Reflection:
Using the Gibb's Reflective Model, i will be reflecting on the practical session we had on the 7th of March, 2016.
Description: In this week, initially, we practiced IV
cannulation. I cannulated twice, once with a 20G and the second time with an
18G needle. I followed the steps for cannulation and both times I got a
flashback instantly. Following this we learned how to perform SC injections. My
teacher demonstrated this skill and then I tried doing it. I used a 2mL
syringe, however, we learned that the maximum volume via SC is 1mL. I withdrew
1 mL of a drug. After this I cleaned the site of injection with an alcohol
swab. After this I grabbed the syringe with the medication in my right hand and
pinched the patient’s skin with my left hand. I inserted the needle at a 45
degree angle to the skin, with the bevel facing upwards. The model we used
showed whether the needle went into the SC layer or not. I had successfully
inserted the needle into the SC layer. I
then slowly injected the medication into the patient’s skin. After this I
removed the needle and pressed on the skin gently in a circular motion to distribute
the medication.
Feelings: This time around I felt very comfortable
and confident to perform the IV cannulation skill. I felt proud of myself for
being able to get a flashback immediately. I was very excited to learn how to
perform the SC injection. I felt it was very easy to grasp and perform. I felt
proud of myself when I was able to perform this skill successfully from the
first time.
Evaluation: The IV cannulation was really good. I
followed the correct steps and got a flow of blood into the cannula. Moreover,
I did a very good job at executing a SC injection. I followed all the steps
correctly and that was great!
Analysis: I am very happy about the backflow of blood
because this means that I entered the cannula into the vein. This makes for a
successful cannulation. I did everything correctly in this lab, and it was
great. Furthermore, for the SC injection, I cleaned the site aseptically, to
ensure asepsis. This is a crucial step, and I did it. Also, after injecting the
patient, I saw that I was able to get the needle into the SC layer of the skin,
which was very satisfying.
Conclusion: I could keep practicing IV cannulation to
keep improving. I became better at this skill just from a few times of
practice. Therefore, any practice will definitely have an impact on my ability
to perform this skill seamlessly. Also, for the SC injection, I did a very good
job for my first time, however, I must continue to practice this skill until it
becomes second nature. I believe I did everything revolving around this skill
the right way and have nothing to add.
Action Plan: I plan to keep up the good work and keep
practicing performing IV cannulation. In
addition, I plan to practice doing SC injections whenever possible. I also plan
to continue following the correct steps for this skill, in accordance with what
is required of me.
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| Image 1: Me cleaning the site before performing SC injection. |
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| Image 2: Me pinching the skin as i insert the needle at a 45 degree angle to the skin. |
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| Image 3: Showing the needle fully inserted. |
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| Image 4: Showing a verification that the needle is in the SC layer. |
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| Image 5: Me disposing of the needle in the sharps box after i was done. |
Learned Concepts
In this week's lecture we learned about occupational lung diseases. These include coal worker's pneumoconiosis, silicosis, asbestosis, hypersensitivity pneumonitis, tumor-related disorders, and other exposures.
Interstitial lung disease is caused by inorganic and organic dusts, chemical exposure, autoimmune, and some unknown causes.
Presents as progressive dyspnea, disease specific symptoms (connective tissue diseases), abnormal pulmonary function test, abnormal CXR.
Diagnosed by complete history taking, physical assessment, CXR, and other tests done in-hospital.
When gathering this patient's history must ask for age, cigarette smoking, prior medication use, duration of symptoms, autoimmune disorders, connective tissue diseases, occupational exposures and home environment.
In interstitial lung disease upon chest auscultation can hear crackles, but no wheezes (large airways not involved), and bronchovesicular breath sounds (high pitch sounds over main bronchi). There will also be digital clubbing.
Coal Worker's Pneumoconiosis is defined as the accumulation of coal dust and the lung tissue's reaction to its presence. Can be simple or complicated. This disease is caused by exposure to coal dust, and geographical location.
Types of coal include Anthracite, Bituminous, Lignite.
Risk factors are:
- Particle size
- Age at first exposure
- Duration and type of exposure
- History of cigarette smoking
- Associated Crystalline Silica exposure
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| Image 6: Note about pathophysiology of CWP. |
CWP clinically presents as progressive dyspnea that worsens with high level of exposure, long duration of exposure, and history of cigarette smoking. Also presents as Caplan syndrome (Positive rheumatoid factor). Simple CWP is usually asymptomatic but complex CWP shows signs of cough, dyspnea, decreased lung function, and RVF.
Diagnosis usually done in- hospital using CXR, complete blood count, and other tests.
Prehospitally we manage this type of patient symptomatically by providing oxygen and bronchodilators as needed. Also, in hospital they must monitor such patients, give them immunizations to limit infections, and monitor for secondary infections.
Asbestosis is pneumoconiosis associated with the inhalation of Asbestos fibers. These fibers can be thin and straight (very poor prognosis since it goes down the airways and stabs the alveoli) or curved( better prognosis).
Caused by occupational exposure (construction industry, ship building), and non-occupational exposure (residential home renovations). High risk occupations include plumbers, electricians, carpenters, boiler makers.
Other risk factors are age at first exposure, Abestos particle type, duration and type of exposure, and history of cigarette smoking.
Pathophysiology is similar to that of CWP except after the Abestos fibers are inhaled there is a latency period before phagocytosis occurs.
Presents as progressive dyspnea that is worse if there is a high level of exposure, long duration of exposure, and history of cigarette smoking. Upon chest auscultation there is bilateral basil crackles and mild expiratory wheezing. A late sign is Cor Pulmonale.
Cor Pulmonale is, as we learned 2 weeks ago, failure of the right side of the heart due to long-term pulmonary hypertension. Marked by edema, cardiac arrhythmias, JVD, and third heart sound.
Asbestosis is diagnosed by a series of tests conducted in the hospital. These tests include complete blood count, CXR, sputum cultures, among others.
To manage this patient supplemental oxygen therapy is required, prevention of further exposure, and bronchodilators.
Silicosis is pneumoconiosis associated with the inhalation of Crystalline Silica dust. Most common is Quartz. Silicosis is classified as chronic, accelerated, or acute.
Silicosis can be caused by occupational and non-occupational exposures. Some high risk occupations include tunneling, steelworks, sand blasting, stone masonry, glass manufacturing, and construction industry.
Other risk factors include age at first exposure, Crystalline Silica type, duration and type of exposure, and history of cigarette smoking.
Pathophysiology of chronic Silicosis same as asbestosis. However, pathophysiology of accelerated Silicosis has a much shorter latency period than chronic silicosis.
Pathophysiology of acute silicosis is caused by extensive Crystalline Silica inhalation. There is Proteinaceous Alveolar Filling which leads to phagocytosis and continues in the same path as the chronic and accelerated silicosis resulting in an immune response.
Chronic and accelerated silicosis present as progressive dyspnea, coughing and wheezing.
Acute silicosis presents as rapidly progressing dyspnea, cough, wheeze, pleuritic pain, and may mimic atypical pneumonia.
Diagnostics of silicosis include CXR, Serologies, sputum cultures, complete blood count, among others.
Management includes prevention of further exposure, oxygen, and bronchodilators. In hospital, immunizations are administered to limit infections and continuous monitoring for secondary TB is done.
We then went on to learning about hypersensitivity pneumonitis which is defined as lung inflammation associated with the exposure to an allergen. This disease is classified as acute, sub acute, and chronic.
The cause of hypersensitivity pneumonitis is widely variable. It is interesting to note that cigarette smokers have a decreased risk of attaining this disease. This is due to the decreased immune response and allergic response of lungs from airway damage.
High risk occupations include farming, bird fanciers, manufacturing, textile workers, and many others.
Other risk factors are allergen type, age at first exposure, duration and type of exposure, and associated immunodeficiency disorders.
Management of Acute Hypersensitivity pneumonitis:Asbestosis is pneumoconiosis associated with the inhalation of Asbestos fibers. These fibers can be thin and straight (very poor prognosis since it goes down the airways and stabs the alveoli) or curved( better prognosis).
Caused by occupational exposure (construction industry, ship building), and non-occupational exposure (residential home renovations). High risk occupations include plumbers, electricians, carpenters, boiler makers.
Other risk factors are age at first exposure, Abestos particle type, duration and type of exposure, and history of cigarette smoking.
Pathophysiology is similar to that of CWP except after the Abestos fibers are inhaled there is a latency period before phagocytosis occurs.
Presents as progressive dyspnea that is worse if there is a high level of exposure, long duration of exposure, and history of cigarette smoking. Upon chest auscultation there is bilateral basil crackles and mild expiratory wheezing. A late sign is Cor Pulmonale.
Cor Pulmonale is, as we learned 2 weeks ago, failure of the right side of the heart due to long-term pulmonary hypertension. Marked by edema, cardiac arrhythmias, JVD, and third heart sound.
Asbestosis is diagnosed by a series of tests conducted in the hospital. These tests include complete blood count, CXR, sputum cultures, among others.
To manage this patient supplemental oxygen therapy is required, prevention of further exposure, and bronchodilators.
Silicosis is pneumoconiosis associated with the inhalation of Crystalline Silica dust. Most common is Quartz. Silicosis is classified as chronic, accelerated, or acute.
Silicosis can be caused by occupational and non-occupational exposures. Some high risk occupations include tunneling, steelworks, sand blasting, stone masonry, glass manufacturing, and construction industry.
Other risk factors include age at first exposure, Crystalline Silica type, duration and type of exposure, and history of cigarette smoking.
Pathophysiology of chronic Silicosis same as asbestosis. However, pathophysiology of accelerated Silicosis has a much shorter latency period than chronic silicosis.
Pathophysiology of acute silicosis is caused by extensive Crystalline Silica inhalation. There is Proteinaceous Alveolar Filling which leads to phagocytosis and continues in the same path as the chronic and accelerated silicosis resulting in an immune response.
Chronic and accelerated silicosis present as progressive dyspnea, coughing and wheezing.
Acute silicosis presents as rapidly progressing dyspnea, cough, wheeze, pleuritic pain, and may mimic atypical pneumonia.
Diagnostics of silicosis include CXR, Serologies, sputum cultures, complete blood count, among others.
Management includes prevention of further exposure, oxygen, and bronchodilators. In hospital, immunizations are administered to limit infections and continuous monitoring for secondary TB is done.
We then went on to learning about hypersensitivity pneumonitis which is defined as lung inflammation associated with the exposure to an allergen. This disease is classified as acute, sub acute, and chronic.
The cause of hypersensitivity pneumonitis is widely variable. It is interesting to note that cigarette smokers have a decreased risk of attaining this disease. This is due to the decreased immune response and allergic response of lungs from airway damage.
High risk occupations include farming, bird fanciers, manufacturing, textile workers, and many others.
Other risk factors are allergen type, age at first exposure, duration and type of exposure, and associated immunodeficiency disorders.
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| Image 7: Note about the pathophysiology of Hypersensitivity Pneumonitis. |
Acute Hypersensitivity pneumonitis presents as abrupt chills/ fever, chest tightness, dyspnea, malaise, cough, and crackles.
Sub acute presents as dyspnea, gradual onset, anorexia, malaise, cough.
Chronic presents clinically as insidious onset, dyspnea, anorexia, malaise, possible digital clubbing, irreversible pulmonary fibrosis and cough.
Diagnostics for acute and sub acute hypersensitivity pneumonitis is CXR, pulmonary function test, high resolution chest CT scan, and pathology.
Diagnostics for chronic hypersensitivity pneumonitis include complete blood count, lung biopsy, CXR, pulmonary function test, and high resolution chest CT scan.
- Prevent further exposure
- Symptomatic (oxygen, bronchodilators)
- Immunizations
Management of chronic hypersensitivity pneumonitis:
- Prevent further exposure
- oxygen + bronchodilators
- Immunizations
- Corticosteroid treatment
After reading the recommended readings this is what i learned.
The best treatment to provide for pneumonia patients found in the community is to transport them to a hospital as soon as possible. In hospital they will conduct tests to pinpoint the cause and treat it (Schmitt, 2010). Therefore, as a paramedic i must provide early and rapid transport to such patients to get them to definitive care.
In one of the readings i found occupational asthma. I found this interesting since it was not covered in the lecture. Occupational asthma has the same symptoms as regular asthma. However, it is triggered by the exposure to an agent that is encountered specifically in the occupational environment. Similarly, occupational COPD is the same as regular COPD except that the inhalation of noxious particles or gases encountered in the occupational setting contribute to the COPD. It was also interesting to learn that occupational asthma is the most common industrial lung disease but it is underestimated (Reid & Reid, 2013).
References
Reid, P.A., & Reid, P.T.
(2013). Occupational lung disease. The Journal of the Royal College of
Physicians of Edinburgh,43, 44-48. doi: 10.4997/JRCPE.2013.111
Schmitt, S. (2010). Community
acquired pneumonia. Retrieved from https://elearning.fchs.ac.ae/mod/resource/view.php?id=33471
Stand Out Moment
Biggest Impression
The biggest impression on me as a paramedic this week was learning SC injections. This is a very important skill that i will definitely need once i become a paramedic.
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