STATUS ASTHMATICUS

Introduction

Bronchial asthma could be defined as a chronic inflammatory disease of the bronchial airways resulting in its hyper-responsiveness which resolves spontaneously or in response to treatment .

It manifest clinically with difficulty in breathing associated with wheezing, cough and chest tightness.

While status asthmaticus is a severe asthma attack that fails to response to conventional therapy after 24hours.

The terminology status asthmaticus is outdated and has been replaced by the term Acute Severe Asthmatic Attack (ASAA). It is a life threatening episode of airway obstruction and is considered a medical emergency.

ETIOLOGY

The precipitating factors in ASAA are usually upper respiratory infections, allergen exposure, or a reduction in anti-inflammatory medications. Other relating factors include- overreliance on bronchodilators, environmental pollutant, failure to identify worsening airflow obstruction and non-compliance with health care regimen.

PATHOPHYSIOLOGY

An asthma attack is initiated when exposure to an irritant or trigger occurs, resulting in the initiation of the inflammatory immune response in the airways. Bronchospasm occurs along with increased vascular permeability and increased mucus production. Mucosal edema and thick tenacious mucus production further increases vascular permeability and increased airway responsiveness.

The combination of bronchospasm, airway inflammation and increased airway responsiveness result in narrowing of airway and obstruction. Causing significant effect explained below.

Pulmonary Effects- As the diameter of airway decreases, airway resistance increases resulting in increased residual volume, hyperinflation of the lungs, increased work of breathing and abnormal distribution of ventilation.

Ventilation mismatch occurs which results in hypoxaemia.

Alveolar dead space increases with hypoxic vasoconstriction resulting in hypercapnia.

CARDIOVASCULAR EFFECT: Inspiratory muscle force increases in an attempt to ventilate the hyper-inflated lungs, resulting in a significant increase in negative intra-pleural pressure. This leads to an increase in venous return and pooling of blood in the right ventricle. The stretched right ventricle causes the intraventricular septum to shift, thereby impinging on the left ventricle. The left ventricle has to work harder to pump blood from the high negative pressure in the thorax to elevate pressure in the systemic circulation. This leads to decrease in CO and a fall in systolic blood pressure on inspiration (pulsus paradoxus).

MANIFESTATION

➡️ Cough

➡️ Inability to make a complete sentence

➡️ Wheezing

➡️ Cyanosis

➡️ Dyspnea

➡️ Tachycardia

➡️ Tachypnea

➡️ Diaphoresis

➡️ Shortness of breath

➡️ Low peak expiratory flow

➡️ Increase use of accessory muscle

➡️ Pulsus paradoxus

➡️ Silent Chest

➡️ Decrease level of consciousness

➡️ Inability to lie supine

INVESTIGATIONS

➡️ Full blood count

➡️ Lung function test

➡️ Blood gases analysis

➡️ Skin sensitivity test

➡️ Electrolyte and urea

➡️ Chest x-ray

➡️ ECG showing deviation at the right side of the heart.

ASSESSMENT/DIAGNOSES

ABGS- initially will indicate hypocapnia and respiratory alkalosis caused by hyperventilation.

As the attack continues  and patient starts to fatigue, hypoxemia and hypercapnia develops.

Lactic acid may result from lactate overproduction by the respiratory muscle. deterioration of pulmonary functions test despite aggressive bronchodilator therapy is diagnostic of ASAA.

MEDICAL MANAGEMENT

1st line mgt is to correct dehydration, provide calories and nutrition and provide an IV line for drugs administration

Bronchodilator – inhaled B2 agonist and anticholinergics are the bronchodilators of choice for ASAA. 500mg of Aminophiline is given slowly.

Parenteral anti-inflammatory drugs e.g. Hydrocortisone; are also given; 500mg of  hydrocortisone is given stat and there after 200-400mg 4hrly depending on severity of the attack.

Anticholinergic are used in combination with B2 agonist

According to wikipedia magnesium sulphate can be used as a bronchodilator after beta agonists and anticholinergic agents has failed in severe excerbation of asthma. Studies conducted have revealed that magnesium sulphate can be nebulized to reduce sypmtoms.

In Rx of status asthmaticus, systemic corticosteroids have antinflammatory effects that limits mucosal edema, decrease mucus production and potentiate b2 agonist.

O2 is commenced to correct cyanosis based on ABGS result. In the absence of ABGS analysis, give 60% o2 by face mask to maintain SaO2 greater than 92%.

Give broad spectrum antibiotics

Mucolytic is given, this helps in the lysing of the mucus plug and thus relieving obstruction.

Indication for mechanical ventilation include cardiac and respiratory arrest, disorientation, failure to respond to bronchodilator and exhaustion.

A large ETT is used to decrease airway resistance and  to facilitate suctioning of secretion. High inflation should be avoided b/cos of potential volutrauma. Sedation and neuromuscular paralysis may be necessary.

If secretion is very thick it may be necessary to do a bronchoalveolar lavage in order to wash all the mucus plug.

 

GENERAL NURSING MANAGEMENT

➡️ Positioning and loose tight clothing

➡️ Administer O2

➡️ Suction PRN

➡️ Monitor V/S

➡️ Monitor ABGS

➡️ Do pulseoxymetry.

➡️Give prescribed drugs

➡️Psychotherapy

➡️ Provide pt education

➡️ Provide comfort and emotional support.

NURSING DIAGNOSIS

➡️ Ineffective breathing pattern related to exposure to irritants (predisposing factors) evidenced by prolonged expiration, tachypnea, respiratory depth change.

➡️ Ineffective airway clearance related to bronchospasm, ineffective cough evidenced by adventitious lung sound, chest tightness.

➡️ Anxiety related respiratory distress and change in health status evidenced by restlessness.

Others include: fatigue, deficient knowledge, activity intolerance.

 

COMPLICATIONS 

➡️ Respiratory arrest

➡️ Cardiac arrest

➡️ Loss of consciousness

➡️ Respiratory alkalosis

➡️ Metabolic acidosis

➡️ Lung atelectasis