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.
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.
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.
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.
So it's a question of which antibiotic to use.
Microbiologic testing and the site of care are usually
determined by the severity of the illness, with most of the testing taking place in the hospital setting.
In mild Severity, with a CURB-65 score of zero, or a PSI score of 1-2, patients are usually treated as an outpatient.
Tests are usually minimal but can include covid 19 testing or influenza testing depending on local incidence levels.
In moderate severity with CURB-65 scores of 1-2
or PSI scores of 3 to 4,
patients are usually usually hospitalized on a general medicine floor.
Tests would include covid 19, rapid PCR or culture for MRSA,
blood cultures (which are taken prior to administration of antibiotics), sputum gram stains or cultures, urine strep antigen,
legionella testing, respiratory virus panels during flu season, and HIV screening.
Finally, in very severy cases with a CURB-65 score of three or more, and a PSI of 4-5,
The reason why is that to actually get a positive
result for serology, you need a matched sample,
these patients are usually treated in the ICU. Testing is similar to that of moderate severity cases
plus the possible addition of a bronchoscopy if the benefits outweigh the risks.
This allows for specimen collection for gram stain and cultures, fungal stains and cultures, and molecular testing.
The Empiric antibiotic guidelines is based on several factors, but for patients without comorbidities,
penicillin allergy, or suspicion of MRSA pr pseudomonas infections, the guidelines are as follows.
antibiotics should be started within 4 hours of presentation or within 1 hour if the patient is in septic shock.
The regimine selected is dictated by both the pathogen and the case severity.
It is usually guided by local susceptibility patterns, drug formularies, and individual patient characteristics.
If a pathogen is subsequently identified,
the susceptibility testing should be used to guide that regime adjustments.
The duration of therapy varies, with Mild CAP cases receiving
5 days or oral antibiotics as an outpatient,
and moderate or severe cases receive 5-7 days of IV antibiotics in the hospital.
Clinical improvement, trending procalcitonin levels (which is a biomarker for active infection),
pathogen, and presence of clinical complications all must be taken into consideration when determening the lengh of therapy.
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.
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.