Management of Patients With Upper & Obstructive Respiratory Disorders

Question 1

Head & Neck Cancers

Answer 1

Squamous cell
Membrane lining respiratory tract
47,000 new cases per year
2% - 3% of all malignancies
Men: 2 – 5 x greater incidence

Risk factors
50 years or older
Prolonged use of tobacco & alcohol
Diet poor in fresh fruits & veggies
HPV infection: About 70% of oropharyngeal cancers are caused by HPV. In the United States, more than half of cancers diagnosed in the oropharynx are linked to HPV type 16

Question 2

Laryngeal Cancer

Answer 2

Glottic (True vocal cords)
Radiation provides 85% - 95% cure
Supraglottic (Above vocal cords)
Radiation
Partial Larygectomy
Subglottic (Below vocal cords)
Metastasis common
Total Laryngectomy

Question 3

Radiation Site Skin Care

Answer 3

Use prescribed lotions / creams
Do not use within 2-hours of treatment
Apply with “patting”, not rubbing motion

Avoid:
Temperature extremes
Rough / tight clothing
Rubbing / scratching treated area

Notify MD of moist skin reaction immediately

Question 4

Dry mouth (Xerostomia)

Answer 4

Pilocarpine hydrochloride (Salagen) to increase saliva production
Increase oral fluids
Always carry a water bottle!
Sugarless gum or candy
Baking soda or glycerin mouth washes
Artificial saliva

Question 5

Stomatitis

Answer 5

Soft, bland foods
Relieve pain
Frequent mouth rinses with water
Suck on ice chips
Rinse & spit: Antacid, Diphenhydramine (Benadryl) & topical Lidocaine
Avoid
Commercial mouthwash
Hot / spicy foods

Question 6

Radical (En bloc) Neck Dissection

Answer 6

All the tissue on the side of the neck from the jawbone to the collarbone is removed. The muscle, nerve, salivary gland, and major blood vessel in this area are all removed.

Removal of:
Lymph channels / nodes (Selective)
Sternocleidomastoid muscle
Spinal accessory nerve (Sternocleidomastoid & trapezius neck muscles)
Modified “spares”
Jugular vein
Sub-mandibular tissue

Question 7

Surgical Complications

Answer 7

Airway obstruction
Hemorrhage
Expect blood-tinged tracheal secretions for 24-48 hours
Observe for: ??
Carotid artery rupture
Fistula

Question 8

Post-Operative Care

Answer 8

Risk for / Potential:
Aspiration
Ineffective airway clearance
Impaired gas exchange
Impaired nutrition (Less than requirements)
Infection

Surgical site
Wound drain; Expect small to moderate sero-sanguinous drainage for 48 – 72 hours
Tube feeding
Communication

Question 9

Parts of Tracheostomy Tube

Answer 9

A variety of tubes are available to meet individual patient needs.

All tracheostomy tubes contain a faceplate or flange, which rests on the neck between the clavicles and outer cannula.

In addition, all tubes have an obturator, which is used when inserting the tube. During insertion of the tube, the obturator is placed inside the outer cannula with its rounded tip protruding from the end of the tube to ease insertion. After insertion, the obturator must be immediately removed so air can flow through the tube. Keep obturator at bedside in case of accidental decannulation.

Tracheostomy tubes have an outer cannula (which keeps the airway patent) and an inner cannula (which can be disposable or nondisposable and removed for cleaning).

Cuffed and uncuffed tracheostomy tubes are available. A tracheostomy tube with an inflated cuff (balloon) is most commonly used, particularly if the patient needs mechanical ventilation or is at risk of aspiration. Cuffless tubes are primarily used for the patient with a long-term tracheostomy, making eating and talking possible.

The outer and/or inner cannula may be fenestrated or nonfenestrated. A fenestrated tube has an opening (a hole) on the surface of the tube. A fenestrated tube will allow the patient to breathe spontaneously.

Question 10

“Fenestrated” Trach tube for speaking:

Answer 10

Cuff deflated
Inner cannula removed
Trach tube capped
Allows air to pass over vocal cords

Question 11

Tracheostomy Safety Precautions

Answer 11

Obturator & tube of equal/smaller size kept at bedside
Tapes/ties not changed for at least 24-hours
First tracheostomy tube change usually performed by MD after 7-days
Once per month
Healed tract well formed after several months
Patient can be taught to change tube using clean technique

Question 12

Tracheostomy Care

Answer 12

Suction to remove secretions
Inner cannula care
Cleanse around stoma
Change ties

Cuffed tube used for risk of aspiration or mechanical ventilation
Minimal occlusive volume (MOV) to create an airway seal
Should not exceed 20 mm Hg or 25 cm H2O

Question 13

Accidental Dislodgment

Answer 13

Priority is to immediately replace tube
Grasp retention (“Stay”) sutures & spread opening
Insert obturator in replacement tube

Another method:
Insert suction catheter to allow for air passage & guide re-insertion
Thread tracheostomy tube over catheter
Remove suction catheter

Cannot replace tube?
Assess level of respiratory distress
Minor dyspnea may be alleviated with Semi-Fowler’s position
Severe distress may progress to respiratory arrest
Cover stoma with sterile dressing
Ventilate with bag-mask over nose & mouth until help arrives

Question 14

Decannulation

Answer 14

When patient can exchange air & manage secretions
Stoma closed with gauze & covered with occlusive dressing (tape)
Tissue forms in 24 to 48 hours
Opening will close in several days
Instruct patient to splint stoma with fingers when coughing, swallowing, or speaking

Question 15

Asthma

Answer 15

Pathophysiology
Reactive airway disease
Reversible in early stages
Characterized by broncho-spasm
Chronic inflammatory lung disease causes varying degrees of pathology - obstruction

Triggers
Drugs & Food Additives
Aspirin, NSAIDs, ACE inhibitors
Gastroesophageal Reflux Disease (GERD)
Psychological / Emotional Stress

Question 16

Asthma: Early-Phase

Answer 16

Inflammatory mediators cause early-phase response
Vascular congestion
Edema formation
Production of thick, tenacious mucus
Bronchial muscle spasm
Thickening of airway walls

Question 17

Asthma: Late-Phase

Answer 17

Late-phase response
Occurs within 4 to 6 hours after initial attack
Occurs in about 50% of patients
Can be more severe than early phase and can last for 24 hours or longer

Late-phase response
If airway inflammation is not treated or does not resolve, it may lead to irreversible lung damage
Structural changes in the bronchial wall known as remodeling

Corticosteroids are effective in treating this inflammation.

Question 18

Clinical Manifestations asthma

Answer 18

Most common manifestations
Cough
Shortness of breath (dyspnea)
Wheezing
Wheezing is an unreliable sign to gauge severity
Severe attacks can have no audible wheezing due to reduction in airflow
“Silent chest”: ominous sign of impending respiratory failure
Severely diminished breath sounds
Chest tightness
Variable airflow obstruction

Unpredictable and variable
Recurrent episodes of wheezing, breathlessness, cough, and tight chest
May be abrupt or gradual
Lasts minutes to hours

Question 19

Asthma: Health Promotion

Answer 19

Identify & avoid known triggers
Use dust covers
Use of scarves or masks for cold air
Avoid aspirin or NSAIDs
Desensitization can decrease sensitivity to allergens
Prompt diagnosis & treatment of upper respiratory infections and sinusitis may prevent exacerbation
Fluid intake of 2L to 3L daily
Adequate nutrition
Adequate sleep
Take -adrenergic agonist 10 to 20 minutes prior to exercising

Question 20

Acute Signs of Hypoxemia

Answer 20

Restlessness
Increased anxiety
Inappropriate behavior
Increased pulse & B/P
Pulsus paradoxus
Drop in systolic BP > 10 mm Hg during inspiration

Question 21

Asthma: Diagnostic Studies

Answer 21

Detailed history & physical
Pulmonary function tests
Peak expiratory flow rate (PEFR)
Chest x-ray
ABGs
Pulse oximetry
Allergy testing
Eosinophil levels
Sputum culture & sensitivity

Question 22

ABG’s

Answer 22

pH 7.35 - 7.45
Pco2 35 – 45 mm Hg
HCO 3 21 – 28 mEq/L
P02 80 – 100 mm Hg
O2 Sat 95% - 100%
O2 Content 15 – 22 vol%
Base Excess 0 +/ 2 mEq/L
Alveolar to Arterial 02 Difference < 10 mm Hg

Question 23

Asthma: Nursing Diagnoses

Answer 23

Ineffective airway clearance
Ineffective therapeutic regimen management
Anxiety
Goal: Decrease patient’s sense of panic
Stay with patient
Encourage slow, pursed lip breathing
Prolongs expiration
Position comfortably

Question 24

Treatment of Acute Asthma

Answer 24

Start O2 & monitor pulse oximetry or ABG’s
Short-acting -adrenergic agonists(SABA’s) by metered dose (Spacer or nebulizer)
Corticosteroids
May be added with insufficient initial response to SABA alone
Continue until patient:
Breathes comfortably
Wheezing has disappeared & signs of good air exchange are present
PFT’s are near baseline values

Question 25

Asthma: Acute Intervention

Answer 25

Monitor respiratory & cardiovascular systems Lung sounds Respiratory rate Pulse BP ABGs Pulse oximetry FEV(forced expiratory volume) and PEFR (peak expiratory flow rate) Work of breathing Administer O2 Bronchodilators Chest physiotherapy Medications (as ordered) Ongoing patient monitoring Response to therapy

Question 26

Status Asthmaticus

Answer 26

Severe attack that does not respond to treatment Life-threatening, risk for respiratory failure Causes: Clinical Manifestations Increased airway resistance (Edema) Mucous plugging Bronchospasm - Air trapping & Hyperinflation Potential complications:??

Question 27

Status Asthmaticus: Treatment

Answer 27

Supplemental O2 Mask or nasal cannula to achieve 90% Increase frequency & dose of bronchodilators Continuous -adrenergic agonist nebulizer therapy Drug delivery at home may have been sub-maximal Higher doses under supervision may be beneficial IV Aminophylline may be added if no response to -adrenergic agonists IV corticosteroids every 4-6 hours Continuous monitoring IV magnesium sulfate (Bronchodilator) IV fluids for insensible fluid loss Bronchoscopy (rare, to remove thick mucous plugs) Move to higher level of care: Arterial catheter; frequent ABG monitoring Mechanical ventilation if no response to treatment Sodium bicarbonate; treat metabolic acidosis

Question 28

Asthma: Other Complications

Answer 28

Rib fractures Pneumothorax Pneumo-mediastinum Atelectasis Pneumonia

Question 29

Patient Teaching: Inhalers

Answer 29

Difficulty using MDI? Spacer or nebulizer Clean by removing dust cap & rinsing with warm water DPI (dry powder inhaler) requires less manual dexterity & coordination Must be kept in dry place Rinse mouth after steroid doses – reduces risk of oropharyngeal candidiasis, hoarseness and dry cough May still be easier if after -adrenergic agonists

Question 30

COPD Description

Answer 30

Airflow limitation not fully reversible Usually progressive Abnormal inflammatory response of lungs, primarily caused by cigarette smoking and other noxious particles or gases Emphysema and chronic bronchitis are similar lung conditions under the umbrella of COPD

Question 31

COPDSignificance

Answer 31

Third leading cause of death in United States Kills more than 133,000 Americans each year

Question 32

COPDEtiology

Answer 32

Risk factors Cigarette smoking Occupational chemicals and dust Air pollution Severe recurring respiratory infections α1-antitrypsin deficiency α1-antitrypsin deficiency (an autosomal recessive disorder) is a risk factor for developing COPD. Some degree of emphysema has been thought to occur as a person ages. It is caused by changes in the lung structure and the respiratory muscles, even in a nonsmoker.

Question 33

A1-Antitrypsin Deficiency

Answer 33

Genetic risk factor Autosomal recessive (Lung/liver) Inhibits breakdown of lung Proteolytic enzymes Neutrophils & macrophages Smoking greatly exacerbates disease process Onset by 40 years Minimal tobacco Family Hx Chronic liver disease (infant/adult) Northern European

Question 34

COPDCigarette Smoking

Answer 34

Clinically significant airway obstruction develops in 15% of smokers COPD should be considered in any person who is over 40 with a smoking history of 10 or more pack-years Effects of nicotine Stimulates sympathetic nervous system

Question 35

COPDOccupational & Environmental

Answer 35

COPD can develop with intense or prolonged exposure to Dusts, vapors, irritants, or fumes High levels of air pollution Fumes from indoor heating or cooking with fossil fuels

Question 36

COPDPathophysiology

Answer 36

Common characteristics Mucus hypersecretion Dysfunction of cilia Hyperinflation of lungs Gas exchange abnormalities

Question 37

COPD Manifestations

Answer 37

Progressive Dyspnea on exertion to Dyspnea at rest Enlarged A-P diameter of chest Percussive hyper-resonance CXR: Over-inflation & flat diaphragm Compensated respiratory acidosis (Late) Cardiac enlargement & Right ventricular lift ECG: Right heart strain pattern and axis deviation Cyanosis, neck vein distention & pitting edema

Question 38

Management of COPD

Answer 38

Prevent respiratory infection Improve ventilation Bronchodilators -adrenergic agonists Methylxanthines (Theophylline) Anti-cholinergics (Ipratroprium) Glucocorticoids Long-term oxygen Remove / control secretions Reduce complications DVT prophylaxis Influenza vaccine Pneumonia vaccine Promote exercise Improve general health / nutrition

Question 39

Other Therapies for COPD

Answer 39

Surgery Lung volume reduction Bullectomy Lesions > 1 cm Lung transplantation Pursed-lip breathing Airway clearance Effective (Huff) coughing Chest PT Postural drainage Airway clearance devices Acapella High-frequency chest wall oscillation

Question 40

COPD Complications

Answer 40

Right-sided heart failure (Cor Pulmonale) Exacerbations Acute respiratory failure Depression Anxiety

Question 41

Chronic Bronchitis

Answer 41

Destruction of cilia in airways of lungs. Airways then become inflamed and narrower, making breathing difficult Inflammation Increased mucous production Chronic cough Scarring At least 3-months for two consecutive years Abnormal V/Q ratio Fall in PaO2 Impaired ventilation may increase PaCO2 Polycythemia Compensation for hypoxemia

Question 42

Emphysema

Answer 42

Obstruction results from destruction of alveolar walls which leads to permanent over-distention of air spaces Destruction of pulmonary capillaries further decreases oxygen V/Q (ventilation-perfusion) Centriacinar (Smokers) Panacinar (alpha-1 antitrypsin deficiency) Paraseptal (Spontaneous pneumothorax) Centriacinar begins in the respiratory bronchioles and spreads peripherally mainly in the upper half of the lungs. Panacinar predominates in the lower half of the lungs and destroys the alveolar tissue. Paraseptal emphysema preferentially localizes around the septae of the lungs or pleura, often associated with inflammatory processes, like prior lung infections.