Dental Management of Patients with Respiratory Disease

-Most common respiratory disease is Airway disease and Chronic infectious disease .
-Asthma and tuberculosis fall under a category called chronic obstructive airway disease
(COPD )
-Most chronic infectious disease is tuberculosis ..
-COPD : chronic irreversible airflow limitation ..
-How to differentiate between Asthma and COPD?
1-Pulmonary function: youll find that the patient has airway obstruction
2-reversibility : give the patient a bronchodilator ( beta2 agonist ) and recheck the function
test once again ..
If it is reversible = then the patient has Asthma
If irreversible ( the airway obstruction is fixed and the bronchi cant be dilated ) the patient
has COPD .
Pulmonary function = the actual values the patient score / the predicted value by the
computer = --%
The value of the irreversibility 12% from the basal of the patient.
when you do the pulmonary function you have to take the patients weight and age and
insert those data into the computer to calculate the (basal or the predicted value) then the
patient do the test and you calculate how much patient got from the expected values ..
For example patient is 80 kg and is 60 years old the computer will calculate the expected
values that the patient should get using those data .. then we do the test for the patient and
see how much he was able to score out of the expected value that the computer estimated
..
After we are done with the test we give the patient a bronchodilator and see if the values
changes this means that the disease he has is reversible and it is asthma ..
Normally ubove 80% if less than 80% do the irreversibility test
COPD : 2 main diseases
1-chronic bronchitis : chronic cough with expatriation for at least 3 months for 2 successive
years
2- emphysema : permanent ( irreversible ) abnormal dilatation of the air spaces distal to the
respiratory bronchiole ( in the alveoli ) which is the last part of the bronchus where gas
exchange occur ..

-The regular episodes of cough accompanied with expatriation of mucous ( for one week of
time or less that 3 months for 2 successive years is called acute bronchitis .
Normally we dont have sputum when we cough . any spetum or secretions is considered an
abnormal thing ..
Causes of COPD :
1-smoking
2- Air pollution
3- Occupational exposure ( works in a factory fll of dust or smoke)
4- Alfa 1- antitrypsin deficiency ( anti-elastiase and protease inhibitor)
-If patient is a female and is not a smoker think of cause number 2+3
-If patient is non-smoker and if about 30 -40 years old with no history of occupational
hazards think of cause number 4 which is something congenital ..
*Blue bloater =
* Pink buffer =
Generally there is no one thats is purely chronic bronchitis nor Emphysema it is always a
mixed condition with one of the diseases having the upper hand or the more dominant one
.. how to know wich one is the dominant one ?
1- The clinical picture
chronic bronchitis : Patient around 50 + overweight +chronic productive cough +
large amount of sputum +dyspnea but less than the patient who is emphysematous
+frequent infections hypoxia ( po2 in the blood is less than normal ) cyanotic patient
due to elevated co2 in the blood + elevated hematocrit value and this is related to
elevated co2 levels this will result in more red blood cells to detoxify the body from
the cos2 .
*po2= oxygen tension . measured using blood gases test . we also can measure
those thing using this test ( PH PCO2 PCO2 )
*So2= oxygen saturation .
Emphysema: a more prominent dyspnea( because the problem is in the alveoli ) =
shortness of breath +infections are normal they come in the winter once per year
with no septum
as normal ppl ..
2- Investigations :
1-Pulmonary function
2- x-ray

3-Blood gases
How to differentiate between dilutional anemia and actual anemia ?
By measuring the hematocrit value ..
dilutional anemia can be due to renal failure ..

- increase hematocrit value: due to decrease in PO2 level (hypoxia), and as a defense
mechanism, the body increases the hematocrit
level (increase in the RBCs number) to increase the PO2 level.
as the pt with anima we do for him hematocrit value to differentiate between the normal
anemia & dilutional anemia (in pt
with kidney failure).

Cor pulmonale: right side heart failure secondary to pulmonary (lung- respiratory ) disease

Why right side ? because the main function of the right ventricle is to pump blood to
the chest so if we have any problem in the chest the back pressure will damage the
right ventricle atrophy dilatation failure so it is a late effect of pulmonary
disease ..
Cor pulmonale is so common with bronchitis and rare with emphysema

Chest x-ray :
1- Bronchitis : congestion .= increase bronchio vascular marking around the haillar
node from repeated infection (will show congestion) .
2- Emphysema : hyperinflation . lung is mostly translucent/radiolucent (not sure,
sorry!) ribbon shape heart .

- in emphysema= -older onset
- barrel chested= wide shoulder & long chest
- sever dyspnea= due to gas exchange problem. at the beging of the disease the dyspnea is
body protective
mechanism to increase the respiratory rate after the problem in the gas exchange

- any pt smoker with cough & mucous production and he might have COPD I should do

1- chest x- ray 2- pulmonary function 3- blood gases

- FEV1 = forced expiratory volume in the 1st sec. FVC= forced vital capacity
FEV1 & FVC we can know if the pt is normal or not
- staging= mild moderate & severe which are different in the management for example:
sever COPD pt can't go under general
anasthesia. Also, pt hypoxic, cianotic,....

spirometry pulmonary function test
:
blood gases -1
2- pulmonary function test= we ask the pt to take deep inspiration the forced expiration to
calculate FEV1 to detect any disease at the 1st sec

obstructive (asthma , COPD) or resrective disease. Also, to know the reversibility ( COPD IS
IRREVERSABLE , but asthma is reversible) in this test we give the pt vasodilator which is short
acting B2 agonist (ventolen) by inhalation (b/c it's early onset and it's local acting )
- medical management
if there is infection we give antibiotic
if the pt is asthmatic we give supportive tx starting with short or long B2 agonist, but if the
asthma is sever we give systemic or local steroids
- dental management
1- if there is infection we give appointment after 1-2 weeks to give time to the infection to
resolve
2- we don't put the pt in supine position, he should be setting or semi setting
3- no rubber dam b/c the pt will feel suffocation & the CO2 level will increase which will lead
to cyanosis
4- we can use local anesthesia but general anesthesia we can use it with mild to moderate
but severe pt WE CAN'T
5- if the pt takes steroids he should take supplementary dose before he come to the clinic
6- the pt should bring his inhaler with him so I can know what he is using and if ER I can give
him
7- my clinic should have O2 supplement & vasodilator

8- I should do pulse oximetry which is non invasive procedure to measure the capillary
pulsation and the O2 SATURATION (not tension which we
can get from blood gases test) if the O2 less than 90 I can proceede but if the O2 is reducing
with time I have to give him low flow O2 to prevent CO2 retention
9- if the pt is on theophylline (ex. aminophylline drug) which has narrow safety marine. I
SHOULD NOT GIVE HIM erythromycin, azithromycin antibiotic because these antibiotic
decrease the metabolism of theophylline which will increase it amount inside the body and
the pt will have toxicity, epilepsy+
, arrhythmia

We will move to part 2

Asthma is reversible air way obstruction . asthma by definition is a chronic inflammatory

disease of the air way , it may happen early onset (children ) or at older age not related to
smoking or air pollution . Asthma comes as an extrinsic factor , the patient is exposed to dust
or infection or exercise or specific drug such as aspirin then it causes bronchospasm.
What is the meaning of Air way hyper responsiveness
normal person + normal stimulation = nothing happen to him
asthmatic person + normal stimulation = something happens to him caused by air way
hyper responsiveness ( many people when they laugh they cough ) .
*not all hyper responsive people are asthmatic , BUT part of asthma characteristic picture is
air way hyper responsiveness
* which means that airway hyper responsiveness alone is a disease but with asthma is a
feature , explanation :
If somebody had an infection and took antibiotic the cough may disappear
BUT with somebody had an infection , the sputum may disappear but cough persists for 10
to 15 days this is called air way hyper responsiveness.
If somebody enters a room closed or contains some dust the normal response is nothing ,
because the respiratory way has a lining where the infections and dust sticks then washed ,
so we dont feel , but is the person is asthmatic he will feel .
Normal stimuli + asthmatic patient = exaggerated response

There main Five types:

-Extrinsic =atopic or IgE mediated

-Intrinsic
Drug induced most famous ones are non-steroidal and aspirin must be avoid
with patients have a history of asthma
-Exercise induced
-Infectious
The first one is mediated by IgE , but the remaining are mediated by Vagus
which is a nerve that has receptors in the air way, the asthmatic patient has
exaggeration or hyper responsiveness. Normally during exercise and change hot
and cold gases nothing happen to him but in asthmatic patient a problem
happens.
What is the meaning of atopic allergic .

Slide 12 pictures : she is comparing :

Normal airway
dilated
no secretion
Muscle relaxed(blue line)

Asthma
constricted
there is a secretion
increase muscle thickness+??min26:27
eosinophil's from IgE the most
important cell in chronic inflammation
(small spots )

Slide 13 picture :
This picture is very important!
The difference between normal and diseased is that the it is sensitized which
means that the antigen when enters the body has the ability to form IgE because
not all antigens are able to form antigens , if the person is normal there should
not be IgE formed or formed in a small percentage , (in CBC the eosinophil's
percentage is from 0-1maxium , normally there should not be .
Normal patient pollen, dust or any antigen enters taken by antigen
presenting cells ( dendritic cells has many progections) dentitic cells
present the antigen to T helper 2T helper 2 secretes L4 , L3,L5
L4 activates B cells B cells form antibodies IgE
L3, L5 actives eosinophil's (main cell in asthma )

(T helper 1 for sarcadosis )but we concentrate in asthma with T helper 2

*the ability of the body to produce IgE in response to antigen the patient is
atopic or sensitized .
Ex , If you have 2 brothers got a mosquito sting , one of them may develop
urticaria (which means that he is sensitized means that the antigens entered
his body has the ability to form IgE )and the other bother not .
After the pervious process the air way is still normal . Why ?? because the
manifestations appears on re-exposure, the first phase is the sensitization= the
body gets ready (forms antibodies that has its receptors rested on mast cells
which is very important because it releases histamine which cause all
manifestations : etching , urticaria , eye gets blurred and excrete a lot of
secretions , bronchospasm thats why in the process of treatment we give
the patient antihistamine that dont decrease the number of cell but
decreases the mediators coming out of the mast cells.(this is the first idea )
(second idea ) there are some patients doing sensitization for asthma they do
skin test then they take repeated vaccinations to decrease the manifestations of
asthma, but first it has to been proved that this specific antigen causes asthma ,
these vaccinations decrease the sensitization of mast cells.
When re exposure to the antigen there will be an ANTIGEN ANTIBODY
REACTION , the antigen which was the patient exposed to and the antibody
which was formed (like key and hole ) Antigen +antibody = mast cell ruptures
and gives out all the mediators inside it especially histamine , also eosinophil's
increase.
Histamine is responsible for early action , while eosinophil's(called recruitment ,
of the eosinophil's in the airway = delayed action . recruitment
If the patient has some symptoms at the beginning , he maybe be rescued with
antihistamine which may cause an improvement , if no improvement we must
give something to antagonist the eosinophil's and its secretions.
*status asthmatics : the patient presents with cough, expectoration, dyspnea
more than normal (not used to it ),that dont improve with current medication ,
the situation must be detected early (you may face t in your dental practice ),
we do broncho dilator , 1, 2, 3 if no improvement that means the patient has
status asthmatics.
How to prove status asthmatics see the venous near the jugular vein if
congested + pulsus paradox .
What is pulsus paradox normally blood pressure during inspiration is less than
normal (the variation not more than 10mmHg if I measure it during inspiration +

expiration) , if the variation more than 10mmHg thats prove that the patient
has status asthmatics .
Pulsus paradox Not specific for status asthmatics it may be found in constricted
pericarditis , or cardiac parmonel in patients in ER after an accident .
Severe dyspnea Not responding to treatment + pulsus paradox status
asthmatics ( feature : the patient is not able to complete a statement,
say stuff infrequent + severe dyspnea) the patient may or may not develop
cyanosis + congestion in jugular vein .
Why it is important to Know status asthmatics to detect and be able to
manage the patient must be sent to the ER , the patient should not stay on
the dental chair and given only broncho dialator , Beccause the patient may
need nebulizer or systemic management .
Some dental material used in the clinic causes this such as Local anesthesia that
contain a preservative that may cause induction of asthma , when we give 2 or 4
cartridges of LA lead to status asthmatics.
So , if the patient is asthmatic I should avoid giving him LA with adrenaline
because it contains the preservative .
Asthma investigations = tha same as COPD investigations + skin test
Skin test we bring the most common antigen and inject it subcutaneous and
see the reaction if there is an induration + redness means that the patient
is sensitized to what was injected .if we know the antigen that causes asthma we
give the patient hypo sensitization or vaccination that reduces the frequency of
asthma .
We also do chest X-ray + blood gases + CBC to see .(can not hear properly )
*specification of asthma :
Intermittent asthma: infrequent asthma , less than 2 per week no need for
regular Tx
Persistent asthma: more frequent , or more daily symptoms with night syndromes (it's when
the pt. wakes up from sleep suffocated and dizzy)
they are mild, moderate and severe, according to the pulmonary function and according to the
symptoms. which would affect the management of the disease.
the management and investigation are similar to the airway as general.
Management: bronchodilators, drugs that decrease the conjunction and lessen muscle spasm.

Bronchodilator:

-long acting.

-short acting.

Steroids: decrease resistance in the airway.

Dental Management: assessment of the condition (occurred at young age or old age), stage (from the
symptoms). know the medication the pt. is taking.

*if a pt. has severe asthma, consult their physician and know at which stage they could be
treated.
*the pt. should bring their medication, for the dentist to see and to give them prophylactic. if
the pt. takes steroids, give supplementation (?) before treatment.

Drugs to be avoided: erythromycin (non-steroidal or aspirin).

You can use local anesthetic but avoid the ones with preservative.
In chronic pt. give them steroid supplementation and avoid stress (give them morning appointment
and make it short)

**IMP.**
*Recognize signs and symptoms of a severe or worsening asthma attack:
-Inability to finish sentences with one breath.
-Ineffectiveness of bronchodilators to relieve
dyspnea.
-Tachypnea equal to or greater than 25 breaths per minute.
-Tachycardia equal to or greater than
110 beats per minute.

* in case it happens (severe asthma): contact the ER, give them short/fast acting drugs. even if there
is no response, repeat administration bronchodilator (inhaler) every 5 minutes.
the bronchodilator used in the inhaler, needs force by the pt. to work it into the lungs and to benefit
from the treatment. however the one used in the ER, is positively carried into the lungs (ie. doesn't
need force)(using ultra-sonic waves)

TB:
*if a pt. is diabetic, pregnant, immunocompromised pt. or on steroids, they could easly catch TB.
*it's common in developing countries (India and bengeladish)
*treatment is prolonged (a year) (the pt. might get bored or dis-continue the treatment when they
feel better).
* if the pt. discontinue the treatment, they would develop resistance to the drug used.
* TB bacilli is rod shaped, aerobic and non-motile.
* ZiehlNeelsen stain is used to investigate TB (cannot be washed) (it's called acid fast, alcohol fast.
that means once we apply the dye, it will stain and cannot be washed)

* it's a chronic infection.

* it could be transferred via milk (but we are not concerned with that so the lecture would focus on
droplet infection)
* the second killer -after aids, is TB. (in regard of chronic infection)
Symptoms: night sweats, fever, cough, general malaise, anorexia, vomiting and loss of weight.
* history of exposure to TB pt.
* for the pt. to get TB, they must be in an immunocompromised state (pregnant, diabetic)
* in children (under 15), the chance of catching infection is scarce because of vaccination and limited
exposure to the community.
* in adolescence (15-25) ==> active stage.
* above 40 if immunocompromised, would catch infection easily.

Carrier or not it will show in other

investigations ( by sputum analysis) to know
if it infectious should be by sputum . if the
mom tuberculosis it can be transmitted by
transmaternal homotegonous route
Tuberculin test : not used now, drop of the
test Purified Protein Derivative PPD in the
TB bacilli wall intradermal injection if there is
indurations after 24 hrs it means +ve TB test
= ( a type of delay hypersensitivity)=
previous exposure to bacilli not infectious
which is known by the sputum positive or
not.
Tx is imp: differs if the patient is 1-fresh case
or 2-resistant.
1- Fresh is easily treated ? response of tx is easier
First 2 months 3 drugs then we remove the one drug? Bacteria resist to response plus
causing liver toxicity. So, total 6 months standard of the fresh case.
2-If the pt. is resistant: it differs if its to drug or more than.
If resistant to more than 1 drug we give a combination of drugs of 7 drugs. ( TB drugs+
cephalosporin and cycloserin ) because we have to do the combination to avoid the
resistance.
For any pt to know if is TB even if its a fresh case I take a sputum to culture (for 2-3 weeks)
How can I know if there is resistant? By test ( a culture) there are 2 types of cultures 1tacktick (name of the machine detect CO2 bacilli release it if positive we proceed with 2nd

stage the culture the culture in a desk with protein medium then they immerge with tablets
of antibiotics then they see the interaction according to the culture they know the drug
resistant it maybe one drug resistant or more than one)
If it is more than one drug resistant we treat it as a new category wich is the third category.
(So, first one is the fresh case second one drug resistant third is the combination 8 months
total or 9-12 months)
TB management is imp:
Hx of TB I have to know its fresh case ( no tx) or hx of TB it differs if active TB sputum +ve
forbidden to treat this pt as a dentist if emergency situations I have to take the precautions.
While if pt previously treated we judge by the symptoms e.g fever, cough is it getting any
better or not if symptoms are getting better 2nd step we take the sputum + or not ( if after 2
weeks of tx the sputum is not transferred to negative then I know there is resistant ) if a pt.
didnt continue the full required period of drug therapy S/he will develop resistanse and not
cured w hya de almushkela !
So if the pt. is active TB we dont tx as dentists if pt. on tx I make sure that symptoms
relieved or not if the pt. is free from symptoms and sputum is negative and ergent dental
case we do it if emergency and active do precautions the mask and vacuum ventilation for
me and the assistant as well.

Group 8. Good luck.

(Please note that illustrations from the internet not from the doctor for better imagination!
Good luck ~ Afnan Aljuaid)

Tuberculosis

Figure 1. Tuberculin test after the PPD injection.

Figure 2. case for us as dentists:1

DX: Tuberculosis, lymph node involvement and fistula formation.

Figure 3: death from TB around the world the darker the higher!

Oral manifestations of tuberculosis are uncommon and present as a wide

spectrum of lesions, usually secondary to pulmonary infection. Regional
lymphadenopathy usually accompanies the oral lesions.
A particular formof cervical lymph-node tuberculosis is known as scrofula.
Clinically, it presents as a swelling of numerous cervical lymph nodes that
occasionally leads to the formation of numerous fistulas though the overlying
skin. The differential diagnosis should include lymphoma, submandibular
sialadenitis, and actinomycosis.