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Acute severe upper gastrointestinal haemorrhage is an important medical emergency.

A sudden loss of 20% or more circulatory blood volume usually produces signs of shock, such as tachycardia, hypotension, faintness and sweating.

Haematemesis: diagnostic strategy model

Probability diagnosis

• Chronic peptic ulcer (stomach and duodenum) 50%

• Acute gastric ulcers/erosions 20%

• Oesophagitis (incl. GORD)

• Mallory–Weiss (emetogenic) syndrome

• Drugs: aspirin, NSAIDs, anticoagulants, clopidogrel

Serious disorders not to be missed

• Vascular:

  • oesophageal varices

  • blood dyscrasias

  • vascular malformation/angiodysplasia

  • hereditary coagulopathy

• Cancer:

  • gastric or oesophageal

• Other:

• chronic liver disease

Pitfalls (often missed)

• Stomach ulcer

• Swallowed blood (e.g. epistaxis)

• Collagen diseases (e.g. scleroderma)

Rarities

• Ruptured oesophagus

• Hereditary haemorrhagic telangiectasia

Key history

• Nature of vomitus from fresh blood to ‘coffee grounds’

• Is bleeding arising from the mouth, nose or pharynx?

• Indigestion, heartburn or stomach pains

• Associated symptoms (e.g. weight loss, jaundice)

• Any bleeding problems

• Drug history including alcohol, NSAIDs, antiplatelet agents, warfarin, steroids

Key examination

• Patient's general state including circulation, vital signs

• Abdominal examination and rectal examination

• Evidence of liver disease

Key investigations

• Upper GIT endoscopy diagnoses bleeding source in 80%

• FBE

• LFTs including γ GT

• Helicobacter pylori tests

• Imaging (e.g. plain erect X-ray, as indicated)

Causes of upper GI bleeding

The major cause of bleeding is chronic peptic ulceration of the duodenum and stomach, which accounts for approx. half of all cases. The other major cause is acute gastric ulcers and erosions, which account for at least 20% of cases. Aspirin and NSAIDs are responsible for many of these bleeds. Causes are illustrated in Fig. H1.

Investigations

Investigations to determine the source of the bleeding should be carried out in a specialist unit. Endoscopy will detect the cause of the bleeding in at least 80% of cases.

Management

The immediate objectives are:

1. restore an effective blood volume (if necessary)

2. establish a diagnosis to allow definitive treatment

All patients with a significant bleed should be admitted to hospital and referred to a specialist unit. Urgent resuscitation is required where there has been a large bleed and there are clinical signs of shock. Such patients require an intravenous line inserted and transfusion with blood cells or fresh frozen plasma (or both) commenced as soon as possible.

In many patients bleeding is insufficient to decompensate the circulatory system and they settle spontaneously. Approximately 85% of patients stop bleeding within 48 hrs. PPIs should be commenced in most cases since most bleeds are from peptic ulceration. Use oral PPIs if possible but IV PPIs can be used.

Most patients require no specific therapy after resuscitation. In some instances haemostasis of bleeding points (via endoscopy) can be achieved with a heater probe (e.g. Gold Probe) or injection of adrenaline or both. Occasionally surgery will be necessary to arrest bleeding but should be avoided if possible in patients with acute gastric erosion.

Haematuria is the presence of blood in the urine and can vary from frank bleeding (macroscopic) to the microscopic detection of red cells.

All patients presenting with macroscopic haematuria or recurrent microscopic haematuria require both radiological investigation of the upper urinary system and visualisation of the lower urinary system to detect or exclude kidney pathology.

The key radiological investigation is the intravenous urogram (pyelogram) and then ultrasound. Common urological cancers that cause haematuria are bladder (70%), kidney (17%), kidney, pelvis or ureter (7%) and prostate (5%).

The commonest cause of glomerulonephritis leading to nephritic syndrome (oedema + hypertension + haematuria) is IgA nephropathy.

A condition in which the total body iron is increased to 20–60 g (normal 4 g). The excess iron is deposited in and damages several organs:

• liver → cirrhosis

• pancreas → ‘bronze’ diabetes

• skin → bronze or leaden grey colour

• heart → restrictive cardiomyopathy

• pituitary → hypogonadism: impotence etc.

• joints → arthralgia (esp. hands); chondrocalcinosis

It is usually primary (hereditary—autosomal recessive) but may be secondary (e.g. chronic haemolysis, ↑ dietary iron, multiple transfusions).

Symptoms

(May be) extreme lethargy, polyuria and polydipsia, arthralgia, loss of libido

Signs

(Look for) hepatomegaly, very tanned skin, cardiac arrhythmias

Diagnosis

• ↑ serum transferrin saturation >70% and ↑ ferritin (>250 mcg/L) (key tests)

• Liver biopsy (if LFT enzymes abnormal) or hepatomegaly

• HFE genetic studies—C282Y and/or H63D mutation

• Screen first-degree relatives (s. transferrin saturation and s. ferritin)

Management

• Refer for specialist care.

• Weekly venesection 500 mL (250 mg iron) until serum iron levels normal and haemoglobin <110 g/L (may take at least 2 yrs), then every 3–4 mths to keep s. ferritin (<100 mcg/L), transferrin saturation and iron normal.

• Normal diet.

• Avoid alcohol.

• Life expectancy is normal if treated before cirrhosis or diabetes develops.

Key facts on hair numbers

• Hair growth is asynchronous (i.e. continuous production and shedding).

• Humans produce 1 km of hair a month.

• Approx. 50–100 hairs are shed daily without a reduction in density.

• The scalp contains, on average, 100 000 hair follicles.

• At least 25% of hair must be shed before a noticeable loss of density occurs.

• Hair loss counts consistently above 100/d indicate excessive hair loss.

• Significant hair loss tends to block the shower drain or be visible all over the pillow.

Hair loss: diagnostic strategy model

Probability diagnosis

• Androgenetic alopecia (male pattern baldness)

• Alopecia areata (diffuse type)

• Telogen effluvium (incl. postpartum)

• Anagen effluvium (esp. cytotoxic therapy)

• Seborrhoeic dermatitis

Serious disorders not to be missed

• Infection:

  • tinea capitis

  • bacterial folliculitis

  • secondary syphilis

  • post-febrile state

• Cancer:

  • treatment for cancer

Other:

• systemic disease (e.g. lupus)

Pitfalls (often missed)

• Nutritional:

  • severe dieting

  • malnutrition

  • zinc/iron deficiency

Key investigations

Consider:

• FBE/ESR

• pituitary hormones (FSH/LH/prolactin/FSH)

• hair pull test

• trichogram

• scalp biopsy

• skin scrapings and hair sample for fungal microscopy and culture

Causes of diffuse hair loss

• Androgenetic alopecia

• Telogen effluvium

• Postpartum telogen effluvium

• Alopecia areata (diffuse type)

• Drugs—cytotoxics, anti-epileptics, various hormones, others

• Hypothyroidism

• Nutritional

  • iron deficiency

  • severe dieting

  • zinc deficiency

  • malnutrition

• Post-febrile state

• Anagen effluvium

Androgenic alopecia

This is the most common form of human hair loss affecting 50% ♂ by 40 yrs and up to 50% ♀ by 60 yrs. It is genetically determined as well as being androgen dependent. In women the pattern of hair loss is different to men. Diffuse thinning occurs on the top of the head (the crown) while the front hairline usually remains (Figure H2).

Treatment, which is difficult, is summarised on Androgenetic alopecia (male pattern baldness).

Alopecia areata, alopecia totalis and alopecia universalis

Alopecia areata is a disorder of the hair follicle causing a sudden onset of localised or diffuse hair loss. The features are complete hair loss (small patch or diffuse), a clean normal scalp, no inflammation and exclamation-mark hairs. Small patches may recover spont. (usu. 80%), while extensive (> 50% loss) has a variable course.

Alopecia totalis, which involves the total scalp, has at best a 50% chance of recovery in a fit adult. In alopecia universalis the eyebrows and eyelashes are also affected.

For treatment, Alopecia areata (patchy hair loss).

Scarring alopecia

In this irreversible condition hair follicles are damaged. A scalp biopsy is essential to determine the diagnosis. Apart from obvious causes, such as trauma, severe burns, a carbuncle and scalp ringworm with kerion, the causes are:

• lichen planopilaris—a variant of lichen planus

• discoid lupus erythematosus

• folliculitis decalvans—probably due to S. aureus

• pseudopelade—a slowly progressive scarring condition

Telogen effluvium

This is increased shedding of telogen hairs, which can be triggered by a variety of stresses, including severe stress, childbirth, febrile illness, trauma, crash dieting and cessation of the OCP.

Typical features: stressful event → 2–3 mth gap to diffuse hair loss with white bulbs on end of the hair.

If uncomplicated, recovery can be expected in 6 months. If there is a concern about non-recovery, an option is the use of topical minoxidil for min. 4 months. Refer if incomplete recovery or relapsing episodes.

Anagen effluvium

This is hair loss during the anagen phase and is typically seen in association with cancer chemotherapy. Anagen hair shafts are identified by their long and pigmented hair bulb (compared with the white bulb of telogen). The follicle may remain in anagen, leading to a quick recovery or move into telogen, thus delaying growth by about 3 months.

Trichotillomania (hair pulling)

This is patchy hair loss caused by deliberate plucking or twisting of hair shafts. It is common (by habit) in young children but in older children and adults it may be an obsessive-compulsive disorder often associated with stress.

Clinical features

• Incomplete patchy alopecia

• Hairs of different length

• Hairs broken and twisted

• Strange pattern of loss

• Tends to occur on side of dominant hand

Hair disorders in children

Hirsuties

This is growth in the female of excess, coarse terminal pigmented hair in androgen dependent sites, namely in a male sexual pattern (e.g. upper lip, beard area and back). For management refer to hirsutism.

Hypertrichosis

This is the increased growth of fine vellus or downy hair over the entire body. The cause is generally unknown. It may be a prepubertal trait. Can be caused by drugs such as phenytoin.

Dry hair

Oily hair

The commonest causes are orodental disease due to poor oral hygiene and inappropriate diet.

• Exclude dental disease, malignancy (esp. nasopharyngeal carcinoma), pulmonary TB, hairy tongue, nasal and sinus infection.

• Consider drugs, e.g. isosorbide dinitrate, antidepressants.

• Avoid or limit onions, garlic, peppers, spicy salami and similar meats.

• Avoid or limit strong cheeses.

• Avoid smoking and excessive nips of alcohol.

• Brush teeth regularly during day—immediately after a meal.

• Rinse mouth out with water after meals.

• Avoid fasting for long periods during the day.

• Gargle with mouthwash regularly (e.g. Listerine, Cepacol Mint mouthwash, 0.2% aqueous chlorhexidine).

• Use dental floss regularly to clean the teeth.

• Chew sugarless gum to moisten mouth.

Tip: Use an oil/water wash (e.g. equal volumes of aqu. Cepacol and olive oil), gargle a well-shaken mixture and spit out, qid.

Preventive advice

• Drink alcohol on a full stomach.

• Select alcoholic drinks that suit you: avoid champagne.

• Avoid fast drinking—keep it slow.

• Restrict the quantity of alcohol.

• Dilute your drinks.

• Drink three large glasses of water before retiring.

Treatment

• Drink ample fluids, preferably water, because of relative dehydration effect of alcohol.

• Take 2 paracetamol tablets for discomfort, esp. for headache.

• Drink orange juice or tomato juice, with added sugar.

• A drink of honey in lemon juice helps.

• Coffee and tea (better) are suitable beverages.

• Have a substantial meal but avoid fats.

Definition:

allergic rhinitis can be either intermittent (lasting for <4 d per week or <4 weeks) or persistent (lasting for >4 d per week or >4 wks).

Suggested management steps

• Patient education

• Allergen avoidance (if possible)

Mild cases:

• Less-sedating antihistamines:

  • fexofenadine 60 mg bd, or desloratadine 5 mg/d or cetirizine 10 mg/d, or levocetirizine 5 mg/d or loratadine 10 mg/d, or

  • levocabastine nasal spray ±

• decongestant, e.g. pseudoephedrine, phenylephedrine

Moderate to severe cases:

• intranasal corticosteroids (the most effective). Select from:

  • beclomethasone dipropinate 100 mcg per nostril bd

  • budesonide 128 mcg per nostril daily

  • ciclesonide 2 sprays per nostril daily

  • mometasone furoate 2 sprays per nostril daily

  • fluticasone furoate 2 sprays per nostril daily

  • fluticasone propriate 2 sprays per nostril daily

  • triamcinolone 2 sprays per nostril daily

• prednisolone 25 mg (o) /d, reducing over 10 d if others ineffective

Use sodium cromoglycate (Opticrom) drops for eye irritation. Can use oral corticosteroids if topicals ineffective. Consider intranasal antihistamines (e.g. levocabastine) to relieve excessive itching and sneezing. Consider immunotherapy if applicable and leukotriene receptor antagonist if concurrent asthma.

The commonest cause of headache presenting in general practice is respiratory infection. Common causes of chronic recurrent headache are tension, so-called transformed migraine and combination (mixed) headaches. Migraine is not as common as in specialist practice.

Headache: diagnostic strategy model

Probability diagnosis

• Acute:

  • respiratory infection

• Chronic:

  • tension-type headache

  • combination headache

  • migraine

  • transformed migraine

Serious disorders not to be missed

• Cardiovascular:

  • subarachnoid haemorrhage

  • intracranial haemorrhage

  • carotid or vertebral artery dissection

  • temporal arteritis

  • cerebral venous thrombosis

• Neoplasia:

  • cerebral tumour

  • pituitary tumour

• Infection:

  • meningitis (esp. fungal)

  • encephalitis

  • intracranial abscess

• Haematoma: extradural/subdural

• Glaucoma

• Benign intracranial hypertension

Pitfalls (often missed)

• Cervical spondylosis/dysfunction

• Dental disorders

• Refractive errors of eye

• Sinusitis

• Ophthalmic herpes zoster (pre-eruption)

• Exertional headache

• Hypoglycaemia

• Post-traumatic headache (e.g. post-concussion)

• Post-spinal procedure (e.g. epidural, lumbar puncture)

• Sleep apnoea

Tension-type headache

Tension or muscle contraction headaches are typically a symmetrical tightness. They can be episodic or chronic. They tend to last for hours and recur each day. They are often associated with cervical dysfunction and stress or tension, although the patient may be unaware of such tension (see Fig. H3).

Management

• Careful patient education.

• Counselling and reassurance.

• Advise stress reduction, relaxation therapy and yoga or meditation classes. Provide mindfulness therapy or CBT.

• Medication—mild analgesics such as aspirin or paracetamol. Avoid tranquillisers and antidepressants if possible but consider these drugs if symptoms warrant medication (e.g. amitriptyline 10–75 mg (o) nocte increasing to 150 mg if nec.).

Migraine

Migraine, or the ‘sick headache’, is derived from the Greek word meaning ‘pain involving half the head’. It affects at least 1 person in 10, ratio ♀:♂ ∼2:1, and peaks between 20–50 yrs. There are various types of migraine with classic migraine (headache, vomiting and aura) and common migraine (without the aura) being the best known.

Management

Patient education—explanation and reassurance about the benign nature of migraine

Counselling and advice

• Avoid known trigger factors, e.g. physical or emotional stress, lack of sleep, bright lights.

• Diet: keep a diary—consider elimination of chocolate, cheese, red wine, walnuts, tuna, Vegemite, spinach and liver.

• Practise a healthy lifestyle, relaxation programs, meditation techniques and biofeedback training.

Treatment of the acute attack

• Start treatment at earliest impending sign.

• Rest in a quiet, darkened, cool room.

• Cold packs on the forehead or neck.

• Avoid moving around too much.

• Do not read or watch television.

• Avoid drinking coffee, tea or orange juice.

• For patients who find relief from simply ‘sleeping off’ an attack, consider prescribing temazepam 10 mg or diazepam 10 mg in addition to the following measures.

First signs of attack:

• 1st line: soluble aspirin, e.g. Dispirin Direct 2–3 tabs or paracetamol/codeine co 2 tabs (o) + metoclopramide 10 mg (o) if nausea a feature or

  consider NSAIDs (e.g. ibuprofen, diclofenac rapid)

• 2nd line: a triptan agent—sumatriptan 100 mg (o) or 6 mg (SCI) or nasal spray 10–20 mg per nostril or

  zolmitriphan 2.5–5 mg (o) repeat in 2 h if nec. or

  naratriptan 2.5 mg (o) repeat in 2–4 h if nec.

  rizatriptan 10 mg wafer, repeat in > 2 hrs if nec.

Established attack:

• metoclopramide 10 mg (2 mL) IM or IV or

• prochlorperazine 12.5 mg IM or 25 mg rectally

The severe attack:

• metoclopramide 10 mg IV or

• prochlorperazine IV or chlorpromazine IM

Practice tip for severe classic migraine: IV metoclopromide or chlorpromazine + 1 L IV N saline in 30 mins + oral soluble aspirin or paracetamol

Prophylaxis (for >2 attacks per mth)

• propranolol 40 mg (o) bd increasing up to 240 mg/d if nec. or

• pizotifen 0.5 mg (o) nocte increasing to 3 mg if nec.

• hormone manipulation, e.g. OCP for menstrual migraine

Consider an antidepressant alone or in combination. Reserve methysergide for unresponsive severe migraine.

Transformed migraine

This term describes the progressive increase in frequency of migraine attacks until the headache recurs daily. The typical migraine features become modified so that the pattern resembles tension headache but with the unilateral focus of migraine. Overuse of analgesics is implicated. A trial of a triptan agent is worthwhile and naproxen for drug withdrawal headache.

Cluster headache

Occurs in paroxysmal clusters of unilateral headache, which typically occur nightly, usually early a.m. A hallmark is the pronounced cyclical nature of the attacks. Occurs typically in males (6:1 ratio). Another feature is ptosis, lacrimation and rhinorrhoea on the side of the pain.

Management

Acute attack:

• consider 100% oxygen 10 L/min for 15 mins by face mask (usually good response)

• sumatriptan 6 mg SCI (or 20 mg intranasal) or

• avoid alcohol during cluster

Prophylaxis (once a cluster starts)—consider the following:

• methysergide 2 mg (o) tds

• prednisolone 50 mg/d for 10 d then reduce

• pizotifen

• indomethacin trial (helps confirm diagnosis)

• sodium valproate

• verapamil SR 160 mg (o) /d ↑ 320 mg

Cervical dysfunction/spondylosis

Headache from neck disorders, often referred to as occipital neuralgia, is far more common than realised and is very rewarding to treat by physical therapy, including mobilisation and manipulation and exercises in particular.

Combination headache

Combined (also known as mixed) headaches are common and often diagnosed as psychogenic headache or atypical migraine. They have a combination of various degrees of:

• tension and/or depression

• cervical dysfunction

• vasospasm (migraine)

• drugs (e.g. analgesics—rebound, caffeine)

• some cases may be transformed migraine

The headache, which has many of the features of tension headache, tends to be constant, being present throughout every waking moment. It can last for weeks or months.

Treatment includes insight therapy, reassurance that the patient does not have a cerebral tumour, and lifestyle modification. Wean the patient off analgesics. The most effective medication is amitriptyline or other antidepressant. Consider physical treatment for a cervical component.

Temporal arteritis

Temporal arteritis (TA), a subset of giant cell arteritis, is also known as cranial arteritis. There is usually a persistent unilateral throbbing headache in the temporal region and scalp sensitivity with localised thickening, with or without loss of pulsation of the temporal artery. Usually >50 yrs; the mean age is 70 yrs.

Diagnosis is by biopsy and histological examination of the superficial temporal artery. The ESR is usually markedly elevated. The CRP is usually elevated.

Treatment

Initial medication is prednisolone 40–60 mg (o) daily, initially for 2–4 wks then gradual reduction (max. 10%) wk intervals. Dose reduction and progress is monitored by the clinical state and ESR levels. Add aspirin.

Frontal sinusitis

Contrary to popular belief, sinusitis is a relatively uncommon source of headache.

Management

Principles of treatment:

• Drain the sinus conservatively using steam inhalations.

• antibiotics: amoxycillin or amoxycillin/clavulanate or cefaclor or doxycycline

• analgesics

Subarachnoid haemorrhage (SAH)

Clinical features

• Sudden onset headache (moderate—to—intense severity)

• Occipital location

• Localised at first, then generalised

• Pain and stiffness of the neck follows

• Vomiting and loss of consciousness often follow

• Kernig's sign +ve

• About 40% die before treatment

• CT scanning is the investigation of choice

Refer urgently to major neurosurgical unit.

Hypertension headache

Tends to occur only in severe hypertension, such as malignant hypertension or hypertensive encephalopathy. The headache is typically occipital, throbbing and worse on waking in the morning.

Benign intracranial hypertension (pseudotumour cerebri)

This is a rare but important sinister headache condition which typically occurs in young obese women. Key features are headache, visual blurring and obscurations, nausea, papilloedema. The CT and MRI scans are normal but lumbar puncture, which relieves the headache, reveals increased CSF pressure and normal CSF analysis.

It is sometimes linked to drugs, including tetracyclines (most common), nitrofurantoin, oral contraceptive pill and vitamin A preparations.

Pharmacological treatment in children

Tension headache and migraine:

• paracetamol 20 mg/kg (o) statim then 15 mg/kg 4–6 hrly (max 90 mg/kg) or

• ibuprofen 5–10 mg/kg (o) statim, up to 40 mg/kg/day (not <6 mths)

The clinical terms used to describe brain injury of concussion, confusion and laceration indicate minor to major degrees of a similar injury. Life-threatening injuries include extradural and subdural haematomas, see Fig. H6. The Glasgow coma scale (see Table H2) can be used as a guide to the conscious state.

Concussion.

Extradural haematoma

Following head injury there may be a short lucid interval followed by loss of consciousness. The patient is restless, confused, irritable (Fig. H7), has severe headache and develops neurological signs.

• Investigation: skull X-ray, CT scan. Lumbar puncture contraindicated

• Management: urgent decompression of haematoma

Subdural (epidural) haematoma

The responsible injury may seem trivial esp. in elderly and the haematoma may be acute, subacute and chronic. Consider it in a person with personality change, headache, slow unsteady movements and fluctuating conscious level. Investigate and treat as above.

Heart failure occurs when the heart is unable to maintain sufficient cardiac output to meet the demands of the body.

Symptoms

• dyspnoea → exertional dyspnoea → dyspnoea at rest → orthopnoea → paroxysmal nocturnal dyspnoea

• lethargy/fatigue

• weight change: gain or loss

• dizzy spells/syncope

• palpitations

• ankle oedema

Investigations

Apart from routine investigations, left ventricular function should be measured by echocardiography (the most important test) or nuclear gated blood pool scanning to determine the ejection fraction, which is usually very low in heart failure. B-type natriuretic peptide is a marker of the severity of CHF. Differentiate between systolic (commonest) and diastolic failure.

Treatment

The treatment of heart failure includes appropriate patient education, determination and treatment of the cause, removal of any precipitating factors, general non-pharmaceutical measures and drug treatment. Studies have shown the benefit of a multidisciplinary approach.

Prevention

The emphasis on prevention is very important since the onset of heart failure is generally associated with a very poor prognosis. Approx. 50% of patients with severe heart failure die within 2–3 years of diagnosis.

General non-pharmacological management

• Refer for a rehabilitation program with interdisciplinary care

• Physical activity: rest if symptoms severe; moderate activity when symptoms are absent or mild

• Weight reduction, if patient obese

• Salt restriction: advise no-added-salt diet (<2 g or 60–100 mmol/d)

• Encourage no smoking and limited alcohol (1 SD/d)

• Water restriction: water intake should be limited to ≤1.5 L/d in patients with advanced heart failure, esp. when the serum sodium falls below 130 mmol/L

• Fluid aspiration if a pleural effusion or pericardial effusion is present

Drug therapy of systolic heart failure

Any identified underlying factor should be treated. Initial drug therapy should consist of an ACE inhibitor and usually a diuretic. Loop diuretics such as frusemide are preferred for acute episodes although other diuretics may be used for long-term maintenance therapy. Atrial fibrillation should be treated with digoxin. Vasodilators are widely used for heart failure and ACE inhibitors are currently the most favoured vasodilator.

Note: Monitor and maintain potassium level in all patients.

ACE inhibitors, β-blockers and spironolactone have been shown to improve survival in CHF and in combination are the gold standard.

Initial therapy of chronic heart failure

1. ACE inhibitor (start low, aim high)

   Dosage of ACE inhibitor: start with ¼ to ½ lowest recommended therapeutic dose and then adjust for the individual patient by gradually increasing it to the maintenance or max. dose (Table H3). Once-daily agents are preferred. Use ARB if cough with ACEI.

2. Diuretic (add this to the ACE inhibitor if congestion only), loop diuretic preferred:

   • frusemide 20–40 mg (o) once or twice daily or

   • butmetanide 0.5–1 mg (o)/d or

   • ethacrynic acid 50 mg (o)/d or

   • (thiazide type diuretic)

   • hydrochlorothiazide 25–50 mg (o) daily (or other thiazide) or

   • indapamide 1.5–2.5 mg (o) daily

ACE inhibitors

• In practice the usual initial treatment of heart failure is an ACE inhibitor, which is the key drug. This optimises response and improves diuretic safety.

• The first dose should be given at bedtime to prevent orthostatic hypotension.

• Potassium-sparing diuretics or supplements should not be given with ACE inhibitors because of the danger of hyperkalaemia.

• Kidney function and potassium levels should be monitored in all patients.

Beta-blockers

Selective β-blockers prolong survival of patients with mild to moderate CHF taking ACE inhibitors. Start with low doses.

Heart failure (unresponsive to first-line therapy)—stepwise strategy

• ACE inhibitor plus

• Frusemide 40–80 mg (o) bd plus

• Selective β-blocker plus

• Digoxin (if not already taking it)

  • 0.5–0.75 mg (o) statim (depending on kidney function) then

  • 0.5 mg (o) 4 h later then

  • 0.5 mg the following day then

  • individualise maintenance plus

• Spironolactone 12.5–25 mg (o) /d (monitor potassium and KFTs)

Severe heart failure

• Seek specialist advice.

• Hospital with bed rest.

• ACE inhibitor (o) to max. tolerated dose

• Frusemide to max. 500 mg/d

• Selective β-blocker plus

• Spironolactone (low dose) 25 mg/d

If poorly controlled, consider adding:

• thiazide diuretic

• spironolactone—doses ↑ 100–200 mg/d

• a β-blocker

• digoxin

• heparin (if confined to bed)

If still uncontrolled, consider other vasodilators:

• isosorbide dinitrate and hydralazine

Consider cardiac transplantation for appropriate patients with end-stage heart failure (e.g. patients <50 yrs with no other major disease). Other surgical options include heart valvular surgery, coronary artery bypass surgery and surgical ventricular restoration (surgical reduction of an enlarged left ventricle).

Pitfalls in management

• Excessive use of diuretics (most common treatment error)

• Giving an excessive loading dose of ACE inhibitor

• Failure to correct remedial causes or precipitating factors

• Failure to measure left ventricular function

• Failure to monitor electrolytes and kidney function

Diastolic heart failure

Management is based on treating the cause such as hypertension, ischaemia and diabetes. The basic treatment is with inotropic agents such as calcium antagonists (verapamil, diltiazem) and β-blockers. If possible, avoid diuretics, digoxin, nitrates and nifedipine.

Acute severe heart failure

(acute pulmonary oedema)

Treatment

(Keep in mind LMNOP—lasix, morphine, nitrates, O₂, CPAP.)

• Prop patient up

• Oxygen (mask or intranasal) 6–8 L/min

• Insert IV line

• Glyceryl trinitrate 300–600 mcg sublingual: can use IV nitrates in preference to morphine (if BP >100 mm Hg)

• Frusemide 40 mg IV, ↑ 80 mg IV as nec.

• Morphine 1–2.5 mg/min IV slowly (↑ 5–10 mg), esp. if chest pain

• CPAP (continuous positive airway pressure) or BiPAP

Give digoxin if rapid atrial fibrillation and patient not taking it.

Note: Morphine is now less favoured. Glyceryl trinitrate IV (in hospital) is preferred. Continuous +ve airway pressure (CPAP) is effective.

Important causes of heel pain include:

• Achilles tendon disorders

  • tendonopathy/peritendonitis

  • bursitis

    • postcalcaneal

    • retrocalcaneal

  • tendon tearing

    • partial

    • complete

• bruised heel

• tender heel pad—usually atrophy

• ‘pump bumps’

• plantar fasciitis

• calcaneal apophysitis

• peroneal tendon dislocation

• posterior tibialis tendonopathy

• tarsal tunnel syndrome

• neuropathies (e.g. diabetic, alcoholic)

US examination is useful to differentiate the causes of Achilles tendon disorders.

Achilles tendon bursitis

Bursitis can occur at two sites:

• posterior and superficial—between skin and tendon

• deep (retrocalcaneal)—between calcaneus and tendon (see Fig. H9)

Treatment

• Avoid shoe pressure (e.g. wear sandals)

• 1–2 cm heel raise inside the shoe

• Apply local heat and ultrasound

• NSAIDs (14-d trial)

• Inject corticosteroid into bursa with a 25 g needle

Plantar fasciitis

This common condition (also known as ‘policeman's heel’) is characterised by pain on the plantar aspect of the heel, esp. on the medial side; it usually occurs about 5 cm from the posterior end of the heel.

History

• Pain:

  • under the heel

  • first steps out of bed

  • relieved after walking about

  • increasing towards the end of the day

  • worse after sitting

• May be bilateral—usually worse on one side

• Typically >40 yrs

• Both sexes

Signs

• Tenderness: deep and localised

• Heel pad may bulge or appear atrophic

• Crepitus may be felt

• No abnormality of gait, heel strike or foot alignment

Treatment

• Heals spontaneously in 12–24 mths

• Consider trial NSAIDs—3 wks

• Therapeutic foot massages

• Exercise program to stretch Achilles tendon & plantar fascia

• US therapy

• Hydrotherapy: place foot alternately 30 secs in hot & cold water for 15 mins

• Protect heel with an orthotic pad to include heel and foot arch (e.g. Rose insole or thick pad of sponge or sorbo rubber).

• Injection of LA and depot corticosteroid into tender site helps for at least 2–3 wks for very severe pain (otherwise avoid).

Achilles tendonopathy/peritendonitis

Clinical features

• History of unaccustomed running or long walk

• Usually young to middle-aged males

• Aching pain on using tendon

• Tendon feels stiff, esp. on rising

• Tender thickened tendon

• Palpable crepitus on movement of tendon

Treatment

• Rest: ? crutches in acute phase, plaster cast if severe

• Cool with ice in acute stage, then heat

• NSAIDs (14-d trial)

• 1–2 cm heel raise under the shoe

• US and deep friction massage

• Mobilisation, then graduated stretching exercises

Avoid corticosteroid injection in acute stages and never give into tendon. Can be injected around the tendon if localised and tender.

Partial rupture of Achilles tendon

Clinical features

• A sudden sharp pain at the time of injury

• Sharp pain when stepping off affected leg

• A tender swelling palpable about 2.5 cm above the insertion

• May be a very tender defect about size of tip of little finger

Treatment

If palpable gap—early surgical exploration with repair. If no gap, use conservative treatment:

• initial rest (with ice) and crutches

• 1–2 cm heel raise inside shoe

• US and deep friction massage

• graduated stretching exercises

Convalescence is usually 10–12 wks.

Complete rupture of Achilles tendon

Clinical features

• Sudden onset of intense pain

• Patient usually falls over

• Feels more comfortable when acute phase passes

• Development of swelling and bruising

• Some difficulty walking, esp. on tiptoe

Diagnosis

• Palpation of gap (best to test in first 2–3 h as haematoma can fill gap)

• +ve Thompson's test (calf squeeze test)

Treatment

Early surgical repair (within 3 wks).

Acute viral hepatitis may be caused by Hepatitis A, B, C, D & E, and less commonly by CMV and EBV. These can cause severe liver disease (esp. Hepatitis B & C) from end stage liver failure to hepatocellular carcinoma. A and D are spread by the faecal–oral route, B and C from blood and possible other body fluids. See also Jaundice.

Diagnostic markers for acute hepatitis

• Hepatitis A: IgM anti-HAV (Ab)

• Hepatitis B: surface antigen (HBsAg)

• Hepatitis C: anti-HCV (Ab)

• IgM antibodies = recent infection

• IgG antibodies = previous exposure

Hepatitis A

Features

• Recovery usu. in 3–6 wks

• Sometimes a subclinical illness

• No carrier state

• Does not cause chronic liver disease

• Fulminant hepatitis with coma & death is rare

• LFTs and viral markers confirm diagnosis

Serology

• IgM anti HAV = active infection

• IgG antibodies = immunity

Treatment

• Rest as appropriate

• Avoid sedatives, NSAIDs

• Cease alcohol until LFTs normal

• Cease OCP

• Fat-free diet

• Advise on infection control

Prevention

• Sanitary health measures

• 2 dose primary vaccine 0 → 6–12 mth

Hepatitis B (HBV)

Features

• Transmission by blood spread, sex, perinatal spread, percutaneous

• 5% become chronic carriers but

• 95% with infant acquired HBV → carriers

• 15–40% of carriers → cirrhosis

• LFTs and viral markers confirm diagnosis

HBV antigens of virus particle

• HBsAg = surface antigens

• HBcAg = inner core antigens

• HBeAg = a soluble protein from pre-core & core

Antibodies develop to each of these (see Fig. H10).

Serology guidelines

• HBsAg = acute/persistent infection

• anti-HBs = past infection & immunity

• HBeAg = highly infective

• HBV DNA = circulating & replicating virus

• anti-HBc IgM = recent infection and earliest indicator

• anti-HBc IgG = past infection

Interpretation

• HBsAg = diagnosis and/or carrier

  • if +ve do full viral profile

Progress is monitored 6–12 mthly with HBeAg, HBV DNA and LFTs:

• HBsAg –ve + HBV DNA + anti-HBe = resolving

• as above + anti-HBs = full recovery

• HBsAg +ve + HBV DNA = replicating & infective, refer

Chronic hepatitis B is defined as the presence of HBsAg for longer than 6 months.

• Monitor LFTs every 6 mths—if abnormal refer to specialist.

Treatment

• As for Hepatitis A

• Advise about transmission

• Address any drug dependence

Medication for chronic Hepatitis B with abnormal LFTs:

• lamivudine 100 mg (o) /d or tenofir or entecavir until HBe Ag undetectable and replaced by anti-HBe twice at least 3 mths apart plus

• pegylated interferon alpha-2a SCI once weekly for 48 wks

Prevention

• Hepatitis B vaccine: 0, 1, 6 mths, or

• Hepatitis A and B combined: 0, 1, 6 mths

Note: Measure severity of any hepatic fibrosis by FibroScan^®(transient elastography) imaging.

Hepatitis C (HCV)

Features

• Mainly acquired from IV drug use & tattooing

• Minimal clinical symptoms—often asymptomatic

• About 70% can progress to chronic hepatitis (see Fig. H11)

• Treatment decisions based on the HCV genotype which should be tested

• Good cure rates now esp. with types 2 & 3

Serology

• HCVAb (anti-HCV) +ve = exposure (current or past)

• HCV RNA (a PCR test) +ve = chronic viraemia

            −ve = spontaneous clearance

• CD4/HCV = viral load

• ALTs in LFTs → indicates disease activity (tested 3 times over next 6 mths)

  • ALT persistently normal = good prognosis

  • ALT ↑↑ = treatment required; refer

• If PCR +ve + significant viral load +↑ ALT, perform genotyping (to determine treatment)

• HCV genotyping—to determine duration of anti-HCV therapy

Note: HCV RNA is present when the ALT becomes abnormal while the anti-HCV rises more slowly and may not be detectable for several weeks.

Follow progress with LFTs and αFP screening. Also check for HBV and HIV (informed consent).

Note: Monitor severity of hepatic fibrosis by FibroScan^® imaging.

Treatment

• As for Hepatitis B

• Education/advice about transmission

• Address opioid dependence

• Shared care with specialist (early referral)

• Best to start antiviral treatment within 12 wks

Acute HVC (if recognised early):

• pegylated interferon alpha SCI weekly, up to 24 wks

Chronic HVC:

• pegylated interferon alpha SCI plus

• ribaviran (o) in 2 divided doses

Length of treatment is determined by genotype & response.

As a rule: genotypes 1, 4, 5, 6—48 wks; genotypes 2, 3—24 wks.

Side-effects of treatment

These can be quite distressing.

Interferon: flu-like illness (constant), insomnia, depression, diarrhoea, leucopenia, thrombocytopenia, thyroid dysfunction, retinopathy, alopecia, neuropsychiatric disturbance, ↑ triglycerides.

Ribavirin: cough, dyspnoea, insomnia, rash, pruritus, ↑uric acid, haemolytic anaemia, teratogenicity, induction of autoimmune diseases.

Herpes labialis (classical cold sores)

The objective is to limit the size and intensity of the lesions.

Topical treatment

At the first sensation of the development of a cold sore (preferably at the prodrome stage):

• apply an ice cube to the site for up to 5 mins every 60 mins (for first 12 h) or

• saturated solution of menthol in SVR or

• other topical applications include:

  • idoxuridine 0.5% preparations (Herplex D liquifilm, Stoxil topical, Virasolve) applied hrly day 1 then 4 hrly or

  • povidone-iodine 10% cold sore paint: apply on swab sticks 4 times a day until disappearance or

  • aciclovir 5% cream, 4 hrly while awake for 4 d

Oral treatment for severe attack

One of:

• famciclovir 125 mg (o) bd for 5 d

• valaciclovir 500 mg (o) bd for 5 d

• aciclovir 200 mg (o) 5 times/d for 5 d

Aciclovir can be used in children.

Oral treatment for immunocompromised patients

One of:

• aciclovir 200 mg (o) 5 times/d for 7–10 d

• famciclovir 500 mg (o) bd for 7–10 d

• valaciclovir 1 g (o) bd for 7–10 d

Prevention

If exposure to the sun precipitates the cold sore, use a 30+ sun protection lip balm, ointment or solastick. Zinc sulphate solution can be applied once a wk for recurrences. Oral aciclovir 200 mg bd or valaciclovir 500 mg/d or famciclovir 250 mg bd (6 mths) can be used for severe and frequent recurrences (>6/yr).

Genital herpes

Topical treatment

The proven most effective topical therapy is topical aciclovir (not the ophthalmic preparation) or 10% povidone—iodine (Betadine) cold sore paint on swab sticks for several days.

Pain relief can be provided in some patients with topical lignocaine. Saline baths and analgesics are advisable.

Oral treatment

For the first episode of primary genital herpes (preferably within 24 h of onset) one of the guanine analogues can be used.

• aciclovir: 400 mg 3 times/d for 5 d or until resolution of infection or

• famciclovir: 250 mg (o) tds for 5 d or

• valaciclovir: 500 mg (o) bd for 5 d

This appears to reduce the duration of the lesions from 14 days to 5–7 d. The drugs are not usually used for recurrent episodes, which last only 5–7 d. A 5-d course of any of the drugs can be used for a severe recurrence. Very frequent recurrences (≥6 in 6 mths) benefit from continuous low-dose therapy for 6 mths (e.g. valaciclovir 500 mg (o) once daily).

Eczema herpeticum

• Aciclovir 400 mg (o), 3 times/d or

• Famciclovir 250 mg (o) bd or

• Valaciclovir 500 mg (o) bd until healed.

Use IV aciclovir for severe cases.

Herpetic whitlow

Drugs and dosage as above for 7–10 d.

Herpes simplex keratitis

• Aciclovir 3% ophthalmic ointment, 5 times/d for 14 d or at least 3 d after healing also

• Atropine 1% 1 drop 12 hrly

Consider specialist referral.

Cranial nerve involvement

The trigeminal nerve—15% of all cases:

• ophthalmic branch—50% affects nasociliary branch with lesions on tip of nose and eyes (conjunctivae and cornea)

• maxillary and mandibular—oral, palatal and pharyngeal lesions

Management

• Appropriate detailed explanation and reassurance. Dispel myths.

• Explain that herpes zoster is only mildly contagious but children can acquire chickenpox after exposure to a person with the disorder.

Topical treatment

For the rash, use a drying lotion such as menthol in flexible collodion. Aciclovir ointment can be used but it tends to sting.

Oral medication

1. Analgesics (e.g. paracetamol or codeine or aspirin)

2. Guanine analogue antiviral therapy for:

   • all immunocompromised

   • any patient provided rash present <72 h (esp. those >60 yrs)

   • ophthalmic zoster (evidence to date—reduces scarring and pain but not neuralgia)

   • severe acute pain

Drugs and dosage

• Aciclovir 800 mg 5 times daily for 7 d or

• Famciclovir 250 mg 8 hrly for 7 d or

• Valaciclovir 1000 mg 8 hrly for 7 d

Postherpetic neuralgia

Definition: pain persisting >4 weeks after vesicles crusted.

Increased incidence with age and debility, with duration greater than 6 mths.

• Resolves within 1 yr in 70–80% but in others it may persist for years.

• Eye complications of ophthalmic zoster, including keratitis, uveitis and eyelid damage.

Treatment options

Oral medication

• Basic analgesics (aspirin or paracetamol or NSAID orally)

• Carbamazepine 50–100 mg (o) bd initially ↑ to 400 mg bd (max) (for lancinating pain)

• Tricyclic antidepressants (e.g. amitryptiline 10–50 mg (o) nocte starting dose)

• Gabapentin 300 mg (o) daily (nocte) initially ↑ as tolerated to tds

Topical medication

• Capsaicin (Capsig) cream. Apply the cream, which can ‘burn’, to the affected area 3–4 times/d (apply ice massage, 20 mins before).

• Lignocaine 5% ointment or 10% gel or

• Lignocaine 5% patch to painful area

Others

• TENS as often as necessary (e.g. 16 h/d for 2 wks) plus antidepressants.

Prevention

Consider giving varicella zoster immune globulin to contacts of patients who are immunosuppressed and have no history of varicella (vaccine ‘Zostavac’):

Simple brief episodes (possible options):

• Valsalva manoeuvre

• rebreathing air in paper bag (as for hyperventilation)

• breath holding

• sucking ice/swallowing iced water

• catheter inserted quickly in and out of nose or nasopharynx

• pressure on the eyeballs

Persistent (assuming exclusion of organic diseases):

• chlorpromazine orally or IV or IM or

• sodium valproate

Consider acupuncture, hypnosis or phrenic nerve block.

Hip and buttock pain: diagnostic strategy model

Probability diagnosis

• Traumatic muscular strains

• Referred pain from spine

• Osteoarthritis of hip

Serious disorders not to be missed

• Cardiovascular:

  • buttock claudication

• Neoplasia:

  • metastatic cancer

  • osteoid osteoma

• Infection:

  • septic arthritis

  • osteomyelitis

  • tuberculosis

  • pelvic and abdominal infections: pelvic abscess, pelvic inflammatory disease, prostatitis

• Childhood disorders:

  • DDH

  • Perthes disease

  • slipped femoral epiphysis

  • transient synovitis (irritable hip)

  • juvenile chronic arthritis

Pitfalls (often missed)

• Polymyalgia rheumatica

• Fractures:

  • stress fractures femoral neck

  • subcapital fractures of femoral head

  • sacrum

  • pubic rami

• Avascular necrosis femoral head

• Femoroacetabular impingement (e.g. exostoses)

• Torn acetabular labrum

• Sacroiliac joint disorders

• Inguinal or femoral hernia

• Bursitis or tendonitis:

  • greater trochanteric pain syndrome

  • ischial bursitis

  • iliopsoas bursitis

• Osteitis pubis

• Neurogenic claudication

• Chilblains

Key features: hip & buttock pain

Key history

Pain analysis, especially exact site and pain radiation. Associated symptoms such as limp, stiffness, night pain, fever. Past history, family history, obstetric history, drug history.

Key examination

• Use the traditional method of look, feel, move, measure, test function and look elsewhere.

• The patient should be stripped to the underwear to allow maximal exposure.

• Also examine lumbosacral spine, sacroiliac joints, groin and knee.

Key investigations

• Serological tests: RA factor

• FBE, ESR/CRP

• Radiological tests: plain X-ray (AP) of pelvis to show both hip joints; lateral X-ray (‘frog’ lateral best in children)

• CT or MRI of hip joint

• Needle aspiration of joint if septic arthritis suspected

Hip pain in children

Children can suffer from a variety of serious disorders of the hip, e.g. developmental dysplasia (DDH), Perthes disease, tuberculosis, septic arthritis and slipped capital femoral epiphysis (SCFE), all of which demand early recognition and management.

Developmental dysplasia of the hip (DDH)

Previously known as congenital dislocation of the hip.

Clinical features

• Females:males = 6:1

• Asymmetry in 40%

• Diagnosed early by Ortolani and Barlow tests (abnormal thud or clunk on abduction); test usually –ve after 2 mths

• US excellent (esp. up to 3–4 mths, ideally 6 wks) and more sensitive than clinical examination

• Plain X-ray difficult to interpret up to 3 mths, then helpful

Treatment (guidelines)

• DDH must be referred to a specialist.

• Placed in an abduction splint or pelvic harness, or other methods if older.

Perthes disease

A juvenile osteochondritis leading to avascular necrosis of femoral head.

Clinical features

• Males:females = 4:1

• Usual age 4–8 (rarely 2–18)

• Sometimes bilateral

• Presents as a limp and aching (hip or groin pain)

• Characteristic X-ray changes

Requires urgent referral: provide crutches.

Transient synovitis

This common condition is also known as ‘irritable hip’ or observation hip and is the consequence of a self-limiting synovial inflammation.

Clinical features

• Children aged 4–8 yrs

• Sudden onset of hip pain and a limp: may be referred knee pain

• Child can usually walk (some may not)

• ± history of recent trauma or URTI

Outcome: settles to normal within 7 d, without sequelae. Treatment is bed rest, crutches and analgesics.

Refer early.

Slipped capital femoral epiphysis

SCFE typically presents in the obese adolescent (10–15 yrs) with anterior hip (groin pain) knee pain and a slight limp.

• Diagnosis before major slipping is vital.

• X-ray pelvis and ‘frog leg lateral’ of affected hip.

• Cease weight-bearing and refer urgently.

Septic arthritis

Septic arthritis of the hip should be suspected in all children with acutely painful or irritable hip problems.

Hip and buttock pain in the elderly

The following conditions are highly significant in the elderly:

• osteoarthritis of the hip

• aortoiliac arterial occlusion → vascular claudication

• spinal dysfunction with nerve root or referred pain

• degenerative spondylosis of lumbosacral spine → neurogenic claudication

• polymyalgia rheumatica

• trochanteric bursalgia (greater trochanteric pain syndrome)

• fractured neck of femur

• secondary tumours

Osteoarthritis of the hip

The most common form of hip disease.

Clinical features

• Usually >50 yrs, increases with age

• May be bilateral: starts in one, other follows

• At first pain worse with activity, relieved by rest, then nocturnal pain and pain after resting

• Stiffness, esp. after rising

• Stiffness, deformity and limp may dominate (pain mild)

Note: May present with knee pain.

• Abnormal gait

• First movements lost are IR and extension

Treatment

• Careful explanation: patients often fear OA of hip

• Weight loss if overweight

• Relative rest

• Complete RIB for acute pain

• Analgesics and NSAIDs (judicious use)

• Aids and supports (e.g. walking stick)

• Physical therapy, including isometric exercises

• Hydrotherapy is useful

• Surgery is very effective

Greater trochanteric pain syndrome

Also known as trochanteric bursalgia, it is very common in mid-age to elderly females presenting with pain over lateral surface of the greater trochanter. Features are:

• female >45–50 years

• pain on outside hip referred to as far as foot

• pain on lying on hip at night

• limp

Treat with trial of physiotherapy and exercises. Trial of NSAIDs and local steroid plus lignocaine injection.

Most cases are due to idiopathic hirsutism along racial or familial lines.

• Exclude adrenal or ovarian pathology (e.g. PCOS).

• Use bleaching, waxing or depilatory creams, or shave.

• Do not pluck hairs, esp. around the lips and chin. Plucking stimulates hair growth but shaving appears to have no effect.

• Electrolysis may help but is expensive and protracted.

• Drug treatment: spironolactone 100–200 mg daily; takes 6–12 mths to respond. Preferred to cyproterone acetate.

Features

• Persistent itchy papules due to hypersensitivity from insect bites

• Any biting insect, esp. fleas, mosquitoes, sandflies, mites, bed bugs

• Commonest in children 2–6 yrs

• Small weals evolving to firm reddish papules grouped together

• Persist for days, sometimes wks

Treatment

• Soothing lotion or cream (in preferred order):

  • phenol 1% or menthol 0.5% in oily calamine lotion or menthol 1% cream

  • crotamiton 10% lotion

  • Ego Soov Bite

• Topical corticosteroids (start with 0.5% hydrocortisone)

• Consider oral antihistamines or corticosteroids in severe cases

Note: Prevention is best, esp. in those prone to hives.

Common causes: viral URTI (acute laryngitis), non-specific irritative laryngitis, vocal abuse, nodules and polyps of cords, intubation, oesophageal reflux.

Chronic:

• children—‘screamer's nodules’

• adults—non-specific laryngitis (e.g. smoking; ‘barmaid’ syndrome)

Exclude: imminent airway obstruction (e.g. croup, epiglottitis, malignancy, hypothyroidism), other severe infections (e.g. diphtheria, TB), foreign body, allergy, goitre.

Diagnosis: larynx must be visualised.

Investigations

• Thyroid function tests

• Chest X-ray-look for bronchogenic cancer

• Indirect laryngoscopy

• Direct laryngoscopy

• Consider CT scan for suspected laryngeal neoplasia or trauma

Management

• Acute:

  • treat according to cause

  • vocal rest or minimal usage at normal conversation

  • avoid irritants (e.g. dust, tobacco, alcohol)

  • consider inhalations and cough suppressants

• Chronic:

  • establish diagnosis

  • consider specialist ENT referral

Laryngitis

About 50% of patients acquiring HIV infection develop an acute infective illness similar to glandular fever within wks of acquiring the virus (the HIV seroconversion illness).

Main features are fever, lymphadenopathy, lethargy and possibly sore throat and a generalised rash.

If these patients have a negative infectious mononucleosis test, perform an HIV antigen–antibody test or HIV rapid test, which may have to be repeated in 4 wks or so if negative.

If positive, confirm diagnosis with western blot test.

Patients invariably recover to enter a long period of good health for 5 yrs or more.

The level of immune depletion is best measured by the CD4 +ve T-lymphocyte (helper T-cell) count—the CD4 cell count. The cut-off points for good health and severe deficiency disease appear to be 500 cells/μL and 200 cells/μL respectively. The level determines when to initiate antiretroviral therapy (ART).

Progress of the disease can be measured with the viral load test.

Clinical stages of HIV disease

• Acute seroconversion illness

• Asymptomatic phase or persistent generalised lymphadenopathy

• Symptomatic:

  • early (e.g. constitutional symptoms, oral candidiasis, herpes zoster)

  • late (e.g. pneumocystis pneumonia, Kaposi's sarcoma)

  • advanced (e.g. CMV retinitis, cerebral lymphoma)

Typical common clinical presentation of HIV/AIDS

• Fever of unknown origin

• Weight loss (usually severe)

• Respiratory: non-productive cough, increasing dyspnoea and fever: due to opportunistic pneumonias (pneumocystis pneumonia may have abrupt or insidious onset)

• Gastrointestinal including oral cavity:

  • chronic diarrhoea (many causes) with weight loss or dehydration

  • oral candidiasis and oral hairy cell leukaemia

• Neurological disorders (e.g. headache, dementia, ataxia, seizures, visual loss)

• Skin—Kaposi's sarcoma and shingles, esp. multi-dermatomal, infections (viral, bacterial or fungal)

Management

Patients with HIV infection require considerable psychosocial support, counselling and regular assessment from a non-judgmental caring practitioner.

The holistic approach to life is recommended

Support groups and continuing counselling.

Medication (current guideline—CD4⁺ cells < 350 µL treat with ART)

If CD4 count 350–500 µL, strongly consider, offer or closely monitor. Current thinking favours early treatment.

Currently the use of three antiretroviral drugs is preferred: usu. 2 from the NRTI class with one from either the NNRTI or the protease inhibitor group. The HAART (highly active antiretroviral therapy) strategy is a combination of 3 (or more) agents with one or more penetrating the blood–brain barrier.

Common regimens

• zidovudine + lamivudine + indinavir or nevirapine

• zidovudine + didanosine + indinavir or efavirenz

• emtricitabine + tenofovir + efavirenz

• emtricitabine + didanosine + indinavir or nevirapine

For updated information check the HIV website (www.aidsinfo.nih.gov). Subcutaneous injections of interleukin have been shown to boost immunity.

Precautions—beware of:

• drug interactions (www.hiv-druginteractions.org)

• contraindicated combinations (eTG complete)

• adverse effects (eTG complete)

Note: Treatment of acute HIV is not of proven clinical benefit, but is optional and some clinics offer it.

Recommended BP measurement

• All people aged 18+ yrs

• Every 2 yrs

Recommended routine basic screening tests

• Ambulatory monitoring

• Urine tests

  • urinalysis (for protein, blood and glucose)

  • micro-urine (casts, red and white cells)

  • urine culture (only if urinalysis abnormal)

• Biochemical tests

  • potassium and sodium

  • creatinine and urea/e GFR

  • uric acid

  • glucose

  • lipids

• Chest X-ray

• ESR

• ECG

Others (e.g. renal ultrasound) only as indicated.

Risk stratification and calculation of cardiovascular risk

Treatment of hypertension is generally indefinite and it is important to establish the risk status and the prognosis before starting therapy, esp. if hypertension is an isolated factor. The WHO-ISH recommendation is that decisions about management of patients with hypertension should not be based on BP alone, but also on the presence or absence of other risk factors, including important factors such as age, diabetes and smoking. Cardiovascular risk should be stratified according to the BP level and the presence of:

• absolute cardiovascular risk factors

• associated clinical conditions

• target organ damage

A practical approach is to stratify total cardiovascular risk in the terms low, moderate (medium), high and very high added risk which are calibrated to indicate an absolute 10-yr risk of cardiovascular disease of <15%, 15–20%, 20–30% and >30% respectively (based on Framingham criteria). For example, low risk indicates starting treatment and monitoring, high risk indicates treat immediately.

Risk estimates can be determined by referring to various cardiovascular risk tables on the website. A commonly used tool in Australia is the modified New Zealand Cardiovascular Risk Calculator (www.nzgg.org.nz or www.heartfoundation.com.au).

It is important to collaborate with patients in decision making and thus discussing cardiovascular risk assessment, and BP level should be the starting point when discussing the risks and benefits of treatment.

Management of essential hypertension

Start with non-drug therapy if diastolic BP >90 mmHg and systolic >140 mmHg.

• Weight reduction (if necessary)

• Reduced alcohol intake to 1–2 SDs/d (max.)

• Reduced sodium intake (avoid excess salt)

• Increased exercise

• Reduction of particular stress

• Smoking cessation

• Consider drug factors (e.g. NSAIDs, steroids)

• Ensure adequate potassium and calcium intake

Drug treatment

Monotherapy

• Start with a single agent at low dose (depends on the individual and risk factors), e.g. diuretic (preferred in elderly) or β-blocker (cardioselective).

• Can use an ACE inhibitor/angiotensin II receptor blocker (ARB) or a calcium channel blocker (CCB) as first line.

Recommended starting medication

1. ACE inhibitor or ARB or

   calcium channel blocker (CCB) or

   low-dose thiazide diuretic (if aged ≥65 years)

2. If target not reached:

   ACE1 or ARB + CCB or

   ACE1 or ARB + thiazide

3. If target not reached: use combination (best evidence)

   ACE1/ARB + CCB + thiazide

Need at least 4–6 wks to test effect.

If partly effective, increase dose to maximum or add on.

If ineffective, substitute a different class.

Combination (for partly effective monotherapy) (Fig. H12)

• Diuretic + β-blocker or ACE inhibitor/ARB

• β-blocker + dihydropyridine Ca antagonist

• ACE inhibitor/ARB + Ca antagonist

• prazosin + others

Example

Start with perindopril 5 mg (o)/d increasing to max 10 mg/d.

If inadequate, add:

• indapamide 1.25 mg (o) d or hydrochlorothiazide 12.5 mg (o)/d.

Note: Monitor electrolytes, esp. s. potassium.

• Rebreathe air from cupped hands over nose and mouth using slow deep breaths.

• Encourage patient to learn to slow down breathing.

• Get patient to breathe in and out of a paper bag (an alternative esp. if tetany develops).

• Investigate the possibility of phobias.

• Advise cutting out caffeine and nicotine.

Symptoms: sweating, tremulousness, palpitations, nausea, anxiety, blurred vision, confusion ± coma.

Causes: insulin toxicity, oral hypoglycaemic toxicity, other drugs (e.g. quinine, salicylates), alcohol, fasting, tumours (e.g. insulinoma), Addison disease, post gastrectomy.

Treatment: glucagon 1 mg SC or IM with sugar under tongue or other sweets, 25–50 mL, 50% dextrose (or glucose) or both if severe.