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Pneumonia: Treatment

by Jeremy Brown, PhD
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    00:01 The other aspect of management is this correction of oxygenation. If you have consolidation, you are placing air in the alveoli with inflammatory fluid. And that causes hypoxia because it generates what we call a right to left shunt. What I mean by that is that blood coming up the pulmonary artery, which is deoxygenated, will reach the area with the consolidation in it, it will go through that area but because there's no air in the alveoli, that blood will not be oxygenated, and therefore, it will reach the pulmonary veins in a deoxygenated state, and you end up mixing the deoxygenated blood coming from the consolidated lung with the oxygenated blood coming from the remaining normal lung. The consequence of that is that you have a mixture of hypoxic blood and normoxic blood, and the combination of the two will dictate how hypoxic the patient will be. So in this example, for example we have a patient who has quite extensive consolidation and therefore, the deoxygenated blood shunting through that consolidated lung has a significant effect on the arterial oxygen concentration, reducing it down to about 80%. So oxygen needs to be corrected and we do that using masks and if necessary mechanical ventilation. Another important physiological upset that occurs in patients with pneumonia is due to the sepsis, due to the septic shock potentially, that can develop in a minority of patients with acute bacterial pneumonia. Before that, actually many patients because they’ve been breathing fast, unable to drink and eat, they are dehydrated. So dehydration is common, and beyond that some patients will develop septic shock with persisting hypotension even after they’ve been rehydrated. An acute kidney injury is very common in these patients as a consequence of these problems. So patients with pneumonia will require intravenous fluids to rehydrate them if they have got a low blood pressure or clinically, they are dehydrated. And if the low blood pressure persist despite rehydration, then you need to consider inotropes and admission to intensive care to treat the septic shock, and to avoid the downstream consequences of having hypotension, increasing kidney injury, etc. etc. Killing the pathogen. Well, when the patient first presents to you with pneumonia, you don't know what the bug is causing that pneumonia, so we treat the patient initially with what we call empirical antibiotics, ones which will cover the common causes of pneumonia. To do that we need to know what the common microbial causes of pneumonia are. And for the industrialized world, these are relatively similar across different countries, and they split down into about 20-25% of cases are just due to viruses, influenza being the commonest one, but occasionally you get other viruses rhinovirus, RSV, parainfluenza, etc. and adenovirus. And then, three quarters of cases are due to bacteria. Those bacteria can be divided into two categories: the pyogenic bacteria the ones that cause a higher inflammatory response, focal consolidation generally speaking.

    03:15 The ones that will cause more acute and severe disease, and that's mainly Streptococcus pneumonia, which is responsible for about half of all cases of community acquired pneumonia.

    03:25 But there are a couple of other bacteria that occasionally come through Haemophilus influenza, Stapylococcus aureus, being the commonest. Fortunately, gram-negative pneumonia is relatively rare. Atypical organisms cause a less aggressive disease, and those are mycoplasma and chlamydophila, and occasionally Legionella, which is an exception and that it can actually cause severe disease despite being part of the atypical category of organisms. An important point is that many patients will have a mixed infection, so they will have a viral infection that allows the bacteria in, so they have a combination of influenza A and say pneumococcal pneumonia.

    04:00 And the same thing happens with mycoplasma and chlamydophila, that allows the bacteria in to cause an infection, so you get a combination of an atypical organism plus Haemophilus, Staphylococcus aerus or Steptococcus pneumonia. A very important point here is that actually, when it comes to the treatment of pneumonia we don't normally treat the viruses, the exception being influenza A which we’ll treat with a neuraminidase inhibitors because there are no good antiviral agents for most of these viruses, but we do have to treat the bacteria.

    04:32 So it's a question of which antibiotic to use. I’ll come back and discuss the antibiotics in a bit more detail in a subsequent slide. Now we do do tests to identify what the pathogen that’s causing pneumonia is. We actually limit these tests in general to patients presenting with moderate or severe disease. So they are in hospital and they have a reasonably high risk of mortality of 15% or more. In these patients we’ll do blood and if possible a sputum culture, although many patients are unable to produce sputum for this. We might do a viral nasopharyngeal aspirate to look for viruses such as influenza A. And there are two urine antigen tests that are used for patients presented with pneumonia: one looks for pneumococcus, and the other looks for legionella. So we may send those as well, and those both have a sensitivity of about 70% for those bacterial pathogens. The serology test for viruses, mycoplasma and chlamydophila, are actually not often particularly useful.

    05:30 The reason why is that to actually get a positive result for serology, you need a matched sample, when the patient is ill and 3 or 4 weeks later when they are recovering. So serology in general does not guide therapy because it's a post disease diagnosis. The changes in serology only really shows that you had that infection only 3 or 4 weeks after you got better.

    05:54 The last test I've put down here is the HIV test. Now that doesn’t tell you the organism that’s causing the disease, but it is an important microbial test because HIV is an important risk factor of community acquired pneumonia. And patients with HIV will develop pneumococcal pneumonia at a much higher rate. Apparently, it’s about 20 times the chance of non-HIV-infected person, and that increase in the chance of getting pneumococcal pneumonia is unrelated to having a low CD4 count. So a pneumonia is an early marker of somebody with HIV infection before they've developed significant immune suppression according to the CD4 count, and therefore an HIV test in any situation where HIV may be relatively prevalent, an HIV test would be useful. So antibiotics. You need to kill the invading pathogen. As I discussed before, it’s the bacteria that we are really targeting, and the one that we really need to kill is Pneumococcus, with some considerations for S. aureus, Haemophilus influenzae if somebody is particularly unwell. So in general, we need –sorry- we need also to cover the atypical organisms, mycoplasma and chlamydophila. Now the problem here is that the antibiotic that kills pneumococcus doesn't kill chlamydophila and mycoplasma necessarily. So the best antibiotics to use against pneumococcus is a penicillin such as amoxicillin, but that does not have any efficacy against chlamydophila or mycoplasma.

    07:30 For those we need a macrolide. So if somebody presents with a mild disease, actually we got a little bit room to maneuver. If the patient doesn't get better with one antibiotic, then we can swap to another. So in general what we do know in those situations is that we treat them with amoxicillin or clarithromycin, and see how they go, and if they are not improving then we would actually need to think about swapping. And the normal situation there is that somebody will receive amoxicillin but it turns out to be a mycoplasma infection, and the amoxicillin as it doesn't kill mycoplasma, the amoxicillin has no effect, therefore we will swap to clarithromycin. Moderate disease. Because the patient is in hospital, because the mortality is now reaching 15% or thereabouts in the CURB65 score 2 or more, that’s the definition of moderate disease, we’d like to make sure that we kill all the most likely pathogens. So amoxicillin is combined with a macrolide such as clarithromycin, so that we cover both the pneumococcus and the mycoplasma and the chlamydophila in those circumstances. Severe disease, when patients are considered for intensive care, and have really quite marked systemic upset, and maybe have a high risk of death, then we just need to be a little careful, and we extend the cover to amoxicillin to coamoxiclav, and the reason why we do that is that coamoxiclav, augmentin is its trade name has better activity against Staphylococcus aureus, and some of the gram-negative bacteria that potentially could be causing infection in these circumstances. And because the patient is terribly ill, we don't have much room for maneuver, we don't have much chance of making a mistake here, and then correcting it later on, so the cover for the potential pathogens needs to be extended accordingly. So in these circumstances is a combination of coamoxiclav and a macrolide, such as clarithromycin. An important point here is that some of the unusual gram-negative pathogens that are very rarely found in community acquired pneumonia, such as Pseudomonas aeruginosa, are not covered by these treatments, and that needs to be thought about if the patient is not getting better.

    09:44 Right, how do we monitor the progress of the disease? Well normally patient with community acquired pneumonia presenting to hospital, coming in, receiving their antibiotics, their IV rehydration, they actually get better within a couple days, from 2 to 3 days.

    10:00 Normally, the pyrexia will go away within 72 hours. The pulse rate and their blood pressure will come back down to normal, and the oxygenation will improve. And, as well we can do a blood test to see whether there's an improvement in whatever parameters that have been abnormal on the initial presentation. So for example, the C-reactive protein, the inflammatory marker which is normally quite high on presentation should usually fall by 50% every 24 hours or so once the stimulation of the inflammation has gone. So once the infecting organisms have been killed by the antibiotics then the CRP will fall by 50% every day or so. So by the day 3 or 4, we expect remitting CRP level to have fallen by over 50%. And the things like the hyponatremia, the abnormal liver function test, the high white cell count, the high urea and creatinine, they should all normalize over the first couple of days of admission. If somebody is not getting better, if the blood tests are persistently abnormal, if they are still hypoxic, there is still pyrexia, you need to think about various things. One is that you need a chest X ray to look for the complications, and if there is a pleural effusion present then you need to tap that pleural effusion to make sure it’s not infected. You need to think about re-culturing to see whether the bacteria that is present might be a resistant organism and I've mentioned pseudomonas already as one of the key organisms we need to consider. And then, we just have to think about the diagnosis. Was this the right diagnosis? Did they have pneumonia or do they have one of the other conditions that I mentioned earlier? Is this a pulmonary embolus for example? Is there a pulmonary oedema complicating this? Is there a cancer that makes the consolidation difficult to treat, as there is no drainage of the area of the lung. Or is this an inflammatory lung disease which is not infective at all, a cryptogenic organizing pneumonia etc. etc.

    12:03 etc. The other issues that you can get with pneumonia,


    About the Lecture

    The lecture Pneumonia: Treatment by Jeremy Brown, PhD is from the course Infections of the Respiratory Tract.


    Included Quiz Questions

    1. Amoxicillin for Chlamydophila pneumoniae
    2. Neuroaminidase inhibitor for Influenza
    3. Amoxicillin for Streptococcus pneumoniae
    4. Clarithromycin for Mycoplasma pneumoniae
    1. Oxygen content is more than the pulmonary artery oxygen content but lesser than the pulmonary vein oxygen content.
    2. Oxygen content is same as in the pulmonary artery.
    3. Oxygen content is lesser than that of the pulmonary artery.
    4. Oxygen content is more than that of the pulmonary vein.
    5. Oxygen content is normal
    1. Start inotropes and intensive care unit referral
    2. Start IV antibiotics
    3. Increase the fluid's rate of flow through the IV line
    4. Wait and watch for improvement.
    1. Urine
    2. Blood
    3. Sputum
    4. Nasopharyngeal swab
    5. Nasal bone cartilage biopsy
    1. Community-acquired pneumonia
    2. Aspiration pneumonia
    3. Hospital-acquired pneumonia
    4. Interstitial pneumonia
    5. Atypical pneumonia
    1. Streptococcus pneumonia
    2. Legionella
    3. Mycoplasma pneumonia
    4. Hemophilus influenza
    5. CMV virus
    1. Amoxicillin and clarithromycin
    2. Amoxicillin or ceftriaxone
    3. Amoxicillin or clarithromycin
    4. Coamoxiclav and clarithromycin
    5. Ceftriaxone
    1. Coamoxiclav 1.2gms tds and clarithromycin 500mg bds for 5 days
    2. Amoxicillin 500 mg tds and clarithromycin 500mg bds for 5 days
    3. Amoxicillin 500 mg tds or clarithromycin 500mg bds for 5 days
    4. Coamoxiclav 1.2gms tds and clarithromycin 500mg bds for 3 days
    5. Amoxicillin 500 mg tds
    1. Pseudomonas
    2. Streptococcus pneumonia
    3. Legionella pneumonia
    4. Mycoplasma pneumonia
    5. Pneumococcus
    1. C- reactive protein decreases to less than 50%
    2. C- reactive protein decreases to less than 30%
    3. C- reactive protein decreases to less than 40%
    4. C- reactive protein decreases to less than 20%
    5. C- reactive protein decreases to less than 10%
    1. All the following options are helpful in monitoring patients who are not recovering post treatment
    2. Perform chest X-ray to rule out other complications
    3. Perform pleural effusions if necessary
    4. Reconsider alternative diagnosis
    5. Re-culture and check for resistant organsims
    1. Interstitial lung disease
    2. DVT
    3. Cardiac ischemia
    4. Atrial fibrillation
    5. Acute respiratory distress syndrome

    Author of lecture Pneumonia: Treatment

     Jeremy Brown, PhD

    Jeremy Brown, PhD


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