Examination Check GCS, pulse rate, respiratory rate, BP, T and SpO 2 : \200 Feel the h ead for muscular tenderness, arterial tenderness, trigger points for neuralgia, and look for evidence of head injury. Examine the eyes for VA, pupil reactions, eye movements. Look at the fundi for papilloedema. Palpate the sinuses for tenderness. \200 Look in the ears for haemotympanum or infection. \200 Check the oral cavity for infection. \200 Look for evidence of purpura/rash of me ningococcal infection. \200 Complete a full neurological examination (include cranial ner ves, limb tone, power, sensation, co-ordination and re \202 exes). Check for Kernig \200\231s sign : straightening the knee whilst the hip is \202 exed prod uces discomfort in the presence of meningeal irritation. Management Investigation and emergency treatment will be tailored according to the presenta tion of the patient, based upon the likely diagnosis. \200 Check FBC, ESR, CRP, U&E, bloo d glucose. \200 If pyrexial and no other obvious source of infection found, take blood cultures and consider IV cefotaxime 2g. Start IV \202 uids and admit. Give paracetamol (oral or IV if vomiting) and an NSAID. \200 An effective treatment for h eadache is IV metoclopramide 10mg with IV \202 uids. Arrange an emergency CT brain for any patient with an acute severe headache, or with a hist ory of seizure, or an abnormal neurological exam. Arrange a CT for any patient with HIV. If subarachnoid hemorrhage is suspected and CT normal, admit for lumbar puncture. It may be safe to discharge home a patient with slow onset headache that has resolved follo wing treatment, with normal examination and blood tests. Arrange GP follow up. Always advis e to reattend if symptoms worsen. 128 CHAPTER 3 Medicine Subarachnoid hemorrhage Consider subarachnoid hemorrhage in any \200\230worst ever \200\231 or sudden onset headac he Atraumatic subarachnoid hemorrhage can occur at any age and is an important cause of sud den collapse and death. Most bleeds follow rupture of saccular ( \200\230berry \200\231) an eurysms in the circle of Willis. Other bleeds may be due to arteriovenous malformations, tu mors, or connective tissue disorders. History Up to 70 % of patients with subarachnoid hemorrhage report rapid onset or \200\230 worst ever \200\231 headache. This is classically described as \200\230like a blow to the back of the head \200\231, accompanied by neck pain, photophobia, and vomiting. In 25 % , e xertional activities precede the event. The patient may present after syncope or \201 ts. Drowsiness and confusion are common. \200\230Warning headaches \200\231 may precede subar achnoid hemorrhage. Unilateral eye pain may occur. Examination Document pulse rate, BP, T o , and GCS. An unconscious patient with signs of Cu shing \200\231s response signi \201 es i intracranial pressure. Perform full cranial and p eripheral nerve examination. There may be focal motor and sensory signs due to intracerebra l extension of the hemorrhage or vasospasm, subhyaloid hemorrhages (blotchy hemorrhages see n in the fundi) or cranial nerve palsies. Oculomotor nerve palsy is characteristic of a ber ry aneurysm involving the posterior communicating artery. Neck stiffness is often absent in ED presentations, either because meningeal irritation has not yet occurred or because the patient is deeply unconscious. Investigation This may need to proceed alongside resuscitation in seriously ill patients: \200 Assess airway and breathing. If the patient is unconscious, open the airway and conta ct ICU. Consider urgent RSI, tracheal intubation and ventilation. Obtain venous access and check BMG, FBC, clotting screen, U&E. \200 CXR may show changes of neurogenic pulmonary oedema. \200 ECG may demonstrate ischaemic changes. \200 Arrang e emergency CT scan for all suspected cases (maximally sensitive within 12hr). Admit for lu mbar puncture (LP) (done > 12hr after head- ache onset) even if CT scan is normal. Involve the neurosurgical team early. It may be useful to use the Hunt and Hess score (see Table 3.8 ) when communicating severity by phone. 129 SUBARACHNOID hemorrhage Table 3.8 Hunt and Hess scale for subarachnoid haemorrahage Grade 1 Asymptomatic, mild headache, slight nuchal rigidity 2 Moderate to severe headache, nuchal rigidity, no neurologic de \201 cit other than cranial nerve palsy 3 Drowsiness/confusion, mild focal neurological de \201 cit 4 Stupor, moderate-severe hemiparesis 5 Coma, decerebrate posturing Treatment Tailor this according to the presentation and the need for resuscitation: \200 Maintain SpO 2 94 \200\22398 % . \200 Provide adequate analgesia and antiemetic. Codeine (30 \200\22360mg PO), paracetamol (1g PO) and/or NSAID may suf \201 ce. Some patients requ ire more potent analgesics (eg morphine titrated in 1mg increments IV according to response ) \200\224 proceed slowly to avoid drowsiness. If unconscious (GCS < 8), severely agitated or combative, tracheal intu- bation (with gener al anesthetic (GA)) will allow IPPV and control of pCO 2 to within normal levels. Insert a urinary catheter and arterial line. Contact neurosurgical team \200\224 further treatment options include: \200 Nimodipine ( 60mg PO every 4hr or 1mg/hr IVI) to prevent and treat ischaemic neurological de \201 cits secondary to vasospasm. \200 Mannitol IV (eg 200mL o f 10 % ) if there is evidence of i ICP. 130 CHAPTER 3 Medicine Migraine Patients with recurrent migraine rarely attend the ED unless symptoms are differen t from usual \200\224 take care to avoid missing more serious condi- tions. The pathogenes is of migraine is not entirely clear, but there is initial vasoconstriction and subsequent vasodilatation of both intracranial and extracranial blood vessels. Presentation Precipitants include fatigue, alcohol, menstruation, oral contraceptive pill ( OCP), hunger, chocolate, cheese, shell \201 sh, and red wine. A prodrome lasting 5 \200\22330min occurs in a third of patients, with blurred vision, phot ophobia, or scintillating scotomata (an area of blurred or absent vision surrounded by movi ng zig-zag lines), malaise, anorexia, and vomiting. A few experience hemiparaesthesiae, mil d unilateral weakness, ataxia, or dysphasia. The following headache may last 4 \200\22372hr , and is usually \200\230throbbing \200\231 and unilateral, but may be generalized. Photop hobia, nausea, or phonophobia is common. Rare forms of migraine Hemiplegic migraine Profound hemiplegia precedes the development of the headache by 30 \200\22360min. The weakness and other focal de \201 cits usually resolv e quickly. Occasionally, they may be slow or fail to resolve. Basilar migraine Brainstem disturbances, with impaired consciousness, vertigo, dysarthria, diplopia, and limb weakness. Ophthalmoplegic migraine Transient unilateral ophthalmoplegia and ptosis, which may last se veral days. Acephalgic migraine Very occasionally, neurological defects may be present without headache . Examination Look for evidence of other serious diagnoses. Treatment of acute attacks \200 Give simple analgesia (eg paracetamol 1g PO PRN qds or NS AID) in combination with an anti-emetic (eg metoclopramide 10mg PO, or IV). \200 Refer fo r admission patients who have neurological signs, altered mental status, or where there is diagnostic uncertainty (including change in severe headache pattern). Acute attacks that fail to respond to simple measures may respond to other drugs, but these are associated with signi \201 cant adverse effects. 5HT 1 agonist sumatriptan (6mg SC or 50mg PO or 20mg intranasally) is effective, but discuss with a senior \201 rst. Sumatriptan causes vasoconstriction and is therefore contraindicated in IHD, uncontrolled h ypertension, basilar, and hemiplegic migraine. Rebound headache may occur in up to 45 % . Ergotamine is best avoided (see BNF ). It causes nausea, vomiting, abdominal pain, and musc ular cramps. It is contraindicated in peripheral vascular disease, IHD, pregnancy, breast f eeding, hemiplegic migraine, Raynaud \200\231s disease, liver and renal impairment, and hyp ertension. This page intentionally left blank 132 CHAPTER 3 Medicine Other causes of headache Cluster headache These are more common in men. Often there is a fa mily history. Headache usually occurs at night, waking the patient. Sometimes alcohol may a ct as a precipitant. Headaches are typically \200\230clustered \200\231 into up to eight a ttacks per day each lasting between 15 and 180min. Pain is usually severe, centered upon th e eye. Associated symptoms, often unilateral, include conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead, and facial sweating, miosis, ptosis. Treatment Hig h \202 ow O 2 (12L/min via reservoir mask) for 15min sometimes provides relief. Otherwise , use paracetamol/NSAID. Consult before contemplating starting ergotamine or sumatriptan. Trigeminal neuralgia Characterized by stabbing unilateral pain within the distribution of t he trigeminal nerves. Stimulation of the \200\230trigger area \200\231 (eg by touching, ha ir brushing, or even chewing) induces very severe pain. Treat with car- bamezepine and oral analgesia. Admit if the pain is severe and unrelieved. Tension headache The diagnosis is only made after exclusion of more serious pathology. The history may be described in a dramatic manner. The headache is usually continuous, pres sing, or tight ( \200\230band-like \200\231) in nature. It is usually bitemporal or occipit al. Usual features of migraine are absent and the headache does not worsen with exertion. Examination often reveals pericranial muscle tenderness, but is otherwise normal. Treat with simple analgesia (eg paracetamol 1g PO qds PRN) and advise GP follow-up. Reassur e the patient that a thorough history and examination have not revealed any worrying featur es. Cranial ( \200\230temporal \200\231 or \200\230giant cell \200\231) arteritis (see b p .541) Consider this in all patients > 50 years with recent onset of headache or change in h eadache pattern. There may be weight loss, night sweats, low grade fever, jaw claudication, ande d vision (up to 10 % present with acute visual loss), shoulder girdle stiffness, and muscular aches (polymyalgia). Involvement of carotid or vertebral arteries may lead to TIAs or stroke. Examination: the temporal arteries may be tender, reddened, pulseless, or thickened. Fundos copy is usually normal, but papilloedema can occur later in the disease. Investigation: i E SR > > 40mm/hr, often with a low grade anemia and leucocytosis. A normal ESR does not exclu de temporal arteritis. Treatment: in view of the serious risk of rapidly progressive visual loss, if suspected giv e 200mg IV hydrocortisone (or 40mg prednisolone PO) immediately. Refer to the neurologist o r ophthalmologist as an emergency \200\224 the diagnosis may be con \201 rmed by temporal artery biopsy. 133 OTHER CAUSES OF HEADACHE Space-occupying lesions If the headache is always located on the same side, consider space occupying lesions and arteriovenous malformations. Headaches that are dull, aching, and mad e worse by lying down or straining are typical of space occupying lesions. Malignant hypertension Hypertension is an unusual cause of headaches, but is seen in patien ts with malignant hypertension and diastolic BP > 130mmHg ( b p.90). Ventricular shunts Assume that any patient who presents with headaches associated with a ve ntricular shunt has infection/blockage and refer as an emergency. Associated drowsiness is a particular pointer to blockage. Analgesic headache Chronic use of simple analgesics, sympathomimetics, ergotamine, or cocai ne is associated with headaches. Stopping or starting certain medications (eg OCP) can also cause headache, as can withdrawal from caffeine. Exclude serious causes and advise GP foll ow-up with advice on medication use. Cerebral venous thrombosis This is more common than was previously realized. It presents in similar fashion to subarachnoid or subdural hemorrhage: sudden onset head- ache with nause a and vomiting. It may be associated with sinus infections, pregnancy and the post-partum p eriod. The diagnosis may be missed on CT, but a clue includes i ICP at LP. Meningitis (see b p.224) Encephalitis Miscellaneous causes Headaches may also result from: \200 Hypoxia and hypercapnoea. \200 Poisons: eg CO and solvents ( b p.208). \200 Drugs: eg nitrates, sildena \201 l. \200 Post-traumatic ( b p.368). 134 CHAPTER 3 Medicine Acute confusional state (delirium) De \201 nition of delirium Delirium is a form of organi c brain syndrome characterized by: \200 Disturbed conscious level and mood (overactivity, excitement, drowsi- ness or stupor). Global disturbance of cognition (memory, orientation, attention, speech, motor function). Rapid onset with \202 uctuating course (often worse at night, with reversal of usual sleep \200\223wake cycle) and brief duration. Perceptual distortions and hallucinations (especially visual). Causes of acute confusion One or more of the following may be the underlying cause of an ac ute confusional state (several causes frequently co-exist): \200 Prescribed medication: d igoxin, cimetidine, steroids, analgesics, diuretics, anticholinergics, antiparkinsonian drugs. Drugs of abuse: opioids, benzodiazepines, ecstasy, amphetamines, hal- lucinogens. Withdrawal: from alcohol, opioids, hypnotics or anxiolytics. \200 Infection: pneumonia, U TI, septicaemia, meningitis, encephalitis. \200 Metabolic: hypoxia, hypercapnia, hypoglyc aemia, acidosis, hyponat- raemia, hypercalcaemia. Cardiac: acute MI, cardiac failure, endocarditis. \200 Neurological: head injury, chronic subdural haematoma, meningitis, post- ictal state. Organ failure: respiratory, renal and hepatic failure. \200 Endocrine: myxoedema, thyroto xicosis, diabetes, Addison \200\231s disease. Differential diagnosis Delirium can occur at any age, but is much more common in the elderl y. It is often misdiagnosed as schizophrenia, depression, or dementia (see opposite). Diffe rentiation can be dif \201 cult, but the following are more suggestive of physical illness : \200 Non-auditory hallucinations. \200 Dysarthria. \200 Ataxia. \200 Gait disturb ance. \200 Incontinence. \200 Focal neurological signs. Approach Search systematically for (and exclude) the physical causes of acute confu- sion o utlined above. 135 DEMENTIA Investigation of acute confusion Perform a thorough, careful physical and mental state exam ination (see b Mental state examination, p.606) on acutely confused patients. It may be imp ossible to obtain an accurate history from the patient, so actively seek other sources of i nformation: relatives, carers, GP, and previous medical records. Look carefully for evidence of alcohol/drug intoxication or evidence of withdrawal states. Examine for focal neurological signs and signs of acute cardiac, respiratory, or abdominal abnormalities (including acute urinary retention). Document basic vital signs (GCS, pulse, BP, respiratory rate and T * ) in all cases. Mandatory basic investigations \200 BMG. \200 U&E, FBC, and blood glucose. \200 Urinalysis. \200 SpO 2 and ABG. \200 ECG. \200 CXR. Adopt a low threshold for additional investigations based on clinical suspicion \200\224 blood cultures, serum paracetamol and salicylate, CT brain scan, and even LP may be indicated. Be careful not to miss: hypoglycaemia, head injury, Wernicke \200\231s encephalopathy, opio id intoxication, acute alcohol withdrawal, CO poisoning. Dementia Dementia is an acquired, progressive decline in intellect, behavior, and personali ty. It is irreversible and typically occurs with a normal level of consciousness. Note that patients with dementia are at risk of delirium resulting from an acute infective or metabo lic origin \200\224 a clue to this may be an acute deterioration in mental state. The commonest causes of dementia are Alzheimer \200\231s disease, vascular dementia, and Le wy body dementia. 136 CHAPTER 3 Medicine The unconscious patient: 1 Uncommon causes \200 Type 2 respiratory failure \200 Cardiac failure \200 Arrhythmias \200 Hypovolaemic shock \200 Anaphylaxis \200 Hepatic/renal failure \200 Hypotherm ia/hyperthermia \200 Meningitis/encephalitis \200 Malaria \200 DKA/HHS \200 Non-con vulsive status epilepticus \200 Wernicke \200\231s encephalopathy Common causes \200 Hypoglycaemia \200 Drug overdose \200 Head injury \200 Stroke \200 Subarachnoid hemorrhage \200 Convulsions \200 Alcohol intoxication Treatment may be needed before any diagnosis is made. Remember: \200 Airway. \200 Breat hing. \200 Circulation. Initial resuscitation Airway and cervical spine Whatever the cause of coma, a patient may d ie or suffer brain damage due to airway obstruction, respiratory depression. or circulatory failure. Clear and protect the airway immediately, and immobilize the cervical spine if tr auma is suspected. Breathing If breathing appears inadequate ventilate with O 2 using a self- in \202 ating b ag with an O 2 reservoir. An uninjured patient who seems to be breathing adequately can be examined supine, but nurse him/her in the recovery position toe d risk of airway obstructio n. Record RR. Circulation Measure pulse and BP. Observe and feel the skin for color, sweati ng and T . Obtain reliable venous access. Monitor ECG. Replace IV \202 uid if indicate d. Conscious level Assess level of consciousness using GCS ( b Head injury: examination, p. 360). Check the blood glucose (initially by BMG) and treat hypoglycaemia immediately ( b p. 150). Record pupil size. Give slow IV thiamine (ie 2 pairs of Pabrinex ampoules in 100mL 5 % glucose over 30min \200\224 see BNF ) to patients with a history of alcoholism or who appear malnourished. 137 THE UNCONSCIOUS PATIENT: 1 History Obtain a history from the ambulance crew and the patient \200\231s relatives and fr iends. Ask: \200 How was the patient found? \200 When was he/she last seen? \200 Is t here any suggestion of trauma? \200 Is there any history of \201 ts? \200 Has there b een recent foreign travel? \200 Previous symptoms and medical history (including depressi on). \200 Note any drugs available. Check previous ED records and hospital notes. Examination Examine thoroughly for illness and injury. Check clothes and possessions for ta blets and cards/bracelets warning of pre-existing disease. i Respiratory rate may re \202 ect obstructed airway, aspiration, pneumonia, DKA, liver/renal failure, salicylate poisonin g, methanol, or ethylene glycol. Respiratory depression may be due to poisoning (eg barbiturates, opioids, tricyclics) or i ICP. Brainstem compression or damage by stroke may cause rapid, irregular or intermittent ( Cheyne \200\223Stokes) breathing. If bradycardic consider: hypoxia, complete heart block, i ICP, digoxin or B-blocker poisoning ( b p.198). If tachycardic consider: airway obstructio n, hypoxia, hypovolaemia, SVT, VT, or anticholinergic overdose. AF may be associated with cerebral emboli. Hypotension suggests hypoxia, shock (hypovolaemic, anaphylactic, septic), or poisoning. Hyp ertension may be due to i ICP. Skin: look for pallor, cyanosis, jaundice, spider naevi, ski n crease/scar pigmentation (Addison \200\231s disease), rashes (eg purpura in meningococcal infection or DIC), injection marks (drug addiction or medical treatment), and signs of tra uma. Erythema or blistering over pressure points indicate the patient has been unconscious for some hours. Measure rectal T with a low-reading thermometer if the skin feels cold. Coma is common at <30 C ( b Hypothermia: presentation, p.254). 138 CHAPTER 3 Medicine The unconscious patient: 2 Neurological examination include GCS, limb strength, muscle tone and re \202 exes, optic fundi, ear drums, neck stiffness (except in neck injury), and pal pation of the fontanelle in babies. Lateralizing signs, such as facial or limb weakness, ma y be caused by a stroke, intracranial bleeding or pre- existing problems (eg previous strok e or Bell \200\231s palsy). Ocular nerve palsy or divergent squint with coma can indicate W ernicke \200\231s encephalopathy, requiring IV thiamine or tricyclic poisoning. Look for su btle signs of seizure activity (eg twitching of ocular muscles or eyelids, unusual limb mov ements), which may indicate non-convulsive status epilepticus. Look at the fundi \200\224 spontaneous central retinal venous pulsations are rare with i ICP. Subhyaloid hemorrhages ( blotchy fundal hemorrhages) suggest subarachnoid hemorrhage. Hypoglycaemia can cause localized weakness/coma and mimic stroke. Coma without lateralizing signs is usually due to poisoning, a post-ictal state, brainstem stroke, or hepatic failure: extensor plantar re \202 exes are common in these conditions. Tricyclic antidepressants often cause coma with dilated pupils, a divergent squint, i muscl e tone, jerky limb movements, and extensor plantars. In severe poisoning, there may be musc le \202 accidity with respiratory depression ande d re \202 exes ( b p.194). Coma with s mall pupils and respiratory depression suggests opioid poisoning ( b p.188). In unexplained coma, give a therapeutic trial of naloxone (0.4 \200\2230.8mg IV), observing for changes i n conscious level, respiratory rate, and pupil size. Investigations \200 BMG and blood glucose. If BMG is low, do not wait for the laboratory result to con \201 rm this before starting treatment. ABG (record FiO 2 and whether breathing spontaneously or IPPV). \200 FBC, prothrombin tim e, U&E. \200 Check paracetamol and salicylate levels if poisoning is suspected: para- cet amol alone does not cause coma (except in late cases with liver failure), but a mixture of drugs may have been taken. Drug screening for sedatives/hypnotics is not needed, but in une xplained coma keep blood for later analysis if necessary. ECG may show arrhythmias ( b Tricyclic antidepressant poisoning, p.194). CXR may show pneumonia, aspiration, trauma, or tumor. \200 CT scan may be needed to diagn ose subarachnoid hemorrhage, stroke, or head injury. Psychogenic coma Patients sometimes pretend to be unconscious. It can be dif \201 cult to be certain of this \200\224 exclude other causes \201 rst. Suspect psychogenic coma if s erious pathology has been excluded and when the eyes are opened, only the sclera show as th e eyes deviate upwards (Bell \200\231s phenomenon). This page intentionally left blank 140 CHAPTER 3 Medicine Collapse and syncope Syncope is a sudden, transient loss of consciousness, with spontaneous recovery. Priorities \200 Identify serious or life-threatening problems and institute treatment. \200 Decide which patients require admission. \200 Decide which patients require follow- up. History of syncopal episode Was it a simple faint? Vasovagal or neurally-mediated syncope i s a common response to an overwarm environment or prolonged standing, and can be precipitat ed by sudden fright or visual stimuli (eg the sight of blood). Other contributors are large meals, prolonged starvation or alcohol. There are usually premonitory symptoms of feeling unwell, nauseated, dizzy, or tired, with yawning, blurred or \200\230tunnel \200\231 visio n, or altered hearing. If the fainter cannot get supine (eg bystanders keeping them upright ), seizure-like twitching may occur ( convulsive syncope ). Vomiting and incontinence may o ccur and do not reliably discriminate seizures from faints. Was it a seizure? Look at the ambulance records. An eyewitness account is crucial. Ask what the witnesses actually saw (do not assume they know what a \200\230 \201 t \200\231 look s like). There should typically be no prodrome, there is often a cry followed by tonic/clon ic movements. Cyanosis, saliva frothing from the mouth, heavy breathing, tongue biting, or incontinence suggest a generalized seizure. Post-ictal drowsiness or confusion is normal \200\224 very rapid recovery questions the diagnosis. Was it a cardiac event? Cardiac syncopal events are also abrupt in onset (eg collapse due t o hypertrophic cardiomyopathy) and may be accompanied by pallor and sweating. Recovery may be rapid with \202 ushing and deep/sighing respiration in some cases (eg Stokes \200\223A dams attacks). Nausea and vomiting are not usually associated with syncope from arrhythmias . Ask about previous episodes and chest pain, palpitations, history of cardiac disease, and family history of sudden death. Syncope associated with exertion is a worrying feature: po ssible causes include aortic or mitral stenosis, pulmonary hypertension, cardiomyopathy, or coronary artery disease. Other causes Carotid sinus syncope is neurally mediated, and often occurs with shaving or t urning the head. Syncope may be secondary to effects of medication (eg GTN, B-blockers, ant i-hypertensive drugs). Syncope may also be the presenting feature of subarachnoid hemorrhag e, ruptured ectopic pregnancy, aortic or carotid dissection, PE, or GI bleed. Syncope is ra rely caused by a TIA. 141 COLLAPSE AND SYNCOPE Assessment and treatment If a patient suddenly loses consciousness in the ED, assess respon siveness and check for a pulse. Keep the airway clear, give O 2 , and monitor pulse and ECG . Note any neurological signs during the episode and obtain BP, SpO 2 , and BMG. Patients s een following syncope Obtain a detailed account from the patient and witnesses. Look for si gns of tongue biting, incontinence, or other injuries, examine the CVS for murmurs, arrhyth mias or abnormalities. Perform a neurological examination and look for focal signs. Do post ural tests (supine and standing or sitting pulse and BP). A degree of postural hypotension is common, but postural symptoms (eg dizziness, weakness, etc.) are always signi \201 cant (look for causes of hypovolaemia eg GI bleed, ectopic pregnancy). Check BMG to exclude hyp oglycaemia and an ECG looking for arrhythmias, LVH, ischaemia, previous or acute MI, and QT prolongation. An abnormal ECG may be the only clue to an underlying hypertrophic cardiomyo pathy (HCM) or Brugada syndrome. Disposal Admit patients for cardiology review within 24 hr if they present with: \200 An ECG abnormality. \200 Heart failure. \200 Loss of consciousness on exertion. \200 Fam ily history of sudden death <40 year or inherited cardiac condition. \200 Age > 65 year w ith no prodromal symptoms. \200 A heart murmur. Refer patients for assessment by a specia list in epilepsy if they present with one or more of: \200 A bitten tongue. \200 Amnesi a, unresponsiveness, unusual posturing, or prolonged limb jerking, head turning to one side. History of a prodrome. \200 Post-ictal confusion. It may be appropriate to discharge pati ents with full recovery, appropriate history for vasovagal syncope and a normal examination . See www.nice.org.uk Diagnoses not to be missed \200 GI bleed: syncope ( postural symptoms) indicate signi \201 cant blood loss and hypovolaemia. Perform PR examination to check for blood/ melaena. Ectopic pregnancy: suspect this in women with syncope and abdominal pain or gynecological symptoms. Do a pregnancy test. Ruptured abdominal aortic aneurysm. \200 PE ( b Pulmonary embolism, p.120). A witness may give a history of cyanosis. Indicative of massive thrombus. 142 CHAPTER 3 Medicine Acute generalized weakness Weakness may be a feature of common neurological problems (eg TI A/ stroke), or accompany many of the causes of collapse (see b Collapse and syncope, p.140) . Less commonly, generalized muscle weakness may be the presentation of a number of other d iseases. Guillain \200\223Barr syndrome Guillain \200\223Barr follows a respiratory or GI viral infection and is character- ized by progressive symmetrical weakness, spreading from distal muscles to involve proximal muscles. Symptoms and signs include muscle tender- ness, back pain, loss of muscle re \202 exes, sensory symptoms (paraesthesiae of \201 ngers and toe s) and disturbance of the autonomic nervous system (hyper- or hypotension, tachy- or bradyc ardia, bladder atony). Beware respiratory failure, which can rapidly progress to respirator y arrest. Serial vital capacity measurements are advised. Refer to the medical team/ICU. Multiple sclerosis Multiple sclerosis (MS) is a demylinating disease of the CNS. It is more common in females and usually presents between ages 20 \200\22350. The disease follows a r elapsing and remitting course with sensory loss, stiffness, and weakness of legs, ataxia, a utonomic impairment (bladder dysfunction), and diplopia. Patients may present with these sy mptoms during their \201 rst exacerbation or with optic neuritis (pain in one eye with vi sual blurring). Arrange admission under neurology. If patient has eye symptoms, arrange urg ent ophthalmology review. Polymyositis Polymyositis is an in \202 ammatory myopathy that presents with symmetrical p roximal muscle weakness, arthritis and sometimes muscular tenderness. Patients report dif \201 culty climbing stairs, standing from a low chair, or lifting arms to brush hair. Creat ine kinase (CK) levels are raised. Refer to a rheumatologist for treatment. Myasthenia gravis This is a rare autoimmune disease, which results in painless weakness in which the muscles are fatiguable, but tendon re \202 exes and pupil responses are normal. Ptosis, diplopia, and blurred vision are the commonest pres- entations. Usually, cranial ne rves are involved to a greater extent than limb muscles and the distribution is asymmetrica l. Crises may present with severe muscle weakness in which the major concern relates to res piratory compromise \200\224 the patient may require emergency temporary ventilatory suppo rt. If the diagnosis is suspected in a patient not known to have myasthenia gravis, refer to a specialist who may wish to perform an edrophonium test . Patients with known myasthenia gra vis may present with weakness due to under-treatment, over-treatment (cholinergic crisis), or an adverse reaction to an unrelated drug. Refer to the medical team for investigation. 143 ACUTE GENERALIZED WEAKNESS Periodic paralysis This encompasses a family of hereditary diseases associated with defects in muscle ion channels. Episodes of weakness can be associated with \202 uctuations in s erum potassium levels lasting a few hours to a week. Patients may develop myotonia between attacks and \201 xed proximal muscle weakness. Treatment tends only to be required for hy pokalaemic periodic paralysis with oral potassium supplementation. Wound botulism Botulism has made a recent come back in the IV drug injecting community. Bot ulinum toxin inhibits the release of acetylcholine at neuromuscular junctions, sympathetic and parasympathetic synapses. Wound infection with Clostridium botulinum presents with dipl opia, blurred vision, ptosis, and neck weakness, which can progress to respiratory failure. Treatment is with antitoxin, benzylpenicillin, and metronidazole, along with respiratory s upport. It is worth remembering that generalized weakness may also be caused by: \200 Spinal cord compression. \200 Tetanus. \200 Alcoholic myopathy. \200 Diphtheria. \200 Lead poi soning. 144 CHAPTER 3 Medicine Stroke A stroke is an acute onset of focal neurological de \201 cit of vascular origin whi ch lasts > 24hr. The blood supply to the brain has two sources \200\224 the internal carot id and the basilar arteries. The internal carotids supply the anterior and middle cerebral arteries, known as the anterior circulation. The basilar artery supplies the posterior cere bral artery in 70 % of people (the posterior circulation). Anterior and posterior communica ting arteries in the circle of Willis provide collateral circulation in cases of carotid ar tery stenosis. Pathogenesis 70 % of strokes occur in those aged > 70yrs, but they can occur at any age. Cerebral infarction (80 % ) Results from: \200 Thrombosis secondary to atherosclerosis, h ypertension and rarely arteritis. Cerebral embolism from AF, valve disease/replacement, post-MI, ven- tricular aneurysm, myxoma, endocarditis or cardiomyopathy. An episode of hypoperfusion. Cerebral hemorrhage (20 % ) Associated with: \200 Hypertensi on (rupture of small arteries in the brain). \200 Subarachnoid hemorrhage (see b p.128). \200 Bleeding disorders (including anticoagulants) and intracranial tumors. Presentation Stroke preceded by neck pain may indicate carotid/vertebral artery dissec- tio n or subarachnoid hemorrhage. Headache is an unusual presentation of stroke and may indicat e cerebral hemorrhage. Be alert to the possi- bility of different pathology requiring urgen t treatment (eg hypoglycaemia, Todd \200\231s paresis, hemiplegic migraine, meningitis, enc ephalitis, brain abscess, head injury, Bell \200\231s palsy, \200\230Saturday night palsy \200\231, tumors). Undertake a thorough examination including: \200 Assessment of mental status/GCS and sign s of meningeal irritation. \200 Evidence of head or neck injury. \200 Examination of pu pils, fundi, and cranial nerves. \200 Assessment of motor function (tone, power, and re \202 exes). \200 Assessment of sensory function (including speech and comprehension). \200 Examination for cerebellar signs (co-ordination, speech). \200 Check for sources of embolism (AF, murmurs, carotid bruits). Localization on clinical grounds alone can be dif \201 cult, and differentiation between infarction and hemorrhage requires CT/MRI. NICE rec ommend the use of the ROSIER score to identify patients presenting with acute stroke (see T able 3.9 ). The ROSIER score will pick up the majority of patients who are having a stroke, but may not identify patients with posterior circulation infarcts. 145 STROKE Table 3.9 ROSIER score for stroke recognition Criteria Points Facial weakness (asymmetrical) 1 Arm weakness (asymmetrical) 1 Leg weakness (asymmetrical) 1 Speech disturbance 1 Visual \201 eld defect 1 Loss of consciousness or syncope \200\2231 Seizure \200\2231 Stroke unlikely if score 0 or less. Investigation Examine and investigate \201 rstly to exclude other conditions and secondly to con \201 rm the diagnosis of stroke. As a minimum requirement: BMG, FBC, ESR, U&E, blo od glucose, ECG, CXR. Monitor with pulse oximeter (if SpO 2 <94 % obtain ABG) and cardiac m onitor. Emergency CT Arrange emergency CT scan where: \200 The patient presents with symp toms under 4hr of duration. They may be eligible for emergency thrombolysis treatment. Time is of the essence. The patient is on warfarin, heparin, or other anticoagulant. \200 There is a known bleedi ng disorder. \200 GCS <13. \200 Unexplained progressive or \202 uctuating symptoms. \200 Papilloedema, neck stiffness or fever. \200 There was a severe headache at onset of symptoms. Management \200 Immediately correct hypoglycaemia if present (see b p.150). \200 Hypert ension and labile BP are common in the early post-stroke period. Do not attempt to reduce the BP on presentation. Give supplemental oxygen only if SpO 2 <95 % . \200 Screen the patient \200\231s ability to swallow (try a teaspoon of water). \200 If intracranial hemorrhage has been excluded, all patients should receive aspirin 300mg as soon as possible. Give this rectally if unable to swallow. Give PPI if there is a history of dyspepsia. If allergic to aspirin, give alte rnative antiplatelet drug such as clopidogrel. Wherever possible, admit patients directly to units where they can be cared for by staff sp ecializing in stroke treatment and rehabilitation. Thrombolysis If intracranial hemorrhage has been excluded within 4hr of onset of symptoms, alteplase may be administered by a trained and supported emergency physician, only where th e patient is managed within a specialist acute stroke service. See local guidelines and htt p://www.nice.org.uk 146 CHAPTER 3 Medicine Transient ischaemic attacks A TIA is an episode of transient focal neurological de \201 ci t of vascular origin lasting <24hr. A TIA gives major warning for the development of stroke (5 % within 48hr, up to 50 % in 5 years). Even in patients with resolution of symptoms/sig ns, most have evidence of infarction on CT/MRI. Presentation Carotid territory involvement produces unilateral weakness or sensory changes, dysphasia, homonymous hemianopia, or amaurosis fugax. Vertebrobasilar territory involvement produces blackouts, bilateral motor or sensory change s, vertigo, and ataxia. Causes Most TIAs result from thrombo-embolic disease involving either the heart (AF, mitral stenosis, arti \201 cial valves, post-MI) or extracranial vessels (carotid artery stenosi s). Other causes include: \200 Hypertension. \200 Polycythaemia/anemia. \200 Vasculit is (temporal arteritis, polyarteritis nodosa, SLE). \200 Sickle cell disease. \200 Hypo glycaemia. \200 Any cause of hypoperfusion (eg arrhythmia, hypovolaemia). \200 Syphilis . Assessment To diagnose a TIA, the symptoms must have resolved within 24hr. Document vital signs and perform a thorough neurological examination. Look for possible sou rces of emboli eg arrhythmias (especially AF), heart murmurs, carotid bruits, MI (mural thr ombus). Investigations \200 Check BMG. \200 Send blood for FBC, ESR, U&E, blood glucose, lipids (INR if on anti- coagulants). Record an ECG to search for MI, arrhythmia. Management \200 Calculate the ABCD 2 score (Table 3.10 ). \200 Admit to a stroke unit p atients scoring 4 or more points, or anyone with more than one TIA in the previous week. Patients scoring 3 or less points, or who present one week after symp- toms have resolved, may be suitable for discharge with stroke team follow-up in the next week. Start the patient on daily aspirin 300mg immediately. \200 Admit patients with continuing symptoms or residual de \201 cit (by de \201 ni- tion, not a TIA). See http://www.nice.org.uk 147 TRANSIENT ISCHAEMIC ATTACKS Table 3.10 ABCD 2 score for TIAs Criteria Points Age Age 60 or over 1 BP at assessment Systolic > 140mmHg or diastolic > 90mmHg at assessment 1 Clinical features Speech disturbance 1 Unilateral weakness 2 Duration of symptoms 10 \200\22359min 1 60 min or more 2 Diabetes 1 Patients scoring > 4 points are at increased risk. 148 CHAPTER 3 Medicine Seizures and status epilepticus First \201 t A \201 rst \201 t has enormous consequen ces \200\224 do not diagnose without good evidence A detailed history from both the patien t and any witnesses is crucial to the diagnosis. The presence of jerking movements or incon tinence does not necessarily re \202 ect epilepsy. Carefully document what was seen, in or der to avoid confusion with vasovagal syncope or other types of collapse. Full rapid recove ry suggests a syncopal event. Always consider alcohol/drug use, withdrawal states, hypoglyc aemia, arrhythmia, head injury, subarach- noid hemorrhage, stroke/TIA, infection (including meningitis) or metabolic disturbance. As part of the general examination, carefully examine the CNS, documenting: GCS, confusion, focal abnormalities, \201 ndings on fundoscopy. Examine the cardiovascular system and ch eck for signs of aspiration. Todd \200\231s paresis may follow seizures \200\224 focal de \201 cit or hemiparesis may persist for up to 24hr and indicates a high chance of structural lesion.