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

Hydrocortisone IV

– What clinical response you expect?

– What continuing clinical observations will you need to undertake?

Answer 1

CLINICAL RESPONSE:

I expect sudden worsening of the condition because the patients is already having respiratory acidosis, low magnesium level, lung hyper inflation and use of accessory muscles and tracheal tug and hypoxia.

I expect a need of mechanical ventillation.

Mechanical ventilation in supports gas-exchange and unloads ventilatory muscles until aggressive medical treatment improves the functional status of the patient. Close monitoring of the patient's condition is necessary to obviate complications and to identify the appropriate time for weaning.

Analysis of arterial blood gases is important in the management of patients with acute, severe asthma, but it is not predictive of outcome. In the early stages of acute, severe asthma, analysis of arterial blood gases usually reveals mild hypoxemia, hypocapnia and respiratory alkalosis

Respiratory acidosis is always present in hypercapnic patients who rapidly deteriorate and in severe, advanced-stage disease, metabolic (lactic) acidosis may coexist.

During an asthma attack, all indices of expiratory flow, including FEV1, FEV1/FVC (forced vital capacity), PEF, maximal expiratory flows at 75%, 50%, and 25% of vital capacity (MEF75, MEF50, and MEF25 respectively) and maximal expiratory flow between 25% and 75% of the FVC (MEF25–75) are reduced significantly. The abnormally high airway resistance observed (5–15 times normal) is directly related to the shortening of airway smooth muscle, edema, inflammation, and excessive luminal secretions, and leads to a dramatic increase in flow-related resistive work of breathing. Although the increased resistive work significantly contributes to patient functional status, however, the elastic work also increases significantly, and enhances respiratory muscle fatigue and ventilatory failure

In asthmatic crisis, remarkably high volumes of functional residual capacity (FRC), total lung capacity and residual volume can be observed, and tidal breathing occurs near predicted total lung capacity. Lung hyperinflation that develops as a result of acute airflow obstruction, however, can also be beneficial since it improves gas exchange. The increase in lung volume tends to increase airway caliber and consequently reduce the resistive work of breathing. This is accomplished, however, at the expense of increased mechanical load and elastic work of breathing.

CONTINUING CLINICAL OBSERVATIONS:

Close monitoring by serial measurements of lung function to quantify the severity of airflow obstruction and its response to treatment are of paramount importance. PEF or FEV1 <30–50% of predicted or personal best indicates severe attack.

Monitor spO2

ABG analysis hourly.

Close monitoring of Vital signs

Physical examination should be especially directed toward the detection of complications of asthma: pneumothorax; pneumomediastinum; subcutaneous emphysema; pneumopericardium; pulmonary interstitial emphysema; pneumoretroperitoneum; tracheoesophageal fistula (in the mechanically ventilated); cardiac arrhythmias, myocardial ischemia or infarction; mucous plugging, atelectasis; pneumonia; sinusitis; coexisting vocal cord dysfunction; theophylline toxicity; electrolyte disturbances (hypokalemia, hypophosphatemia, hypomagnesemia); lactic acidosis; and hyperglycemia.

Blood tests needed in patients excessive use of β2-agonists may decrease serum levels of potassium, magnesium, and phosphate.