Essential human disease for dentists Flashcards
Which ASA grades (American Society of Anaesthesiologists) can be treated in general practice and which should be treated by specialists?
ASA 1 and 2 in general practice
ASA 3 and 4 by specialists
What does ASA I stand for?
ASA 1 = healthy
What does ASA II stand for?
ASA 2 = presence of systemic disease with no effect on normal function, e.g. well controlled diabetes
What does ASA III stand for?
ASA 3 = Presence of systemic disease which limits function, e.g. poorly controlled epilepsy
What does ASA IV stand for?
ASA 4 = Presence of systemic disease which is a constant threat to life, e.g. severe coronary artery disease
What does ASA V stand for?
ASA 5 = Patient not expected to survive more than 24 hours
Is a pt who has recently had an operation under GA without complication a risky pt for dental tx under LA?
No
They are unlikely to present a serious risk for dental tx under LA
Why should all pts be asked about their ‘risk habits’ (smoking and alcohol)?
These pose a significant general health risk and increase the risk of oral cancer, periodontal disease and delay wound healing post-surgery.
What questions can be useful when assessing for cardiovascular diseases?
- Are you generally fit and well?
- Do you have any heart problems?
- Do you have high blood pressure?
- What medications are you taking?
- How far can you walk unaided without stopping?
- Can you climb stairs?
- What prevents you from going further?
What may breathless at rest (RR >12/min) indicate?
Heart failure or respiratory problems
What may an abnormal appearance indicate?
Any underlying syndrome associated with congentital heart defects (e.g. Down’s syndrome)
What may an apprehensive, sweaty, pained expression indicated?
Angina or myocardial infarction
What may a) finger clubbing b) pale nail bed c) splinter haemorrhages indicate?
1) finger clubbing = congenital heart defect
2) pale nail bed = anaemia
3) splinter haemorrhage = bacterial endocarditis
What may a) cyanosis b) gingival hypertrophy c) xanthelasma (yellow plaques around eyes) indicate?
a) cyanosis = poor oxygenation of the blood and may have a cardiac cause
b) gingival hypertrophy = nifedipine (Ca Ch blocker) antihypertensive medication, phenytoin anti-epileptic, cyclosporine
c) xanthelasma = elevated cholesterol
What may an irregular pulse indicate?
A cardiac rhythm abnormality, most commonly atrial fibrillation
What is the normal resting heart rate?
60-100 beats per min
> 100 = tachycardia
<60 = bradycardia
What is hypertension?
A persistently raised blood pressure (BP) >140/90 mmHg.
- Both diastolic and systolic components are important
In 90% of cases no cause can be found and its called primary hypertension.
What may dental procedures cause in hypertension pts?
Further rise in blood pressure and lead to acute complications
What is the epidemiology of hypertension?
Affects 5-10% of general pop and is most common cause of preventable disease in the developed world.
Normally detected btw 20 and 50 years.
What is the aetiology of hypertension?
Primary hypertension = no specific cause, likely origin is multifactorial
Secondary hypertension = cause known and include renal disease, pregnancy, coarctation of the aorta, endocrine tumours and drugs (e.g. steroids)
What organs are commonly affected by hypertensions?
Brain (stroke)
Eyes (retinal haemorrhages)
Aorta (aneurysm)
Heart (IHD, MI, HF, left ventricular hypertrophy)
Kidney (renal failure)
Legs (peripheral vascular disease)
What are clinical features of hypertension?
Primary hypertension is asymptomatic until complications develop in target organs.
In severe hypertension (>180/110mmHg) there may be dizziness, headache and epistaxis.
Any untreated hypertensive pt is at risk of developing left ventricular failure, MI, stroke or renal failure.
What is the most common cause of death among hypertensive patients and what is hypertension the most important predisposing factor for?
Most common cause of death = coronary artery disease
Hypertension is most important predisposing factors for = stroke
What is the tx for hypertension?
Secondary hypertension - tx of the cause if possible.
Primary hypertension - cannot be cured but BP can be reduced to acceptable level.
Lifestyle advise - weight loss reduction, increased exercise, decreased alcohol consumption, stopping smoking and a low salt diet.
Medical management - diuretics, B-blockers, Ca antagnosist, ACE inhibitor, Angiotensin II receptor blocker, Adrenergic inhibitors
What are the different drug classes of antihypertensives?
1) ACE inhibitors
2) Angiotensin II receptor blockers (ARBs)
3) Adrenergic inhibitors/Alpha blockers
4) Beta blockers
5) Calcium channel blockers
6) Diuretics
ACE inhibitors:
- drug names
- examples
- MoA
- Main effect on BP
ACE inhibitor:
- “pril”
- Lisinopril, Enalapril, Ramipril
- Inhibit ACE
- Decrease SVR, SV
ARBs
- drug names
- examples
- MoA
- Main effect on BP
ARBs:
- “sartan”
- Losartan, Valsartan, Candesartan
- Block Angiotensin II receptors
- Decrease SVR, SV
Adrenergic inhibitors/Alpha blockers:
- drug names
- examples
- MoA
- Main effect on BP
Adrenergic inhibitors/alpha blockers:
- “osin”
- Doxazosin, Terazosin, Prazosin
- Block alpha receptors
- Decrease SVR
Beta blockers:
- drug names
- examples
- MoA
- Main effect on BP
Beta blockers:
- “lol”
- Atenolol, Bisoprolol, Propranolol
- Block beta receptors
- Decrease HR, SV
Calcium channel blockers:
- drug names
- examples
- MoA
- Main effect on BP
Calcium channel blockers:
- “dipine” + others
- Amlodipine, Nifedipine, Diltiazem, Verapamil,
- Block calcium channels
- Decrease SVR
Diuretics:
- drug names
- examples
- MoA
- Main effect on BP
Diuretics:
- “ide”
- Furosemide (loop diuretic), Spironolactone (potassium sparing diuretic), Hydrochlorothiazide (Thiazide diuretic)
- Facilitates diuresis, decrease fluid volume
- Decrease SV
Should you treat hypertensive pts under LA?
Yes. Reliable and complete analgesia is desirable to avoid distress to pts, which will induce increased sympathetic output and further increased blood pressure.
The careful use of adrenaline containing LA causes minimal increases in BP so long as it is not given intravascularly or in excessive doses.
What are dental complications in hypertensive patients? (4)
1) Stressful situations may cause an additional rise in BP which could precipitate systemic problems (e.g. stroke or myocardial infarction)
2) Post-operative bleeding is more likely to complicate surgical procedures in hypertensive pts.
3) There may be interactions between pt’s hypertensive meds and drugs you with to prescribe
4) Many hypertensive have oral side-effects
- xerostomia (diuretics)
- gingival hyperplasia (nifedipine)
- salivary gland swelling (clonidine)
- lichenoid drug reactions (angiotensin-converting enzyme inhibitors)
- altered taste (diuretic, ACE, ARBs, B-blockers?)
What oral side-effects could anti-hypertensives have? (5)
- xerostomia (diuretics)
- gingival hyperplasia (nifedipine)
3) salivary gland swelling (clonidine)
4) lichenoid drug reactions (angiotensin-converting enzyme inhibitors)
5) altered taste (diuretics, ACE, ARBs, B-blockers?)
- What is the dental relevance of hypertension? *
- Hypertension is common, affecting between 5 and 10% of the population.
- Do not carry out routine treatment on pts whose BP is greater than 160/110
- May be detected first in dental practice
- Increased post-operative bleeding
- Patients may also be taking aspirin as part of their management and thus suffer increased post-operative oozing.
- Many antihypertensive medications have oral side effects
- Check for drug interactions between antihypertensive meds and drugs prescribed as part of dental treatment
- Hypertensive pts are at increased risk of cardiovascular disease (angina and myocardial infarct)
What is the epidemiology of ischaemic heart disease?
Ischaemic heart disease is the most common cause of death, accounting for 35% of total mortality, in the western world. 3% of adults suffer with angina, and 1% have had a myocardial infarction in the last 12 months.
What is the aetiology of ischaemic heart disease?
Coronary atheroma is the most common cause of IHD.
What are risk factors for ischaemic heart disease?
Fixed: age, male, family.
Modifiable (hard): hyperlipidaemia, smoking, hypertension, diabetes
Modifiable (soft): obesity, lack of exercise, high intake of alcohol, personality, oral contraceptive.
What is the pathogenesis of IHD?
Formation of an atheromatous plaque within the coronary arteries which produces a fixed constriction to blood flow.
The plaque consists of a necrotic core containing cholesterol surrounded by increased smooth muscle and fibrous tissue.
Endothelial lining is disrupted, thrombus formation occurs due to platelet adhesion and vessel lumen becomes narrowed.
How does a myocardial infarction. (MI) occur?
Acute thrombus which completely occludes the vessel causes an MI.
What are clinical features of angina?
Symptoms: severe, crushing, central chest pain that radiates down the left arm. Usually provoked by physical exertion and resolves with rest.
What are clinical features of IHD? When do you consider an MI?
Can have severe, crushing, central chest pain that radiates down the left arm.
IHD does not always cause chest pain; the pt may become breathless, feel nauseous, sweat or complain of pain in the right arm, neck or even jaw.
If symptoms persist for longer than 15 mins and do not respond to rest of anti-anginal meds, then consider a possible MI
What is treatment for IHD?
Conservative: modifying risk factors (e.g. cease smoking, lose weight, take sensible exercise)
Medical: decrease myocardial oxygen demand (e.g. by using nitrates).
Surgical: dilate affected vessels (angioplasty) and insert stents, or bypass the affected areas with vascular grafts (coronary artery bypass graft).
How do dental treatments affects pts with IHD?
- Dental tx may provoke an angina attack or an MI.
- As a dentist, need to establish the severity of the pt’s symptoms, provoking factors and whether their angina is stable or unstable.
Stable angina is predictable; occurs under reproducible conditions, response to rest and medication.
Unstable angina is unpredictable: may get progressively worse and occur at rest. - It is good practice to request pt takes GTN (glyceryl trinitrate) before you commence tx.
- Avoid prolonged procedure
- Minimise stress.
What LA can you treat pts with stable angina with?
2% lidocaine with adrenaline 1:80 000.
Should pts with unstable angina be treated?
No until their condition has been brought under control. Pts should be referred to doctor for management.
What implications does decubitus angina have?
Pt who suffer with decubitus angina, which is brought on by lying flat, must not be treated supine.
What should you do if a pt develops central chest pain or other anginal symptoms during tx?
- Stop what you’re doing
- Reassure pt
- Summon help
- Place pt in comfortable position
- Give GTN sublingually
If no response then consider possibility of unstable angina or MI:
6. call an ambulance
7. place oxygen high flow
8. repeat GTN sublingual
9. Give aspirin 300mg chewed
- Dental relevance of ischaemic heart disease *
> It is very common within the population, with 20% of males under 60 years affected.
> It may present with toothache or pain in the jaw
> Dental treatment may provoke symptoms or acute complications.
> Determine whether symptoms are stable or unstable; stable pts can be treated in dental practice
- preventative dentistry
- plan short treatments
- keep stress to minimum
- give GTN pre-treatment
- adequate local analgesia
> Unstable pts should be referred to their doctor before any dental treatment.
> In emergency stop tx, give GTN and consider the possibility of an MI.
> There is no requirement for antibiotics cover for coronary artery bypass grafts of coronary artery stents. (if in doubt, liaise with cardiologist)
What is rheumatic fever (RF)?
An acute inflammatory disease which primarily affects the joint and the heart. It is an autoimmune disorder that is usually preceded by a streptococcal sore throat. The heart valves can be damaged and become vulnerable to endocarditis.
What is the epidemiology of rheumatic fever?
Rheumatic fever affects 3% of pts following a group A B-haemolytic streptococcal sore throat.
It is most common in childhood between 5 and 15 yers of age and is rare in adults.
Poor socioeconomic groups are at increased risk.
What is the pathogenesis of rheumatic fever?
Not fully understood but there are four absolute requirement for RF to occur:
- A B-haemolytic streptococcal infection, a susceptible host, pharyngeal site and persistence of infection.
- RF occurs 2 to 3 weeks after a streptococcal sore throat.
- Connective tissues of heart, including valves, are susceptible to damage from autoimmune response.
What are clinical features of rheumatic fever?
“RF licks the joints and bites the heart”
Most pts have a fever and a flitting polyarthritis. If heart is involved there may be a murmur, pericarditic pain or acute heart failure.
Heart is the only tissue to suffer permanent damage and may lead to endocarditis or HF in the future.
How do you treat rheumatic fever?
Bed rest, analgesia, and eradication of the streptococcal infection.
Dental relevance of rheumatic fever
1) Pts with a history of rheumatic fever have an increased risk of developing bacterial endocarditis following invasive dental treatment.
2) Antibiotic prophylaxis is required prior to invasive dental tx (check current guidelines!!!)
Invasive dental tx includes
> Tooth extraction
> Tooth reimplantation
> Implant placement
> Subgingival scaling and probing
> Endodontic treatment beyond the apex
> Placement of matrix or orthodontic bands
> Intraligamentary local anaesthetic
What is infective endocarditis?
Condition caused by infection of the endocardium and heart valves, which is some cases is fatal.
Commonly due to blood-borne bacterial infection but may be fungal in the immunocompromised.
50% of cases are due to Streptococcal viridans and, as a result, dental treatment is often implicated as the causal event.
What is the epidemiology of infective endocarditis?
Primarily affects older patients with degenerative valvular heart disease.
Used to be common in pt who suffered valve damage due to rheumatic fever.
Now there is an increased incidence in IV drug users.
What is the pathogenesis of infective endocarditis?
Damaged or prosthetic heart valves are usually involved, as are areas affected by abnormal flow jets from heart defects (e.g. ventral septal defect).
Normal valves on right side of heart can be affected in IV drug users.
Mitral valve most often affected, with the formation of adherent vegetations along the damaged valve cusps. These consist of clumps of organisms, fibrin and platelets.
What are clinical features of infective endocarditits?
Local valvular damage causes incompetence or stenosis of valve, producing a new heart murmur that may change as the damage progresses.
Distant effects occur as parts of the vegetation break away and pass in the blood stream to lodge at distant sites (e.g. kidney and brain) where they cause further local infection (septic emboli).
Immune complexes are deposited at various sites in the body and causes rashes, nail splinter haemorrhages and rarely, Olser’s nodes in the skin of the fingers. Finger clubbing also occur later in the process.
Systemic effects include ‘flu-like’ illness and weight loss.
How do you diagnose infective endocarditis?
Primarily from the history, the results of multiple blood cultures and visualising the cardiac vegetations using ultrasound.
How do you prevent IE?
CHECK GUIDELINES FOR ABX PROPHYLAXIS.
- Dental relevance of infective endocarditis *
> 10% of cases are thought to follow dental treatment.
> 50% of cases are due to streptococcus viridans, an oral commensal.
> Antibiotic prophylaxis should be given prior to invasive dental tx as per guidelines.
> At risk pts include those with:
- previous rheumatic fever
- congenital heart disease
- significant heart murmur
- heart valve replacement
- degenerative valvular disease
- past episode of endocarditis
What is the epidemiology of heart failure?
Increased prevalence in the elderly
Affects 1% of people age 50 years increasing to 5% by age 75.
2/3rd of pts with HF will die within 5 years of diagnosis.
What is the aetiology of heart failure?
HF is due to a problem with either contraction (systole) or relaxation (diastole) of the heart muscles. There are three common causes:
> hypertension
> valvular heart disease
> ischaemic heart disease
What is the pathogenesis of HF?
Left or right or both ventricles may be affected, depending on the cause.
Failure of the left ventricle decreases the ability to pump blood to the body (poor tissue and organ perfusion) and causes fluid to build up in the lungs (pulmonary congestion).
Failure of the right ventricle leads to build up of fluid in the periphery of the body (dependent oedema).
Left ventricular failure often leads to right ventricular failure and then it is called congestive cardiac failure.
What are clinical features of HF?
Depends on which side of the heart is affected!
> shortness of breath which is worst on laying flat (orthopnoea)
quick weight gain due to fluid retention
swelling in ankles, legs and abdomen (dependent oedema)
fatigue and weakness
other symptoms, such as nausea, palpitations, chest pain, waking suddenly at night unable to breath and changes in sleep pattern.
How do you diagnose HF?
Confirm with a chest x-ray which reveals any cardiac enlargement or fluid build up in the lungs.
An echocardiogram may be carried out to measure the pumping efficiency of the heart (ejection fraction)
What is treatment for heart failure?
lifestyle changes, medical treatments and, rarely, surgery:
Lifestyle: weight loss, exercise, cessation of smoking, low-salt diet.
Medical:
- Diuretics reduce fluid overload
- Inotropic drugs to increase cardiac contractility
- ACE inhibitors to decrease cardiac workload
Surgery:
- valvular surgery
- heart transplant (rare)
- Dental relevance of heart failure *
1) Most pts can be treated safely in dental practice under local anaesthetic
2) It is very common within the population, with 5% of over-75s affected.
3) Dental tx may provoke symptoms and pts may become breathless if laid flat in the dental chair.
4) Determine whether their symptoms are stable or unstable.
Stable pts can be treated in dental practice:
- preventative dentistry
- plan short treatments
- keep stress to a minimum.
Unstable pts should be referred to their doctor before any dental treatment.
5) Use sedation with caution
What are congenital heart defects?
Structural, functional or positional defects of the heart that are present at birth in approximately 1% of population.
They may manifest at any time after birth or may never be detected at all.
Must liaise with cardiologist before dental tx.
What is the epidemiology of congenital heart defects?
1% of live births are affected. 8 common lesions:
1) Ventricular septal defect
2) Patent ductus arteriosus
3. Atrial septal defect
4. Pulmonary valve stenosis
5. Aortic valve stenosis
6. Coarctation of the aorta
7. Tetralogy of Fallot
8. Transposition of the great vessels
Familial tendency, males and females effected equally, and more than one defect may be present in an individual
What is the aetiology of congenital heart disease?
No specific causes are found and it is likely that the aetiology is multifactorial.
What is the pathogenesis of congenital heart disease?
Most heart defects either obstruct blood flow in the heart or great vessels or cause blood to flow through the heart in an abnormal way.
Obstructive defects, Septal defects, Cyanotic defects, Shunts.
What are clinical features of congenital heart disease?
- Cyanosis if blood is not properly oxygenated.
- HF due to abnormal pressures or volumes within the heart
- Heart murmur if there is turbulent flow
- Growth failure
- Chest infections
How can dental treatment affect pts with congenital heart defects?
Dental tx should not be undertaken without consultation with the patient’s medical practitioner.
May require antibiotic prophylaxis as they have an increased risk of developing endocarditis. (CHECK GUIDANCE)
Pts with heart failure may not tolerate supine position in a dental chair and become breathless
- Dental relevance of congenital heart defects *
> These defects are common within the population, affecting 1%
> Many will require antibiotic prophylaxis before high-risk dental procedures (see endocarditis guidelines)
> Liaise with the patient’s doctor before embarking on treatment.
> Preventive dental treatment should be a priority in order to avoid excessive antibiotic prescription and reduce dental sepsis.
What is deep vein thrombosis?
DVT is due to the formation of a blood clot in the deep veins of the lower limbs. These clots may release fragments (emboli) which travel to the lungs, causing a pulmonary emboli.
What is the epidemiology of DVT?
DVT is very common but often asymptomatic problem. It can occur at any age, but is more common in those over 60.
What is the aetiology of DVT?
This is due to one of three factors, known as Virchow’s triad
- Stasis of normal blood flow due to:
> prolonged bed rest
> general anaesthesia
> long-distance economy travel
> pregnancy - Damage to blood vessel wall due to:
> trauma
> inflammation - Composition change of the blood due to:
> lupus erythematosus
> antithrombin III
> malignancy
> oral contraceptive
What is the pathogenesis of DVT?
Once formed, the blood clot enlarges and obstructs the local venous blood flow and may release fragments in to the systemic circulation.
What are clinical features of DVT?
Usually only one lower limb is affected and the symptoms include:
> swelling
> tenderness and pain
> erythema of the overlying skin
How can you prevent a DVT during an operation?
- Identification of high-risk pts and procedures
- Prophylactic anticoagulation
- Careful positioning and padding of patients on the operating table
- Use of compression stocking and boots
- Adequate fluid replacement
- Early postoperative mobilisation
How do you treat pts with DVT?
Most pts are anti-coagulated using warfarin to facilitate the resorption, prevention of extension and reformation of the DVT
- Dental relevance of DVT *
> DVT may lead to pulmonary embolism
> Pts are often anti-coagulated, with warfarin, and require special care before invasive procedures are carried out - BLEEDING RISK CHECK GUIDELINES.
What questions can you ask a pt to assess for respiratory diseases?
- Are you generally fit and well?
- Do you have any chest problems?
- Do you suffer with shortness of breath?
- What are your current medications?
What is haemoptysis?
Coughing up blood from the respiratory tract.
May be caused by chest infection, inhaled foreign body, pulmonary oedema or lung cancer.
What is dyspnoea?
The sensation of shortness of breath.
The speed of onset and duration may indicate the cause.
Rapid onset: asthma, pulmonary embolus or inhaled foreign body.
Gradual onset: obstructive airway disease or malignancy.
What is orthopnoea?
If dyspnoea (sensation of shortness of breath) is increased by lying flat.
This may indicate a cardiac cause.
At what respiratory rate is breathlessness?
> 12 breaths per minute
- may indicate respiratory or cardiac problems.
What is stridor?
A harsh, rasping sound on inspiration and is indicative of upper airway obstruction such as laryngeal oedema due to allergy swelling or a foreign body in the larynx.
What is cyanosis?
Blue discoloration of the skin and mucous membranes.
Only in extremities indicates poor perfusion (cold) or cardiac output.
Detected centrally reflects hypoventilation, parenchymal lung disease, heart failure.
What is Horner’s syndrome?
Unilateral dropping of upper eye lid, constriction of the pupil and lack of facial sweating.
May be due to infiltrative spread of lung tumour to the cervical sympathetic chain.
What is asthma?
An increasingly common, reversible, obstructive airway condition affection 5% of UK population.
There are three characteristic features:
1) Hyper-responsive airways
2) Inflammation
3) Excess mucous production.
Care must be taken not to provoke an acute attack or further suppress respiration during dental tx by inappropriate prescribing, excessive stress or the indiscriminate use of sedation.
What is the aetiology of asthma?
Extrinsic: pollen, salivary proteins, pet fur
Intrinsic: atopy with raised IGE levels, asthma gene (chromosome 11), bronchial hyper-reactivity
Lifestyle/environmental: exercise (>cold air), stress, smoking, drugs (NSAIDs, B-blockers), pollution, viral infection (upper respiratory tract infections)
What is the pathogenesis of asthma?
There is a triad of oedema, broncho-constriction and mucous plugging, affecting the bronchioles.
This is reversible and causes a variable degree of obstruction. It is caused by mast cell degranulation and release of vasoactive amine (e.g. histamine and prostaglandin)
What are clinical features of asthma?
Depend of the severity of disease.
Polyphonic expiratory wheeze to inability to breath, with cyanosis and coma.
In children may be nocturnal cough which keeps the child awake.
When severe asthma, pt may not be able to complete sentences and become increasing panicked and anxious.
Life-threatening features: cyanosis, absent breathing sounds, confusion, exhaustion.
How do you treat asthma?
Stepwise tx of asthma of increasing severity.
Step 1. Occasional B2 agonist (e.g. salbutamol)
Step 2. Add B2 agonist + inhaled steroid.
Step 3. Add long-acting B2 agonist.
Step 4. Add a combination of theophylline leukotriene agonist. High-does inhaled steroid.
Step 5. Add oral steroids and nebulisers.
Prevention: avoid house dust, pet fur, and cold air and smoking cessation.
Tx measured by assessment of symptoms and measurement of peak expiratory flow rate using peak flow meter.
- Dental relevance of asthma *
> Most asthmatics can be treated safely under LA
> Non-steroidal anti-inflammatory drugs may precipitate or worsen an asthma attack in sensitive patients.
> Inhaled steroids may cause changes in the oral mucosa, e.g. candida infection in the palate. Advise patients to rinse with warm water after using their steroid inhaler.
> Postpone treatment during exacerbations of the condition.
> Use sedation with care.
> Advise patient to use their inhaler at the beginning of each treatment session.
> Patients who are taking steroids no longer need steroid cover for dental treatment under LA.
What is chronic obstructive pulmonary disease?
COPD is caused by a group of lung diseases that lead to damage of lung tissue with persistent and progressive limitation of air flow.
Chronic bronchitis and emphysema are the two most common cause of COPD and often coexist.
Smoking is implicated in 95% of cases.
What is the aetiology of COPD?
4 major agents are involved:
1. Smoking (95%)
2. Atmospheric pollution
3. Respiratory infection
4. a1-antitrypsin deficiency (pulmonary protective protease).
What is the pathogenesis of bronchitis?
In chronic bronchitis there is damage to the respiratory epithelium with ulceration, excess mucus production and variable airway narrowing.
What is the pathogenesis of emphysema?
Air-space dilation and loss of elastic tissue within the alveolar walls - leading to gas trapping, over inflation and limitation of expiratory airflow
What are the clinical features of COPD?
Many pts are not aware of problem until significant damage has occurred.
Chronic cough, production of excess sputum, shortness of breath and an expiratory wheeze.
(In contrast to asthma, bronchodilators do not offer the same degree of relief).
Potential complications include:
- respiratory failure
- right heart failure
- pneumothorax
What is treatment of COPD?
- Cessation of smoking
- Drug therapy - targeted Abx, bronchodilators, inhaled and oral steroids.
- Non-invasive ventilation
- Breathing exercises and chest physiotherapy.
Why should COPD pts not be given high-flow oxygen? (exception, emergencies?)
These pts rely on low oxygen tension to drive their respiration, so should not be given high-flow oxygen over long periods of time.
(in emergency use 100% oxygen at a high flow rate?)
- Dental relevance of COPD *
- Most pts with COPD can be treated safely under LA.
- Keep tx sessions short.
- Pts may find it difficult to cope with rubber dam due to increased airway obstruction.
- Inhaled steroids may cause changes in the oral mucosa, i.e. Candida infection in the hard palate. Advise pts to rinse with warm water after using their steroid inhaler to prevent this occurring.
- Postpone tx during exacerbations of the condition.
- DO NOT SEDATE THESE PTS OR USE RELATIVE ANALGESIA.
- Advise pt to use their inhaler at the beginning of each tx session.
What is lung cancer?
The most common malignancy in the western world and third most common cause of death in the UK. Pts may present with head and neck symptoms.
What is the aetiology of lung cancer?
Lung cancer is the main cause of lung cancer, accounting for up to 90% of cases. The risk increases with the intensity, quantity and duration of smoking.
What is the pathogenesis of lung cancer?
Small-cell lung cancer (SCLC) - commonly occurs centrally in the lungs, has a rapid growth rate and metastases early.
Non-small-cell lung cancer (NSCLC) - tends to have a slower rate of growth and tenancy to metastasise later.
What is the clinic features of lung cancer?
Local: persistent cough, prolonged chest infection, chest pain increased by breathing and coughing, haemoptysis (coughing up blood), progressive shortness of breath, hoarse voice, horner’s syndrome.
Systemic: finger clubbing, weight loss, malaise, anaemia.
Metastatic spread to bone, brain and liver causing: bone pain, neurological deficits, jaundice.
What is the treatment of lung cancer?
Depends on tumour histotype, location, degree of spread and fitness of the pt.
In most pts, only palliative tx can be offered, including radio- and chemotherapy, supportive therapy and analgesia.
- Dental relevance of lung cancer *
- Advice on how to stop smoking, and support, should be given to all smokers.
- Lung cancer can present with:
> cervical lymphadenopathy
> distended neck veins
> horner’s syndrome - meiosis, ptosis and anhydrosis.
What is the aetiology of inhaled foreign body?
Increased risk of inhalation of foreign bodies during dental tx due to:
- the close proximity between the operative field and the airway
- small instruments used in dentistry
- supine position of the patient
- sedation-induced reduction in reflex airway protection
What is the pathogenesis of inhaled foreign body?
Typically objects pass down the most direct route from the pharynx into the right main bronchus and the right lower lobe of the lung.
If the object is not retrieved rapidly, there is a risk of lung abscess or pneumonia.
Impacted objects may irritate the respiratory tract and obstruct the airflow, causing cough, stridor and wheeze.
What are the clinical features of inhaled foreign body?
Majority of foreign bodies will be swallowed and pass into the alimentary tract, carrying a small risk of perforation as they pass through.
If inhaled, large objects are likely to impact above the vocal cords, whereas smaller objects are more likely to pass into the lung. The patient may cough and choke but this is not always the case and inhalation may occur asymptomatically.
Presentation may be delayed, with signs and symptoms of chronic lung infection.
How do you diagnose inhaled foreign body?
Need high degree of clinical suspicion.
If cannot locate missing object it is mandatory to refer pt for a chest x-ray in an attempt to exclude inhalation.
How do you tx inhaled foreign body?
- Look for it, around pt or in oral cavity.
- If not found, consider inhalation. Ask pt to cough and turn their head to the side to aid location of the object. Use suction and good lighting to examine the oropharynx and carefully retrieve any objects with forceps.
- If emergency, call ambo and give high flow oxygen. Consider sharp blow to back or heimlich manoeuvre.
- Most objects retrieved using a bronchoscope.
- Dental relevance of inhaled foreign body *
> Up to 27% of inhalation incidence occur during dental tx.
> The risk of inhalation is increased when consciousness if impaired e.g. sedation
> Inhalation may occur asymptomatically.
> You are obliged to ascertain the location of objects ‘lost’ during dental tx.
> If you cannot locate a missing object a chest x-ray should be carried out to attempt to exclude inhalation.
> If there are signs of airway obstruction the emergency services should be called and high-flow oxygen administered.
- DO NOT ATTEMPT A SURGICAL AIRWAY UNLESS APPROPRIATELY TRAINED
- Pts who have ingested sharp objects e.g. endodontic files, should be referred to hospital for assessment.
How can you prevent inhalation of foreign bodies?
Use of rubber dam
Restraining cords on instruments
Avoiding over sedation
What is pulmonary embolism?
This occurs due to the blockage of a portion of the arterial system in the lungs. It is most commonly due to a blood clot shed from a DVT.
What is the aetiology of PE?
Most commonly due to emboli released from blood clots formed in the lower limbs as a result of deep vein thrombosis.
What is the pathogenesis of PE?
The embolus impacts and obstructs a portion of the pulmonary arterial circulation, resulting in collapse of the alveoli in the area and decreasing the efficiency of gas exchange.
What are clinical features of PE?
Depends on size and position of the area obstructed:
- sudden onset of chest pain
- acute shortness of breath
- haemoptysis (coughing up blood)
- collapse
- sudden death
How do you treat PE?
Dissolved using thrombolytic drugs and then further thrombosis is prevented by anti-coagulation, mostly with warfarin/(DOACs?).
- Dental relevance of pulmonary embolism *
- Patients are often anticoagulated with warfarin, and required special care before invasive dental procedures are carried out (cf. haemotology)
What is sarcoidosis?
Sarcoidosis is a common chronic granulomatous condition of unknown origin that may cause cervical lymph node enlargement and parotid gland swelling.
Affects more females than males, increased incidence in Afro-Caribbean origin. Most commonly diagnosed between 20-40.
Lungs and lymph nodes are commonlly affected, but any tissue or organ may be involved.
Most pts are asymptomatic. Those who develop symptoms usually recover spontaneously; some may follow a relapsing, remitting course.
Only 40% of those pts with symptoms require treatment with immune suppression.
- Dental relevance of sarcoidosis*
Some 4% of pts with sarcoidosis develop parotid gland enlargement and a dry mouth.
Cervical lymph node enlargement occurs in 15%. Sinus involvement may lead to repeated sinusitis.
Patients may treat with immune suppressant drugs, increasing their risk of infection.
Acute breathlessness: anxiety
Dental anxiety may cause breathlessness. In most cases careful explanation and reassurance is all that is required to prevent any complications.
In cases of severe anxiety, it may be better to carry out the tx using supplemental therapy to aid relaxation, eg. hypotherapy, acupuncture, IV/oral sedation or relative analgesia.
Acute breathlessness: hyperventilation
Extreme over-breathing - may occur in pts who are anxious or phobic.
pH of plasma is increased as CO2 is blown off. This causes the Ca2+ in the plasma to be reduced and as a result muscle and nerve transmission are affected causing the pt to experience tingling of their extremities of muscle spasm.
Treat by making pt re-breathe from a paper bag to raise their CO2 level. Further tx may require supplemental relaxation therapy.
Acute breathlessness: pain
Inadequate analgesia may cause the pt to become short of breath. This is best remedied by supplemental anaesthetic or, on occasion, it may be necessary to delay tx and give the pt a course of antibiotics to settle any acute infection.
Acute breathlessness: asthma
Asthma may be provoked by anxiety, stress or the inappropriate prescription of NSAIDs to sensitive pts. It is characterised by difficulty in breathing out with an expiratory wheeze.
Acute breathlessness: COPD
Pts with COPD tend to be chronically short of breath but the situation may be made worse by the use of a rubber dam, for example, which may further restrict air flow. If the pt has developed heart failure, they may become acutely breathless in the supine position.
Acute breathlessness: anaphylaxis
Swelling of the tongue and laryngeal tissues may occur during anaphylaxis, causing acute airway obstruction. In addition to this, bronchospasm causes an asthma-like state with reduced airway patency and an expiratory wheeze.
Acute breathlessness: inhaled foreign body
Pt will often cough at time of inhalation - depending on where object impacts - may become acutely short of breath.
Acute breathlessness: heart failure
When affecting the left ventricle, HF causes fluid to accumulate in the lungs, leaving the pt short of breath. This is often made worse by lying the pt backwards during tx.
Acute breathlessness: angina
Angina may manifest as acute shortness of breath without the classical signs of central chest pain. Pts often have a history of cardiovascular problems e.g. MI
Acute breathlessness: myocardial infarction
Often causes central crushing chest pain leading to acute shortness of breath. In addition to this the pt may develop sudden left heart failure and pulmonary oedema, making the situation worse.
Acute breathlessness: pulmonary embolus
Often causes acute shortness of breath with chest pain that is increased by the act of breath. There may be a recent history of CVT or prolonged immobility.
Acute breathlessness: pneumothorax
This is due to the escape of air into the pleural space, causing the affected lung to collapse.
May occur spontaneously or, more commonly, is due to trauma or lung pathology.
Those with history of chronic lung disease, e.g. emphysema, are at higher risk.
Acute breathlessness: lung cancer
This cause progressive shortness of breath but there may be an acute exacerbation if there is an associated pneumothorax or haemorrhage from the tumour leading to acute obstruction of the airway of haemothorax.
- Dental relevance of acute breathlessness *
> If not due to anxiety, sudden onset of shortness of breath is a serious sign.
> In all cases stop tx and assess the pt.
> Administration of high-flow oxygen 15L/min will do no harm.
> If there is no immediate resolution the emergency services should be called.
How can GI disorders and diseases be divided? (3)
- Inflammatory: peptic ulcer disease, coeliac, Crohn’s and Ulcerative colitis
- Neoplastic: carcinoma of the oesophagus, stomach and colon
- Functional: achalasia, diverticulosis and irritable bowel syndrome.
What do oesophageal disorders usually present with?
Dysphagia (difficulty swallowing)
Pain - may result from acid reflux of spasm
Cough or vomit - if food or liquids do not pass normally to the stomach they may reflux back to the pharynx, overflow into the lungs or present as a cough.
What is achalasia?
Loss of ganglia from intramural plexus leads to a failure of relaxation of the gastro-oesophageal sphincter. This produces a functional obstruction to oesophageal emptying with dysphagia for solids and liquids. Failure of peristalsis leads to progressive dilatation of the oesophagus.
What is aetiology of carcinoma in the oesophagus?
History of smoking increases risk fivefold.
Heavy consumption of alcohol raises it 20-fold.
What is the pathogenesis of carcinoma of the oesophagus?
Majority are squamous cell carcinomas while in the lower third they may be adenocarcinomas.
Can spread to adjacent structures, including lymph nodes.
What are the clinical features of carcinoma of the oesophagus?
Usually present with dysphagia of gradual onset, which is initially to solids and later fluids.
May also have pain on swallowing or effects of local spread e.g. recurrent laryngeal nerve palsy.
How do you diagnose carcinoma of the oesophagus?
History, barium swallow test, endoscopy, biopsy.
CT to stage disease and plan tx.
- Dental relevance of carcinoma of the oesophagus *
Patients may present with dysphagia which may be due to malignancy.
Medicines may need to be prescribed in elixir form.
What is peptic ulcer disease and oesophageal reflux?
Acid refluxing into the oesophagus may cause pain, ulceration and spasm. Peptic ulcers can affect the oesophagus, stomach or duodenum.
What is the aetiology of peptic ulcer disease and oesophageal reflux?
Commonly due to mucosal inflammation caused by acid and pepsin, with Helicobacter pylori infection and stress.
In the oesophagus ulceration is usually related to acid reflux while in the stomach it occurs due to decreased mucosal resistance, induced by smoking and/or NSAIDS.
Duodenal ulceration is related to increased gastric acid production, which the duodenal secretions are unable to neutralise.
In all cases, stress may play an important role.
What is the pathogenesis of peptic ulcer disease and oesophageal reflux?
Ulcers in the oesophagus usually affect the lower part, pyloric antrum is common in stomach and first part of duodenum.
The natural history of the ulcers may lead to healing with scarring which may cause strictures.
Complications of acute bleeds or perforation.
What are the clinical features of peptic ulcer disease and oesophageal reflux?
Classical presenting features are pain, which is relieved by eating.
If a stricture develops this may be replaced by vomiting while and active bleed is a cause of haematemesis (vomiting of blood).
How do you treat peptic ulcer disease and oesophageal reflux?
Modify risk factors and medical therapy with antacids, H2 blockers, e.g. ranitidine and proton pump inhibitors, e.g. omeprazole.
- Dental relevance of peptic ulcer disease *
Prescription of NSAIDs must be avoided.
What is the aetiology of coeliac disease?
Sensitivity to gluten (wheat, barley, rye, oats) and has an HLA associated with B8.
What are the clinical features of coeliac disease?
The disease classically presents with a change in bowel habit (COBH).
There is an increased frequency and bulky, offensive frothy greasy stool which flush with difficulty.
There is often associated abdominal colic, weakness and weight loss.
If the onset is in childhood this results in short stature and a ‘failure to thrive’.
How do you diagnose coeliac disease?
Presence of antibodies to gliadin and endomysium.
Augmented by an endoscopic biopsy.
- What is the dental relevance of coeliac disease *
Malabsorption of B12, folate and iron causing:
- oral ulceration
- glossitis
- angular cheilitis
- anaemia
Bleeding tendency due to malabsorption of vitamin K.
Enamel defects may occur in the permanent dentition if the onset is in childhood.
What is Crohn’s disease?
A chronic granulomatous disease that may affect any part of the GI tract from the mouth to the anus. The terminal ileum is most commonly involved.
What is the aetiology of Crohn’s disease?
Unknown, usually starts in teens or early twenties with a second peak in old age
What is the clinical presentation presentation of Crohn’s disease?
Intermittent abdominal pain, diarrhoea, abdominal distention (90%), anaemia and weight loss (50%), clubbing (50%), fresh blood or melaena (40%), fever (30%), fistulae and perinasal sepsis (20%), uveitis, arthritis, skin rashes (erythema nodosum).
How do you diagnose Crohn’s disease?
Based on the appearance seen on barium enema, endoscopic examination, colonoscopy/ileoscopy and biopsy.
The differential diagnosis included other granulomatous conditions such as tuberculosis and sarcoidosis.
Can have labial swelling in Crohn’s disease.
What is the treatment of Crohn’s disease?
Correction of any nutritional deficiencies and the use of immunosuppressives such as prednisolone (acutely), azathioprine (long-term disease modifying) as well as other immunomodulating medications such as sulphasalazine and mesalazine.
Surgical interventions may be necessary.
- Dental relevance of Crohn’s disease *
Oral manifestations are likely to occur at some stage in most patients and include:
- Ulceration
- Cobblestone mucosa
- Facial and labial swelling
- Mucosal tags
- Pyostomatitis vegetans
Malabsorption (particularly B12) may lead to oral complications.
Immunosuppression increases the infection risk.
What is ulcerative colitis?
A chronic inflammatory bowel disease that affects the colon with backwash involvement of the terminal ileum.
What is the aetiology of ulcerative colitis?
Unknown, but usually present in the age group of 20-40 years. There is probably a genetic basis with a close link to ankylosing spondylitis and HLA-B27.
What are the clinical presentations of ulcerative colitis?
At presentation 30% are localized to the rectum while 20% are widespread.
The presenting symptoms include painless, bloody diarrhoea with mucus which may be associated with fevers and periods of near normality (remissions).
Superficial ulceration in the colon.
How do you diagnose ulcerative colitis?
Diagnosis is from the history and by endoscopic examination (colonoscopy) which revels superficial ulceration and contact bleeding.
The differential diagnosis includes carcinoma of the colon, food poisoning and pseudomembranous colitis.
How do you treat ulcerative colitis?
Medical management includes a high-protein, high-fibre diet and immunomodulation with corticosteroids (acutely), azathioprine (long term), sulphasalazine and mesalazine.
Surgical intervention may be required, particularly in the case of toxic megacolon.
- Dental relevance of ulcerative colitis *
Oral ulceration may occur.
Immunosuppression increases the infection risk
How common is carcinoma of the colon?
Third commonest cancer in the UK
What are predisposing factors of carcinoma of the colon?
These include neoplastic polyps, long-standing ulcerative colitis (and possible crohn’s), a positive family history, familial polyposis coli and previous cancer.
What are the clinical presentations of carcinoma of the colon?
Often detected during investigation of unexplained anaemia. In 60% there is a mass on rectal examination. Presentation depends on site of the tumour in the colon:
- left: bleeding PR, COBH, and tenesmus
- right: anaemia, weight loss and abdominal pain
- both: obstructive, perforation, haemorrhage or fistula.
How do you diagnose carcinoma of the colon?
Colonoscopy and biopsy. CT scan to determine seize and liver ultrasound to detect metastasis.
How do you treat carcinoma of the colon?
Primary surgery with adjuvant chemotherapy.
- Dental relevance of carcinoma of the colon *
Oral manifestations of anaemia may occur.
What is diverticular disease?
A diverticulum is a herniation of the bowel mucosa through the bowel wall, which occurs at a weak point where it is pierced by blood vessels. Inflammation of a diverticulum results in diverticulitis which most commonly presents with abdominal pain.
Treatment is with a high-fibre diet and may involve surgery if recurrent.
What is irritable bowel syndrome (IBS)?
IBS is the commonest diagnosis made at gastrointestinal clinical and is characterised by intermittent diarrhoea, abdominal pain and bloating relieved by bowel action.
Psychological factors account for most cases while some may relate to specific food intolerances. Women are more commonly affected than men.
What is the treatment of IBS?
Reassurance and explanation. A high-fibre diet and avoidance of dietary triggers may help.
- Dental relevance or irritable bowel syndrome *
May be associated with psychogenic oral symptoms such as chronic (atypical) facial pain, burning mouth syndrome and temporomandibular joint dysfunction.
What is haematemesis?
This is vomiting of blood, most commonly from the upper gastrointestinal tract. This myst be distinguished from haemoptysis (coughing up blood).
Vomited blood is usually partially digested and dark, resembling coffee grounds, and it may be mixed with food.
If severe this can be life threatening, e.g. bleeding oesophageal varices.
Causes:
> congenital (haemophilia, ehlers-danlos syndrome, peutz-jeghers syndrome)
> infective (helicobacter pylori-induced ulceration)
> Inflammatory (peptic ulceration, gastritis, oesophagitis)
> Trauma (surgery, swallowed blood from epistaxis)
> Venous engorgement (oesophageal varices)
> Neoplasia (oesophageal SCC, Gastric CA)
> Drug induced (warfarin, NSAID induced gastric erosion)
How do you test cranial nerve I?
Sense of smell
How do you test cranial nerve II?
Visual acuity using Snellen chart
Visual field
How do you test cranial nerves III, IV and VI?
Assess eye movements. Lateral and vertical movements.
How do you test cranial nerve V?
Facial sensation in the territories of the trigeminal nerve (frontal V1, maxillary V2, and mandibular V3) tested and mapped using a pin or cotton wool.
Masseter and temporalis muscles can be palpated while pt clenches their teeth to assess the motor division of trigeminal
How do you test cranial nerve VII?
Facial movements - raise eyebrow, smile
Where to lower motor neurones lesions affect compared to upper motor neurones?
VII lower motor neurones affect movement of both forehead and mouth whereas an upper motor neurone lesion affects just the mouth.
How do you test cranial nerve VIII?
Hearing tested by whispering a number in one ear while masking the other.
How can you test cranial nerve IX and X?
speech, swallow and palatal movements.
IX = glossopharyngeal
X = vagus
Lesion in either may result in dysarthria.
Palatal movement to test vagus nerve
How can you test cranial nerve XI?
Shoulder shrug
Accessory (XI) nerve supples sternocleidomastoids and part of the trapezius.
How can you test cranial nerve XII?
Tongue should be observed at rest for wasting or fasciculations.
Stick tongue out, and watch if it deviates.
What are the effects of XII motor neurone lesions?
Hypoglossal (XII) lower motor neurone lesions cause the tongue to be wasted and to deviate to the side of the lesion.
In bilateral upper motor neurone lesions the tongue becomes spastic and its movements slow and limited. Alternating tongue movements will be slow and irregular with a cerebellar lesion.
What may LMN bulbar palsy be a feature of?
May be a feature of motor neurone disease, myasthenia gravis or a tumour in the medulla. Here the tongue is wasted.
Can cause slurred speech, difficulty swallowing, choking and a hoarse voice.
What is UMN bulbar palsy be caused by?
UMN bulbar palsy is due to bilateral lesions (stroke, multiple sclerosis, motor neurone disease). Here the tongue is not wasted but movements are slow and stiff.
What is the pathogenesis of Bell’s palsy?
Bell’s palsy is the most common cause of facial nerve paralysis.
Pathogenesis is not fully understood but the condition is probably caused by latent Herpes viruses (Herpes Simplex Virus type 1 and Herpes zoster virus), which are reactivated from cranial nerve ganglia. Inflammation of the nerve results in nerve damage and a lower motor neurone (LMN) weakness that involves the whole musculature of one side of the face.
What are upper motor neurone (UMN) weakness usually cause by and what part of the face does it spare?
By contrast, upper motor neurone (UMN) weakness spares the forehead muscles and is usually due to a stroke or tumour of the cerebral hemisphere.
What are causes of lower motor neurone facial palsy?
- Belly palsy caused by reactivation of HSV-1 or HZV from the cranial nerve ganglia causing inflammation of the nerve, causing nerve damage and LMN weakness.
- Tumours of the eighth nerve or skull
- Parotid tumour, inflammation, injury
- Sarcoidosis (often bilateral weakness)
- Middle ear or mastoid infections
- Pontine lesions (demyelination of infarction)
- The Ramsay Hunt syndrome due to herpes zoster infection of the geniculate ganglion produces severe facial palsy with a painful vesicular eruption on the palate and external auditory meatus; acyclovir should be given.
- Melkersson’s syndrome: association of recurrent facial nerve palsy, inflammatory swelling of the face and a geographical tongue.
- Traumatic injury (parotid surgery and skull base fractures).
What is Ramsay Hunt syndrome?
It is due to herpes zoster infection of the geniculate ganglion of the facial nerve and produces a severe facial palsy with a painful vesicular eruption on the palate and external auditory meatus; aciclovir should be given.
What are clinical features of Melkersson’s syndrome?
Association of recurrent facial nerve palsy, inflammatory swelling of the face and a geographical tongue.
What are the clinical features of Bell’s palsy?
> Ear pain may precede the attack then facial weakness develops over 1 to 5 days and is often complete.
The face feels stiff and the patient has difficulty closing the eyelids, and difficulty with eating and smiling.
Altered taste can also occur due to involvement of the chorda tympani nerve.
Hyperacusis (distortion of sound in the ipsilateral ear) indicates involvement of the nerve supplying the stapedius muscle.
A branch also innervates the lacrimal glands and decreased production of tears on the affected side may result.
After recovery of a proximal lesion there may be synkinesia (a blink causing ipsilateral movement of the lips) or crocodile tears (lacrimation accompanies salivation during eating) due to aberrant innervation.
What is treatment of Bells palsy?
Eighty percent fully recover in 1-2 months, but a small number, particularly diabetics and the elderly, have permanent facial weakness.
**The risks of this may be reduced by a short course of high-dose prednisolone and aciclovir if started within the first few days of symptom onset. **
To prevent drying and other corneal injury, lubricating eye droops may be necessary and the eyelids should be taped closed during sleep.
- Dental relevance of Bell’s palsy *
A parotid tumour may present as facial palsy
Occasionally dental treatment may cause facial nerve palsy. Accidental injection into the parotid gland during a misdirected mandibular block may anaesthetize the facial nerve. The condition will only last for the duration of the anaesthetic, but the eye must be protected with an eye patch.
What type of nerve is the facial nerve and what is its nucleus and route?
The facial nerve is predominantly motor and the nucleus is in the pons. It leaves the brainstem to pass through the cerebello-pontine angle into the internal auditory canal (with the VIII cranial nerve). It lies close to the inner and middle ear in the temporal bone. It leaves the skull via the stylomastoid foramen to supply the muscles of facial expression and platysma.
What is trigeminal neuralgia?
Trigeminal neuralgia is a sudden, severe, brief stabbing, recurrent pain in the distribution of one of the division of the trigeminal nerve.
What is the epidemiology of trigeminal neuralgia?
Usually occurs in the elderly; in younger people it can be secondary to multiple sclerosis.
What is the pathophysiology of trigeminal neuralgia?
This remains unknown but it is thought to be related to compression of the trigeminal nerve by blood vessels.
What are differential diagnoses to trigeminal neuralgia?
Dental: exposed dentine, fracture tooth, periodontitis, osteomyelitis
Trigeminal neuropathy (e.g. compression of trigeminal roots from tumour or aberrant vessels)
Glossopharngeal neuralgia
Postherpetic neuralgia
Cluster headaches
Cranial arteritis
Temporomandibular joint disorders
Atypical facial pain
What are the clinical features of trigeminal neuralgia?
- Spasms of pain occur in the face, usually radiating from the corner of the mouth or from the gingivae toward the cheek and ear.
- It is often triggered by touch, chewing, shaving or even cold wind.
- The pain is severe and occurs hundred of times a day.
- Facial sensation and the other cranial nerves are normal.
What is the treatment of trigeminal neuraglia?
Carbamazepine is usually effective in controlling the pain, although dosages associated with drowsiness are often needed.
Alternatives include phenytoin, lamotrigine, valproate and gabapentine.
If the condition fails to respond to medical treatment, various surgical interventions are available, including cryotherapy, microvascular decompression, percutaneous balloon compression, radiofrequency thermocoagulation, and glycerol infection.
- Dental relevance of trigeminal neuralgia *
> Trigeminal neuralgia may occur after dental treatment.
> Many patients attribute their pain to dental causes and will initially seek dental treatment
> The pain can be confused with dental pain. A marcaine block can be very successful at producing immediate and even long-term relief of this painful condition.
> Dental care may be difficult not only due to the pain experienced by the patient but also because of depression related to chronic pain and diminished salivation due to the use of tricyclic antidepressants.
> Trigeminal neuralgia is rare in young people.
What is a stroke?
A stroke is a sudden neurological disturbance due to blockage or rupture of a brain blood vessel.
What are the classifications of a stroke?
- Ischaemia stroke (85% of all strokes) due to blockage of a cerebral artery by an embolus or by thrombus. If the neurological deficit last for less than 24 hours, it is called a transient ischaemia attack (TIA).
- Haemorrhagic stroke due to intracerebral bleed
- Subarachnoid haemorrhage due to rupture of a blood vessel (often an aneurysm or arteriovenous malformation) into the cerebrospinal fluid within the subarachnoid space.
What is the pathogenesis of ischaemic stroke?
Most ischaemic stroke is due to emboli arising from an internal carotid artery stenosed (narrowed) by atheroma.
Occasionally emboli come from the heart affected by mitral valve disease, right to left shunts, bacterial endocarditis, or a mural thrombosis following myocardial infarction or atrial fibrillation.
What are the risk factors for stroke?
- Age > 60 years
- Diabetes mellitus
- Cardiac disease
- Smoking
- Peripheral vascular disease
- Oral contraceptive pill and pregnancy
- Crack and cocaine
- Hypertension
- Polycythaemia
- Hyperlipidaemia
How do you diagnose strokes?
Diagnosis is by CT or MRI. Carotid stenosis is imaged by Doppler ultrasound.
What is the treatment of ischaemic stroke?
Involves reduction of risk factors and rehabilitation.
Aspirin 150mg daily should be given and surgical endarterectomy considered for symptomatic carotid artery stenosis >70%.
What is a haemorrhagic stroke?
This is much less common than ischaemic stroke and is immediately visible on CT scan.
It usually occurs in hypertensives or those with coagulation disorders.
What is a subarachnoid haemorrhage?
This presents with a severe headache ‘like being hit on the back of the head with a cricket bat’. It may be provoked by exertion, sexual inter-coarse, or while straining. About 1/3 become unconscious and have a high risk of death or disability.
- Dental relevance of stroke *
> Patient will often be taking anti-platelet medication or be anticoagulated.
> Oral hygiene may be compromised due to weakness of the facial area or paralysis of extremities.
> Swallowing may be compromised; adjust head position and ensure thorough, constant evacuation during dental procedures.
> Communication may be difficult as speech and/or understanding may be affected.
> Mobility may be affected.
What is epilepsy?
Epilepsy is a central nervous system disorder in which seizures recur, usually spontaneously.
What is the classification of epilepsy?
This involves differentiating between attacks that start all over the brain (generalised) and those that start in a focal area. A focal seizure can remain localised or may spread to involve the whole brain (secondary generalised).
What is the pathogenesis of epilepsy?
This is not fully understood but patients with primary generalised epilepsy are more likely to have a family history of the disorder.
Focal epileptic attacks arise from brain abnormalities such as tumours, infections, infarctions, after head injury, or from hippocampal sclerosis associated with frequent childhood febrile convulsions.
Isolated non-recurrent seizures are commonly caused by metabolic disturbances (hypoglycaemia, hyponatraemia, uraemia, and liver failure), hypotension, alcohol and drugs.
How do you diagnose seizures?
Convulsions can be tonic (generalised stiffness) or clonic (repetitive shaking of the limbs); most seizures are tonic then clonic. Other features that point strongly to a diagnosis of epilepsy are:
1. Postictal (after fitting) confusion lasting 5-20 mins
2. Incontinence of urine
3. Biting the tongue or cheek
4. Inability to remember the onset
5. Stereotyped auras (hallucinations)
What is the classification of seizures?
Generalised seizures
- tonic-clonic (grand mal)
- absence (petit mal) - common in children
- myoclonic: shock-like jerks of the limbs.
Focal seizures
- simple - consciousness not impaired
- complex - consciousness impaired
What are the treatments of epilepsy?
Anti-epileptic drugs (AEDs) are indicated for recurrent seizures. The choice of drug depends on the type of epilepsy and the side-effect profile of the drug.
> cosmetic side-effects include weight gain, acne, hair loss and gingival hypertrophy.
= e.g. phenytoin induced gingival hypertrophy
> There are many drug interactions, e.g. phenytoin and carbamazepine are enzyme inducers.
> Most AEDs cause delayed healing and increased risk of microbial infections.
> Excessive bleeding can occur with carbamazepine and sodium valproate.
Most seizures will terminate on their own, but prolonged seizures (>5-10 mins) should be terminated using intravenous or rectal diazepam. In practice use buccal midazolam 10mg in 1ml of liquid.
- Dental relevance of epilepsy *
> Patients who have seizures need referral to specialist services and must stop driving.
Stress may precipitate seizures
Drug interactions are common with antiepileptic medications; always check in the BNF.
Most anti-epileptic drugs cause delayed healing and increased risk of infection, and some cause excessive bleeding. Oral manifestations from the use of AEDs include:
- gingival hypertrophy (phenytoin)
- xerostomia (carbamazepine)
In the event of seizure:
- protect the airway
- protect the patient from the surrounding environment but do not restrain.
Most seizures will stop on their own. Once the seizure has stopped the patient is likely to be drowsy so do not continue their dental treatment but briefly examine for dental trauma. They will need an escort home.
What is dementia?
Dementia is characterised by gradual deterioration of intellect, memory and cognitive function in the absence of a disturbance of consciousness.
What is the aetiology (causes) of dementia?
- Most common cause is Alzheimer’s disease. Alzheimer’s is associated with the formation of neurofibrillary tangles and amyloid plaques in the brain.
- Degenerative disease (e.g. Alzheimer’s disease)
- Genetic (e.g. Huntington’s chorea)
- Vascular (e.g. multi-infarct dementia)
- Metabolic (e.g. Wilson’s disease)
- Toxic (e.g. alcoholic dementia)
- Deficiency. (e.g. Wernicke-Korsakoff syndrome in thiamine deficiency)
- Mass lesion (e.g. cerebral tumour)
- Infection (e.g. CJD, AIDS)
- Inflammation (e.g. SLE)
- Trauma
- Hydrocephalus
What are the clinical features of dementia?
These depend on the area of the cortex affected but may result in impairment of:
- Intellect: e.g. impaired reasoning and calculation
- Language e.g. difficulty reading, writing and disordered speech
- Social function e.g. loss of personality, inability to work, withdrawn
- Visuospatial function
- Memory and concentration e.g. inattentive, difficulty retaining new information.
Dementia is NOT associated with impaired consciousness
What is the treatment of dementia?
Depends on the cause of dementia but in all causes social support for patients and their families is essential.
