4. Individuals with a history of atopy, hay fever, rhinitis,
asthma or eczema.
Latex proteins can permeate
following contact through both skin and mucosa or via
lungs
Type of reactions:
Type I
a. Hives, erythema, urticaria which may be localized or
generalized.
b. Upper respiratory symptoms, including stuffy or runny
nose, cough, asthma.
c. Red, itchy eyes, angioedema of eyelids.
d. GI symptoms, including diarrhea, nausea, vomiting,
cramping.
e. Headache, anxiety, shortness of breath, itching.
g. Anaphylaxis, tachycardia, hypotension, cardiovascular
collapse.
Testing for type I natural rubber latex allergy is through
blood testing, such as RAST (radioallergosorbent test)
identifies what types of IgE proteins trigger allergic
reactions. This is caused from IgE (immune) mediated
reactions to proteins found in a type of rubber tree.
Type IV (allergic contact dermatitis)Also known
as allergic contact dermatitis. This involves a
delayed skin rash with blistering and oozing of
the skin. Type IV reactions are caused by the
chemicals used to process the rubber. Patch
testing needs to be done to verify which type
of chemical triggers the reaction.
Irritant contact dermatitis:It can also cause
irritant contact dermatitis: The most common
type of reaction.
This causes dry, itchy, irritated areas on the skin, most
often on the hands. It can be caused by the irritation of
using gloves, or it can also be caused by exposure to other
workplace products. Frequent washing of the hands,
incomplete drying, exposure to hand sanitizers, and the
talc-like powder coatings (zinc oxide, etc.) used with
gloves can aggravate symptoms. Irritant contact dermatitis
is not a true allergy.
Identification of High-Risk Groups
1. Patients with a history of multiple surgical procedures,
including those with
myelomeningocoele (spina bifida) and congenital
genitourinary tract anomalies.
2. Health care personnel with occupational exposure.
3. Other individuals with occupational exposure to
natural rubber latex, including
hairdressers, greenhouse workers and those in latex product
manufacturing.
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5. Individuals with a history of food allergy to
tropical fruits (such as avocado, kiwi,banana),
chestnuts, stone fruits and additional specific
foods
FITkit is a latex allergen testing method for
quantification of the major natural rubber latex
(NRL) specific allergens
Operating Room Management of the Patient
With Latex Allergy
Identify each patient who is at risk. A careful
history frequently will elicit episodes
of previous allergic reactions or risk factors.
2. Patients who have a suggestive history and
confirmatory laboratory findings must be
managed with complete latex avoidance.
3. When possible, the patient should be scheduled
for elective surgery as the first case of the day.
Airborne latex-laden particles are presumed to be
at their minimum levels at that time.
4. No one should enter the surgery with latex
gloves, without scrubbing after taking off latex
gloves or while wearing latex-laden clothing
from previous latex exposure. Some patients'
sensitivity is so extreme that replacement of
Latex products with non-latex products may still
result in a reaction if the products are
manufactured in the same facility as the Latexcontaining products.
5. Preview all equipment to be used, looking for
possible latex-containing products.Latex is
present in a number of items found in the dental
surgery besides gloves. These include latex dam,
gutta percha, some prophylaxis cups, mixing
bowls, orthodontic elastics, some suction tips,
bite blocks, amalgam carriers, gas tubing, IV
tubing, emergency resuscitation masks and blood
pressure cuffs.
6. To prevent aerosolization of latex particles and
transfer between patients, non-powdered gloves
must be used in the surgery and a good
ventilation system is required.
7.The surgery must be damp wiped down before
the patient arrives and ensure that all staff is
aware that the patient is latex allergic.
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8.Latex gloves can be replaced by substitutes
such as nitrile and neoprene gloves. Other
materials such as prophylaxis cups and bite
blocks are available in plastic
or silicone.Non latex dental dam is available
made from silicone and synthetic elastomers.
Latex free disposable syringes are available
Facemasks can be obtained which
are latex free.
Local anesthetics known to be latex-free
can be used. Protective eyewear needs to be
checked for any rubber nosepieces and avoided.
The only issue is with using gutta percha for
endodontics which is probably the most effective
obturating material and there are no good
alternatives so one has to ensure that there is no
overfill of the root canal system.
9. The details of any allergic reaction should be
clearly documented on the patient’s chart.
10. MANAGEMENT (SPECIFIC)
1. Contact dermatitis and Type IV reactions:
a. Avoid irritating skin cleansers.
b. Topical corticosteroids can be applied locally
for rashes or hives.
2. Type I latex reactions:
a. Mild reactions respond well to antihistamines,
and topical nasal steroids may be
useful.
b. Hives are treated with antihistamines and
systemic steroids.
c. A reaction with airway involvement may
require the use of systemic steroids,
bronchodilators, endotracheal intubation and
epinephrine.
d. In the case of anaphylaxis, a formal
anaphylaxis protocol is advisable. Adrenaline
should be kept in the surgery for an emergency
and in case of anaphylaxis, 0.5 to 1.0mg for an
adult or 0.01mg/kg up to 30kg for a child should
be administered.
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106. How to manage patient on Tranquiliser therapy?
68. From the medical history you find the patient is on
Tricyclic Anti-depression medication. How would you
manage this patient? 10. Mgt. Of pt. Under tri cyclic
anti depressants?
Taking a detailed medical history to reach a proper
diagnosis, aetiology of the chief complain and essential for
safe prescribing of dental drug.
- Consult the patient’s GP if any precautions should be
taken or any modification to the treatment should be
followed
- Reconfirm the definitive treatment plan and make sure the
patient’s expectations are what the result would be.
- The adverse effects of psychotrophic drugs and their
management:
1. Xerostomia:
• It is the most important adverse effect
• Pt has dry mouth and lack of saliva leading to caries and
candidosis
• It has major effect on salivary function
• If change in pt’s treatment not possible, following long
term management should be followed: dietary
modification, salivary substitutes, regular sipping of water,
salivary flow stimulants, sialogogues
• Increase recall visits for oral hygiene instructions, fluoride
application n early intervention.
2. Bruxism :
• It is forceful excursive movement of jaw with grinding of
teeth.
• Occasionally seen in pt’s on antidepressant drugs
• It may also occur independent of medications in pt’s with
severe anxiety.
• This complication can be reduced with occlusal splints
3. Surgical bleeding:
• Pt’s on anticonvulsants have relative high incidence of
thrombocytopenia.
• There are chances of bleeding in dental treatments.
• Get appropriate lab investigations before the procedures.if
any abnormal results pt should be referred to medical
practioner for management.
• Some antidepressants also impair platelet aggregation,
thus precautions need to be taken
4. Drug induced- excessive salivation:
• Anticholinergic drugs induce hypersalivation.
• Due to excess salivation in dental procedure compromises
dental material creating difficulty in working environment.
• Hyoscine hydrobromide 300 microgram chewed and
swallowed before dental work, in addition to standard
measures for maintaining a dry field, may be helpful.
5. Operative use of vasoconstrictors :
• Sympathomimetic vasoconstrictors such as adrenaline,
used in conjunction with local anaesthetics to prolong
anaesthetic effect and control local bleeding, are generally
safe, but there are interactions with MAO inhibitors.
• The antidepressants may potentiate the action of
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adrenaline and possibly increase the patient's blood
pressure. If adrenaline is necessary, consider using about
one-third of the normal amount.
• The interaction might lead to peripheral vasodilation
resulting in prolonged bleeding, hypotension and reflex
tachycardia
• If there is concern about interactions with
sympathomimetic vasoconstrictors, felypressin may be an
alternative.
6. Awareness of the patients psychological status is
necessary, and interactions of practitioner and staff with the
patient must be appropriate. Certain patients might never be
satisfied with the appearance of prosthesis of treatment.
7.Patients with anxiety or phobic states can be difficult to
manage and may only present themselves when an
emergency arises.
8.Routine sedatives might be ineffective. A referral for
General anesthesia or to a specialist might be advised.
9.caution while giving medication to a patient who has no
apparent symptoms and demands analgesic drugs with a
good knowledge or preference of the drug.
10. Dental pt’s may be prescribed with psychotrophic drugs
for a mental illness or to manage severe anxiety associated
with dental procedure. A detailed medical history is
essential to prevent unnecessary drug interactions.
104.How do you manage a patient on steroid therapy
and long standing rheumatoid arthritis? 75. Acute
Adrenal Insufficiency
Rheumatoid arthritis
RA is a chronic, systemic disease. RA is a member of a
family autoimmune diseases with a high level of
rheumatoid factor which gives the condition its name. High
rheumatoid factor diseases include lupus erythematosis,
scleroderma, and sjorgren's syndrome.
RA is characterized by a pattern of swollen tender joints.
The joints most often include the small joints of the hands
and feet, wrists and knees.
Diagnosis
interviewing the patient to determine their history of
disease, testing the blood for rheumatoid factor and other
effects of the disease, physical examination to determine
the pattern of inflamed joints, and to look for lumps under
the skin (rheumatoid nodules), and imaging exams (x-ray,
CAT scan, and others).
As a systemic disease, RA may affect multiple organs
including the lungs, kidneys, even the tissue surounding the
heart. RA becomes active or flares up and then becomes
silent or goes into remission.
There is no cure for RA. Patients primarily take a variety of
anti-inflamatory drugs to ease the pain and inflamation of
RA. Aspirin is a time-tested non-steroidal anti-inflamatory
drug (NSAID). Newer NSAIDs including Ibuprofen and
Naproxophen are alternatives.
Steroids are very strong inflamation fighters. Prednisone is
a good choice to gain control of an especially bad flare.
There are other medications known as disease modifying
anti-rheumatic drugs or DMARDs. Gold, methotrexate, and
hydroxychloroquine slow the progress of the disease. These
medications carry their own serious side effects.
ORAL HEALTH
1)Part of the reason that RA patients have more serious
tooth decay and gum disease is that swollen, inflamed hand
and wrist joints make oral hygiene (brushing and flossing)
tedious and painful.
Electric toothbrushes provide larger, more comfortable
handles for patients who loose the ability to grasp the thin
handle of standard toothbrushes.
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There are a few useful devices available for interdental
cleaning. There is a popular device that streaches any floss
across the ends of a "Y" shaped handle. Also, a Waterpik,
an interdental cleaner can be used.
2)RA often affects salivary glands causing inflamation and
dryness. Sjorgren's syndrome the combination of dry eye
(keratoconjunctivitis sicca) and dry mouth (xerostomia) is
common in RA.
In some cases, medications that increase the effectiveness
of the salivary glands such as pilocarpine
Artificial saliva products
Use of a gentle toothpaste formulation as Biotene
Drinking plenty of water and stimulating the salivary
glands by chewing sugar free gum or sucking on sugar free
hard candies.
Without the cleansing and antibacterial effects of saliva,
teeth are much more likely to decay. Fight rampant decay
with maximal use of fluoride, impeccable oral hygiene and
decreasing sugar consumption.
3)Thrush, oral yeast infection, frequently accompanies long
standing xerostomia. Symptoms of thrush include a burning
sensation especially in the tongue and sores in the corners
of the mouth. Effective treatment includes presciptions of
antifungal tablets, rinses and salves.
4) There is a strong link between periodontal disease and
RA as the two diseases result from a poorly regulated
immune system.
5)The temporomandibular joint (jaw joint or TMJ) is the
most complicated joint in the human body.
RA will cause swelling and pain. Pain may become severe
when chewing and speaking.
relief with the usual treatments such as anti-inflammatory
medications, exercise and heat.
RA sometimes damages the TMJ. Then, it is necessary to
replace all or part of the joint with an analog made of
titanium and plastic.
6)Many of the medications that patients take to treat RA
and the pain associated with it have oral side effects.
a)NSAIDs such as aspirin and ibuprofen, cause stomach
irritation which may lead to nausea and vomiting. The acid
of the stomach causes erosion of the enamel, the hard outer
covering of teeth.
if aspirin is being used, hemostasis might be affected.
b)Steroids cause a lower resistance to infection.
7)Patients with RA may require antibiotic prophylaxis
owing to joint replacement and/or immune suppression,
glucocortico-steroid replacement therapy.
Glucocorticoids play a critical role in the body's
response to stress. Stress results in release
of cytokines, and in particular the cytokine
interleukin-1, which causes cortisol levels
to rise from adrenal gland cortex thereby mobilising the
body's glycogen and fat stores.
Exogenous steroids suppress the hypothalamopituitary–
adrenal (HPA) axis. Such patients lack the capacity to
respond with the normal physiological output of
endogenous corticosteroids in response to the stress
Treatment with a dosage of 5-10 mg /day for a few weeks
can cause adrenal suppression
1) a detailed medical history is required.The underlying
disease should be found out.
2) consultation with the specialist about dosage, time
period
3)Dental treatment might be stressful. (extractions, root
planning) If sufficient adrenocorticoids (mainly
glucocorticoids) aren’t produced following stress, adrenal
crisis migh occur.
4)Too reduce stress, morning appointments are preffered so
pt can be monitored till evening.
5)Patients having minor dental procedures (e.g. filling
replacement) do not usually require steroid
supplementation, but a ‘top-up’ dose prior to the procedure
may be needed if they find dental procedures emotionally
stressful.
6)Patients having minor oral surgery that causes physical
stress, such as tooth extraction, require steroid
supplementation prior to the procedure, and possibly for up
to 24 hours afterwards.
7) those patients taking high doses of steroid should double
the usual dose on the day
8) If adrenal insufficiency is suspected,
follow-up with an endocrinologist is
important, as secondary adrenal disease
needs to be ruled out.
9) For surgical procedures under general
anaesthesia, the need for peri-operative
glucocorticoid supplementation, for
patients on exogenous steroids, should be
determined by the severity of the surgery
and the pre-existing glucocorticoid dose,
*For surgical procedures under general anaesthesia, the
need for peri-operative glucocorticoid supplementation, for
patients on exogenous steroids, should be
determined by the severity of the surgery
and the pre-existing glucocorticoid dose.
for patients undergoing general anesthesia for minor
surgery 100 mg hydrocortisone intramuscularly
should be administered and the usual glucocorticoid
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medications maintained. For major surgery 100 mg
hydrocortisone delivered as a bolus pre-operatively
followed by 50 mg 8-hourly for 48 hours is
adequate.
Patients might be predisposed to infection.
ADRENAL CRISIS
Three clinical states associated with adrenal failure
are considered to occur.
1) Acute adrenal crisis, with insufficiency of
mineralocorticoids and glucocorticoids, is a medical
emergency. The patient presents with abdominal pain,
weakness, hypotension, dehydration, nausea and
vomiting.13 Laboratory findings may include decreased
sodium (hyponatraemia), elevated potassium
(hyperkalaemia), decreased blood glucose (hypoglycemia),
acidosis and uraemia.
2)Patients with secondary Addison's disease
3. Patients taking exogenous glucocorticoids.
Exogenous glucocorticoids can cause adrenal gland
suppression and resultant atrophy. With atrophy of the
adrenal glands there is a decreased glucocorticoid
response to stress, and this may precipitate an adrenal crisis
Many patients are on, or have been treated with,
corticosteroids and often appear healthy. Acute adrenal
insufficiency (Addisonian crisis) may present with:
- Nausea (with or without vomiting)
- Weakness
- Hypotension
- Weak and rapid pulse
- Confusion
- Hypoglycaemia
- Collapse (may resemble a faint, but hypotension that does
not respond
to lying the patient flat)
- Coma (if untreated)
Management
- Lay the patient flat, with the legs raised.
- Summon medical assistance.
- Give 200 mg hydrocortisone IV or 500 mg
methylprednisolone IV
(slowly).
- Give oxygen (10–15 L/min)
- Take blood for glucose and electrolyte estimation.
- Put up an intravenous infusion:
- Initially give colloid solution and monitor BP.
- When BP stable, continue with normal saline or dextrosesaline.
- Give glucose (orally or IV), if there is hypoglycaemia.
- Determine and deal with the underlying cause once BP
has been stabilized.
Control of pain and infection are particularly important.
- Steroid supplementation (100 mg hydrocortisone at 6hourly intervals)
must be continued for at least 3 days after the BP has
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returned to
normal.
96.Discuss the effects of cigarette smoking on general
health and its impact on oral health. What would you
tell your patients to encourage them to stop smoking?
81. smoking and its effects and how to motivate patient
to leave the habit.
30. Discuss the effects of cigarette smoking on general
health and its impact on oral health. What would you
tell your patients to encourage them to stop smoking?
Tobbaco can be taken in two forms:
Smokeless and smoking form
ORAL
1)The smoking and chewing of tobacco products can have
a dramatically negative impact on a person’s
appearance.Smoking and chewing tobacco stains and
discolours teeth, dentures and restorations. Smoked tobacco
staining of dentures is a special problem because it is often
too heavy and too deeply embedded to be removed by
denture cleansers
2) TOOTH AND PROSTHETIC STAINS. Tobacco
stain, a brown/black extrinsic stain, is typically found on
the enamel surfaces of smokers and tobacco chewers. It is
especially pronounced in cervical areas and the lingual
aspects of the mandibular incisors.
3) HALITOSIS. Both smoked and smokeless tobacco
usage produce unpleasant breath odors or "bad breath".
With smoking the halitosis is produced predominantly by
the retention and subsequent exhalation of inhaled smoke in
the lungs. Regardless of the method of absorption,
however, numerous noxious elements characteristically
escape from the lungs via the blood/air interchange. Pipe
and cigar tobacco contains more sulfur than cigarettes,
hence users tend to have a more offensive halitosis than
cigarette smokers.
4) ABRASION. Tooth abrasion resulting in a notching of
incisal edges and cusp tips is a well-established
consequence of holding a pipe in the same location while
smoking.
EROSION. The chemical dissolution of enamel has
occasionally been reported in tobacco smokers and
chewers, but only as a secondary consequence of using
breath mints or as idiopathic cases
5) Dental implants :Tobacco can be damaging to both the
initial and long-term success of dental implants. Smoking is
the most significant risk factor in the failure of dental
implants.
6) Oral cancer: All forms of tobacco use are known to
cause oral cancer. Smokers who consume alcohol are at an
even higher risk of oral cancer due to the synergistic
effects.
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7) Oral mucosal diseases: Tobacco use is associated with a
range of changes to the oral mucous membrane cells. The
diseases most commonly associated with smoking are:
• Smoker’s palate (nicotinic stomatitis): A change in the
hard palate caused by heavy smoking.
The palate turns white and can be littered with red dots
located within small raised lumps.
This condition is not pre-malignant and disappears after
smoking is stopped.
• Smoker’s melanosis: Smokers are more likely to develop
local areas of melanin pigmentation
• Oral Candidosis: An opportunistic mucosal infection
caused by the Candida albicans fungus. it has been
suggested that tobacco use depresses the immune system,
making smokers more susceptible to infection.
Smoking is a risk factor for this infection
8)Periodontal diseases: the attachment of fibroblasts to
cementum is altered by nicotine and new investigations are
underway to further evaluate the local effects of tobacco
cytotoxins.
• Smokers have decreased levels of salivary and serum
immunoglobulin which affects wound
healing in the oral cavity and the mouth’s ability to clear
pathogens.
•dry sockets or localised osteitis occurs four times more
frequently in smokers than in non-smokers.
Routine periodontal surgery and tooth extraction are also
adversely affected, possibly because of the direct contact of
smoke constituents on open wounds, or reduced blood flow,
or impaired leukocyte function, or diminished fibrinolytic
activity, or the drying effect of mouth-breathing, or the clotdisrupting effect of the negative intraoral pressure produced
during tobacco smoking
• There is also evidence which suggests that smoking
inhibits healing through the effects of
decreased oxygenation in the blood and tissues, and
constriction of blood vessels.
Carbon monoxide binds to hemoglobin in red blood cells,
preventing affected cells from carrying a full load of
oxygen.
• Tobacco smoking and chewing is a risk factor associated
with chronic destructive periodontal disease.
• It has been estimated that a smoker has between a 5 fold
and 20 fold increased risk of periodontal disease.
• The risk of alveolar bone loss is seven times greater
amongst smokers than non smokers.
•The severity of periodontal disease increases with the
number of cigarettes smoked.
Smokers exhibit higher rates of tooth loss than nonsmokers.
• The outcome of periodontal treatment is less favourable
or unfavourable in smokers.
12) SINUSITIS. Tobacco smokers are much more prone
to maxillary sinusitis than nonusers and this condition
typically resolves or is significantly reduced when the
smoking habit is discontinued. This effect is probably
secondary to a tobacco-induced edema of the sinus
membranes and by diminished ciliary activity of respiratory
epithelial cells.
14)ALTERED TASTE. Tobacco smoking diminishes our
ability to detect various tastes and smells.
GINGIVITIS. Frequent studies have concluded that
tobacco smokers are more likely to demonstrate gingival
redness, hemorrhage and inflammatory enlargement
(edema) than nonsmokers with similar oral hygiene habits.
9)Smokers have decreased levels of salivary and serum
immunoglobulins which impairs their ability to fight the
bacteria in the oral cavity. Tobacco smoking, furthermore,
also suppresses human immune responses, including
responses to oral microbial toxins. Oral leukocytes,
especially neutrophils, have a diminished ability to move,
to phagocytize, or to secrete enzymes in smokers.
10) Dental caries: Smokers have a significantly greater
number of carious or repaired tooth surfaces than
nonsmokers, and heavy smokers are more affected than
light smokers. Smokers also have higher plaque rates than
nonsmokers. It has been suggested that smokers as a group
have poorer oral hygiene habits and skills, make fewer
visits to dentists, and have lesser overall health standards
than nonsmokers
. This is especially true for persons with poor oral hygiene,
possibly because of the softening of plastics secondary to
plaque-produced acids. Smoking is also known to
contribute to or accentuate the staining properties of
chlorhexidine solutions and gels.
Effects of smoking on the respiratory system
ï‚·
Irritation of the trachea (windpipe) and larynx
(voice box)
ï‚·
Reduced lung function and breathlessness due to
swelling and narrowing of the lung airways and
excess mucus in the lung passages
ï‚·
Impairment of the lungs’ clearance system,
leading to the build-up of poisonous substances,
which results in lung irritation and damage
ï‚·
Increased risk of lung infection and symptoms
such as coughing and wheezing
ï‚·
Permanent damage to the air sacs of the lungs.
11) Wound healing: Tobacco use is known to impair wound
healing.
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Effects of smoking on the circulatory system
ï‚·
Raised blood pressure and heart rate
ï‚·
Constriction (tightening) of blood vessels in the
skin, resulting in a drop in skin temperature
ï‚·
Less oxygen carried by the blood
ï‚·
Stickier blood, which is more prone to clotting
ï‚·
Damage to the lining of the arteries, which is
thought to be a contributing factor to
atherosclerosis (the build-up of fatty deposits on
the artery walls)
ï‚·
Reduced blood flow to extremities like fingers
and toes
ï‚·
Increased risk of stroke and heart attack due to
blockages of the blood supply.
Effects of smoking on the immune system
ï‚·
The immune system doesn’t work as well
ï‚·
The person is more prone to infections such as
pneumonia and influenza
ï‚·
Illnesses are more severe and it takes longer to
get over them.
ï‚·
Lower levels of protective antioxidants (such as
Vitamin C), in the blood.
Effects of smoking on the musculoskeletal system
ï‚·
Tightening of certain muscles
ï‚·
Reduced bone density.
Other effects of smoking on the body
ï‚·
Irritation and inflammation of the stomach and
intestines
ï‚·
Increased risk of painful ulcers along the
digestive tract
ï‚·
Reduced ability to smell and taste
ï‚·
Premature wrinkling of the skin
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ï‚·
Higher risk of blindness
Effects of smoking on the male body
ï‚·
Lower sperm count
ï‚·
Higher percentage of deformed sperm
ï‚·
Genetic damage to sperm
ï‚·
Impotence, which may be due to the effects of
smoking on blood flow and damage to the blood
vessels of the penis.
Effects of smoking on the female body
ï‚·
Reduced fertility
ï‚·
Menstrual cycle irregularities or absence of
menstruation
ï‚·
Menopause reached one or two years earlier
ï‚·
Increased risk of cancer of the cervix
ï‚·
Greatly increased risk of stroke and heart attack if
the smoker is aged over 35 years and taking the
oral contraceptive pill.
Effects of smoking on the unborn baby
ï‚·
Increased risk of miscarriage, stillbirth and
premature birth
ï‚·
Low birth weight, which may have a lasting
effect of the growth and development of children.
Low birth weight is associated with an increased
risk for heart disease, stroke, high blood pressure,
being overweight and diabetes in adulthood
ï‚·
Increased risk of cleft palate and cleft lip
ï‚·
Paternal smoking can also harm the fetus if the
non-smoking mother is exposed to second-hand
smoke.
If the mother or father continues to smoke during their
baby’s first year of life, the child has an increased risk of
ear infections, respiratory illnesses such as pneumonia and
bronchitis, sudden infant death syndrome (SIDS) and
meningococcal disease.
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Diseases caused by long-term smoking
A lifetime smoker is at high risk of developing a range of
potentially lethal diseases, including:
ï‚·
Cancer of the lung, mouth, nose, voice box,
tongue, nasal sinus, oesophagus, throat, pancreas,
bone marrow (myeloid leukaemia), kidney,
cervix, ovary, ureter, liver, bladder, bowel and
stomach
ï‚·
Lung diseases such as chronic obstructive
pulmonary disease, which includes chronic
bronchitis and emphysema
ï‚·
Coronary artery disease, heart disease, heart
attack and stroke
ï‚·
Ulcers of the digestive system
ï‚·
Osteoporosis and hip fracture
ï‚·
Poor blood circulation in feet and hands, which
can lead to pain and, in severe cases, gangrene
and amputation.
Smoking cessation
There are 5 crucial steps in advising people to stop
smoking:
• Ask
• Assess
• Advise
• Assist
• Arrange
Ask
Ask the patient if he/she smokes. This information should
be recorded in the patient’s notes.
Smoking status should be kept up to date.
Assess
Assess the patient’s willingness to quit as well as recording
any previous quit attempts. This will help identify the best
means of quitting.
Advise
Advise smokers to quit. Most smokers are aware of the
dangers of smoking but may not appreciate the degree of
risk. There is good evidence that brief advice by dental
professionals is effective,
particularly for users of smokeless tobacco.
Dentists should stress to patients who have made
unsuccessful quit
attempts that it is common to make several attempts before
succeeding.
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To help smokers overcome nicotine cravings, dentists can
recommend following the “Four Ds”, aimed at reducing the
urge to smoke:
• Delay: Don’t act on the urge to smoke by opening a pack
or lighting a cigarette because even after a few minutes this
urge will reduce.
• Deep Breaths: Take three deep, slow breaths in and out.
• Drink water: Sip it slowly and enjoy the taste.
• Do something else: Take your mind off smoking by doing
some exercise, listen to music or go for a walk.
A quit date should be arranged during this brief advice
session.
Assist
Discuss the benefits of various stop smoking aids such as
Nicotine Replacement Therapy (NRT), Zyban (bupropion)
or Champix (varenicline). Remind the patient that these
pharmacotherapies are
available on prescription.
Arrange
Patients may also be referred to their local Stop Smoking
Service.
The dentist should arrange a follow-up appointment to
discuss the outcome or issues faced by the patient during
the quitting process.
47. Changes in oral mucosa caused by smoking
ORAL CANCER : oral cancers develop by way of
cocarcinogenesis, multiple factors are usually involved.
Tobacco chewers also develop oral carcinomas. The oral
cancer risk for these users is about 4 times greater than
nonusers, although the data proving this is very sparse.
A very unique low-grade oral malignancy, verrucous
carcinoma, is so seldom diagnosed in nonchewers that it is
aptly called the "snuff dipper's cancer" This carcinoma
typically develops in the exact site of chronic tobacco
placement. It differs from the usual oral cancer in that it
enlarges very slowly, is essentially nonmetastasizing, and
consists of very mature epithelial cells, i.e. has little
dysplasia.
LEUKOPLAKIA. Approximately 80% of leukoplakia
patients are smokers and when large groups of adults are
examined we find that smokers are much more likely to
have leukoplakia than nonsmokers .smoke-induced
leukoplakias may disappear 6-12 months after affected
patients stop smoking.
Speckled leukoplakia (erythroleukoplakia), for example has
a cancer potential of at least 25%, in some studies as high
as 41%.
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NICOTINE PALATINUS (STOMATITIS). A white
keratotic change, it does not transform into malignancy and
is a response to the heat of tobacco smoke rather than the
chemicals in the smoke. It is completely reversible within a
few months of quitting the smoking habit, even when
present for many decades before the habit is stopped.
ACUTE NECROTIZING ULCERATIVE
GINGIVITIS (ANUG). ANUG is strongly correlated with
tobacco use. it occurs most frequently in teenagers and
young adults and may result from defective neutrophil
function allowing bacterial and possibly viral
(cytomegalovirus) invasion of gingival tissues. The
vasoconstrictive action of nicotine and other tobacco
components is thought to contribute strongly to the painful
tissue necrosis and ulceration seen in this disease, but
emotional stress and poor oral hygiene appear to play roles
almost as important.
HAIRY TONGUE. The condition of elongated filiform
papillae mimicking hair on the dorsum of the tongue is
frequently seen in heavy smokers .
Theoretically tobacco smoke prevents the epithelial cells
from sloughing in a normal fashion and they accumulate
into a very thickened and white (unless stained brown,
black, etc.) surface which extends as long "hairs" at the tips
of the papillae.
CANDIDIASIS AND MEDIAN RHOMBOID
GLOSSITIS. The great majority (83%) of oral candidiasis
patients are moderate to heavy cigarette smokers. Median
rhomboid glossitis, a candida-induced tongue change, is
most frequently (85%) seen in smokers and is markedly
improved upon smoking cessation.
99. Management of patient with heart disease.
HYPERTENSION
SMOKELESS TOBACCO KERATOSIS. Snuff pouch,
like nicotine palatinus, no longer considered to be a true
leukoplakia. It is a white keratotic plaque, as is It typically
has a semitranslucent appearance rather than a flat
whiteness, and it has a microscopic appearance different
from the simple excessive keratin by which leukoplakia is
characterized. It also is located only in areas of direct
contact with snuff or chewing tobacco and is almost always
completely reversible when the affected patient quits his or
her habit.
SMOKER'S MELANOSIS. Smoking is capable of
stimulating oral mucosal melanocytes to produce excessive
melanin, thereby creating patches of brown pigmentation
on gingival or buccal mucosae . The number and intensity
of these smoker's melanoses are dose-dependent and
smoking cessation seems to reverse the process completely.
Nicotine itself activates one of the steps in melanin
production. An occasional lesion may have leukoplakia
superimposed on it,the term "melanoleukoplakia" (or
"leukomelanosis")
SUBMUCOUS FIBROSIS. Oral submucous fibrosis is a
precancerous condition characterized by a progressive
stiffening of the oral mucosa to the point wherein affected
persons have difficulty opening their mouths.
LEUKOEDEMA. A poorly demarcated, grayish-white,
opalescent change of the buccal mucosa, bilaterally, is
frequently seen in persons with darkly pigmented skin .
Always a benign lesion and usually considered a simple
variation of normal, it is nevertheless capable of an
increased whiteness and size in smokers.
Aditi Khamar
CLASSIFICATION
• Primary (essential) hypertension - 80-90% of
hypertensive patients are in this group, where no known
cause can be identified.
• Secondary hypertension - 10-20% of patients are
hypertensive because of underlying disease:
renal - renal artery stenosis
endocrine - thyrotoxicosis
vascular - coarctation of the aorta
gynaecological - eclampsia and pre-eclampsia of pregnancy
COMPLICATIONS OF LONGSTANDING
HYPERTENSION
1. Cerebrovascular accident - thrombosis or aneurysm.
2. Cardiac - heart failure or myocardial infarction.
3. Renal failure.
4. Retinopathy - papilledema.
5. Headache - hypertensive encephalopathy.
MANAGEMENT OF ESSENTIAL HYPERTENSION
• Non-drug measures - weight reduction, decreased salt
intake, stopping smoking, stress reduction, stopping oral
contraceptive drugs.
• Medication - once commenced, drug therapy is continued
for life. The following broad categories of medication may
be used, sometimes in combinations depending on the
patient's response:
diuretics - for fluid overload, e.g. chlorothiazide
beta-blockers - to dampen the sympathetic input that
increases the activity of the heart, e.g. propranolol (Inderal)
vasodilators - to decrease peripheral vascular resistance,
e.g.hydralazine
centrally acting drugs which compete with neurotransmitter
chemicals of the sympathetic nervous system responsible
for increased
heart activity, thereby reducing sympathetic mediated
increased heart activity, e.g. methyldopa (Aldomet).
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MINOR ORAL SURGERY IN HYPERTENSIVE
PATIENTS
1. Minimize stress levels - adjunctive sedation may be
useful. Severe dental problems might increase
hypertension.
2. Avoid adrenaline-containing local anaesthetic solutions
since adrenaline is a cardiac stimulant, although this may
have little bearing on wellcontrolled hypertensive patients.
Although adrenaline increases the systolic pressure, the
mean arterial blood pressure remains virtually unaffected
because the diastolic pressure is concomitantly reduced.
Using an LA without a vasoconstrictor might be less
effective for pain control, resulting in pain which might
increase the blood pressure.
3. It is safer to perform surgery under local anaesthesia
wherever possible, since general anaesthesia may evoke
wild fluctuations in blood pressure that can be dangerous
for the hypertensive patient.
4. Primary and reactive bleeding from a surgical wound can
be a problem, where there is undiagnosed or poorly
controlled hypertension.
5.NSAIDS should be used with caution, there is aa
probability of renal impairment.
Increased risk in patients taking ACE inhibitor or
angiotensin II receptor antagonist and a diuretic.
CORONARY ISCHEMIC DISEASE
Ischaemic heart disease is the result of insufficient blood
flow through the coronary arteries which supply the
nutrients and oxygen essential for normal myocardial
function.
The main reason is atherosclerosis-restricting myocardial
blood flow-demand cannot be met with exertion.
• Angina pectoris - chest pain, particularly on exertion, that
is readily relieved by rest and nitroglycerine medication.
Medications used are: glyceryl trinitrate, antiplatelet drugs
• Myocardial infarction - persistent and severe chest pain
lasting longer than 30 minutes that is not relieved by rest or
nitroglycerine medication.
Referred to as a 'heart attack' .
Atherosclerosis-plaque becomes active abruptly becomes
active with endothelial rupture, vasoconstriction, platelet
adhesion, thrombosis and inflammation.
The syndromes depend on the
Thrombosis, distal platelet and thrombus embolisation, and
myocardial necrosis.
• Major risk factors:
hypereholesteraemia occurring below the age of 45 years
hypertension occurring below the age of 45 years
smoking
diabetes.
• Minor risk factors:
lack of exercise
stressful 'type A' personality
oral contraception
obesity.
Aditi Khamar
MINOR ORAL SURGERY IN PATIENTS WITH
ISCHAEMIC HEART DISEASE
Ensure that current condition is stable. And rehab program
being followed.
1. Minimize stress levels - adjunctive sedation may be
useful.
Minimum stress, pain and time.
2. Use short appointments, relaxation techniques and
effective LA with vasoconstrictors, sedation if required.
3. It is safer to perform surgery under local anaesthesia and
sedation wherever possible, since general anaesthesia may
evoke wild fluctuations
in cardiac rhythm that can be dangerous for the patient with
ischaemic heart disease. When a general anaesthesia is
planned, warn the anaesthetist,
who may request further investigations such as an
electrocardiogram and chest X-ray prior to surgery.
4. Avoid elective surgery, in patients who have had a
myocardial infarct, stent placement or coronary bypass
surgery within the last 6 months.
When extractions are required, antibiotics are warrented as
damaged epithelium is present.
5. Patients should bring their anti-angina medication with
them and take a sublingual tablet immediately prior to
surgery to minimize the cardiac symptoms that may arise
from the stress of surgery.
6. Some patients may be on low-dose aspirin which will
create persistent bleeding from surgical wound. If aspirin
therapy is not stopped at least 7-10 days prior to surgery, in
consultation with the patient's physician, then strict
attention to local haemostasis is warranted.
7. consult with the physician if any doubt about patients
condition persists.
8. periodontal disease may be a risk factor for cv disease.
Keep periodontal health impeccable.
HEART DISEASE
It could be: due to left ventricular failure with pulmonary
congestion and dyspnoea, or right ventricular failure with
high venous pressure, hepatic congestion and peripheral
edema.
CARDIOMYOPATHY
Progressive failure of contractility of cardiac muscle.
MANAGEMENT
1)Condition should be stable and treatment simplified.
2)short duration
3)head higher than heart, not horizontal position.
4)antibiotic prophylaxis
Plus answer below
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76.Patient gives history of Warfarin treatment in the
assessment. What will be the considerations in the
dental management of such patient?
There has to be a balance between the increasd risk of
blleding (if drug is not stopeed) and the risk of
intravascular thrombi and emboli (if drug is stopped)
The effect of an intravascular event is much more.
A thorough medical history is required for drugs,
underlying condition and medication taken.
Commonly used drugs:
Aspirin
Warfarin
5) The normal INR for an individual without taking
warfarin is 1.0.
6) The INR should be checked before any dental surgery.
7) Minor dental surgical procedures like simple extraction
of up to 3 teeth, gingival surgery, crown and bridge
procedures, dental scaling etc.. can be carried out on dental
patients taking warfarin if the INR is within therapeutic
range i.e., 2.0 - 4.0.Whenever the INR is above 4 it is
preferred to refer the patient back to his physician.
8) Local anaesthetic should be given cautiously avoiding
venepuncture. A local anaesthetic containing
vasoconstrictor should be administered by infiltration or
intraligamentary injections and try to avoid regional nerve
blocks when possible.
9) Bleeding can be controlled in a reasonable time by
minimising the extent of surgery to one site or quadrant
local bleeding control measure like 4.8%tranexamic acid
protocol should be used after extraction only, loosely
packing the site with haemostatic agents like
surgicel(spongostan) or gelfoam and using sutures or firm
post operative packs over the wound.
Heparin
Clopidogrel
PATIENTS TAKING ASPIRIN
patients have a normal INR, prolonged bleeding time.
10) Preferably surgery should be performed in the morning
to facilitate post operative observation.
Usually don’t bleed much from extraction wounds
11) For extensive surgery the assistance of physician is
required.
In case dosage not stopped pt must be warned about1
1)excess bruising
2)Discuss risks..embolism is a major problem if drug is
stopped.
3)locally applied treatments for hemostasis.
If aspirin is to be stopped, it must be done atlest 10 days
before the procedure.
Ideal=14
Restart 2 days after surgery.
12) Also consider the possible drug interactions with
warfarin.Medications including antibiotics like
metronidazole, amoxicillin, aspirin and alcohol may
unpredictably alter the INR and increase the risk of
bleeding.
WARFARIN
1) Warfarin is a common oral anticoagulant prescribed for
patients with conditions like deep vein thrombosis, stroke,
pulmonary embolism, atrial fibrillation, prosthetic heart
valves.
2) So discontinuing warfarin for few days prior to dental
surgery in order to limit bleeding problems increases the
risk of thromboembolic events.
3) The possibility of post operative bleeding in patients
taking warfarin concerns the dentist. However, before
deciding if warfarin therapy should be interrupted , the risk
of post operative bleeding must be balanced against the risk
of thromboembolism.
4) The activity of warfarin is expressed using the INR(ratio
of PTtime of the patient to mean of Normal inr).
Aditi Khamar
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95.Management of patient with diabetes and allergy to
penicillin.
89.A controlled, non-insulin dependant diabetic patient
requires extraction of tooth 47. What are the treatment
precautions, if any?
74. Diabetic coma
42. 45 year old male diabetic on insulin is scheduled for
upper and lower denture in preparation for full u/l
denture how would you manage?
25. A controlled non - insulin diabetic (niddm) pt
requires extraction of tooth 47. What are the treatment
precautions if any?
Enlarged velvety-red gingival tissues that bleed easily (Fig
1).
Vascular changes that can give the gingivae a distinct
purple /bluish
hue (Fig 2).
Multiple periodontal abscesses.
Mobile teeth indicating bone loss.
Proliferative tissue at the gingival margin.
Inflammation spreading through the attached gingiva.
Lack of resolution of gingival signs after conventional
treatment.
Severe, aggressive periodontitis relative to patient’s age.
Delayed wound healing following oral surgical procedures.
* the diabetic patient with poor oral hygiene, a history of
smoking, infrequent dental visits, and a high fermentablecarbohydrate intake is more likely to experience oral
diseases such as caries and periodontitis and to respond
Aditi Khamar
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poorly to dental treatment than a diabetic patient without
these factors.
*Well-controlled diabetic patients with periodontitis have
positive responses to nonsurgical therapy, periodontal
surgery, and maintenance that are similar to those of people
without diabetes.
*poorly controlled diabetic patients respond much less
favorably, and short-term improvements in periodontal
health are frequently followed by regression and by
recurrence of disease.
*undiagnosed diabetic patients include enlarged gingival
tissues that bleed easily upon manipulation and the
presence of multiple periodontal abscesses.
*If the clinician suspects an undiagnosed diabetic state, the
patient should be questioned to elicit a history of
polydipsia, polyuria, polyphagia, or unexplained weight
loss.
The patient should be questioned about a family history of
diabetes.
If diabetes is suspected, laboratory evaluation and
physician referral are indicated.
*The clinician should
determine the patient's recent
glycated hemoglobin values.
HbA1c values of less than 8%
indicate relatively good glycemic control; values greater
than 10% indicate poor control.
*stress reduction, treatment setting, the use of antibiotics,
diet modification, appointment timing, changes in
medication regimens, and the management of emergencies.
*Endogenous production of epinephrine and cortisol
increase during stressful situations. These hormones elevate
blood glucose levels and interfere with glycemic control.
Adequate pain control and stress reduction are therefore
important in treating diabetic patients.
*Conscious sedation should be considered for extremely
anxious patients.
*Patients with very poor glycemic control, severe head and
neck infections, other systemic diseases or complications,
and dental-treatment needs that will require long-term
alteration of medication regimens or diet may be
considered for treatment in a more controlled medical
environment.
*The use of systemic antibiotics for routine dental
treatment is not necessary for most diabetic patients.
Antibiotics may be considered in the presence of acute
infection.
Aditi Khamar
*In patients with severe periodontitis, adjunctive use of
tetracycline antibiotics in conjunction with mechanical
periodontal therapy may have beneficial effects on
glycemic control as well as on periodontal status.
*Dental treatment can result in postoperative discomfort.
Because diet is a major component of diabetes
management, diet alterations that are made because of
dental treatment may have a major impact on the patient.
*Another diet change occurs when patients are placed on
orders to take nothing by mouth (NPO) before dental
treatment, a common recommendation before conscious
sedation. Consultation with the patient's physician may be
needed to adjust the dose of insulin or oral agents in this
situation;
*Appointment timing for the diabetic patient is often
determined by the individual's medication regimen.
It is generally best to plan dental treatment to occur either
before or after periods of peak insulin activity.
For those who take insulin, the greatest risk of
hypoglycemia will thus occur about 30 to 90 minutes after
injecting lispro insulin, 2 to 3 hours after regular insulin,
and 4 to 10 hours after NPH or Lente insulin. For those
who are taking oral sulfonylureas, peak insulin activity
depends on the individual drug taken. Metformin and the
thiazolidinediones rarely cause hypoglycemia.
* The greatest risk would occur in a patient who has taken
the usual amount of insulin or oral agent but has reduced or
eliminated a meal prior to dental treatment.
*It is helpful to check the pretreatment blood glucose level
(using the patient's glucometer) and to have a source of
carbohydrates readily available.
If the level is near the lower end of the normal range, a
small amount of pretreatment carbohydrate may prevent
hypoglycemia during the appointment.
Diabetic Emergencies in the Dental Office
The most common diabetic emergency in the dental office
is hypoglycemia, a potentially life-threatening complication
that must be managed accordingly. Signs and symptoms
include confusion, sweating, tremors, agitation, anxiety,
dizziness, tingling or numbness, and tachycardia. Severe
hypoglycemia may result in seizures or loss of
consciousness.
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As soon as a patient experiences signs or symptoms of
possible hypoglycemia, he or she should check the blood
glucose with a glucometer. If a glucometer is unavailable,
the condition should be treated presumptively as a
hypoglycemic episode. The dental practitioner should give
the patient approximately 15 g of oral carbohydrate in a
form that will be absorbed rapidly.
If the patient is unable to take food by mouth and an
intravenous line is in place, 25 to 50 mL of a 50% dextrose
solution (D50) or 1 mg of glucagon can be given
intravenously.
If an intravenous line is not in place, 1 mg of glucagon can
be injected subcutaneously or intramuscularly at almost any
body site. Glucagon injection causes rapid glycogenolysis
in the liver, releasing stored glycogen and rapidly elevating
blood glucose.
Following
treatment, the signs and symptoms of hypoglycemia should
resolve in 10 to 15 minutes. The patient should be observed
for 30 to 60 minutes after recovery. Evaluation by
glucometer can ensure that normal blood glucose levels
have been achieved before the patient is released.
of the diabetic state. The mechanisms underlie the oral
effects of diabetes share many similarities with the
mechanisms that are responsible for the classic diabetic
complications. The intimate relationship between oral
health and systemic health in individuals with diabetes
suggests a need for increased interaction between the dental
and medical professionals who are charged with the
management of these patients. Oral health assessment and
treatment should become as common as the eye, foot, and
kidney evaluations that are routinely performed as part of
preventive medical therapies. Dental professionals with a
thorough understanding of current medical treatment
regimens and the implications of diabetes on dental care are
able to help their diabetic patients achieve and maintain the
best possible oral health.
In some instances, marked hyperglycemia may present with
symptoms mimicking hypoglycemia. If a glucometer is not
available, these symptoms must be treated as
hypoglycemia. If the event was actually hyperglycemia, the
small amount of extra glucose derived from treatment will
generally not have a significant effect.
On the other hand, if glucose-elevating emergency
treatment was withheld from a patient in a mistaken belief
that the emergency was related to
elevated glucose levels when
hypoglycemia was in fact
present, severe adverse outcomes are possible. The best
means of determining the true nature of a glucose-related
emergency is to check the blood glucose level with a
glucometer.
Because hyperglycemic emergencies develop more slowly
than does hypoglycemia, they are less likely to be
encountered in the dental office. Diabetic ketoacidosis and
hyperosmolar nonketotic acidosis require immediate
medical evaluation and treatment. In the dental office, care
is limited to activating the emergency medical system,
opening the airway and administering oxygen, evaluating
and supporting circulation, and monitoring vital signs. The
patient should be transported to a hospital as soon as
possible.
o
Diabetic coma
hypoglycemia in a patient on insulin or
insulin secretogogues occurs when the
blood glucose level falls low enough to
cause symptoms and signs
adregenic symptoms
pale skin
sweating
shaking
palpitation
anxiety
neuroglycopenic symptoms
Conclusion
hunger
suboptimal intellectual function
confusion
coma
seizure
Diabetes mellitus is a metabolic condition affecting
multiple organ systems. The oral cavity frequently
undergoes changes that are related to the diabetic condition,
and oral infections may adversely affect metabolic control
imp points to be consider
patient medical history
Aditi Khamar
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dental history
3. Apt in morning- increase glucose
decrease insulin activity/afternoon
-decrease glucose and increase insulin
4. Instruct patient to tell ,if they feel
any symptom
oral surgery-prophylactic antibiotic
therapy
consultation with a patients physician
before conducting extensive
periodontal or oral surgery
management
-reassure the patient
-assess vital signs ,blood pressure,
pulse and respiratory rate
-defer dental treatment
-call 000
-or organise transport to medical
facilities
if patient is semi conscious will able to
drink then give a glucose drink
unconscious patient give 1mg glucagon
im or give 50ml of 50% glucose iv or
give 100ml of 20%glucose iv
there r some precaution we should take
in managing diabetic patients for
surgery
1. Perform the surgery soon after meal
time
2. Try to manage patient in short apt
3. A morning apt should be better
4. Patient should maintain oral
hypoglycemic drugs and carbohydrate
intake as usual
5. Ensure emergency glucose and drugs
to hand
6. Prescribe antibiotic and analgesic for
prophylaxis to prevent infection
secondary to delayed healing
7. Premedication in anxious patient
with benzodiazepines
8. Use gradual position changes to
avoid postural hypotension
medical considerations
• take a thorough medical history for all
patients
• obtain information concerning the
type of diabetes ,the severity and
control of the diabetes and presence of
cardiovascular or neurological
complications.
Refer any patient with the cardinal
symptoms of diabetes or finding that
suggest diabetes to physician for
diagnosis and treatment.-- headache,dry
mouth ,repeated skin infection,blurred
vision,paresthesia,progressive
periodontal disease
food intake and apt scheduling
1. Verify that the patient has taken
medication
2. Verify that the patient has had
adequate intake of food
Aditi Khamar
Diabetic coma is a reversible form of coma[1] found in
people with diabetes mellitus. It is a medical emergency.
Three different types of diabetic coma are identified:
1.
Severe diabetic hypoglycemia
2.
Diabetic ketoacidosis advanced enough to result
in unconsciousness from a combination of severe
hyperglycemia, dehydration and shock, and
exhaustion
3.
Hyperosmolar nonketotic coma in which extreme
hyperglycemia and dehydration alone are
sufficient to cause unconsciousness.
In most medical contexts, the term diabetic coma refers to
the diagnostical dilemma posed when a physician is
confronted with an unconscious patient about whom
nothing is known except that he has diabetes. An example
might be a physician working in an emergency department
who receives an unconscious patient wearing a medical
identification tag saying DIABETIC. Paramedics may be
called to rescue an unconscious person by friends who
identify him as diabetic. Brief descriptions of the three
major conditions are followed by a discussion of the
diagnostic process used to distinguish among them, as well
as a few other conditions which must be considered.
An estimated 2 to 15 percent of diabetics will suffer from at
least one episode of diabetic coma in their lifetimes as a
result of severe hypoglycemia.
Contents
ï‚·
1 Types
o
1.1 Severe hypoglycemia
o
1.2 Advanced diabetic ketoacidosis
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o
1.3 Nonketotic hyperosmolar coma
ï‚·
2 Identifying the cause
ï‚·
3 Treatment
ï‚·
4 References
when coma is reached. However these features are variable
and not always as described.
If the patient is known to have diabetes, the diagnosis of
DKA is usually suspected from the appearance and a
history of 1–2 days of vomiting. The diagnosis is confirmed
when the usual blood chemistries in the emergency
department reveal hyperglycemia and severe metabolic
acidosis.
Treatment of DKA consists of isotonic fluids to rapidly
stabilize the circulation, continued intravenous saline with
potassium and other electrolytes to replace deficits, insulin
to reverse the ketoacidosis, and careful monitoring for
complications.
Types
Severe hypoglycemia
People with type 1 diabetes mellitus who must take insulin
in full replacement doses are most vulnerable to episodes of
hypoglycemia. It is usually mild enough to reverse by
eating or drinking carbohydrates, but blood glucose
occasionally can fall fast enough and low enough to
produce unconsciousness before hypoglycemia can be
recognized and reversed. Hypoglycemia can be severe
enough to cause unconsciousness during sleep.
Predisposing factors can include eating less than usual or
prolonged exercise earlier in the day. Some people with
diabetes can lose their ability to recognize the symptoms of
early hypoglycemia.
Unconsciousness due to hypoglycemia can occur within 20
minutes to an hour after early symptoms and is not usually
preceded by other illness or symptoms. Twitching or
convulsions may occur. A person unconscious from
hypoglycemia is usually pale, has a rapid heart beat, and is
soaked in sweat: all signs of the adrenaline response to
hypoglycemia. The individual is not usually dehydrated and
breathing is normal or shallow. Their blood sugar level,
measured by a glucose meter or laboratory measurement at
the time of discovery, is usually low but not always
severely, and in some cases may have already risen from
the nadir that triggered the unconsciousness.
Unconsciousness due to hypoglycemia is treated by raising
the blood glucose with intravenous glucose or injected
glucagon.
Advanced diabetic ketoacidosis
Nonketotic hyperosmolar coma
Nonketotic hyperosmolar coma usually develops more
insidiously than DKA because the principal symptom is
lethargy progressing to obtundation, rather than vomiting
and an obvious illness. Extreme hyperglycemia is
accompanied by dehydration due to inadequate fluid intake.
Coma from NKHC occurs most often in patients who
develop type 2 or steroid diabetes and have an impaired
ability to recognize thirst and drink. It is classically a
nursing home condition but can occur in all ages.
The diagnosis is usually discovered when a chemistry
screen performed because of obtundation reveals extreme
hyperglycemia (often above 1800 mg/dl (100 mM)) and
dehydration. The treatment consists of insulin and gradual
rehydration with intravenous fluids.
Identifying the cause
Diabetic coma was a more significant diagnostic problem
before the late 1970s, when glucose meters and rapid blood
chemistry analyzers became universally available in
hospitals. In modern medical practice, it rarely takes more
than a few questions, a quick look, and a glucose meter to
determine the cause of unconsciousness in a patient with
diabetes. Laboratory confirmation can usually be obtained
in half an hour or less. Other conditions that can cause
unconsciousness in a person with diabetes are stroke,
uremic encephalopathy, alcohol, drug overdose, head
injury, or seizure.
Diabetic ketoacidosis (DKA), if it progresses and worsens
without treatment, can eventually cause unconsciousness,
from a combination of severe hyperglycemia, dehydration
and shock, and exhaustion. Coma only occurs at an
advanced stage, usually after 36 hours or more of
worsening vomiting and hyperventilation.
Fortunately, most episodes of diabetic hypoglycemia,
DKA, and extreme hyperosmolarity do not reach
unconsciousness before a family member or caretaker seeks
medical help.
In the early to middle stages of ketoacidosis, patients are
typically flushed and breathing rapidly and deeply, but
visible dehydration, pallor from diminished perfusion,
shallower breathing, and tachycardia are often present
Treatment depends upon the underlying cause:
Aditi Khamar
Treatment
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ï‚·
Ketoacidotic diabetic coma: intravenous fluids,
insulin and administration of potassium and
sodium.
ï‚·
Hyperosmolar diabetic coma: plenty of
intravenous fluids, insulin, potassium and sodium
given as soon as possible.
ï‚·
Hypoglycaemic diabetic coma: administration of
the hormone glucagon to reverse the effects of
insulin, or glucose given intravenously.
Coma may be due to a variety of causes not directly related
to diabetes. Diabetic coma is a state of unconsciousness
that can put a patient at risk of brain damage or even death.
It is triggered by either persistent and extreme elevations in
glucose (blood sugar) levels (hyperglycemia) or abnormally
low glucose levels (hypoglycemia).
A coma is a deep, prolonged state of unconsciousness
caused by an injury or disease. A region deep within the
brain stem stimulates the brain to
various levels of wakefulness and
alertness, depending on signals
received from the eyes, ears, skin and other sensory organs.
When this area of the brain is disturbed, a person’s
consciousness may be impaired.
In most cases, a diabetic coma lasts a few days. Rarely,
some patients may remain in a persistent coma (sometimes
called “awake coma”). Patients in this state may have open
eyes, and they may make grunting sounds or other
vocalizations. However, the higher brain functions are
absent.
Diabetes review 2004
If the glucose level is too low, the person has hypoglycemia
and if the level is too high, the person has hyperglycemia.
Hyperglycemia is just a term for raised blood glucose but in
some cases it can lead to a life-theathening condition called
diabetic ketoacidosis. Patients with diabetes mellitus type 1
are especially prone to this condition.
Causes for this condition vary; in the case of diabetes, it
could be due to too much food too quickly or forgetting to
inject oneself with insulin, while in the case of
hypoglycemia it could be due to a lack of food, too much
exercise for current conditions, or to an insulin or other
medication overdose.
Controlling glucose is the best way to prevent diabetic
coma. Patients should consult with a physician about their
appropriate glucose level and closely monitor this level to
make sure it is not too high or too low. Changes in diet,
exercise and medication may be necessary to manage
glucose. A sick-day plan devised by a physician can also
help prevent diabetic coma.
Certain causes directly related to diabetes require
differentiation: (1) Hypoglycemic coma resulting from
excessive doses of insulin or oral hypoglycemic agents. (2)
Hyperglycemic
coma associated
with either
severe insulin deficiency (diabetic ketoacidosis) or mild to
moderate insulin deficiency (hyperglycemic hyperosmolar
state). (3) Lactic acidosis associated with diabetes,
particularly in diabetics stricken with severe infections or
with cardiovascular collapse.
Diabetic coma is a condition in which a patient loses
consciousness because of excessively high or excessively
low glucose (blood sugar). A person in a diabetic coma is
still breathing but is in a profound state of unconsciousness
and cannot be aroused by stimuli.
91.Patient had hepatitis 10 years ago. What would be
your additional information that you have to get from
patient and how can that effect your dental
management of that patient? 61. Hepatitis, 10yrs ago,
what additional information you get from pt. And how
it influences his treatment?
Hepatitis oral manifestations:
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1)higher incidence of dental caries and periodontal
involvement
2)salivary flow reduced
3)healing response of tissues poorer
4)Hep C has greater manifestations
5)healing response of soft tissue to surgery is poorer
6)heavy emphasis on preventive care
7) extractions are the best treatment
8)advanced hep C or antiviral drugs, use antibacterial
prophylaxis
9)excess alcohol consumption, drug use may interfere
with treatment
10) If patient with related cirrhosis, excess bleeding
tendency, due to lack of coagulation and
thrombocytopenia. Consult specialists and realted
precautions
(tranexemic mouthwash rinse)
These drugs should be avoided, a sthey are
metabolized in liver and may burden it further.
1.Ensure all the members in the dental unit is
vaccinated against hepatitis b.
booster dose is given every 5yrs.
3.take proper measures and protocols to prevent
needlestick and sharps injury
2.patients blood must be screened for hep b antigen
and antibody
4.use double gloves in performing treatments
5.use of high vacuum suction to prevent the spread of
aerosols contaminated with patients saliva
6.use face shields
7.prescribe medications on the consent of general
physician of the patient….the drug might cause
toxicity if not effectively processessed in th liver
8.Lookback investigations
‘Lookback investigation’ refers to the process of
identifying, tracing, recalling,counselling and testing
patients or HCWs who may have been exposed to an
infection in a health care setting.
9. no dental treatment other than urgent care
should be rendered for a patient with acute viral
hepatitis
10.aerosols should be minimized
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Antigen or antibody
When found
Significance for infectivity
HBs(surface)antigen or australian
antigen
Becomes detectable in late incubation and is
present during acute hepatitis.declines over 36months but persists in carriers,whether
asymptomatic or with chronic active hepatitis
Indicates infectivity,though not
necessarily a high infectivity
Antibody to HBs(surface)antigen
Seen in recovery,reflecting immunity against the
virus.also found in those immunised against
hepatitis b
Probably indicates no risk of
infection.denotes past ecposure and
immunity(incl active vaccination)to
the virus and possible need for
further investigation to determine
infectivity
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HBc(core)antigen
Only present in the liver,not used to determine
infectivity
Antibody to HBc antigen
Found in acute disease,recovery and in carriers,
whether asymptomatic or with chronic active
hepatitis
Indicates past infection but a high
level indicates an infection risk
Hbe(envelope) antigen
Becomes detectable in late incubation and is
present during acute hepatitis. persists in
carriers, with chronic active hepatitis but not
usually in asymptomatic carriers
Indicates acute infection or a carrier
state of high infectivity
Antibody to HBe antigen
Develops as Hbedisappears.sometimes persists
in chronic asymptomatic carriers
Indicates either recovery from acute
infection or a carrier state of low
infectivity
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a)
Fibrotic : caused by drug.
b)
Inflammatory : induced by bacterial plaque.
•
The role of plaque in overall pathogenesis of drug
– induced gingival enlargement is not clear.
•
TREATMENT : FIRST OPTION
1.
Discontinuing the drug or changing the drug with
the physician’s consultation.
2.
If substitution of drug is attempted, 6- 12 month
period of time is allowed to elapse between
discontinuation of drug and possible resolution of
gingival enlargement before a decision to
implement surgical treatment is made.
4)The presence of the enlargement makes plaque control
difficult, often resulting in a secondary inflammatory
process that complicates the gingival overgrowth caused by
the drug.
3.
Alternative medicine to phenytoin sodium
include, carbamazepine and valproic acid, both
are reported to have a lesser impact in inducing
gingival enlargement.
5)The enlargement more severe in the maxillary and
mandibular anterior regions.It occurs in areas in which
teeth are present, not in edentulous spaces, and the
enlargement disappears in areas from which teeth are
extracted.
4.
For patients on nifedipine, 44% chances of
gingival enlargement occurs, diltiazem or
verapamil may be alternatives, their reported
prevalence of gingival enlargement is 20% & 4%,
respectively.
5.
Cyclosporin – induced gingival enlargement can
spontaneously resolve if substituted by
tacrolimus.
6.
The antibiotic azithromycin may aid in
decreasing the severity of cyclosporin- induced
gingival enlargement.
88. patient presents with gingival enlargement. he is on
nifedipine for blood pressure. how to manage?
1)The growth starts as a painless, beadlike enlargement of
the interdental papilla and extends to the facial and lingual
gingival margins.
As the condition progresses, the marginal and papillary
enlargement unite; they may develop into a massive tissue
fold covering a considerable portion of the crowns, and
they may interfere with occlusion
2)When uncomplicated by inflammation, the lesion is
mulberry shaped, firm, pale pink, and resilient, with a
minutely lobulated surface and no tendency to bleed.
3) The enlargement characteristically appears to project
from beneath the gingival margin, from which it is
separated by a linear groove.
6)Drug-induced enlargement may occur in mouth with little
or no plaque and may be absent in mouths with abundant
deposits.
7)An inflammatory infiltrate may be found the bottom of
the sulcus, or pocket. Cyclosporine enlargements usually
have a more highly vascularized connective tissue with foci
of chronic inflammatory cells, particularly plasma cells.
SECOND OPTION :
1.
The clinician should emphasize plaque control as
first step in the treatment of drug- induced
gingival enlargement.
2.
A good oral hygiene and frequent professional
removal of plaque decreases the degree of
gingival enlargement present and improves
overall gingival health.
3.
Drug- induced enlargement is associated with
pseudo- pocket formation, frequently with
abundant plaque accumulation and periodontitis,
meticulous plaque control aid in maintaining
attachment levels.
4.
Also, adequate plaque control may aid in
preventing or retarding the recurrence of gingival
enlargement in surgically treated cases.
Oxytalan fibers are numerous beneath the epithelium and in
areas of inflammation.
TREATMENT OF DRUG- ASSOCIATED GINGIVAL
ENLARGEMENT :
1.
2.
Gingival enlargement has been associated with
three different types of drugs : anticonvulsants,
calcium channel blockers, and
immunosuppressant.
The overgrown tissue shows two components :
THIRD OPTION :
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1.
Surgery either gingivectomy or the periodontal
flap.
2.
Elimination of local irritants early in pregnancy is
preferable to treatment of gingival enlargement.
2.
Small areas (upto 6 teeth) of drug-induced
gingival enlargement with no evidence of
attachment loss (no need for osseous surgery),
treated with the gingivectomy technique.
3.
Marginal and interdental gingival inflammation
and enlargement are treated by scaling and
curettage.
4.
3.
3mm of keratinized tissue should remain in
apicocoronal direction after surgery is completed.
Surgical excision of tumorlike enlargement and
scaling and planing of the tooth surface.
5.
Enlargement recurs unless all irritants are
removed.
6.
Food impaction is frequently an inciting factor.
Gingivectomy / gingivoplasty can be performed via
electrosurgery or a laser device.
Recurrence is aproblem, but it can be minimized with
proper attention to
daily plaque control and regular professional cleanings.
Some clinicians use positive-pressure appliances after
surgery to help discourage recurrence.
TREATMENT OF LEUKEMIC GINGIVAL
ENLARGEMENT :
WHEN TO TREAT :
1.
Gingival lesions in pregnancy should be treated
as soon as detected.
2.
Scaling and root planing procedures and adequate
oral hygiene measures reduce the size of the
enlargement.
3.
Gingival enlargements do shrink after pregnancy,
but usually do not disappear.
4.
Lesions should be removed surgically during
pregnancy only if they interfere with mastication
or produce an esthetic disfigurement.
1.
Leukemic enlargement occur in acute or subacute
leukemia and is uncommon in the chronic state.
2.
The medical care of leukemic patients is
complicated by gingival enlargement with
superimposed painful ANUG, which interferes
with eating and creates toxic systemic reactions.
3.
BT, CT and platelet count is checked and
hematologist consulted before periodontal
treatment is instituted.
4.
After the acute symptoms subside, gingival
enlargement correction is done.
a)
Preventing gingival disease before it occurs.
TREATMENT :
b)
Treating existing gingival disease before it
worsens.
1.
Scaling and root planing carried out under topical
anesthesia.
5.
2.
The initial treatment consists of removing all
loose accumulations with cotton pellets,
performing superficial scaling, and instructing the
patient in oral hygiene for plaque control, which
includes use of chlorhexidine mouthwashes.
Every pregnant patient should be scheduled for
periodic dental visits, the importance of which in
the
prevention of serious periodontal disturbances
should be stressed
3.
Deeper scalings are carried out at subsequent
visits, treatment confined to small area of the
mouth to control bleeding.
4.
Antibiotics are administered systemically the
evening before and for 48 hrs. after to reduce risk
of infection.
TREATMENT OF GINGIVAL ENLARGEMENT IN
PREGNANCY :
1.
In pregnancy, the emphasis should be on :
6.
7.
In pregnancy, the emphasis should be on :
c)
Preventing gingival disease before it occurs.
d)
Treating existing gingival disease before it
worsens.
6.
Every pregnant patient should be scheduled for
periodic dental visits, the importance of which in the
prevention of serious periodontal disturbances should be
stressed
Treatment requires elimination of all local
irritants responsible for precipitating the gingival
changes in pregnancy.
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86. 65 year old female patient on oral bisphosphonates .
She has several grossly carious posterior teeth. how to
manage?
Cyclosporine-induced gingival enlargement is more
vascularized than the phenytoin enlargement, occurs in
approximately 30% of patients receiving the drug, is
more frequent in children, and its magnitude appears to
be related more to the plasma concentration than to the
patient's periodontal status. Gingival enlargement is
greater in patients who are medicated with both
Cyclosporine
and calcium channel-blocking drugs
Bisphosphonates slow bone loss and iomprove bone
density.
Drugs reduce bone turnover. Adsorbed on bone surfaces.
Remain.
Taken up by osteoclasts_interfere with ATP metabolism or
membrane function.
Osteoclasts die or are unable to function.
Bone formation exceeds resorption and density increases or
stabilizes.
Used for : Osteoporosis, Pagets, bone metastasis
stopped, multiple myeloma,increase bone mass in OI,
enlargement of metastasis arrested.
drug –dronate
Risk because of:
interfere with signalling between cells and new blood
vessel growth..tissue of marrow becomes avascular and
dies..bone devoid of osteoclast
Osteoblast and clast are interdependent..osteocytes are not
replaced by clasts and ultimately die.
Bone and soft tissue necrosis.
CLINICAL FEATURES
1)pain, which arises mainly from soft tissue as bone is
insensitive.
2)bone exposed because overlying muco periosteum is
dependent on blood supply from bone
more in prominent areas like tori or posterior lingual aspect
of the mandible.
3)draining sinus at to=imes.
4)Extensive soft tissue infection possible
5)mobility of teeth
6)exposed bone
Radiograph might be completely normal
As medullary space of marrow is affected.
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the risk of BON, other risks associated with various
treatment options, and the risk of foregoing treatment, even
temporarily.
3)The patient should be encouraged to consult with his or
her treating physician about any health risks. However,
patients with possible risk factors for BON may benefit
from assessment by an expert in metabolic bone diseases.
Bis phosphonates can remain in the bone for a long time.
Risk of BON dependent on dosage potency and length of
time along with medical factors and nature of bone.
BON can occur spontaneously, owing to dental disease or
secondary to dental therapy. Therefore, patients taking oral
bisphosphonates should be instructed to contact their
dentist if any problem develops in the oral cavity.
4)Routine dental treatment generally should not be
modified solely on the basis of oral bisphosphonate
therapy.
If you have a history of multiple myeloma, metastatic
cancer, Paget’s disease and osteoporosis you may need to
check to see if you received i.v. bisphosphonates during
treatment
General recommendations.
As with all dental patients, routine dental examinations are
recommended.
1)A comprehensive oral evaluation should be carried out of
all patients about to begin therapy with oral
bisphosphonates
2)The dentist should inform the patient taking oral
bisphosphonates that
ï‚·
there is a very low risk of developing BON;
ï‚·
there are ways to minimize the risk, but not to
eliminate the already low risk;
ï‚·
the consensus is that good oral hygiene along
with regular dental care is the best way to lower
risk;
ï‚·
there are no diagnostic techniques to identify
those at increased risk of developing BON.
The patient also should be informed of the dental treatment
needed, alternative treatments, how any treatment relates to
Aditi Khamar
5)Before undergoing any invasive procedure that involves
manipulation of the bone or periosteum, patients should
again be informed about the implications of oral
bisphosphonate therapy and the risk of BON.
6)When the treatment plan dictates that the medullary bone
and/or periosteum is going to be involved in multiple
sextants, the dentist should treat one sextant or tooth first, if
dentally possible.
At that point, the dentist should allow for a two-month
disease-free follow-up, treating the patient with
antimicrobials, before other sextants are treated with
similar therapy.
7)Chlorhexidine is used two times per day for two months
after surgery.
8)periapical pathoses, sinus tracts, purulent periodontal
pockets, severe periodontitis and active abscesses already
involve the medullary bone and may cause osteonecrosis by
themselves. These areas should be treated immediately,
because the medullary bone already is involved in the
pathologic process.
9)If medication is discontinued, bone might gradually
recover.Very slow process
Medication options..if BISP are discontinued..strontium
ranalate and Teraparatide.
Managemant of Caries (extensive)
1)efforts made to preserve teeth.
2)RCT preferred
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3)point 8) above explain to patient.
4)retain decoronated roots as overdenture abutmants5)CHX
rinses to prevent soft tissue infection
5)If soft tissue infection exists concurrent medication
Dentists should check and adjust removable dentures to
avoid soft-tissue injury.
6) LA without adrenaline
3)Maintenance of implants should follow accepted
mechanical and pharmaceutical methods to prevent periimplantitis, with regular monitoring of the patient.
4)Appropriate forms of nonsurgical therapy combined with
a prolonged phase of initial therapy should be considered
for patients with peri-implantitis.
5)If the disease does not resolve, surgical revision of soft
tissues around the implant(s) may be appropriate and, when
necessary, modest bone recontouring may be considered.
Management of periodontal diseases.
1)patients with destructive periodontal diseases who are
receiving oral bisphosphonate therapy should receive
appropriate forms of nonsurgical therapy, which should be
combined with a prolonged phase of initial therapy for
observation.
2)If the disease does not resolve, surgical treatment should
be aimed primarily at obtaining access to root surfaces,
with modest bone recontouring being considered when
necessary.
3) guided bone regeneration or guided tissue regeneration
should be judiciously considered, in view of the fact that
bisphosphonates have been shown to decrease the
vascularity of tissues, which may have a negative effect on
grafted sites.
6)Monitoring of implants essential. Loss of osseintegration
might occur.
Oral and maxillofacial surgery
Temporary 3 month withdrawal befor and 3 months after
might reduce risk of bone necrosis developing.1)When
dental and/or periodontal disease treatment has failed,
surgical intervention may be the only alternative.
2)Patients taking oral bisphosphonates who are undergoing
invasive surgical procedures should be informed of the risk,
albeit small
3)Alternative treatment plans consisting of endodontics
instead of extraction and bridges and partial dentures versus
implant reconstruction should be discussed with the patient.
4)Patients without periodontal disease should receive
accepted mechanical and pharmaceutical methods to
prevent periodontal disease, and they should be monitored
on a regular basis as determined by their dentists.
4)If extractions or bone surgery are necessary, conservative
surgical technique with primary tissue closure should be
considered, when possible.
4) mobile teeth need to be extracted if non vital, as
prognosis is poor.
5) immediately before and after surgical procedures
involving bone, the patient should rinse gently with a
chlorhexidine-containing rinse. Typically, chlorhexidine is
used two times per day for two months after surgery.
5)keep exposed bone and mucosa as clean as possible
using CHX and oral hygiene methods
Prominent bone edges to be removed without LA to prevent
trauma to soft tissues.
If bone is removed the surrounding bone is not healthy.
(Unlike ORN and OM)
Implant placement and maintenance.
1)treatment plans for patients taking bisphosphonates
should be considered carefully, since implant placement
requires the preparation of the osteotomy site.
2) The patient may be at increased risk of developing BON
when extensive implant placement or guided bone
regeneration to augment the deficient alveolar ridge before
implant placement is necessary.
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6)Prophylactic antibiotics may be utilized during the
healing/wound closure phase for procedures that involve
extensive manipulation of the bone
As blood supply is limited systemic medications might not
reach.
Topical is preferable with good oral hygiene.
7) healing may be slow. If 6 weeks later healing not
complete, refre to specialist= BON. DO NOT CURETTE.
8) Alternative to extraction is elastic band extraction. @-4
weeks.
Aggressive Infection
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If present, culture taken
Metronidazole and amoxiciilin
If sequestration occurs, open surgical debridement
necessary.
84. HIV positive patient with caries. How to manage during
your treatment.
ADD PREVENTION
Factors, which predispose expression of oral lesions,
include:
–CD4 counts less than 200 cells/mm3
–Viral load greater than 3,000 copies/mL
–xerostomia (dry mouth)
–poor oral hygiene
–smoking
Use of crystal methamphetamine is associated with
increased risk of HIV acquisition, and its use by infected
individuals can be associated with
rapid dental decay known as “meth mouth”
These lesions frequently develop at the cervical region of
the tooth, where the crown meets the root. formation of an
abscess.
It is important to receive care at an early stage of this
disease in order to avoid abscesses.
Treatment includes the use of techniques such as “scoop
and fill,” in which the bulk of the
decayed material is scooped out — usually without
anesthesia, using hand instruments —
and replaced with a temporary filling that contains fluoride
to inhibit further decay. The filling material of choice is
glass ionomer.
This treatment requires a dentist, who can restore each
tooth in a traditional manner after the scoop and fill
process. Infections of the pulp of the tooth should be
treated with an antibiotic, preferably penicillin.A
Artificial saliva products can be effective in people who
have active tooth decay resulting in part from drug related
dry mouth.
Every patient should receive a comprehensive
initial evaluation.
To provide the best oral health care possible, oral health
care professionals should perform a medical and social
history along with a comprehensive medical systems
review at recall visits for stable patients and at each visit
for unstable patients.
The dental provider should determine and document the
patient’s chief complaint(s) and health history.
Common
or notable HIV-related oral conditions include 1)xerostomia
2) candidiasis
3) oral hairy leukoplakia
4) periodontal diseases such as linear gingival erythema
and necrotizing ulcerative periodontitis,
5) Kaposi’s sarcoma,
6)human papilloma virus-associated warts, and 7)ulcerative
conditions including herpes simplex
virus lesions, recurrent aphthous ulcers, and neutropenic
ulcers.
Xerostomia
Xerostomia is a major contributing factor in dental decay in
HIV-infected individuals.
experience moderate to severe xerostomia in association
with the effects of medications (eg, didanosine) or the
proliferation of CD8+ cells in the major salivary glands.
Changes in the quantity and
quality of saliva, including diminished antimicrobial
properties, lead to rapidly advancing dental decay and
periodontal disease
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Patients with HIV infection may develop associated skin
manifestations and cervical lymphadenopathy; therefore,
extraoral head and neck examinations and oral soft-tissue
examinations should be performed at each visit.
A comprehensive treatment plan that includes preventive
care and maintenance should be developed and discussed
with the patient.
Medications may interfere with dental treatment and cause
adverse effects, such as decreased salivary flow, altered
liver function, and bone marrow suppression, resulting in
anemia, thrombocytopenia, and neutropenia
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Drug-drug interactions also may occur.
When there are non-cavitated lesions, remineralization
should be performed with fluoride varnishes and homecare
fluoride products.
A higher risk of dental caries in patients with HIV may be
caused by decreased salivary flow, which may occur as a
result of salivary gland disease or as a side effect of a
number of medications.
Also, some topical antifungal medications have high
sugar content, possibly resulting in increased caries
susceptibility.
As in all patients, prevention and management of carious
lesionsin individuals with HIV/AIDS should include
diagnosis, caries risk assessment, and behavior
modification to reduce caries activity.
Treatment should include remineralization of noncavitated, smooth-surface lesions and restorative treatment
of cavitated lesions.
Establishment of recall intervals should be based on
caries risk status, with high-risk patients being seen more
frequently.
Caries risk should be reassessed at each recall visit, and
future care should be planned accordingly. In addition to
fluoride varnishes, therapy in adults should include pit and
fissure sealants and proper use of certain sugarless chewing
gums that may provide protection.18
.
Because a significant number of HIV patients have a
history of substance use or are active substance users, the
following oral complications, which may be related to drug
addiction, should be
considered: xerostomia, rampant dental caries (especially
cervical caries), poor oral hygiene, gingival and periodontal
disease, and
occlusal wear as a result of bruxism.
Injection drug users (IDUs) have a high incidence of
bacterial endocarditis. Oral health care providers should
address this issue with respect to antibiotic prophylaxis
before performing dental
procedures.19,20
Candidiasis
The 3 common presentations of oral
candidiasis are angular cheilitis, erythematous
candidiasis, and pseudomembranous
candidiasis.
Angular cheilitis presents as erythema
or fissuring of the corners of
the mouth. Treatment involves
the use of a topical antifungal cream
Erythematous candidiasis
presents as a red, flat, subtle lesion on the dorsal surface of
the tongue or on the hard or soft
palates. It may present as a “kissing” lesion—if a lesion is
present on the tongue, the palate should be
examined for a matching lesion
patients complaining of oral burning
Pseudomembranous candidiasis (or
thrush) appears as creamy, white, curdlike
plaques on the buccal mucosa,
tongue, and other oral mucosal surfaces.
The plaques can be wiped away,
typically leaving a red or bleeding
underlying surface.
Topical treatments for mild to moderate
cases of both erythematous and
pseudomembranous candidiasis
include clotrimazole troches, nystatin
oral suspension, and nystatin pastilles
treatment must be continued for at
least 2 weeks in order to reduce organism
colony-forming units to levels low
enough to prevent recurrence.
Topical agents (mild to moderate oral candidiasis)
Clotrimazole troches
Nystatin oral suspension
Nystatin pastilles
Systemic agents
Fluconazole
Itraconazole oral suspension
Voriconazole
Oral Hairy Leukoplakia
Oral hairy leukoplakia, which is caused by Epstein-Barr
virus, presents as a white, corrugated lesion
on the lateral borders of the tongue; the lesion cannot be
wiped away
patients presenting with it while on antiretroviral therapy
may be experiencing failure of their current regimen.
Periodontal Disease
Linear gingival erythema
Linear gingival erythema, or “red band gingivitis,” presents
as a red band along the gingival margin
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commonly extends to the posterior teeth. It can also present
on attached
and non-attached gingiva as petechialike
patches.
Necrotizing Ulcerative
Periodontitis
rapid destruction of soft tissue in the former condition and
hard tissue in the latter.
The condition is characterized by severe pain,
loosening of teeth, bleeding, fetid odor, ulcerated gingival
papillae, and rapid loss of bone and soft tissue
Patients often refer to the pain as “deep jaw pain.”
Treatment includes removal of dental plaque, calculus, and
necrotic soft tissues utilizing
a 0.12% chlorhexidine gluconate or 10% povidone-iodine
lavage, and institution of antibiotic therapy
Management of Necrotizing
Ulcerative Periodontitis
Initial visit
• Prescribe narrow spectrum antibiotics
such as metronidazole 500 mg, dispense
14 to 20 tablets, take 1 tablet twice
daily for 7 to 10 days. Other antibiotic
options include clindamycin and amoxicillin
• Pain management is extremely important
• Nutritional supplementation or counseling
may be necessary
Follow-up visits
• Detailed periodontal care, such as scaling
and root planing
to persist for longer than the 7- to 14day period observed in immunocompetent
individuals. Treatment for
milder cases involves the use of topical
corticosteroids such as dexamethasone
elixir (0.5 mg/5 mL) 5 mL
swished for 1 minute and then
expectorated, 2 to 3 times daily until
symptoms resolve. For more severe
occurrences, systemic corticosteroids
such as prednisone are used.
Kaposi’s Sarcoma
Kaposi’s sarcoma is the most frequent HIV-associated oral
malignancy, Kaposi’s sarcoma-associated herpesvirus
(KSHV) is the etiologic agent.
Kaposi’s sarcoma can be macular, nodular, or raised and
ulcerated, with color ranging from red to purple
early lesions tend to be flat, red, and asymptomatic, with
the color becoming darker as the lesion
ages.
Treatment ranges from localized injections of
chemotherapeutic agents, such as vinblastine sulfate, to
surgical removal. Oral hygiene must be
stressed. Systemic chemotherapy may be the treatment of
choice.
The warts may be cauliflower-like, spiked, or
raised with a flat surface.
Treatment may involve surgery, laser
surgery, or cryotherapy.
HPV survives in aerosol.
Topical 5-fluorouracil treatment has
been used on external lesions
Ulcerative Diseases
Herpes simplex virus
Recurrent intraoral HSV outbreaks
start as a small crop of vesicles
that rupture to produce small, painful
ulcerations that may coalesce. Lesions
on the lip are fairly easy to recognize.
In the mouth, lesions on keratinized,
or fixed, tissues, including the hard
palate and gums, should prompt suspicion
of HSV infection
Herpetic ulcerations are often self-limiting,
although the use of an antiviral medication such as
acyclovir is sometimes necessary to control the outbreak.
Aphthous ulcerations
Recurrent aphthous ulcerations appear on non-keratinized,
or non-fixed, tissues, such as the labial or buccal mucosa,
floor of the mouth, ventral surface of the tongue, posterior
oropharynx, and maxillary and mandibular vestibules .
The lesions are characterized by a halo of inflammation and
a yellow-gray pseudomembranous covering.
They are very painful, especially during consumption of
salty, spicy,or acidic foods and beverages, or
hard or rough foods.
Neutropenic ulcerations
Neutropenic ulcerations are very painful ulcerations that
can appear on both keratinized and non-keratinized tissues,
and are associated with absolute
granulocyte counts of less than 800/μL
Patients should receive granulocyte colony-stimulating
factor treatment prior to systemic or
topical steroid treatment
Pain in ulcerative disease
Pain management is a crucial component
of treating ulcerative oral diseases.
Pain usually is treated with topical anesthetics or systemic
analgesics.
However, relief provided by topical anesthetics is usually
of short duration.
Anesthetic mouth rinses numb the taste buds, resulting in a
decreased desire to eat, and diminished nutritional intake
can have a significant negative impact on overall wellbeing for many patients.
a rinse composed of polyvinylpyrrolidone, hyaluronic acid,
and glycyrrhetinic acid.
Oral Warts—Human Papilloma
Virus
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2nd ideal time fetus not very large
prevention of disease progression
-up- plus Routine dental care
83.A patient comes to you for a recall visit and informs
you she is 3 months pregnant. What is your line of
management? 38. Dental treatment in pregnant
women?
3rd Uncomfortable for patient
-same as 1Elective care avoided after first half
Potential problems related to dental Treatment
re-constructive procedures (crown & bridge
fabrication & significant surgical procedures) are
best delayed until after pregnancy
1.
2.
3.
Dental procedures can potentially cause harm to a
developing fetus via:
a. Radiation
b. Drugs
c. Stress
Supine hypotension in late pregnancy
Poor nutrition
Prevention of medical complications
1.
Women of childbearing age
a. Always use contemporary radiographic
techniques including lead apron when
performing radiographic examination
b. Avoid prescribing drugs that are known to
be harmful to fetus or whose effects as yet
unknown
c. Encourage patient to maintain a balanced,
nutritious diet
2.
Pregnant women
a. Contact patient’s physician to verify
physical status, present management plan,
ask for suggestions regarding patient’s
treatment and to obtain history of previous
pregnancies
b. Maintain optimum oral hygiene, including
prophylaxis, throughout pregnancy
c. Avoid elective dental care during 1st
trimester & ½ of 3rd trimester
d. 2nd trimester is the best time for elective
treatment
e. Avoid radiographs during 1st trimester;
thereafter take only those necessary for
treatment, always using lead apron
f. Avoid administration of drugs known to be
harmful to fetus
g. In advanced stages of pregnancy (3rd
trimester), avoid placing patient in supine
position for prolonged periods of time
3.
Trimester wise
1st..spontaneous miscarriages occur
avoid elective treatment
Plaque control,
Oral hygiene
Sc, pol, Cur
Avoid elective treatment, only urgent
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Dental treatment during pregnancy
PERIO
1) minimize systemic infection and disease is of utmost
importance during this period
2)bacteria associated with periodontal disease have been
associated with low birth weights and premature birth
Porphyromonas
gingivalis,
Actinobacillus actinomycetemcomitans, Bacteroides
forsythus,
and Treponema denticola
the bacteria associated with periodontal disease increases
prostaglandin E2, tumor necrosis factor a, and interleukin
1-B. These in turn set up an inflammatory response that
may stimulate cervical dilation and labor, leading to
premature birth.
3)Dental hygiene procedures, such as prophylaxis, deep
scaling, or root planning are allowable in any trimester of a
normal pregnancy.
Dental prophylaxis is encouraged to not only minimize the
bacterial load of periodontal pathogens, but also to
reinforce good oral hygiene habits for the patient.
4)Dental hygiene should be encouraged during pregnancy
due to the high incidence of gingivitis
in pregnant patients.
5) Pregnancy gingivitis
Due to hormonal and vascular changes
2-8 months
Bleeds easily
treated by sc, RP,
6)pregnancy tumors in areas of gingivitis.
Buccal maxillary anterior areas.
purple-blue
ulcerated, bleeds
sc, RP
can be a painful, nonesthetic soft tissue growth that is
frequently removed either during the patient’s pregnancy or
recent postpartum period
might regress spontaneously
CARIES
*Saliva changes-decreased buffers, minerals
decrease flow 1st, 3rd sem
increased 2nd
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More acidic
*esophageal relux-acid exposure
1)most gestational women must increase their caloric
intake during pregnancy. Frequently, this intake is in the
form of multiple, small meals, or increased carbohydratebased food, which exposes the patient’s teeth to higher acid
levels and caries risk
2)If dental caries is a source of pain or acute infection
dentist should provide invasive care no matter what the
patient’s phase of pregnancy.
3) Dental decay also presents an additional source of
bacterial load on the patient.
4)Oral-maxillofacial abscesses may release various
exotoxins, cytolytic enzymes, as well as grampositive and
gram-negative bacteria.
muscle cramps, back pain, or positional hypotension when
reclined in the dental chair, which may lead to an
uncomfortable environment to deliver elective care.
4)Bouts of great joy, anxiety, or fear can be common during
pregnancy. When combined with dental fears or phobia,
pregnant patients may delay or avoid dental care. Anxiety
may lead to transient increases in blood
pressure, gastrointestinal upset, hyperventilation, or uterine
cramping.
Often, counseling and addressing the causes of the patient’s
fears help relieve
the symptomology.
5)there is no contraindication to using diagnostic
procedures deemed necessary, such as appropriate
radiographs, during a patient’s pregnancy, as long as
normal safety precautions are followed.
6)These precautions includes beam collimation, high-speed
film, limited exposures, and lead-apron protection for the
patient. It is estimated that the average full-mouth dental
film series may expose the fetus to 1 _ 10 rads of radiation,
far below the tetratogenic risk to the unborn child
Fetus susceptible 2-6th week
MANAGEMENT
1)SUPINE HYPERTENSIVE SYNDROME
In supine position uterus compresses inf vena cava –
decreased return to heart-also fetal hypoxia
-sweating,weakness,nausea, lack of air
-bradycardia-drop in BP- Loss of consciousness
RX-lift right hip 10-12 cm to take weight off major blood
vessels
-raise head above feet
-patient made to lie on left side
2)EXCESSIVE VOMITING
-seated in semi supine position
-if nauseous,treatment stopped, patient repositioned upright
-rinse mouth with mouthwash
-morning appointments avoided
-advise not to brush immediately after vomiting.
use antacid, water and baking soda
eat cheese
1)It is best not to expose a pregnant woman
to medical risks unnecessarily, which is why elective care is
often postponed until gestation has concluded.
2)the second trimester of pregnancy is usually devoted to
maturation and not commonly associated
with preterm birth in healthy pregnancies, many dentists
feel comfortable delivering elective dental care during this
period.
3)Even though the third trimester is also devoted to fetal
maturation, gestational women may be more prone to
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Local Anesthetics
Antifungals
Antibiotics
Ulcer healing
NSAIDS
Opiods
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Lidocaine and prilocaine,
B
first-line choices for local anesthesia for pregnant
women who do not have any contraindication
etidocaine
Bupivicaine, mepivicaine
Procaine
C
nystatin, chlorhexidine
B
the use of vasoconstrictors, such as epinephrine or
levonorderfrin, is not contraindicated. avoiding
injection within blood vessels and maintaining total
dosages at or below therapeutic ranges
Doxycycline = D
Clotrimazole
ketoconazole
fluconazole
the penicillin family, the
erythromycins
azithromycin,
clindamycin,
metronidazole
cephalosporins
C
B
estolate (erythromycin) causes hepatitis
tetracycline, minocycline,
and doxycycline
D
likelihood of chelating in bones and teeth.
Omeprazole
esmoprazole
lansoprazole
B
Pantoprazole
Misoprostol
teratogenic
Aspirin and diflusinal
associated with prolonged
gestation and labor, anemia, increased bleeding
potential, and premature closure of the ductus
arteriosus of the heart
Even ibuprofen,
ketoprofen, and naproxen
B for first two trimesters
D for third trimester
Acetaminophen
B
C (with codeine,hydroxyl
codeine or oxycodone)
Naproxen
Oxycodone
B
B
meperidine,
hydrocodone,
propoxyphene, and
codeine
C
are contraindicated due to their risks of
prolonged labor, hemorrhage risk during delivery,
and premature closure
of the ductus arteriosus.
1st line of choice
long-term narcotic usage is ill-advised as the fetus
may develop either neonatal depression or
withdrawal symptoms
Avoid codeine late in gestation-fetal resp depression
withdrawal symptoms
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Anxiolytic
Triazolam,
X
Most benzodiazepines for anxiolytic relief must be
administered with extreme caution and consultations
with the patient’s physician because most drugs in
this class are classified in categories C or D
Diazepam
Controversial
the risk of oral cleft
developments during the
first trimester and the risk
of neonatal toxicity and
withdrawal symptoms
during the third trimester
Controversial
risk of reduced uterine blood flow or tetratogenic
effects when used in high concentrations. Short-term
use of nitrous oxide when used in combination with
O50% oxygen for nonelective dental procedures
management is not possible without anxiolytic
management.
NO
Antacids
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Aluminium and mg
hydroxide
Simethecone
calcium carbonate
Not to be used in 1st
2nd, 3rd use with enough oxygen
B
C
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43. Your nurse sustains an LA needle stick injury how
would you proceed? 16. Discuss the procedure for
managing an operation needle stick injury following
infiltration anesthesia?
73.Emergency Treatments Cardiac Arrest
63.. emergency on the dental chair. Patient is unconscious
with no pulse, no breath. What’s your management?
54. Anaphylactic shock??
Q. preventing endocarditis