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Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always … More Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.
Principal sources
C. Scully 2010 Medical Problems in Dentistry (6e), Churchill Livingstone
.
M. Longmore  et al. 2014 Oxford Handbook of Clinical Medicine (9e), OUP
.
D. Mitchell 2006 An Introduction to Oral and Maxillofacial Surgery, OUP
.
M. Lubin  et al. 2006 Medical Management of the Surgical Patient, Cambridge University Press
(comprehensive but entirely North American perspective). Various 1995 Procedures in Practice, BMJ. BNF 67.
Note

NB All drug doses relate to fit, adult patients ~770kg in weight. Always check doses for children, the elderly, and those with other medical conditions.

Anaemia is a ↓ in the level of circulating haemoglobin to below the normal reference range for a patient’s age and sex. It indicates an underlying problem and, as such, the cause of the anaemia should be diagnosed before instituting Rx.

graphic Never rush into transfusing patients presenting with a chronic anaemia. Perform basic blood investigations before giving iron or transfusing. Elective surgery in patients with an Hb <10g/dL is rarely appropriate.

of anaemia are notoriously unreliable, but beloved of examiners and include: general fatigue, heart failure, angina on effort, pallor (look at conjunctivae and palmar creases, but unreliable), brittle nails &/or spoon-shaped nails (koilonychia), oral discomfort &/or ulceration, glossitis, and classically angular cheilitis.

See Chapter 19.

(MCV < 78fL) Iron-deficiency anaemia is by far the commonest cause. Causes: chronic blood loss (gastrointestinal or menstrual), inadequate diet. FBC and biochemistry show microcytic, hypochromic anaemia with a low serum iron and a high total iron binding capacity (TIBC). ↑ RBC zinc protoporphyrin is a fast and sensitive early test. Thalassaemia and sideroblastic anaemia are rare causes of microcytosis.

Commonly, anaemia of chronic disease. Other causes: pregnancy, acute blood loss, haemolytic anaemia, and aplastic anaemia. Once pregnancy is excluded, the patient needs investigation by an expert. The TIBC is usually ↓.

(MCV > 100fL) Low vitamin B12 &/or low folate are the common causes. Vitamin B12 is ↓ in pernicious anaemia (deficit of intrinsic factor), alcohol abuse, small gut disease, and chronic exposure to nitrous oxide. Low folate is usually dietary, but may be caused by illness (e.g. coeliac disease, skin disease) or drugs such as phenytoin, methotrexate, trimethoprim, and co-trimoxazole.

In all cases the cause must be sought; this may necessitate referral to a haematologist. Drugs used in iron deficiency: ferrous sulfate 200mg tds. Transfusion of packed cells covered with furosemide 40mg PO if elderly or ↓ cardiac function, indicated rarely for severe microcytic anaemia. Lifelong IM hydroxocobalamin 1mg 3-monthly is used to treat vitamin B12 deficiency, and folic acid 5mg od for folate deficiency.

graphic Never use folate alone to treat ‘macrocytosis’ unless it is proven to be the only deficiency. NB Folic acid is not the same as folinic acid.

A homozygous hereditary condition causing red cells to ‘sickle’ when exposed to low O2 tensions, resulting in infarctions of bone and brain. In sickle cell trait (heterozygous form) the cells are less fragile and sickle only in severe hypoxia. Management: perform haemoglobin electrophoresis (or Sickledex if result needed urgently) on all Afro-Caribbean (and consider Mediterranean, Middle Eastern, and Indian) patients planned for GA.

are a neoplastic proliferation of white blood cells. Acute leukaemias are characterized by the release of primitive blast cells into the peripheral blood and account for 50% of childhood malignancy. Acute lymphoblastic leukaemia, the commonest childhood leukaemia, now has up to 90% cure rate in favourable cases. May present as gingival hypertrophy and bleeding. Acute myeloid leukaemia is the commonest acute leukaemia of adults, with high remission rates possible but a tendency to relapse. Chronic leukaemias have cells that retain most of the appearance of normal white cells. Chronic lymphocytic leukaemia is the commonest and has a 5yr survival of >50%. Chronic myeloid leukaemia is characterized by the presence of the Philadelphia chromosome, a fact beloved by examiners. Affects the >40s. Rx: interferon &/or bone marrow transplant (BMT) or stem cell transplantation. Remissions are common, although a terminal blast crisis usually supervenes at some stage.

are proliferation of non-leukocyte marrow cells, with a wide range of behaviour and presentation, including anaemia, bleeding, and infections.

Monoclonal gammopathies such as multiple myeloma are B-lymphocyte disorders characterized by production of a specific immunoglobulin by plasma cells. Multiple myeloma is also a differential ∆ of lytic lesions of bone, particularly the skull. ∆: monoclonal paraprotein band on plasma electrophoresis, Bence Jones proteins in urine.

are solid tumours arising in lymphoid tissue. Their classification is confusing; previously divided into Hodgkin’s or non-Hodgkin’s lymphomas, the latter group was so diverse as to be meaningless. The current (2008) WHO classification attempts to define them by cell type, and recognizes 4 broad categories—mature T cell, mature B and NK cell, Hodgkin’s, and those associated with immunodeficiency. Prognosis is highly variable and type-dependant. Lymphoma should always be considered in the differential ∆ of neck swellings.

Has been the mainstay of Rx for these diseases, with supplemental radiotherapy for masses or prior to BMT. It is essential to remember that any patient receiving these drugs will be both immunocompromised and liable to bleed.

In haematological malignancy, anaemia, bleeding, and infection are the overwhelming risks. Look for and treat anaemia. Avoid aspirin, other NSAIDs, trauma, and IM injections. Prevent sepsis, and if it occurs treat very aggressively with the locally recommended broad-spectrum antibacterials and antifungals, e.g. piperacillin/tazobactam 2.25g and gentamicin 80mg IV tds plus fluconazole up to 100mg daily. Liaise with haematologist urgently.

Characterized by deposits of fibrillar eosinophilic hyaline material in a wide range of organs and tissues. Two types:1°amyloidosis (AL amyloid), a plasma cell dyscrasia. Signs and symptoms include peripheral neuropathy, renal involvement, cardiomyopathy, xerostomia, and macroglossia. Rx: immunosuppression (rarely helps). 2°amyloidosis (AA amyloid). It reflects an underlying chronic disease: infection, rheumatoid, neoplasia. May respond to Rx of underlying disease. ∆: biopsy of rectum or gingivae—stain with Congo red.

For the practical management of a bleeding patient, see graphic Post-operative bleeding, p. 360.

May present as nosebleeds, purpura, or post-extraction bleeding. Remember that aspirin is the most common acquired cause, its effect being irreversible for 1 week. Other causes include diseases such as Von Willebrand’s disease; immune thrombocytopenic purpura (ITP); virally associated (especially HIV) thrombocytopenic purpura; thrombocytopenia secondary to leukaemia; cytotoxic drugs; or unwanted effects of drugs, notably aspirin and chloramphenicol. Management: ensure platelet levels of >50 × 109/L, preferably 75 × 109/L for anything more than simple extraction or LA. If actively bleeding, use a combination of local measures (graphic Post-operative bleeding, p. 360), tranexamic acid, and platelet transfusion. Platelet transfusions are short-lived and if used prophylactically must be given immediately prior to or during surgery. Liaise closely with the lab. The quality of preparation varies by locality. Tranexamic acid mouthwash may ↓ oral bleeding.

Present as prolonged wound bleeding &/or haemarthroses. Causes include the haemophilias, anticoagulants, liver disease, and von Willebrand’s disease.

Less common causes include: hereditary haemorrhagic telangiectasia, aplastic anaemia, chronic renal failure, myeloma, SLE, disseminated intravascular coagulation, and isolated deficiency of clotting factors.

The commonest clotting defect. Inherited as a sex-linked recessive, it affects males predominantly, although female haemophiliacs can occur. All daughters of affected males are potential carriers. Usually presents in childhood as haemarthroses. Bleeding from the mouth is common. Following trauma, bleeding appears to stop, but an intractable general ooze starts after an hour or so. Severity of bleeding is dependent on the level of factor VIII activity and degree of trauma.

Clinically identical to haemophilia A; also known as Christmas disease.

A combined platelet and factor VIII disorder affecting males and females. Mucosal purpurae are common, haemarthroses less so. Wide range of severity. May improve with age &/or pregnancy.

The haemophilias and Von Willebrand’s disease should always be managed at specialist centres. Check the patient’s warning card for the contact telephone number.

Given IV or high-dose SC for therapeutic anticoagulation. Its effect wears off in ~8h although it can be reversed by protamine sulfate in an emergency. Measure in activated partial thromboplastin time (APTT).

Given orally; effects take 48h to be seen. Normal therapeutic range is an international normalized ratio (INR) of 2–4. Simple extractions are usually safe at a level within therapeutic range. Reverse the effects of warfarin with vitamin K &/or fresh frozen plasma if needed, but consider why the patient is anticoagulated in the first place. See graphic Prophylaxis, p. 566.

Given SC, these are small fractions of heparin salts commonly used for short-term prevention of deep vein thrombosis or, in higher doses, for full anticoagulation. Measuring or reversing activity are rarely required but differ from heparin—anti-factor Xa assay is used to measure activity and reversal with protamine sulphate is only partially effective.

This is the commonest cause of death in the UK.

is a consistently raised BP (>140 systolic, >90 diastolic >3 months) and is a risk factor for ischaemic heart disease, cerebrovascular accidents, and renal failure. Up to 95% of hypertension has no definable cause: essential hypertension. 5% is secondary to another disease such as renal dysfunction or endocrine disorders.

is ↓ of the blood supply to part of the heart by narrowing of the coronary arteries, usually by atheroma, causing the pain of angina pectoris. If myocardial cells die as a result, acute coronary syndrome (MI) occurs (graphic Acute chest pain, p. 537).

is the end result of a variety of conditions, not all of them cardiovascular. Basically, the heart is unable to meet the circulatory needs of the body. In right heart failure, dependent oedema and venous engorgement are prominent. In left heart failure, breathlessness is the principal sign. The two often coexist. There is an ever-present risk of precipitating heart failure, even in treated patients, by ↑ the demands on the heart, e.g. by fluid overload or excessive exertion.

is collapse of the peripheral circulation due to a sudden ↓ in the circulating volume. If this is not corrected there can be failure of perfusion of the vital organs, resulting in heart failure, renal failure, and unconsciousness ending in death.

are disturbances of blood flow which are audible through a stethoscope. They may be functional or signify structural disorders of the heart. Echocardiography will differentiate. They are of great relevance to dentists as their presence warns of the potential for colonization of damaged valves by blood-borne bacteria. Such a bacteraemia can be caused by dental procedures.

Patients with a PMH of rheumatic fever are very likely to have some damage to a heart valve, usually the mitral valve. Traditionally advice has been to provide antibiotic prophylaxis for invasive dental procedures, but more recent guidance has advised against this.1 The risk of precipitating heart failure or MI in patients with compromised cardiovascular systems is ever-present. Prevent by avoiding GA, especially within 3 months of an MI, using adequate LA with sedation if necessary, and avoid excessive adrenaline loads. Consider potential drug interactions (graphic Alarm bells, p. 600) and remember some of these patients will be anticoagulated.

Exclusion of septic foci may be requested in patients at high risk from bacteraemia, e.g. heart transplant recipients, those with prosthetic valves or valvular damage, or those with a history of IE. It is prudent to err on the side of caution with these individuals and some will need dental clearances.

Disease of the chest is an everyday problem in developed countries. The principal symptoms are cough, which may or may not be productive of sputum, dyspnoea (breathlessness), and wheeze. The coughing of blood (haemoptysis) mandates that malignancy be excluded.

Include the common cold, sinusitis, and pharyngitis/tonsillitis (which may be viral or bacterial), laryngotracheitis, and acute epiglottitis. All are C/I to elective GA in the acute phase. Sinusitis (graphic Maxillary sinusitis, p. 396). Penicillin is the drug of choice for a streptococcal sore throat. Avoid amoxicillin and ampicillin, as glandular fever may mimic this condition and these drugs will produce a rash, of varying severity, in such a patient. Epiglottitis is an emergency, and if suspected the larynx should NEVER be examined unless expert facilities for emergency intubation are to hand.

Both viral and bacterial lower tract infections are debilitating and constitute a C/I to GA for elective surgery. Bear in mind TB and atypical bacteria, e.g. legionella, mycoplasma, and coxiella. Open TB is highly infectious and cross-infection precautions are mandatory (graphic Prevention of cross-infection, p. 744).

A very common condition usually caused by a combination of bronchitis (excessive mucus production, persistent productive cough >3 months per year for 3yrs) and emphysema (dilation and destruction of air spaces distal to the terminal bronchioles). Smoking is the prime cause and must be stopped for Rx to be of any value. Be aware of possible systemic steroid use.

Reversible bronchoconstriction causes wheezing and dyspnoea. Up to 8% of the population are affected; there is often an allergic component. Patients complain of the chest feeling tight. May be precipitated by NSAIDs. Penicillin and aspirin allergies are more common. Management of acute asthma graphic Management, p. 548.

An inherited disorder whereby viscosity of mucus is ↑. Patients suffer pancreatic exocrine insufficiency and recurrent chest infections. ∆: by history and sweat sodium measurement.

Causes >20% of cancer deaths. Principal cause is smoking. ↓ incidence in females, though not by much. Symptoms are persistent cough, haemoptysis, and recurrent infections. 2yr survival is only 10%. Mesothelioma is an industrial disease caused by asbestos exposure.

Most commonly presents as hilar lymphadenopathy in young adults. Oral lesions can occur. Erythema nodosum common.

Avoid GA. Use analgesics and sedatives with caution; opioids and sedatives ↓ respiratory drive, NSAIDs may exacerbate asthma. Advise your patients to stop smoking (and if you are a smoker, stop). Refer if suspicious, especially in the presence of confirmed haemoptysis.

The mouth and its mucosal disorders and disorders of the salivary glands are covered in Chapter 10.

Presents symptoms which can be confused with those originating from the mouth, the most important being dysphagia. Difficulty in swallowing may be caused by conditions within the mouth (e.g. ulceration), pharynx (e.g. FB), benign or malignant conditions within oesophagus, compression by surrounding structures (e.g. mediastinal lymph nodes), or neurological causes. It is a symptom which should be taken seriously and investigated by at least CXR, barium swallow, &/or endoscopy. Reflux oesophagitis is a common cause of dyspepsia, sore throat, cough, and bad taste.

(duodenal malignancy rare) May present with epigastric pain, vomiting, haematemesis, or melaena.

Commonly due to infection with Helicobacter pylori and usually responds to H. pylori eradication therapy (combination of proton pump inhibitor/broad-spectrum antibiotic/anaerobicidal, i.e. metronidazole). Other causes include stress ulceration in critically ill or major surgical patients, and elderly people on NSAIDs. Prophylaxis is with H2 antagonists or proton-pump inhibitors to reduce acid secretion or sucralfate, a mucosal protectant, which maintains the protective gastric pH barrier but is a problem practically as it clogs fine-bore NGT. Symptomatic relief of dyspepsia without significant ulceration is with antacids and alginates. Persisting epigastric pain or other symptoms must be investigated as gastric carcinoma requires early surgery and carries a poor prognosis.

graphic Endoscopic investigation of patients >40yrs with persisting epigastric symptoms is mandatory.

Non-malignant, Helicobacter-negative ulceration (oesophagitis, gastritis, duodenitis) clears with 1 month of proton pump inhibitor Rx (e.g. omeprazole 10–20mg od) and can often be maintained with H2 antagonists (ranitidine or cimetidine).

This has a multitude of associated disorders which tend to present in a similar manner; namely, malabsorption syndromes, diarrhoea, steatorrhoea, abdominal pain, anaemia, and chronic deficiencies. Coeliac disease and Crohn’s disease are the best known conditions. Coeliac disease is a hypersensitivity response of the small bowel to gluten and treated by strict avoidance. A number of oral complaints are related, typically ‘cobblestoning’ of the mucosa. Crohn’s disease may affect any part of the gastrointestinal tract but has a preference for the ileo-caecal area. It is a chronic granulomatous disease affecting the full thickness of the mucosa and may result in fistula formation. Ulcerative colitis is often mistaken for Crohn’s disease initially, but affects the colorectum only. Treatment with systemic steroids and other immunosuppressants is common.

Diverticular disease is a condition with multiple outpouching of large bowel mucosa which can become inflamed, causing diverticulitis. The irritable bowel syndrome is a condition associated with ↑ colonic tone, causing recurrent abdominal pain; there may be some psychogenic overlay.

Colonic cancer is common in older patients; it may present as rectal bleeding, a change in bowel habit, intestinal obstruction, tenesmus (wanting to defecate but producing nothing), abdominal pain, or anaemia. It is treated surgically, with up to 90% 5yr survival if diagnosed early (Duke’s A). Familial polyposis coli is associated with the Gardener syndrome (graphic Gardener syndrome, p. 755). Antibiotic-induced colitis results from overgrowth of toxigenic Clostridium difficile after use of antibiotics, commonly ampicillin and clindamycin. It responds to oral vancomycin or metronidazole.

Malignancy has the worst prognosis of any cancer and most Rx is essentially palliative.

Often a manifestation of alcohol abuse. Aetiology is not entirely clear. Causes acute abdominal pain. Amylase levels are a guide but not infallible. Patients need aggressive rehydration, maintenance of electrolyte balance, and analgesia, in high-dependency or ICU setting.

The main problems presented by patients with liver disease are: the potential for ↑ bleeding, inability to metabolize and excrete many commonly used drugs, and the possibility that they can transmit hepatitis B, C, &/or D (Hep A and E are spread by faecal–oral route). The liver is also a site of metastatic spread of malignant tumours. Patients in liver failure needing surgery, especially under GA, are a high-risk group who should have specialist advice on their management.

The prime symptom of liver disease. It is a widespread yellow discoloration of the skin (best seen in good light, in the sclera), caused by the inability of the liver to process bilirubin, the breakdown product of haemoglobin. This occurs either because it is presented with an overwhelming amount of bilirubin to conjugate (e.g. haemolytic anaemia), or it is unable to excrete bile (cholestatic jaundice). Cholestatic jaundice in turn may be either intrahepatic or extrahepatic.

represents hepatocyte damage; this is reflected by ↑ aspartate transaminase levels on liver function tests, and results in impaired bile excretion, as indicated by ↑ plasma bilirubin. Causes include alcohol and other drugs, toxins, bacterial and viral infections. A degree of hepatitis is present with these causes, whereas primary biliary cirrhosis and anabolic steroids cause a specific intrahepatic cholestasis without hepatitis.

is caused by obstruction to the excretion of bile in the common bile duct by gallstones, tumour, clot, or stricture. Carcinoma of the head of the pancreas, or adjacent lymph nodes, may also compress the duct, and must be excluded.

Ascertain a ∆ for the cause. Do hepatitis serology. Cross-infection precautions (graphic Prevention of cross-infection, p. 744).

Do coagulation screen. May need correction with vitamin K or fresh-frozen plasma.

Always warn the anaesthetist, as it will affect the choice of anaesthetic agents.

If a jaundiced patient must undergo surgery correct fluid and electrolyte balance, and ensure a good peri-operative urine output by aggressive IV hydration with 5% glucose and mannitol diuresis to avoid hepato-renal syndrome (see OHCM).

Do not use IV saline in patients in fulminant hepatic failure, as there is a high risk of inducing encephalopathy.

Know which disease you are dealing with. If Hep B or C employ strict cross-infection control (graphic Prevention of cross-infection, p. 744).

Be cautious in prescribing drugs (consult the BNF/DPF) and with administering LA.

Do not administer GAs.

Take additional local precautions against post-op bleeding following simple extractions (graphic Post-operative bleeding, p. 360). A clotting screen should be obtained for anything more advanced, and in all patients with severe liver disease.

The commonest urinary tract problems, infections, are of relevance only to those who manage in-patients. Rarer conditions such as renal failure and transplantation are, surprisingly, of more general relevance because these patients are at ↑ risk from infection, bleeding, and iatrogenic drug overdose during routine Rx.

This is tested in all in-patients. ‘Multistix’ will test for glycosuria (diabetes, pregnancy, infection), proteinuria (diabetes, infection, nephrotic syndrome), ketones (diabetic ketoacidosis), haematuria (infection, tumour), and bile as bilirubin and urobilinogen (cholestatic jaundice).

A common cause of toxic confusion in elderly in-patients, especially females. Send a mid-stream urine (MSU) for culture and sensitivity, then start trimethoprim 200mg bd PO or ampicillin 250mg qds PO and ensure a high fluid intake. Minimal investigations of renal function are U&Es, creatinine, and ionized Ca2+.

A syndrome of proteinuria (>3.5g/day), hypoalbuminaemia, and generalized oedema. Facial oedema is often prominent. Glomerulonephritis is the major precipitating cause and investigations should be carried out by a physician with an interest in renal medicine.

A medical emergency causing a rapid rise in serum creatinine, urea and K+. It may follow surgery or major trauma and is usually marked by a failure to PU. Remember the commonest causes of failing to PU post-op are under-infusion of fluids and urinary retention. Rx: ↑ IV fluid input and catheterize (graphic Catheterization, p. 560). If ARF is suspected get urgent U&Es, ECG, and blood gases. Obtain aid from a physician. Control of hyperkalaemia, fluid balance, acidosis, and hypertension are the immediate necessities.

Basically the onset of uraemia after gradual, but progressive renal damage, commonly caused by glomerulonephritis (inflammation of the glomeruli following immune complex deposits), pyelonephritis (small scarred kidneys due to childhood infection, irradiation, or poisoning), or adult polycystic disease (congenital cysts within Bowman’s capsule). It has protean manifestations, starting with nocturia and anorexia, progressing through hypertension and anaemia to multi-system failure. Continuous ambulatory peritoneal dialysis, haemodialysis, and transplants are the mainstays of Rx.

↑ risk of infection, worsened by immunosuppression.

↑ bleeding tendency.

↓ ability to excrete drugs.

Veins are sacrosanct; never use their A-V fistula.

Bone lesions of the jaws (renal osteodystrophy, 2° hyperparathyroidism).

Generalized growth impairment in children.

Potential carriage of Hep B, HIV.

An increasingly common final Rx of renal failure, and when successful renal function may reach near normal levels. Kidneys are, however, immunosuppressed and at greatly ↑ risk from infection. They may share the problems associated with chronic kidney disease depending on the level of function of the transplant.

Take precautions against cross-infection (graphic Prevention of cross-infection, p. 744).

Treat all infections aggressively and consider prophylaxis.

Use additional haemostatic measures (graphic Post-operative bleeding, p. 360).

Be cautious with prescribing drugs (graphic Prescribing, p. 576).

Never subject these patients to out-patient GA.

Remember veins are precious.

Try to perform Rx just after dialysis if possible.

1° hypoadrenocorticism. Atrophy of the adrenal cortices causes failure of cortisol and aldosterone secretion. 2° hypoadrenocorticism is far commoner, due to steroid therapy or ACTH deficiency (graphic Management of patients requiring steroid supplementation, p. 570). All need steroid cover.

Primary hyperaldosteronism causes hypokalaemia and hypernatraemia with hypertension.

These are due to excess corticosteroid production. The disease refers to 2° adrenal hyperplasia due to ↑ ACTH, whereas the syndrome is a 1° condition, usually due to therapeutic administration of synthetic steroid or adenoma. Classical features are obesity (moon face, buffalo hump) sparing the limbs, osteoporosis, skin thinning, and hypertension.

Production of copious dilute urine due to ↓ ADH secretion or renal insensitivity to ADH. May occur temporarily after head injury.

Persistent hyperglycaemia due to a relative deficiency of insulin (graphic Management of the diabetic patient undergoing surgery, p. 568).

Excess production of growth hormone, before and after fusion of the epiphyses, respectively.

A large thyroid gland, of whatever cause.

Symptoms of heat intolerance, weight loss, and sweating occur. Signs are tachycardia (may have atrial fibrillation), lid lag, exophthalmos, and tremor. Commonest cause is Graves disease (graphic Graves disease, p. 756). Functioning adenomas are another cause.

Can be 1° due to thyroid disease, or 2° to hypothalamic or pituitary dysfunction. 1° disease is often an autoimmune condition. Symptoms are poor tolerance of cold, loss of hair, weight gain, loss of appetite, and poor memory. Signs are bradycardia and a hoarse voice.

1° is caused by an adenoma. 2° is a response to low plasma Ca2+, e.g. in renal failure, and 3° follows on from 2° when the parathyroids continue ↑ production, even if Ca2+ is normalized.

Usually 2° to thyroidectomy, when parathyroid glands inadvertently removed. Plasma Ca2+ ↓, resulting in tetany. Chvostek’s sign is +ve if spasm of facial muscles occurs after tapping over the facial nerve.

Can lead to 2° hypothyroidism or 2° hypoadrenocorticism.

Caused by certain tumours (e.g. bronchial carcinoma), head injury, and some drugs. Hyponatraemia, overhydration, and confusion occur.

May be the only functioning thyroid the patient has; do not excise lightly. Do pre-op isotope scan.

A very rare tumour of the adrenal medulla, secreting adrenaline and noradrenaline. Symptoms are recurring palpitations and headache with sweating. Simultaneous hypertension with a return to baseline on settling of symptoms, is a good marker.

May erode the pituitary fossa (seen on lateral skull X-ray) and can cause blindness via optic chiasma compression.

graphic Always ask yourself: ‘Is she, or can she be, pregnant?’

is a C/I to elective GA, the vast majority of drugs (graphic Prescribing, p. 576), and non-essential radiography (the most vulnerable period being in the first 3 months). Elective Rx is best performed in the mid-trimester.

The end of a woman’s reproductive life and her periods. It is often associated with hot flushes and other relatively minor physical problems. Emotional disturbances may coexist, and the incidence of psychiatric disorders increases at this time.

Around 1:3000 people have an inherited defect of plasma cholinesterase. These families are absolutely normal in every respect except in their ability to metabolize suxamethonium. This leaves them unable to destroy the drug which, normally wearing off in 2–4min, produces prolonged muscle paralysis. This paralysis requires ventilatory support until the drug wears off, which, in the homozygote, may take as long as 24h.

A rare, potentially lethal reaction to, usually, an anaesthetic agent. Characterized by ↑ pulse, muscle rigidity, and ↑ temperature. Dantrolene sodium and cooling may be life-saving.

Secretes glucagon causing hyperglycaemia.

Secrete insulin. Causes sporadic hypoglycaemic episodes.

Secrete gastrin causing duodenal ulcers and diarrhoea (Zollinger–Ellison syndrome).

A rare group of endocrine tumours. MEN IIb is medullary thyroid cancer, phaeochromocytoma, and oral mucosal neuromas.

Pathology of the bones of the facial skeleton is covered in Chapter 9.

(brittle bone disease) An autosomal dominant type 1 collagen defect. Multiple # following slight trauma with rapid but distorted healing is characteristic. Associated with blue sclera, deafness, and dentinogenesis imperfecta (graphic Dentinogenesis imperfecta (hereditary opalescent dentine), p. 69). The jaws are not particularly prone to # following extractions.

(marble bone disease) There is an ↑ in bone density and brittleness, and a ↓ in blood supply. Prone to infection which is difficult to eradicate. Bone pain, #, and compression neuropathies may occur. Anaemia can complicate severe disease. Facial characteristics are frontal bossing and hypertelorism.

An inherited defect in cartilaginous bone formation, usually autosomal dominant. Causes skull bossing; many have no other problems. Best known current representative would be Tyrion Lannister, the character from A Game of Thrones.

An inherited defect of membranous bone formation, usually autosomal dominant. Skull and clavicles are affected. Multiple unerupted teeth with retention of 1° dentition is characteristic.

Failure of bone mineralization in, respectively, children and adults. Can be caused by deficiency, failure of synthesis, malabsorption, or impaired metabolism of vitamin D, and also hypophosphataemia or ↑ Ca2+ requirement in pregnancy.

A lack of both bone matrix and mineralization. Important causes are steroid therapy, post-menopausal hormone changes, immobilization, and endocrine abnormalities. HRT in post-menopausal women appears helpful. Results in ↑ incidence of #, especially femoral neck and wrist. Bisphosphonates are being aggressively promoted in the treatment of osteoporosis resulting in some of the noted increase in BRON graphic Dento-alveolar surgery: bisphosphonates, p. 364.

Replacement of a part of a bone or bones by fibrous tissue with associated swelling. It usually starts in childhood and ceases with completion of skeletal growth. Termed monostotic if one bone is affected, polyostotic if more than one bone, and Albright syndrome if associated with precocious puberty and café au lait areas of skin hyperpigmentation.

A bilateral variant of fibrous dysplasia.

A common disorder of the elderly, where the normal, orderly replacement of bone is disrupted and replaced by a chaotic structure of new bone, causing enlargement and deformity. The hands and feet are spared. Complications include bone pain and cranial nerve compression, or, more rarely, high output cardiac failure or osteosarcoma. Another condition treated with bisphosphonates.

These are mainly vasculitides (inflammation of vessels).

Giant cell vasculitis of the craniofacial region. Presenting symptom is unilateral throbbing headache. Signs are high ESR with a tender, pulseless artery. Major complication of temporal arteritis is optic nerve ischaemia causing blindness, so start high-dose steroids (60mg prednisolone PO od) and monitor using ESR. Biopsy confirms.

More generalized vasculitis affecting proximal axial muscles. Accounts for 25% of cases of cranial arteritis. Responds to steroids; gradual improvement with time.

A collection of inherited diseases characterized by muscle degeneration. Duchenne’s is the most common and is usually fatal in early adulthood.

Distinguished by delayed muscle relaxation after contraction. They are genetically determined in a complex fashion.

A generalized immune-mediated inflammatory disorder of muscle. If a characteristic rash is present the condition is known as dermatomyositis and has an association with occult malignancy.

1° degeneration of articular cartilage, cervical and lumbar spine, hip and knee joints, commonly affected or 2° to trauma or other joint disease, resulting in pain and stiffness. Osteophyte formation and subchondral bone cysts, which collapse leading to deformity, are characteristic. Physiotherapy, weight loss, and analgesia are the mainstays of Rx. Joint replacement is definitive Rx.

Immunologically mediated disease where joint pain and damage are the most prominent symptoms. Morning pain and stiffness in the hands and feet, usually symmetrical, is characteristic. There may be systemic upset and anaemia. Ulnar deviation of the fingers is patho-gnomonic. Rx includes NSAIDs, steroids, and physiotherapy. Second-line or disease-modifying antirheumatic drugs (DMARDs) may favourably influence outcome at expense of unwanted effects, e.g. penicillamine, antimalarials, immunosuppressants (including TNFαchimeric monoclonal antibody—infliximab). Dry eyes and mouth may be associated with rheumatoid arthritis (Sjögren syndrome graphic Sjögren syndrome (secondary Sjögren syndrome), p. 434). TMJ symptoms are rare in rheumatoid arthritis, although up to 15% of patients have radiographic changes in the joint.

Rarer form of the disease affecting children. It can be much more severe than the adult condition and can cause TMJ ankylosis.

Associated with the skin condition and affects the spine and pelvis. It is usually milder than rheumatoid arthritis and has no serological abnormalities. The TMJ can be affected, but symptoms are usually mild despite some isolated case reports to the contrary.

Urates are deposited in joints, causing sudden severe joint pain, often in the great toe. Affected joints are red, swollen, and very tender. Gout 2° to drugs, radiotherapy, or haematological disease is commoner than that caused by an inborn error of metabolism.

Affects the spine, usually in young men. Inflammation involves the insertion of ligaments and tendons. It is associated with HLA-B27. Later, kyphotic deformity and ↑ risk of cervical fractures.

Seronegative arthritis, urethritis, and conjunctivitis, usually in response to an infection. Oral lesions are often present. Genital and intestinal variants.

Osteochondritis of the femoral head in, mainly, boys aged 3–11yrs. No systemic implications.

I Olfactory. Sense of smell is rarely tested, although damage is quite common following head &/or mid-face trauma.

II Optic. Examine the pupils for both direct and consensual reflex; assess the visual fields; check visual acuity and examine the fundus with an ophthalmoscope (graphic Eyes, p. 9).

III Oculomotor. The motor supply to the extra-ocular muscles except lateral rectus and superior oblique. It supplies the ciliary muscle, the constrictor of the pupil, and levator palpebrae superioris. A defect therefore causes impairment of upward, downward, and inward movement of the eye, leading to diplopia, drooping of the upper eyelid (ptosis), and absent direct and consensual reflexes.

IV Trochlear. Supplies superior oblique, paralysis of which causes diplopia; worst on looking downward and inward.

V Trigeminal. The major sensory nerve to the face, oral, nasal, conjunctival, and sinus mucosa, and part of the tympanic membrane. It is motor to the muscles of mastication. Sensory abnormalities are mapped out using gentle touch and pin-prick. Motor weakness is best assessed on jaw opening and excursion.

VI Abducens. Supplies lateral rectus. A defect causes paralysis of abduction of the eye.

VII Facial. Motor to the muscles of facial expression. Supplies taste from the anterior 2⁄3 of tongue (via chorda tympani) and is secretomotor to the lacrimal, sublingual, and submandibular glands. It innervates the stapedius muscle in the middle ear. The lower face is innervated by the contralateral motor cortex, whereas the upper face has bilateral innervation. Assess by demonstrating facial movements.

VIII Vestibulocochlear. Is sensory for balance and hearing. Deafness, vertigo, and tinnitus are the main symptoms.

IX Glossopharyngeal. Supplies sensation and taste from the posterior 1⁄3 of the tongue, motor to stylopharyngeus, and secretomotor to the parotid. Lesions impair the gag reflex in conjunction with X

X Vagus. Has a motor input to the palatal, pharyngeal, and laryngeal muscles. Impaired gag reflex, hoarseness, and deviation of the soft palate to the unaffected side are seen if damaged. The vagus has a huge parasympathetic output to the viscera of the thorax and abdomen.

XI Accessory. Is motor to sternomastoid and trapezius, causing weakness on shoulder shrugging and on turning the head away from the affected side.

XII Hypoglossal. Motor supply to the tongue. Lesions cause dysarthria (impaired speech) and deviation towards the affected side on protrusion.

The vast majority of headaches are benign; the secret is to pick out those which are not. Read on.

Commonest type. Due to muscle tension in occipitofrontalis. Usually worse as the day progresses; may feel ‘band-like’. Responds to reassurance, anxiolytics, and analgesics.

A distinct entity characterized by a preceding visual aura (fortification spectra). Severe, usually unilateral headache with photophobia, nausea, and vomiting. Thought to be due to cerebral vasoconstriction, followed by reflex vasodilation (the latter is the cause of the pain). 5HT agonists, e.g. sumatriptan (C/I: ischaemic heart disease, cerebrovascular disease) abolish an attack if used early, and many drugs are used to prevent attacks (such as propranolol or pizotifen). F > M, the oral contraceptive being a contributing factor. There are many variants of classical migraine.

Rarer than migraine and causes localized pain, usually around the eye, with associated nasal stuffiness. M > F. There is a typical time of onset, often in early morning, which recurs for several weeks: ‘clustering’. Alcohol is a common precipitant. 5HT agonists (sumatriptan) to treat and calcium channel blockers (verapamil) for prophylaxis.

A cause of headache demanding urgent further investigation. Pointers are headache, worse on waking, irritation, ↓ level of consciousness, vomiting, sluggish or absent pupillary reflexes, bulging of the optic disc (papilloedema). Rising BP and slowing pulse are late premorbid signs of ↑ ICP.

Affects up to 1:50. Presents as daily headache due to excessive or regular use of OTC analgesics (especially codeine-containing) and some antimigraine preparations. Pain pathways may be altered and after withdrawal of the drug the headache may be slow to resolve.

Ice-cream headache, post-coital headache, needle-through-eye headache, and many other distinctive and benign headaches are described.

Must be considered in the differential ∆ of headache with photophobia and neck stiffness. Organisms are Haemophilus influenzae, Neisseria meningitidis (meningococcus), N. gonorrhoeae, and Streptococcus pneumoniae. In children, the meningococcus is especially important and classically associated with a non-blanching purpuric rash. This is one of the very few indications for instituting immediate blind antibiotic therapy (parenteral penicillin).

Usually mild and self-limiting. Distinguished from bacterial meningitis by lumbar puncture.

A rare manifestation of infection with the herpes simplex virus. Can be distinguished from drunkenness or dementia by history and rapid onset. Parenteral aciclovir can be curative.

Most brain tumours are 2° deposits. Although both benign and malignant primary tumours are found, they are rare. Despite this, they are the commonest cause of cancer death in children after leukaemia.

An episodic outflow from the brain causing disturbances of consciousness, motor, and sensory function. Most causes are idiopathic but those with onset in adult life must be investigated for local or general cerebral disease. Major or grand mal epilepsy is characterized by an aura and loss of consciousness, and followed by tonic and clonic phases. Incontinence is a good guide to a genuine seizure. The fit rarely lasts >5min, if it does the patient has entered status epilepticus (graphic Fits, p. 546).

(absence attacks) Are epileptic attacks usually confined to children, taking the form of a short absence when movement, speech, and attention cease.

Characterized by hallucinations of the special senses.

Affects limbs in isolation. Patients with established epilepsy (once any treatable cause has been excluded) must be maintained on adequate levels of antiepileptic drugs.

Fits, usually in children >5yrs old, 2° to pyrexia.

A very common cause of death in the elderly. A stroke is basically death of part of the brain following cerebral ischaemia, either due to bleeding into the brain or occlusion of vessels. It is often clinically difficult to distinguish these different types of stroke. As for acute coronary syndromes, rapid thrombolysis may be indicated, as may interventional endovascular procedures.

A disorder characterized by demyelination in multiple ‘plaques’ throughout the CNS. Symptoms are multiple and disseminated in both time and place. It is the commonest neurological disease of young adults, and the most common form is relapsing/remitting. Parenteral interferon treatment can reduce recurrences.

Muscle weakness due to inadequate response to, or levels of, acetylcholine. Extra-ocular muscles are often first affected.

A disease affecting the basal ganglia associated with a ↓ in the local levels of dopamine. Characterized by a ‘pill-rolling’ tremor, ‘cog-wheel’ rigidity, and bradykinesis with a shuffling gait.

graphic The skin of the face is the commonest site of curable skin cancers, so look and think (graphic Skin cancer, p. 492).

An indolent skin cancer which very rarely metastasizes. If it kills it usually does so by local destruction. Chronic exposure to sunlight is a major aetiological factor. There are various forms, the commonest being an ulcerated nodule with raised pearly margins and a telangiectatic surface. Rx: excision (micrographic or conventional), radiotherapy (especially electron beam), cryotherapy, curettage, topical immune modulation, photodynamic therapy, and electrodessication.

of the skin is surprisingly indolent in comparison to SCC of mucosa but beware the external ear which can be aggressive in 40%. Presents as an ulcerated lesion with raised edges. Keratin horns may be present, and it may arise in areas of previously sun-damaged skin or in gravitational leg ulcers. Surgical excision or radiotherapy is Rx of choice.

This condition is being increasingly diagnosed, with a doubling of the incidence in the last 20yrs. The prognosis is dependent primarily on the depth of the tumour (Breslow thickness), as the thicker the lesion the poorer the prognosis. Early metastasis is common. Sunlight is a major aetiological factor, possibly due to burning at early age. Suspect if a pigmented lesion rapidly enlarges, bleeds, ulcerates, shows ‘satellite’ lesions or changes colour. Prompt referral for specialist management is needed. Lots of ‘sun aware’ campaigns emphasize prevention.

Areas of skin containing a disproportionate number of melanocytes.

A freckle.

Premalignant lesions often found in patients with malignant melanoma. They should be excised and patients advised to use high-factor sunscreens.

A premalignant pigmented lesion of the elderly.

Presents as a scaly, red plaque. It is basically a squamous carcinoma which has not yet penetrated beyond the basal layer.

Persistently sun-damaged areas of skin in which cancer may arise.

A purple, vascular, multifocal malignant tumour typically seen in AIDS and other immunocompromised patients. Also seen intraorally.

to the skin occur most frequently from breast, kidney, and lung, but skin secondaries from oral cancer are increasingly being seen.

A common, relapsing proliferative inflammatory skin disease. Appears as a red plaque with silvery scale, chiefly on extensor skin of knees and elbows, although any area can be affected. Can be associated with systemic disease, particularly arthropathy (graphic Diseases of connective tissue, muscle, and joints, p. 522). Rx is mainly topical: steroids, coal tar, dithranol &/or UVB radiation, or psoralen-sensitized UVA radiation (PUVA). Rarely, methotrexate can be used.

Also called dermatitis. Has several variants according to aetiology.

Starts in the 1st year of life with a red symmetrical scaly rash. Emulsifying ointments help prevent fissuring, although steroids are sometimes needed. Up to 90% grow out of it by age 12.

Can be produced in anyone exposed to a sufficient irritant. The hands are the usual target, with blistering, erythema, and cracking of skin.

A genuine allergic response, e.g. to nickel.

A fungal infection mainly affecting the scalp (‘cradle cap’) in neonates.

Fungal infections are particularly common, causing angular cheilitis, athlete’s foot, paronychia, vaginitis, etc. Furuncles are staphylococcal boils. Erysipelas is a streptococcal cellulitis. Viruses cause herpes zoster and simplex infections, molluscum contagiosum, and warts.

of the skin bring a shudder to most people, but they are also a hazard of working closely with patients! Head lice respond to malathion. Flea bites, as well as being unpleasant, can spread plague, among other serious diseases. Scabies is an infestation with a mite which creates a characteristic itchy burrow in the finger webs.

Acne vulgaris is characterized by the blackhead (comedone), and is an inflammatory condition caused by ↑ sebum secretion. Hormone-dependent, although superinfection with the acne bacillus is a contributing factor. Tends to scar. After proprietary lotions, low-dose tetracyclines help. Dianette®, a combined oral contraceptive, is a useful alternative in women. The teratogenic retinoid, isotretinoin, is particularly useful in severe and late onset acne unresponsive to other Rx.

The skin, like the mouth, acts as an outside indicator for many internal diseases.

Painful, red, nodular lumps on the shins.

Circular target lesions.

Vanishing and recurring pink rings. These are all non-specific markers for a variety of diseases.

An autoimmune hypopigmentation, associated with other autoimmune conditions.

Blue-edged ulcers, especially on the legs; associated with ulcerative colitis and Crohn’s disease.

Subcutaneous circular thickening and necrobiosis lipoidica (yellow plaques on the shins) are associated with diabetes.

Vesicular rash of knees, elbows, and scalp. Associated with coeliac disease.

Red swellings above the ankle. Associated with hyperthyroidism.

Skin diseases associated with malignancy are acanthosis nigricans (rough, pigmented, thickened areas of skin in axilla or groin) and thrombophlebitis migrans (tender nodules within blood vessels which move from site to site).

One way of getting to grips with a new subject—and to virtually all dentists psychiatry as opposed to psychology is new—is to categorize. The major adult psychiatric diagnoses are listed in order of severity. This is known as the ‘hierarchy of diagnosis’.

(delirium, toxic confusion) Clouding of consciousness and disorientation in time and place are major symptoms. Mood-swings are common, and visual hallucinations, rare in other psychiatric conditions, can be present.

graphic There is an underlying, frequently treatable cause to this condition (infection, hypoxia, drugs, dehydration, alcohol withdrawal, etc.). Rx: find the cause and correct it, using sedation until the cause is identified and Rx has taken effect.

(dementia) A global intellectual deterioration highlighted by a worsening short-term memory. Never label someone as demented until all other possible causes, including depression, have been excluded. They may require evaluation by a psychiatrist. Alzheimer’s disease and multi-infarct dementia are the commonest causes. There is no cure, although effective support services and psychosocial interventions can improve the quality of life considerably. Anticholinesterase inhibitors, e.g. donepezil, and memantine, may slow the rate of cognitive decline.

See graphic Dentistry for the disabled, p. 46.

Contact with reality is lost and normal mental processes do not function. There is loss of insight. If an organic condition is excluded, the ∆ is one of four.

A disorder where the victims live in an incomprehensible world full of vivid personal significance. First-rank symptoms are a good guide to ∆: delusions, thought insertion, broadcasting and withdrawal, passivity feelings, visual and auditory hallucinations.

Mania, hypomania, manic-depressive psychosis, and depression. Mania and hypomania are characterized by euphoria, hyperactivity, overvalued ideas or grandiose delusions, and pressure of speech. They differ only in degree. Cyclical mania and depression is known as bipolar affective disorder. Rx is with major tranquillizers and prophylaxis with lithium carbonate.

May be either psychotic or neurotic. Markers of major depressive illness are anhedonia (failure to find pleasure in things which once did please), anorexia, especially with weight loss, early morning wakening, tearfulness, inability to concentrate, feelings of guilt and worthlessness, and suicidal ideation.

are psychoses where paranoid symptoms predominate and, despite lack of insight, other diagnoses do not apply.

graphic The commonly abused drugs can all mimic or precipitate psychotic states, as can giving birth—puerperal psychosis.

A neurosis is a maladaptive psychological symptom in the absence of organic or psychotic causes of the symptom and after exclusion of a psychopathic personality. Insight is present.

frequently coexists with depression. These patients often have physical symptoms for which there is no physical explanation.

Intrusive thoughts or ideas which the subject recognizes as coming from within themselves, but resents and is unable to stop. May be associated with compulsive behaviour where repeated purposeless activity is carried out due to an inexplicable feeling that it must be done.

is the generation of fear or anxiety out of proportion to the stimulus. Numerous stimuli exist, including dentists.

The development of weight reduction as an overvalued idea. Associated with weight ↓ of >25% of ideal body weight and obsessive food avoidance. Commonest in females, it is also associated with amenorrhea. Has a significant mortality rate; binge-eating followed by vomiting &/or laxative abuse can occur. Bingeing without weight loss is bulimia nervosa. Dental effects graphic Erosion, p. 244.

These are not illnesses but extremes of normal personality traits, e.g. obsessional, histrionic, schizoid (cold, introspective), borderline (black-and-white thinking). The most important is the psychopathic (sociopathic) individual who has no concept of affection, shame, or guilt, and is characterized by antisocial behaviour. They are often superficially personable, highly manipulative, and totally irresponsible. They have insight and are responsible for their own actions (bad not mad).

These are a group of individuals who present special problems because of defects in, or suppression of, their immune system. The condition with the highest profile among these is AIDS.

The chief effect of being immunocompromised is an ↑ susceptibility to infection, often due to opportunistic organisms. Anything which changes the host environment in favour of opportunistic pathogens (e.g. surgery, broad-spectrum antibiotics) can lead to potentially fatal infection with rare or otherwise innocuous organisms.

which suppress the immune response: corticosteroids, ciclosporin, azathioprine, cytotoxics, etc., are now in common use therapeutically. Cross-infection graphic Prevention of cross-infection, p. 744. Aggressive Rx of infections and antimicrobial prophylaxis are needed graphic Principles of antibiotic prophylaxis, p. 566.

There are at least 18 of these. The commonest is selective IgA deficiency, which affects ~1:600; it has a wide spectrum of severity but may remain asymptomatic.

e.g. SLE, rheumatoid arthritis, carry a minor ↑ risk of infection.

(graphic Chronic kidney disease (formerly chronic renal failure), p. 516.) Moderately ↑ risk.

e.g. anaemia. Carry a minor ↑ risk.

is common and carries a moderate ↑ risk of infection.

Severe viral infections, TB, AIDS (specific defect).

All haematological malignancies severely ↑ risk of infection.

Caused by infection with human immunodeficiency virus (HIV). CD4 T-lymphocyte defect ensues with failure of (mostly) cell-mediated immunity. HIV antibody useful as a marker of infectivity but absence does not guarantee no infection. Infection causes short flu-like illness, then variable latent period while CD4 cells ↓ in number. Full-blown AIDS develops when CD4 levels fall critically low. Infections characteristic of AIDS are Pneumocystis jirovecii pneumonia and disseminated mycobacterial infection. Kaposi’s sarcoma is the tumour most often associated with the condition. The mode of transmission, for those visiting from another planet, is essentially, exchange of bodily fluids: unprotected sex, as a recipient of contaminated blood or blood products, or mother to fetus transmission. Treatment is with highly active antiretroviral therapy (HAART) and measures to prevent opportunistic infections. Oral manifestations of AIDS graphic Oral manifestations of HIV infection and AIDS, p. 452. Practical procedures for control of cross-infection graphic Prevention of cross-infection, p. 744.

depends on estimation of the likely HIV exposure risk. Triple therapy guidelines in the US. Local implementation via genito-urinary consultant in UK.

Every practice should possess portable apparatus for delivering high-flow O2. In addition, the facility to deliver nitrous oxide and O2 mixture, e.g. via an anaesthetic or relative analgesia machine, can be invaluable.

The following should be readily available:2

Automated external defibrillator.

Basic set of oro-pharyngeal airways, with a self-inflating bag and mask system, e.g. ambu-bag.

Non-rebreathing oxygen mask with tubing.

Pocket mask with oxygen port.

Portable high-vacuum suction.

‘Spacer’ device for inhaled bronchodilators.

Automated blood glucose measuring device.

Disposable syringes (2, 5, and 10mL), needles (19 and 21G), and a tourniquet. Butterfly needles and IV cannulae are great assets to those familiar with their use.

Alcohol wipes.

Adrenaline, 1:1000 solution (1mg adrenaline in 1mL saline). Auto-injectors (0.3mg) often held by high-risk patients. Salbutamol aerosol inhaler (100 micrograms/actuation).

Midazolam 10mg buccal.

Oral glucose solution/tablets/gel/powder.

Flumazenil 100 micrograms/mL 5mL ampoule (only if providing IV sedation).

Glucagon 1mg IM injection.

Aspirin dispersible (300mg).

Glyceryl trinitrate (GTN) spray (400 micrograms/dose).

This list of drugs really is a minimum for any professional performing invasive Rx. Ideally, all public areas, let alone dental practices, should have access to an automated external defibrillator as this is the most valuable single piece of equipment in a cardiac arrest (graphic Cardiorespiratory arrest, p. 538). All drugs should be in pre-filled syringes where possible. In hospital, check your ‘crash cart’ and be amazed at its contents.

graphic If you buy something learn how to use it!

Fainting (vaso-vagal syncope) is innocuous providing it is recognized. It is easily the most common cause of sudden loss of consciousness, with up to 2% of patients fainting before or during dental Rx. The possibility of vaso-vagal syncope while under GA, and hence failure to recognize the condition and correct cerebral hypoxia, is the major reason for recommending the supine position.

Predisposing factors are: pain, anxiety, fatigue, relative hyperthermia, and fasting. Characteristic signs and symptoms are: a feeling of dizziness and nausea; pale, cold, and clammy skin; a slow, thin, thready pulse which rebounds to become rapid; and loss of consciousness with collapse, if unsupported.

A faint may mimic far more serious conditions, most of which can be excluded by a familiarity with the patient’s PMH. These include strokes, corticosteroid insufficiency, drug reactions and interactions, epileptic fit, heart block, hypoglycaemia, and MI.

Avoid predisposing factors.

Treat patients in the supine position unless specifically contraindicated (e.g. heart failure, pulmonary oedema).

Lower the head to the level of, or below, the heart. Best achieved by laying the patient flat with legs slightly elevated.

Loosen clothing (in the presence of a witness!).

Monitor pulse. If recovery does not occur rapidly, then reconsider the ∆.

Determine the precipitant and avoid in the future.

If bradycardia persists with no evidence of recovery to rapid full pulse, try tiny dose of atropine (100 micrograms IV). Dose may be repeated up to 600 micrograms.

Severe, acute chest pain is usually the result of ischaemia of the myocardium. The principal differential ∆ is between stable angina and an acute coronary syndrome/myocardial infarction. Both exhibit severe retrosternal pain described as heavy, crushing, or band-like. It is classically preceded by effort, emotion, or excitement, and may radiate to the arms, neck, jaw, and, occasionally, the back or abdomen. Angina is usually rapidly relieved by rest and glyceryl trinitrate (0.5mg) given sublingually, or GTN spray (400 micrograms per spray), which most patients with a history of angina carry with them.

Failure of these methods to relieve the pain, and coexisting sweating, breathlessness, nausea, vomiting, or loss of consciousness with a weak or irregular pulse, suggest an infarct.

Management depends on your immediate environment, but always ensure the patient is placed in a supported upright position if conscious, as the supine position increases pulmonary oedema and hence breathlessness.

Summon help (ambulance). Administer analgesia; the most appropriate form available here will be nitrous oxide/O2 mixture (50% O2). Don’t panic. Be prepared should cardiac arrest supervene. Give aspirin 300mg PO. Tell ambulance staff what you have done.

Nurse upright. Give O2. Establish IV access and give an opioid analgesic if available (2.5–5mg of diamorphine is most useful). Get ECG, U&Es. Summon help; in units integrated into general or teaching hospitals this may best be achieved by contacting the medical on-call team via the switchboard urgently, as thrombolysis or primary endovascular intervention, if appropriate, improve outcome.

graphic Don’t await ‘expertise’. ACT.

Ninety per cent of deaths from cardiac arrest occurring outside hospital are due to ventricular fibrillation (VF). This is also the commonest arrest pattern seen in hospital. It is potentially reversible by prompt (<90sec) defibrillation. The commonest underlying cause is ischaemic heart disease, but other causes may exist, especially in younger people. Acute asthma, anaesthesia, drug overdose, electrocution, immersion, or hypothermia often precipitate pulseless electrical activity (PEA) arrests. These are treatable conditions and potentially reversible.

In certain instances properly performed cardiopulmonary resuscitation (CPR) can sustain life for up to an hour while a precipitating condition is being treated.

These proceed simultaneously (see Fig. 12.1).

 Adult basic life support. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (  http://www.resus.org.uk).
Fig. 12.1

Adult basic life support. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (graphic  http://www.resus.org.uk).

Protect yourself! Do not become another casualty, whether in the street, practice, or hospital environment. Gently ‘shake and shout’ to assess the person’s level of consciousness. If there is no response, shout for help (and ask whoever goes for help to come back to tell you if help is coming). Then:

In witnessed and monitored arrests a single sharp blow over the heart (precordial thump) is worthwhile.

Airway—carry out a chin lift or jaw thrust, and clear oropharynx. Remove loose dentures, but retain if they are well fitting (it gives a better mouth seal).

Breathing—look, listen, and feel for breathing for no more than 10sec (if hypothermia suspected, up to 1min). If the person is breathing normally, place in recovery position. If not, get help even if this means leaving the patient yourself to do it.

Commence chest compressions, at the middle of the lower half of the sternum, delivering 30 compressions in the first instance, before providing 2 rescue breaths.

Remember, statistically the patient’s best chance at survival once absence of breathing is confirmed is defibrillation, therefore getting early help may be the most useful thing you can do. Children and victims of trauma or drowning are exceptions and may benefit from 1min of resuscitation before you leave to get help.

CPR, single and two rescuers: 30 compressions to 2 ventilations.

Aim for 100–120 compressions/min.

For those working in an environment where facilities for advanced life support (defibrillation, intubation/ventilation) exist, the 2010 UK Resuscitation Council/ILCoR Guidelines are reproduced in Fig. 12.2 and Fig. 12.3.

 Algorithm for advanced cardiac life support. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (  http://www.resus.org.uk).
Fig. 12.2

Algorithm for advanced cardiac life support. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (graphic  http://www.resus.org.uk).

 Algorithm for automated external defibrillation. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (  http://www.resus.org.uk).
Fig. 12.3

Algorithm for automated external defibrillation. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (graphic  http://www.resus.org.uk).

Penicillins are the commonest offender, but it is worth remembering that there is a 10% cross-over in allergic response between penicillins and cephalosporins.

An anaphylactic reaction is not an all-or-nothing response, and grades of severity are seen. Generally, the reaction starts a few minutes after a parenteral injection, and not immediately as does a simple faint. Some caution should be exercised, though, as the quicker the onset of an anaphylactic reaction the more severe it is likely to be. Some patients with known severe allergic reactions/previous anaphylaxis will carry an auto-injector (0.3mg adrenaline) to self-administer at the first sign of symptoms.

Principal symptoms are facial flushing, itching, numbness, cold extremities, nausea, and sometimes abdominal pain. Signs include wheezing, facial swelling and rash, and cold clammy skin with a thin thready pulse. Loss of consciousness may occur, with extreme pallor which progresses to cyanosis as respiratory failure develops.

It can be difficult to distinguish anaphylaxis from acute asthma in, e.g. an asthmatic given an NSAID they are allergic to. Don’t panic, just go through management for acute asthma, then start on management for anaphylaxis (Fig. 12.4). Adrenaline is a bronchodilator anyway. Befriend this drug!

 Treatment for anaphylaxis algorithm. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (  http://www.resus.org.uk).
Fig. 12.4

Treatment for anaphylaxis algorithm. Reproduced from UK Resuscitation Council 2010 Guidelines, with permission (graphic  http://www.resus.org.uk).

is sudden onset, with severe face and neck allergic swelling. The airway is at risk and therefore should be managed as for anaphylaxis.

Place patient supine with legs raised, if possible.

Check ABCDE (Airway, Breathing, Circulation, Disability + Expose) and administer O2 (15 litres/min).

0.5mL of 1:1000 adrenaline IM. Repeat after 5 min, then every 5min until improved. Do not give IV—this concentration will induce ventricular fibrillation.

If in practice, an ambulance should be called and the patient transferred to hospital, where the following may be carried out:

Fluid challenge—500–1000mL rapidly—the type of fluid isn’t important, just plenty and fast.

200mg of hydrocortisone IV.

10mg of chlorphenamine slowly IV (if available).

O2 by mask.

Salbutamol 0.5mg/mL (1mL) as IM or SC injection in patients on non-cardioselective beta-blockers if no response to adrenaline.

While there are a multitude of drug interactions which the dental surgeon should be aware of as a prescriber, the drugs most liable to present an emergency problem to the dentist are those which we administer as LAs.

Although it is possible to achieve toxic levels of lidocaine, adrenaline, prilocaine, or felypressin without intravascular injection, this generally requires a particularly cavalier attitude to the administration of LA. Commonly, this effect is due to intravascular injection of a substantial proportion of a cartridge of LA. Confusion, peri-oral tingling, drowsiness, agitation, fits, or loss of consciousness may occur. Do not use more than 10 × 2.2mL cartridges of lidocaine/adrenaline (440mg lidocaine). In practice, you will rarely consider coming near this amount.

Stop procedure! (They won’t be numb.)

Place supine.

Maintain airway, give O2.

Await spontaneous recovery (in ~30min) unless tragically a serious event such as MI supervenes, in which case treat as indicated.

The use of corticosteroids therapeutically or otherwise for whatever cause may suppress the adrenal response to stress. The longer the course of Rx and the higher the dose used the more likely this is to occur. It is almost certain that a large number of people have unnecessary ‘prophylaxis’ with hydrocortisone and many would now argue that without evidence (short synacthen test) of adrenocortical insufficiency it is unnecessary. However, we take the view that you are less likely to cause harm by a brief supplementation of steroid than you are by ignoring the potential problem because it happens to be rare in reality.

It is worth remembering that virtually all serious steroid unwanted effects are from chronic usage (acute steroid-induced psychosis being the exception—a risk from the high-dose orthognathic regimens).

The prime aim is to prevent the occurrence of stress-induced collapse; therefore, if patients have received steroids in the past year or are on steroids at present, cover any stressful procedure, anaesthetic, infection, or episode of trauma with 25–50mg hydrocortisone IM (IV if under GA) 30min prior to elective stress. Seriously ill patients require IV qds doses covering the period of admission. It is a fallacy to believe you are ↓ risk of steroid unwanted effects by trying to avoid giving prophylactic steroids. Doubling the oral dose may work but is rather hit and miss. Calculating an ‘exact’ dose is unnecessarily complicated and risks people ‘forgetting’. Stick to sticking them with 25–50mg hydrocortisone IM unless you have a very valid reason to change.

In patients presenting acutely, treat immediately. If collapse occurs in such a patient, ∆ is established by pallor, rapid, thin pulse with a profound and sudden ↓ in BP, and loss of consciousness.

Place in supine position. Maintain airway. Give O2. Obtain IV access.

200mg hydrocortisone IV immediately.

Ensure help (i.e. an ambulance) is requested.

Exclude other causes of collapse.

The majority of epileptic fits do not require active intervention as the patient will usually recover spontaneously. All that is needed is sensible positioning to prevent the patient from damaging himself. Fits may be precipitated in a known epileptic by starvation, flickering lights, certain drugs such as methohexitone, tricyclics, alcohol, or menstruation. They may also follow a deep faint.

Many epileptics have a preceding aura followed by sudden loss of consciousness with a rigid extended appearance and generalized jerking movements. Frequently, they are incontinent of urine and may bite their tongue. There is a slow recovery with the patient feeling sleepy and dazed. There may be a cause for the fitting: trauma, tumour, and alcohol withdrawal are common. There are numerous others, any adult should have a first fit fully investigated by a neurologist.

graphic Should the fitting be repeated or last >5min, the patient has entered the state of status epilepticus. This is an emergency and requires urgent control.

Get help. In a simple major fit the patient should be placed in the recovery position when practicable and allowed to recover. If they enter status epilepticus, 10mg midazolam IV/buccal/nasal usually aborts the fit; beware respiratory depression. Assess cardiorespiratory function; clear and maintain airway, and give O2 if available. It is worthwhile considering placing an IV cannula or a butterfly in any epileptic patient with less than perfect control, as stress is an important precipitant. Status epilepticus should not be allowed to continue for more than 20min as the mortality rate (up to 30%) and chance of permanent brain damage ↑ with the length of attack.

Get help. After giving IV benzodiazepines (lorazepam 4mg, midazolam or 10mg diazepam as emulsion 10–20mg) and maintaining an airway, give an IV bolus of up to 50mL of 20–50% glucose unless certain blood glucose (BM stick) is >5mmol/L. Establish a 0.9% saline infusion and repeat the benzodiazepines if necessary. If the fits are not controlled it may be necessary to use a phenytoin infusion or induce anaesthesia with thiopental, an intravenous barbiturate, paralyse, and ventilate.

Hypoglycaemia is the diabetic emergency most likely to present to the dentist. It is an acute and dangerous complication of diabetes and may result from a missed meal, excess insulin, or ↑ calorific need due to exercise or stress. Most diabetics are expert in detecting the onset of hypoglycaemia themselves; however, a small number may lose this ability, particularly if changed to a new form of insulin. Recognition of this state is essential and an acutely collapsed diabetic should be assumed hypoglycaemic until proven otherwise, e.g. by ‘BM’ sticks or blood-glucose levels.

Disorientation, irritability, increasing drowsiness, excitability, or aggression in a known diabetic, suggest hypoglycaemia. They often appear to be drunk.

If conscious, give glucose orally in any available form. Repeat if necessary every 10–15min. Get help.

If impaired consciousness, give buccal glucose gel and/or1mg of IM glucagon.

If unconscious, protect airway, place in recovery position. If the correct kit is available, establish IV access and give up to 50mL of 20–50% glucose.

An acute asthmatic attack may be induced in a patient predisposed to bronchospasm by exposure to an allergen, infection, cold, exercise, or anxiety. Characteristically, the patient will complain of a tight chest and shortness of breath. Examination will reveal breathlessness, with widespread expiratory wheezing. The accessory muscles of respiration may be used to support breathing. If the patient is unable to talk, you are dealing with a potentially fatal episode.

Make use of the patient’s own anti-asthmatic drugs, such as salbutamol inhalers. Ideally, this should be administered in the form of a nebulizer using 24% O2 and nebulized salbutamol. A do-it-yourself nebulizer can be fabricated from the patient’s own inhaler pushed through the base of a paper cup. Repeated depressions of inhaler plunger will create an aerosol inside the cup which the patient can inhale. This will relieve most reversible airways obstruction. Steroids should be administered either as oral prednisolone, if the patient carries these with them, or as IV hydrocortisone up to 200mg IV, if available. This combination of salbutamol, steroids, and O2 will often completely resolve an attack; however, in individuals who do not respond, an urgent hospital admission is required. Patients who are only partially responsive must have underlying irritants such as a chest infection either excluded or treated.

graphic Be aware of the possibility of anaphylaxis mimicking acute asthma. Remember adrenaline 0.5mL 1:1000 IM.

Keep the patient upright.

Administer salbutamol by inhaler and a spacer device. Repeat every 10min until resolved (or ambulance arrives).

Give O2.

If a complete response takes place it is reasonable to allow the patient to return home. If there is any doubt, arrange for the patient to be seen at the nearest emergency department.

Nurse patient upright.

Give nebulized salbutamol 5mg (with O2) at 15–30min intervals, continuously if necessary.

Give nebulized ipratropium 500 micrograms (with O2).

Establish IV access and give up to 200mg hydrocortisone IV or prednisolone 40mg PO.

Monitor peak expiratory flow, arterial blood gases, and pulse oximetry.

Obtain a CXR; exclude infection, pneumothorax.

If incomplete response, obtain expert help rather than embarking on alternative Rx such as aminophylline.

The combination of delicate instruments and the supine position of patients for many dental procedures inevitably ↑ the risk of a patient inhaling a FB. Patients with facial trauma often have missing teeth—always think where could they be? Two basic scenarios are likely, depending on whether or not the item impacts in the upper or lower airway.

This will stimulate the cough reflex, which may be sufficient to clear the obstruction. A choking subject should be bent forward to aid coughing. If the obstruction is complete or there are signs of cyanosis in:

Conscious patient—support chest with one hand, strike between the scapulae with the heel of your other hand. Repeat up to 5 times if needed. If this fails carry out abdominal thrusts (Heimlich manoeuvre) by encircling victim with your arms from behind and deliver sharp upward and inward squeeze to create sudden expulsion of air. Repeat up to 5 times. Alternate 5 back blows with the 5 abdominal thrusts. First attempt is most likely to succeed and they may vomit.

Unconscious patient—CPR should be commenced; this will provide circulatory support as well as help dislodge the FB.3

If all else fails cricothyroid puncture may preserve life if the obstruction lies above this level.

As only a segment of the lungs will be occluded this presents a less acute problem. It is also easier to miss. Classically, this involves a tooth or tooth fragment slipping from the forceps and being inhaled. With the patient in a semi-upright position the object ends up in the right posterior basal lobe. Should this happen, inform the patient and arrange to have a CXR taken ASAP. If the offending item is in the lungs (Fig. 12.5), removal by a chest physician by fibre-optic bronchoscopy is indicated, as failure to remove the tooth is inevitably followed by collapse and infection distal to the obstruction. Rarely, lobectomy may be needed.

 When a lost tooth cannot be located it must be searched for, ingestion is not a real problem but inhaled teeth must be removed.
Fig. 12.5

When a lost tooth cannot be located it must be searched for, ingestion is not a real problem but inhaled teeth must be removed.

When presented with a suddenly collapsed patient the first thing to assess is your own response. Don’t panic.4 You are only of value to the patient if you can function rationally. Always instigate a call for help—we are all useless without it. If presented with a case of sudden loss of consciousness, in the absence of an obvious ∆, the following steps should be followed.

Maintain the airway and provide O2 if available.

Place in supine position. If the patient has simply fainted they will recover virtually immediately.

Are they breathing? If not then get help before starting CPR (graphic Cardiorespiratory arrest, p. 538). If they are breathing normally:

If in dental practice, give glucagon 1mg IM.

If in hospital, establish IV access and give up to 20mL 20–50% glucose IV.

Give hydrocortisone up to 200mg IV.

If unable to get access, use glucagon 1mg IM.

These measures will usually resolve most cases of sudden, non-traumatic loss of consciousness.

If the patient is acutely distressed and breathless they should be treated in an upright position and given O2 while you try to differentiate between an acute asthmatic attack, anaphylaxis, and heart failure, and treat as indicated.

Always ensure that someone has requested assistance in the form of an ambulance or, if in hospital, that the appropriate staff have been contacted. If at all possible, try to speak to the receiving doctor yourself.

Immediately after resolution of an emergency there tends to be a period of numb inactivity amongst the staff involved. Use this period to review your management of the situation and carefully document what happened. If the patient has been transferred to hospital or another department a brief, legible account of proceedings must accompany them. Include drugs used, their dosages, and when they were given. Try to ensure that a friend or relation of the patient is aware of the situation.

The vast majority of in-patients will experience considerable anxiety on being admitted for operation, including about those procedures which are in themselves ‘routine’. In addition, as dentists have little training in medical clerking and ward work, there is a substantial risk of compounding an already stressful situation by being overly stressed yourself. Minimize this by preparation. Learn about the ward(s) you will work on before taking up a post. Never be afraid to ask nursing staff if you are unsure, and try to know a day in advance what cases are coming in.

All patients attending as in-patients for operation must (i) be examined and ‘clerked’, and (ii) have consented to surgery. In addition, many will require a variety of pre-op investigations; these vary widely from consultant to consultant, so get to know the local variations. Common investigations and their indications are listed in the following paragraphs. Sampling techniques graphic For sampling, p. 556; samples graphic Investigations—general, p. 12.

This basically consists of taking a complete medical and dental history from the patient, including any drugs they are taking at present (which you must remember to continue while in hospital by writing up in the drug ‘kardex’), a family history for inherited disease, and a social history for problems related to smoking, alcohol, drug abuse, and ability to cope at home post-op. This is followed by a systematic clinical examination (graphic Medical examination, p. 8). Any special investigations are then arranged, and the results of these should be seen before the patient goes to theatre. Any problems uncovered should be relayed to the anaesthetist, who is the only person capable of saying whether or not the patient is ‘fit for anaesthesia’. Any required pre-, peri-, or post-op drugs are written up graphic Prescribing, p. 576.

All patients undergoing GA or sedation must give written, informed consent. It is advised that patients receiving interventions under LA also do so. Every hospital has its own surgical consent form which you complete. After having the procedure and its likely potential risks explained, the patient also signs. It is essential that you are happy in your own mind that you understand what the operation entails, current UK regulations suggest the surgeon who will operate or someone who is capable of doing the operation should take the consent. Obtain consent only for procedures with which you are familiar.

(See graphic Investigations—general, p. 12.)

Elderly patients. Any suspicion of anaemia.

All Afro-Caribbeans for GA. Consider also those of Mediterranean, Arabic, or Indian origin. There may be a local policy but usually not. Ask your anaesthetist.

All patients needing IV fluids, on diuretics, diabetics, or with renal disease. Have a low threshold for doing this test.

All major surgery, any past history of bleeding disorders, liver disease, or history of ↑ alcohol, anticoagulants.

Liver disease, alcohol, major surgery.

Major surgery, trauma, shock, anaemia.

all major surgery, most patients >50.

active chest disease, possible metastases.

and HIV markers Varies; usually at-risk groups only; pretest counselling now considered mandatory. Check local hospital policy.

Immediately post-op, patients are resuscitated in a recovery room adjacent to theatre, with a nurse monitoring cardiorespiratory function. Once recovered, unless they are to be monitored in the ICU/HDU they will be returned to the ward. In all patients, ensure a patent airway and consider:

may take the form of LA (should be given post-anaesthetic/pre-surgery), oral or parenteral NSAIDs, or oral or parenteral opioids. Immediately post-op, analgesia is best given parenterally. Antiemetics such as cyclizine 50mg oral, IM, or IV, or ondansetron 4mg IM or IV should be given if nausea or vomiting is present. Many anaesthetists consider this their responsibility—ask.

are given in accordance with the selected regimen (graphic Principles of antibiotic prophylaxis, p. 566). Certain patients may benefit from corticosteroids pre- and post-op to ↓ oedema; regimens vary.

is a problem principally for patients undergoing major head and neck cancer surgery (graphic Oral cancer, p. 494), who should have had a dietetic assessment pre-op and a decision made about postop feeding (NGT, gastrostomy) but it is worthwhile reminding nursing staff to order soft diets for all oral surgery patients who can feed by mouth and to have liquidizers available for patients in IMF.

is covered in graphic Intravenous fluids, p. 557.

Special consideration needs to be given to patients in IMF and those with tracheostomies. Immediate post-op rigid IMF is now rare however post-op elastic IMF is common. These patients need to be specially attended by a nurse looking after that patient only, for the first 12–24h (‘specialed’). Lighting, suction, and the ability to place the patient head-down if they vomit, is mandatory. Other techniques include tongue suture, prolonged retention of a nasopharyngeal airway, elective prolonged intubation, and tracheostomy. Avoiding this situation, see graphic Treatment of facial fractures, p. 476. Tracheostomy is a great aid to secure airway management, but enormously inconvenient for patients and has its own complications. If indicated it is essential to care for the tube by suction and humidification to ensure patency.

To become proficient in the skills of venepuncture you must practise the art in all its forms. To develop the skill of placing IV cannulae, cultivate a sympathetic anaesthetist, as anaesthetized patients are venodilated and will not feel pain! When carrying out cannulations and arterial punctures on patients in the ward, a drop or two of 2% plain lignocaine deposited SC with a fine needle will aid both your peace of mind and the patient’s comfort. While most hospitals have phlebotomy services you will be asked to get blood and cannulate out of hours and when the phlebotomists fail so learn as soon as you can.

Tourniquet, alcohol wipes, cotton wool. Green (21G) needles and butterflies are commonly used. Many hospitals have adopted sealed ‘vacutainer’ systems which are convenient but fiddly to use. Learn the basics first, then your hospital’s system. Sometimes finer needles or butterflies are needed, e.g. blue (23G). Many hospitals now have sealed sterile ‘cannulation packs’ for bedside use. Patients who are difficult to cannulate can have fluids and certain drugs through fine (20G) or even 22G IV cannulae; most have 18G. Shocked patients or those needing blood should have at least a 16G and preferably a 14G cannula inserted. Note that gauges and colours are not consistent between needles and cannulae.

First choice is the cubital fossa. Inspect and palpate; veins you can feel are better than those you can only see. Insert the needle at a 30–40° angle to the skin and along the line of the vein. If no veins are found in the cubital fossa try the back of the hand with a butterfly and use a similar approach. The veins of the dorsum of the foot are a last resort before the femoral vein lying just medial to the femoral artery in the groin.

Single-bolus injections; use a 21G butterfly in a vein on the back of the hand.

For IV fluids or multiple IV injections place a 18G IV cannula in a straight segment of vein in the forearm, hand, or just proximal to ‘anatomical snuffbox’. Try to avoid crossing a joint as the cannula tissues more quickly if subjected to repeated movements. When inserting the cannula ensure the skin overlying the vein is fixed by finger pressure; pierce the skin, and move the stilette along the line of the vein until it enters the vein and blood flows into the cannula. As soon as you enter the vein, pull the stilette back into the cannula to minimize the risk of going through the vein. Insert the full length of the cannula into the vein and secure. Keep patent with saline flush.

Whenever possible, obtain an arterial sampling syringe. Use LA unless patient anaesthetized. The syringe and needle must be flushed with heparin. Use radial, brachial, or femoral arteries. Palpate, prepare area with alcohol wipe, and insert needle at 30–60° to skin. When the needle enters the artery, blood pulsates into the syringe. Only 1–2mL are needed. All ITUs have a blood gas analyser and some other areas of your hospital will have one too, find out where it is and how to use it. If not the specimen goes in a chilled bag to the biochemist. The puncture site needs to be firmly pressed on for 2–3min to prevent formation of a painful haematoma.

The maintenance of daily fluid requirements plus replacement of any abnormal loss by infusion of (usually) isotonic solutions. Normal requirements are ~2.5–3L in 24h. This is lost via urine (normal renal function needs an absolute minimum of 30mL/h, but aim for 60mL/h), faecal loss, and sweating. Where possible replace with oral fluids; IV fluids are a second best.

1L normal saline (0.9%) and 2L 5% glucose in 24h (‘2 sweet and 1 salty’). Add 20mmol potassium chloride per litre after 36h, unless U&Es suggest otherwise. Hartmann’s solution/Plasma-Lyte 148 are more expensive but the most physiological crystalloids. Increase these in the presence of abnormal losses, burns, fever, dehydration, polyuria, and in the event of haemorrhage or shock.

For burns, start with Hartmann’s and be guided by the Burns Centre.

For fever, use saline.

For dehydration or polyuria, use 5% glucose, unless hyponatraemic. Exception is ketoacidosis: use saline.

Haemorrhage demands replacement whole blood if available (rarely is); packed cells are what you will be offered in most hospitals in most countries. Shock needs, crystalloid challenge (not 5% glucose—use saline/Hartmann’s), blood and control of haemorrhage. Be guided by the pulse, BP, urine output, haemoglobin, the haematocrit, and the U&Es.

↓ fluid load in heart failure, and avoid saline. Shock and dehydration are rare complications of maxillofacial trauma or any other condition principally presenting to the dentist; therefore in their presence consider damage to other body systems and seek appropriate advice.

Post-op, is usually due to over-transfusion. Review anaesthetic notes, and if this is the case simply catheterize and observe.

Post-op, is usually due to under-transfusion or dehydration pre- or peri-operatively. First, palpate abdomen for ↑ bladder and listen to chest to exclude pulmonary oedema. Then catheterize the patient to exclude urinary retention and allow close monitoring of fluid balance. Then ↑ rate of infusion of fluid (max 1L/h) unless the patient is in heart failure or bleeding. The former needs specialist advice, the latter needs blood or an operation. In an otherwise healthy post-op patient, if this does not produce a minimum of 30mL/h of urine, a diuretic (20–40mg furosemide PO/IV) may be tried. Take care when using fluid challenges, as if failure to PU is renal it is possible to fluid overload the patient quickly. Review the fluid balance, U&Es, over several days for an overview.

graphic Group and save—you won’t get blood; group and cross-match—you will get blood in ~1h; type specific group—you will get blood urgently.

Blood may be required for patients in an acute (e.g. traumatized) situation, electively (e.g. peri-operatively) during major surgery, or to correct a chronic anaemia (graphic Anaemia, p. 504). In practice, the former two are much more commonly encountered by junior dental staff.

is indicated in patients who have lost >20% blood volume, exhibit signs of hypovolaemic shock, or in whom this appears inevitable.

graphic Remember maxillofacial injuries alone only rarely result in this degree of blood loss (graphic Bleeding, p. 466).

Always take blood for grouping in severely traumatized patients, and proceed to cross-match as indicated by the clinical signs. Always use cross-matched blood, except in utter extremis when O rhesus –ve blood can be used. Massive transfusions create problems with hyperkalaemia, thrombocytopenia, and low levels of clotting factors; therefore in patients with severe haemorrhage, simultaneous fresh frozen plasma (4–6 units) and platelets (6 units) will be needed. Most labs only provide packed cells.

is blood donated by a patient prior to elective surgery for use only on themselves. It avoids risks of cross-infection but requires a specially interested haematology department, so check locally. Autotransfusion is sometimes used in vascular surgery.

are used for the correction of anaemia if too severe for correction with iron, or if needed prior to urgent surgery. This ↓ the fluid load to the patient, but elderly individuals and those in heart failure should have their transfusion covered with a small dose of furosemide PO or IV.

Cross-match one patient at a time and be sure you are familiar with local procedures.

Nurse will perform regular observations of temperature, pulse, respiration, and urine output during transfusion—look at them!

Don’t use a giving set which has contained dextrose, as the blood will clog.

Except in shock, transfuse slowly (1 unit over 2–4h; >4h the cannulae start to clog).

1 unit of blood raises the Hb by 1g/dL = 3% haematocrit.

ABO incompatibility. Causes anaphylaxis; manage accordingly (graphic Anaphylactic shock and other drug reactions, p. 542).

Cross-infection.

Heart failure can be induced by over-rapid transfusion.

Milder allergic transfusion reactions are the commonest problem; Rx by slowing the transfusion. If progressive or temperature >40°C stop transfusion and inform lab to check cross-matching. IV hydrocortisone 100mg and chlorphenamine 10mg are useful standbys.

Citrate toxicity is a hazard of very large transfusions and can be countered by 10mL of calcium gluconate with alternate units.

Learning Point:

Summary of your first attempts at venepuncture—what went right and what could be better

Your own hospital will have a protocol

This is not a topic normally covered by the dental syllabus, but the dental graduate may find him- or herself confronted with a patient needing urethral catheterization if working on an oral and maxillofacial surgical ward. The only procedure they are likely to need to be able to perform is temporary urethral catheterization. This is indicated for urinary retention (almost always post-op), for precise measurement of fluid balance, or, rarely, to avoid use of bedpan or bottle. Avoid catheterization if a history of pelvic trauma is present, as an expert is needed. Catheters are associated with a high incidence of UTIs, and presence of a UTI is a relative C/I.

Most wards have their own; ask for it and ensure you have an assistant available. It should contain a tube of local anaesthetic gel, a dish with some aqueous chlorhexidine, swabs, a waterproof sheet with a hole in the middle, sterile gloves, a 10-mL syringe filled with sterile water, and a drainage bag. In most cases a 14–16 French gauge Foley catheter will suffice. Use a silicone catheter if you anticipate it being in situ for more than a few days.

Explain what you are going to do and why. If catheterizing for post-op fluid balance, do it in the anaesthetic room after intubation (ask the anaesthetist first!). The operating theatre is the best place to learn. The procedure can be made both aseptic and aesthetic by wearing two pairs of disposable gloves; one pair is discarded after achieving analgesia, which is done by instillation of lidocaine gel (also acts as a lubricant). Find the urethral opening and, using the nozzle supplied, squeeze in the contents of the tube. In the female, finding the opening is the only significant problem and most women are catheterized by female nursing staff. In the male, it is necessary to massage the gel along the length of the penis and leave in situ for several minutes before progressing. Once analgesia is obtained, the female urethra is easily catheterized; if you have been unable to find the meatus to instil LA you should not proceed but get help. In the male, hold the penis upright and insert the tip of the catheter; pass it gently down the urethra until it reaches the penoscrotal junction, pull the penis down so that it lies between the patient’s thighs, thereby straightening out the curves of the urethra, and advance the tip into the bladder until urine flows.

Once urine flows, the catheter balloon can be inflated with sterile water. In the conscious patient it should be painless; if not, deflate the balloon and reposition the catheter. In the anaesthetized patient, insert the catheter all the way, inflate, then pull back. Connect the drainage bag and remember to replace the foreskin over the glans to avoid a paraphimosis.

graphic If, in the presence of adequate analgesia, you are unable to pass the catheter do not persist, but get expert assistance.

Learning Point:

Try reflecting on how your first catheterization went, write it down

The main role for this type of feeding, as far as dental staff are concerned, is in the care of debilitated patients and those undergoing surgery for head and neck cancers. In view of the latter, it is worthwhile having a basic understanding of the subject.

is providing liquid, low-residue foods either by mouth, fine-bore nasogastric tube, or gastrostomy. A range of proprietary products are available for these feeds. Be guided by the local dietitian, who has expertise in this area which you will lack. The major problem is osmotic diarrhoea, which can be ↓ by starting with dilute solutions.

are the mainstay in enteral nutrition for patients undergoing major oropharyngeal surgery. In many institutions, nurses are not allowed to pass these tubes, although they are allowed to pass standard nasogastric tubes for aspirating stomach contents. You can therefore find yourself asked to pass such a tube by someone who is more proficient but forbidden to do so. Gastrostomy tubes are placed by the relevant specialists (and have higher complication rates).

Wear gloves. Explain the procedure to the patient and have them at 50–60° upright with neck in neutral position. Place a small amount of lidocaine gel in the chosen nostril after ensuring it is patent. Keep a small drink of water handy. Select a tube; check the guidewire is lubricated and does not protrude. If a tracheostomy tube is present the cuff should be deflated to allow passage of the tube. Lubricate the tube and introduce it into the nostril; pass it horizontally along the nasal floor. There is usually a little resistance as the tube reaches the nasopharynx; press past this and ask the patient to swallow (use the water if this helps). The tube should now pass easily down the oesophagus, entering the stomach at 40cm. Secure the tube to the forehead with sticky tape and only now remove the guidewire, being careful to shield the patient’s eyes. Inject air into the tube and listen for bubbling over the stomach. Confirm position with a CXR. (Some systems require leaving a radio-opaque guidewire in prior to X-ray: check the tube you are using.)

Nasal patency. Select the least narrow nostril, use a lubricant, and, if necessary, a smaller tube and topical vasoconstrictor.

Gagging/vomiting. Press ahead; all sphincters are open.

Tube coiling into mouth. Cooling the tube makes it more rigid and often helps. As a last resort, topical anaesthesia and direct visualization with a laryngoscope or nasendoscope, while an assistant passes the tube, may be necessary.

Tube pulled out by patient. If they must have the tube, consider a nasogastric tube ‘bridle’ designed for this problem or a stitch to the septum or soft tissue of the nose.

Hazardous and expensive. Central or peripheral lines are required and need to be maintained. Neither as safe nor efficient as enteral feeding. Avoid if at all possible.

Patients who have been starved for >5 days and are then fed enterally or parenterally risk this electrolyte and fluid imbalance characterized by severe hypophosphataemia with other biochemical disturbances. Avoid by supplementation with B vitamins and gradated biochemical correction.5

Feeding tube placed directly in stomach through abdominal wall at endoscopy.

X-ray (or ultrasound) guided version of a PEG. Needs NGT in place to inflate stomach.

LA (graphic Local analgesia—tools of the trade, p. 606); RA (graphic Sedation—relative analgesia, p. 612); IV sedation (graphic IV sedation, p. 614); cryoanalgesia (graphic Cryosurgery, p. 387).

Pain control aims to relieve symptoms while identifying and removing the cause; the exception is when the cause is not treatable, as in palliative and terminal care. Then, the approach is to deal with the symptoms to enable the patient to have a quality to their life.

May often be well controlled by LA (graphic Local analgesia—tools of the trade, p. 606), but it is often necessary to use systemic analgesics. Useful analgesics in this situation include paracetamol (1000mg PO/PR/IV 4-hourly) and ibuprofen (400–600mg 8-hourly). Both these can be combined with codeine (8–30mg). NSAIDs such as diclofenac (50mg PO 8-hourly or 75mg IM perioperatively, followed by one further dose of 75mg IM). These drugs are all simple analgesics and, with the exception of paracetamol, have the advantage of an anti-inflammatory action which is at least as important as their central analgesic effect. In post-op pain, opioid analgesics are helpful when used parenterally and short term. Morphine 10mg 3–4-hourly combined with an antiemetic such as metoclopramide (10mg IM/IV) is useful in the immediate post-op period. PCA systems (see later in this topic) after major surgery are commonly used. They are set up by the anaesthetists.

is a problem, as these patients must be assessed neurologically for evidence of head injury which C/I opioids. The addition of codeine phosphate (60mg IM) to a NSAID is often effective and does not significantly interfere with neurological observations. Alternatively, PR or IM diclofenac sodium may suffice. There is often a hospital acute pain team who will be happy to advise in difficult cases.

not of dental or iatrogenic origin is covered in graphic Facial pain, p. 438. These conditions often require the use of co-analgesics such as antidepressants, antiepileptics, and anxiolytics.

An important subject in its own right. Points to note include: aim for continuous control using oral analgesia; use regular, not on demand, analgesia titrated to the individual; diagnose the cause of each pain and prescribe appropriately (e.g. steroids for liver secondaries or ↑ intracranial pressure, NSAIDs &/or radiotherapy for bone metastases, co-analgesics for nerve root pain, etc.). Remember that psychological dependence is very rare in advanced cancer patients using long-term opioids, and analgesic tolerance slow to develop. When starting patients on opioid analgesia, always consider using an antiemetic (graphic Antiemetics, p. 585) and a laxative. OH may be incredibly difficult for patients with oral cancer or following head and neck surgery. Use of chlorhexidine gluconate and metronidazole (200mg bd) ↓ the smell associated with wound infection or tumour fungation even when there is no prospect of eliminating it entirely. Patients rarely develop the disulfiram reaction to metronidazole on this regimen that occurs with higher doses.

Surgery is painful. Providing LA (consider the long-acting agent bupivacaine/levobupivacaine) or systemic analgesia before surgery begins may ↓ overall requirements for analgesia.

The optimal technique for severe post-op pain. Small machine delivers a bolus (1–2mg morphine) when patient presses a button. Can be repeated as needed.

Two variables: (i) bolus dose; (ii) ‘lock out time’ time during which machine will not respond (allows time for opioid to achieve maximum effect and prevents overdosage).

Learning Point:

What analgesics are available and work in your area?

Prophylaxis is the prevention of an occurrence. In surgery this is usually infection or thromboembolism. Prophylaxis used to prevent the occurrence of bacterial infection is quite different from treating an established infection. There are two broad categories of patients requiring antibiotic prophylaxis: (i) those who have it to prevent a minor local bacteraemia causing a serious infection out of all proportion to the procedure, e.g. the immunocompromised; (ii) those who receive it to prevent local septic complications of the procedure, e.g. wisdom-tooth removal.

The regimen should be short, high dose, and appropriate to the potential infecting organisms. The aim is to prevent pathogens establishing themselves in surgically traumatized or otherwise at-risk tissues, therefore the antimicrobial must be in those tissues prior to damage or exposure to the pathogen. It must not, however, be present too long before this, as there is then a risk of pathogen resistance and damage to commensal organisms. The regimen should therefore start immediately pre-op (i.e. <6h) or perioperatively (e.g. with anaesthetic induction) and should be continued for 24–48h maximum. When practicable, select an antimicrobial as specific to the common pathogens for that procedure as possible, except in the immunocompromised, where broad-spectrum prophylaxis is appropriate.

Prophylaxis against infective endocarditis is no longer indicated on a routine basis.6

Immunocompromised (e.g. severe leukopenia)—2.25g piperacillin/tazobactam plus 120mg gentamicin IV pre-op. Repeat qds for 24h.

Dento-alveolar surgery—simple extractions need not be covered but third-molar surgery often is. Regimens: metronidazole 400mg PO (500mg IV) pre-op followed by 400mg tds for 24h, amoxicillin 1g PO/IV followed by 500mg tds for 24h.

Prevention of DVT &/or pulmonary embolus in susceptible patients (e.g. women on the pill, prolonged surgery, iliac crest grafts) can be achieved using daily low-molecular weight heparin SC od (various types available—check which one your hospital favours). Thromboembolic antiembolism (TED) stockings will also ↓ DVT. Rx of pulmonary embolus graphic DVT, p. 572.

Learning Point:

Every hospital has its own regimens (sometimes one for each consultant)

graphic Many hospitals have a diabetic team who will advise on the management of these patients. Find out if this happens in your locality and make use of them. Type 2 diabetics are an increasing group in the developed world and have a plethora of health problems.8

Know the type and severity of the diabetes you are dealing with.

Inform the anaesthetist (and diabetic team if available).

Remember these patients are more likely to have occult heart disease, renal impairment, and ↓ resistance to infection, so get an ECG, U&Es, and use antibiotics prophylactically.

If nursing staff are experienced with blood glucose estimation using blood glucose testing strips or similar, 2–4 hourly tests will suffice for monitoring control. Otherwise pre-, peri-, and post-op blood glucose estimation is needed.

If in doubt and you are on your own (although you never should be) use a GKI (see graphic Management: insulin-dependent, p. 568).

Always have diabetics first on the operating list, in the morning if possible. Admit to hospital the day before surgery if insulin regimen is to be used.

If anything other than a minor, short procedure, treat as insulin-dependent. If random blood glucose is >15mmol/L treat as insulin-dependent.

Patients being treated under LA, or LA and sedation should maintain their carbohydrate intake and any oral hypoglycaemic drugs as normal. Plan surgery to fit their regular mealtimes. Have carbohydrate readily to hand if needed, and ensure adequate post-op analgesia, as pain or trismus can easily interfere with their usual intake. Remember antibiotic prophylaxis.

Halve the dose of oral hypoglycaemic 24h prior to surgery and omit on day of surgery. Do blood glucose pre- and post-op (if >15 go to GKI). Halve normal dose of oral hypoglycaemic until able to take normal diet, then back to normal dose. Keep an eye on the K+ concentration (U&Es pre- and post-op) and keep well hydrated. If in doubt, manage as for insulin dependent.

Admit 24–48h pre-op to optimize control. If glycaemic control poor, involve diabetic team early. Examine the patient carefully. Get an ECG, FBC, U&Es, and random blood glucose. Look for heart and respiratory disease, leucocytosis indicating infection, anaemia, hypo- or hyperkalaemia, and renal impairment. If these are acceptable, normal insulin/carbohydrate intake up to and including evening meal the day before surgery. Omit long-acting insulin on the day before surgery. Starve following this, and place on an IV infusion of glucose (glucose 5–10% 500mL), potassium (10mmol K+ injected into bag of glucose) infused via a controlled rate device over 5h, i.e. 100mL/h. This is infused via three-way tap into a peripheral cannula. Simultaneously, short-acting insulin is infused via a pump through the three-way tap into the same cannula at a rate indicated by the sliding scale (Table 12.1). The insulin is normally made up as 49.5mL N saline with 50IU of short-acting insulin giving 50mL = 50IU insulin, but always check your local nurses’ policy.

Table 12.1
Sliding scale
BMInsulin IU/h

>22

8

18–22

6

14–18

4

10–14

3 Target zone

6–10

2

2–6

1

<2

Stop and give glucose

BMInsulin IU/h

>22

8

18–22

6

14–18

4

10–14

3 Target zone

6–10

2

2–6

1

<2

Stop and give glucose

The original GKI had a fixed amount of insulin injected into the 500mL of glucose but the flexibility of sliding scale delivery has made this technique the most frequently used.

The scale details will vary according to the type of fingerprick glucose tests available in your locality; numbers are not absolute but the principle will always work. Choice of crystalloid is variable; 10% glucose ↑ carbohydrate and anabolism but tends to tissue veins quickly.

Once the patient can eat and drink, resume normal insulin regimen and discontinue infusion as BMs normalize.

These patients are unable to respond to the stress of surgery due to depletion or absence of their endogenous corticosteroid response.

Patients with Addison’s disease, patients prescribed corticosteroids for modulation of the immune system, and steroid abusers from various ‘sports’.

The rarest of these groups but requires the most aggressive supplementation as sufferers are entirely reliant on prescribed steroids. Minor surgery can safely be covered with IM hydrocortisone sodium succinate 100mg qds the day of surgery. Major surgery should be covered for 3 days using the same regimen. IV administration is kinder over the longer period.

Do you know why they are on these drugs? Consider the underlying disease and whether it has any bearing on your Rx plan; e.g. a patient receiving steroids as part of a cytotoxic regimen will also be at risk from bleeding and infection. In an uncomplicated case before minor surgery, all that is needed is a single IM injection of hydrocortisone 50mg 30min prior to the procedure. Alternatives are an IV injection immediately pre-op followed by double the normal oral dose of steroid. Another way is to ask the patient to take a double dose on the day of the operation, normal dose plus 50% the day after, and normal plus 25% on the third day, thereafter returning to their usual dose. Those undergoing major surgery should have the IM/IV regimen over 24h or longer.

Unfortunately these are a real and ↑ problem.9 Although these drugs are taken for their androgenic effect, few ‘sportspersons’ have access to appropriate advice or drugs and many users will have a degree of suppressed steroid response. It is probably safest to cover procedures using the IM regimen as for those on prescribed steroids, although this could be considered overkill. Remember the risk of shared needles.

Learning Point:

Write some notes on the steroid regimens used in your hospital/department/practice

Use appropriate analgesia (graphic Analgesics in hospital practice, p. 580).

A small physiological ↑ in temperature occurs post-op. Other causes: atelectasis, infection (wound, chest, urine), DVT, incompatible transfusion, allergic reactions.

Antiemetics, e.g. IM/IV cyclizine 50mg. Prochlorperazine 12.5mg or metoclopramide 10mg. Ondansetron for the recalcitrant (4mg IV/IM, 8mg PO).

Common after intubation; needs reassurance and simple analgesia. Cold water ↓.

Often follows suxamethonium use in anaesthetic induction. Again, reassurance and simple analgesics.

Usually caused by autonomic suppression by a GA. Treat by placing ‘head-down’. If necessary, speed up IV infusion for a short while.

CXR, culture sputum, and start on ampicillin or cefuroxime until culture results available.

A symptom, therefore look for the cause, e.g. infection, electrolyte imbalance, alcohol withdrawal, hypoxia, or dehydration, and correct. Only consider sedation, e.g. haloperidol 1–5mg (care in the elderly), after action has been taken to deal with the cause and the patient constitutes a threat to themselves or others.

Comparatively rare, even after major maxillofacial surgery. Early mobilization and adequate analgesia helps; if not, use temporary catheterization (graphic Catheterization, p. 560).

Follows ‘tissued’ cannulae or irritant IV injections. Observe for infection, treat pain, and consider supportive strapping.

Signs are painful, shiny, red, swollen calf, usually unilaterally but may be bilaterally. ‘At risk’ are immobile patients especially following pelvic surgery, patients with cancer, women on the pill, the elderly, and the obese. Confirm by Doppler US or ascending venography. Prevent by using a low-molecular-weight heparin (dalteparin, enoxaparin) pre-op and 5 days post-op &/or pressure stockings, and ensure early mobilization. Stop the pill prior to any major surgery. Rx: bed rest, leg strapping and elevation, analgesia and heparinization (give 5000 units stat IV followed by 50 000 units in 50mL normal saline by syringe driver infusion starting at 1000 units/h (1mL/h) and adjust according to the KCT/APTT, keep between 1.5–2.5 times the control values). The major risk of DVT is the development of pulmonary embolus. This classically presents 10 days post-op when the patient has been straining at stool and may occur despite no apparent DVT. Symptoms are pleuritic chest pain, dyspnoea, cyanosis, haemoptysis, and an ↑ jugular venous pressure. Signs of shock are often present, ranging from very little in the young who can compensate, to cardiac arrest! Usually a clinical ∆, confirmed after heparinization, analgesia, and O2 have been instituted, by CXR, blood gases, spiral CT, or lung ventilation—perfusion scan &/or pulmonary angiography. ECG will sometimes show deep S waves in I, pathological Q waves in III, and inverted T waves in III (SI, QIII, TIII). Must be followed up by 3–6 months anticoagulation with warfarin, so involve a haematologist.

Less serious but more common are post-phlebitic limb, varicose veins, limb swelling, and skin discoloration. May lead to varicose eczema.

Local pain, swelling, infection, and trismus are the commonest. Antral complications may follow maxillary surgery. These are considered in the relevant chapters.

Notes
1

NICE Guidance 2008 (UK) graphic  http://www.nice.org.uk/060

3

Resuscitation Council (UK) 2006 Guidelines
.

4

Thank you Douglas Adams!

5

H. Melena  et al. 2008 BMJ  336 1495
.

7

J. Hill & T. Treasure 2007 BMJ  334 1053
.

8

P. Home  et al. 2008 BMJ  336 1306
.

9

HMSO 2004 Drug Ther Bull  42 1
.

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