Respiratory - Noninfectious Pulmonary Parenchymal Disease Flashcards
(41 cards)
1
Q
What happens when Carbon monoxide (CO) is inhaled?
A
- Forms Carboxyhemoglobin
- CO has 200x greater affinity for hemoglobin
- Less O2 carried in blood
- Less O2 released at tissues (holds on tight)
- Mucus membranes can be red but oxygen is not as available to tissues
2
Q
What is Cyanide Toxicosis?
A
- Produced by combustible items as they burn
- Cyanide inhibits cytochrome oxidase
- inhibits aerobic metabolism
- CNS and heart depend on aerobic ATP production
- Almond odor
3
Q
What are the respiratory concerns with fire patients?
A
- Tissue Hypoxia:
- ⇣ inspired, carrying, and release of O2
- Cardio (arrhythmias), Neuro (sedate, seizures, coma)
- Thermal Damage
- Upper respiratory tract and larynx
- Dermal burns
- Pulmonary Irritation
- Toxins cause chemical or thermal-induced bronchoconstriction, inflammation, necrosis, pulmonary edema
- Signs range from ⇡RR to fatal respiratory dysfunction
4
Q
What can be seen on radiographs of fire patients?
A
- Can be normal in mild cases (20%)
- Can show bronchial disease from toxin irriation
- Can show pulmonary edema
- inflammation and oxidant injury damage alveoli and increase permeability
- blood flow increased and lymphatics impaired
- Can show alveolar pattern
- pneumonia can occur after smoke inhalation
5
Q
What are the treatments for Fire patients?
A
- Respiratory Tract:
- O2 supplementation to eliminate CO
- hyperbaric oxygen chamber can help
- Bronchodilators
- Nebulization and coupage
- Other potential therapies
- Antibiotics if documented pneumonia
- Steroids if obstructive airway edema/inflammation
- Tracheostomy f obstruction
- +/- mechanical ventilation
- Burns: wound care, antibiotics, IV fluids, analgesia
- Eyes: Topical antibiotics and atropine
- O2 supplementation to eliminate CO
6
Q
What does a Hyperbaric Oxygen Chamber do?
A
- Patient breathes 100% Oxygen intermittently inside a chamber with increased pressure
- More O2 dissolved in blood
- ⇡ availability to tissues (12-15x)
- Allows CO elimination too
7
Q
What is Pulmonary edema? causes?
A
- Pulmonary Edema = increased fluid in the extravascular pulmonary parenchyma
- Cardiogenic (congestive heart failure)
- increased hydrostatic pressure due to falling heart and fluid overload
- Non-cardiogenic
- increased permeability of vessels from damage to microvascular barrier, causes leaking fluid and protein into interstitium and alveoli
- Cardiogenic (congestive heart failure)
8
Q
What is the clinical presentation of Pulmonary edema?
A
- Dyspnea, cough
- may cough up pinkish foam
- Harsh and moist sounding lungs (crackles)
- listen closely for murmur
9
Q
How should a patient with pulmonary edema be radiographed?
A
- DV less stressful than VD
- Have oxygen available
10
Q
What are the differentials for Noncardiogenic Pulmonary Edema?
A
- Stepwise Diagnostics as needed O2 in between
- Radiographs confirm edema and help with cardiac/noncardiogenic
- Echo to confirm/ruleout cardiac disease if in question
- Hx ad PE help prioritize/ruleout many noncardiogenic differentials
- Oral ulcerations - think electrocution
- Signs of infection/sepsis - CBC, Chem, cultures, titers
- Non of the above? - is there systemic inflammation, neoplasia, neurologic disease
11
Q
What is the treatment for noncardiogenic pulmonary edema?
A
- Oxygen and low stress
- Treat underlying disease
- Furosemide:
- helps if cardiac edema (congestive heart failure)
- Ok to try 1 dose while sorting out reason for edema
- willl not help noncardiogenic edema cases
- may be harmful if patient is hypovolemic
- Ventilator for severe cases
12
Q
What is Acute Respiratory Distress Syndrome (ARDS)?
A
- Exaggerated inflammatory response in the lungs
- sequelae to acute lung injury, systemic inflammation or sepsis
- Cytokines infiltrate, chemotaxis of neutrophils and macrophages
- Permeability of pulmonary vessels keeps increasing
- Non-cardiogenic edema worsens
13
Q
What is Pulmonary Thromboembolism?
A
- Obstruction of a pulmonary vessel with a blood clot originating at some distant site
- Risk factors:
- Virchow’s Triad-
- vascular injury
- Impaired blood flow (stasis)
- hypercoagulability
- Virchow’s Triad-
14
Q
What conditions result in hypercoagulable patients?
A
- Protein losing nephropathy/enteropathy
- Immune mediated hemolytic anemia
- Neoplasia
- Necrotizing pancreatitis
- Cushing’s and steroid patients
- Diabetes mellitus
- Sepsis
- Trauma
- Cardiac Disease - not truly hypercoagulable, but ⇡ risk for emboli
- heartworm, endocarditis, cardiomyopahty
15
Q
What happens to pulmonary thromboembolisms?
A
- Normal coagulation - clot starts lysing within several hours
- Abnormal coagulation - existing clots can grow and more clots can form and travel
16
Q
What are the clinical signs of Pulmonary Thromboembolism?
A
- Vary from subclinical to acutely fatal
- Acute onset dyspnea, tachypnea
- Ventilation/perfusion mismatch
- Hypoxia
- Signs of underlying disease elsewhere
17
Q
How is pulmonary Thromboembolism diagnosed?
A
- Often suspected but hard to prove
- Chest Radiographs
- areas of hypovascular lung (VD/DV views)
- Pulmonary infiltrates (hemorrhage, atelectasis, infarct)
- Coagulation Testing
- PT/PTT/platelets - no correlation between these and thromboembolism
- Low antithrombin III concentration increases thrombotic risk
- Higher D-Dimer concentration is consistent with PRE
- D-dimer = plasmin-mediated break
- Try to confirm with:
- pulmonary angiography
- Nuclear scintigraphy
18
Q
What is the treatment for Pulmonary thromboembolism?
A
- Oxygen supplementation
- IV fluids to optimize perfusion
- Bronchodilator may help
- Theophylline ⇢ pulmonary vasodilation
- Prevent more Clots
- Heparin 100 U/kg SQ TID
- Aspirin 0.5-1.0mg/kg PO q24hrs
- Clopidogrel 0.5-1mg/kg PO q24hrs
- Treat underlying disease
19
Q
What are pulmonary contusions
A
- Compression injury w/hemorrhage
- injury to vessel walls causes non-cardiogenic edema and loss of lung compliance
- Can be progressive in first 24-48hrs
- may present with decent or good respiratory function
- Can deteriorate quickly
- if survive - resolve over 7-10days
- most common thoracic injury in dogs/cats
- Car accidents, falls, fights, abuse
20
Q
What are the clinical signs of pulmonary contusions
A
- Can be mild at first
- Then tachypnea, dyspnea, open-mouth breathing
- Crackles, cyanosis, hemoptysis, ⇡HR, arrhythmias
21
Q
How are pulmonary contusions diagnosed?
A
- Radiographs- patchy alveolar or interstitial pattern
- may take 48hrs to appear
- CT documents changes earlier
- may take 48hrs to appear
22
Q
What is the treatment for Pulmonary Contusions?
A
- Treat life-threatening injuries
- Oxygen supplementation
- Pain control
- Fluids to optimize perusion, but avoid fluid overload
- may have increased vascular permeability ⇢ non-cardiogenic pulmonary edema
- Monitor closely for 48hrs (may worsen quickly)
- Ventilator for severe cases
23
Q
What is the pathophysiology of Lung lobe torsions
A
- Lung torses and vein collapses but artery stays open
- severe congestion causes fluid to leak into interstitium
- lung consolidates, fluids leaks out, pleural effusion forms
- Why?
- Spontaneous, underlying respiratory disease, surgical trauma
- Anything that causes consolidation or atelectasis in cobco with extra fluid or air surrounding the lobe could increase risk of torsion
- Spontaneous, underlying respiratory disease, surgical trauma
24
Q
Which breeds have an increased risk of lung lobe torsions?
A
- Large deep-chested dogs
- Afgan hound 133x more likely than other breeds
- Pugs increased risk
25
What is the clinical presentation of patients with lung lobe torsion?
* Dyspnea
* coughing
* depression
* Dull lung sounds due to consolidation and effusion
26
How is Lung lobe torsion diagnosed?
* Thoracocentesis to improve breathing, fluid analysis
* Radiographs - consolidation with air bronchogram
* right middle or left cranial lobes (due to shape and looseness)
* Ultrasound w/ Doppler: torsed hilus obstructed with fluid and lack of venous flow
* Fluid Analysis (variable)
* Clear
* Serosanguinous/hemorrhagic
* Chylous
* Cytology:
* neutrophils and lymphocytes
* check for neoplasia and fungal disease
* Culture usually negative
27
What is the treatment for lung lobe torsion?
* Remove fluid prior to surgery
* Some dogs need chest tubes
* Oxygen and IV fluids as indicated
* Sx for lung lobectomy
28
What is the prognosis for patients with lung lobe torsion
* Most dogs do well if spontaneous or non-neoplastic
* Afgans ⇡ risk for persistent chylothorax post-op
29
What is the common signalment of Pulmonary Fibrosis patients?
* Middle to older age dogs and cats
* No sex predilection
* Breeds:
* West highland white terriers
* Staffordshire bull terriers
* Other terrier breeds
* Miniature poodles
* No specific cat breeds
30
What is the Etiology of Pulmonary Fibrosis?
* Primary Idiopathic
* Genetic predisposition
* Secondary
* infectious
* FIV, herpes, calicivirus, toxoplasmosis, histoplasmosis, COVID
* Toxin- paraquat is a classic offender
* Neoplasia
* Systemic lupus erythematosus
31
What is the pathophysiology of Pulmonary Fibrosis?
* Damage to alveolar epithelium and Type I pneumocytes
* Type II pneumocytes are more compact and less sensitive to injury - so they proliferate to fill in denuded areas
32
What is the history and PE associated with Pulmonary Fibrosis?
* Hx:
* usually slowly progressive respiratory signs
* BAR, good appetite
* Exercise intolerance, tachypnea, dyspnea, cough
* PE:
* Abnormal auscultation
* Crackles common, wheezes may be present
33
How is Pulmonary Fibrosis diagnosed?
* Radiographs
* pronounced patchy diffuse pattern
* Equal number of interstitial, alveolar, bronchial patterns; some mixed
* Investigate other differentials or triggers that may be treatable (infectious) or not so treatable (neoplasia, paraquat)
* Echo: may have pulmonary hypertension that we can treat
* CT: classic honeycomb appearance in people
* Lung aspirate:
* not very helpful, unless able to assess architectural changes or degree of fibrosis
* helps ID other diseases (cancer, fungal)
* Lung biopsy:
* Gold standard, but not always definitive
* Patchy distribution means you can miss it
* Dx is often presumptive based on breed and consistent signs and findings
34
What is the treatment for Pulmonary Fibrosis?
* Supplemental oxygen as needed
* Immunosuppressive therapy (steroids, azathioprine - dogs only)
* Anti-fibrotic therapy (steroids, +/- -colchicine)
* Anti-pulmonary hypertension (sildenafil)
35
What is Pulmonary Hypertension? Why does it occur?
* Increase in pulmonary arterial pressure
* sources:
* ⇡ left atrial pressure
* Pulmonary over-circulation
* ⇡ pulmonary vascular resistance
36
What leads to pulmonary hypertension?
* Severe respiratory disease
* Decreased oxygen exchange ⇢ Hypoxia
* Hypoxia ⇢ vascular constriction and hypertrophy of pulmonary arterial walls
* Underlying respiratory causes
* Fibrosis, pneumonia, chronic bronchitis
* Also seen with PTE, HW, shunts, mitral disease
37
What are the clinical signs of pulmonary hypertension
* Cough
* Dyspnea
* Cyanosis
* Collapse
38
What are the diagnostic tests for pulmonary hypertension
* Thoracic radiographs - assess lungs for primary respiratory disease
* Echocardiogram is most practical way
* measure increased pulmonary artery pressure
39
What is the treatment for Pulmonary Hypertension?
* Sildenafil to relax pulmonary vasculature
40
What primary lung tumors are found in dogs? signs? treatment?
* Single mass, often incidental finding
* Usually carcinomas, spread locally
* Clinically normal or cough, dyspnea, hemoptysis
* Often can be surgically removed
41
What primary lung tumors are found in cats? signs? treatment?
* Bronchogenic carcinomas, metastasize to digits
* Radiographs extremely variable
* Present with progressive dyspnea, increased effort
