Anthonisen severity scale for ABECB

Anthonisen severity scale for ABECB

ABECB = acute bacterial exacerbations of chronic bronchitis

-dyspnea
-increased sputum volume
-increased sputum purulence.

type I (severe) 3 ข้อ
type II (moderate) 2 ข้อ
type III (mild) 1 ข้อ + one of the following
-an upper respiratory tract infection in the past 5 days
-fever without any other apparent cause
-increased cough or wheezing
-20% increase in the respiratory rate or heart rate above baseline

Acute exacerbation COPD

Thai guideline 2553

Mild
-OPD
-increase frequency bronchodilartor
-oral prednisolone (พิจารณาเป็นรายๆไป) 20-30 mg/day (5-7 day)
-ATB only when suspected infection

Severe
-Accessory muscle
-HR >120
-Hemodynamic not stable
-PEFR < 100
-O2 sat < 100 PaO2 45 or pH < 7.35
-drowsiness alteration of concious
-Rt Heart failure

Admit criteria
-above
-severity stage 4
-Heart failure
-not response to treatment
-ขาดคนดูแล

Treatment
-O2 keep sat 90%
-Bronchodilator beta2 or anticholinergic MDI spacer 4-6 puff or nebulizer
q 20 min till improve or have side effect
-corticosteroid dexa 5-10 q 6 or pred 30-60/day or hydro 100-200 (total 7-14 day)
-ATB ("to all")
-Theophylline IV if intractible case
-NIPPV (not response to above,PCO2 45-60, pH 7.25-35)

contraindicate NIPPV
-apnea
-BP drop
-Arrythmia
-conscious not full
-abn face structure
-just face surgery , GI
-too much sputum
-GI bleed

Invasive MV
-contraindicate NIPPV
-not improve with NIPPV
-Acute resp acido pH<7.25
-severe hypoxemia

AIRWAY DISEASE IN RHEUMATOID

AIRWAY DISEASE IN RHEUMATOID

1. UPPER AIRWAY
-cricoarythenoiditis
-ankylosing of cricoarrythenoid
-vasculitis of recurrent laryngeal nerve
-rheumatoid nodule on vocal cord

2.LOWER AIRWAY
–airway obstruction (RA+Smk : 60 %),(RA non smk 0-24%)
–association with sjogren peribronchial lymphocytic inflammation
–Bronchiolitis obliteran both from disease and drug
–centrilobular emphysema
–Bronchiectasis

Resistance of the airways

Resistance of the airways describes the obstruction to airflow provided by the conducting airways, resulting largely from the larger airways (down to division 6-7), plus a contribution from tissue resistance resulting produced by friction as tissues of the lung slide over each other during respiration

Airway diameter depends on the level of the airway in the tracheobronchial tree, airway smooth muscle tone, traction on the air- way from surrounding lung tissue, and internal and external pressures on the airway.

ABPA diagnostic criteria and staging

Skin prick testing (SPT) for Aspergillus fumigatus (AF) as a screening tool

Early diagnosis is responsive to steroids.

CT allows precision in the diagnosis of central bronchiectasis (which is virtually pathognomonic of ABPA) and may enable earlier diagnosis.

But in CF is different
-Thymus- and activation-regulated chemokine (TARC)
-serum total immunoglobulin (Ig)E
-specific Aspergillus fumigatus IgE and IgG
-specific IgE against recombinant A. fumigatus allergens (rAsp f) 1, 3, 4 and 6

Diagnostic accuracy was greater for TARC (93%) than for total IgE (74%), or rAsp f 4 (75%) or f 6 (79%)

Cystic Fibrosis Foundation has proposed a new set of criteria for ABPA diagnosis in cystic fibrosis patients (53):
• clinical deterioration (coughing, wheezing, increased sputum production, exercise intolerance and decrease in pulmonary function);
• immediate hypersensitivity to A. fumigatus (positive skin test or IgE response);
• total serum IgE concentration >1000 kUI/l;
• precipitating antibodies to A. fumigatus;
• abnormal chest roentgenogram (infiltrate, mucus
plugs or unexplained changes compared to previous chest X-ray).

Staging of ABPA

Churg-strauss

จำไว้ Eo 2 + asthma + neuropathy + (upper + lower –> คล้าย wegner)

สูตรจำ ” P E V ” or ” A E V ”

Bleb Bullae Cyst

BLEB

1 cm
-Pathology.—An airspace measuring more than 1 cm usually several centimeters in diameter, sharply demarcated by a thin wall that is no greater than 1 mm in thickness. A bulla is usually accompanied by emphysematous changes in the adjacent lung.
-Bullae may contain nothing but gas or may contain overdistended and ruptured alveolar septa and blood vessels
Radiographs and CT scans.—A bulla appears as a rounded focal lucency or area of decreased attenuation, 1 cm or more in diameter, bounded by a thin wall.Multiple bullae are often present and are associated with other signs of pulmonary emphysema

CYST

-Pathology.—A cyst is any round circumscribed space that is surrounded by an epithelial or fibrous wall of variable thickness (51).
-Radiographs and CT scans.—A cyst appears as a round parenchymal lu- cency or low-attenuating area with a well-defined interface with normal lung. Cysts have variable wall thickness but are usually thinwall (<2 mm) and occur without associated pulmonary emphysema (Fig 21). Cysts in the lung usually contain air but occasionally contain fluid or solid material. The term is often used to describe enlarged thin walled airspaces in patients with lymphangioleiomyomatosis (52) or Langer- hans cell histiocytosis (53); thicker walled honeycomb cysts are seen in patients with end-stage fibrosis

EMPHYSEMA

-Pathology.—Emphysema is characterized by permanently enlarged airspaces distal to the terminal bronchiole with destruction of alveolar walls (42,43). Absence of “obvious fibrosis” was his- torically regarded as an additional crite- rion (42), but the validity of that criterion has been questioned because some interstitial fibrosis may be present in emphysema secondary to cigarette smoking (56,57). Emphysema is usually classified in terms of the part of the acinus predominantly affected: proximal (centriacinar, more commonly termed centrilobular, emphysema), distal (paraseptal emphysema), or whole acinus (panacinar or, less commonly, panlobular emphysema).
-CT scans.—The CT appearance of emphysema consists of focal areas or regions of low attenuation, usually without visible walls (58).presenting bronchovasular bundle in central area. In the case of panacinar emphysema, decreased attenuation is more diffuse

Bronchiectasis three layers phlegm

Bronchiectasis three layers phlegm

1.the upper for bubble-like, frothy, faomy (partly from saliva)
2.middle-level for thin sero-mucus liquid
3.the underlying base = pus ,necrotic tissue , cell debris

Co2 Narcosis in COPD

Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by central chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr. The hypoxic drive is so weak that unconsciousness will develop before respiratory distress is noted and is therefore a risk for high altitude flying pilots. For this reason, supplemental oxygen is required by Federal Aviation Regulations[1] for pilots flying above about 12,500 feet altitude in unpressurized airplanes.

In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respiration.

Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as “CO2 Retainers”) are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself.

The respiratory drive is normally largely initiated by PaCO2 but in chronic obstructive pulmonary disease (COPD) hypoxia can be a strong driving force and so if the hypoxia is corrected then the respiratory drive will be reduced. There will also be a loss of physiological hypoxic vasoconstriction which is partly protecting the patient from the effects of areas of gross alveolar hypoventilation

Lung transplant in COPD

Guidelines for timing a referral for a transplant evaluation for patients with COPD and emphysema due to alpha-1 antitrypsin deficiency include [90]:

BODE index >5
Post-bronchodilator FEV1 <25 percent of predicted
Resting hypoxemia, defined as PaO2 <55 to 60 mmHg
Hypercapnia
Secondary pulmonary hypertension
Accelerated decline in FEV1