Christian Sonnier MD - PowerPoint Presentation

Slide1

Christian Sonnier MD

Introduction to hospital medicine:

Common respiratory admitsSlide2

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

Recognizing

respiratory distress and failure

When to consider ICU

When to consider

intubation

RSI basicsSlide3

Community acquired pneumonia

Not all CAP needs hospitalization. Need to use clinical judgment when deciding if admission is needed

Admit if:

Failed outpatient therapy

hemodynamically

unstable

Sepsis

Pneumonia severity index

Curb-65 score

Severe community acquired pneumonia score

SMART-COPSlide4

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

70

pts

and under= class II

71-90

pts

= class III

91-130

pts

= class IV

130+

pts

= class VSlide5

PSI step 1

Age over 50

Presence of any of the following comorbid conditions

Cancer

Heart failure

Stroke

Renal

dz

Liver

dz

Presence of any of the following physical exam

Ams

Pulse over 125

Resp

rate over 30

Sbp

under 90

feverSlide6
Slide7
Slide8

Psi strategy

The higher the class the greater the indication for admissionSlide9

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 5Slide10

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

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 pointsSlide11

SMARt-COP

Uses set of clinical criteria to predict who needs ICU care (score of 3+=increasing need for ICU)

Age

Albumin

Resp

rate

Arterial pH

PaO2 on room air

Sbp

Multilobar

infiltrates

Pulse

confusionSlide12

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

Leukocytosis

Sputum cx

Blood cx

Urine studies (cx and legionella antigen)Slide13

Community acquired pneumonia

Can be caused by variety of pathogens including viral

Most commonly but not limited to

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 reportsSlide14
Slide15
Slide16
Slide17
Slide18

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 studiesSlide19

Community acquired pneumonia

Prevention

Vaccination in patients 65+

Smoking cessationSlide20
Slide21

Health care associated pneumonia

HCAP= pneumonia in non-hospitalized patient who has extensive healthcare contact

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 intubationSlide22

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 daysSlide23

HCAP

Tips: consider the following (for any pneumonia)

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.Slide24

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 feedingSlide25

Aspiration pneumonia

Clinical signs of anaerobic bacterial infection

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)Slide26

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 bronchoscopySlide27

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.Slide28

copd

GOLD ClassificationSlide29

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 Slide30

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”Slide31

copd

Mild exacerbations can be managed at home by providing:

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 exacerbationsSlide32

copd

Moderate to severe exacerbations as well as any exacerbation with hemodynamic instability need hospital treatment.

Oxygen therapy

Beta-adrenergic agonists

Anticholinergic agents

Systemic glucocorticoids

Antibiotics and antiviral agents

Supportive care

Bipap

vs

mechanical ventilationSlide33

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.Slide34

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 hospitalSlide35

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 dischargeSlide36

copd

Systemic glucocorticoids

Shown to improve the following when added to bronchodilator therapies

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-

qidSlide37
Slide38

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 presentationSlide39
Slide40

copd

Supportive care during exacerbation

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 supportSlide41
Slide42
Slide43

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

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

ectSlide44
Slide45
Slide46

asthma

Rest of treatment is similar to COPD exacerbation

Oxygen therapy (with out the risk of respiratory depression)

Systemic steroids

Antibiotics, antivirals

Progressive vent support

Chest physiotherapy

Mucolytic

Supportive therapySlide47

Chf

See cardio lecture

Goal here is to provide oxygen/ventilator support until

chf

exacerbation is resolving

Take the opportunity to optimize therapy

ACE/ARB

B-Blocker

Diruetics

(especially

lasix

)

Digoxin

Acid

Salt restrictionSlide48

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 PESlide49

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

malignancySlide50

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 signSlide51

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 sobSlide52

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 itSlide53

DVT/PE

Manage

ment

Prophylaxis

Scd

Compression hose

Lovenox

30-40mg (1mg/kg)

subq

qday

Treatment

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 legSlide54

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.Slide55

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,

broncoscopySlide56

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

.Slide57

Hypoxemic respiratory failure

Hypoxemia is the

most immediate threat to life

, more immediately life threatening than

hypercapnea

Pathophysiologic causes of

hypoxemic respiratory failure

Shunting

V/Q mismatch

Diffusion limitation

Dead spaces

Low FiO2

Low atmospheric pressure

Hypoventilation of alveoliSlide58

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 mismatchSlide59

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 consolidationSlide60

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 alveoliSlide61

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 diffusingSlide62

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. Slide63

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

Brain

Spinal cord

Peripheral nerves

Neuromuscular junction

Muscles

Thorax

lungsSlide64

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.Slide65

Other resp failures

Trauma, obstruction

ectSlide66

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.Slide67

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 codeSlide68

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 supportSlide69

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 setSlide70

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

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 ventSlide71

references

Cecil’s medicine

Harrison’s textbook of medicine

Uptodate

Ardsnet

protocol