Download Introduction to hospital medicine: Common respiratory

INTRODUCTION TO
HOSPITAL MEDICINE:
COMMON RESPIRATORY
ADMITS
CHRISTIAN SONNIER MD
LEARNING OBJECTIVES
• Discuss common respiratory admits and their
management
• Pneumonia: community acquired vs HCAP vs aspiration
pneumonia
• COPD exacerbation
• Asthma exacerbation
• CHF exacerbation (“cardiac asthma”)
• Pulmonary embolism/dvt
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Recognizing respiratory distress and failure
When to consider ICU
When to consider intubation
RSI basics
COMMUNITY ACQUIRED PNEUMONIA
• Not all CAP needs hospitalization. Need to use
clinical judgment when deciding if admission is
needed
• Admit if:
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Failed outpatient therapy
hemodynamically unstable
Sepsis
Pneumonia severity index
Curb-65 score
Severe community acquired pneumonia score
SMART-COP
COMMUNITY ACQUIRED PNEUMONIA
• PSI (pneumonia severity index
• If one or more Step 1 risk factors are present then proceed
to step 2
• Step 2 stratifies risk into class II, III, IV or V based on total
points
• Total point score is calculated by adding:
• Male: pt age in years
• Female: pt age in years -10
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70 pts and under= class II
71-90 pts= class III
91-130 pts = class IV
130+ pts= class V
PSI STEP 1
• Age over 50
• Presence of any of the following comorbid conditions
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Cancer
Heart failure
Stroke
Renal dz
Liver dz
• Presence of any of the following physical exam
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Ams
Pulse over 125
Resp rate over 30
Sbp under 90
fever
PSI STRATEGY
The higher the class the greater the indication for
admission
CURB-65 SCORE
• Similar validation to PSI and simpler to use
• C confusion
• Based on specific mental status test or any altered mentation
• U urea
• BUN over 7 mmol/L or 20mg/dL
• R respiratory rate
• Over 30/min
• B Blood pressure
• Sbp under 90 or dbp under 60
• 65 age 65 or over
• Score of 0-1= outpatient
• Score of 2= admission
• Score of 3+= strongly consider ICU especially if 4 or 5
SEVERE COMMUNITY ACQUIRED
PNEUMONIA SCORE
• SCAP
• Score 10+ points = admission and likely ICU
• Has the worst validation of all scores…needs more study
• Major criteria
• Arterial pH <7.30 = 13 points
• Sbp < 90mmHg = 11 points
• Minor criteria
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Resp rate >30 bpm = 9 points
PaO2/FiO2 <250 = 6 points
BUN >30 mg/dL or > 10.7mmol/L = 5 points
AMS = 5 points
Age 80+ = 5 points
Multilobar or bilateral infiltrates cxr = 5 points
SMART-COP
• Uses set of clinical criteria to predict who needs ICU
care (score of 3+=increasing need for ICU)
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Age
Albumin
Resp rate
Arterial pH
PaO2 on room air
Sbp
Multilobar infiltrates
Pulse
confusion
COMMUNITY ACQUIRED PNEUMONIA
• Dx: clinical, imaging and lab based
• Clinically:
• Cough, rhonchi, rales, fever, chills
• No long term hospital or health care exposure in past 30-90
days
• Imaging
• Evidence of infiltrates on cxr
• Lab
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Leukocytosis
Sputum cx
Blood cx
Urine studies (cx and legionella antigen)
COMMUNITY ACQUIRED PNEUMONIA
• Can be caused by variety of pathogens including
viral
• Most commonly but not limited to
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Strep pneumo
H influ
Mycoplasma pneumonia
Chlamydia pneumo
Legionella
Just as with any infection start with broad abx coverage and
decrease as needed based on culture reports
COMMUNITY ACQUIRED PNEUMONIA
• Additional tips
• Duration of therapy is usually 5-7 days of po abx
• Cxr may lag by 24-48 hours behind clinical picture
• Upon admission if patient is dehydrated, rehydration may
“fluff out” infiltrates and make them more apparent
• If patient does not respond to tx, may need stronger abx
coverage and mechanical ventilation
• The more co-morbidites the greater the re-admission risk
• Glucocorticoids have some evidence in shortening hospital
stays
• Tissue factor pathway inhibitors do not show benefit
• Statins have limited anti-inflamatory properties and show
limited benefit in studies
COMMUNITY ACQUIRED PNEUMONIA
• Prevention
• Vaccination in patients 65+
• Smoking cessation
HEALTH CARE ASSOCIATED
PNEUMONIA
• HCAP= pneumonia in non-hospitalized patient who
has extensive healthcare contact
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IV therapy, wound care, chemo with in 30 days
Resident of long term care facility (pinecrest, nh ect)
Hospitalization for acute care for 2+ days with in last 90 days
HD in clinic or hospital within past 30 days.
Some argue hospital employees qualify
• HAP: hospital acquired (nosocomial) pneumonia:
pneumonia that occurs 48 hrs or more after
admission and was not noted on admission
• VAP: ventilator-associated pneumonia: HAP that
develops 48-72 hours after intubation
HCAP
TX
• Patients are usually septic therefore begin EGDT asap
• Obtain cbc, cmp, lactic acid, procalcitonin, bld cx,
urine cx, sputum cx
• Begin empiric abx therapy
• Vancomycin, levaquin, zosyn
• Goal is to cover MRSA and double cover pseudomonas
• Maintain these meds until specific organism has been
identified then de-escelate to monotherapy if possible
• Then to po and discharge
• Once de-escelating from empiric to focused therapy the tx is
very similar to CAP (see prior slides)
• Usually duration of therapy is at least 14-15 days
HCAP
• Tips: consider the following (for any pneumonia)
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Albuterol, duonebs, xopenex (q4q2prn)
Incentive spirometry
Chest physiotherapy
Lactinex
Pneumovax if age appropriate
Smoking cessation
Good pulm hygiene and toilet (suctioning ect)
If copious secretions mucomyst and or robinol may be
helpful.
ASPIRATION PNEUMONIA
• Definition: pneumonia following aspiration of gastric
contents
• Difficult to distinguish between chemical
pneumonitis and true pneumonia therefore we
usually treat as pneumonia
• If aspiration pneumonia occurs always get a
swallow study or evaluate for dysphagia before
feeding
ASPIRATION PNEUMONIA
• Clinical signs of anaerobic bacterial infection
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Indolent/smoldering sx (low grade fevers ect)
Absence of chills/rigors
Foul odor to sputum
Infiltrates worse on the right (remember anatomy…right
mainstem is straight shot)
ASPIRATION PNEUMONIA
• If anaerobic organisms are suspected/assumed
• First line is clindamycin 600mg iv q8hrs then 300mg po qid
• Alternatives
• Augmentin 875mg po bid
• Flagyl (500mg po/iv tid) +amoxicillin (500mg tid) or penicillin G
(1-2million units IV q4-6hrs)
• If hcap suspected: go to vanc, levaquin and zosyn as
discussed earlier
• Duration of tx: 7-10 days unless case becomes more
complicated
• In the event of mechanical obstruction may need
bronchoscopy
COPD
• Chronic obstructive pulmonary disease: group of
related disorders that all cause airflow limitation
• Emphyseme
• Chronic bronchitis
• Chronic obstructive asthma
• Main difference between copd and asthma is airway
(bronchial constriction is more reversible in asthma.
COPD
• GOLD Classification
COPD
• For the purposes of this lecture we will not discuss dx
of copd as this usually is an outpatient event and
chronic management of the disorder is also
outpatient.
• We will focus on how to tell a patient may have
copd and how to handle acute exacerbations
COPD
• Copd patient:
Usually heavy smoking history
Usually have sedintary lifestyle due to respiratory limitations
Have baseline non-productive cough, wheeze
Barrel chest, blue bloater, pink puffer is not a reliable
characteristic
• Intermittent exacerbations caused by physiological stress
(cold, flu, pneumonia) “peaks in symptoms however upon
resolution patient is never quite back to baseline”
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COPD
• Mild exacerbations can be managed at home by
providing:
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Bronchodilator
Oral glucocorticoids
Antibiotics
Continuation of chronic meds
• Inhaled short acting beta-agonists (albuterol)
• Inhaled short acting anticholinergic agents (ipratropium)
• Nebulizers may be easier for patient’s with exacerbations
COPD
• Moderate to severe exacerbations as well as any
exacerbation with hemodynamic instability need
hospital treatment.
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Oxygen therapy
Beta-adrenergic agonists
Anticholinergic agents
Systemic glucocorticoids
Antibiotics and antiviral agents
Supportive care
Bipap vs mechanical ventilation
COPD
• Oxygen therapy
• Critical component of acute therapy however care should
be taken to avoid excess oxygen therapy
• Excess oxygen can worsen condition because COPD
patient’s tend to be CO2 retainers
• These patient’s have a baseline hypercapnia which supports
their respiratory drive.
• Excess O2 over 60-70mmHg causes decrease in hypercapnia
which results in respiratory depression
• Pox goal of 88-92% is adequate for copd patient’s
• Nurses and RT may not understand this, specify to them that
this is adequate and not to be concerned.
• DO NOT PLACE COPD PATIENT ON HIGH FLOW O2 THERAPY
AND LEAVE THEM ALONE… THEY WILL STOP BREATHING.
COPD
• Every copd exacerbation should receive inhaled
short acting beta adrenergic agonists
• Albuterol
• Use caution as albuterol can cause tachyarrhythmias such as
afib. In patient’s prone to these arrythmias use levalbuterol
• Levalbuterol (xopenex)
• These agents are commonly combined with anticholinergic
agents such as ipratoprium
• This is duoneb
MDI therapy has equal efficacy as nebulizers however patients
are often comforted by nebulizer therapy and this therapy can be
combined with oxygen therefore we tend to use these more in
the hospital
COPD
• Albuterol, duonebs, xopenex are usually dosed as
follows
• Q4q2prn
• Scheduled every 4 hours while awake
• Every 2 hours as needed
• There has not been shown to be a difference in preventing
hospital admission using duonebs vs albuterol in an outpatient
bases therefore which ever is cheaper for the patient is the right
answer at discharge
COPD
• Systemic glucocorticoids
• Shown to improve the following when added to
bronchodilator therapies
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Improve lung function
Decrease hospital lenghts of stay
Reduced failure rate of therapies
Does not matter if it is oral or IV
Doses (optimal doses are unknown) the following are common
doses
• Prednisone 40mg qday (this is the prototypical dose)
• Methylprednisolone 60-125mg bid-qid
COPD
• Anti-microbial therapy
• If suspected infection is cause exacerbation then treat
accordingly
• this could be anything from pneumonia, uri, flu, cellulitis or any
other infection…the physiological stress can trigger an
exacerbation
• In case of pneumonias see earlier sections of this
presentation
COPD
• Supportive care during exacerbation
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Stop smoking
Dvt/pe prevention
Nutritional support
Mucolytic agents
Rehydration
Pain control (specifically for air-hunger)
Chest physiotherapy
Mechanical ventilation (progressive support from
cpapbipapintubation and vent support
ASTHMA
• Definition: reversable bronchoconstriction and
inflammation. An allergic reaction usually.
• Exacerbation is characterized by
• Sob, wheezing
• Cough, chest pain
• Fatigue
• Risk factors for fatal asthma
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Previous severe episodes requiring ICU and intubation
Hospitalization/ER within past year the more the worse
Not on inhaled steroids
More than 1 canister of SABA a month
Comorbidities such as CAD, copd, drug abuse ect
ASTHMA
• Rest of treatment is similar to COPD exacerbation
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Oxygen therapy (with out the risk of respiratory depression)
Systemic steroids
Antibiotics, antivirals
Progressive vent support
Chest physiotherapy
Mucolytic
Supportive therapy
CHF
• See cardio lecture
• Goal here is to provide oxygen/ventilator support
until chf exacerbation is resolving
• Take the opportunity to optimize therapy
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ACE/ARB
B-Blocker
Diruetics (especially lasix)
Digoxin
Acid
Salt restriction
PE/DVT
• DVT is the leading cause of PE
• Deep vein thrombosis
• Most commonly occurs in the lower extremity however upper
extremity and deep abdominal vessels are possible as well
• Pieces of the clot can dislodge and travel via venous system
through right side of heart and lodge in the pulmonary arteries
causing PE
DVT/PE
• Diagnosis
• Providers in the ER/hospital must have high index of
suspicion…this means always look for it!
• Classic triad: hemostasis, endothelial injury,
hypercoagulable states
• Immobility
• Trauma
• malignancy
DVT/PE
• Physical exam findings
• Disproportionate swelling of the limbs
• Measure above and below the knee/elbow
• Difference of 2 or more cm between limbs
• Pain on deep palpation of the limb
• Palpable cord
• Homan sign
DVT/PE
• Diagnosis
• Well criteria (there is one for both dvt and pe)
• D-dimer
• Only clinically useful if it is negative as this effectively rules out
clot
• Positive d-dimer should always prompt further investigation with
bilateral venous ultrasound
• ct pe protocol or vq scan if pt is also sob
DVT/PE
• Ct pe protocol
• Useful in actually visualizing the clot
• Will yield a definitive yes or no answer
• Vq scan
• Useful if iv contrast can not be used or not available
• Will yield a probability but can not 100% rule out a clot
• If clinical suspicion still remains then treat for it
DVT/PE
• Management
• Prophylaxis
• Scd
• Compression hose
• Lovenox 30-40mg (1mg/kg) subq qday
• Treatment
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Lovenox 1mg/kg subq bid while bridging to warfarin
Xarelto
Heparin
Direct TPA per catheter placed by IR
• Indicated for
• Saddle embolism
• Hemodynamic instability with large clot
• Compartment syndrome of the leg
ACUTE RESPIRATORY FAILURE
• Definition: Inability of the respiratory system to meet
the oxygenation, ventilation and metabolic
demand of the patient’s current condition
• Two types of failure per definition above
• Oxygenation failure: aka Type 1:
• PaO2 less than 60mmhg therefore first priority is to correct
hypoxemia
• Ventilation failure: aka Type 2:
• PACO2 over 50mmhg with pH under 7.3. need to determine if
patient has chronic failure like copd or if this is acute.
ACUTE RESPIRATORY FAILURE:
• Dx is clinical: too fast, too slow, unable to protect
airway, hypoxic or hypoxemia
• Hypoxic: refers to the POX monitor or cyanosis
• Hypoxemia: is on the ABG
• Dx is also lab based:
• ABG, CXR, CT scan, broncoscopy
ACUTE RESPIRATORY FAILURE
• In reference to the two types mentioned earlier;
these are also referred to as hypoxemic respiratory
failure vs Hypercapnic respiratory failure.
• each of these has several possible causes therefore
early in the tx course it is important to determine
what you are dealing with, thus the importance of
the abg ect.
HYPOXEMIC RESPIRATORY FAILURE
• Hypoxemia is the most immediate threat to life,
more immediately life threatening than
hypercapnea
• Pathophysiologic causes of hypoxemic respiratory
failure
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Shunting
V/Q mismatch
Diffusion limitation
Dead spaces
Low FiO2
Low atmospheric pressure
Hypoventilation of alveoli
HYPOXEMIC RESPIRATORY FAILURE
• In any respiratory failure it is important to calculate
the A-a gradient because a normal gradient means
there is no problem with the lungs or pulmonary
circulation and you should start looking else where
for the problem ie cardiac or muscular fatigue
• An increased A-a gradient means there is a venous
admixture and can only have one of 3 causes
• Shunt
• Deadspace
• V/Q mismatch
HYPOXEMIC RESPIRATORY FAILURE:
SHUNT
• Shunt: blood goes through pulmonary circulation
without being exposed to oxygen areas of lung
have no ventilation
• Can be intracardiac: ASD, VSD ect
• Can be pulmonary: something is preventing inspired
gas from reaching the alveoli
• Atelectasis, ARDS, pulmonary edema, pneumonia
consolidation
SHUNT
• Main characteristic is hypoxemia resistant to
increased FIO2
• PaO2/FIO2 ratio is lower the worse the shunt gets
• Shunts do respond well to positive pressure
ventilation to recruit alveoli
HYPOXEMIC RESPIRATORY FAILURE:
VQ MISMATCH
• Blood is not flowing to an area of the lung that is
being ventilated:
• asthma, copd, interstitial lung disease, pneumonitis can also
cause this
• Readily corrects with increased FIO2 as there is
nothing wrong with the oxygen reaching the alveoli
and diffusing
HYPOXEMIC RESPIRATORY FAILURE:
DEAD SPACE VENTILATION
• Opposite of a shunt, the air is getting to the alveoli
but the blood isn’t. Think PE!
• If no blood can get to the alveoli then it doesn’t
matter how good they are…there is no gas
exchange.
HYPERCAPNIC/HYPERCARBIC
RESPIRATORY FAILURE
• Type II failure: too much PaCO2 and low pH
• There is an inability of the body to rid itself of
enough CO2.
• Can have a variety of different causes
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Brain
Spinal cord
Peripheral nerves
Neuromuscular junction
Muscles
Thorax
lungs
HYPERCAPNIC RESPIRATORY FAILURE:
• Easiest way to find the problem is by physical exam
and history looking for problems with any of the
systems listed previously.
• It is important to remember that COPD pt will be
chronic CO2 retainers and can mimic lab values of
this respiratory failure as a base line. However COPD
exacerbation can be hypercapnic respiratory
failure.
OTHER RESP FAILURES
• Trauma, obstruction ect
GENERAL TX OF RESPIRATORY FAILURE
• Identify and treat underlying cause
• Provide simple/non-invasive support and move up
towards mechanical ventilation as needed.
• Always be on the look out for progression to ARDS
or other severe manifestations of respiratory failure.
WHEN TO CONSIDER ICU
• Profound hemodynamic instability
• AMS in the presence of respiratory distress
• Intubated patient or patient with high likelihood of
sudden decompensation
• Use your clinical judgement…if the patient makes
you nervous it is better to move to ICU early then to
have them decompensate and code
WHEN TO CONSIDER INTUBATION
• Impending respiratory failure
• Gcs less than 8 (or if you feel patient is unable to
adequately protect airway)
• Worsening abg
• Severe respiratory distress or depression that is not
responding to non-invasive support
INTUBATION
• For the purpose of this lecture we will not go into
specifics of intubation. At this point (beginning of
intern year) you should have an upper level resident
or attending with adequate experience assist you
with intubation and vent setup/management
• For further information please review the respiratory
failure and mechanical vent lectures in the ICU
lecture set
BASICS OF RSI
• Determine need for intubation
• If patient is coding or there is no time for admit of
meds then proceed with intubation
• If time
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Sedation ie etomidate, versed, ativan
Paralytic ie succynocholine, vecuronium, rocuronium
Directly or indirectly visualize the vocal cords
pass et tube cuff just beyond vocal cords
Inflate tube and check for placement
Verify with cxr
Set the vent
REFERENCES
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Cecil’s medicine
Harrison’s textbook of medicine
Uptodate
Ardsnet protocol