Patients particulars

Name:

A. M.

Age:

50years

Sex:

Male

Op No:

3228710-53

Diagnosis: Asthmatic attack

Chief Complain
The relatives gave a history of patient inability to talk since that morning, deep breathing,
and inability to feed, inability to talk. He had not received any insulin which he was
supposed to receive once daily, since he complained of feeling sick after injecting himself
and taking anti malaria drugs he was receiving for three days.
History of presenting illness
breathing fast and deeply. The history from the relatives indicated that the patient has
been unable to feed and feeling unwell for about four days. She had not injected himself
for three days since he said he had been taking some anti malarias he had received from a
Dispensary which was making feel worse when taken when he was still receiving the
insulin. The mother tried to wake him up that morning but she was unable to wake up or
even talk and she was
Past health history
A. M. has been admitted a year before when he was newly diagnosed with chronic
Asthma , in March 2012, and has been on ventolin tablets and inhaler since then. He was
being followed up at K District Hospital medical outpatient clinic. He has no other
history of any other major medical illness
Family social history
The patient is a married man with two children; 23 20 and 17years respectively who are
all in good health. He is a businessman and the wife a housewife who also takes care of
their shamba.
Physical assessment
On general appearance, the patient appeared quite sick, could not respond to calls. On
system review;
respiratory system: Had kussmal kind of breathing

Cardiovascular system: there was tachycardia,

Central nervous system: the patient was agitated
The rest of the systems were normal.
Vital signs: temperature 39.50c, pulse 100 beats per minutes, respiration 16 per minutes,
blood pressure 90/60mmHg.
Medical Management
The patient was started on intravenous normal saline. Two Intravenous lines were started
and the fluid left to run freely. She was also given insulin soluble 10 IU intravenously and
10 IU intramuscularly. Blood sugar was being monitored hourly. Patient was
Nursing management
Patient was positioned in
The prescribed drugs were administered

LITERATURE REVIEW
STATUS ASTHMATICUS
Status asthmaticus is an acute exacerbation of asthma that remains unresponsive to
initial treatment with bronchodilators. Status asthmaticus can vary from a mild form to a
severe form with bronchospasm, airway inflammation, and mucus plugging that can
cause difficulty breathing; carbon dioxide retention; hypoxemia; and respiratory failure.
Risk factors
Asthma results from a number of factors, including genetic predisposition and
environmental factors.
Risk factors for asthma also include the following:

Viral infections

Air pollutants - Eg, dust, cigarette smoke, and industrial pollutants

Medications - Including beta-blockers, aspirin, and nonsteroidal antiinflammatory drugs (NSAIDs)

Cold temperature

Exercise

Etiology
Exposure to an allergen or trigger causes a characteristic form of airway inflammation in
susceptible individuals, exemplified by mast cell degranulation, release of inflammatory
mediators, infiltration by eosinophils, and activated T lymphocytes. Multiple
inflammatory mediators may be involved, including interleukin (IL)3, IL-4, IL-5, IL-6,
IL-8, IL-10, and IL-13; leukotrienes; and granulocyte-macrophage colony-stimulating
factors (GM-CSFs). These, in turn, incite involvement of mast cells, neutrophils, and
eosinophils. See the diagram below

The figure depicts antigen presentation by the dendritic cell, with the lymphocyte and
cytokine response leading to airway inflammation and asthma symptoms.
Physiologically, acute asthma has 2 components: an early, acute bronchospastic aspect
marked by smooth muscle bronchoconstriction and a later inflammatory component
resulting in airway swelling and edema.
Early bronchospastic response
Within minutes of exposure to an allergen, mast cell degranulation is observed along with
the release of inflammatory mediators, including histamine, prostaglandin D2, and
leukotriene C4. These substances cause airway smooth muscle contraction, increased
capillary permeability, mucus secretion, and activation of neuronal reflexes. Early
asthmatic response is characterized by bronchoconstriction that is generally responsive to
bronchodilators, such as beta2-agonist agents.
Later inflammatory response
The release of inflammatory mediators primes adhesion molecules in the airway
epithelium and capillary endothelium, which then allows inflammatory cells, such as
eosinophils, neutrophils, and basophils, to attach to the epithelium and endothelium and
subsequently migrate into the tissues of the airway. Eosinophils release eosinophilic
cationic protein (ECP) and major basic protein (MBP). Both ECP and MBP induce
desquamation of the airway epithelium and expose nerve endings. This interaction
promotes further airway hyperresponsiveness in asthma. This inflammatory component
may even occur in individuals with mild asthma exacerbation.
Bronchospasm, mucus plugging, and edema in the peripheral airways result in increased
airway resistance and obstruction. Air trapping results in lung hyperinflation,
ventilation/perfusion (V/Q) mismatch, and increased dead space ventilation. The lung
becomes inflated near the end-inspiratory end of the pulmonary compliance curve, with
decreased compliance and increased work of breathing.
The increased pleural and intra-alveolar pressures that result from obstruction and
hyperinflation, together with the mechanical forces of the distended alveoli, eventually

lead to a decrease in alveolar perfusion. The combination of atelectasis and decreased

perfusion leads to V/Q mismatch within lung units. The V/Q mismatch and resultant
hypoxemia trigger an increase in minute ventilation.
CLINICAL MANIFESTATION
Physical Examination
Patients are usually tachypneic upon examination and, in the early stages of status
asthmaticus, may have significant wheezing. Initially, wheezing is heard only during
expiration, but wheezing later occurs during expiration and inspiration.
The chest is hyperexpanded, and accessory muscles, particularly the sternocleidomastoid,
scalene, and intercostal muscles, are used. Later, as bronchoconstriction worsens, the
wheezing may disappear, which may indicate severe airflow obstruction.
Normally, the difference in systolic blood pressure between inspiration and expiration
does not exceed 15mm Hg. In patients with severe asthma, a difference of greater than
25mm Hg usually indicates severe airway obstruction.
An inability to speak more than 1 or 2 words at a time may also be observed in the later
stages of an acute asthma episode. Ventilation/perfusion ratio (or V/Qratio) mismatch
results in decreased oxygen saturation and hypoxia.
Vital signs may show tachycardia and hypertension. The peak flow rate should be
included in the vital signs in patients who are able to cooperate and who are able to
tolerate the peak flow maneuver without significant distress.
The patients level of consciousness may progress from lethargy to agitation from air
hunger and even syncope and seizures.
If untreated, prolonged airway obstruction and marked increase in the work of breathing
may eventually lead to bradycardia, hypoventilation, and even cardiorespiratory arrest.
General examination

The peak flow rate is a standard measure of airflow obstruction and is relatively simple to
perform. Most patients with more than a mild exacerbation of asthma have hypoxia and
decreased oxygen saturation due to V/Q mismatch. Some patients prefer to remain seated
and leaning forward, rather than assuming a supine position.
Retractions (ie, intercostal, subcostal, use of abdominal muscles) may be observed in
patients with status asthmaticus. The use of accessory muscles has been shown to
correlate with the severity of airflow obstruction. An abnormally prolonged expiratory
phase with audible wheezing can be observed. Patients with moderate to severe asthma
are often unable to speak in full sentences.
Children with status asthmaticus may appear dehydrated as a result of poor intake,
vomiting, and increased work of breathing. This can occur in adults, but less frequently.
Cardiovascular symptoms may include tachycardia or hypertension in mild to moderate
asthma. With worsening hypoxemia, hypercarbia, marked air trapping, and
hyperinflation, stroke volume is compromised and hypotension and bradycardia may be
observed.
Central Nervous System(CNS) status ranges from wide awake to lethargic and from
agitated to comatose. As hypoxemia progresses, lethargy progresses to agitation caused
by air hunger. As more lung units become obstructed, hypoxemia worsens and
hypercarbia develops. Both hypoxemia and hypercarbia can lead to seizures and coma
and are late signs of respiratory compromise.
Examination of the respiratory system
Wheezing occurs from air moving through narrowed, obstructed airways. This exhalation
results in turbulent airflow and produces wheezes. Although asthma is the most common
cause of wheezing, anything that causes airway obstruction and narrowing that results in
turbulent airflow may generate wheezes. Therefore, not all wheezing is asthma.
Auscultation often reveals bilateral expiratory and possibly inspiratory wheezes and
crackles; air entry may or may not be diminished or absent, depending on severity.

Remember, the silent chest may herald impending respiratory failure in a patient too
obstructed or fatigued to generate wheezing.
If tension pneumothorax develops, signs of tracheal deviation to the opposite side,
decreased or absent air entry on the affected side, shift of the location of heart sounds,
and hypotension may be evident. Air leaks may also include pneumomediastinum and
subcutaneous emphysema.
In moderate to severe status asthmaticus, abdominal muscle use can cause symptoms of
abdominal pain.
Pulsus paradoxus (a decrease in the systolic blood pressure during inspiration) results
from a decrease in cardiac stroke volume with inspiration due to greatly increased leftventricular afterload. This increase is generated by the dramatic increase in negative
intrapleural and transmural pressure in a patient struggling to breathe against significant
airways obstruction. Pulsus paradoxus of greater than 20mm Hg correlates well with the
presence of severe airways obstruction (ie, forced expiratory volume in 1 second [FEV1]
< 60% predicted).
DIAGNOSTIC CONSIDERATIONS
Status asthmaticus can be misdiagnosed when wheezing occurs from an acute cause other
than asthma, such as aspiration of a foreign body or congestive heart failure (CHF) that
may require urgent treatment. These alternative causes are discussed below.
Viral infections/bronchiolitis
Common respiratory viral infections, such as infection with respiratory syncytial virus
(RSV), may cause airway swelling and narrowing in infants and children, giving rise to
inflammation and swelling of the bronchioles and resulting in bronchiolitis. Although
viral infections may clearly trigger asthma, typical bronchiolitis results from airway
swelling and edema, not from bronchospasm, and is generally unresponsive to treatment
with bronchodilators.

Foreign body
Aspiration of a foreign body is a particularly important consideration in toddlers. These
episodes are generally unwitnessed. When the foreign body lodges in the right or left
mainstem bronchus or beyond, the child may present with a cough and wheezing, often
unilaterally. When suspected, a chest radiograph should be obtained.
Cystic fibrosis
Airways are obstructed with thick, inspissated secretions.
Extrinsic compression
Airways can be compressed from vascular structures, such as vascular rings,
lymphadenopathy, or tumors.

Congestive heart failure

Airway edema may cause wheezing in CHF. In addition, vascular compression may
compress the airways during systole with cardiac ejection, resulting in a pulsatile wheeze
that corresponds to the heart rate. This is sometimes erroneously referred to as cardiac
asthma.
Tracheomalacia
Although the airway sounds are slightly different from those of asthma, they are often
referred to as wheezes.
Differential Diagnoses

Airway Foreign Body

Aspiration Syndromes

Bronchiectasis

Bronchiolitis

Croup

Gastroesophageal Reflux

Heart Failure, Congestive

Idiopathic Pulmonary Arterial Hypertension

Inhalation Injury

Pulmonary Artery Sling

APPROACH CONSIDERATIONS
The selection of laboratory studies depends on historical data and patient condition. Tests
that can be performed in patients with status asthmaticus include the following:

i.

Chest radiography

Obtain a chest radiograph to evaluate for pneumonia, pneumothorax,

pneumomediastinum, congestive heart failure (CHF), and signs of chronic obstructive
pulmonary disease, which would complicate the patient's response to treatment or reduce
the patient's baseline spirometry values.
Chest radiography is indicated in patients who have an atypical presentation or in those
who do not respond to therapy
ii.

Complete blood count (CBC)

Obtain a CBC and differential to evaluate for infectious causes (eg, pneumonia, viral
infections such as croup), allergic bronchopulmonary aspergillosis, and Churg-Strauss
vasculitis. When elevated, serum lactate levels (when obtained early at the onset of status
asthmaticus) can correlate with improved lung function.
A CBC and differential may demonstrate an elevated white blood cell count, with or
without a shift to the left. The CBC count may also indicate a bacterial infection;
however, beta-agonists and corticosteroids may result in demargination of white cells
with an increase in the peripheral white cell count.
iii.

Arterial blood gas (ABG)

An ABG value can be obtained to assess the severity of the asthma attack and to
substantiate the need for more intensive care. However, the use of blood gas
determination is controversial. The information generated by this measurement may be
helpful in determining whether or not to intubate a patient with asthma. However, such
decisions are usually made on the basis of clinical grounds in a patient who is either in
respiratory arrest or impending respiratory arrest.
If a patient with acute asthma has adequate peripheral oxygen saturation, is receiving
further therapy, and does not warrant immediate intubation, then the usefulness of blood
gas data should be weighed against the potential pain and agitation that running this test
may cause in a child. Improvement or deterioration in acute asthma can generally be
followed clinically. Indwelling arterial catheters reduce the pain issue and generate highly
reliable and reproducible information.
ABG determinations are indicated when the peak expiratory flow (PEF) rate or the forced
expiratory volume in 1 second (FEV1) is less than or equal to 30% of the predicted value
or when the patient shows evidence of fatigue or progressive airway obstruction despite
treatment.
The 4 stages of blood gas progression in persons with status asthmaticus are as
follows:

Stage 1 - Characterized by hyperventilation with a normal partial pressure of

oxygen (PO2)

Stage 2 - Characterized by hyperventilation accompanied by hypoxemia (ie, a low

partial pressure of carbon dioxide [PCO2] and low PO2)

Stage 3 - Characterized by the presence of a false-normal PCO2; ventilation has

decreased from the hyperventilation present in the second stage; this is an
extremely serious sign of respiratory muscle fatigue that signals the need for more
intensive medical care, such as admission to an ICU and, probably, intubation
with mechanical ventilation.

Stage 4 - Characterized by a low PO2 and a high PCO2, which occurs with
respiratory muscle insufficiency; this is an even more serious sign that mandates
intubation and ventilatory support.

Staging
The 4 stages of status asthmaticus are based on ABG progressions in status asthma.
Patients in stage 1 or 2 may be admitted to the hospital, depending on the severity of their
dyspnea, their ability to use accessory muscles, and their PEF values or FEV1 after
treatment (>50% but < 70% of predicted values).
Patients with ABG determinations characteristic of stages 3 and 4 require admission to an
ICU. The PEF value or FEV1 is less than 50% of the predicted value after treatment.
Stage 1
Patients are not hypoxemic, but they are hyperventilating and have a normal PO2. Data
suggest that to possibly facilitate hospital discharge, these patients may benefit from
ipratropium treatment via a handheld nebulizer in the emergency setting as an adjunct to
beta-agonists.
Stage 2

This stage is similar to stage 1, but patients are hyperventilating and hypoxemic. Such
patients may still be discharged from the emergency department, depending on their
response to bronchodilator treatment, but will require systemic corticosteroids.
Stage 3
These patients are generally ill and have a normal PCO2 due to respiratory muscle
fatigue. Their PCO2 is considered a false-normal value and is a very serious sign of
fatigue that signals a need for expanded care. This is generally an indication for elective
intubation and mechanical ventilation, and these patients require admission to an ICU.
Parenteral corticosteroids are indicated, as is the continued aggressive use of an inhaled
beta2-adrenergic bronchodilator. These patients may benefit from theophylline.
Stage 4
This is a very serious stage in which the PO2 is low and the PCO2 is high, signifying
respiratory failure. These patients have less than 20% lung function or FEV1 and require
intubation and mechanical ventilation.
Patients in stage 4 should be admitted to an ICU. Switching from inhaled beta2-agonists
and anticholinergics to metered-dose inhalers (MDIs) via mechanical ventilator tubing is
indicated. Parenteral steroids are essential, and theophylline may be added, as with
patients in stage 3.
iv.

Serum Electrolyte

Serum electrolyte measurement, particularly of serum potassium levels, is important.

Medications used to treat status asthmaticus may cause hypokalemia. A low pH may
result in a transient elevation of potassium.
v.

Serum Glucose Levels

Serum glucose levels may become elevated from stress; the use of beta-agonist agents,
such as epinephrine; and the use of corticosteroids. Because of poor stores, however,
hypoglycemia may develop in younger children in response to stress.
vi.

Blood theophylline levels

Blood theophylline levels provide an important monitoring component in patients taking

theophylline (either at home or while hospitalized) and especially in patients who have
received a bolus infusion of theophylline followed by continuous intravenous (IV)
infusion. The volume of distribution of theophylline is 0.56 mg/L in children and adults.
A dose of 1 mg/kg of theophylline raises the serum level by approximately 2 mg/dL.
If the patient has been receiving theophylline at home, obtain a serum theophylline level
before therapy. Following a loading dose (if needed), obtain a serum level 30 minutes
after the end of the infusion. For serum theophylline steady-state levels, obtain a serum
sample at 24-36 hours in children younger than 6 months, at 12-24 hours for those aged 6
months to 12 years, and at 24 hours for children aged 12 years and older.
Factors that decrease theophylline clearance (increase levels) include cimetidine,
erythromycin and other macrolide antibiotics, viral infections, cirrhosis, fever,
propranolol, and ciprofloxacin.
Factors that increase theophylline clearance (decrease levels) are IV isoproterenol,
phenobarbital, smoking, phenytoin, and rifampin.
vii.

Pulmonary Function Testing

PEF and FEV1

The most important and readily available test to evaluate the severity of an asthma attack
is the measurement of PEF. PEF monitors are commonly available to patients for use at
home, and they provide asthmatic patients with a guideline for changes in lung function
as they relate to changes in symptoms. In most patients with asthma, a decrease in peak
flow as a percentage of predicted value correlates with changes in spirometry values.
Although FEV1 is also used to monitor the degree of airway obstruction, in patients who
are acutely ill, peak flow monitoring is more commonly performed.
According to the guidelines of the National Heart, Lung, and Blood Institute/National
Asthma Education and Prevention Program, hospitalization is generally indicated when
the PEF or FEV1 after treatment is greater than 50%, but less than 70%, of the predicted

value. Hospitalization in an ICU is dependent on the severity of symptoms, use of

accessory muscles, and ABG results, as well as an FEV1 less than 50%.
A drop in the FEV1 to less than 25% of the predicted value indicates a severe airway
obstruction. A patient with an FEV1 of greater than 60% of the predicted value may be
treated in an outpatient setting, depending on the clinical situation. However, if the
patient's FEV1 or PEF rate drops to less than 50% of predicted, admission to the hospital
is recommended.

Pulse oximetry and spirometry

Pulse oximetry and spirometry values should be used to monitor the progression of
asthma. As the results indicate improvement, treatment may be adjusted accordingly.
If a portable spirometry unit is not available, a PEF rate of 20% or less of the predicted
value (ie, usually < 100 L/min) suggests severe airflow obstruction and impending
respiratory failure.
Pulse oximetry provides a continuous evaluation of oxygen saturation, which is vitally
important because the primary cause of death in status asthmaticus is hypoxia.
The advantages of pulse oximetry are that pulse oximetry is readily available, it is
noninvasive, it provides continuous monitoring, and it is a good indicator of hypoxemia
resulting from V/Q mismatch.
The disadvantages of pulse oximetry are that movement artifact can be significant and the
modality may provide an erroneous reading when pulsatile flow is inadequate (ie, shock
with poor perfusion) or in the presence of anemia.

MANAGEMENT OF STATUS ASTHMATICUS

Approach Considerations
After confirming the diagnosis and assessing the severity of an asthma attack, direct
treatment toward controlling bronchoconstriction and inflammation. Beta-agonists,
steroids, and theophylline are mainstays in the treatment of status asthmaticus.
Treat pregnant women with acute asthma in the same aggressive manner as nonpregnant
women.Respiratory acidosis can be detrimental to the fetus and the mother. Use special
abdominal shielding during chest radiography or sinus imaging.
Treat children with acute asthma in manner similar to that for adults, except when
children are mechanically ventilated, because their chests are more compliant and require
special attention.
According to guidelines from the National Asthma Education and Prevention Program
(NAEPP) Expert Panel, overall care for a child with asthma includes intensive outpatient
treatment with medications and alteration of the environment.Admission to the hospital
represents a failure of outpatient management.
Fluid replacement
Hydration, such as normal saline at a reasonable rate (eg, 150 mL/h), is essential. Special
attention to the patient's electrolyte status is important.
Hypokalemia may result from either steroid use or beta-agonist use. Correcting
hypokalemia helps to wean an intubated patient with asthma. Hypophosphatemia may
result from poor oral intake and is also an important consideration when weaning such
patients.
Antibiotics
The routine administration of antibiotics is discouraged. Patients are administered
antibiotics only when they show evidence of infection (eg, pneumonia, sinusitis). In some
situations, sinus imaging using computed tomography (CT) scanning or plain
radiography may be essential to help rule out chronic sinusitis.

Oxygen monitoring and therapy

Monitoring the patient's oxygen saturation is essential during the initial treatment of
status asthmaticus. Arterial blood gas (ABG) values are usually used to assess
hypercapnia during the patient's initial assessment. Oxygen saturation is then monitored
via pulse oximetry throughout the treatment protocol.
Oxygen therapy is essential, with hypoxia being the leading cause of death in children
with asthma. Oxygen therapy can be administered via a nasal canula or mask, although
patients with dyspnea often do not like masks. With the advent of pulse oximetry, oxygen
therapy can be easily titrated to maintain the patient's oxygen saturation above 92%
(>95% in pregnant patients or those with cardiac disease).
In the event of significant hypoxemia, non-rebreathing masks may be used to deliver as
much as 98% oxygen. Tracheal intubation and mechanical ventilation are indicated for
respiratory failure.
Chest tube placement
Chest tube placement may be necessary in the management of pneumothorax.
Leukotriene modifiers
Leukotriene modifiers are useful for treating chronic asthma but not acute asthma. This
treatment may be beneficial if used via a nebulizer, but it remains experimental.
ICU admission criteria
Indications for ICU admission include the following:

Altered sensorium

Use of continuous inhaled beta-agonist therapy

Exhaustion

Markedly decreased air entry

Rising PCO2 despite treatment

Presence of high-risk factors

Failure to improve despite adequate therapy

Surgery
Status asthmaticus is generally managed by means of medical therapy, with some
exceptions. For example, thoracentesis or thoracostomy is indicated in pneumothoraces.
Some children may have asthma that is primarily exacerbated by gastroesophageal reflux
disease. Some can be treated with a combination of antireflux and histamine 2 (H2)
receptor antagonist agents; however, surgery, such as Nissen fundoplication, is
occasionally required.
Anesthesia support is needed if inhaled anesthetic agents are considered for refractory
severe intubated status asthmaticus.
If all other support modalities fail and extracorporeal membrane oxygenation (ECMO) is
required, surgical support for cannula placement should take place at an established
pediatric ECMO center.
Diet
Some children with asthma may have episodes triggered by food allergies. Consultation
with a nutritionist may be necessary to provide appropriate dietary management.
Medication
The following agents are used in the pharmacologic treatment of status asthmaticus:

Beta2-Agonists

The first line of therapy is bronchodilator treatment with a beta2-agonist,these agents

relax airway smooth muscle, thus causing bronchodilation in patients with reversible
airway obstruction, such as asthma.

Albuterol (Proventil HFA, Ventolin HFA, ProAir HFA)

Albuterol relaxes bronchial smooth muscle by action on beta2 receptors with little effect
on cardiac muscle contractility. Administer continuous nebulization with a pump-driven
aerosol or via a small-particle aerosol generator
Levalbuterol (Xopenex, Xopenex HFA)
Levalbuterol is a selective beta2-agonist. Albuterol is a racemic mixture, while
levalbuterol contains only the levo isomer of albuterol. The safety and efficacy of
levalbuterol have not been determined in children under 12 years; multicenter trials in
children aged 12 years and younger are ongoing.