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Urinary symptoms and haematuria
Decision algorithm for the investigation and referral of haematuria.
Visible haematuria (VH)
Plasma creatinine/eGFR
Exclude transient cause
including UTI
Symptomatic nonvisible
haematuria (s-NVH)
Urology assessment
• Imaging and cystoscopy
Non-visible haematuria (NVH)
Exclude transient causes, including UTI
Asymptomatic non-visible haematuria (a-NVH)
Blood pressure
Plasma creatinine/eGFR
Send urine for ACR or PCR
40 yrs <40 yrs
All of:
• eGFR 60 ml/min AND
• ACR <30 or PCR <50 AND
• BP <140/90
2 of 3 dipstick tests positive
YesNo Stop
Normal Abnormal
Any one of:
• eGFR <60 ml/min
• ACR 30 or PCR 50
• BP 140/90
Nephrology assessment
No cause established
Primary care monitoring
Annual assessment (whilst haematuria persists) of BP, eGFR and ACR/PCR
Referral or re-referral to urology if:
• Development of VH or s-NVH
Referral to nephrology if:
• Significant or increasing proteinuria (ACR >30 or PCR >50)
• eGFR <30 ml/min (confirmed on at least 2 readings and without an identifiable reversible cause)
• Deteriorating eGFR (by >5 ml/min fall within 1 year, or >10 ml/min fall within 5 years)
N.B. Direct referrals between urology and nephrology will depend on local commissioning guides
Cause establishedCause established
Fig.15.3 Decision algorithm for the investigation and referral of haematuria. BAUS/RA Guidelines: Initial assessment of haematuria July 2008. ACR, Albumin/creatine ratio; BP, blood pressure; eGFR, estimated glomerular filtration rate, PCR, protein/creatinine ratio; UTI, urinary tract infection.
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Introduction
1515
Imaging
In urological practice, imaging is of most use when you sus­pect structural lesions. Renal tract ultrasound scanning is useful to assess the size and cortical structure of the kidney and visualize the ureters and bladder to guide further imag­ing. This may include:
• Abdominal CT scan: to visualize the kidneys, adjacent organs and other abdominal masses. Noncontrast CT of the kidneys/ureters/bladder is now the gold standard for the diagnosis of renal calculi (99% sensitive).
• Abdominal magnetic resonance imaging is superior to CT for some solid lesions and for staging of renal cell carcinoma.
Other investigations
• Cystoscopy: bladder lesions.
• Ureteroscopy: ureter lesions.
RED FLAG
Visible asymptomatic haematuria in patients older than 45years and persistent nonvisible haematuria in patients older than 60years needs urgent urological investigation to exclude a renal tract malignancy (see Fig.15.3).
Proteinuria
Small amounts of proteinuria can occur in non-renal dis­ease such as urinary tract infection and with vaginal mu­cus; however, significant proteinuria of more than 1 g/day usually indicates primary renal pathology. Proteinuria is discussed in further detail in Chapter30.
Chapter Summary
• Urinary symptoms include symptoms of irritation, such as frequency and dysuria or obstructive symptoms, including hesitancy, poor stream, postmicturition dribbling and incomplete voiding.
• Polydipsia and polyuria can be driven by high glucose levels, hypercalcaemia and diabetes insipidus.
• Diabetic insipidus can be cranial or nephrogenic; focus your history taking and examination on potential causes.
• Haematuria can occur from anywhere in the urogenital tract. It can be classified into visible and nonvisible, painful and painless. Painless visible haematuria in patients older than 45years and persistent nonvisible haematuria in patients older than 60years should prompt urological referral to exclude an underlying malignancy.
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Headache and facial pain

16

INTRODUCTION

Headache is one of the most common presenting symp­toms. There are often few clinical signs, and the history is the main diagnostic tool. Many different pathological processes can result in headache and facial pain. The International Headache Society classification divides headache into primary (where the headache is itself the disease; e.g. migraine), secondary (where the headache is due to other conditions; e.g. infection, trauma, vascular disorder) and other headaches, facial pains and cranial neuropathies.
The differential diagnosis of headache and facial pain is
summarized in Table16.1.
History and examination findings
History
Characteristics of the headache will point towards the diagnosis.
Solitary acute episode
This pattern is seen in vascular events, infection and trauma. It may also be the first presentation of the other causes of headache.
Subarachnoid haemorrhage presents with a sudden on­set of severe pain ‘as if someone had hit them on the head’. Often most severe occipitally, it usually reaches maximal severity at onset or within seconds. Nausea, vomiting, neck stiffness and photophobia can occur and can result from meningeal irritation. Subarachnoid haemorrhage can be associated with altered level of consciousness, seizures and focal neurological deficits.
Seizures, focal neurological signs and symptoms of raised intracranial pressure (see later) can also result from cerebral venous sinus thrombosis. Causal factors include inherited disorders of coagulation, pregnancy, oral contraceptive pill use, dehydration, extension of local infection (e.g. of para­nasal sinuses or middle ear) and severe intercurrent illness. Dissection of a carotid or vertebral artery can also cause a sudden onset of pain associated with focal neurology.
Patients with infective meningitis present with a short history of headache, symptoms of infection (malaise, fever, rigors), symptoms of meningeal irritation (vomiting, pho­tophobia, neck pain and/or stiffness) and possibly a rash or altered mental state. ‘Aseptic’ meningitis that can occur because of tuberculosis or carcinoma presents in a more subacute manner and can go unnoticed. Encephalitis, acute inflammation of the brain, may present with headache, fe­ver and altered mental status.
Table16.1 Differential diagnosis of headache and facial pain (see Chapter32)
Pattern Causes
Solitary acute episode Infection: meningitis, encephalitis, abscess
Vascular event: intracranial haemorrhage (especially subarachnoid), venous sinus thrombosis, occasionally infarction (especially if arterial dissection occurred) Trauma First migraine or benign thunderclap headache
Progressive headache Raised intracranial pressure (including idiopathic intracranial hypertension)
Giant cell arteritis
Episodic headache/facial pain Migraine
Cluster headache and other trigeminal autonomic cephalalgias Trigeminal neuralgia Coital cephalalgia
Chronic headache/facial pain Tension headache/analgesic rebound headache
Postherpetic neuralgia Head injury Paget disease of the skull
Other causes of facial pain Dental problems
Temporomandibular joint Ears/nose/sinuses Cervical spine Eye—especially acute or intermittent angle-closure glaucoma Myocardial ischaemia (rarely)
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Headache and facial pain
Cerebral abscess may cause fevers, rigors, headaches, seizures and symptoms of raised intracranial pressure as the lesion enlarges. The infection may have spread from a local or distant primary focus, such as lung (bronchiectasis, ab­scess), heart (endocarditis), middle ear or sinuses (paranasal sinusitis).
Acute angle-closure glaucoma can cause a severe headache associated with blurred vision, eye pain, cloud­iness of the cornea, conjunctival injection and a dilated pupil. There may be nausea and vomiting. It should be considered in hypermetropic, middle-aged or elderly patients. It may occur intermittently with repeated acute attacks.
Progressive headache
A headache that comes on gradually over days or weeks and increases in severity is often a feature of a ‘space- occupying lesion’ (such as a tumour or abscess), idiopathic intracranial hypertension, chronic subdural haematoma or hydro­cephalus. Hydrocephalus can be due to either blockage of cerebrospinal fluid (CSF) flow (‘noncommunicating’, e.g. haemorrhage, cysts, malformations) or failure of CSF reab­sorption (‘communicating’, e.g. following meningitis or sub­arachnoid haemorrhage).
In these, the headache results from raised intracranial pressure, and has the characteristic features shown below.
CLINICAL NOTES
SYMPTOMS OF RAISED INTRACRANIAL PRESSURE
• Headache worse on coughing, sneezing, stooping down.
• Headache worse in the morning.
• Visual disturbance due to papilloedema.
• Nausea and vomiting.
• Diplopia (false localizing cranial nerve VI palsy).
Headache associated with temporal arteritis is also of gradual onset; however, the nature of it is different from that described above. The condition predominantly af­fects older people (mean age at onset is over 70 years). Presentation is with superficial headache overlying the temporal arteries; scalp tenderness which may be exac­erbated by brushing or combing the hair is often present. Jaw claudication, and occasionally tongue claudication, may arise because of inflammation of the branches of the external carotid artery. Visual loss may be temporary (amaurosis fugax) or permanent if the ciliary or central retinal arteries are affected. Weight loss, anorexia, fever and proximal muscle stiffness (but not tenderness) may also occur.
HINTS AND TIPS
Consider temporal arteritis in any patient older than 50years with a headache.
Recurrent episodic headache and facial pain
Migraine and cluster headaches present with episodes of pain (often severe) interspersed with long symptom-free periods. Paroxysms of pain are also a feature of trigeminal neuralgia and other cranial neuralgias.
Although, classically, migraine is preceded by aura, migraine without aura is more common. Premonitory symptoms precede both types, occur hours to days before the migraine and include fatigue, nausea and sensitiv­ity to light and noise. Aura can consist of visual features (positive, e.g. flickering lights, spots or lines, or nega­tive, e.g. visual loss), sensory symptoms (paraesthesiae or numbness), speech disturbance and focal neurology. These symptoms can occur with or without a headache, and are fully reversible. The headache can be unilateral or bilateral. It is often pulsating in nature, and can be associated with nausea, photophobia, phonophobia and aversion to physical activity. The attack resolves sponta­neously after 4–72 hours in adults.
Cluster headache is a severe unilateral pain centred around one eye. The pain lasts for 15–180 minutes if un­treated, and occurs up to eight times per day for several weeks, often waking the patient from sleep. There may be ipsilateral nasal congestion or rhinorrhoea, and the eye can become watery and red; miosis and ptosis can also develop, and occasionally will become permanent. Symptom-free periods of many months occur between attacks. Cluster headache is more common in men, and may be precipitated by alcohol.
Trigeminal neuralgia is characterized by paroxysms of lancinating pain in the distribution of cranial nerve V. It is often stimulated by the touching of ‘trigger zones’ on the face such as the lips, or by eating or drinking, but can oc­cur spontaneously. The pain does not occur during sleep. Spontaneous remissions can last several months.
Chronic headache and facial pain
Persistent pain is a feature of postherpetic neuralgia, post­traumatic headache, Paget disease of the skull and tension headache.
Postherpetic neuralgia is persistent burning pain in the distribution of the trigeminal nerve that develops following infection of the nerve by varicella zoster virus (commonly known as ‘shingles’). Facial scarring is usually apparent, and the pain may disturb sleep. It is uncommon in the young.
Tension-type headache is often described as ‘a tight band around the head’. It is most often constant and
102
Eyes
— Papilloedema — Subhyaloid haemorrhage — Horner's syndrome — 3rd, 6th cranial nerve palsies — Optic atrophy
Meningism
— Neck stif — Kernig sign — Brudzinski’
TMJ
Tenderness and
Temporal artery
movement
fness
s sign
Introduction
— Tenderness — Loss of pulsation
Sinuses and teeth
— Dental hygiene — Sinus tenderness
Cervical spine
— Movement and tenderness
Pulse and blood pressure
— Septic shock — Cushing reflex
1616
Fig.16.1 Examining the patient with headache and facial pain. AVM, Arteriovenous malformation; TMJ,
temporomandibular joint.
bilateral, and tends to be worse towards the end of the day or at times of stress.
Following head injury, a few patients develop persistent headache, like a tension headache. It is associated with poor memory and concentration, dizziness, irritability and symptoms of depression.
People in whom headache developed or worsened while they were using analgesic medication for more than 3months may have a medication-overuse headache. It can occur with practically any of the medications commonly used for treatment of headache including NSAIDs, parac­etamol, aspirin and triptan, opioid and ergot drugs.
Examination
On examination, look for evidence of the pathological pro­cesses, such as raised intracranial pressure and meningism.
General
— Altered consciousness level — Photophobia — Phonophobia — Fever — Audible bruit over AVM — Facial herpetic scarring — Purpuric rash — Focal neurological signs — Paget disease/bony deformity
Focal neurological deficits, if present, help to determine the site of the lesion. Fig.16.1 summarizes the examination approach.
CLINICAL NOTE
SIGNS OF RAISED INTRACRANIAL PRESSURE
• Papilloedema.
• False localizing sign (ipsilateral then bilateral cranial nerve VI palsy).
• Altered level of consciousness.
• Bradycardia with hypertension (the Cushing reflex – a late sign); may indicate imminent brain herniation and death.
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Headache and facial pain
CLINICAL NOTES
SIGNS OF MENINGISM
• Irritability: with a preference for a quiet, darkened room.
• Neck stiffness and photophobia.
• Positive Kernig sign: spasm and pain in hamstrings on knee extension.
• Positive Brudzinski sign: neck flexion causes hip and knee flexion.
• Delirium, fever and petechial rash: may be present in infectious meningitis.
CLINICAL NOTE
SUBARACHNOID HAEMORRHAGE
Look for subhyaloid (retinal) haemorrhage, bruit of an arteriovenous malformation and a cranial nerve III palsy caused by direct pressure from a posterior communicating artery aneurysm.
CLINICAL NOTE
SIGNS OF TEMPORAL ARTERITIS
• Temporal artery tenderness.
• Loss of temporal artery pulsation – there may be overlying erythema.
• Optic atrophy (seen as optic disc pallor).
• Low-grade pyrexia.
Investigations
An algorithm for the investigation of the patient with head­ache and facial pain is shown in Fig.16.2. Investigations in­clude the following.
Blood tests
• Full blood count: normochromic normocytic anaemia suggests chronic disease (e.g. temporal arteritis, tuberculous meningitis); leucocytosis in infection.
• Erythrocyte sedimentation rate: high in temporal arteritis but may also be raised in infection and malignancy.
• Clotting studies may be important in the context of intracerebral bleeding.
Imaging
• CT or magnetic resonance imaging scans of the head: presence of blood, space-occupying lesion (tumour, abscess) or hydrocephalus. Contrast enhancement may help determine the nature of a lesion.
• CT angiography, magnetic resonance angiography or digital subtraction angiography: to identify the precise cause (e.g. berry aneurysm or arteriovenous malformation) in subarachnoid haemorrhage.
Further tests (Fig.16.2)
• Temporal artery biopsy: temporal arteritis. This is a definitive test but, as there is often patchy vascular involvement (‘skip lesions’), a negative result does not exclude the diagnosis.
• Lumbar puncture: this should never be performed when raised intracranial pressure is a possibility, as it may cause cerebellar tonsil herniation (‘coning’). CSF should be sent to the laboratory for assessment of glucose and protein, microscopy, culture and cytology (see Chapter22). CSF sampling and spectrophotometry may also diagnose subarachnoid haemorrhages not detected on CT.
• Visual fields: these should be serially measured in patients with idiopathic intracranial hypertension (because of the risk of optic nerve infarction).
• Electroencephalography: herpes simplex encephalitis shows abnormal patterns.
• Intraocular tonometry: pressure will be raised in glaucoma.
Chapter Summary
• Tension headache is the most common type of headache.
• The history and examination are the most useful diagnostic tools in a patient presenting with headache.
• Brain imaging is not routinely performed in patients with no worrying features.
• Raised intracranial pressure is a contraindication to performing a lumbar puncture.
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Headache
Facial pain
History
Examination
Introduction
1616
Suggestive of
temporal arteritis
ESR
Temporal artery biopsy
CSF
Leucocytosis
Meningitis
Diagnosis unclear
or suggestive of
intracranial disease
CT head scan
or MRI scan
Normal Abnormal
Lumbar
puncture
Xanthochromia
Subarachnoid
haemorrhage
Benign intracranial
Diagnosis clear
Migraine
Tension headache
Coital cephalagia
Cluster headaches
Temporomandibular
joint pain
Blood Tumour Abscess
Hydrocephalus
High CSF
pressure
hypertension
Dural sinus thrombosis
Angiography
Berry aneurysm
Arteriovenous
malformation
No abnormality
Fig.16.2 Algorithm for the investigation of the patient with headache and facial pain. CSF, Cerebrospinal fluid; CT, computed tomography; ESR, erythrocyte sedimentation rate; MRI, magnetic resonance imaging.
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Goitre, thyroid disease and
thyroid malignancy

INTRODUCTION

‘Goitre’ means an enlarged thyroid gland. It may be a single enlarged gland or composed of a single nodule or multiple nodules. The leading cause of a goitre worldwide is iodine deficiency; in the United Kingdom, where iodine is added to foods as a supplement, autoimmune conditions (e.g. Hashimoto thyroiditis and Graves disease) are the most common causes. Thyroid nodules are common, and are often incidental findings on ultrasonography or at autopsy. In adults, only around 5% of these nodules are malignant. Thyroid nodules are less common in children but a greater proportion are malignant.
History and examination findings
Most patients are asymptomatic. The goitre may be noticed by someone else or may be seen by the patient in the mirror. The history taking should aim to reveal any features of com­pression from the goitre, whether the metabolic function of the gland is altered and to elucidate whether a malignant cause is likely:
• Local symptoms: ask about dysphagia, dyspnoea and hoarseness.
• Symptoms of hypothyroidism or hyperthyroidism.
• Previous or current use of goitrogenic drugs (e.g. lithium, amiodarone).
• Diet, lack of iodine or conversely very high iodine intake (e.g. seaweed); both can lead to goitre formation.
• Exposure to environmental factors such as previous radiotherapy or environmental radiation such as fallout from the Hiroshima or Chernobyl disasters, or living in an area of high volcanic activity such as Iceland or Hawaii (all are risk factors for benign and malignant thyroid nodules).
• Family history: ask about a history of goitre (suggesting autoimmune disease) or of thyroid cancer (suggesting familial thyroid cancer or multiple endocrine neoplasia).
• Smoking (the evidence is conflicting but smoking is certainly a risk factor for other malignancies which may cause neck lumps).
• Duration of goitre and rate of change: long-standing goitres suggest benign disease.
• Tenderness: subacute thyroiditis.
• Pregnancy/menopause (associated with thyroid enlargement).
Physical examination should look for:
17
CLINICAL NOTES
The incidence of thyroid cancer peaks between 30 and 50years and is around three times more common in women.
• signs related to the patient's thyroid status;
• whether the goitre is smooth or nodular;
• whether there are nodules and whether these are multiple nodules or a single nodule;
• whether the nodule is hard or soft, regular or irregular and fixed or mobile, and whether there is lymphadenopathy.
HINTS AND TIPS
On examination, ask the patient to drink some water, and note the thyroid moving as the patient swallows. Does the mass move with swallowing? If it does, this suggests it is part of the thyroid. Look for enlargement and asymmetry. Stand behind a seated patient and use your fingers to examine the gland as the patient swallows. Feel for lumps and tenderness. Percuss down below the thyroid onto the anterior chest wall to detect any retrosternal thyroid mass.
RED FLAGS
The presence of stridor, signifying partial airway obstruction, requires immediate referral.
Other red flags include any child with a thyroid nodule, unexplained hoarseness or voice change associated with a goitre, a painless rapidly enlarging thyroid mass and a thyroid mass in a patient with a history of previous radiation therapy.
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