Medical surgical nursing 1

1. RESPIRATORY DISORDERS

2. Introduction
 Breathlessness is common among patients
and can indicate a physiological problem in
any body system, not just the respiratory
system.
 An increase in RR is a compensatory
mechanism in DKA. Conversely, a reduced
RR is often seen in CNS depression or
opiate drug overdose

3. Introduction
 Deep sighing respirations are seen in an
attempt to increase the elimination of CO2.
 A change in RR indicates either a physiological
or psychological problem.
 The respiratory system is the first system in
the body to respond to altered homeostasis.
 Changes in the rate and depth of respiration
occur within seconds of a problem that may
be remote from the respiratory system.

4. Introduction
 The measurement of RR in clinical practice
continues to be omitted or, if recorded at all,
serial measurements are often absent.
 Some patients with respiratory problems
require immediate resuscitative interventions.
 Always undertake an ABCDE assessment.
 This will identify those patients with actual or
impending airway obstruction and those with
absent or ineffective respirations

5. Nursing Assessment
History:
 Clinical features to be obtained from history
include:
 When the difficulty in breathing started
 Breathlessness on exertion
 Nocturnal dyspnea; orthopnoea; cough
 Sputum - colour, amount and presence
of blood
 Breathlessness or inability to take a deep
breath due to chest injuries and related pain

6. Nursing Assessment
History:
 Chest pain - site and quality
 Any trauma - elicit the clear mechanism of
injury
 Fever, smoking
 Exercise tolerance - how many stairs can be
climbed, or how far the patient can walk on
the flat without breathlessness
 Treatment at home or on the way to hospital.

7. Nursing Assessment
History:
 Patients with asthma or COPD may have
increased their own medications before
coming.
 If there was no improvement after increasing
their own inhaled therapy, this is significant.
 For patients with existing respiratory
diseases, ensure to document: medications;
recent admissions; any ICU admissions,
intubation, non-invasive ventilation; previous
pneumothoraces.

8. Nursing Assessment
 Respiratory distress or difficulty among
patients with respiratory problems may
present acutely with shortness of breath.
 They may also exhibit the following signs and
symptoms, which require immediate
intervention:
◦ Marked tachypnoea (RR >30 breaths/min);
altered level of consciousness, agitation,
confusion; marked accessory muscle use;
inability to speak due to breathlessness;
cyanosis and exhaustion

9. Nursing Assessment
Physical Examination:
Inspection:
 Observe for pursed lip breathing.
 Drooling indicates an upper airway problem
and cyanosis (central or peripheral) require
immediate intervention
 Check the patient’s ability to talk and
complete sentences.
 RR, respiratory depth and pattern.

10. Nursing Assessment
Physical Examination:
 Note the patient’s posture. Patients with
partial or impending upper airway
obstruction will adopt a posture that
maximizes ventilation. Usually they lean
forward.
 Observe chest rise and fall, noting any
asymmetry or paradoxical movement.
 Inspect the chest wall for trauma e.g.
abrasions, bruises, wounds, FBs, and scars.
 Observe for accessory muscle usage

11. Nursing Assessment
Physical Examination:
 Observe and document the patient’s
conscious level and degree of agitation,
confusion, and restlessness.
Palpation:
 Feel the position of the trachea to check that
it is in the midline.
 Palpate the clavicles, sternum, and ribs in
patients with a chest injury.This may reveal
crepitus, surgical emphysema or tenderness.

12. Nursing Assessment
Palpation:
 Patients with a lower chest injury may also
have sustained a significant upper abdominal
or retroperitoneal injury.
Auscultation and percussion:
 Listen for breath sounds.Are they equal and
clear bilaterally? Are there any added sounds
such as wheeze or crepitations?
 A silent chest in an asthmatic patient is life-
threatening and requires immediate action.

13. Nursing Assessment
Auscultation and percussion:
 Is there any stridor or an audible wheeze?
 Is the percussion note normal? Dullness
indicates fluid or consolidation, whereas
hyper-resonance indicates air in the pleural
cavity.
 Vital signs: Record the RR; pulse; BP; Oxygen
saturations; temperature; peak flow (in
patients with asthma); GCS score.

14. Diagnostic Investigations
 ABGs in patients with SpO2 of <93% on air.
 Sputum for culture and susceptibility
 FBC if there is a clinical indication (e.g. infection,
anaemia).
 U&E if there are signs of dehydration (may be seen
in asthma through insensible losses).
 Blood cultures, if indicated.
 Pain score.
 CXR.
 ECG, if indicated.

15. Nursing interventions
 Positioning – should be nursed in an upright
position.
 Those with severe respiratory distress often
want to sit with their legs over the side
 Venous access - some patients will require
administration of I.V bronchodilators.
 Analgesia - pleuritic chest pain responds well
to NSAIDs.
 Patients with severe pain may require opiate
analgesia.

16. Nursing interventions
 Inhaled therapies – steroids /bronchodilators.
 Psychological support - it can be extremely
distressing to be breathless.
 A calm, reassuring manner will help to reduce
the patient’s anxiety.
 Oxygen therapy - all patients who are unable
to maintain normal O2 saturations on air will
require O2 therapy.
 Administer supplemental O2 by mask to all
patients with SpO2 of <95%.

17. Nursing interventions
 In patients with known COPD, give a
controlled amount of O2 by mask, starting at
24 – 28% and gradually increase to achieve a
target saturation range of 88– 92%.
 O2 concentrations should be reduced if the
patient becomes drowsy or saturations reach
≥93%.
 Obtain an ABG values immediately as O2
therapy should be titrated to ABGs, not
saturations.

18. Airway obstruction
 Upper airway obstruction is an
interruption in the flow of air through
the nose, mouth, pharynx or larynx.
 Obstruction of the upper airway is
considered a life-threatening situation
that can progress to respiratory arrest.
 Respiratory arrest will lead to cardiac
arrest, that requires cardiopulmonary
resuscitation (CPR).

19. Etiology
 A patient’s airway can become obstructed by
vomitus; food; edema or his tongue, teeth or
saliva.
 The commonest cause of upper airway
obstruction is the tongue.
 Partial airway obstruction is commonly
caused by edema or a small foreign object
that doesn’t completely obstruct the airway.

20. Etiology
 Edema of tongue (caused by trauma), laryngeal
edema and smoke inhalation edema—in anatomical
structures of the upper airway can lead to an
obstruction.
 Other potential causes of airway obstruction
include: anaphylaxis; aspiration of a foreign object;
burns to the head, face or neck area; epiglottitis;
laryngospasms; peritonsillar or pharyngeal
abscesses; tenacious secretions in the airway;
trauma of the face, trachea or larynx; tumors of the
head or neck.

21. Mechanism of obstruction
Once an airway obstruction
occurs, the patient is partially able
or not able to take in oxygen
through inhalation.
This state leads to hypoxemia the
longer the obstruction remains.

22. Clinical Manifestations
 Signs of a partial airway obstruction
include restlessness, agitation and
anxiety, diaphoresis, tachycardia,
coughing, stridor, respiratory distress
and elevated blood pressure.
 Patients with a partial obstruction may
also experience no symptoms.

23. Clinical Manifestations
 With a complete airway obstruction, the following
symptoms may be observed:
◦ universal choking sign—patient clutches throat
with hands
◦ inability to speak
◦ Sudden onset of choking or gagging
◦ Stridor
◦ Cyanosis
◦ Wheezing or any other unusual breath sound that
indicates breathing difficulty
◦ Diminished breath sounds (bilateral or unilateral)
◦ Sense of impending doom
◦ Progression to unconsciousness.

24. Diagnostic Evaluation
 Physical examination may indicate
decreased breath sounds.
 Tests to diagnose an upper airway
obstruction but may include X-rays,
bronchoscopy and laryngoscopy.
 If there are persistent symptoms of an
upper airway obstruction, a chest X-ray,
neck X-rays, laryngoscopy or CT scan may
be ordered to rule out the presence of a
tumor or foreign body.

25. Management
 Rapidly assess the airway patency, breathing,
and circulation.
 Assess the patient’s breath sounds bilaterally.
 Quickly assess the obstruction’s cause.
 When an obstruction relates to the tongue
or an accumulation of tenacious secretions,
place the head in a slightly extended position
and insert an oropharyngeal airway.
 Head tilt, chin lift method; Jaw thrust to be
considered if neck trauma is suspected

26. Oropharyngeal Airways

27. Management
Sizing the
Oropharyngeal
Airway
Measure from
corner of mouth
to angle of jaw
Indications/cont
raindications

28. Management
 Quickly remove objects visible in the mouth
with suction, fingers or Magill forceps.
 If the patient can breathe (partial obstruction),
encourage them to sit forward and cough to
relieve the obstruction.
 Note that coughing might worsen the
obstruction and may totally occlude the airway.
 ET intubation and removal of the foreign object
during insertion of the laryngoscope enables
visualization of the obstruction.
 If an oral or ET airway doesn’t provide
ventilation, patient is prepared for emergency
cricothyroidotomy.

29. Management
 Monitor oxygen saturation (using pulse
oximetry) and cardiac rhythm continuously.
 Continually assess for stridor, cyanosis and
changes in LOC and notify the doctor.
 Monitor chest X-ray and ABG results after
the obstruction is relieved.
 Anticipate cardiac arrest if the obstruction
isn’t cleared promptly.

30. Oxygen therapy
 It is the administration of oxygen at concentrations
greater than that in ambient air to treat or prevent
symptoms and manifestations of hypoxia.
 The aim is to provide adequate transport of oxygen
in the blood; decreasing the work of breathing and
reducing stress on the myocardium.
 A change in the patient’s respiratory rate or pattern
is the earliest indicator of the need for oxygen
therapy.
 These changes may result from hypoxemia or
hypoxia.
 Hypoxemia, a decrease in the arterial oxygen
tension in the blood. Hypoxemia usually leads to
hypoxia, a decrease in oxygen supply to the tissues

31. Oxygen therapy
 Indications: respiratory failure; acute
myocardial infarction; cardiac failure; shock;
anaemia; during anaesthesia; post-operatively;
sleep apnoea; severe pain; asthma; pulmonary
embolus; conditions that affect the
neuromuscular control of breathing e.g.
muscular dystrophy, Guillain–Barré; severe
trauma to diaphragm, ribs, lungs or trachea;
tension pneumothorax; pleural effusion

32. Oxygen delivery
Any oxygen delivery system will include these basic
components:
 Oxygen supply, from either a piped supply or a
portable cylinder
 A reduction gauge: to reduce the pressure to
atmospheric pressure
 Flow-meter: a device that controls the flow of oxygen
in litres per minute
 Tubing: disposable tubing of varying diameter and
length
 Mechanism for delivery : a mask or nasal cannulas
 Humidifier: to warm and moisten the oxygen before
administration
 Water trap if humidifier in use

34. Oxygen delivery
 Nasal cannulas consist of two plastic prongs that
are inserted inside the anterior nares and
supported on a light frame.
 Nasal cannulas can be used only where the
patient requires a low percentage of oxygen and
are used with flow rates of 1–4 litres of oxygen
per minute and provide 28–35% oxygen
 They are well tolerated and are useful post-
operatively or where the patient requires
minimal support.
 They are also used in chronic settings where a
patient at home requires long-term oxygen
therapy

36. Oxygen delivery
 Simple semi-rigid plastic masks are low-flow (5–
10 L/ min) masks which entrain the air from the
atmosphere and therefore are able to deliver a
variable oxygen percentage (from 40% to 60%).
 Oxygen concentrations vary depending on the
flow rate and the patient’s rate and depth of
breathing
 Useful for patients who need a higher
percentage of oxygen temporarily as the cause of
their hypoxia is treated.
 This type of mask may be worn for hours or
several days, but with a humidifier if used for
more than 12 hours.

37. Simple oxygen face mask

38. Oxygen delivery
 Non-rebreathing masks are similar to the simple
semi-rigid plastic masks with the addition of a
reservoir bag.
 This allows the oxygen to be delivered at higher
concentrations (60% - 90%) when used at flow
rates of 10–15 L/min
 Oxygen flows into the bag and mask during
inhalation and the valve prevents expired air
from flowing back into the bag.
 This device should only be used in the presence
of expert nursing and medical support and
during emergency intervention or before more
invasive ventilatory therapy is instituted

39. Non-rebreathing masks

40. Management
 Venturi-type oxygen masks deliver high-flow
oxygen via aVenturi adaptor.
 The adaptors are colour coded according to
the percentage of oxygen they deliver with
different oxygen flow rates.
 Venturi masks are available in the following
concentrations: 24%, 28%, 35%, 40% and 60%.
 Venturi masks with 24% and 28% are suited
to those at risk of CO2 retention

42. Management
 Tracheostomy masks perform in a similar way to
the simple semi-rigid plastic facemask
 The mask is placed over the tracheostomy tube
or stoma.
T
-piece circuit is a simple, large-bore, non-
rebreathing circuit which is attached directly to an
endotracheal or tracheostomy tube.
 Humidified oxygen is delivered through one part
of the T and expired gases leave through the
other part.
 Used as part of the weaning process when a
patient has been ventilated previously by a
mechanical ventilator

43. ASTHMA
 Definition: it is a chronic inflammatory
disease of the airways that is associated
with airway hyper responsiveness,
mucosal edema and mucus production.
 Asthma literally means ‘panting’ and is
characterized by acute exacerbations
interspersed by symptom- free periods.
 The airways become inflamed, narrow,
and hyper-responsive.

44. Introduction
 Airway hyper responsiveness implies that the
airways will narrow easily and too much in response
to various stimuli.
 The chronic airway inflammation is associated
with airway hyper responsiveness that leads to
recurrent episodes of wheezing, breathlessness,
chest tightness and coughing particularly at night
or in the early morning.
 These symptoms are variable, intermittent and
often reversible either spontaneously or with
treatment.

45. Introduction
Estimated that 10% of Kenyan
population have asthma.
The prevalence of asthma in older
children between ages of 12-14 years
may be increasing
Asthma is more prevalent in urban as
opposed to rural areas in Kenya

46. Introduction
 Intrinsic asthma has no known allergic
cause and tends to occur later in life.
 Extrinsic asthma has allergic triggers
such as pollen, animal hair, certain foods,
or certain drugs. Emotion and exercise
can also trigger an exacerbation.

47. Risk factors to development of
asthma
They include:
Genetic predisposition
Atopy
Airway hyperresponsiveness
Early in life common in boys than
girls
Obesity
Exposure to tobacco smoke

48. Trigger factors for asthma attacks
They include:
 Exposure to allergens
 URT viral infections
 Tobacco smoke
 Irritants like paint fumes and household sprays
 Air pollution
 Cold air
 Excessive exercise
 Stress/intense emotional reactions
 Drugs e.g. beta blockers, aspirin
 Menses

49. Pathophysiology
 Chronic inflammation of the airways which is
present even when patients are symptom free.
 A wide array of inflammatory cells are involved
in asthma inflammation including mast cells,
eosinophils,T lymphocytes, dendritic cells,
macrophages and neutrophils
 These cells further produce chemical mediators
like chemokines, leukotrienes, cytokines etc and
their involvement leads to the damage of the
airways causing structural changes e.g. basement
membrane thickening

50. Pathophysiology
 The airway inflammation causes airway hyper
responsiveness, airway narrowing due to
airway smooth muscle contraction,
overproduction of airway mucus, airway
edema and airway remodeling from
deposition of collagen in the basement
membrane.
 The resultant effect is airway limitation that
leads to wheezing, cough, dyspnea and chest
tightness

53. Clinical manifestations
 3 main symptoms occur,
 Cough -with or without mucus production
 Dyspnoea-breathlessness
 Wheezing-airflow through narrow airways
 Chest tightness
 Diaphoresis
 Tachycardia
 Hypoxemia
 Central cyanosis

54. Assessment of the asthmatic
patient
 Initial assessment- History of episodic symptoms
include severe breathlessness (including too
breathless to complete sentences in one breath),
tachypnoea, tachycardia, silent chest, cyanosis or
collapse.
 None of these symptoms singly or together is
specific and their absence does not exclude a
severe attack
 Positive family history and environmental factors
 Presence of other comorbidities associated with
asthma e.g. GERD, drug induced asthma, allergic
reactions e.g. eczema

55. Assessment of the asthmatic
patient
 The following observations are important and they
help to establish the severity of asthma and also
enable the success of treatment interventions to be
evaluated:
 Pulse oximetry-Oxygen saturation (SpO2)
determines the adequacy of oxygen therapy and the
need for arterial blood gas measurement (ABG).
 Arterial blood gases-Patients with SpO2 <92% or
other features of life-threatening asthma require
ABG measurement

56. Assessment of the asthmatic
patient
 RR; pulse; temperature; BP; pain score; GCS score.
 Elevated serum IgE levels in cases of allergy
 Chest X-ray is not routinely recommended in
patients in the absence of:
 Suspected pneumothorax or consolidation
 Life-threatening asthma or failure to respond to
treatment;
 Requirement for mechanical ventilation

57. Assessment of the asthmatic
patient
 Forced ExpiratoryVolume in 1 second and Peak
Expiratory Flow (PEF/FEV) are useful and valid
measures of airway calibre. PEF expressed as a % of
the patient’s previous best value is most useful
clinically.
 PEFR must be measured on arrival in the hospital
and documented.
 Assessment to determine the severity of the asthma
will guide treatment and the need for admission.
 Presence of any features of severe or life-
threatening asthma requires calling for help
immediately.

58. Levels of severity of acute asthma
exacerbations
Moderate asthma:
 Increased symptoms
 PEF >50–75% best or predicted
 No features of acute severe asthma
Acute severe asthma:
Any one of the following:
 PEF 33–50% best or predicted
 RR ≥25/min
 HR ≥110/min
 Inability to complete sentences in one
breath

59. Levels of severity of acute asthma
exacerbations
Life- threatening asthma:
Any one of the following in a patient with severe asthma:
 PEF <33% best or predicted
 SpO2 <92%
 PaO2 <8 kPa
 ‘Normal’ PaCO2 (4.6–6.0 kPa)
 Silent chest
 Cyanosis
 Poor respiratory effort
 Arrhythmia
 Exhaustion
 Altered level of consciousness
 Hypotension

60. Complications
 Status asthmaticus
 Respiratory failure
 Pneumonia
 Atelectasis
 Hypoxemia

61. Treatment
Goals:
 Prevent chronic and troublesome symptoms
 Maintain near normal pulmonary function
 Maintain normal activities
 Prevent recurrent episodes and emergency
hospitalisation
 Provide optimal pharmacotherapy

62. Medical management
 Two classes of asthma medications exist:
Quick relief meds and long acting meds to
achieve and maintain control of persistent
asthma
 Quick relief meds include Short-acting
beta2-adrenergic agonists (SABA) are used
for acute symptoms a they relax airway
smooth muscles e.g. albuterol, ventolin,
levalbuterol; Anticholinergics e.g.
ipratropium bromide can also be used

63. Medical management
 Long acting control meds are mainly anti-
inflammatory drugs. Corticosteroids are
initially used by inhalation e.g.
Beclomethasone Dipropionate, budesonide,
fluticasone; systemic forms e.g. prednisolone
are used to rapidly control asthma and
manage severe, persistent asthma.
 Long-Acting Beta2-Agonists (LABAs) –
inhaled: salmeterol, formoterol; orals:
albuterol are used with AIDs to control
asthma

64. Medical management
 Cromolyn sodium and nedocromil are
alternative anti-inflammatory drugs
 Methylxanthines e.g. aminophylline a
bronchodilator are used with inhaled
corticosteroid (ICS) for nighttime symptom
relief
 Leukotriene inhibitors e.g. montelucast can
also be used

65. Nursing Diagnoses
 Impaired gaseous exchange related to airway
obstruction as evidenced by difficulty in
breathing
 Ineffective airway clearance related to
increased mucus production as evidenced by
productive cough
 Ineffective tissue perfusion related to
hypoxemia as evidenced by cyanosis

66. Nursing interventions
Management priorities will depend on the severity
of the asthma.
 Nurse the patient in high fowlers position to ease
breathing
 Continuous SpO2 and HR monitoring.
 RR should be recorded every 30min at the very
minimum, until it is stable.
 Administer supplemental high-flow oxygen to all
hypoxaemic patients with acute severe asthma to
maintain an SpO2 level of 94–98%.
 Lack of pulse oximetry should not prevent the use
of oxygen.
 ABG analysis and monitoring

67. Nursing interventions
 Administer high-dose inhaled beta-2 agonists as
first line agents in patients with acute asthma and
administer as early as possible.
 In patients with acute asthma with life-threatening
features the nebulization (oxygen-driven) with
ventolin 2mls:3mls N/saline is recommended.
 In severe asthma that is poorly responsive to an
initial bolus dose of beta-2 agonist, consider
continuous nebulization with an appropriate
nebulizer.

68. Nursing interventions
 Add nebulised ipratropium bromide (0.5 mg 4–6
hourly) to beta-2 agonist treatment for patients with
acute severe or life-threatening asthma or those
with a poor initial response to beta-2 agonist
therapy.
 Steroid therapy-administer steroids in adequate
doses in all cases of acute asthma attack. Continue
prednisolone 40–50 mg daily for at least five days or
until recovery.
 Consider giving a single dose of IV magnesium
sulfate to patients with acute severe asthma (PEF
<50% best or predicted) who have not had a good
initial response to inhaled bronchodilator therapy.

69. Nursing interventions
 Monitor PEFR 30minutes post-nebulization.
 Administer prescribed analgesics to manage pain.
 Administer intravenous fluids in cases of
dehydration
 Teach the patient on self care with emphasis on
adherence to prescribed therapy; preventive
measures and need to keep follow up appointments
with health care providers
 Self care includes inhaler use, reduced exposure to
allergens, ability to recognize signs of asthma attack,
performance of coughing and deep breathing
exercises

70. How to use an inhaler

71. Nursing interventions
Refer any patient:
◦ Requiring ventilatory support
◦ With acute severe or life-threatening asthma,
who is failing to respond to therapy, as evidenced
by:
- Deteriorating PEF
- Persisting or worsening hypoxia; hypercapnia
- ABG analysis showing decreasing pH or
increasing H+
- Exhaustion, feeble respiration; drowsiness,
confusion, altered conscious state
- Respiratory arrest.

72. Status asthmaticus
 It is a severe and persistent form of asthma that is
unresponsive to conventional therapy.
 The attacks occur without warning and rapidly
progress to asphyxiation
 Possible causes include:Anxiety, nebulizer abuse,
dehydration, increased adrenergic blockage, irritants,
drug hypersensitivity.
 It is associated with severe bronchospasms and
mucus plugging leading to asphyxia
 The ventilation-perfusion mismatch causes
hypoxemia. Initially the patients have respiratory
alkalosis but later progresses to respiratory acidosis

73. Status asthmaticus
 Signs and symptoms include labored breathing,
prolonged exhalation, engorged neck veins and
wheezing.
 Hospitalization may be required and pulmonary
function studies are accurate in assessing acute
airway obstruction
 Patient is initially treated with inhaled SABA with
systemic corticosteroids (to decrease intense
airway inflammation and swelling). Nebulization
of the medications is required.
 Magnesium sulfate a calcium antagonist may be
administered to induce smooth muscle
relaxation hence bronchodilation

74. Status asthmaticus
 High flow supplemental oxygen using non-rebreather
mask to treat dyspnea, hypoxemia and central
cyanosis
 Intravenous fluids are also administered to hydrate
the patient
 If there is no response to repeated treatments,
mechanical ventilation may be required
 The nurse is expected to constantly monitor the
patient for the first 12-24 hours until control is
achieved
 Blood pressure and cardiac rhythm are also closely
monitored
 Patient should be nursed in a quiet room, free of
respiratory irritants.

75. PNEUMONIA

76. Introduction
 Pneumonia is an inflammation of the lung
parenchyma (respiratory bronchioles and
alveoli) caused by various microorganisms.
 It is the leading cause of death among
infectious diseases.
 Accounts for about 10% of hospital
admissions.
 Pneumonia may be infectious when it is
caused by bacteria, viruses, fungi and
protozoa or non-infectious when it is caused
by aspiration of gastric content and irritating
gases.

77. Risk factors
 Lung cancer
 Cigarette smoking
 Chronic obstructive pulmonary disease
 Depressed cough reflex
 Immunosuppression
 Prolonged immobility
 Unconsciousness
 Drugs – anaesthetic, sedatives, opioids
 Advanced age

78. Classification of infectious Pneumonia
 Community acquired pneumonia (CAP)
 Hospital acquired pneumonia (nosocomial )
 Pneumonia in the immunocompromised host
(Opportunistic)
 Aspiration
Another categorization
Primary-occuring in previously healthy person living
in the community, usually lobar pneumonia due to
pneumococci.
Secondary-develops in association with prior
respiratory, immunocompromised patient,

79. Community acquired pneumonia
Occurs in the community or within 48 hours after
hospitalization.The common causative agents
include
Streptococcus pneumonia-causes 66% of infections
• Haemophylus influenza
• Psedomonas Aeruginosa
• Legionnella pneumophila
• Mycoplasma pneumoniae
• Viruses – cytomegalovirus, adenovirus, herpes simplex
virus and respiratory syncytial virus

80. Hospital acquired pneumonia
 Also called nosocomial pneumonia. It is the onset of
pneumonia symptoms more than 48 hours after
admission for patients with no evidence of infection
on admission.
 HAP is usually contracted by patients who are
already vulnerable to infection (e.g.
immunocompromised, critically ill, intubated or
ventilated).
 Common organisms causing HAP include:
 Staphylococcus aureus

81. Pneumonia in Immunocompromised
host
 Mortality from all pneumonias continues to be
significant in the elderly population and those
with HIV
 Common organisms include:
 Pneumocystis jiroveci
 Fungal pneumonia.
 It can also be caused by organisms observed in CAP
and HAP

82. Aspiration Pneumonia
 This type of pneumonia results from entry of
endogenous or exogenous substances into the
lower airway
 Common pathogens include:
 Staphylococcus aureus.
Streptococcus pneumonia
• Haemophylus influenza

83. Pathophysiology Of Pneumonia
• Entry of microbes into the lower respiratory
tract can be through:Aspiration of oropharyngeal
secretions containing microbes, inhalation of
microbes from the environment or bloodborne
organisms from infections elsewhere in the body.
• Invading micro-organisms colonize the alveoli
initiating an inflammatory and immune response.
• The inflammatory and immune response
produces exudates that impairs diffusion of
oxygen and carbon dioxide in the alveoli
• Inadequate ventilation also occurs due to

84. Patterns of lung involvement
1. Lobar Pneumonia: Involves an entire lobe of a lung.
2. Bronchopneumonia: is distributed in a patchy fashion,
having originated in one or more localized areas within the
bronchi and extending to surrounding areas of lung
parenchyma. Exudates remain in the bronchi and bronchioles.
There is less mucosal edema and congestion of the alveoli
unlike in lobar pneumonia.
3. Interstitial Pneumonia: involves the interstitium i.e. the
alveoli wall and the connective tissue. Involvement may be
diffuse or patchy.Alveoli do not contain significant exudates.
Protein rich hyaline membrane lines the alveoli interfering
with gaseous exchange.
4. Milliary Pneumonia: Discrete inflammatory lesions in the
lung due to hematologic spread. Common in people with
severe immunocompromise.

85. Clinical manifestations
 Chills and fever
 Rapid bounding pulse
 Cough- sputum is of rusted color or purulent.
 Chest pain- pleuritic in nature, sharp, localized,
increases with breathing.
 Tachypnea
 Use of accessory muscles in breathing
 Orthopnea may be present
 Diaphoresis
 Fatigue

86. Diagnosis of pneumonia
 History esp. of a recent URTI
 Physical examination
 Chest x-ray: determines the extent of lung
involvement, lung consolidation, atelectasis
 CT scan gives more details on pulmonary tissue.
 Sputum Examination: gram staining identifies
gram positive and gram negative bacteria
 Fiber optic bronchoscopy- done to obtain
sputum or remove secretions from the bronchial
tree

87. Diagnosis cont…………….
 Complete Blood Count withWBC differential –
WBC of 11,000/mm3 or higher is indicative of
bacterial pneumonia.
 WBC changes are minimal in viral and other
pneumonias.
 Serology testing-detects antibodies of causative
micro-organism. Used when blood and culture
tests are neg.
 Pulse oximetry measures arterial blood oxygen
concentration.
 Arterial blood gas analysis if SpO2 is <93% on air.

88. Prevention of Pneumonia
 Pneumococcal vaccine provides protection
against pneumococcal pneumonia and other
strains of Strep. pneumoniae.
 Recommended for people with high risk of
infection.
 Influenza vaccine- a new vaccine is prepared
annually, useful against viral pneumonia

89. Medical management
Previously healthy and no antibiotics in past 3
months;-
 Outpatients- IM benzyl penicillin 2 mu STAT then
amoxicillin 500mg tds for 7 dys
 If peniciliin allergy is present: erythromycin 500mg
QDS for 7 days.Alternative antibiotics include
cotrimoxazole
For in-patients, treat with IV/IM crystalline penicillin 2
mu QDS until response , then discharge on
amoxicillin 500mg tds; if allergic , erythromycin
500mg qds or cotrimoxazole for 5days

90. Medical management
For secondary pneumonia treat with benzyl
penicillin 2 mu IM/IV QDS plus gentamycin 240
mg IV/IM OD for 5 days or IV ceftriaxone 2 g
OD or Erythromycin 500mg QDS for 5 days
In case of aspiration add metronidazole 500mg IV
TDS or amoxiclavulanate 1.2 g TDS in place of
benzyl penicillin
If staphylococcus is suspected add flucloxacillin
500mgTDS

91. Medical management
For patients receiving intensive care
 A beta-lactam agent plus azithromycin or a
fluoroquinolone is recommended
In cases of MRSA,Add linezolid or vancomycin to the
regimen
In cases of comorbidities or history of antibiotic use
in the past 3 months, select an alternative from a
different class:
 A fluoroquinolone [moxifloxacin, gemifloxacin and
levofloxacin] OR A beta-lactam agent [preferred:
high-dose amoxicillin or amoxicillin/clavulanate;
alternatives: ceftriaxone, cefpodoxime, cefuroxime]
plus a macrolide

92. Other therapies
 If no response consider investigating for TB
 Analgesics e.g. paracetamol or acetyl salicylic
acid
 Antipyretics to treat headache and fever
 Antitussives for the associated cough
 Hydration by increasing fluid intake 2500 to
3000mls per day
 Oxygen administration for patients with
hypoxemia.
 Chest physiotherapy that includes chest
percussion and vibration to move the

93. COMPLICATIONS
• Shock
• Respiratory failure
• Atelectasis
• Empyema and pleural effusion- identified
by chest x-ray.

94. Nursing Management
Assess the patient through history taking, physical
examination, and other diagnostic tests.
Major nursing diagnoses include
 Ineffective airway clearance related to copious
tracheobronchial secretions
 Decreased activity tolerance related to impaired
respiratory function
 Risk for deficient fluid volume related to fever and
a rapid respiratory rate
 Imbalanced nutrition: less than body requirements
 Deficient knowledge about the treatment regimen

95. Nursing management
 Admit for inpatient care in the presence of the
following:
◦ Cyanosis, respiratory distress(RR>25), heart failure or
pleural effusion, more than one lobe is involved, poor
response as outpatient, patient is dehydrated
 Position in semi-fowler’s position but promote
frequent position changes to enhance clearance of
secretions and pulmonary ventilation
 Encourage coughing, deep breathing, endotracheal
suctioning- to remove the secretions and clear the
airway.
 Hydrate the patient by administering I.V fluids

96. Nursing management
 Assess for pleuritic discormfort- administer
prescribed analgesics, reassure patient during periods
of respiratory distress to allay anxiety.
 Analgesics are also vital for deep breathing exercises
and expectoration.
 Administer and titrate oxygen therapy as prescribed
 Schedule activities, planning for rest periods and avoid
overexertion - to reduce metabolic demands and
promote effective breathing pattern.
 Assist patient with ADLs- to reduce energy demand
 Provide assistive devices e. g. trapeze to encourage
movement in bed.

97. Nursing management
 Encourage ambulation and exercises either passive
or active.
 Provide emotional support and reassure that
strength and energy will return to normal when
infection resolves.
 Encourage nutritionally enriched drinks to maintain
the nutritional status of the patient
Provide health education on
 Importance of adherence to medication, resting,
adequate fluid and nutritional intake, signs that
should make patient report to a health care

98. TUBERCULOSIS

99. INTRODUCTION
DEFINITION
 Tuberculosis (TB) is an airborne chronic
infectious disease caused by Mycobacterium
tuberculosis.
 It usually infects the lungs, but it can infect
any part of the body such as the kidney,
spine, and brain except the nails, hair and
teeth.
 If not treated properly,TB disease can be
fatal.

100. Aetiology
 TB disease is caused by a pathogenic bacteria
called Mycobacterium tuberculosis (M.
tuberculosis) from the family
Mycobacteriaceae.
 M. tuberculosis complex species include M.
bovis, M. africanum, M. microti, M. caprae, M.
pinnipedii, M. canetti and M. mungi.
 Most, but not all, of these species have been
found to cause disease in humans.

101. Aetiology
 The majority ofTB cases are caused by M.
tuberculosis.
 M. tuberculosis organisms are also called
tubercle bacilli.

102. Mode of transmission
 TB spreads from person to person by
airborne transmission
 An infected person releases droplet nuclei
through talking, coughing, sneezing, laughing
and singing
 An infectious patient is one with a positive
sputum smear.
 Majority of those infected with theTB bacilli,
their immune system contains the infection &
the bacilli remain dormant for the rest of a
person’s life and do not lead to disease

103. RISK FACTOR FOR TB
 Close contact with someone who has
active TB
 Immunosuppression
 Substance abuse
 Immigration from countries with high
incidences of TB
 Institutionalization
 Overcrowding
 Health care workers

104. CLASSIFICATION OF TB
The following are case definitions used to
classifyTB cases initially:
a) A presumptiveTB case: one who
presents with symptoms or signs suggestive
ofTB
b) Bacteriologically confirmedTB case:
one from whom a biological specimen is
positive by smear microscopy, culture or
WHO-approved rapid diagnostics e.g.
GeneXpert MTB/RIF.

105. CLASSIFICATION OF TB
c) A clinically diagnosedTB case: is one
who does not fulfill the criteria for
bacteriological confirmation but has been
diagnosed with activeTB by a clinician or
other medical practitioner who has decided
to give the patient a full course ofTB
treatment.
◦ This definition includes cases diagnosed on
the basis of X-ray abnormalities or
suggestive histology and extra-pulmonary
cases without laboratory confirmation.

106. CLASSIFICATION OF TB
All bacteriologically confirmed or
clinically diagnosed cases of TB are also
classified according to the following:
1.Anatomical site of disease
2. History of previous treatment
3. HIV status
4. Drug resistance

107. Classification based on anatomical sites
 PulmonaryTB (PTB): Any
bacteriologically confirmed or clinically
diagnosed case ofTB involving the lung
parenchyma or the tracheobronchial tree.
This exclude pleural effusion
 Extra pulmonaryTB (EPTB): Any
bacteriologically confirmed or clinically
diagnosed case ofTB involving organs other
than the lung parenchyma, e.g. pleura, lymph
nodes, abdomen, genitourinary tract, skin,
joints and bones, meninges

108. Classification based on history of
previousTB treatment
a)New patients: one who has never
been treated for TB or has taken anti-
TB drugs for less than one month.
b)Previously treated patients: one
who has received one month or
more of anti-TB drugs in the past.

109. Classification based on history of previousTB
treatment
The previously treated patients are further classified by
the outcome of their most recent course of treatment as
follows:
◦ Relapse patients: previously treated for TB, declared
cured or treatment completed at the end of their most
recent course of treatment, and are now diagnosed
with a recurrent episode of TB.
◦ Treatment after failure patients: previously treated
for TB and whose treatment failed at the end of their
most recent course of treatment.
◦ Treatment after loss to follow-up patients:
previously treated for TB, and declared lost to follow-up
at the end of their most recent course of treatment.

110. Classification based on HIV status
1. HIV-positiveTB patient: Any bacteriologically
confirmed or clinically diagnosed case of TB who has
a positive result from HIV testing conducted at the
time of TB diagnosis or evidence of enrolment in HIV
care.
2. HIV-negativeTB patient: Any bacteriologically
confirmed or clinically diagnosed case of TB who has
a negative result from HIV testing conducted at the
time of TB diagnosis.
3. HIV status unknownTB patient: Any
bacteriologically confirmed or clinically diagnosed
case of TB who has no result of HIV testing and no
evidence of enrolment in HIV care.

111. Classification based on drug resistance
 Drug SusceptibleTB: Any bacteriologically
confirmed case ofTB with no evidence of
resistance to any of the first line anti-TB
medicines
 Drug ResistantTB: Any bacteriologically
confirmed case ofTB with confirmed
resistance to any of the first line medicines.
 It also includes cases with confirmed
resistance to second line anti-TB medicine

112. Pathophysiology
•After inhalation the bacilli passes down the bronchial
system and implant at alveoli where multiplication
takes place.
•The bacilli also spreads to other body regions through
lymph and circulating blood.
•The immune system responds by initiating an
inflammatory reaction
•Phagocytes i.e. neutrophils and macrophages engulf
the bacteria whileTB specific lymphocytes lyse/destroy
the bacteria and normal tissue.
•This tissue reaction results in the accumulation of
exudate in the alveoli.

113. Pathophysiology
•Granulomas, new tissue masses of live and dead bacilli are
surrounded by macrophages which form a protective
wall.
•The new tissue masses are transformed to a fibrous
tissue mass with a central portion called a ghon tubercle.
•The material (bacteria and macrophages) becomes
necrotic forming a cheesy mass.The bacteria become
dormant
•Active disease may occur with reinfection or activation of
dormant bacteria/immunocompromised states.
•The ghon tubercle ulcerates, releasing the cheesy material
into the bronchi.The bacteria becomes airborne, resulting
in the further spread of the disease

114. Clinical manifestations
•Cough of any duration, may be
associated with sputum production that is
blood stained
•Hotness of the body/body temperature
> 37.50 C
•Drenching night sweats
•Unintended weight loss/BMI less than
18.5 of z-score ≤ -2
•Chest pain

115. Clinical manifestations
For children, in addition to the above, the
following should be considered:
•History of frequent respiratory tract
infections
•Failure to Thrive
•Reduced Playfulness
•Lethargy and irritability
•History of contact with a known TB case

116. Diagnosis
•History:TB should be ruled out in any person
presenting with any of the signs and symptoms
ofTB, and history of contact with aTB patient.
The aim of history taking is to rule out other
differential diagnoses ofTB disease – Fungal
pneumonia, COPD, lung abscess, lung cancer,
bronchiectasis, heart failure, sarcoidosis
•Physical signs of TB on respiratory
examination may include tachypnea, bronchial
breath sounds, dullness on percussion, reduced
air entry, fever > 37.50 C, wasting, haemoptysis
and pallor

117. Diagnosis
•Sputum smear microscopy exam – SM
collection procedure
•Sputum culture exam – DST; relapses,
retreatments
•Chest X-rays: consolidation and/or focal
infiltration of upper zones of lobes; patchy
shadows/opacification evidence of cavitations
and scarring (fibrosis), enlarged mediastinal LN
•GeneXpert-a molecular catridge based
automated diagnostic test that can identify M.
tuberculosis and resistance to rifampicin.

118. Diagnosis
•GeneXpert is indicated forTB diagnosis in
HIV+ withTB symptoms; children under 15
yrs withTB symptoms and all smear negative
TB cases

119. Complications of PTB
•Massive haemoptysis
•Chronic pulmonary Aspergillosis
• Lung abscess
• Bronchiectasis
• Spontaneous pneumothorax
• Lung fibrosis

120. TREATMENT OF TB
Aims of treatment
1) Cure patients and therefore prevent
suffering.
2) Prevent transmission of the infection.
3) Prevent death.
4) Prevent long-term complications or
sequelae ofTB.
5) Prevent relapse of the disease.
6) Prevent the development of drug resistant
TB.

121. The principles of TB treatment
1) Never use single drugs
2) Always use drugs in combinations - using
Fixed Dose Combinations (FDCs) to avoid
selection of naturally occurring resistant
mutants to M. tuberculosis
3) Drug dosage is based on weight - to
achieve therapeutic drug levels in the body
and prevent medication side effects

122. The principles of TB treatment
4) Drug intake should be directly observed for
all patients - to ensure adherence, prevent
emergence of drug resistance, assess for
medication side effects and to follow clinical
response closely
5) Ensure the entire treatment is taken as
recommended

123. First line Anti-Tuberculosis Drugs
 Anti-TB drugs should have these properties:
 Bactericidal - the ability to kill the rapidly
dividing, metabolically active bacilli found in
the walls of cavities and in the sputum of
patients with microscopy smear-positive PTB.
E.g. Isoniazid
 Sterilization - the ability to kill the persisting,
dormant or intermittently active bacilli,
responsible for relapses. E.g. Rifampicin and
Pyrazinamide leads to the shortening of
treatment.

124. First line Anti-Tuberculosis Drugs
 There are four drugs used in the first line
treatment ofTB and they include:
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

125. First line Anti-Tuberculosis Drugs
These drugs are given in two phases of
treatment:
 Intensive phase - lasts two months and
usually consists of four drugs.
 Aim is to achieve a rapid killing of actively
dividing bacteria, resulting in the reduction of
bacillary load, negativization of sputum
(within two weeks) and eradication of clinical
symptoms.

126. First line Anti-Tuberculosis Drugs
These drugs are given in two phases of
treatment:
 Continuation phase - lasts four months to
ten months and usually consists of two
drugs.
 Aim is to kill any remaining or dormant
bacilli and preventing subsequent relapse

127. First Line Anti-tuberculous regimen
for Adult Patients
 All forms ofTB exceptTB Meningitis and
osteoarticularTB is 2 RHZE/4 RH
 An intensive/bactericidal phase of 2 months’
of treatment and a continuation/sterilizing
phase of 4 months’ of treatment.
 TB Meningitis and osteo-articularTB has a
regimen of 2 RHZE/10 RH

128. FDC treatment dosage for adults
 Rifampicin 150 mg + Isoniazid 75 mg +
Pyrazinamide 400 mg + Ethambutol 275 mg
(4-FDC tablet RHZE)
 Rifampicin 150 mg + Isoniazid 75mg
(2-FDC tablet RH)
 30-39kg – 2 tablets
 40-54 kg – 3 tablets
 55 - 69 kg – 4 tablets
 Over 70 Kg – 5 tablets

129. First Line Anti-tuberculous regimen
for Adult Patients
 Monthly monitoring of patient weight should
be done and doses adjusted accordingly.
 No trial of therapy should be done to
minimize the emergence of drug resistance.
 For children or adolescents above 30kg treat
as adults
 Administer daily pyridoxine to reduce the
risk of developing peripheral neuropathy.
However, lack of pyridoxine should not stop
TB therapy.

130. First Line Anti-tuberculous regimen
for Adult Patients
Weight (kg) vis dose of pyridoxine
 1-13.9 kg - 12.5mg
 14-25 kg - 25mg
 >25 kg - 50mg

131. Patients withTB may require hospitalization in
certain circumstances:
 Severe forms of PTB and EPTB (e.g.TB
meningitis and pleural effusion)
 Severe malnutrition
 Severe pneumonia
 Other comorbidities e.g. severe anemia,
severe diarrhea, etc
 Court ordered patients to ensure adherence
 Severe adverse reactions such as
hepatotoxicity, severe cutaneous reaction

132. SteroidTherapy
Evidence shows that corticosteroids improve the
morbidity and mortality outcomes in patients
with:
1) TB meningitis
2) TB pericarditis
3) TB Immune Reconstitution Inflammatory
Syndrome in PLHIV
◦ For TB meningitis, dexamethasone in the dose
of 0.4 mg/kg/day is recommended in adults
(>14 years) in conjugation with antitubercular
drugs.
◦ The dose should be reduced over 6–8 weeks.

133. SteroidTherapy
In other conditions, Prednisolone is the preferred
corticosteroid used. It is administered in a
tapering dosage over 7 weeks
Adult and Children>30kg
Weeks 1-4 : 1mg/kg (max 60mg)
Weeks 5-6 : 0.5mg/kg
Week 7 : 0.25mg/k
Adult and Children< 30kg
Weeks 1-4 : 1-2mg/kg (max 60mg)
Weeks 5-6 : 0.5-1mg/kg
Week 7 : 0.25-0.5 mg/kg

134.  Read and make notes on the most
common adverse effects to first line anti-
TB medicines and their management

135. Nursing management
Nursing diagnoses
 Ineffective breathing pattern related to decreased
lung capacity
 Nutrition imbalance less than body requirements
related to chronic poor appetite, fatigue and
productive cough
 Non compliance related to lack of knowledge of
disease process, lack of motivation and long term
nature of treatment
 Decreased activity tolerance related to fatigue,
decreased nutritional status and chronic febrile
episodes

136. Nursing management
 Promote airway clearance by increasing fluid
intake.
 Advocating adherence to treatment regimen
through patient teaching
 Progressive activity schedule that enhances
tolerance to activities
 A nutritional plan that allows for small,
frequent meals is required

137. Nursing management
 Educate patient on Cough hygiene and hand
washing to minimize spread of infection.
 Initiate contact tracing
 Need to isolate the infectious cases; well
ventilated rooms. High Efficiency Particulate
Air (HEPA) masks