CLINICAL NURSE SPECIALIST :CLINICAL NURSE SPECIALIST Abstract The role of the clinical nurse

specialist is critical to improving patient care and staff development and linking professional practice
to evidenced-based outcomes at the patient, unit, and organizational levels. Today more than ever,
the role of the clinical nurse specialist is vital to insuring the provision of quality patient care. As a
member of the leadership team, the clinical nurse specialist is able to directly affect patient care by
responding to the needs of the patient, novice clinician, and expert practitioner LaSala, C. A., Connors,
P. M., Pedro, J. T., Phipps, M. (2007).

Clinical nurse specialist requirements:Clinical nurse specialist requirements A clinical nurse specialist
(CNS) is an advanced practice nurse who has completed a specialized graduate degree
program—either a master's degree or a doctorate to become an expert in a particular type of nursing

STRENGHTS:STRENGHTS • Knowledge of relevant trends in their specialty area Use of Evidence Based
Practice • Understanding of and closeness to patient care, that is the core business of the
organization • Ability to see the big picture, and also specific details within a patient’s care plan, or
unit situation • Ability to network across the organization, in nursing and with other disciplines and
departments Henderson, S. (2004).

opportunities:opportunities Increased autonomy, greater access to reimbursement, and the

increasing demand for cost-effective quality care will lead to greater opportunities for all advanced
practice nurses, including the clinical nurse specialist. With legislative changes and acquisition of new
skills and knowledge, the CNS will assume increased responsibility as a member of the health care
team. Henderson, S. (2004).

weakness:weakness Lack of knowledge from other healthcare disciplines of the importance of the
CNSs contribution to the Healthcare System. CNS’ need to be able to defend their services through
the production of business plans demonstrating the benefits of their role in terms of national policy
and patients outcomes. (Fletcher, 2011).

THREADS:THREADS The clinical nurse specialist must remain vigilant against cost-containing actions
and those who are inclined to view the retention of the clinical nurse specialist as a luxury . They must
clearly establish the importance or their role in the health care system. Redekopp, 1997 .

REFERENCE:REFERENCE Buppert, C- (2002). Billing for nurse practitioner services. Retrieved October
26, 2003, from http://www.meciscape.com/ newarticle/422935 Henderson, S. (2004). The role of the
clinical nurse specialist in medical-surgical nursing. MEDSURG Nursing, 13(1), 38-41 LaSala, C. A.,
Connors, P. M., Pedro, J. T., Phipps, M. (2007). The Role of the Clinical Nurse Specialist in Promoting
Evidence-Based Practice and Effecting Positive Patient Outcomes. The Journal of Continuing Education
in Nursing, 38(6), 262-270. McMyler. E.T, S Milier, D.J. (1997). Two graduating master's students
struggle to find meaning. Clinical Nurse Specialist, 11, 169-172. Redekopp, M.A. (1997). Clinical nurse
specialist role contusion: The need for identity. Clinical Nurse Specialist. 11. 87-90.

Background: Definition and R equirements A CNS is defined as: Advanced practice nurses that bring
specialized knowledge to the practice setting Requirements: Study and supervised clinical practice at
the graduate level, and has become an expert in a defined area of knowledge and practice in a
selected clinical area of nursing. (American Association of Colleges of Nursing, 2017), (Cockerham,
2014)

Background: Specialities and Scope of Practice:Background: S pecialities and S cope of P ractice

Specialities : Oncology, pediatrics, geriatrics, psychiatric/mental health, adult health, acute critical
care , community health , etc. Scope of Practice: Autonomy Leadership Present within many
Jurisdictions (American Association of Colleges of Nursing, 2017), (Cockerham, 2014)

Competencies/Standards of Care::Competencies/Standards of C are : Direct care Consultation

Systems Leadership Collaboration Coaching Research Ethical Decision-Making, Moral Agency and
Advocacy

Roles: :Roles: Optimize patient care Make decisions Develop specialized treatment plans Educate
Promote Teamwork Analyze Data Research

Challenges::Challenges: Role clarity Moving evidence into practice Effective change management
Prioritization and time management Demonstrating benefits to the organization

Future Role Development: :Future R ole D evelopment : Research has indicated CNS roles have
assisted with: Improving patient outcomes Enhancing Nursing Practice based upon EBP research
Providing an additional resource for nursing staff Facilitating multidisciplinary approaches with
complex cases Utilizing enhanced skillsets to educate nursing staff with a goal of optimizing patient
outcomes and patient safety (NACNS, 2017), (LaSala, Connors, Pedro, & Phipps, 2007)

Summary: :Summary: A CNS-APN offers a wide variety of enhanced patient care knowledge/skills and
is apparent across many sub-specialties of patient care Despite its challenges, a CNS can assist with: (1)
Optimizing patient outcomes, (2) Enhance nursing practice through EBP research, and (3) Assist with
utilizing a multidisciplinary approach to assist with complex patient cases

References: :References: American Association of Colleges of Nursing . (2017, June 12). Retrieved
from http://www.aacn.nche.edu/publications/position/CNS.pdf Cockerham, A., Keelling, A (2014). A
Brief History of Advanced Practice Nursing in the United States (Ed.), Advanced practice nursing: an
integrative approach (5 th ed.) (pp. 1-21). St Louis, MI: Elsevier. CNS Careers | Clinical Nurse Specialist
Job Duties and Career Paths. (n.d.). Retrieved June 16, 2017, from
http://www.allnursingschools.com/clinical-nurse-specialist/job-description/ Home. (n.d.). Retrieved
June 16, 2017, from
http://nacns.org/professional-resources/practice-and-cns-role/cns-competencies/core-competencies
/ LaSala, C., Connors, P., Pedro, J., & Phipps, M. (2007). The role of the clinical nurse specialist in
promoting evidence-based practice and effecting positive patient outcomes. Journal Of Continuing
Education In Nursing , 38 (6), 262-270. Retrieved from
http://web.b.ebscohost.com.ezproxy.morningside.edu:2048/ehost/pdfviewer/pdfviewer?vid=3&sid=
950d03c3-9e12-480f-b5a4-c47f3c57c7c8 %40sessionmgr103&hid=123 National Association of Clinical
Nurse Specialists (NACNS) . (2017). What is a CNS? Retrieved from
http://nacns.org/about-us/what-is-a-cns/ (n.d.). Retrieved June 16, 2017, from
http://www.nursingworld.org/MainMenuCategories/ANAMarketplace/ANAPeriodicals/OJIN/TableofC
ontents/Vol-19-2014/No2-May-2014/Challenges-in-CNS-Education-and-Practice.html

The role of Advanced Nurse Practitioner is invaluable. It provides opportunity for patients to receive
timely care and negate unnecessarily delay in receiving treatment, especially with the growing
shortage of GPs in primary care. ANPs in the community and primary care are able to develop close,
long-term relationships with their patients and work in partnership with them to achieve optimum
health. Advanced Nurse Practitioners are autonomous in making decisions based on assessment,
diagnosis and interpretation of test results. ANPs are able to independently prescribe appropriate
medication, evaluate or refer to other specialists if necessary.

While I acknowledge the fact that Health Education England has now developed a definition of
Advanced Nurse Practice and the Royal College of Nursing has developed a credentialing system as
steps to formal recognition of the individual nurse’s or midwife’s practice at ANP level, more needs to
be done.

There are still some big issues in terms of lack of full recognition of the role, and lack of appropriate
remuneration compared to similar jobs of equal value. There is also the need for registration of ANPs
on the NMC professional register in order to give public assurance and safeguard patient safety. I call
on the RCN and the Queen’s Nursing Institute to lobby the government for proper recognition of the
role of the ANPs and demand for appropriate remuneration with similar weighting, to match similar
jobs of equal value.

I am an advocate of the ANP role as I have worked and led on developing the role within the
community, primary, urgent and emergency care for several years. I have been instrumental in
shaping workforce transformation including teaching and mentoring nurses and allied healthcare
professionals including pharmacists and physiotherapists.

Coping with a complex and evolving environment like the NHS demands expertise in evidence-based
practice, service transformation, and implementation of new strategies in managing patient care and
healthcare workforce through traditional and non-traditional ways. We need to have practitioners
with advanced nursing, leadership and management skills. Do not be afraid to stand up and be
counted amongst them.

EFINITION:DEFINITION It is an inflammation of lung parenchyma i.e caused by microbial agent It is

usually associated with increased in interstitial & alveolar fluid. Currently pneumonia is the sixth most
common cause of death for all ages. I

Etiology:Etiology There are many causes of pneumonia & it include: Bacterial: pneumococcal
pneumonia : caused by– streptococcus pneumoniae. Staphylococcus pneumonia: caused by—
staphylococcus aureus . Gram –ve bacterial pneumonia: caused by- klebsiella pneumonia . Anaerobic
bacterial pneumonia: caused by normal oral flora.
Cont……….d:Cont……….d b) Viruses: Viral pneumonia: caused by influenza a virus . c) Mycoplasm :
mycoplasma pneumonia: caused by mycoplasma microorganism . d) Fungal agents : Fungal
pneumonia: caused by histoplasmosis ,candidiasis. e) Protozoa : parasitic pneumonia common
organism is pneumocystis carinii .

Cont………d:Cont………d Nosocomial pneumonia is acquired within a hospital in a patient admitted to

the hospital for something else. Risk increased with an underlying illness, recent surgery, recent
intubation, and in persons already on antibiotics for something else.

Etiology :Etiology Pneumonia may also result from aspiration of food ,fluid ,vomitus ,inhalation of
toxic or caustic chemicals ,smoke ,dust or gases. OTHER RISK FACTORS Advanced age A history of
smoking URTI Prolonged Tracheal intubation Prolonged bed rest & immobility. Chronic disease. HIV
infection.

Cont…………..d:Cont…………..d Immunosuppressive therapy Nonfunctional immune system

Malnutrition Dehydration chronic lung disease Additional risk factor : exposure to air
pollution ,alcoholism ,inhalation of noxious substances ,aspiration of food ,liquid ,foreign or gastric
material.

Segments affected from pneumonia :Segments affected from pneumonia a) BRONCHIAL PNEUMONIA
it involves the terminal bronchial and alveoli.

b) LOBAR PNEUMONIA:b) LOBAR PNEUMONIA It involves one or more entire lobes.

3)Segmental pneumonia:3)Segmental pneumonia It involves the a segment of lobes.

4) Bilateral pneumonia:4) Bilateral pneumonia It affects the lobes in both lungs.

5) Interstitial pneumonia:5) Interstitial pneumonia It is also called reticular pneumonia. It involves

inflammatory response within the lung tissues surrounding the airspaces.

6) Alveolar pneumonia:6) Alveolar pneumonia It is also acinar pneumonia. There is fluid accumulation
in a lung distal air spaces. 7) Necrotizing pneumonia : it causes the death of a portion of lung tissues. X
ray examination reveal cavity at the formation at the site of necrosis. Necrotic lung tissue ,which does
not heal constitutes a permanent loss of functioning parenchyma.

PATHOPHYSIOLOGY:PATHOPHYSIOLOGY Invasion of microbes . Inflammation of airway . Filling of

inflammatory exudates in alveolar air spaces. Lung consolidation .( The process of becoming a firm
solid mass, as in an infected lung when the alveoli are filled with exudate ) Impaired gas exchange .
Hypoxia

CLINICAL MANIFESTATION:CLINICAL MANIFESTATION Rapidly rising fever. sweats Shaking chills.

Pleuritic chest pain. Tachypnoea. Cough & sputum production

Cont……….d:Cont……….d Hemoptysis ,dyspnea ,headache ,fatigue Chest auscultation reveals bronchial

breathe sounds Tactile fremitus is usually increased .

DIAGNOSTIC EVALUATION.:DIAGNOSTIC EVALUATION. Lab investigations Gram staining Chest X-ray

Sputum culture analysis Hypersensitivity test ABG analysis to asses the need for supplemental o2.

Medical management :Medical management May need admission to hospital if patient has a high
fever, shortness of breath, or in shock. Bed rest, plenty of fluids, and Tylenol for pain are usually
sufficient for mild uncomplicated cases.

CONT.:CONT. Antibiotic therapy are used for treatment such as penicillin , amoxicillin , augmentin ,
erythromycin , zithromax , cephalosporin , depending upon the causative bacteria. General antibiotics
(e.g., erythromycin) may be given until the cultures come back from the lab, then changed to the
appropriate antibiotic.

CONT..:CONT.. Antivirus medications such as Amantadine ( Influenza A and B) or Ribavirin are

available . Postural drainage Chest physiotherapy Tracheal suctioning

CONT.:CONT. Intravenous (IV) fluids should be started. Oxygen should be administered as ordered.
Bronchodilator medication If one has TB or other dangerous forms of Pneumonia , isolate from other
patients. If unable to breathe, respiratory support is provided .

CONT.:CONT. Follow up laboratory tests and X-Ray s are done to check treatments. Medical follow up
after discharge and a repeat X-Ray in 6-9 weeks.

COMPLICATIONS:COMPLICATIONS Shock & Respiratory failure Atelectasis & Pleural effusion

NURSING MANAGEMENT:NURSING MANAGEMENT NURSING ASSESSMENT 1.Change in temperature.

2.Amount, odour & colour of secretions. 3.Frequency & severity of cough. 4.Changes in chest X-ray
finding. .

CONT.:CONT. 5.Change in physical assessment findings. 6.Changes in chest X-ray finding. 7.Altered
mental status , dehydrations , excessive fatigue , heart failure.
DIAGNOSIS:DIAGNOSIS Ineffective airway clearance related to copious tracheobronchial secretions.
Activity intolerance related to impaired respiratory function. Risk for deficient fluid volume related to
fever & dyspnea.

CONT.:CONT. Imbalanced nutrition less than body requirements. Deficient knowledge about the
treatment regimen & preventive heath measures.

NURSING INTERVENTIONS:NURSING INTERVENTIONS Improving airway patency Removing secretions

that interfere gas exchange. Encourage hydration. Coughing can be initiated Encourage increased
fluid intake

CONT..:CONT.. Employ postural drainage to loosen &mobilize secretions. Auscultate the chest for
crackles & rhonchi.

CONT.:CONT. Administer cough suppressants if cough is non-productive. Mobilize the patient to

improve secretion clearance & reduce risk of atelectasis . & worsening pneumonia.

MAINTAINING NUTRITION:MAINTAINING NUTRITION Provide fluid with electrolyte. Enriched drinks or

shakes may be helpful.

PROMOTING REST & CONSERVING ENERGY:PROMOTING REST & CONSERVING ENERGY Give
ventilated room for rest. Give comfort position. Change the position periodically.

PROMOTING PATIENT’S KNOWLEDGE:PROMOTING PATIENT’S KNOWLEDGE Instruct the cause of

pneumonia , management , complication ,need for follow up. Instruct how he can recover from it.

Monitor for complications:Monitor for complications Monitor vital signs, oximetry at regular intervals
to assess the patient’s response to therapy .

Cont……….:Cont………. Assess for resistance fever or returns of fever , potentially indicating bacterial
resistance to antibiotics. Auscultate lungs and heart. Heart murmurs or friction rub may indicate acute
bacterial endocarditis , pericarditis or myocarditis .

Relieving pleuritic pain:Relieving pleuritic pain Place in a comfortable position for resting & breathing.
Encourage frequent change of position to prevent pooling of secretions. Demonstrate how to splint
the chest while coughing. Avoid suppressing a productive cough .
Cont…..:Cont….. Administer prescribed analgesics agent to relief pain. Encourage modified bed rest .
Watch for abdominal distension ,which may be due to swallowing of air during intervals of severe
dysponea.

EXPECTED OUTCOMES:EXPECTED OUTCOMES Cyanosis and dyspnoea reduced,ABG levels improved.

Coughs effectively,absence of crackles. Appears more comfortable. Free from pain. Fever controlled.
No signs of resistant infection.

PATIENT EDUCATION & HEALTH MAINTAINENCE:PATIENT EDUCATION & HEALTH MAINTAINENCE

Advice the patient that fatigue & weakness may be prolonged after pneumonia.

Cont…….:Cont……. Encourage chair rest after fever subsides , Encourage breathing exercise.

Cont…..:Cont….. Explain that a chest X- ray is taken 4 to 6 weeks after recovery to evaluate lungs for
clearing & detect any tumour or cause. Advice smoking & alcohol cessation.

Cont….:Cont…. Advice to take good nutrition. Encourage yearly immunization. Practice frequent hand
washing. Advice avoidance of contact with people who have upper respiratory infection

PREVENTION:PREVENTION Vaccination -- against measles, Influenza , Pneumococcal p., especially in

those over age 65 and other diseases Bed-ridden individuals -- avoid prolonged bed rest, perform
exercises in bed, breathing and coughing exercises before and after an operation.

CONT…:CONT… Avoid alcohol, drugs, NGT feeding Avoid smoking Avoid taking antibiotics for viral
Pneumonia Foods high in vitamins, minerals, and other nutrients.

BIBLIOGRAPHY:BIBLIOGRAPHY Sandra m et al,” manual of nursing practice “. Vol 1, 8 th ed, Jaypee

brothers medical publishers; India , 286 -2 89. Smeltzer, c.suzanne, Bare,G.Brenda, “medical surgical
nursing”, 10 th ed :lippincott raven publishers; Pp-520-532 Joyce M Black & J. Hawks,”medical surgical
nursing”,vol 2,7 th ed, Elsavier publishers, Pp -1710-1720. www.goggle.com
omicillary treatment of pneumonia :
Domicillary treatment of pneumonia Give Cotrimoxazole (trimethoprim[T] + Sulfamethozazole[S]) (5-7 mg/kg/day of T + 25-35
mg/kg/day of S) in two divided doses for 5 days OR Amoxicillin (30-40 mg/Kg/day) in 2-3 divided doses for 3-5 days Follow-up after 2
days Ask: Is the child breathing slower? Is there less fever? Is the child eating better? YES ---- complete 5 days of cotrimoxazole or 3-5
days of Amoxicilin *Check for danger signs NO CONTINUE ANTIBIOTICS x 5 day * Assess difficult breathing and Chest Indrawing
YES REFER CONTINUE ANTIBIOTICS for 5days REFER FOR HOSPITILIZATION COMPLETE 5 days of Cotrimozazole OR 3- 5
days Amoxicili

Definition • Is an inflammatory process of the lung parenchyma that is commonly caused by infectious agents. OR • Pneumonia is
inflammation (swelling) of the tissue in one or both of your lungs. It is usually caused by an infection

7. Classification of pneumonia According to causes • Bacterial (the most common cause of pneumonia) • Viral pneumonia • Fungal
pneumonia • Chemical pneumonia (ingestion of kerosene or inhalation of irritating substance) • Inhalation pneumonia (aspiration
pneumonia). •

8. According to areas involved • Lobar pneumonia; if one or more lobe is involved. • Broncho-pneumonia; the pneumonic process has
originated in one or more bronchi and extends to the surrounding lung tissue.
9. Conti… • According to the manner in which the infection was acquired: This type of infection is acquired in the community and the
causative organism is one that is prevalent in the community at the time. • • Hospital acquired /nasocomian pneumonia:-this type of
infection is acquired in a health care institution due to cross infection and the causative organism is one that lead to infection. •

10. Predisposing factors • Immuno-suppresed patients. • Cigarette smoking. • Difficult swallowing (due to stroke, dementia,parkinsons
disease, or other neurological conditions). • Impaired consciousness ( loss of brain function due to dementia, stroke, or other
neurological conditions).

11. Conti…. • Chronic lung disease (COPD, bronchostasis) • Frequent suction • Other serious illness such as heart disease, liver
cirrhosis, and DM, recent cold, laryngitis or flu.

12. Pathophysiology • The streptococci reach the alveoli and lead to inflammation and pouring of exudates into the air spaces. WBCs
migrate to alveoli, the alveoli become thicker due to its filling consolidation, and involved areas by inflammation are not adequately
ventilated, due to secretion and edema.

13. Conti…. • This will lead to partial occlusion of alveoli and bronchi causing a decrease in alveolar oxygen content. Venous blood that
goes to affected areas without being oxygenated and returns to the heart. This will lead to arterial hypoxemia and even death due to
interference with ventilation.

14. Sign and Symptoms • Shaking chills • Rapidly rising fever ( 39.5 to 40.5 degree) • Stabbing chest pain aggravated by respiration
and coughing • Tachypnea, nasal flaring • Patient is very ill and lies on the affected side to decrease pain • Use of accessory muscles of
respiration e.g. abdomen and intercostals muscles • Cough with purulent, blood tinged, rusty sputum. • Shortness of breath. • Flushed
cheeks. • Loss of appetite, low energy, and fatigue. • Cyanosed lips and nail beds.

15. Physical Examination • • Chest x-ray • Blood test • History taking • Sputum culture •

16. Nursing management • Maintain a patent airway and adequate oxygenation. • Obtain sputum specimens as needed. • Use suction
if the patient can’t produce a specimen. • Perform chest physiotherapy. • Provide a high calorie, high protein diet of soft foods. • To
prevent aspiration during nasogastric tube feedings, check the position of tube, and administer feedings slowly. • Provide a quiet, calm
environment, with frequent rest periods. • Monitor the patient’s ABG levels, especially if he’s hypoxic. • Assess the patient’s respiratory
status, auscultate breath sounds at least every 4 hours

17. Preventive measures • You can help stop germs spreading to others by practising good hygiene, For example: When you cough or
sneeze, cover your mouth and nose with a tissue to catch the germs Throw used tissues away immediately, in a bin or toilet – germs
can live for several hours after they leave your nose or mouth. Wash your hands regularly, to avoid transferring germs to anyone else
or other objects. • Frequent turning of bed ridden patients and early ambulation as much as possible. • Coughing and breathing
techniques. • Sterilization of respiratory therapy equipment • Suctioning of secretion in the unconscious who have poor cough and
swallowing reflexes, to prevent aspiration of secretions and its accumulation.

18. Conti…. Vaccinations To help protect against pneumonia, people in higher risk groups should be vaccinated. The recommended
vaccinations are: The pneumonia jab (pneumococcal vaccination), which protects against pneumococcal infection Life style Smoking,
alcohol misuse and intravenous drug abuse can increase your risk of developing pneumonia.

19. Conti… Smoking • Smoking damages your lungs, which means they become infected more easily. • If you smoke, the best thing
you can do to prevent pneumonia is quit smoking.

20. Conti…. • Alcohol misuse Excessive and prolonged alcohol misuse is known to weaken your lungs' natural defenses against
infections, making you more vulnerable to pneumonia. One study found 45% of people admitted to hospital with pneumonia had an
alcohol misuse problem. Alcohol misuse is defined as regularly drinking over the recommended weekly limits (21 units of alcohol for
men and 14 units of alcohol for women). • Not only does alcohol misuse increase your risk of developing pneumonia, it also increases
your risk of it being more serious. It is estimated that people who misuse alcohol are three to seven times more likely to die from
pneumonia than the general population. If you drink alcohol, do not exceed recommended daily limits (three to four units a day for men
and two to three units a day for women).

21. Prognosis With treatment, most patients will improve within 2 weeks. Elderly or very sick patients may need longer treatment.

22. Treatment • Antibiotic, depending on sputum and blood culture • Oxygen therapy • Chest physiotherapy • Monitor the patient’s ABC
levels, especially if he’s hypoxic. • Monitor fluid intake and output.

23. Complication • Acute respiratory distress syndrome (ARDS) • Pleural effusion • Lung abscesses • Respiratory failure (which
requires mechanical ventilator) • Sepsis, which may lead to organ fail

24. Refference 1. Bickey L.S. (2003), Bates Guide to Physical Examination. Textbook. 2. (8th Ed): Elsevier St Louis, Missouri. 3.
Dirksen.L.H (2004), Medical Surgical Nursing. Textbook. (3th Ed): Elsevier St Louis, Missouri. 4. Fausi. B. (1998), Principles of internal
medicine. Volume 2, page 1419-1426. Textbook. (14th Ed): New York. St Louis. 5. Luckman J. (2004) Medical- Surgical
Nursing.Volume 4, page 550-557. Textbook. (4th Ed): Elsevier St Louis, Missouri.

Definition • Is an inflammatory process of the lung parenchyma that is commonly caused by infectious agents. OR • Pneumonia is
inflammation (swelling) of the tissue in one or both of your lungs. It is usually caused by an infection

7. Classification of pneumonia According to causes • Bacterial (the most common cause of pneumonia) • Viral pneumonia • Fungal
pneumonia • Chemical pneumonia (ingestion of kerosene or inhalation of irritating substance) • Inhalation pneumonia (aspiration
pneumonia). •

8. According to areas involved • Lobar pneumonia; if one or more lobe is involved. • Broncho-pneumonia; the pneumonic process has
originated in one or more bronchi and extends to the surrounding lung tissue.

9. Conti… • According to the manner in which the infection was acquired: This type of infection is acquired in the community and the
causative organism is one that is prevalent in the community at the time. • • Hospital acquired /nasocomian pneumonia:-this type of
infection is acquired in a health care institution due to cross infection and the causative organism is one that lead to infection. •
10. Predisposing factors • Immuno-suppresed patients. • Cigarette smoking. • Difficult swallowing (due to stroke, dementia,parkinsons
disease, or other neurological conditions). • Impaired consciousness ( loss of brain function due to dementia, stroke, or other
neurological conditions).

11. Conti…. • Chronic lung disease (COPD, bronchostasis) • Frequent suction • Other serious illness such as heart disease, liver
cirrhosis, and DM, recent cold, laryngitis or flu.

12. Pathophysiology • The streptococci reach the alveoli and lead to inflammation and pouring of exudates into the air spaces. WBCs
migrate to alveoli, the alveoli become thicker due to its filling consolidation, and involved areas by inflammation are not adequately
ventilated, due to secretion and edema.

13. Conti…. • This will lead to partial occlusion of alveoli and bronchi causing a decrease in alveolar oxygen content. Venous blood that
goes to affected areas without being oxygenated and returns to the heart. This will lead to arterial hypoxemia and even death due to
interference with ventilation.

14. Sign and Symptoms • Shaking chills • Rapidly rising fever ( 39.5 to 40.5 degree) • Stabbing chest pain aggravated by respiration
and coughing • Tachypnea, nasal flaring • Patient is very ill and lies on the affected side to decrease pain • Use of accessory muscles of
respiration e.g. abdomen and intercostals muscles • Cough with purulent, blood tinged, rusty sputum. • Shortness of breath. • Flushed
cheeks. • Loss of appetite, low energy, and fatigue. • Cyanosed lips and nail beds.

15. Physical Examination • • Chest x-ray • Blood test • History taking • Sputum culture •

16. Nursing management • Maintain a patent airway and adequate oxygenation. • Obtain sputum specimens as needed. • Use suction
if the patient can’t produce a specimen. • Perform chest physiotherapy. • Provide a high calorie, high protein diet of soft foods. • To
prevent aspiration during nasogastric tube feedings, check the position of tube, and administer feedings slowly. • Provide a quiet, calm
environment, with frequent rest periods. • Monitor the patient’s ABG levels, especially if he’s hypoxic. • Assess the patient’s respiratory
status, auscultate breath sounds at least every 4 hours

17. Preventive measures • You can help stop germs spreading to others by practising good hygiene, For example: When you cough or
sneeze, cover your mouth and nose with a tissue to catch the germs Throw used tissues away immediately, in a bin or toilet – germs
can live for several hours after they leave your nose or mouth. Wash your hands regularly, to avoid transferring germs to anyone else
or other objects. • Frequent turning of bed ridden patients and early ambulation as much as possible. • Coughing and breathing
techniques. • Sterilization of respiratory therapy equipment • Suctioning of secretion in the unconscious who have poor cough and
swallowing reflexes, to prevent aspiration of secretions and its accumulation.

18. Conti…. Vaccinations To help protect against pneumonia, people in higher risk groups should be vaccinated. The recommended
vaccinations are: The pneumonia jab (pneumococcal vaccination), which protects against pneumococcal infection Life style Smoking,
alcohol misuse and intravenous drug abuse can increase your risk of developing pneumonia.

19. Conti… Smoking • Smoking damages your lungs, which means they become infected more easily. • If you smoke, the best thing
you can do to prevent pneumonia is quit smoking.

20. Conti…. • Alcohol misuse Excessive and prolonged alcohol misuse is known to weaken your lungs' natural defenses against
infections, making you more vulnerable to pneumonia. One study found 45% of people admitted to hospital with pneumonia had an
alcohol misuse problem. Alcohol misuse is defined as regularly drinking over the recommended weekly limits (21 units of alcohol for
men and 14 units of alcohol for women). • Not only does alcohol misuse increase your risk of developing pneumonia, it also increases
your risk of it being more serious. It is estimated that people who misuse alcohol are three to seven times more likely to die from
pneumonia than the general population. If you drink alcohol, do not exceed recommended daily limits (three to four units a day for men
and two to three units a day for women).

21. Prognosis With treatment, most patients will improve within 2 weeks. Elderly or very sick patients may need longer treatment.

22. Treatment • Antibiotic, depending on sputum and blood culture • Oxygen therapy • Chest physiotherapy • Monitor the patient’s ABC
levels, especially if he’s hypoxic. • Monitor fluid intake and output.

23. Complication • Acute respiratory distress syndrome (ARDS) • Pleural effusion • Lung abscesses • Respiratory failure (which
requires mechanical ventilator) • Sepsis, which may lead to organ fail

24. Refference 1. Bickey L.S. (2003), Bates Guide to Physical Examination. Textbook. 2. (8th Ed): Elsevier St Louis, Missouri. 3.
Dirksen.L.H (2004), Medical Surgical Nursing. Textbook. (3th Ed): Elsevier St Louis, Missouri. 4. Fausi. B. (1998), Principles of internal
medicine. Volume 2, page 1419-1426. Textbook. (14th Ed): New York. St Louis. 5. Luckman J. (2004) Medical- Surgical
Nursing.Volume 4, page 550-557. Textbook. (4th Ed): Elsevier St Louis, Missouri.

Introduction

Pneumonia is defined as "inflammation of the lung caused by bacteria, in which the air sacs (alveoli)
become filled with inflammatory cells and the lungs become solid"[1]

https://www.slideshare.net/ksuneet/lung-cancer-8943833

. ymptoms - Signs of Lung Cancer Symptom / Signs Cough 74% Dyspnea 37% Hemoptysis 57% Recurrent
Pneumonia Chest Pain, Wheezing 25% Dysphagia Laryngeal Nerve Paralysis 18% Horners Syndrome
Pancoast Syndrome Superior Vena Cava Syndrome Atelectasis Pleural Effusion
. 8. Pathological ClassificationNon Small Cell Lung Cancer Small Cell Lung Cancer(NSCLC)
(SCLC)Squamous Cell Carcinoma 25 – 30% Oat Cell CarcinomaAdenocarcinoma 35-40% Intermediate Cell
CarcinomaLarge Cell Carcinoma 10-15% Combined Cell Carcinoma
. 9. TNM Staging (AJC CS ERR)Primary Tumor - TT1 Tumor <3cm without invasion more proximal than lobar
bronchusT2 Tumor >3cm OR of any size with any of the following - Invades Visceral Pelura - Atelectasis of
less than entire lung - Proximal extent of at least 2cm from carinaT3 Tumor of any size with any of the
following - Invasion of Chest Wall - Invasion of Diaphragm, Mediastinal Pleura, Pericardium - Atelectasis
involving entire lung - Proximal extent within 2cm of carinaT4 Tumor of any size with any of the following -
Invasion of mediastinum - Invasion of heart or great vessels - Invasion of vertebral body - Presence of
malignant pleural or pericardial effusion - Satellite tumor nodes within same lobe as primary tumor
. 10. TNM StagingNodal Involvement - NN0 No regional node involvementN1 Involvement of ipsilateral hilar
or ipsilateral peribronchial nodesN2 Involvement of ipsilateral mediastinal or subcarinal nodesN3
Involvement of contralateral mediastinal or hilar nodes OR Ipsilateral or contralteral scalene or
supraclavicular nodesMetastasis - MM0 Distant Metastasis absentM1 Distant Metastasis present
. 11. Stage IStage IA T1 N0 M0Stage IB T2 N0 M0
. 12. Stage IIStage IIA T1 N1 M0Stage IIB T2 N1 M0, T3 N0 M0
. 13. Stage IIIa Stage IIIA T3 N1 M0, T1-3 N2 M0
. 14. Stage IIIb Stage IIIB Any T N3 M0, T4 Any N M0
. 15. Stage IV Stage IV Any T Any N M1
. 16. Investigations for Lung Cancer
. 17. InvestigationsDiagnostic Tests Staging TestsChest X-Ray CT Scan - Chest, Brain,
AbdomenBronchoscopy PET ScanUltrasound Guided Biopsy Bone ScintigraphyCT guided Biopsy
Mediastinoscopy Bone Marrow Biopsy
. 18. Chest X-Ray – Diagnostic
. 19. Fiberoptic Bronchoscopy - Diagnostic Bronchoscopy Video
. 20. Ultrasound Guided Biopsy - Diagnostic
. 21. CT Guided Biopsy - Diagnostic
. 22. CT Scan - STAGING
. 23. PET Scan for STAGING
. 24. Fused PET and CT Scan
. 25. Mediastinoscopy for STAGING
. 26. Bone Scintigraphy for STAGING
. 27. Bone Marrow Aspiration - STAGING
. 28. Current Treatments for NSCLC
. 29. Treatment Options SURGERY TARGETED RADIOTHERAPY THERAPY CHEMOTHERAPY
. 30. Treatment by Stages of CancerStage Description Treatment OptionsStage Ia – Ib Tumor localized in
lung Surgical resectionStage IIa – IIb Tumor spread to local lymph nodes Surgical resectionStage IIIa Tumor
spread to regional lymph Chemotherapy followed nodes in trachea, chest above by radiation or surgery
diaphragmStage IIIb Tumor spread to contra lateral Combination of lymph nodes Chemotherapy and
RadiationStage IV Tumor metastasis to organs outside Chemotherapy and or chest palliative care
. 31. Surgery – Wedge, Lobectomy, Pneumonectomy
. 32. Radiation Therapy Treatment of stage I and stage II NSCLC, radiation therapy alone is considered
when surgical resection is not possible. Role of radiation therapy as surgical adjuvant therapy after
resection of the primary tumor is controversial. Radiation therapy reduces local failures in completely
resected (stages II and IIIA) NSCLC but has not been shown to improve overall survival rates. Radiation
therapy alone used as local therapy has been associated with 5-year survival rates of 12-16% in early-stage
NSCLC (ie, T1 and T2 disease). No randomized trials have directly compared radiation therapy alone with
surgery in the management of early- stage NSCLC
. 33. Chemotherapy Only 30% of patients with NSCLC become eligible for surgical resection 50% of
patients who undergo resection experience either a local or systemic relapse of cancer 80% of patients with
NSCLC end up taking some sort of chemotherapy Combination chemotherapy has better survival rates
than single agent chemotherapy, which has potentially no role in curative therapy of NSCLC. Adjuvant
chemotherapy (after surgery) has failed to elicit any benefits, however neoadjuvant chemotherapy (given
prior to surgery) has improved survival in patients with Stage IIIa disease.
. 34. Chemotherapeutic AgentsDrug Mechanism of Action ToxicityCisplatin / Carboplatin Causes intrastrand
and interstrand cross- Tinnitus, Hearing Loss, linking of DNA, - strand breakage Toxic Neuropathy,
MyelotoxicVinorelbine It inhibits tubulin polymerization during G2 Granulocytopenia, phase of cell division
Constipation, FatigueGemcitabine Antimetabolite that acts as inhibitor of DNA Myelosuppression, Flu
synthesis like symptoms, Hemolytic Uremic Syndrome, Lung toxicityPaclitaxel Inhibits tubulin
depolymerization in spindle Myelosuppression, during cell division neuropathy, hypersensitivityPemetrexed
disodium Disrupts folate-dependent metabolic Fatigue, processes essential for cell replication.
myelosuppression, Infection, GI toxicityDocetaxel Inhibits cancer cell growth by promoting Myelosuppression,
fluid assembly and blocking disassembly of retention, HSN rxns microtubulesEtoposide Causes single
strand breaks in DNA, inhibits Myelosuppression, repair of DNA Transient Hypotension
 . 35. Targeted Therapy
. 36. What are “targeted therapies”? Cytotoxic vs. Cytostatic Primarily target malignant cells Target
molecules involved in: ◦ cell growth signal transduction ◦ angiogenesis ◦ metastasis Generally less toxic at
therapeutic doses Many are oral agents
. 37. Targeted Therapies Targets the HER2 receptor that is over-expressed in 25% of breast cancers
. 38. Targeted TherapiesTargets the VEGF and inhibits angiogenesis in NSCLC and colorectal cancer
. 39. Epidermal Growth Factor Receptor EGFREGFR is over-expressed in:• many tumour typesincluding
NSCLC
. 40. Tyrosine Kinase Inhibitor

Pneumonia is "a severe form of acute lower respiratory infection that specifically affects the lungs".
The lungs consist of bronchi, which divide into bronchioles that end in alveoli. The small blood vessels
in the lungs are responsible for gaseous exchange (oxygen moving into the lungs and carbon dioxide
moving out of the lungs).[2] During a Pneumonia infection, the alveoli of one or both lungs fill up with
pus or fluid. This increases the labor of breathing, and thus gaseous exchange cannot occur as it
normally would[3]

Prevalence of Pneumonia

According to UNICEF/WHO (2006) Pneumonia kills more children than any other illness -- more than
AIDS, malaria and measles combined and it accounts for nearly one in five child deaths globally.[3] It
has been found that 1,6 million people die from pneumonia world wide each year. It should also be
noted that pneumonia is one of the leading causes of deaths for children under the age of 5.

In South-East Asia, in the Pacific, and in Sub-Saharan Africa about 433 million young children contract
the disease annually.[4] Amongst children under the age of 5, these two regions have the highest
incidence of pneumonia cases and when combined, they "bear the burden of more than half the total
number of pneumonia episodes worldwide".[3] Pneumonia accounts for approximately 5% of deaths
in Ireland.

Types of Pneumonia

Aspiration Pneumonia

Aspiration Pneumonia results when food, drink, vomit, secretions or other foreign material is inhaled
and causes an inflammatory response in the lungs and bronchial tubes.

Aspiration Pneumonia occurs predominantly in the right lung because its total capacity is greater than
that of the left lung[5]

Aspiration of large amounts of gastric contents can cause acute respiratory distress within 1 hour

Immediate physiotherapy is required to help with secretion clearance

Atypical Pneumonia

This term refers of Pneumonia caused by the following bacteria: Legionella pneumophila,
Mycoplasma pneumoniae, and Chlamydophila pneumoniae.
Atypical pneumonia is caused by bacteria and does not respond to the normal antibiotics used for
treatment[5][6]

Bacterial Pneumonia

Bacterial Pneumonia occurs when pneumonia-causing bacteria masses and multiplies in the lungs.
The alveoli become inflamed and pus is produced, which spreads around the lungs. The bacteria that
caused Bacterial Pneumonia are: streptococcus pneumonia, hemophilus influenza, legionella
pneumophilia and staphylococcus aureus[7]

Bronchial Pneumonia

Bronchopneumonia is “a descending infection starting around the bronchi and bronchioles.[8] The
terminal bronchioles become blocked with exudates and form consolidated patches. This results in
atelectasis.

Community-acquired Pneumonia

Most common type of pneumonia

This means the infection was acquired at home in a person who has not recently been hospitalised

With this type of pneumonia the most common cause is 'Streptococcus Pneumonia'[9]

Hospital-acquired Pneumonia

Patients develop features during or after hospitalisation for another illness or procedure with a
latency period of 72 hours

Infectious agent is often Gram-negative bacteria such as 'Escherichia coli or Klebsiella' [9]

5% of patients are reported to develop hospital-acquired pneumonia

Mycoplasmal Pneumonia (also known as 'walking pneumonia')

It is similar to bacterial pneumonia, whereby the mycoplasmas proliferate and spread - causing
infection.[7]

Pneumocystis carinii Pneumonia

Pneumocystis carinii pneumonia is the result of a fungal infection in the lungs caused by the
Pneumocystis carinii fungus.

This fungus does not cause illness in healthy individuals, but rather in those with a weakened immune
system.[5]

Ventilator Associated Pneumonia (VAP)

This type of pneumonia usually occurs two days after a hospitalised patient has been intubated and
been receiving mechanical ventilation.[10]

This is especially a life-threatening infection as patients who require mechanical support are already
critically ill.[11]

Viral Pneumonia

Viral Pneumonia is believed to be the cause of half of all pneumonias. The viruses invade the lungs
and then multiply- causing inflammation.[7]

Stages of Pneumonia

Pneumonia has four stages, namely consolidation, red hepatization, grey hepatization and resolution.
Consolidation

Occurs in the first 24 hours

Cellular exudates containing neutrophils, lymphocytes and fibrin replaces the alveolar air

Capillaries in the surrounding alveolar walls become congested

The infections spreads to the hilum and pleura fairly rapidly

Pleurisy occurs

Marked by coughing and deep breathing[12][13]

Red Hepatization

Occurs in the 2-3 days after consolidation

At this point the consistency of the lungs resembles that of the liver

The lungs become hypeaemic

Alveolar capillaries are engorged with blood

Fibrinous exudates fill the alveoli

This stage is "characterized by the presence of many erythrocytes, neutrophils, desquamated

epithelial cells, and fibrin within the alveoli"[12][13]

Grey Hepatization

Occurs in the 2-3 days after Red Hepatization

This is an avascular stage

The lung appears "gray-brown to yellow because of fibrinopurulent exudates, disintegration of red
cells, and hemosiderin"

The pressure of the exudates in the alveoli causes compression of the capillaries

"Leukocytes migrate into the congested alveoli"[12][13]

Resolution

This stage is characterized by the "resorption and restoration of the pulmonary architecture"

A large number of macrophages enter the alveolar spaces

Phagocytosis of the bacteria-laden leucocytes occurs

"Consolidation tissue re-aerates and the fluid infiltrate causes sputum"

"Fibrinous inflammation may extend to and across the pleural space, causing a rub heard by
auscultation, and it may lead to resolution or to organization and pleural adhesions"[12][13]

Causes

There are many different causes of pneumonia which can be classified as infective or aspiration
pneumonia.
Infective pneumonia:

the infection and inflammatory response of the lungs and bronchial tubes when bacteria or a virus
enters the lung and proliferates

can occur through inhaling small droplets containing pneumonia

causing organisms such as Streptococcus pneumoniae.[10]

Aspiration pneumonia:

caused by inhaling vomit, mucous, bodily fluids, or certain chemicals

causing the lungs and bronchial tubes to become inflamed[5]

Risk factors

The elderly, infants and young children are more at risk of contracting community-acquired
pneumonia than young and middle-aged adults. Underlying health problems such as:

Flu

Cancer

Age >65years

Smoking

AIDS

heart disease

Diabetes

Asthma

chronic bronchitis

Emphysema

Chronic obstructive pulmonary disease

Bronchiectasis

Immunosuppressive disorders and therapy

Debility or stroke

Coma

Problems with swallowing

Alcoholism

Intravenous drug abuse

Cause a person's immune system to be weakened - thus leaving them at risk of contracting
Pneumonia. It has also been found that frequent exposure to cigarette smoke increases the risk of
developing Pneumonia (Health24.com)

Signs and symptoms

Initially symptoms are similar to that of a cold followed by:

A high fever (pyrexia)

Chills

Productive cough

Sputum may be discoloured and may become blood-stained as the pneumonia progresses. The
following may also occur:

Dyspnoea

Sharp chest pain

Worsening cough

Fever/chills

Tachycardia

Pleuritic chest pain

Headaches

Malaise

Muscle pains

Cyanosis due to poorly oxygenated blood

Loss of appetite

Rapid breathing

Wheezing or grunting during breathing

Intercostal muscle recession during breathing

Vomiting[14]

Chest X-rays often lag behind the clinical presentation.The X-ray will show decreased lung expansion
and patchy opacity on the affected side with ill defined margins[15][11]

Diagnosis

Physical examination

Auscultation- Bronchial breath sounds or fine cracks over the affected area
? Pleural rub

Chest X-ray

usually done to confirm the diagnosis

Sputum samples and blood tests

done to diagnose the type of pneumonia that is present

sputum test is done to determine whether it is a fungal or bacterial infection

blood test is done to examine the White Blood Cell count of the involved patient

this can be used to indicate the severity of the pneumonia, as well as to determine whether it is a viral
or bacterial infection.

bacterial infection would result in a blood count that has an increased amount of neutrophils

a blood count that has an increased amount of lymphocytes would indicate a viral infection.

Increased CRP

Complications

Pleural effusion

When fluid accumulates between the pleura and the chest wall due to the large amount of fluid
already present in the lungs.

As a result of the Pneumonia, a pleural effusion may develop which could lead to the collapse of the
lungs if not treated appropriately[5]

Empyema

Pus may be present in the lungs due to the infection.

Thus pockets of pus may develop in the cavity between the pleura and the chest wall, or in the lung
itself which is otherwise known as empyema[5]

Lung abscess

A lung abscess develops when the infection has destroyed lung tissue and a cavity filled with pus is
formed[5]

Bacteremia

This occurs when the infection is no longer contained within the lungs and moves into the
bloodstream, thus the blood is infected[5]

Septicemia

When bacteremia occurs septicemia can follow, as this is an infection that is spread throughout the
body.

The infected blood is the best way for the infection to manifest in other parts of the body
(Health-cares.net, 2005).

Meningitis

The infection may spread to the meninges that cover the brain and spinal cord, leading to
meningitis[5]
Septic arthritis

When bacteremia has occurred septic arthritis is also a danger, as the bacteria manifests in the joints
through which blood passes[5]

Endocarditis or pericarditis

As blood is also circulated through the heart muscles and the pericardium, the risk of developing an
infection there is very high if bacteremia is present[5]

Treatment

Treatment will vary depending on how bad the symptoms are, and what the cause of the infection is.

Bacterial Pneumonia can be treated with penicillin and/or anti-biotics

Viral Pneumonia cannot be treated with anti-biotics, as they have no effect. This type of pneumonia
normally resolves over time.

Mycoplasma Pneumonia is usually treated with anti-biotics.

Doctors will also include the following when treating patients with pneumonia:

Breathing exercises

Analgesic administration

Cough suppressant medication

Fever-reducing medication (i.e.: Aspirin)

Oxygen therapy (when indicated)

Physiotherapy Management

Modified postural drainage - this allows gravity to drain secretions from specific segments of the lungs

Shaking and vibes - to mobilize secretions

Coughing and huffing exercises - to expectorate secretions

Administer humidification - to mobilize secretions

Breathing exercises - Localized and Diaphragmatic

IPPB administration - to increase lung volumes

Mobilization of the patient - done to increase air entry, increase chest expansion, and to loosen
secretions[16]

Clinical Guidelines for Physiotherapy management of Community-Acquired Pneumonia[17]

For Patients admitted to hospital;

CPAP should be considered for patients with type 1 respiratory failure who remain hypoxaemic
despite optimum medical therapy and oxygen. (Grade C)
NIV can be considered for selected patients with type II respiratory failure, especially those with
underlying COPD. (Grade C)

Medical conditions permitting, patients should;

Sit out of bed for at least 20mins within the first 24hours

Increase mobility each subsequent day of hospitalisation (Grade B)

The regular use of PEP should be considered (Grade B)

Patients should NOT be treated with traditional airway clearance, +/- IPPB routinely. (Grade B_

Children and Pneumonia

Why are children vulnerable?

Unlike healthy children with many natural defenses to protect them against the invasion of pathogens
in the lungs, the unhealthy children with a compromised immune system has weak defenses.

Children who suffer from malnutrion, particularly inadequate zinc intake and lack of exclusive
breastfeeding have a higher risk of developing pneumonia.

Other risk factors include:

Being born premature

Having asthma or genetic disorder such as sickle-cell disease

Having heart defects such as ventricular septal defect (VSD), atrial septal defect (ASD) or patent
ductus arteriosus (PDA)[18]

Several environmental factors such as overcrowding homes and exposure to parental smoke
increases a child's susceptibility to pneumonia and its complications.[19]

Signs & Symptoms in children

In children the signs and symptoms are similar to that of adults.

Sometimes a child's only sign may be rapid breathing and often when pneumonia exist in the lower
part of the lungs, no breathing problems may be present but rather fever, abdominal pain or
vomiting.

If pneumonia is caused by bacteria, the infected child becomes sick relative quickly and is prone to
developing high fever and rapid breathing.

If pneumonia is caused by viruses, symptoms may appear gradually and less severe than the bacterial
pneumonia.[20]

Parents should be aware of the following signs and symptoms:

Nostril flaring

Sternal retraction

Increased breath rate

> 60 breaths/min for newborns up to 2 months

> 50 breaths/min for 2 months to 12 months

> 40 breaths/min for a child older than 1 years of age[21]

Prevention

Vaccines are usually administered to prevent infection by viruses and bacteria.

Kids usually receive routine immunisation against Haemophilus Influenzae and Pertussis at the age of
2 months of age.

Some vaccines are also administered against pneumococcus organism, a common cause of
pneumonia[20]

Transmission of pneumonia - Infection may occur in different ways may it be through contaminated
air droplets, blood-born infection or from coming into contact with contaminated substances during
delivery. Either way it is believed that babies already have the bacterial pathogens causing pneumonia
in their nose and/ or throat and are inhaled into the lungs.

Related articles

Bronchopulmonary Dysplasia - Physiopedia

Condition/Definition Bronchopulmonary Dysplasia on X-ray Bronchopulmonary dysplasia (BPD) is a

chronic lung condition that is caused by tissue damage to the lungs.[1] It usually occurs in immature
infants who have had severe lung disease at birth, such as respiratory distress syndrome, and have
needed to receive mechanical ventilation and supplemental oxygen as treatment for more than a few
weeks after birth. The delicate tissues of the lungs can become injured when the alveoli (air sacs) are
hyper inflated (over-stretched) by the ventilation or by high oxygen levels. As a result, the lungs
become inflamed and additional fluid accumulates within the lungs.[2] BPD is marked by
inflammation, exudates, scarring, fibrosis, and emphysema, and most commonly presents itself in
pre-term infants to 21 days post natal.[3] Pathophysiology The pathophysiology of BPD is
multifactorial and is not yet fully understood. It is believed that a variety of toxic factors contribute to
the formation of BPD by injuring the small airways, eventually resulting in a reduction of the alveolar
surface area. This affects gaseous exchange which further compromises blood oxygenation.[4] Stages
of BPD BPD is believed to be a disease of scarring and repair. Even though the exact pathophysiology
is still unclear, 4 stages in the development of BPD have been identified. In stage 1 (1-3 days), the
pathologic appearances of BPD are identical to those of respiratory distress syndrome where there is
not enough surfactant in the lungs. Surfactant helps to lower surface tension in the airways and this
helps keep the lung alveoli open. It involves the presence of hyaline membranes, atelectasis, vascular
hyperemia, and lymphatic dilatation.[4] In stage 2 (4-10 days), lung destruction resulting in ischeamic
necrosis of airways occurs due to stretching of the terminal bronchioles. Immediate reparative
changes in the lungs as well as bronchiolar obstruction are also seen in this stage. Hyaline membranes
can persist into this stage and emphysematous coalescence of the alveoli is seen.[4] Stage 3 (11-20
days) involves progressive repair of the lung, with a decreased number of alveoli. There is
compensatory hypertrophy of the remaining alveoli, and hypertrophy of bronchial-wall muscle and
glands. Regenerating clear cells are seen, along with exudation of alveolar macrophages and
histiocytes into airways. Airtrapping, pulmonary hyperinflation, tracheomegaly, tracheomalacia,
interstitial edema, and ciliary dysfunction may also be present.[4] In stage 4 (>1 month),
emphysematous alveoli are seen. Chronic lung damage eventually causes Pulmonary hypertension
(caused by thickening of the inner-most lining of pulmonary arterioles), and results in cor pulmonale.
Fibrosis, atelectasis, a cobblestone appearance due to uneven lung aeration, and pleural
pseudofissures are often seen. Marked hypertrophy of peribronchiolar smooth muscle is present.[4]
Causes and Risk Factors BPD occurs in severely ill infants who have received high levels of oxygen for
long periods of time or who have been on a ventilator during treatment for respiratory distress
syndrome. It is more common in infants born early (premature) whose lungs were not fully developed
at birth.[1] The following risk factors have been identified: Premature birth. Respiratory Infection.
Meconium aspiration. Congenital heart disease. It may also occur as a secondary problem for the
neonate attached to a mechanical ventilator.[1][5] Signs and Symptoms The most noted signs in an
infant with BPD.[1][5] The most Common signs of BPD are: Shortness of breath Cough Wheezing If
BPD worsens, the infant will present with: Severely difficult breathing with grunting The chest and
abdomen move in opposite directions with every breath Rib retractions: ribs are visible during each
breath Nasal flaring: nostrils open wide during each breath Use of accessory muscles: neck muscles
are prominent during each breath Rapid breathing rate Complications of BPD Pulmonary Edema
Despite overcoming the most serious stages of BPD, some infants still suffer long term complications.
The possibility of obtaining serious long-term complications however is minute. These complications
include: They are often more susceptible to respiratory infections such as influenza and pneumonia.
The infection is worse in children with BPD than in normal infants. Pulmonary oedema, an excess fluid
build-up in the lungs, which decreases air entry into the lungs and infants cannot breathe which
results in respiratory distress. Infants with a history of BPD may also develop a rare complication in
their circulatory system known as pulmonary hypertension. This occurs when the blood vessels
carrying blood from the heart to the lungs become narrowed, resulting in high blood pressure. Infants
with BPD have stunted growth and have problems gaining weight. They also tend to lose more weight
when they are sick. Premature infants with severe BPD also have a higher incidence of cerebral palsy.
Diagnosis It is difficult to determine whether or not a baby has bronchopulmonary dysplasia (BPD)
before he or she is about 14 to 30 days old. By this time the baby should be showing improvement in
breathing problems, instead the condition seems to be getting worse and the baby requires more
oxygen and assistance from a ventilator.[6] According to kidshealth.com when making a diagnosis the
following factors should be taken into account: Prematurity Infection Mechanical Ventilator
dependence for a prolonged period BPD is confirmed as a diagnosis if the infant requires additional
oxygen and continues to shows signs of respiratory distress after 28 days of age. A number of tests
are also conducted on newborns with breathing problems to make sure they diagnose their condition
correctly. According to the National heart, lung and blood institute these tests include: Blood tests.
Blood samples are checked to see whether the baby has enough oxygen in his or her blood. Chest
x-rays. It shows larger areas of air and changes from inflammation or infection. It also shows areas of
the lung that have collapsed and may help confirm that the lungs aren't developing normally. On a
chest x – ray, the lung tissue appears spongy. Echocardiogram. The use of sound waves to create a
moving picture of the heart. Echocardiogram is used to rule out congenital heart defects or
pulmonary arterial hypertension as the cause of the breathing problems. Doctors grade BPD as mild,
moderate, or severe, depending on how much supplemental oxygen the baby needs and how long he
or she needs it.[6] Prevention There are a number of things a mother can do to prevent her baby from
being born before their lungs have fully developed: During pregnancy, regular check ups with the
doctor should be done. Dietary supplements are essential, along with good, healthy eating habits.
Avoid smoking, consuming alcohol and taking illegal drugs. It is vital that the mother-to-be is
controlling any chronic diseases (e.g. Diabetes, Hypertension etc.) with proper medication.
Mothers-to-be must make sure that they attend to all cuts and bruises as soon as possible to prevent
infections and other easily attainable communicable diseases. Medical Management Doctors begin
treatment for respiratory distress at birth and before they even know whether the baby has BPD.
According to the National Heart, Lung and Blood Institute, medical management of a child with RDS
and possibly BPD includes:[6] Breathing Support The baby is usually put on a mechanical ventilator.
The ventilator, which is connected to a breathing tube that runs through the baby's mouth or nose
into the windpipe, can be set to help a baby breathe or to completely control a baby's breathing. It
also is set to give the amount of oxygen the baby requires. With help breathing, the baby's lungs have
a chance to develop.[6] Surfactant Replacement Therapy The baby is given surfactant to open his or
her lungs until the lungs have developed enough to start making their own surfactant. Surfactant is
given through a tube that is attached to the ventilator, which pushes the surfactant directly into the
baby's lungs.[6] Medication Medication is usually prescribed to reduce swelling in the airways and
improve the flow of air in and out of the lungs. These medications include: Bronchodilators –
Bronchoconstriction and airway hyper reactivity. Diuretics - Pulmonary edema, and removal of extra
fluid in the lungs. Steroids - To decrease airway inflammation. Vasodilators - Cor pulmonale.
Antibiotics - Control infections Supportive Therapy Treatment in the NICU is designed to limit stress
on the baby and meet his or her basic needs of warmth, nutrition, and protection. According to the
National Heart, Lung and Blood Institute, such treatment usually includes:[6] Using a radiant warmer
or incubator to keep your baby warm and reduce the chances of infection. Ongoing monitoring of
blood pressure, heart rate, breathing, temperature and the amount of oxygen in the baby's blood.
Monitoring fluid intake to make sure that fluid doesn't build up in the baby's lungs. Physiotherapy
Management It must be noted that infants with Bronchopulmonary Dysplasia are cared for in the
Neonatal Intensive Care Unit. The mainstay of physiotherapy treatment is to clear the chest of
secretions. This can be done by: Vibrations and light percussions. Changing positions helps to mobilise
secretions out of the small airways. Suctioning and mucolytics may be an option for tenacious sputum
and when the child has difficulty coughing. [7] [8] Evidence There is limited evidence for the role of
physiotherapy in the treatment of BPD. A study carried out by Gomez-Comesa et al, reported that
physiotherapy treatment in the NICU was effective in improving BPD in prematurely born children
with respiratory distress syndrome. Physiotherapy assisted in reducing the number of days that
ventilation and hospitalization were required and favoured the prevention of future disabilities.[9]

Hospital Acquired Pneumonia - Physiopedia

Definition/Description “Pneumonia is an infection of the lung tissue. It is defined as "inflammation of

the lung caused by bacteria, in which the air sacs (alveoli) become filled with inflammatory cells and
the lungs become solid". When a person has pneumonia the air sacs in their lungs become filled with
microorganisms, fluid and inflammatory cells and their lungs are not able to work properly. Diagnosis
of pneumonia is based on symptoms and signs of an acute lower respiratory tract infection, and can
be confirmed by a chest X-ray showing new shadowing that is not due to any other cause (such as
pulmonary oedema or infarction)." [1] (NICE clinical guidelines 2014) Hospital-acquired pneumonia
"Hospital-acquired pneumonia is defined as pneumonia that occurs 48 hours or more after hospital
admission and is not incubating at hospital admission. Early-onset (occurring within 4 days of
admission) hospital-acquired pneumonia is usually caused by the same bacteria and viruses as
community-acquired pneumonia and has a good prognosis. Late-onset (starting 5 days or more after
admission) hospital-acquired pneumonia has a worse prognosis and is usually caused by
micro-organisms that are acquired from the hospital environment. MRSA, Pseudomonas aeruginosa
and other non-pseudomonal Gram-negative bacteria are the most common causes."[2] (NICE
Guidelines. Published: 15 July 2014) Epidemiology “At any time 1.5% of hospital inpatients in England
have a hospital-acquired respiratory infection, more than half of which are hospital-acquired
pneumonia and are not associated with intubation. Hospital-acquired pneumonia is estimated to
increase hospital stay by about 8 days and has a reported mortality rate that ranges from 30–70%.
Variations in clinical management and outcome occur across the UK.”[1] HAP and VAP together are
the second most common cause of hospital-acquired infection and have been associated with a
higher mortality than any other nosocomial infection.[3] HAP is the second most common nosocomial
infection with a crude overall rate of 6.1 per 1000 discharges[4] Ventilator-acquired pneumonia (VAP)
has been studied more comprehensively than HAP. A clear reason for this is VAP is responsible for
86% of the HAP reported[5]. The incidence rate of HAP is between 3 and 10 per 1000 hospital
admissions[6][7]. Mortality rates from VAP are between 24 and 50% but it is reported to jump to 76%
if it is caused my multi drug resistant pathogens that are often linked to later stage pneumonia (>
5days in hospital)[5]. Although it is difficult to determine the exact cause of death in critically ill
patients, which will cause discrepancies in any date, Accurate antibiotics taken at the right time has
shows to lower mortality rate for HAP. The chance of infection is estimated to be 3%/day during the
first 5 days of ventilation, followed by 2%/day up to day 10 of ventilation and there- after 1%/day.[8]
Aetiology The most common cause is an accumulation of bacteria, most ordinarily gram-negative
bacilli and staphlycoccus aureus, which inhabit the oropharynx and upper airways in seriously ill and
ventilated patients[9]. A less common cause is seeding of the lung due to bacteremia; a bacterium
that originates in the patients’ blood supply and can transferred to the lungs during gas exchange.
Finally inhalation of bacterially contaminated aerosols which transport airborne particles containing
Legionella sp, Aspergillus sp, or influenza virus, although this is a relatively unfamiliar form of
contracting hospitalized pneumonia[9]. Endotracheal intubation with mechanical ventilation poses
the greatest overall risk[10]. Ventilation Associated Pneumonia is a subcategory of hospitalized and
contributes more than 85% of all cases, with pneumonia occurring in up to 27% of ventilated
patients[10]. Endotracheal intubation related bacteria embed themselves deep into the endotracheal
tube cuff enabling them to avoid the body' nature immune response while also providing a biofilm of
protection from antibiotics[9]. In non-intubated patients, risk factors include previous antibiotic
treatment, high gastric pH, resulting from cardiac, pulmonary, hepatic, or renal deficiencies[9]. Major
risk factors for postoperative pneumonia are patients older than 70, abdominal or thoracic surgery,
and cardiorespiratory functional depletion[9]. Many patients at risk for HAP and VAP have underlying
medical conditions that put them at higher risk for acquiring antibiotic-resistant organisms (AROs).[3]
Investigations HAP or VAP should be suspected in all patients, whether ventilated or not, if two or
more of the following clinical features are present: temperature greater than 38°C or less than 36°C;
leukopenia or leukocytosis; purulent tracheal secretions and decreased partial pressure of oxygen in
arterial blood (PaO2).[3] General investigations are not necessary for the majority of patients who are
managed in the community. Pulse oximeters allow for simple assessment of oxygenation. When a
patient is admitted to hospital: FBC with differential white cell count: Total white blood cells: All the
white cell types are given as a percentage, and as an absolute number per liter. A high WBC is often
an indicator of infection[11]. CRP (to aid diagnosis and as a baseline measure). The C-reactive protein
(CRP) test is a diagnostic tool that identifies regions of inflammation[12]. CRP is a protein
manufactured in the liver before dispersal into the blood which occurs a few hours after any form of
tissue injury, an acute manifestation of infection, or inflammation caused by another source[12]. The
CRP test can be used in adjunction with signs, symptoms and other tests in order to fully evaluate
patients with HAP[12]. Blood cultures: Blood culture is a microbiological culture of blood. It is
employed to detect infections that are spreading through the bloodstream (such as bacteremia,
septicemia amongst others). Pneumococcal and legionella urinary antigen tests: Urine tests are
administered and designed to locate the presence of both Streptococcus pneumoniae and Legionella
species[13]. Two major pathogens in HAP, which also play a key role in community acquired
Pneumonia. The tests are usually in conjunction with both sputum examination and blood testing due
to their high specificity[13]. CXR: HAP may deliver signs of abnormal opacity in specific areas of the
lungs, or even clear consolidation due to inflammation causing abnormal positioning of structures,
such as the trachea and mediastinum[14]. Sputum examination and culture. Sputum Examination is a
diagnostic tool used to identify bacteria and fungi located in the pulmonary facet[15]. Samples are
often obtained through expectorating or in some cases an induced saline can produce the required
volumes from lab testing. HAP normally produces sputum in a thick and purulent form, which is
common in more cases of infection[15]. Blood gases: Blood gases will demonstrate how well both the
respiratory and the renal systems are functioning[16]. In terms of HAP ABG’s can be used to gain
insight into the patient’s oxygen saturation levels as well as demonstrate incidences of both acidosis
and alkalosis, both of which can occur due to poor ventilation[16]. Aspiration of pleural fluid (for
biochemistry and culture). Chest aspiration is a diagnostic tool used to investigate the cause of pleural
fluid or to improve respiration rates that have dropped due to accumulated fluid[17]. Samples of the
pleural fluid are sent for analysis which includes cytology for malignant cells and bacteriology for
identification of foreign bacteria[17]. Clinical Manifestations A patient that develops new or extra
pulmonary infiltrates and a fever are signs of HAP. In order to differentiate HAP and other pathologies
diagnosis should be based on a radiographic x-ray. To diagnose HAP radiological opacity with alveolar
condensation must be present.[18] The time of onset of HAP is a large determinate of the type of
bacteria causing the infection: Early-onset HAP occurring in the first 4 days of hospitalization) is often
caused by community-acquired pathogens such as: Haemophilus influenzae, Streptococcus
pneumoniae, or methicillin-susceptible S aureus (MSSA). In this context, pathogens with strong
intrinsic or acquired antimicrobial resistances are rarely causative. Late-onset HAP developing ≥ 5
days after hospitalization is often caused by aerobic Gram-negative bacilli such as: P aeruginosa,
Enterobacteriaceae, or Acinetobacter) or Methicillin-resistant Staphylococcus aureus (MRSA)
Late-onset pneumonia is due to P aeruginosa, Acinetobacter, or MRSA in 30 to 71% of cases.
Physiotherapy and Other Management Other health professionals will be treating your patient. What
is their input?When addressing HAP, respiratory physiotherapy interventions should be individually
tailored around the patient’s symptoms, observing aspects such as degree of pain, mobility
capabilities and an array of complex factors[19]. Therefore techniques may include positional
manipulations (addressing V/A matching and attempting to uses gravity to potentially enable
drainage), manual hyperinflation, percussion, shaking, vibrations, suctioning (if huffing or cough
promoting techniques are proving ineffective in regards to sputum extraction), breathing exercises
including thoracic expansion and relaxing tidal volumes, while also engaging sputum reduction
through active cycle and autogenic drainage techniques) as well as mobilization[19]. The later of
course demonstrating great importance not only in terms of improving the patients’ respiratory
distress, but also in reducing overall hospitalization. Published substantial evidence very much
supports the role of physiotherapy in the respiratory managing HAF, demonstrating both short-term
and longer term benefits[19]. However, its essential to promote physiotherapy treatment as part of a
multi-disciplinary approach as aspects including pharmaceutical interventions play an integral part in
controlling bacterial diseases, promoting lung function and reducing problematic symptoms[20].
Prevention Three European societies, (European Respiratory Society (ERS), European, Society of
Clinical Microbiology and Infectious Diseases (ESCMID) and European Society of Intensive Care
Medicine (ESICM), in 2008 produced a report to further the clinical guidelines of HAP and VAP. Within
these guidelines they outline several measures that can have proven to reduce the likelihood of HAP.
Generally recommended general measures: Alcohol-based hand disinfection Use of microbiologic
surveillance Monitoring and early removal of invasive devices Programs to reduce antimicrobial
prescriptions Generally recommended specific measures Avoidance of endotracheal intubation
Avoidance of reintubation Preference of noninvasive ventilation (NIV) Preference of orotracheal
intubation and orogastric tubes Maintenance of the ET cuff pressure at approximately 20 cmH2O
Avoidance of flushing the condensate into the lower airway or to in-line medication nebulizers Patient
positioning (semirecumbent position)[21] Additional measures which might be helpful in distinct
settings and populations: Continuous aspiration of subglottic secretions Endotracheal tubes coated
with antiseptics or silver Preference of heat-moisture exchangers (HMEs) over heater humidifiers (HH)
Oral decontamination Selective decontamination of the digestive tract (SDD)[21] The VAP Guidelines
Committee and the Canadian Critical Care Trials group in 2008 recommended several approaches to
encourage a reduction in incidences[22]: The orotracheal route of intubation should be used when
intubation is necessary There should be no scheduled ventilator circuit changes but new circuits for
each patient, and changes if the circuits become soiled or damaged Changes of heat and moisture
exchangers with each patient, also every 5-7 days and as clinically indicated Closed endotracheal
suctioning system, and that the system is changed for each patient and as clinically indicated. The use
of subglottic secretion drainage in patients expected to be mechanically ventilated for > 72hrs Bed
head to be elevated to 45°. If this angle is not possible then as much elevation as possible is
recommended The use of oral antiseptic chlorhexidine The use of oral antiseptic povidone-iodione
should be considered with patients with severe head injury Rotating beds should be considered
Resources NHS website http://www.nhs.uk/conditions/pneumonia/Pages/Introduction.aspx Patient
website http://www.patient.co.uk/health/pneumonia-leaflet

Bronchitis - Physiopedia

Condition Bronchitis can be defined as an inflammation of the bronchi. It is also noted to be an

infection of the lower respiratory tract which, in general, will follow an upper respiratory tract
infection. Acute bronchitis is caused either by a viral or bacterial infection. It is characterized by
coughing, the production of excessive amounts of mucopurulent sputum and narrowing of the
bronchi due to spasmodic contractions. The respiratory passages also become inflamed and irritated.
This illness is commonly one of a viral nature and is usually self-limiting. It may progress to pneumonia
if unaddressed or if treatment is not effective. Episodes of this disease mainly occur in middle and
adult life, however, both adults and children can acquire bronchitis. It is more common in males than
females and is also more common amongst smokers than non-smokers. Symptoms are noted to be
similar for both age groups. Bronchitis is usually a progressive disease and could possibly lead to
respiratory failure if not treated effectively. Pertussis, commonly known as whooping cough, can also
be seen to mimic acute bronchitis and is often under-diagnosed, leading to the need for differential
diagnosis. Infants usually get bronchiolitis, which involves the smaller airways and causes symptoms
similar to asthma. In general, an infant will lead a relatively protected life. It is therefore noted that
respiratory infections will usually only become common once the child starts school. These infections
may also be seen to be recurrent through the early school-going years as the body's defence
mechanisms are still developing as the child grows. Pathology Acute bronchitis is generally caused by
a viral infection. In patients younger than 1 year, the respiratory syncytial virus, parainfluenza virus
and the coronavirus are noted to be the most common causes. In patients between 1 and 10 years,
the parainfluenza virus, enterovirus, respiratory syncytial virus and rhinovirus dominate the causes of
acute bronchitis. In patients older than 10 years, the influenza virus, respiratory syncytial virus and
adenovirus are the most common causes. Acute bronchitis was first described in the 1800’s as the
inflammation of the bronchial mucous membranes. Subsequently this inflammation has been noted
to be the end result of a complex series of events. These events include an infectious or
non-infectious trigger. This leads to the injury of the bronchial epithelium resulting in an inflammatory
response with hyper-responsiveness of the airways and mucous production. Bronchial wall repair
takes a few weeks to occur. The patient will still suffer from a cough during these weeks. Half of the
patients suffering from acute bronchitis will continue to cough for longer than 2 weeks and in a
quarter of patients the cough will last for more than a month. Chronic bronchitis in children can be as
result of two things: Excessive inflammation or continuous exposure to allergens or irrtants. This will
result in a bronchospasm and cough. Later the airway will become inflamed with oedema and there
will be mucous production(due to overactivity of mucous secreting glands. This mucous production
can build up, covering the bronchial walls and in turn results in an obstruction being formed in the
bronchioles. Therefore it can be said that chronic bronchitis in children is most probably diagnosed as
asthma. General pathology: Hypertrophy of the mucous glands in the bronchial wall. Increased
number of goblet cells. Recurrent infection, especially in childhood could lead to chronic
inflammatory changes, fibrosis, distortion and even ulceration. The small airways are often affected
which is partly due to a loss of elastic support from the surrounding alveoli. Risk Factors Exposure to
second-hand smoke Contact with someone already infected with bronchitis A viral upper respiratory
tract infection Asthma Enlarged tonsils and or adenoids Sputum retention Unexplained weight loss
Cor pulmonale Ventilatory failure Weakened immune system Repeated exposure to lung irritants
Causes Acute bronchitis is caused by viral and bacterial infections. This form of the disease may last
up to several days, or even weeks. Viruses, which include the influenza A and B, adenovirus,
rhinovirus and the respiratory synctial virus Acute exacerbations of chronic lung disease may be
caused by bacteria, which include Streptococcus, Haemophilus, Moraxella catarrhalis and
Mycoplasma pneumonia Atypical pathogens such as Mycoplasma pneumonia, Chlamydia pneumonia
and Chlamydia psittaci Bacteria such as Streptococcus pneumonia and Moraxella Contributory or
Predisposing Factors Bronchiectasis Cystic Fibrosis Congestive heart failure Some children may be
more prone to the contraction of acute bronchitis than others and these include children with
respiratory illnesses such as asthma and children exposed to high levels of airborne pollutants. Signs
and Symptoms The signs and symptoms of this disorder will depend on the severity of the disease as
well as considering which stage the disease has been diagnosed. This just means that some symptoms
may be present in some cases and may be absent in others. General Symptoms Coughing which will
be dry, hacking and painful in the initial stages. Coughing later becomes productive with purulent
sputum. Sputum may also contain blood Coughing may last for more than two weeks Continued
forceful coughing may cause chest and abdominal muscle pain Coughing can be severe enough at
times to injure the chest wall or even cause the child to pass out Wheezing Coarse crackles may be
heard on auscultation. Difficulty in breathing due to narrowing of the bronchi. General physical signs
Barrel chest (increased anteroposterior diameter) Diaphragm appears lower and flatter Paradoxical
inward movement of the lower ribs and visible interspaces during inspiration Sternum appears
elevated The liver may become palpable as it is displaced downwards due to overinflation. The breath
sounds have a longer expiratory phase and there may be decreases air entry. Other added sounds
that may be heard on auscultation include rhonchi and crackles. Symptoms for Viral Acute Bronchitis:
Non-productive cough Purulent sputum Symptoms will be aggravated by cold/dry/dusty air
Symptoms for Bacterial Acute Bronchitis: Productive cough Pyrexia Pain behind the sternum, which
will be aggravated by coughing Runny Nose Chills Slight fever Back and muscle pain Sore throat
Prevalence/Incidence A study done by the School of Public Health and Family Medicine at the
University of Cape Town (UCT), revealed that out of the sample population 2,3% of males and 2,8% of
females had bronchitis. It was also found that the strongest predictor of this disease was a history of
tuberculosis. Other predictors include smoking, occupational exposure, and other domestic exposure
e.g exposed to smokey fuel and being underweight. The incidence rate of acute bronchitis in the
United States of America (USA), according to www.wrongdiagnosis.com is approximately 1 in 21 or
4.60%, this is extrapolated out to 23 new cases per minute. The following statistics about acute
bronchitis were posted on www.wrongdiagnosis.com and are all from the Hospital Episode Statistics,
England Health Department and were all for the year 2002-2003. It was found that 0.017% of hospital
consultant episodes were for acute bronchitis. 52% of hospital consultant episode were for men. The
mean stay in hospital was 4.3 days and the mean age of hospitalised patients diagnosed with acute
bronchitis was 40 years. The following results are shown as extrapolations of the research done in the
USA and therefore the results are based on these methods. Chronic Bronchitis in Southern Africa
(Extrapolated Statistics) ( Extrapolated Prevalence --- Population Estimated Used) Angola -- 488,384 ---
10,978,5522 Botswana -- 72,921 --- 1,639,2312 South Africa -- 1,977,303 --- 44,448,4702 Swaziland --
52,014 --- 1,169,2412 Zambia -- 490,481 --- 11,025,6902 Zimbabwe -- 163,343 --- 1,2671,8602
Diagnosis Just like any respiratory disorder, the diagnosis will start with the history of the patient,
including all details pertaining to the disorder (exposure to irritants, including being exposed to
second-hand smoke). Upon physical examination, decreased breath sounds, wheezing, rhonchi and
prolonged expiration will be evident. Various tests can be used to diagnose bronchitis in patients who
present with prolonged coughing and shortness of breath. Chest X-ray This test is used to rule out
pneumonia. In bronchitis, the x-ray will show no evidence of lung infiltrates or consolidation. Sputum
Culture This allows the doctor to check for signs of inflammation or a bacterial infection Blood Tests
These tests include arterial blood gasses to test for levels of oxygen, carbon dioxide and acidity of the
blood. Pulse Oximetry This test will determine the amount of oxygen in the blood. An arterial blood
gas test is more exact, but will be more painful and traumatic for the child. Pulmonary lung functions
Pulmonary function tests are also known as lung function tests. These tests measure the amount of
air ones' lungs can hold, the way your lungs function(moving oxygen into the lungs and carbon dioxide
out of the lungs) and how quickly you can move air in and out of your lungs. The other advantages of
these tests are that it can diagnose lung diseases, measure how severe the lung disease is and also
evaluate how effective the treatments that have been administered are noted to be. Medical
Management The physical examination of patients presenting with symptoms of acute bronchitis
should focus on the vital signs. These should include the presence or absence of pyrexia and
tachypnea, and pulmonary signs such as wheezing, rhonchi, and prolonged expiration. Evidence of
consolidation must be absent, or a diagnosis of pneumonia can be made. In general, the patient
needs to rest, may need the use of antipyretics, should have adequate hydration, and should avoid
smoke where possible. Some of the main objectives of treatment for this disorder will be to keep the
bronchioles open and functioning, to facilitate the removal of secretions, to prevent disability and to
improve one's quality of life as much as possible. It is extremely important to correctly manage cases
of bronchitis. In the case of an emergency, a child suffering from acute bronchitis or the exacerbation
of chronic bronchitis should be adequately oxygenated as this would be the primary medical
intervention at the time, and most important. Antibiotics can be used to treat acute bronchitis caused
by a bacterial infection. They are ineffective in the treatment of acute bronchitis caused by a virus
however. The treatment for the viral form is commonly symptomatic, and can include analgesics for a
sore throat, antipyretic medication for fever, and cough suppressants where deemed necessary and
effective. A humidifier may also be used in order to increase the humidity of the air and ease dryness
of the respiratory passages, which can cause excessive coughing due to irritation. In rare cases, the
patient may be hospitalized if they experience breathing difficulty that doesn't respond to treatment.
This usually occurs because of a complication of bronchitis, not bronchitis itself. Pharmaceuticals
Aspirin, Paracetamol, Ibuprofen or Acetaminophen These are used for the treatment of pain and
fever and can be used to ease headaches caused by excessive coughing. Pertussives Pertussive
therapy is used in order to induce coughing as an aid for expectoration. Antitussives Antitussives are
used to control coughing, especially in cases if the cough is creating significant discomfort. The
selection of an antitussive medication is dependent upon the cause of the cough. An antihistamine
would be made use of to treat a cough caused by allergic rhinitis. A decongestant or an antihistamine
would be utilized to treat a cough caused by a postnasal drip. And a bronchodilator when a cough
results from the exacerbation of asthma. Non-specific antitussives are made use of to just suppress an
unproductive, ineffective cough while not hampering the resolution of the infection. Bronchodilators
These prevent excessive coughing which would lead to pain and fatigue. Antibiotics Used in the
treatment of acute bronchitis caused by a bacterial infection.In paediatrics ,antibiotics will only be
used for bronchitis related to bacteria.Physicians will prescribe Amoxicillin to children younger than 8
years old. Expectorants These may be beneficial in removal of sputum by mobilizing and aiding
expectoration, preventing atelectasis and bronchospasm. Steroid Therapy This form of medical
managemnet may be considered if conservative measures fail. Immunizations An important aspect of
child care and is an important defence mechanism against viral agents of disease and illness.
Physiotherapy Management According to Shepherd (1995)[1], bronchitis is one of the main
respiratory disorders during which a child will be referred for physiotherapy treatment. Postural
Drainage This can be exercised at an angle of 45º in prone and in side lying. This must first be cleared
with the institution as necessary, as well as considering possible contra-indications such as a head
injury. Manual Techniques Percussions, shaking and vibrations can be used to mobilize secretions and
aid expectoration. Once again, precautions and contra-indications are to be observed. Breathing
Exercises Active Cycle of Breathing Techniques(ACBT) could be used in order to mobilize secretions.
Teaching relaxed breathing techniques as well as diaphragmatic breathing to aid oxygenation and
prevent respiratory distress. Full thoracic expansion must be emphasized which will aid oxygenation.
The patient should be encouraged to aid the mobilization of secretions through coughing and deep
breathing during the day. The patient, and family, should be advised that the patient needs to rest
and avoid bronchial irritants where possible. This, however, does not exempt the patient from
partaking in physiotherapeutic activities. Education Teaching the importance of nose blowing into a
tissue and not swallowing the secretions as well as discarding the tissue safely after blowing their
nose is important,s as this will prevent the spread of infection. The patient and family/caregiver
should be advised that a dry cough may persist after the bronchitis has resolved due to irritation of
the respiratory passages. A humidifier at the bedside may be useful in combating the negative
after-effects as it will saturate the air that is breathed in. Treatment Schedule and Home Advice
Treatment should be carried out 3 to 4 times a day depending on the severity of the condition. If an
upper respiratory tract infection is contracted again, treatment should be started as soon as possible
to prevent it from developing into bronchitis or further severe complications. The patient and/or
family should be able to recognize early signs and symptoms of acute bronchitis and report them
immediately. [2] [3] [4] Prognosis If an underlying lung disorder is not present, symptoms of acute
bronchitis will usually subside within 7 to 10 days. A dry, hacking cough may however be present for
several months after this allotted time. Acute bronchitis usually heals completely, therefore leading to
an excellent prognosis. Bronchitis commonly begins with a dry cough, which can wake the patient up
at night. This will progress to a cough, which is productive in nature, and may accompany symptoms
such as pyrexia, malaise and a headache. These symptoms will only last for a few days, but the
productive cough will last for several weeks. If any of the symptoms associated with this disorder
should remain untreated or uncontrolled it could lead to secondary complications such as pneumonia.
This would thus lead to a poorer prognosis. Prevention In paediatric bronchitis as well as other
medical conditions, prevention is always better than cure. Hands should be washed regularly to avoid
the spreading of any viruses and other infections. A hand should be placed over the mouth during
coughing, and the washing ones' hands after a cough will aid in the removal of any viruses or germs
on the hands. If this is not observed, it may lead to the spread of infection. If and where possible,
exposure to air pollution should be reduced. Smoking near children should be prevented as secondary
smoke can damage the bronchial tree and makes it easier for viruses to cause an infection. If the child
is easily susceptible to contracting infections, contact with people who are already suffering from
bronchitis should be avoided. Antimicrobial therapy should be administered at the first sign of
purulent sputum. Children suffering from bronchitis should always have a balanced diet and healthy
eating plan in order to keep their immune system in an optimal condition. This allows it to fight off
infection and prevent the development of acute bronchitis, disrupting daily life along with general
well-being.

Today is World Pneumonia Day – Physiospot – Physiotherapy and Physical Therapy in the Spotlight

Today is “World Pneumonia Day” which was first hosted in 2009 when over 100 organisations joined
to form the Global Coalition against Child Pneumonia. It’s marked every year on 12 November with
the aim of: Raising awareness about pneumonia, the world’s leading killer of children under the age
of five; Promoting interventions to protect against, prevent and treat pneumonia; and Generating
action to combat pneumonia. Pneumonia is one of the most solvable problems in global health and
yet a child dies from the infection every 20 seconds. Together, as physiotherapists, we can ensure the
fight against pneumonia is won. Pneumonia is “a severe form of acute lower respiratory infection that
specifically affects the lungs”. The lungs consist of bronchi, which divide into bronchioles that end in
alveoli. The small blood vessels in the lungs are responsible for gaseous exchange (oxygen moving into
the lungs and carbon dioxide moving out of the lungs). During a Pneumonia infection, the alveoli of
one or both lungs fill up with pus or fluid. This increases the labor of breathing, and thus gaseous
exchange cannot occur as it normally would. Learn More About Pneumonia Why are children
vulnerable? Unlike healthy children with many natural defenses to protect them against the invasion
of pathogens in the lungs, the unhealthy children with a compromised immune system has weak
defenses. Children who suffer from malnutrion, particularly inadequate zinc intake and lack of
exclusive breastfeeding have a higher risk of developing pneumonia. Other risk factors include: Being
born premature Having asthma or genetic disorder such as sickle-cell disease Having heart defects
such as ventricular septal defect (VSD), atrial septal defect (ASD) or patent ductus arteriosus (PDA)
Several environmental factors such as overcrowding homes and exposure to parental smoke
increases a child’s susceptibility to pneumonia and its complications. Through the use of simple
physiotherapy treatments such as manual techniques, active cycle of breathing, IPPD breathing and
exercises perhaps we could reduce this mortality rate even just a little bit. To do this we much enable
those in developing countries, where antibiotic and healthcare accessibility is poor, to gain the
knowledge of how to manage the condition. It is our duty, those with understanding and knowledge
of this condition, to do so.

Pneumothorax - Physiopedia

Definition According to the Oxford Concise Medical Dictionary[1], a pneumothorax can be defined as
"Air in the pleural cavity". This occurs when there is a breach of the lung surface or chest wall which
allows air to enter the pleural cavity and consequently cause the lung to collapse. Types of
Pneumothorax Various causes of a pneumothorax[2] exist and each pneumothorax is classified
according to its cause. Primary pneumothorax: also referred to as a spontaneous pneumothorax or
primary spontaneous pneumothorax, It is characterised by having no clear cause or no known
underlying lung pathology. There may be contributing factors, such as cigarette smoke, family history,
the rupture of bulla (small air filled sacs in the lung tissue) but these will not cause pneumothorax
itself. Secondary pneumothorax: also referred to as a non-spontaneous or complicated
pneumothorax. It occurs as a result of an underlying lung pathology such as COPD, Asthma,
Tuberculosis, Cystic Fibrosis or Whooping Cough. A pneumothorax can further be classified as a
tension or non-tension pneumothorax. A tension pneumothorax is caused by excessive pressure build
up around the lung due to a breach in the lung surface which will admits air into the pleural cavity
during inspiration but will not allow any air to escape during expiration. The breach acts as a one-way
valve. This leads to lung collapse. The removal of the air is through surgical incision by inserting a
under water drain in the pleural cavity. This excessive pressure can also prevent the heart from
pumping effectively which may lead to shock. A non-tension pneumothorax is not considered as
severe as there is no ongoing accumulation of air and therefore there is no increasing pressure on the
organs and the chest. Other causes of a pneumothorax can be trauma or incorrect medical care.A
traumatic pneumothorax is caused by trauma to the lungs. Some of the causes are the following:
Stabwound, gunshot or injury from a motor vechicle accident or any other traume to the lungs. A
pneumothorax which develops as a result of a medical procedure or incorrect medical care i.e.
accidental puncture to the lung during surgery, is termed as an iatrogenic pneumothorax. Causes and
Risk Factors The cause of primary spontaneous pneumothorax is unknown (idiopathic), but
established risk factors[3] include: Sex Smoking (cannabis or tobacco) and, Family history of
pneumothorax. Secondary spontaneous pneumothorax occurs in the setting of a variety of lung
diseases. The most common is chronic obstructive pulmonary disease (COPD), which accounts for
approximately 70% of cases. Known lung diseases that may significantly increase the risk for
pneumothorax are: Chronic obstructive pulmonary disease. Cystic fibrosis. Lung cancer. Asthma.
Tuberculosis. Emphysema. Bacterial pneumonia: Certain forms of pneumonia caused by
staphylococcus, streptococcus and other types of bacteria may cause a lung to collapse Other factors
may also cause collapsed lung. These include: Injury or trauma to the chest area: Bullet or stab
wounds, fractured ribs, or a blunt force injury can cause the lungs to collapse. Certain medical
procedures: These include procedures in which the lung may inadvertently be punctured (needle
aspiration to drain fluid from the lung, biopsy or the insertion of a large intravenous catheter into a
neck vein). Activities in which there are sharp changes in air pressure: Flying in an airplane or
deep-sea diving may result in collapsed lung Signs and Symptoms Symptoms of pneumothorax include:
Sudden onset of chest pain (This is a sharp pain, which may lead to a feeling of tightness in the chest)
Dyspnoea (shortness of breath) Tachycardia (rapid heart rate) Tachypnoeas (rapid respiration rate)
Coughing (dry) Fatigue Signs of respiratory distress (nasal flaring, anxiety etc) Hypotension
Subcutaneous emphysema Prevelance Around the World Primary spontaneous pneumothorax occurs
most often in people between age 18 - 40 and Secondary spontaneous pneumothoraces occur more
frequently after age 60 years.Prevalence of a pneumothorax in a newborn is a potentially serious
problem and it occurs in about 1-2% of all births. According to Ch[4]ang and Mukherji (2007) the
incidence of primary spontaneous pneumothorax in the USA (age-adjusted) is 7.4-18 cases per
100,000 persons per year for men and 1.2-6 cases per 100,000 persons per year for women. Incidence
of secondary spontaneous pneumothorax (age-adjusted) is 6.3 cases per 100,000 persons per year for
men and 2 cases per 100,000 persons per year for women. Chronic obstructive pulmonary disease
(COPD) is a common cause of secondary spontaneous pneumothorax that carries an incidence of 26
cases per 100,000 persons. The incidence of iatrogenic pneumothorax is not known, but it probably
occurs more often than primary and secondary spontaneous pneumothoraces combined.Incidence is
higher in men than in women, at a ratio of 6.2:1 for primary pneumothorax and 3.2:1 for secondary
pneumothorax. Although some view primary spontaneous pneumothorax as more of a nuisance than
a major health threat, deaths have been reported. Secondary spontaneous pneumothorax can be life
threatening, depending on the severity of the underlying disease and the size of the pneumothorax.
Mortality percentages in patients with COPD and spontaneous pneumothorax vary from 1-17%.
Iatrogenic pneumothorax may cause substantial morbidity and, rarely, death (Chang[4] & Mukerji,
2007). Pathology The lungs are located inside the chest cavity and air is drawn into the lungs by the
diaphragm. The pleural cavity is the region between the chest wall and the lungs. If the air enters the
pleural cavity, either from the outside (open pneumothorax) or from the lung (closed pneumothorax),
the lung collapses and it becomes impossible for the person to breath, even if they have an open
airway. If a piece of tissue forms a one way valve which allows air to enter the pleural cavity, but not
to escape, overpressure can build up with each breath (tension pneumothorax). This leads to severe
shortness of breath and circulatory collapse. Air leaks from the lungs into other parts of the chest
cavity can occur in newborns. Babies are normally born with collapsed lungs, and a large amount of
pressure is generated as the newborn's body works to inflate their lungs with the first few breaths.
For 98% of newborns there is no problem at all, but for some (2%)the lungs do not immediately open
completely and the strong pressures generated to inflate the lung may cause small ruptures in the
alveoli. The leaked air can be removed by the physician, and continual removal of this leaked air is
required until the ruptures have healed. There is a loss of intrapleural negative pressure that can
result in a lung collapse. Due to this there is a decrease in vital capacity as well as a decrease in PaO2
which is the main consequence of a pneumothorax. The decrease in PaO2 results from various factors
i.e low ventilation-perfusion ratios, anatomic shunts and alveolar hypoventilation. Most patients that
suffer from a pneumothorax also have an increase in alveolar-arterial oxygen tension. Diagnosis
Initially a complete medical and physical examination needs to be conducted. On examination of the
chest with a stethoscope it will be noted that there is either decreased or absent breath sounds over
the area of the affected lung, which may indicate that the lung is not unfolded in the pleural cavity.
There is hyperresonance (higher pitched sounds than normal) with percussion of the chest wall which
is suggestive of pneumothorax diagnosis. Chest x- rays will then be used to confirm the diagnosis of
the pneumothorax. In a supine chest x-ray, a deep sulcus sign is diagnostic and this is characterised by
a low lateral costophrenic angle on the affected side. Also the presence of air outside normal lung
airways and movement or shifting of the organs away from the air leak in the thoracic cavity will be
indicative of the presence of a pneumothorax. Diagram showing a neonate with a right tension
pneumothorax. Note the tracheal deviation to the left. Another procedure used is Transillumination.
This is a procedure used in an emergency situation and makes use of a fiberoptic light probe that is
placed on the baby's chest wall i.e. the side with the air leak will transmit a brighter light. Prognosis
Up to 50% of patients who suffer from a pneumothorax will have another or a recurring
pneumothorax. However, there are no long-term complications after successful treatment. Medical
and Surgical Management The main aim is to relieve the pressure on the lung and allow it to expand.
It is of vital importance to try and prevent the recurrence of a pneumothorax. Treatmen[5]t is
determined by the severity of symptoms and indicators of acute illness, the presence of underlying
lung disease, the estimated size of the pneumothorax on X-ray, and – in some instances – on the
personal preference of the person involved. There are a variety of treatment options for a
spontaneous pneumothorax including simple observation, chest tube placement, chemical
pleurodesis through a chest tube, and surgery. Conservative management with observation until air is
naturally resorbed by the body or simple chest tube placement alone has a very high rate of
recurrence (about 65%) in patients with LAM. Because of this, most thoracic surgeons recommend
pleurodesis (a procedure which obliterates the pleural space to prevent future pneumothoraces) after
the first episode of pneumothorax. Pleurodesis can be done mechanically (using physical abrasion) or
chemically (using talc, doxycycline, bleomycin or other agents). While chemical pleurodesis through a
chest tube can be successful, this may result in incomplete pleurodesis due to uneven distribution of
the chemical. Surgical treatment, using video-assisted thoracoscopy (VATS), is the preferred approach.
For patients with recurrent pneumothorax[6] after surgical intervention, there are several options.
For patients with a total or near total collapse, repeat surgical intervention is recommended. Options
include a repeat mechanical pleurodesis if it is unclear whether an appropriate mechanical
pleurodesis was done initially or pleurectomy in which the pleura overlying the ribs is actually
removed. Another option to consider for refractory pneumothorax is chemical pleurodesis in which a
drug or other agent is used to create an inflammatory response that results in pleurodesis. Talc is the
most commonly used agent due to its effectiveness. Historically, talc pleurodesis was considered a
contraindication to future lung transplantation because of the intense inflammatory response that
made surgery very difficult. However, in the 2014 consensus document for the selection of patients
for lung transplant by the International Society for Heart and Lung Transplantation, pleurodesis was
not considered a contraindication for transplantation. They recommended that “pneumothorax in a
patient who may become a future transplant recipient should be given the best immediate
management… and “the choice of intervention is unlikely to affect future acceptance for
transplantation.” Patients who undergo lung transplantation after a pleural intervention are at higher
risk of bleeding complications; therefore, a strategy of optimizing successful treatment of
pneumothorax while minimizing the impact on potential future lung transplantation should be
undertaken. Given the potential that any intervention could have an impact on future lung
transplantation should this become necessary, it is critical that the patient, pulmonologist and
surgeon work together to develop the best treatment plan for each individual patient. Physiotherapy
Management Indications for Physiotherapy[7] Lung collapse Increased work of breathing Thick
sputum plugs predisposing to ventilation difficulty Blood gas abnormalities Sputum retention Goals
for Physiotherapy To reinflate atelectatic lung areas To improve ventilation To increase oxygenation
Maintain airway clearance Improve exercise tolerance Physiotherapy Management To reduce work
and difficulty of breathing Body positioning Breathing control Relaxation technique To improve
ventilation Localised thoracic expansion exercise Sputum mobilisation techniques Postural drainage
Deep breathing exercise Percussion, shaking and vibrations Sputum removal techniques Coughing and
huffing Airway suctioning Physiotherapy outcome evaluation includes Respiratory rate Breathing
pattern Sputum quantity Ausculatation Cough sound Oxygen requirement SpO2 Arterial blood gases
Chest x-ray changes Muscle strength Functional performance

References

Martin, E.A. (Ed.). (2003). Oxford Concise Medical Dictionary, 6th Edition. Oxford, United Kingdom.
Oxford University Press.

Health24. (2008). Pneumonia. Retrieved February 13, 2009 from

http://health24.com/medical/Head2Toe/777-778-782,13491.asp

https://www.unicef.org/health/index_91917.html

AFP. (2009). 1.6 million die of pneumonia annually: studies. Retrieved April 8, 2009 from
http://www.google.com/hostednews/afp/article/ALeqM5j9-UqSxOOJLWxxBUz1lv9HR5YTgg

Health-cares. (2005). What is pneumonia? Retrieved February 13, 2009 from

http://respiratory-lung.health-cares.net/pneumonia.php

Bartleby. The Lungs. Retrieved April 8, 2009 from

http://education.yahoo.com/reference/gray/subjects/subject/240

Healthscout. (2009). Health Encyclopedia - Diseases and Conditions: Pneumonia. Retrieved April 8,
2009 from http://www.healthscout.com/ency/68/205/main.html

Weller, B.F. (Ed.). (2000). " Bailliere's Nurses' Dictionary", 23rd Edition. London, Harcourt Publishers
limited.

Smith, B., & Ball, V. (1998). Cardiovascular/Respiratory Physiotherapy. Mosby International Limited:
Italy

Koenig, S., & Truwit, J. (2006). Ventilator-associated pneumonia: Diagnosis, treatment and
prevention. Clin Microbiol Rev. 2006 October; 19(4): 637–657. Retrieved April 12, 2009 from
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1592694

Torpy, J. (2007). Ventilator associated pneumonia. Retrieved April 12, 2009 from
http://jama.ama-assn.org/cgi/content/full/297/14/1616

Atkuri, L.V., & King, B.R. (2006). Pediatrics, Pneumonia. Retrieved April 10, 2009, from
http://emedicine.medscape.com/article/803364-overview

Steyl, T. (2007). Applied Physiotherapy 403 notes: Intensive Care Notes. University of the Western
Cape.

Schiffman, G., & Stoppler, M. (2009). Pneumonia. Medicine Net. Com. Retrieved April 12, 2009 from
Causes, Symptoms, Signs and Treatment (Viral, Bacterial) on MedicineNet_com.mht

Klein, J. (2008). Pneumonia. Retrieved February 13, 2009 from

http://kidshealth.org/PageManager.jsp?dn=KidsHealth&lic=1&ps=107&cat_id=20043&article_set=23
001

Madjoe, L., & Marais, M. (2007). Applied Physiotherapy 203 notes: Physiotherapy in Respiratory Care.
University of the Western Cape.
 BTS Guidelines for the Physiotherapy Management of the Adult, Medical, Spontaneously Breathing
Patient 2009

PDR health. (2009). Pneumonia in children. Retrieved April 11, 2009 from
http://www.pdrhealth.com/disease/mono.aspx

Unicef (2006). Pneumonia: The Forgotten Killer of Children. Retrieved April 8, 2009, from
http://www.childinfo.org/pneumonia.html

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Drugs information online. (2009). Pneumonia in children care Guidelines information. Retrieved April
11, 2009 from http://www.drugs.com/cg/pneumonia-in-children.html

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Emergency management. –Nasal oxygen to relieve hypoxemia, respiratory distress, and central
cyanosis. –Intravenous infusion lines to administer medications or fluids. –Hypotension is treated by a
slow infusion of dobutamine . –The ECG is monitored continuously for dysrhythmias which may occur
suddenly. – Intravenous diuretics, and antiarrhythmic agents may be indicated. –Blood is drawn for
serum electrolytes and CBC –Intubation and mechanical ventilation may be performed based on
clinical assessment and arterial blood gas analysis

78. Emergency management. Aggressive volume expansion is of no benefit and may even worsen RV
function by causing mechanical overstretch Modest (500 mL) fluid challenge may help to increase
cardiac index in patients with PE, low cardiac index, and normal BP. vasopressors is often necessary,
Norepinephrine appears to improve RV function via a direct positive inotropic effect. It also increases
right coronary perfusion.

79. Emergency management. •Dopamine and dobutamine are first-line inotropic agents for the
treatment of PE-related shock. Both agents increase cardiac output. •Norepinephrine increases both
cardiac output and systemic vascular resistance and may be beneficial as monotherapy or in
combination with dopamine or dobutamine.

80. –. As soon as massive PE is suspected, high-dose unfractionated heparin should be administered in

larger-than-usual doses. Most patients should receive at least a 10 000-U bolus of heparin, followed
by a continuous intravenous infusion of at least 1250 U/h, with a target activated partial
thromboplastin time (aPTT) of at least 80 seconds Emergency management.

81. Medical Management •General measures to improve respiratory and vascular status •
Anticoagulation therapy • Thrombolytic therapy • Surgical intervention

82. GENERAL MANAGEMENT Oxygen therapy is administered to correct the hypoxemia, relieve the
pulmonary vascular vasoconstriction, and reduce the pulmonary hypertension.
83. Parenteral anticoagulation Immediate anticoagulation can be achieved with IV UFH,
subcutaneous LMWH, or SC fondaparinux. LMWH or fondaparinux are preferred over UFH for initial
anticoagulation in PE, as they have lower risk of inducing major bleeding and heparin-induced
thrombocytopenia. UFH is recommended for patients in whom primary reperfusion is considered, as
well as for those with serious renal impairment (creatinine clearance,30 mL/min), or severe obesity.

84. Anticoagulant Therapy Heparin •Heparin augments the activity of antithrombin III and prevents
the conversion of fibrinogen to fibrin. •5000-10000 Units IV Loading Dose, Then 1000 Units/hr IV
infusion drip • Duration: 7-10 days OR till clinical improvement • Follow up by PTT (1.5-2.5)

85. LMWH . •It should be used whenever possible for the initial inpatient treatment of DVT & PE.
Outpatient of DVT, and possibly PE ,is safe and cost-effective for carefully selected patients.

86. Fondaparinux •Anticoagulant pentasaccharide that specifically inhibits activated factor X •By
selectively binding to antithrombin, fondaparinux potentiates (about 300 times) the neutralization of
factor Xa by antithrombin •Fondaparinux does not cross-react with Heparin induced antibodies •FDA
has approved fondaparinux for initial treatment of acute PE and acute DVT as a bridge to oral
anticoagulation with warfarin

87. Vitamin K antagonists Gold standard’ in oral anticoagulation. •Warfarin prevents activation of
factor II, VII, IX and X. •. •Heparin is continued for 4–5 days to overlap with warfarin therapy to
counter paradoxical hypercoagulability that occurs with warfarin monotherapy.

88. Vitamin K antagonists Anticoagulation with UFH, LMWH, or fondaparinux should be continued
for at least 5 days and until the (INR) has been 2.0–3.0 for two consecutive day. Warfarin can be
started at a dose of 10 mg in younger otherwise healthy outpatients, and at a dose of 5 mg in older
patients and in those who are hospitalized.

89. Novel Anticoagulants Promise immediate onset of action and administration in fixed doses
without routine laboratory coagulation monitoring •These drugs have few drug-drug or drug-food
interactions, making them more “user friendly” •Dabigatran is a direct thrombin inhibitor
•Rivaroxaban is a factor Xa inhibitor •Both are approved in Canada and Europe for VTE prevention
after knee or hip arthroplasty

90. Thrombolytic treatment Thrombolytic treatment of acute PE restores pulmonary perfusion more
rapidly than anticoagulation with UFH alone Thrombolytic therapy has replaced surgical embolectomy
as the treatment for hemodynamically unstable patients with massive pulmonary embolism
Accelerated regimens administered over 2 hours are preferable to prolonged infusions of
first-generation thrombolytic agents over 12–24 hours.

91. Unfractionated heparin infusion should be stopped during administration of streptokinase or

urokinase; it can be continued during rtPA infusion. In patients receiving LMWH or fondaparinux at
the time that thrombolysis is initiated, infusion of UFH should be delayed until 12 hours after the last
LMWH injection (given twice daily), or until 24 hours after the last LMWH or fondaparinux
injection(given once daily).

92. Thrombolysis Indications: •Massive PE •Sub-massive PE where risk of bleeding low (in RVD)

93. THROMBOLYTIC THERAPY Dose Schedules in PE 1. Streptokinase (STK) • I V bolus 250,000 units
over 30’ followed by infusion of 100,000 units/hr for 12-24 hours 2.Recombinant tissue plasminogen
activator (rtPA) • IV bolus of 15 mg in 10’ followed by 85 mg in next 2 hours (total =100 mg) • To be
followed by heparin infusion on completion of TPA

94. THROMBOLYTIC THERAPY Alteplase •Indications: •Documented PE with: – Persistent hypotension

– Syncope with persistent hemodynamic compromise – Significant hypoxemia – +/- patient with acute
right heart strain •Approved Alteplase regimen is 100mg as a continuous IV infusion, in 2hr.
95. Before After

96. Potential benefits of TLT •More rapid resolution of symptoms (eg, dyspnea, Chest pain and
psychological distress) •Stabilization of respiratory and cardiovascular function without need for
mechanical ventilation or vasopressor support •Reduction of RV damage •Improved exercise
tolerance •Prevention of PE recurrence •Increased probability of survival

97. Potential harm •Disabling or fatal hemorrhage including intracerebral hemorrhage •Increased risk
of minor hemorrhage, resulting in prolongation of hospitalization and need for blood product
replacement

98. Use of Heparin Before and After Thrombolysis:

99. IVC filter • Indications: - DVT with massive pulmonary embolus - Recurrent PE not treatable with
anticoagulation - Absolute contra-indications for anti-coagulation - Chronic thromboembolic
pulmonary hypertension • Not used in: - Patients with free-floating thrombi in the proximal veins -
Patients scheduled for systemic thrombolysis, surgical embolectomy

100. Complications associated with IVC filter Early complications • Device malposition (1.3%) •
Pneumothorax(0.02%), • Hematoma (0.6%) • Air embolism (0.2%) • carotid artery puncture (0.04%) •
Arteriovenous fistula Late complications • Recurrent DVT (21%) • IVC thrombosis (2% to 10%), • IVC
penetration (0.3%) • Filter migration (0.3%) • Recurrent PE (2-5%) •

101. Catheter Embolectomy Interventional catheterization techniques Another approach is

mechanical clot fragmentation and aspiration. Pulmonary artery balloon dilation and stenting
Successful catheter embolectomy rapidly restores normal blood pressure and decreases hypoxemia.

102. Surgical Embolectomy When contraindications preclude thrombolysis. Surgical excision of a

right atrial thrombus. Rescue patients whose condition is refractory to thrombolysis Older case
series suggest a mortality rate between 20% and 30%

103. Massive Pulmonary Embolism – Management •Begin bolus high-dose IV unfractionated heparin
as soon as massive PE is suspected. • Begin continuous infusion of heparin to achieve a target aPTT of
at least 80 sec. •Volume resuscitation with no more than 500 to 1000 mL of fluid.( Excessive volume
resuscitation will worsen right ventricular failure. • Have a low threshold for administration of
vasopressors and inotropes.

104. Massive Pulmonary Embolism – Management • If thrombolysis is risky, consider placement of an

inferior vena caval filter, catheter embolectomy, or surgical embolectomy. •Do not use a combination
of thrombolysis and vena caval filter insertion. (The prongs of the filter insert into the caval wall.
Concomitant thrombolysis predisposes to caval wall Hemorrhage.) •Consider immediate referral to a
tertiary care hospital

105. Pulmonary Embolism in Pregnancy Leading cause of death in pregnancy. DVT and PE are
common during all trimesters of pregnancy and for 6-12 weeks after delivery. Heparin and
fibrinolysis are safe in pregnancy. LMWH can be given throughout their pregnancy Warfarin is
contraindicated Women experiencing a thromboembolic event during pregnancy should receive
therapeutic treatment with UFH or LMWH during pregnancy,

106. Pregnancy & Postpartum •Pregnant women who are in a hypercoagulable state or who have had
previous venous thromboembolism should receive prophylactic anticoagulation during pregnancy
•Anticoagulation may be restarted with UFH or LMWH 4- 6 hours following vaginal delivery or 6- 12
hours following cesarean delivery. •Anticoagulation continuing for 4-6 weeks postpartum and for a
total of at least 6 months.

107. Thrombolysis in pregnancy Streptokinase (and probably other thrombolytic drugs) does not cross
the placenta because of its high molecular weight. •However in the mother, bleeding is the major side
effect, usually from the genital tract and often severe. incidence of bleeding is about 8%. • Because of
the risk of bleeding, thrombolysis should not be used routinely in pregnancy. •Should not be used at
the time of delivery unless it appears that the patient is likely to die

108. Malignancy •Four- to sevenfold higher risk of thrombosis compared with patients without cancer.
•Caused by prothrombotic effects of the tumor and also because of treatment, particularly with
surgery, use of a central venous catheter,and chemotherapy. •~20% of patients presenting with VTE
have active cancer, associated with reduced survival. •Initial treatment with heparin and warfarin is
given in the standard manner.

109. Complications • Instant Death • Chronic pulmonary hypertension • Respiratory failure •

Congestive heart failure • Recurrence

110. PREVENTION BEFORE SURGERY GENERAL SURGERY • Unfractionated heparin 5000 units SC bid
or tid or •Enoxaparin 40 mg SC qd or •Dalteparin 2500 or 5000 units SC qd NEURO SURGERY
•Unfractionated heparin 5000 units SC bid or •Enoxaparin 40 mg SC qd and •Graduated compression
stockings or intermittent pneumatic compression

111. Prevention Prevent deep venous thrombosis. • Active leg exercises •The intermittent pneumatic
leg compression device •Use of elastic compression stockings •Anticoagulant therapy, Low molecular
weight heparin prophylaxis. •Avoid oral contraceptive pill

112. Intermittent pneumatic compression

113. Genetic Blood Tests 25-50% of patients with VTE have an inherited disorder There are genetic
causes of metabolism which may be tested for Factor V Leiden – causes increased clotting as variant
cannot be inactivated Factor Protein C Deficiency – results in normal cleaving of Factor Va and Factor
VIIIa

114. Prevention while traveling •Drink plenty of fluids. Preven dehydration, which can contribute to
the development of blood clots.. •Take a break from sitting. Move around the airplane cabin once an
hour or so., •Fidget in your seat. Flex your ankles every 15 to 30 minutes. •Wear support stockings.

115. Prognosis •5 to 10% of symptomatic PEs are fatal within the first hour of symptoms. •Prognosis
depends on the amount of lung that is affected and on the co-existence of other medical conditions;
•chronic embolisation to the lung can lead to pulmonary hypertension. •Once anticoagulation is
stopped, the risk of a fatal pulmonary embolism is 0.5% per year

116. NURSING MANAGEMENT

117. NURSING MANAGEMENT Impaired gas exchange related to decreased perfusion to lung tissues
in pulmonary vascular bed by embolus as manifested by dyspnea, hypoxemia.

118. •Auscultate breath sounds, noting crackles, wheezes. •Administer supplemental oxygen as
indicated. •Look for indication of mechanical ventillator •Treat underlying causes ( eg- respiratory
acidosis) •Monitor pulse oximetry and report O2 saturation <92%. •Encourage frequent position
changes. •Maintain chair or bed rest in semi-Fowler’s position. Support arms with pillows. Outcome-
Weaning from invasive to non invasive MV Normal bilateral entry breath sound Normal ABG findings.

119. Potential for decreased cardiac output related to heart failure as evidenced by increased
CVP ,engorged neck veins, pedal edema •Auscultate apical pulse, assess heart rate, rhythm. •Inspect
skin for pallor, cyanosis. •Monitor urine output, noting decreasing output and concentrated urine.
•Note changes in sensorium: lethargy, confusion, disorientation, anxiety, and depression. •Encourage
rest, semi recumbent in bed or chair. •Elevate legs, avoiding pressure under knee. Encourage active
and passive exercises. •Administer IV solutions, restricting total amount as Outcome- Vitals signs are
within normal range Intake output level maintained
120. Pain related to pulmonary embolism as verbalized by the patient •Asses the nature of the pain
•Asses related factors •Provide comfortable position •Relieve anxiety •Provide psychological support
•Administer oxygen therapy •Administer analgesics

121. Potential for impaired skin integrity RT edema, immobility etc. •Asses for the presence of related
factor •Observe condition of skin; pressure sore •Implement pressure relieving mattresses • Maintain
functional body alignment •Provide skin care •Encourage adequate hydration and nutrition
•Encourage ambulation if patient is able

122. Potential for bleeding RT anticoagulant/thrombolytic therapy •Asses signs and symptoms of
bleeding •Asses patient for high risk for bleeding condition like liver disease, kidney disease, severe
hypertension •Monitor PT level •Monitor IV dosage and delivery system to minimize the risk of over
coagulation / under coagulation. •Institute safety precautions- Pad the side rails •Avoid IM inj.

123. Cont… •Provide gentle oral care •Avoid constipation •Limit physical manipulation •Compress IV
sites for at least 10 min and arterial sites for 30 min •Draw all laboratory samples through existing line
•Send specimens for cross matching •Don’t give foods rich in vitamin K

124. Anxiety related to threat of death , change in health habits, increase in respiratory difficulty
•Asses the level of anxiety. •Encourage patient to ventilate feelings of anxiety. •Asses patient’s
normal coping mechanisms •Support previously effective coping mechanisms - Be empathetic
•Provide adequate rest, Organize activities •Decrease sensory stimulation

125. •The importance of continued warfarin administration for 3 to 6 months to prevent further
thrombus development. •Foods high in vitamin K, such as dark green vegetables and apricots, must
be limited during this time period to prevent decreased warfarin action. •Therapeutic INR value
should be checked . •Not to use warfarin with acetaminophen, nonsteroidal anti-inflammatory drugs
because such combinations can quickly elevate the INR. •To wear a Medic-Alert bracelet indicating
her history Knowledge deficit regarding management of bleeding , embolism & homecare

126. Facilitate learning processes; inform patient and significant others of the following • Etiology •
Effects • Common risk factors • Inform patient and significant others about medications, side effects,
dosage, action etc. • Discuss and give patient list of signs and symptoms of excess of anticoagulation

127. Health Education •Look for bleeding esp., with falls •Avoid use of sharps •Use soft tooth brush
•Don’t take aspirin and other O.T.C. drugs while taking warfarin •Avoid use of laxatives •Report
occurrence of dark /tarry stool to health care provider immediately

128. Health Education •Describe strategies to prevent recurrent DVT/PE •Avoid sitting with legs
crossed or sitting for prolonged periods of time •Follow the medication regimen •When traveling
change position regularly, walk occasionally, do active movement of legs and ankles while sitting
•Drink fluids esp. while traveling and in warm weather, to avoid hemoconcentration due to fluid
deficit

129. Health Education •Describe signs and symptoms of lower extremity compromise; Homan’s sign,
calf pain, edema, increased local temperature etc. •Describe how and when to contact the health
care provider if signs and symptoms of circulatory compromise or pulmonary compromise are
identified.

130. Discharge and Home Care Guidelines Prevent recurrence. The nurse should instruct the patient
about preventing recurrence and reporting signs and symptoms. Adherence. The nurse should
monitor the patient’s adherence to the prescribed management plan and enforces previous
instructions. Residual effects. The nurse should also monitor for residual effects of the PE and
recovery. Follow-up checkups. Remind the patient about follow-up appointments for coagulation
tests.