NU 735 Pulmonary Flashcards
1
Q
**Ventilator Associated PNA
Overview **
A
Community Rate VAP
- Ventilated >/= 30 days, 70 % acquired
- VAP >/= 48 HRS after Intubation
**Mortaligy **
- 50 to 70%
- Underlying disease plays a role
2
Q
VAP : Etiology AKA
Bacteria
A
MDR & non-MDR bacterial pathogen
- **Non-MDR like CAP /gm negative : **
- Pseudomonas aeruginosa ,
- E.coli;
- klimseala pneumonia )
**MDR /gram positive
MRSA or Steph aurous
Atypical Bacteria: Lower incidence
Accept Legionella
3
Q
VAP
Three factors to Pathogenies of VAP
A
* Colonization of the oropharynx (from pathogenic organisms )
* Aspiration of these organisms (lower respiratory tract )
* Compromise of the normal host defense
*
4
Q
Ventilator Associated Pneumonia
Risk Factors
A
* Endotracheal tube : Prolonged intubation
**Bypass normal mechanical factors to prevent aspiration **
- Macro Aspiration: High air flow
- Micro aspiration can occur exacerbation by secretion above the cuff
**Oropharynx flora replaced by pathogenic microorganisms
Glycocalyx biofilm
Protect bacteria
Risk for inoculation
Immunoparalysis: Corresponds with VAP
**Antibiotic selection pressure: Poses Greater Risk **
* Cross infection
* Contaminated equipment
*** Malnutrition **
5
Q
Ventilator Associated Pneumonia
**Complications **
A
- **Prolonged Ventilation and ICU Stay **
*** Nectrotizinet Pneumonia **
- Pulmonary Hemoragged
- Bronchietasis
- Parenchymal Scarring
*Result i Catabolic State:
-Nurtitional Risk muscle waist Rehab
**Permanently Impact the Elderly: **
Unable to return to Independent Living
6
Q
PNA
Clinical Manifestations
A
***** Symtoms ca indolent or Fulinant
* Febrile, ST, Chills, Night Sweats, HA, Malgias, and or arthragias
- Caugh
- Nonproductive
- Productive mucoid, Purulent, or Blood tinged Sputum
Gross Hemotysis: CA-MRSA
Pleural Chest Pain: Pleural Involvement
GI: N/V/D
Dull to flat percussion
Crackles, bronchial breath sounds and pleural friction rub
Elderly Display AMS and few other manifestations
AMS may be 1st
7
Q
Hospital & Ventilator Acquired Pneumonia
Empiric Treatment Plan
A
** Importance of antibiogram ( consult pharmacy _ **
* Plan treatment based on risk factors
** Risk factors: **
* prolonged hospitalization,
* recent antibiotic use,
* intubation,
* immunocompromised,
* ARDS,
No MDR risk factors <10%
8
Q
VAP TX Empirical
No MDR Risk Factors
A
- **Treat with single agent **
- Zosyn 4.5 mg Q 6 hrs ,
- Cefepime 2gm Q 8 hrs or
- Levofloxacin
- Zosyn and Cefepime ( more common for TX b/c of gr negative coverage)
9
Q
VAP TX Empirical
MDR
A
**Antibiotic coverage: 3 different antibiotics
2 will be directed for Pseudomonas ariginosis and
1 MRSA ) **
- Cover for P. aeruginosa & MRSA
- P Aeruginosa: Zosyn, Cefepime or Merrem
-
Consider double coverage if severely ill
Aminoglycoside or Fluoroquinolone
+/- Zyvox or Vancomycin for MRSA**
10
Q
VaP
Specific Treatment Plan
A
- Narrow Down ABT
- Negative Tracheal Aspirate Culture or Growth
-Consider Stoping ABT
- look for Alternative Dx - D/C Combo Therapy for most Pseudomonas Pneumonia
11
Q
Lung Abcess
Overview
A
- Necrosis and Cavitation of Lung
-Caused By Microbial Infection
12
Q
Lung Abscess
Microbes
A
- Anaerobs Associated with** Aspiration **
- Ca-MRSA
- Pseudomonas Aruginosa: Worsen Prognosis in Community
- Strepntococcus Pneumonia
*
13
Q
Lung Abcess
**Risk Factors **
A
**Aspiratin is major risk factor contributed by **
* AMS
* ETOH
* Drug overdose
* Seizures
* Stroke
* Neuromuscular Disease
* Esophageal Dysmotility
14
Q
Lung Abcess
Decreased Incidence
A
Significan
Mortality and Morbidity
15
Q
Lungs Abcess
Characterization
A
- Primary VS Secondary
- Acute vs Chronic
16
Q
Lungs Abcess
Acute
A
Less <4 to 6 wks
17
Q
Lung Abcess
Chronic
A
40% cases
18
Q
Lung Abscess
Typically Single dominant
A
> 2cm (can be single or multiple )
19
Q
Lung Abcess
Primary
A
- **Anaerobic Bacteria **
- Produce extensive Tissue Necrosis
- **Absence of underlying pulmonary or sytemic Condition **
20
Q
Lung Abcess
Primary /clinical Manifestation
A
- Pneumonitis (Gastric acid )
- Parencymal necrosis and vaitatio develop 7 tp 14 days
- Posterior Upper
- Superior lower
- Right lung field (effective more b/c Rt bronchi less angulated )
- Putrid Abscess: Foul smelling breath, sputum or empyema
- Anaerobic Etiology
21
Q
Lung Abscess
Secondary
A
*** Underlying Condition **
- Post obstruction process (bronchial foreign body or tumor )
- Systemic process (HIV or other immune compromised conditions )
22
Q
Lung Abcess
Secondary /Organisms
A
- Pseudomonas aeruginosa & GNR (other gm – rods) most common
- Staphylococcus aureus (septic Emboli)
- Legionella spp.
- Pneumocystitis jirovecii
- Fungal (imuno compromised like bone marrow or organ transplant pt )
*
- Fungal (imuno compromised like bone marrow or organ transplant pt )
23
Q
Lung Abcess
DX
A
- CT chest: Air fluid levels with Development Abcess
- Putrid Sputum Odor: Virtually dx for Anaerobes
- **Sputum Culture and Gram’s Stain:
- Failure of treatment b/c does not show anerobic culture
Yield Polymicrobial
24
Q
Lungs abcess
Secondary Abscess specific
A
present and Faile of tx to Epirical Therapy
* Sputum and BC : Need for target therapy in addition to serologic study for opportunistc pathogenns
* Bronchoscopy with Bronhoaveolar Lavage
* CT guided percutaneous needle aspitration
25
Lung Abcess TX
Primary Lung Abcess
* **Clindamycin 600 mg IV TID **
* Duration TX
-Clinical Improvement
-No Fever
**Transition to Clindamycin 300 mg PO QID ****
26
Lung Abcess TX
Primary Lung Abcess
Alternative: Bat Lestin Combination
Unasyn
Transitio to Augmentin
Duration : 14 wks
3 to 4 wks or 14 wks duration
27
Secondary Lung Abscess
Specific Coveragr for pathogens
Abcess: > 6 to 8 cm diameter
Less likely to respond to aBX alone
Surgical resection
Percutaneous drainage
28
Pleural Effisin
Starts Here
29
Pleural Effusion
Overview
**What is Pleural Space ?
What is Pleural Effusion ?
**Pleural Space **
-Lies between **lung **and **chest wall
- Normally contains thin layer of fluid
**Fluid enters pleural space from capillaries **
- Removed from lymphatics in parietal pleura
**The pleural fluid formation exceeds pleural fluid absorption**
-Excess quantity of fluid in pleural space
**Pleural effusion occurs**
30
Pleural Effusion
Initiating Treatment Plan
**Suspect pleural effusion**
- Chest imaging to diagnose the extent
-Chest ultrasound,
-CT scan (no contrast ) or
-chest x-ray (Pick up sometimes 1st )
**Significant pleural effusion**
-**Thoracentesis**: Bedside or IR
-**Chest tube or
VATs**: (video assistant **thoracotomy ) : **
Late treatment or difficult cases
-** Pleural fluid analysis** : once pleural fluid obtained
31
Pleural Effusion
Etiology
Transudate
VS
Exudate
32
# TEST
** Trasudate **
Effusion develop when change in** systemic factorss such as increase in capillary Hydrostatic pressure or decrease collide pressure
* CHF (left Ventrical Failure )
* Cirrhosis
* Nephrotic Syndrome
* Peritoneal Dialysis
* SVC onstruction
* Myxedema
* Urinothorax (urine in pleural due to retropinnind leaking of urine occumulation
33
**Exudate **
**Result of pleaural inflammation, Infection, injury, or Lymphatic obstruction**
* Neoplastic diseases
* Infectious disease: TB, , pNA
* Inflammation :
* Pulmonary embilism or infarction
* Trauma
34
**Normal Pleural Fluid **
## Footnote
Pleural Effusio Fluid Analysis
- Appears Clear
- PH: 7.60 to 7.64
- Protein: <2% (1-2)
- WBC <1000
- Glucose : Similar to Plasma
- LDH: <50% plasma concetration
- Amylase: 30 to 110
- Triglycerides: <2
- Cholesterol : 3.5 to 6.5
35
Light's Criteria
## Footnote
Pleural Effusio Fluid Analysis
**Light’s Criteria
Exudate vs TRAnsudate
- Exudate = meet at least one -
1. Pleural fluid protein/serum **protein >0.5 **
2. * Pleural fluid LDH/serum **LDH >0.6 **
3. * Pleural fluid LDH >2/3 normal upper limit for serum
* **Serum protein/pleural fluid protein differnts **
Gradient >3.1 g/dL: Transudate
Exudated ruled out It will be Transudate
36
Trasudate
** **Serum protein/pleural fluid protein differnts **
Gradient >3.1 g/dL: Transudate
37
EXudate
Light Criteria 1 out 3
**Serum protein/pleural fluid protein differnts
Glucose < 60
Protein : <3.0
38
Pleural Effsuon
Diagnostic Approach
**Transudate:
- TP >3.1;
- due to disease like CHF, Cirrhosis,
- Treat underlying condition (CHF, Cirrhosis….. )
- -----------------------------------------------------------------------------
**Exudate
- Less 3.0;
-glucose <60
- Inflammation, Bacteria (TB), Immune (HIV )
Further diagnostic procedures needed
* Pleural fluid glucose, cytology, cell count, culture & stain, TB marker
-Glucose <60 mg/dL
* **Consider malignancy vs bacterial infections vs rheumatoid pleuritis**
* Work up coming back negative
-Consider PE work up ( CT contrast of + TX as PE result to fluid 2/2 escemia )
* Work up negative again
-Consider tuberculosis
* Work up still negative
-Consider thoracoscopy or pleural biopsy
* Absolute Findings
pH <7.2, Glucose <60 mg/dL, LDH >1000 U/L, bacteria cultured
-Complete drainage needed MUST
39
Absolute Findings
Must complete drainage : Bacteria
**PH: <7.2**
****Glucose: <60**
**LDH: >1000 **
Bacteria Culture
Must Complete drainage needed Must
40
Pleurla Effusion
Due to Heart Failure
* Most common cause of pleaural effusion: **Left Ventricular HF**
* Abnormal Presentation
** -Throacetesis needed**
Not Bilaterial and Comparable
Febrile
Pleuritic chest Pain
* Treat Underlying heart Failure
-Failure of therapy (Lasix not helping )
Thoracentesis
* Fluid Analysis :
*
**NT-proBNP >1500 (this case you DX Pleural effusion secondary CHF) **
41
Pleural Effusion
Due to Hepatic Hydrothorax
*** Cirrhois **
-5% develop effusion exudated ruled out it al be *
*TRansulate **
* Predominant Mechanism
- Direct Movement of peritoneal fluid into pleural space thru diaphragm
* **Right Sided Effusion (predomi) : large enougth to produce SOB**
42
****Pleural Effusion
**Due to Parapneumonic (should be consider with pt Bacteria PNA )
Overveiw
**Most common exudative pleural effusion USA
- Should consider Bacteria
- **Underlying Causes: **
-Bacterial pneumonia, lung abscess, or bronchiectasis
43
Parapneumonic
Clinical Presentation
**Aerobic Infectio**
- Acute Febrile Illness
- Chest Pain
- Sputum Production
- Leukocytois
44
Parapneumonic
Clinical Presentatio :
**Anaerobic Infection**
Subacute illness
Weight loss
Mild Anemia
Aspiration factor
45
Parapneumonic: Clinical Presentation
**Grossly Purulent Effusion**
Refer to Empyema (puss )
46
Pleural Effusio
Parapneumonic Treatment
**Management Considerations**
-** Free fluid serparting lung frm chest wall >10mm**
-Throracentesis needed
-Loculated Pleural fluid
-PH<7.20, Glucose<60 mg/dl, Gram's stain (+) or pus pleural space
Invasive approach needed ( Get Cardothoraci)
- Reoccurrence Effusion after initial thoracentesis then
-Thoracentesis (repeat thoracentesis should be done)
-Chest tube & instilling **fibronolytic agent (if pleaural fluid cannot be remvoed with Thoracentesis )
-Tissue Plaminogen Activator (tPA )10 mg
Deoxyribonuclease (DNASE)5mg
**Further Meausres : **
-Thoracoscopy with breakdown of adhesions (chest tube insertion )
-Decortication ( remove fibrous tissue )
47
Pleural Effusion
Due to **Malignansy (**Due to Metastatic Disease )
Overview
* **Second most common exudate effusion type (poor prognosis ) **
* Malignancy progress: Not going to be curable by chemotherapy
* Tumor Causes (3 Tumor 75% lead to Malignant effusions)
-Lung cA
-Breast CA
-Lymphoma
* Clinical Findings
-Dyspnea out of propotion (SOB)
-DX supported by cytology
if Cytologic exa are : **Negative Results **
-Consider throacoscopy like **west procedure **
-West Procedure: when malignancy suspected
-Cardithorsurgery on board
48
****Pleural Effusion
Due to **Malignancy **
Treatment
* **Confirming DX:**
*
-**Thoracoscopy **
* Pleurodisis (result in adhesion ....
-CT or US guided needle biopsy of pleural space or nodels
***Treatment **
- Symptomatic relief
- Thoracostomy tube
* **Sclerosis Agent **
- Docxycycline 50 0 mg (can cause inflammation )
- Just symptomatic recommendation Hospice
49
Pleural Effusio
Chylothorax > Etiology
-**Discrutpion of thoracid duct**
-**Chyle (mily fluid that contain fat drops in lymph)accumulatio in pleural space **
50
Pleural Effusio
Chylothorax
Most Common Cause
-Trauma
Thoracis surgery
**Madeastinal Tumors ** :
Lymphangiogram and dediastinal CT Scan
51
Pleural Effusion
Chylothorax
Clinical Findings
Need Thoracentesis
-Dyspnea
-Large Milky effusion
Trigceride >110
52
Pleural Effusion
Chylothorax
Treatment
Medical management
* Chest tube
Avodi prolog insertion
* **Octreotide 50 to 100 mcg SW TID **
* Ocreotide Function By
- Minimizes Lymphatic fluid Excretion
- Do not keep chest tube bor long time b/c excess drainage lead to malnutrition immunologic
* Nutriton: TPN VS Oral feeding
* Surgical Approach:
-Percutaneous transabdominal throracid duct blockage (will control chyle thoresc
-Ligation of throracid duct
53
TB: Overview
Bacteria: Mycobaterium Tuberculosis
Common amongs HIV
Main Cause of all HIV infeted Population and Main cause of death
Foreign born Population
Disadvantaged or Marginalized Population
54
TB : Primary
Limited to no Clinical Findings
Limited infection and spread of the disease
55
TB
Progressive -Primary
Inadequate immune response to contain the primary infection
1/3 of new cases of TB caused by person to person
56
TB Laten
Do not have Active disease
**Cannot transmit to other**
57
Active TB
****Can occur within 2 yrs following primary infection
Reactive to diseases
laten not adequately treatment
contagius
58
COPD
Start Here
59
COPD : Statistics
6th leading cause of death in US
10 mil dx USA
60
COPD
what is that
***** Persistent respitory Symptoms and **Airlow Limitation**
-Not fully reversible (problem happen no going back )
**Airlow limitation** is major physiologic changes in COPD that result in :
- Small airway disease > **Emphysema **
- Narrowed ariways : **Mucus and Fibrosis **
**- Hallmark of Advanced CoPD**: **Exensive Small airway destruction**
COPD: persistent RR symptoms > Airway Limitation .> Extensive Small Airway Detruction
61
COPD
Airway obstruction (chronic )
Determine?
Cause ?
Determined by Spirometry
Usually caused by Smoking
62
COPD Classification
**Ephysema
Chronic Bronchitis
Small airway disease
Gentic Consideration **
63
COPD : **Enphysema **
* Lung Alveoli destruction
* Airway Elargement
* smoking
*
64
Chronic Bronchitis
Chronic Cough and
Phlem
65
Small Airway Disease
Narrowed Smal Bronchioles
Reduced in Number
66
Genetic Considerations
Alpha 1 Atitrypsins Deviciensy
67
COPD : Emphysema
4 Charatetistics
* Chronic exposure t Cigarette smoke
* Compromised Airway Vasculature and Gas exchange
* Structural cell death
* Disordered repair and other component
68
Emphysema " Primary Mechanism
* Elastin degradation and disordered Repair
* Auto Immune : promotes progression
69
COPD
Small Airway Disease
**Major stie of Increase Resistance: **Small airway <2mm
**Characteristics: **
-Cellular Changes: Goblet cell Metaplasia
-smooth muschle Hypertrophy
-Luminal Narrowing: Firbrosis, excessive mucous, edema and cellular infiltration
-Hallmark of advanced COPD: Extensive small airway destruction
70
COPD
Chronic Bronchitis
**Characteritics **
-Mucus Gland Enlagement
-Goblet cell Hyperplasia
Leading t cough and mucouse production
**Bronchi undergo Squamous Metaplasia **
- Predisposed to carcinogenesis and mucociliary clearance
-
-** Smooth muschle herptrophy and brochial hyperactivity**
- Lead to air flow limitation
**Neutrophil influx**: Associated wiht purulent Sputum
71
COPD
Clinical Manifestations
Prologned Expiratory Phase
Expiratory Wheezes
Barrel chest
Accessory Muschle use
Tripod POstion: Faciliates accessory mushcle use
Cyanosis in the lips and nailbeds
Digital clubbin - CA
Hyperinflation of the chest Xray
72
COPD
Lab Test
* ABG
- Resting or Exertional Hypoxemia
-** pCO2 >45** ( norm 35 to 45)
- Presence /impending acute exacerbation
- Elevated Hcg and RVH: Chronic Hypoxia
73
COPD
Lung Studies
**CXR**: increase lung volumes and flatten diaphragm
**CT scan of chest**
Definitive to establish presence /absence of **ephysema **
Determine any coexisting diseases
74
COPD
TX Goal
* Systemic Relief
* Reduce Future risk
* Quit smoking most improtant
75
Articholinertic Muscartinit agent
SAMA (Atrovent )
LAMA (Spiriva)
76
Inhaled Beta Agonist
SABA (Albuterol )
LABA (Brovana )
77
Inhaled Corticosteroids
Pulmicort
78
Combo Therapy
Advair
Symbicort
or Trelegy
79
Severe COPD
Theophilline
and
Daliresp
80
Acute Exacerbation
COPD TX
**Dual SABA/SAMA (Duoneb)**
Brovana 15mcg Nebs Q 12 HRS and
Pulmicort 0.5 Neb Q 12
**Solumedrol: **
Transtiton to oral dosing 24 hrs prior to d/c
Avoid chronic use
Long Acting Muscarnic Anagonist (Seebri Neoinhaler )
Zyrtec and dingulair
81
Asthma
* Syndrome Aiflow Obstruction
* Occur any age
* Adult onset usually permanent
* Severty does not vary for patients
- Mild asthma rarely progresses to more severe disease
82
Asthmatics Inflammation Airway different from
NON Asthmatics
Narrowing with consequent reduced air flow
usualy reversible
chronic asthma with irreversible airway obsutrucion
83
Asthma
Risk Factors
**Major Risk Factor **
-Atopy major RF
Allertic Rhinitis
Atopic deramatitis
Genetic Predispostion
Environmental: Sulfur Dioxide, OZone, Diesel
Obesity: BMI >30
84
Asthma Clinical Findings
Eosinophil Infilaration
85
Asthma DX
Symptoms
**Confirmed :** PFT
**Spirometry**: **Confirme Air flow Limitation **
-Reduced FEF1 and FEV 1/FVC
-Reduce Peak Expiration flow (PEF)
86
Asthma Treatment
Maintenace
* **Maintenance **
-Bronchodialtors
-Anticholinergic
*** LAMA **
Inhaled Corticosteroids
Most effective controler
87
Asthma Exacerbatio
Duonebs
Solumedrol
Ihaler : Brovana and Pulmocort
singular and Zyrtec
O2 Ensure no mucus plug
88
Bronchiectasis
**IIrreversible airway dilation** : Focal Or Diffuse
**Classic Categorization: **
- Cylindrical, tubular, varicose, cystic
- Most common is tubular
**Focal Bronchiectasis**
Changes in localized area
* **Consequence of airway obstruction **: Extrinsic vs intrinsic
* **Diffuse Bronchiectasis: **
- Widespread bronchiectasis
- Underlying systemic or infectious disease
Etiology
Infectious or noninfectious
Nontuberculous mycobacteria (NTM) infection
Affects non-smoking women >50 years
Cystic fibrosis
Late adolescence or early adulthood
Mutation in cystic fibrosis conductance regulator (CFTR)
Leads to infections, inflammation, respiratory failure
89
Bronchietasis
Etiology
I**nfectious or noninfectious**
Nontuberculous mycobacteria (NTM) infection
- Affects non-smoking women >50 years
**Cystic fibrosis **
* Late adolescence or early adulthood
* Mutation in cystic fibrosis conductance regulator (CFTR)
**Leads to infections, inflammation, respiratory failure**
90
Bronchiectais
Causes and Risks
Poor Mucciliary clearance
Microbial colonization of bronchial treee
Damage larger Airway
**Upper LUngs **: post radiation
**Middle lungs ** Non TB Mycobacteria
**Lower Lung field ** chronic Espiration
91
Bronchiectais
Clinical Findigns
SOB, Productve Cough, Thick tenacious sputum
Crackels and Wheezing
Clubbin g
Detected PFT
