Emergencies

113 Latex allergy

Latex proteins can permeatefollowing contact through both skin and mucosa or via lungsType of reactions: Type Ia. 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 Groups1. Patients with a history of multiple surgical procedures, including those withmyelomeningocoele (spina bifida) and congenital genitourinary tract anomalies.

2. Health care personnel with occupational exposure.

3. Other individuals with occupational exposure to natural rubber latex, includinghairdressers, greenhouse workers and those in latex product manufacturing.

4. Individuals with a history of atopy, hay fever, rhinitis, asthma or eczema.

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 episodesof 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 Latex-containing 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.

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

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http://en.wikipedia.org/wiki/FITkit

http://en.wikipedia.org/wiki/Zinc_oxide

http://en.wikipedia.org/wiki/Talc

http://en.wikipedia.org/wiki/Contact_dermatitis

http://en.wikipedia.org/wiki/Rash

http://en.wikipedia.org/wiki/Contact_dermatitis

http://en.wikipedia.org/wiki/RAST_test

http://en.wikipedia.org/wiki/Blood_testing

or silicone.Non latex dental dam is available made from silicone and synthetic elastomers. Latex free disposable syringes are available Facemasks can be obtained whichare latex free. Local anesthetics known to be latex-freecan 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 beuseful.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.

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 splints3. 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 taken4. 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 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.

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'sresponse to stress. Stress results in releaseof cytokines, and in particular the cytokineinterleukin-1, which causes cortisol levelsto 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 stressTreatment 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 isimportant, as secondary adrenal diseaseneeds to be ruled out.9) For surgical procedures under generalanaesthesia, the need for peri-operativeglucocorticoid supplementation, forpatients on exogenous steroids, should bedetermined by the severity of the surgeryand the pre-existing glucocorticoid dose,

*For surgical procedures under general anaesthesia, the need for peri-operative glucocorticoid supplementation, for patients on exogenous steroids, should bedetermined by the severity of the surgeryand the pre-existing glucocorticoid dose.

for patients undergoing general anesthesia for minor surgery 100 mg hydrocortisone intramuscularlyshould be administered and the usual glucocorticoidmedications 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 failureare 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 theadrenal glands there is a decreased glucocorticoidresponse to stress, and this may precipitate an adrenal crisisMany 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 respondto 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 dextrose-saline.- 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 6-hourly intervals)must be continued for at least 3 days after the BP has returned tonormal.

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 formORAL1)The smoking and chewing of tobacco products can have a dramatically negative impact on a person’sappearance.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. 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.

• 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 non-smokers.• The outcome of periodontal treatment is less favourable or unfavourable in smokers.

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

11) Wound healing: Tobacco use is known to impair wound healing.• 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 clot-disrupting effect of the negative intraoral pressure produced during tobacco smoking• There is also evidence which suggests that smoking inhibits healing through the effects ofdecreased 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.

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.

. 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

Irritation of the trachea (windpipe) and larynx (voice box)

Reduced lung function and breathlessness due to swelling and narrowing of the lung airways and excess mucus in the lung passages

Impairment of the lungs’ clearance system, leading to the build-up of poisonous substances, which results in lung irritation and damage

Increased risk of lung infection and symptoms such as coughing and wheezing

Permanent damage to the air sacs of the lungs.

Effects of smoking on the circulatory system

Raised blood pressure and heart rate Constriction (tightening) of blood vessels in the

skin, resulting in a drop in skin temperature Less oxygen carried by the blood Stickier blood, which is more prone to clotting


http://quitsmoking.about.com/cs/nicotineinhaler/g/carbonmonoxide.htm

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)

Reduced blood flow to extremities like fingers and toes

Increased risk of stroke and heart attack due to blockages of the blood supply.

Effects of smoking on the immune system

The immune system doesn’t work as well The person is more prone to infections such as

pneumonia and influenza Illnesses are more severe and it takes longer to

get over them. Lower levels of protective antioxidants (such as

Vitamin C), in the blood.

Effects of smoking on the musculoskeletal system

Tightening of certain muscles Reduced bone density.

Other effects of smoking on the body

Irritation and inflammation of the stomach and intestines

Increased risk of painful ulcers along the digestive tract

Reduced ability to smell and taste Premature wrinkling of the skin Higher risk of blindness

Effects of smoking on the male body

Lower sperm count Higher percentage of deformed sperm Genetic damage to sperm 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

Reduced fertility Menstrual cycle irregularities or absence of

menstruation Menopause reached one or two years earlier Increased risk of cancer of the cervix 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

Increased risk of miscarriage, stillbirth and premature birth

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

Increased risk of cleft palate and cleft lip 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.

Diseases caused by long-term smoking

A lifetime smoker is at high risk of developing a range of potentially lethal diseases, including:

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

Lung diseases such as chronic obstructive pulmonary disease, which includes chronic bronchitis and emphysema

Coronary artery disease, heart disease, heart attack and stroke

Ulcers of the digestive system Osteoporosis and hip fracture Poor blood circulation in feet and hands, which

can lead to pain and, in severe cases, gangrene and amputation.

Smoking cessationThere are 5 crucial steps in advising people to stop smoking:• Ask• Assess• Advise• Assist• ArrangeAskAsk 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.AdviseAdvise 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 quitattempts that it is common to make several attempts before succeeding.

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.

AssistDiscuss the benefits of various stop smoking aids such as Nicotine Replacement Therapy (NRT), Zyban (bupropion) or Champix (varenicline). Remind the patient that these pharmacotherapies areavailable on prescription.

ArrangePatients 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%.

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.

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.

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

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 stenosisendocrine - thyrotoxicosisvascular - coarctation of the aortagynaecological - eclampsia and pre-eclampsia of pregnancy

COMPLICATIONS OF LONGSTANDING HYPERTENSION1. 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. chlorothiazidebeta-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.hydralazinecentrally 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).

MINOR ORAL SURGERY IN HYPERTENSIVE PATIENTS1. 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 theThrombosis, distal platelet and thrombus embolisation, and myocardial necrosis.

• Major risk factors:hypereholesteraemia occurring below the age of 45 yearshypertension occurring below the age of 45 yearssmokingdiabetes.• Minor risk factors:lack of exercisestressful 'type A' personalityoral contraception


obesity.

MINOR ORAL SURGERY IN PATIENTS WITH ISCHAEMIC HEART DISEASEEnsure 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 fluctuationsin 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 DISEASEIt 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.

CARDIOMYOPATHYProgressive failure of contractility of cardiac muscle.

MANAGEMENT

1)Condition should be stable and treatment simplified.2)short duration3)head higher than heart, not horizontal position.4)antibiotic prophylaxis

Plus answer below

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

Heparin

Clopidogrel

PATIENTS TAKING ASPIRINpatients have a normal INR, prolonged bleeding time.

Usually don’t bleed much from extraction wounds

In case dosage not stopped pt must be warned about11)excess bruising2)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=14Restart 2 days after surgery.

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).


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.

10) Preferably surgery should be performed in the morning to facilitate post operative observation.

11) For extensive surgery the assistance of physician is required.

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.


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 coma42. 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 /bluishhue (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 fermentable-carbohydrate intake is more likely to experience oral diseases such as caries and periodontitis and to respond 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 shoulddetermine 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.

*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.

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.

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.

Conclusion

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 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.

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 symptomspale skinsweatingshakingpalpitationanxiety

neuroglycopenic symptoms

hungersuboptimal intellectual functionconfusioncomaseizure

imp points to be considerpatient medical historydental history

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 drinkunconscious 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 time2. Try to manage patient in short apt3. A morning apt should be better4. Patient should maintain oral hypoglycemic drugs and carbohydrate intake as usual5. Ensure emergency glucose and drugs to hand6. Prescribe antibiotic and analgesic for prophylaxis to prevent infection


secondary to delayed healing7. Premedication in anxious patient with benzodiazepines8. Use gradual position changes to avoid postural hypotensionmedical 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 medication2. Verify that the patient has had adequate intake of food3. Apt in morning- increase glucose decrease insulin activity/afternoon -decrease glucose and increase insulin4. Instruct patient to tell ,if they feel any symptomoral surgery-prophylactic antibiotic therapy consultation with a patients physician before conducting extensive periodontal or oral surgery

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 hypoglycemia2. 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

1 Types o 1.1 Severe hypoglycemia o 1.2 Advanced diabetic ketoacidosis o 1.3 Nonketotic hyperosmolar coma

2 Identifying the cause 3 Treatment 4 References

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


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.

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 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.

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.

Fortunately, most episodes of diabetic hypoglycemia, DKA, and extreme hyperosmolarity do not reach unconsciousness before a family member or caretaker seeks medical help.

Treatment

Treatment depends upon the underlying cause:

Ketoacidotic diabetic coma: intravenous fluids, insulin and administration of potassium and sodium.

Hyperosmolar diabetic coma: plenty of intravenous fluids, insulin, potassium and sodium given as soon as possible.

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).

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.

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

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:

1)higher incidence of dental caries and periodontal involvement2)salivary flow reduced3)healing response of tissues poorer4)Hep C has greater manifestations5)healing response of soft tissue to surgery is poorer6)heavy emphasis on preventive care7) extractions are the best treatment8)advanced hep C or antiviral drugs, use antibacterial prophylaxis9)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.


2.patients blood must be screened for hep b antigen and antibody

3.take proper measures and protocols to prevent needlestick and sharps injury

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 aninfection 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


Antigen or antibody When found Significance for infectivityHBs(surface)antigen or australian antigen

Becomes detectable in late incubation and is present during acute hepatitis.declines over 3-6months 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

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

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.

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.

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.

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.

Oxytalan fibers are numerous beneath the epithelium and in areas of inflammation.

TREATMENT OF DRUG- ASSOCIATED GINGIVAL ENLARGEMENT :

1. Gingival enlargement has been associated with three different types of drugs : anticonvulsants, calcium channel blockers, and immunosuppressant.

2. The overgrown tissue shows two components :

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.

3. Alternative medicine to phenytoin sodium include, carbamazepine and valproic acid, both are reported to have a lesser impact in inducing gingival enlargement.

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.

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.

THIRD OPTION :

1. Surgery either gingivectomy or the periodontal flap.

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. 3mm of keratinized tissue should remain in apicocoronal direction after surgery is completed.

Gingivectomy / gingivoplasty can be performed via electrosurgery or a laser device. Recurrence is aproblem, but it can be minimized with proper attention todaily plaque control and regular professional cleanings.Some clinicians use positive-pressure appliances aftersurgery to help discourage recurrence.

TREATMENT OF LEUKEMIC GINGIVAL ENLARGEMENT :

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.

TREATMENT :

1. Scaling and root planing carried out under topical anesthesia.

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.

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. Treatment requires elimination of all local irritants responsible for precipitating the gingival changes in pregnancy.

2. Elimination of local irritants early in pregnancy is preferable to treatment of gingival enlargement.

3. Marginal and interdental gingival inflammation and enlargement are treated by scaling and curettage.

4. 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.

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.

In pregnancy, the emphasis should be on :

a) Preventing gingival disease before it occurs.

b) Treating existing gingival disease before it worsens.

5. Every pregnant patient should be scheduled for periodic dental visits, the importance of which in the

6. prevention of serious periodontal disturbances 7. should be stressed

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

Cyclosporine-induced gingival enlargement is morevascularized than the phenytoin enlargement, occurs inapproximately 30% of patients receiving the drug, ismore frequent in children, and its magnitude appears tobe related more to the plasma concentration than to thepatient's periodontal status. Gingival enlargement isgreater in patients who are medicated with both Cyclosporineand calcium channel-blocking drugs


86. 65 year old female patient on oral bisphosphonates . She has several grossly carious posterior teeth. how to manage?

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 bonemore in prominent areas like tori or posterior lingual aspect of the mandible.3)draining sinus at to=imes.4)Extensive soft tissue infection possible5)mobility of teeth6)exposed bone

Radiograph might be completely normalAs medullary space of marrow is affected.

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

there is a very low risk of developing BON; there are ways to minimize the risk, but not to

eliminate the already low risk; the consensus is that good oral hygiene along

with regular dental care is the best way to lower risk;

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 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.

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 processMedication options..if BISP are discontinued..strontium ranalate and Teraparatide.

Managemant of Caries (extensive)

1)efforts made to preserve teeth.2)RCT preferred3)point 8) above explain to patient.4)retain decoronated roots as overdenture abutmants5)CHX rinses to prevent soft tissue infection5)If soft tissue infection exists concurrent medication

Dentists should check and adjust removable dentures to avoid soft-tissue injury.6) LA without adrenaline

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.

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) mobile teeth need to be extracted if non vital, as prognosis is poor.

5)keep exposed bone and mucosa as clean as possibleusing CHX and oral hygiene methodsProminent 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.

3)Maintenance of implants should follow accepted mechanical and pharmaceutical methods to prevent peri-implantitis, 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.

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)If extractions or bone surgery are necessary, conservative surgical technique with primary tissue closure should be considered, when possible.

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.

6)Prophylactic antibiotics may be utilized during the healing/wound closure phase for procedures that involve extensive manipulation of the boneAs 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

If present, culture takenMetronidazole 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

Commonor notable HIV-related oral conditions include 1)xerostomia2) candidiasis3) oral hairy leukoplakia4) 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 simplexvirus lesions, recurrent aphthous ulcers, and neutropenic ulcers.

XerostomiaXerostomia 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 andquality of saliva, including diminished antimicrobial properties, lead to rapidly advancing dental decay and periodontal disease Use of crystal methamphetamine is associated with increased risk of HIV acquisition, and its use by infected individuals can be associated withrapid 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 thedecayed 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 comprehensiveinitial 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.

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

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 highsugar 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 non-cavitated, smooth-surface lesions and restorative treatment of cavitated lesions.

Establishment of recall intervals should be based oncaries risk status, with high-risk patients being seen more frequently.

Caries risk should be reassessed at each recall visit, andfuture 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 beconsidered: xerostomia, rampant dental caries (especially cervical caries), poor oral hygiene, gingival and periodontal disease, andocclusal 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 dentalprocedures.19,20


CandidiasisThe 3 common presentations of oralcandidiasis are angular cheilitis, erythematouscandidiasis, and pseudomembranouscandidiasis.Angular cheilitis presents as erythemaor fissuring of the corners ofthe mouth. Treatment involvesthe use of a topical antifungal creamErythematous candidiasis presents as a red, flat, subtle lesion on the dorsal surface of the tongue or on the hard or softpalates. It may present as a “kissing” lesion—if a lesion is present on the tongue, the palate should beexamined for a matching lesion patients complaining of oral burning

Pseudomembranous candidiasis (orthrush) appears as creamy, white, curdlikeplaques on the buccal mucosa,tongue, and other oral mucosal surfaces.The plaques can be wiped away,typically leaving a red or bleedingunderlying surface. Topical treatments for mild to moderatecases of both erythematous andpseudomembranous candidiasisinclude clotrimazole troches, nystatinoral suspension, and nystatin pastilles

treatment must be continued for atleast 2 weeks in order to reduce organismcolony-forming units to levels lowenough to prevent recurrence.Topical agents (mild to moderate oral candidiasis)Clotrimazole troches Nystatin oral suspension Nystatin pastilles Systemic agentsFluconazole Itraconazole oral suspension Voriconazole

Oral Hairy LeukoplakiaOral hairy leukoplakia, which is caused by Epstein-Barr virus, presents as a white, corrugated lesionon the lateral borders of the tongue; the lesion cannot be wiped awaypatients presenting with it while on antiretroviral therapy may be experiencing failure of their current regimen.

Periodontal DiseaseLinear gingival erythemaLinear gingival erythema, or “red band gingivitis,” presents as a red band along the gingival margincommonly extends to the posterior teeth. It can also present on attachedand non-attached gingiva as petechialikepatches.

Necrotizing Ulcerative

Periodontitisrapid 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 tissuePatients often refer to the pain as “deep jaw pain.” Treatment includes removal of dental plaque, calculus, and necrotic soft tissues utilizinga 0.12% chlorhexidine gluconate or 10% povidone-iodine lavage, and institution of antibiotic therapy Management of NecrotizingUlcerative PeriodontitisInitial visit• Prescribe narrow spectrum antibioticssuch as metronidazole 500 mg, dispense14 to 20 tablets, take 1 tablet twicedaily for 7 to 10 days. Other antibioticoptions include clindamycin and amoxicillin• Pain management is extremely important• Nutritional supplementation or counselingmay be necessaryFollow-up visits• Detailed periodontal care, such as scalingand root planingto persist for longer than the 7- to 14-day period observed in immunocompetentindividuals. Treatment formilder cases involves the use of topicalcorticosteroids such as dexamethasoneelixir (0.5 mg/5 mL) 5 mLswished for 1 minute and thenexpectorated, 2 to 3 times daily untilsymptoms resolve. For more severeoccurrences, systemic corticosteroidssuch as prednisone are used.

Kaposi’s SarcomaKaposi’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 purpleearly lesions tend to be flat, red, and asymptomatic, with the color becoming darker as the lesionages. Treatment ranges from localized injections ofchemotherapeutic agents, such as vinblastine sulfate, to surgical removal. Oral hygiene must bestressed. Systemic chemotherapy may be the treatment of choice.

Oral Warts—Human PapillomaVirusThe warts may be cauliflower-like, spiked, orraised with a flat surface.Treatment may involve surgery, lasersurgery, or cryotherapy. HPV survives in aerosol.Topical 5-fluorouracil treatment has


been used on external lesions

Ulcerative DiseasesHerpes simplex virusRecurrent intraoral HSV outbreaksstart as a small crop of vesiclesthat rupture to produce small, painfululcerations that may coalesce. Lesionson the lip are fairly easy to recognize.In the mouth, lesions on keratinized,or fixed, tissues, including the hardpalate and gums, should prompt suspicionof 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 ulcerationsRecurrent 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, orhard or rough foods.

Neutropenic ulcerationsNeutropenic ulcerations are very painful ulcerations that can appear on both keratinized and non-keratinized tissues, and are associated with absolutegranulocyte counts of less than 800/μL Patients should receive granulocyte colony-stimulating factor treatment prior to systemic ortopical steroid treatment

Pain in ulcerative diseasePain management is a crucial componentof 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 well-being for many patients.a rinse composed of polyvinylpyrrolidone, hyaluronic acid, and glycyrrhetinic acid.

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?

Potential problems related to dental Treatment

1. Dental procedures can potentially cause harm to a developing fetus via:a. Radiation b. Drugs c. Stress

2. Supine hypotension in late pregnancy3. Poor nutrition

Prevention of medical complications

1. Women of childbearing agea. 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 womena. 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 wise1st..spontaneous miscarriages occuravoid elective treatmentPlaque control,Oral hygiene Sc, pol, CurAvoid elective treatment, only urgent

2nd ideal time fetus not very large prevention of disease progression -up- plus Routine dental care


3rd Uncomfortable for patient-same as 1-Elective care avoided after first half

re-constructive procedures (crown & bridge fabrication & significant surgical procedures) are best delayed until after pregnancy

Dental treatment during pregnancyPERIO1) 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 Porphyromonasgingivalis, 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 topremature 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 gingivitisin pregnant patients. 5) Pregnancy gingivitisDue to hormonal and vascular changes2-8 monthsBleeds easilytreated by sc, RP,6)pregnancy tumors in areas of gingivitis.Buccal maxillary anterior areas.purple-blueulcerated, bleedssc, RPcan be a painful, nonesthetic soft tissue growth that is frequently removed either during the patient’s pregnancy or recent postpartum periodmight regress spontaneously

CARIES*Saliva changes-decreased buffers, mineralsdecrease flow 1st, 3rd semincreased 2nd

More acidic*esophageal relux-acid exposure1)most gestational women must increase their caloric intake during pregnancy. Frequently, this intake is in the form of multiple, small meals, or increased carbohydrate-based 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.

5)there is no contraindication to using diagnosticprocedures 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 sodaeat cheese1)It is best not to expose a pregnant womanto 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 associatedwith 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 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 relievethe symptomology.

Local Anesthetics Lidocaine and prilocaine,

etidocaine

B first-line choices for local anesthesia for pregnant women who do not have any contraindication

Bupivicaine, mepivicaine Procaine

C 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

Antifungals nystatin, chlorhexidine B Doxycycline = D

Clotrimazoleketoconazolefluconazole

C

Antibiotics the penicillin family, the erythromycins azithromycin, clindamycin, metronidazole cephalosporins

B estolate (erythromycin) causes hepatitis

tetracycline, minocycline, and doxycycline

D likelihood of chelating in bones and teeth.

Ulcer healing Omeprazoleesmoprazolelansoprazole

B

PantoprazoleMisoprostol

teratogenic

NSAIDS Aspirin and diflusinal associated with prolongedgestation 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 trimestersD for third trimester

are contraindicated due to their risks ofprolonged labor, hemorrhage risk during delivery, and premature closureof the ductus arteriosus.

Acetaminophen

Naproxen

BC (with codeine,hydroxyl codeine or oxycodone)

B

1st line of choice


Opiods Oxycodone B long-term narcotic usage is ill-advised as the fetus may develop either neonatal depression or withdrawal symptoms

meperidine,hydrocodone, propoxyphene, and codeine

C Avoid codeine late in gestation-fetal resp depressionwithdrawal symptoms

Anxiolytic Triazolam, X Most benzodiazepines for anxiolytic relief must be administered with extreme caution and consultations with the patient’s physician because most drugs inthis class are classified in categories C or D

Diazepam Controversialthe risk of oral cleft developments during the first trimester and the risk of neonatal toxicity and withdrawal symptoms during the third trimester

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 Controversial Not to be used in 1st

2nd, 3rd use with enough oxygen

Antacids Aluminium and mg hydroxideSimetheconecalcium carbonate

B

C


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


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