
TYPES OF PLEURAL EFFUSION OR ASSOCIATED CONDITIONS
o Empyema = infection of pleural space
o Parapneumonic = pleural effusion secondary to bacterial pneumonia
o Hemothorax = gross blood (from chest trauma or malignancy)
o Chylothorax = lymph fluid due to impaired lymphatic drainage
If pneumonia + fever –>shows effusion on CXR but will not drain from thoracentesis = suspect EMPYEMA = will need surgical removal
**biggest way to distinguish between transudative + exudative fluid = is that exudative fluid will have high amounts of protein + LDH from leaking out of inflamed damaged capillaries
- use LIGHT CRITERIA- exudative if > 1 of the following
⦁ fluid protein : serum protein > 0.5
⦁ fluid LDH : serum LDH > 0.6
⦁ fluid LDH > 2/3 of upper limit of serum LDH - exudative also has high cholesterol level > 45
SYMPTOMS ⦁ Asymptomatic - small effusion may go unnoticed ⦁ dyspnea / SOB ⦁ cough ⦁ pleuritic chest pain *** ⦁ fever (infection) ⦁ hemoptysis ⦁ weight loss (malignancy)
- large effusions ==> pain with inhalation (pleurisy) and SOB, worse when laying flat
PHYSICAL EXAM
⦁ decreased breath sounds
⦁ dullness to percussion (unlike pneumothorax)
⦁ decreased tactile fremitus (like pneumothorax)
- can have so much fluid accumulate that it causes pneumothorax / pushes trachea over / mediastinal shift
- if effusion is large enough, can put pressure on lungs and push trachea to other side (like tension pneumothorax)
DIAGNOSIS
⦁ CXR (standing + laying flat) = INITIAL TEST
- standing = fluid will settle in costophrenic angle (bottom is white)
- laying flat = will settle all over chest wall, creating a layering effect (whole side is white)
- **BLUNTING OF COSTOPHRENIC ANGLES **
- ** positive menisci sign **
- lateral decubitus films = best
⦁ can detect smaller effusions
⦁ can differentiate loculations + empyema (whether fluid shifts when laying down or not)
⦁ CT scan can help determine lung disorders and presence of loculation
⦁ Ultrasound can determine presence of loculation and fibrin stranding; also aids in thoracentesis procedure
⦁ THORACENTESIS + ANALYSIS OF PLEURAL FLUID = ** DIAGNOSTIC TEST OF CHOICE ***
PLEURAL FLUID ANALYSIS ⦁ differential cell count ⦁ cytology ⦁ protein (helps determine transudate vs exudate) ⦁ LDH (helps determine transudate vs exudate) ⦁ gram stain ⦁ culture ⦁ pH ⦁ glucose
EXUDATIVE EFFUSION WILL HAVE HIGH AMOUNTS OF PROTEIN + LDH IN PLEURAL FLUID
LIGHT’S CRITERIA: EXUDATE IF >/= 1
o fluid protein : serum protein > 0.5
o fluid LDH : serum LDH > 0.6
o fluid LDH > 2/3 the upper normal limit of serum LDH
pleural fluid protein needs to be more than half of serum protein
ALTERNATIVE CRITERIA: TRANSUDATE IF ⦁ LDH % = 45% ⦁ cholesterol = 45 mg/dL ⦁ protein = 2.9 g/dL
EXUDATE IF
⦁ LDH% = > 45%
⦁ cholesterol > 45 mg/dL
⦁ protein > 2.9 g/dL
Exudates = HIGH PROTEIN, HIGH LDH, low glucose
TREATMENT
- the treatment of underlying conditions may often resolve pleural effusions (don’t drain all of them!)
⦁ thoracentesis if needed
- Thoracentesis = diagnostic + therapeutic
- not all pleural effusions need to be drained with a needle (thoracentesis); often will resolve on their own
SMALL EFFUSIONS from CHF
- may be treated with diuretics or sodium restriction
- Remove fluid via thoracentesis (max amount removed at one time = 1.5L - don’t want to remove too much, because relieving too much pressure at once can lead to compensatory pulmonary edema)
- thoracentesis guided via ultrasound
- needle inserted above rib to avoid vasculature / nerve underneath ribs
- may have placement of chest tube for continued drainage
Hemothorax, with persistent bleeding is an indication for thoracotomy. If on initial placement of the chest tube 1000-1500cc of blood drains or if the chest tube continues to drain over 200cc/hr over 4-5 hours, it is unlikely that the bleeding will stop with a chest tube, or systolic pressure < 70
Emergency thoracotomy = at 5th intercostal space
- chronic effusion may require pleurodesis (induced scarring - with talc or doxycycline)
- empyema may require surgical removal - can be too thick to be drained via thoracentesis
hemothorax can cause mediastinal shift and can lead to collapse
Patient presents as → a 58-year-old female who returns to the hospital with chest pain and difficulty breathing several weeks after being discharged following a myocardial infarction requiring immediate cardiac catheterization. She has been coughing up frothy sputum for the past three days. The patient complains of a sharp pain that worsens during inspiration. Physical exam reveals decreased tactile fremitus, dullness to percussion and diminished breath sounds on the left side
PNEUMOCYSTIS JIROVECII (PJP)
or PCP pneumocystis carinii pneumonia
= Yeast-like fungus - but doesn’t respond to antifungals!!
TRANSMISSION = INHALATION
- ** MC OPPORTUNISTIC INFECTION IN HIV ***
- especially if CD4 < 200***
SYMPTOMS ⦁ fever ⦁ dyspnea on exertion ⦁ nonproductive dry cough ⦁ *** O2 desaturation with ambulation ***
DIAGNOSIS ⦁ CXR - ** BILATERAL diffuse interstitial infiltrates ** - Ground glass opacification - may also be normal - bat appearance
⦁ ** ELEVATED LDH ** = > 2000
⦁ Bronchoalveolar lavage or induced sputum =
** definitive diagnosis **
TREATMENT
⦁ ** BACTRIM ** X 21 days
- add prednisone if hypoxic (PaO2 < 70mmhg, A-a gradient > 35)
If allergic to sulfa = DAPSONE-Trimethoprim
PROPHYLAXIS
⦁ If CD4 < 200 = give bactrim
LUNG ABSCESS
** ALCOHOL ABUSE **
** anaerobic bacteria **
Patients with lung abscess classically present with several weeks of cough, fever, pleuritic chest pain, weight loss, and night sweats.
There may be cough productive of putrid sputum.
Because the progression of lung abscess is indolent, tachycardia, tachypnea, or fever may be absent.
The chest radiograph often shows an area of dense consolidation with an air-fluid level inside a thick-walled cavitary lesion.
Those who abuse alcohol or have other conditions associated with the potential for aspiration are at greatest risk for lung abscess development.
** MC CAUSE OF LUNG ABSCESS = ASPIRATION PNEUMONIA ** = anaerobic bacteria
TREATMENT
- ampicillin-sulbactam, carbapenems, clindamycin
PEDIATRIC PNEUMONIA
Pediatric Pneumonia 0 - 3 weeks: GBS 3 weeks - 3 months: C. trachomatis 1 month - 5 years: RSV 6 - 8 years: M. pneumoniae
C. trachomatis: staccato cough, eye findings
S. pneumoniae: rust-colored sputum
M. pneumoniae: bullous myringitis (or strep)
- used to think it was mycoplasma, but is actually strep!
TUBERCULOSIS TREATMENT
Isoniazid (INH) x 9 months
- give with pyridoxine (vitamin B6) supplementation to prevent peripheral neuropathy
alternative = Rifampin x 4 months
Latent TB: INH for 6 or 9 months, rifampin for 4 months, or INH/rifapentine for 3 months
Active/reactivation TB: rifampin, INH, pyrazinamide, ethambutol (RIPE)
⦁ Rifampin = orange discoloration of body fluids, including urine, tears, sweat and sputum
⦁ Isoniazid = hepatitis and peripheral neuropathy
⦁ Pyrazinamide = hepatotoxicity and polyarthralgias
⦁ Ethambutol = Optic neuritis and color-blindness
PNEUMONIA ETIOLOGY AFTER INFLUENZA
STAPH AUREUS
S. pneumonia: most common, rust-colored sputum, rigors, gram+ paired lancets
Klebsiella: alcoholics, currant jelly sputum, bulging fissures
S. aureus: IVDA, post-influenza, elderly, gram+ cocci in clusters
H. influenzae: COPD, gram-negative pleomorphic rods
Pseudomonas: cystic fibrosis, nursing home resident and cyanosis
Healthcare-associated pneumonia: pseudomonas, MRSA
