Question

Case study

Poppy is a 9 year old female, weight 40Kg.

She presented to ED with worsening respiratory symptoms over the past few hours. Her parents state she is unable to

talk in full sentences or undertake a peak flow. In ED Poppy has been given 3 x 20 minutely nebulised Salbutamol with

6LPM of O2, IVF commenced, Stat dose of Prednisone administered, Chest X-ray shows hyperinflation of both lung

fields. She was admitted to ICU due to her deteriorating respiratory function with a diagnosis of acute exacerbation

of asthma.

EXCERPT OF RELEVANT ICU NOTES

Past History

Diagnosed with asthma age 2 (infrequent intermittent asthma).

7

Current medications: - Ventolin PRN.

IUTD (immunisations up to date)

Nursing Assessment

A. Clear, speaking in single words

B. RR 42bpm, SpO2 87% RA, 92% on 6LPM O2 + nebuliser, auscultation decreased AE bibasally, inspiratory and

expiratory wheeze

C. HR 160bpm, ST, peripherally warm

D. GCS 14/15 (E4, V4, M6)

E. Accessory muscle use, shoulder shrugging on inspiration, tracheal tug

F. IVF NaCl 53 ml/hr

G.

a. Mg- low 0.60mmol/L (0.70-1.10mmol/L) all other pathology is normal.

b. BGL 9.0mmol/L

c. Beta-agonist- Salbutamol

d. Anticholinergic - Atrovent

e. IV Hydrocortisone

f. ABG shows respiratory acidosis, (PH 7.32, PaCO2 49, PaO2 70, HCO3 27, BE -2.1, Lactate

1.4)

Plan

- Keep SpO2 92-95%%

- Beta- antagonist Salbutamol continuous via nebuliser

- Anticholinergic Ipratropium bromide (Atrovent) 500ug 4/24

- Hydrocortisone 100mg 6/24

- MgSO4 6.4mmol/20 minutes

- IVF 53ml/hr

- Repeat ABGs in 1hour

- Monitor BGL

- Peakflow /spirometry

Question:

Explain the pathogenesis causing the clinical manifestations with which Poppy presents.

Answer 1

The symptoms of poppy are

• Inability to talk in full sentences
• Respiratory distress
• Hyperinflation of the lungs
• On examination there is expiratory wheeze,accessory muscle use, shoulder shrugging on inspiration and tracheal tug.
• ABG values show respiratory acidosis.

The case is diagnosed as acute exacerbation of asthma or also can be termed as status asthmaticus. It can be defined as severe bronchospasm that does not respond to aggressive therapies within 30 to 60 minutes.

These symptoms and findings we see here are due to the Pathophysiology of asthma that include

• Airflow obstruction ( inability to talk and wheeze)
• Bronchial hyperresponsiveness due to histamine.
• Inflammation due to increase in immune cells.

To accommodate the respiratory distress, there is hyperinflation of the lungs, accessory muscle use and there is respiratory acidosis due to impaired breathing or hypoventilation.

Why it is actually happening?

Basically there are few components that play a major role in the exacerbation of asthma. They are IgE antibodies that bind to mast cells and form a IgE-mast cell complex (this basically senses the allergen in a sensitized individual and releases various substances), Eosinophils, Dendritic cells and T-helper cells. There are two types of T-helper cells T-helper cell type 1 and T-helper cell type 2. Type 1 is predominant in the lungs and any inflammation is carried out by CMI.However, in asthma there is increased amounts of type 2 cells which are not normally found in lungs, they bring about the inflammation in lungs by humoral immunity, that causes the antibody production here.

So what happens is, the individual first gets sensitized to a allergen. When the allergen is inside the body, it is engulfed by dendritic cells and also the dendritic cells are now activated. Now the columnar epithelial cells will recognize this situation here and will secrete what is called thymic stromal lymphocytes which condition activated dendritic cells to produce chemokines to specifically attract helper T cells type 2 . Also the activated dendritic cells will itself activate the T helper cells to differentiate into type 2 helper T cells and also will secrete chemokines to attract these T helper cells type 2 into the bronchioles.
Type 2 helper T cells produce interleukin-9 that promote mast cell activity and also produce interleukin-5 that causes eosinophil production and chemotactic movement of these eosinophils to lungs.
Helper T cells type 2 will promote humoral immunity and produce IgE via plasma cells. Now IgE and mast cells will form a complex. The individual is now sensitized.

After sensitization, the response to the allergen when it enters again is quite fast and causes all the symptoms of asthma.

The mast cell-IgE complex binds with the allergen. And causes the mast cell to release histamine, prostaglandins and leukotrienes. These are the substances that cause smooth muscle constriction in the airway, edema in the airways , inhibit mucociliary clearance. Hence all these causes an attack of asthma.

autogen Lumen allengen mucus GULEG U M columnar cells . occurs after Sensih'sa hon endritic THYMIC STROMAL LYMPHOCYTE IVATED DENDRTIC CEU eosinchi) going' to the larea I CHEMOATTRACTANT. IGE ANTIBODIES HELPER T CEUL TYPE-2 Histamine, leukotriener, Prostaglandins. HO EOSINO PHILS PROMOTE EOSINOPHIL PRODUCTION 22 ASTHMA MANIFESTATION