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. Investigations BMG, glucose, FBC, U&E, blood cultures if pyrexial, ECG, and if there are ch est signs, a CXR. Check urine pregnancy test if of child- bearing age. All patients with ne w onset seizures need brain imaging at some stage: a signi \201 cant number have structura l CNS abnormalities. Arrange emergency CT scan for patients with focal signs, head injury, known HIV, suspected intracranial infection, bleeding disorder (including anticoagulants), or where conscious le vel fails to improve as expected. Disposal A patient presenting with a \201 rst seizure may be discharged home, accompanied by an adult, if they have normal neurological and cardiovascular examinations, the ECG and electrolytes are normal, and there is an appointment with an epilepsy specialist in the co ming week. Admit any patient with more than one seizure that day or who does not \201 t t he above criteria. Ensure clear documentation of follow-up arrangements, including booked c linic appointment. Meantime, advise the patient not to drive or use machinery and to take s ensible precautions, with supervision when performing activities, such as swimming/bathing until reviewed. Document this advice in the notes. Seizures in known epileptics Ask about any change from the patient \200\231s normal seizure pattern. Possible causes of poor seizure control include: poor compliance with medica- tio n, intercurrent illness/infection, alcohol, or drug ingestion. Examine to exclude any injur y occurring from the \201 t, especially to the head. Occult dislocations (eg shoulder) ma y occur. Check vital signs, BMG and anticon- vulsant levels if toxicity or poor compliance is suspected. Refer patients with a signi \201 cant change in seizure pattern to the medic al team. Discharge to the care of a responsible adult those patients who are fully recovere d with no injuries, symptoms or other concerns. 149 SEIZURES AND STATUS EPILEPTICUS Status epilepticus This is continuous generalized seizures lasting > 30min or without inter - vening recovery. Cerebral damage i with duration. Precipitants include cerebral infection , trauma, cerebrovascular disease, toxic/metabolic dis- turbances, childhood febrile seizur es. Mortality is 8 10 % (due to underlying pathology). Although seizures typically start as generalized, tonic/clonic, these features may gradually diminish, making diagnosis dif \201 cult (coma with virtually no motor evidence of seizure, eg minimal twitching of ocular muscles only). Complications include hypoglycaemia, pulmonary hyper- tension, pulmonary oe dema and precipitous i ICP can also occur. Treatment of status epilepticus \200 Establish a clear airway (a nasopharyngeal airway ma y help). \200 Give high \202 ow O 2 . \200 Monitor ECG, SpO 2 , T , pulse rate, an d BP. \200 Obtain IV access, check BMG and correct hypoglycaemia if present (50mL of 20 % glucose IV). Give IV lorazepam 4mg slowly into a large vein (diazepam 10mg is an alternative). Repeat IV lorazepam 4mg slowly after 10min if seizures continue. Buccal midazolam 10mg (can be repeated once) or rectal diazepam solution 10 \200\22320mg (c an be repeated up to total 30mg) are alternatives if there is no venous access. If alcohol abuse or malnutrition is suspected, give slow IVI thiamine in the form of Pabrin ex 2 pairs of ampoules in 100mL of 0.9 % saline (this occasionally causes anaphylaxis; b e prepared to treat \200\224 see BNF ). Consider the possibility of pregnancy-related \201 ts (eclampsia) in women of childbearin g age and treat accordingly (with IV magnesium sulfate \200\224 \200\224 as outlined on b p.592). Check ABG and save blood for cultures, FBC, U&E, glucose, calcium, magnesium, LFTs, clottin g, drug levels (and toxicology screen if poi- soning/overdose is suspected). Search for features of injury (especially head injury) and infection (look for a rash). If seizures continue despite above therapy, call ICU and consider the use of phenytoin (18m g/kg IV, 50mg/min) with ECG monitoring, or fosphenytoin (20mg/kg phenytoin equivalent IV, < 150mg/min). A 70kg patient would require 1400mg phenytoin equivalent of fosphenytoin (28mL Pro-Epanutin ) diluted in 100mL 0.9 % saline or 5 % glucose, given over 10 \200\22315min . After 30min, contact ICU and proceed without delay to rapid sequence induction (ideally wit h thiopental), tracheal intubation, and continue anticonvulsant medication. 150 CHAPTER 3 Medicine Hypoglycaemia Hypoglycaemia can mimic any neurological presentation including coma, seizure s, acute confusion, or isolated hemiparesis. Always exclude hypoglycaemia in any patient with coma, altered behavior, neurological sympt oms, or signs Plasma glucose is normally maintained at 3.6 \200\2235.8mmol/L. Cognitive fun c- tion deteriorates at levels <3.0mmol/L, but symptoms are uncommon > 2.5mmol/L. In diabet ics, however, the threshold for symptoms can be very variable. Hypoglycaemia is potentially fatal, and accounts for 2.4 % of deaths in diabetics on insulin. Even mild episodes aggrav ate pre-existing microvascular complications and lead to cumulative brain damage. Causes In diabetics, the commonest cause is a relative imbalance of administered versus req uired insulin or oral hypoglycaemic drug. This may result from undue or unforeseen exertion , insuf \201 cient or delayed food intake, excessive insulin administration (due to time, dose or type of insulin). Other causes are: \200 Alcohol (in addition to alcohol directly causing hypoglycaemia, the features of hypoglycaemia may be mistaken for alcohol intoxicat ion or withdrawal). Addison \200\231s disease. \200 Pituitary insuf \201 ciency. \200 Post-gastric surgery . \200 Liver failure. \200 Malaria. \200 Insulinomas. \200 Extra-pancreatic tumors. \200 Attempted suicide or homicide with large doses of insulin or oral hypoglycaemic drug. Symptoms and signs Common features: sweating, pallor, tachycardia, hunger, trembling, alter ed or loss of consciousness, irritability, irrational or violent behavior, \201 tting, fo cal neurological de \201 cit (eg hemiplegia). Look for Medic-Alert bracelet/ chain. Diagnosis Check venous or capillary blood with glucose oxidase strip (BMG). If <3.0mmol/L, take a venous sample for a formal blood glucose level, but give treatment without waiting f or the result. Take appropriate samples if overdose of insulin, oral hypoglycaemic agent, o r other drugs is suspected. 151 HYPOGLYCAEMIA Treatment This depends upon the conscious state and degree of co-operation of the patient. Choose the appropriate option from the following: \200 5 \200\22315g of fast-acting oral carbohydrate (eg Lucozade , sugar lumps, Dextrosol , followed by biscuits and milk). Glucagon 1mg: SC, IM, or IV. Can be administered by relatives, ambu- lance crew and when ve nous access is dif \201 cult. Glucagon is not suitable for treatment of hypoglycaemia due to sulphonylurea drugs, liver failure or in chronic alcoholism (as there may be little live r glycogen available for mobilization). Glucose 10 % solution 50mL IV, repeated at 1 \200\2232min intervals until the patient is fully conscious or 250mL (25 g) has been given. Glucose 50 % solution (25 \200\22350mL IV) is hypertonic, liable to damage veins and no mor e effective than glucose 10 % . If glucose 50 % is used, give it into a large vein and foll ow with a saline \202 ush. The time taken for return of consciousness and the incidence of nausea, vomiting and other adverse effects are similar for IV glucagon and glucose. The persistence of an altered conscious level suggests another underlying pathology (eg str oke), or may re \202 ect the development of cerebral oedema due to hypoglycaemia, which ha s a high mortality. Maintain plasma glucose at 7 \200\22311mmol/L, contact ICU and consider mannitol and/ or dexamethasone. Arrange urgent investigation (eg CT scan) and search for o ther causes of altered consciousness. Overdose Glucose infusions may be needed for 24hr or longer after poisoning with insulin or oral hypoglycaemic drug, depending upon exactly what and how much has been taken. Hypokala emia may be a problem. Block excision of the injection site has been used as successful tre atment for insulin overdose. Octreotide may be helpful in recurrent hypoglycaemia due to ov erdose of a sulphonylurea drug ( b p.197). Discharge 90 % of patients fully recover in 20min. Provided that the cause for the episode has been identi \201 ed and fully corrected, it is reasonable to discharge the patient aft er observation in the ED, with appropriate follow-up. Arrange follow up having considered the following: \200 Why did this episode occur? \200 Has there been a recent change of regimen, other drugs, alcohol, etc.? \200 Is the pati ent developing hypoglycaemic unawareness or autonomic dysfunction? 152 CHAPTER 3 Medicine Hyperglycaemic crises Diabetic keto-acidosis (DKA) is caused by absolute or relative d insu lin levels. Plasma glucose i causes an osmotic diuresis, with Na + and water loss (up to 8 \200\22310L), hypotension, hypoperfusion, and shock. Normal compensatory hormonal mechanism s are overwhelmed and lead to i lipolysis. In the absence of insulin this results in the pr oduction of non- esteri \201 ed fatty acids, which are oxidized in the liver to ketones. Younger undiagnosed diabetics often present with DKA developing over 1 \200\2233 days. Plas ma glucose levels may not be grossly i ; euglycaemic ketoacidosis can occur. Urinalysis dem onstrates ketonuria. Hyperosmolar hyperglycaemic state (HHS) is caused by intercurrent illness, inadequate diabe tic therapy and dehydration. It develops over days/weeks, and is more common in the elderly . HHS is characterized by i glucose levels ( > 30mmol/L), i blood osmolality, and a lack of urinary ketones. Mortality is 85 \200\22310 % , but may be even higher in the elderly. Causes Think of the four \200\230I \200\231s separately or (often) in combination: \200 Infection: common primary foci are urinary tract, respiratory tract, skin. \200 Infarctio n: myocardial, stroke, GI tract, peripheral vasculature. \200 Insuf \201 cient insulin. \200 Intercurrent illness: many underlying conditions precipitate or aggravate DKA and HHS. Clinical features Hyperglycaemic crisis may present in various ways. Some of the following are usually present: Signs of dehydration thirst, polydipsia, polyuria, d skin turgor, dry mouth, hypotension, tachycardia. GI symptoms are common in DKA with nausea, vomiting, and a bdominal pain. This can be severe and mimic an \200\230acute surgical abdomen \200\231. Hy perventilation (respiratory compensation for the metabolic acidosis) with deep rapid breath ing (Kussmaul respiration) and the smell of acetone on the breath, is pathognomonic of DKA. True coma is uncommon, but altered conscious states and/or focal neurological de \201 cit s (which may correct with treatment) are seen particularly in older patients with HHS. Diagnosis and investigations Aim to con \201 rm the diagnosis and search for possible unde rlying cause(s): \200 Check BMG and test the urine for glucose and ketones. \200 Send b lood for U&E, blood glucose, creatinine, osmolality (or calculate it): mOsm/L= (2 \227 Na + ) + glucose (mmol/L) + urea (mmol/L). Check ABG (look for metabolic acidosis respiratory compensation). \200 FBC and CXR (to search for pneumonia). \200 ECG and cardiac monitoring (look for evidence of hyper/hypok alaemia). \200 Blood cultures and if appropriate, throat or wound swabs. \200 Urine/spu tum microscopy and culture. 153 HYPERGLYCAEMIC CRISES Treatment \200 If altered consciousness/coma is present, provide and maintain a patent airway. Give high FiO 2 by mask. Consider the possible need for GA and IPPV for coma severe shock. Commence IV infusion with 0.9 % saline (if the lab result subsequently shows initial plasma Na + to be > 150mmol/L, give 0.45 % saline). Give 1000mL of 0.9 % saline over 0.5 \200\223 1hr, then 500mL/hr for next 2 \200\2233hr. Persistent hypotension may require i in infusion rate and/or colloid administration. Avoid over-rapid infusion with the risks of pulmonary oedema and ARDS, especially in the elderly and patients with IHD. \200 Insulin: start an infusion of soluble insulin using an IV pump or pediatric burette at 6U/hr. No loading dose is required. Check plasma glucose levels every hour initially. When plasma glucose <14mmol /L, d insulin infusion rate to 4U/hr and replace the saline solution with 10 % dextrose to help ketone clearance and acid-base state. Electrolyte balance: although total body K + is low, plasma K + may be normal, i or d . Wit h treatment, K + enters cells and plasma levels d : therefore unless initial K + levels are > 5.5mmol/L, give 20mmol/hr of KCl, monitor ECG, and check K + levels hourly. Despite the presence of metabolic acidosis, do not give sodium bicarbonate. Other electrolytes such as Ca 2 + , Mg 2 + , and PO 4 2 \200\223 are commonly disturbed, but rarely need emergency co rrection. Consider an NG tube to d risk of gastric dilation and aspiration. \200 Monitor urine outp ut (most accurate with urinary catheter). \200 Consider a central venous catheter to moni tor CVP to guide treatment in the elderly or severe illness. Arrange admission to ICU, HDU, or acute medical admissions unit. Other aspects of treatment Signs of infection are often masked. T is rarely i , and i WC C may only re \202 ect ketonaemia. If in doubt, treat with a broad-spectrum antibiotic. Over-rapid \202 uid replacement can cause cardiac failure, cerebral oedema, and ARDS, esp ecially in patients with underlying cardiac disease or the elderly. CVP monitoring may be n eeded. Clotting Hyperglycaemia causes a hypercoagulable state: DVT or PE may occur. Administer pro phylactic anticoagulation with LMWH in DKA or hyperosmolar states. 154 CHAPTER 3 Medicine Sodium derangements Abnormal sodium states can occur with hypervolaemia, euvolaemia, or hyp ovolaemia, depending on the underlying pathophysiological process. Hypernatraemia Causes include diabetes insipidus (lack of ADH or lack of renal response to ADH), diarrhea, vomiting, diuretics, hypertonic saline, sodium bicarbonate administration, or Cushing \200\231s syndrome. Treatment should not correct the Na concentration faster than 1mmol/L/hr. Use 0.9 % saline to correct hypovolaemia (patients who have tachycardia, hypotension, or postural hypotensio n). Once the patient is euvolaemic, use an infusion of 0.45 % saline, or 5 % dextrose. The free water de \201 cit can be calculated using the formula: Free water de \201 cit (in litres) = 0.6 \227 weight (kg) \227 (serum Na/140 \200\2231) and should be replaced over 48hr (in addition to normal maintenance \202 uids). Check ser um Na + after 2 \200\2233hr to monitor correction rate. Complications of hypernatraemia inc lude seizures, subdural and intra- cerebral hemorrhages, ischaemic stroke, and dural sinus thrombosis. Rapid correction of sodium levels (particularly in chronic hypernatraemia) can cause cerebral oedema and further neurological complications. Hyponatraemia Causes include excessive \202 uid loss replaced by hypotonic \202 uids (d iarrhea, burns, prolonged exercise, such as marathon running), polydypsia, ecstasy ingestio n, syndrome of inappropriate ADH secretion, nephrotic syndrome, renal impairment, hepatic c irrhosis, cardiac failure, and many prescription drugs (including diuretics, heparin, and A CE inhibitors). Treatment of acute hyponatraemia (<24hr duration) Those with mild symptoms can be effective ly treated by \202 uid restriction. Patients who present with seizures or signs of raised intracranial pressure are at risk of death and should be treated more aggressively. Serum Na + <120mmol/L is associated with risk of brain herniation. Give up to 200mL of 2.7 % sali ne IV over 30min and recheck serum Na + levels. Treatment of chronic hyponatraemia ( > 24hr duration) is associated with central pontine my elinolysis, particularly in patients with low K + levels or alcoholic patients. Chronic hyp onatraemia should be corrected no faster than 10mmol/L in 24hr. Treat the underlying cause. This may be as simple as discontinuing a diuretic. Patients with cardiac failure, cirrhosi s, or nephrotic syndrome (hypervolaemic patients) should be \202 uid restricted. Severe h yponatraemia in association with seizures or d GCS may be cautiously treated with hypertoni c saline (2.7 % saline 200mL over 30min and recheck serum Na + ). Aim to increase serum Na + by no more than 5mmol/L using this method. See www.gain-ni.org 155 ADDISONIAN CRISIS Addisonian crisis Acute adrenocortical insuf \201 ciency is rare and easily missed. The mo st common cause is sudden withdrawal of chronic steroid therapy (delib- erately or inadvert ently). An Addisonian crisis may also be precipitated in these patients by intercurrent inj ury, infection or stress \200\224 increasing steroid requirement. 80 % of Addison \200\231 s disease in the UK is idiopathic (autoimmune), and may be associated with Graves \200\231 disease, Hashimoto \200\231s thyroiditis, insulin dependent diabetes mellitus (IDDM), perni cious anemia, hypoparathyroidism, and ovarian failure. Other causes include TB, fungal infe ctions, metastatic disease, congenital adrenal hyperplasia, drugs (eg metyrapone or cytotox ic agents), hemorrhage into the adrenal glands occurring as a complication of anticoagulati on or meningococcal septicaemia (Waterhouse \200\223Friderichsen syndrome). Look for a Medi c \200\223 Alert bracelet indicating that the patient is taking steroids. Precipitating factors Infection, trauma, MI, cerebral infarction, asthma, hypothermia, alco hol, pregnancy, exogenous steroid withdrawal or reduction. Clinical features Addison \200\231s disease frequently has an insidious onset with weakness , apathy, anorexia, weight loss, abdominal pain (which may be severe enough to mimic an acu te abdomen), and oligomenorrhoea. In crisis, the main fea- tures may be shock (tachycardia, peripheral vasoconstriction, severe pos- tural hypotension occasionally with syncope, olig uria, profound muscle weakness, confusion, altered consciousness leading to coma), and hypo gly- caemia. Chronic features of Addison \200\231s disease are: areas of vitiligo and hyper pigmentation in the palmar creases, buccal mucosa, areolae, scars, and in the axillae. Investigations Hyperkalaemia, hyponatraemia, hypoglycaemia, uraemia, mild acidosis, hyperca lcaemia, and eosinophilia may be present. If Addisonian crisis is suspected, take appropria te blood samples, but start treatment without waiting for results. Management \200 Obtain IV access. \200 Take blood for cortisol (10mL in a heparinized t ube) and ACTH if pos- sible. Contact the biochemistry lab to warn them that these tests wil l be required. If features of haemodynamic compromise are present, commence volume replacement with IV 0.9 % saline if shocked. \200 Give hydrocortisone sodium succi nate 100mg IV stat. \200 Take blood, urine, and sputum for culture and sensitivity. \200 Check BMG and blood glucose, and treat hypoglycaemia with 50mL of 10 % glucose IV (repeated if necessary). If infection is suspected as a precipitating cause, consider giving broad spectrum antibiotics. \200 Refer for admission. 156 CHAPTER 3 Medicine Thyrotoxic crisis A rare condition, occurring in 1 \200\2232 % of patients with established hyperthyroidism (usually toxic diffuse goiter \200\230Graves \200\231 disease \200\231). Mortality is signi \201 cant (810 % ). Causes It is often precipitated by a physiological stressor: \200 Premature or inappropriate cessation of anti-thyroid therapy. \200 Recen t surgery or radio-iodine treatment. \200 Intercurrent infection (especially chest infect ion). \200 Trauma. \200 Emotional stress. \200 DKA, hyperosmolar diabetic crisis, ins ulin-induced hypoglycaemia. \200 Thyroid hormone overdose. \200 Pre-eclampsia. Clinical features Onset may be sudden with features of hyperthyroidism and adrenergic overactivity. Fever, cardiovascular, and neurological symptoms are common. Weight loss, i appetite, trem or, irritability, emotional lability, heat intolerance, sweating, itch, oligomenorrhoea, ag itation, anxiety, confusion, coma, palpitations, tachycardia, AF (rarely, complete heart bl ock). It may mimic an \200\230acute abdomen \200\231, with abdominal pain, diarrhea, and v omiting. Differential diagnosis Includes acute pulmonary oedema, neuroleptic malignant syndrome, sep tic shock, anticholinergic or sympathomimetic overdose, drug withdrawal, or acute anxiety s tates. Investigations \200 U&E, BMG, and blood glucose, Ca 2 + (hypercalcaemia occurs in 810 % ) . \200 FBC, differential WCC, coagulation screen. \200 Screen for infection: MSU, blood cultures, sputum. \200 T 4 and T 3 (for later analysis), TSH. \200 CXR (searching for pulmonary infection or congestive heart failure). \200 ECG (looking for arrhythmias). Tre atment \200 Manage the airway and give O 2 if indicated. \200 Obtain IV access and comm ence IVI 0.9 % saline (initially 500mL 4-hourly). \200 Pass NG tube if vomiting. \200 I f sedation is required, give small titrated amounts of benzodiazepine (eg diazepam 5 \200\22320mg PO/IV) or haloperidol. Commence dexamethasone 4mg 6 hourly PO or give hydrocortisone 100mg IV. Give broad spectrum antibiotic if infection is suspected. \200 Consider cooling measures in hyperthermia. \200 Refer for admission (consider admission to ICU). \200 Once admitt ed, propranolol (or esmolol) and carbimazole will normally be given together with iodine. Do not give aspirin (this can exacerbate the clinical problem by dis- placing thyroxine from thyroid binding globulin). This page intentionally left blank 158 CHAPTER 3 Medicine Urinary tract infection The urinary tract is normally bacteriologically sterile. Urine infe ction is present if > 10 5 colony-forming units are present per mL of urine. Except at the extremes of age, urinary tract infections (UTIs) are much more common in females due to the shorter urethral length. Most UTIs occur because of organisms invading the bladder via the urethra. Proximal invasion via the ureter may result in acute or chronic pyelonephritis, p articularly if anatomical derangement exists with impaired ureteric or bladder emptying. In both sexes, underlying structural abnormality i UTI risk. Blood-borne spread of infection to the urinary tract can occur, (eg in bacterial endocarditis or systemic Gram \200\223ve infection). UTI is usually caused by a single organism. The commonest organism (90 % ) at a ll ages is E. coli. Proteus, Klebsiella, and saprophytic staphylococci account for most of the remainder in adults. Other organisms (eg Pseudomonas ) more commonly cause UTI in hospi talized patients or following instrumentation. Urinary tract infection: presentation UTIs usually present to the ED in one of two ways Lower UTI (cystitis) Dysuria, frequency, haematuria, suprapubic discomfort, urgency, burnin g, cloudy urine with an offensive smell. Patients with acute urethral syndrome have identic al symptoms, but \200\223ve urine culture. Upper UTI (acute pyelonephritis) Often systemically unwell with malaise, fever, loin and/or back pain, vomiting, rigors and occasionally Gram \200\223ve septicaemia. Investigations Reagent strip (dipstix) urinalysis may show haematuria, proteinuria, + ve ni trite, and leucocyte esterase tests. A patient with clear urine, \200\223ve on dipstix tes ting, is extremely unlikely to have a UTI. False + ve results may be secondary to urinary t ract tumors or excessive exercise. A false \200\223ve nitrite test may re \202 ect pathog ens that do not convert dietary nitrates to nitrites. Urine microscopy may show leucocytes ( > 100/mL correlates well with infection, but may be due to contamination or other urinary tract pathology). RBCs are commonly seen on microscop y, but in isolation have a low degree of sensitivity or speci \201 city for UTI. Underlyin g renal pathology is suggested by \201 nding urinary crystals, RBC, or granular casts. MSU for culture and sensitivity. Transportation the sample to the laboratory without delay to ensure that bacterial overgrowth does not arti \201 cially i the count. Dipslides dippe d into freshly passed urine and transported in a plastic container to the laboratory are an alternative. 159 URINARY TRACT INFECTION Treatment \200 It is usually reasonable to discharge female patients with uncomplicated l ower UTIs with antibiotics . Commence a 3 \200\2236 day course of trimetho- prim or nitrofu rantoin. Provide advice regarding \202 uid intake, no \200\230holding on \200\231, and v oiding after intercourse. Drinking barley water is as effective as attempts at urinary alka linization with sodium bicarbonate. ( Note: urinary alkalinization renders nitrofurantoin i neffective). Advise the patient to see her GP for review, MSU result, and repeat MSU. Elderly men and women with asymptomatic bacteriuria should not receive antibiotic treatment unless they show signs of being unwell. \200 In pregnancy, both symptomatic and asymptom atic bacteriuria should be treated with an antibiotic such as amoxicillin. Given the dif \201 culty in distinguishing prostatitis from simple UTI in men, they should receive a 2-week course of cipro \202 oxacin, trimethoprim, or co-amoxiclav. Arrange GP f ollow-up. Treat catheterized patients with symptoms or signs of UTI for 7 days with cipro \202 oxaci n or co-amoxiclav. Treatment is more effective if the catheter is changed in the ED prior t o commencing antibiotics. Do not treat catheterized patients with asymptomatic bacteriuria with antibiotics. Refer for investigation and treatment all male patients and females with recurrent infectio ns, pregnancy, GU malformation, immunosuppression, or renal impairment. Patients with acute pyelonephritis usually require admission for parenteral antibiotics, \202 uid replacement, and analgesia. Assess and treat for severe sepsis ( b Shock, p.60). See http://www.sign.ac.uk 160 CHAPTER 3 Medicine Chronic renal failure Patients with established chronic renal failure (CRF) are likely to b e very well known to the hospital. Obtain old notes and recent blood results, and liaise ea rly with in-patient specialist teams. Established chronic renal failure (not on dialysis) Patients with mild CRF (glomerular in \201 ltration rate (GFR) > 40mL/min \200\224 100mL/min) are unlikely to have speci \201 c problems related to their underlying renal failure. With GFR <40mL/min, and especially if GFR <10mL/min, complications may in \202 uence presentation and treatment. These patients are prone to pathological fractures. Secondary hyperparathyroidism and osteomalacia (lack of active vitamin D) occur in moderate GFR. In severe CRF, aluminum bone disease, and B 2 - microglobulin related amyloidosis may be associated with pathological fractures. \200\230Pseudo-gout \200\231 due to high Ca 2 + /PO 4 \200\223 production and twitching/tetany due to hypocalcaemia may occur. Other problems include: Defective regulation of extra-cellular \202 uid volume There is a n i risk of \202 uid depletion in moderate CRF and \202 uid retention in severe CRF. Hi gh dose diuretics may be required in severe disease: the combination of furosemide and meto lazone may be effective even with very low GFRs. Hyperkalaemia Most patients preserve potassium balance, but cannot deal with sudden K + loa ds (eg dietary, tissue damage/catabolism, GI bleed). Associated d Ca 2 + compounds the card iac effects. Plasma K + may i very quickly, so monitor ECG and check K + frequently. Hypert ension Often severe and resistant, with an i incidence of accelerated phase. Ciclosporin an d erythropoietin i BP, and can precipitate hypertensive encephalopathy. Drug effects Drugs may accumulate (eg opioids, acyclovir, some antibiotics), worsen renal f ailure (eg NSAIDs, ACE inhibitors, which d renal perfusion), cause hyperkalaemia (eg K + sp aring diuretics, ACE inhibitors, NSAIDs). Infections Impaired WBC function, with i risk of severe infection and features of infection (eg pain, fever) may be masked by the relative i mmuno-compromised state. Bleeding Platelet function is impaired. Pericarditis A sign of severe CRF, indicating the need for dialysis. Neurological dysfunction Usually a sign of severe uraemia \200\224 convulsions and/or alte red conscious state indicate a global metabolic disturbance. 161 CHRONIC RENAL FAILURE Common emergency presentation in haemodialysis patients Pulmonary oedema Usually occurs sho rtly before the next dialysis session and may re \202 ect \202 uid overload due to non-c ompliance with diet and \202 uid restriction. Most are virtually anuric, so diuretics are ineffective. Get the patient on dialysis without delay. While this is being arranged give high \202 ow O 2 and SL buccal or IV nitrates. Pre-dialysis hyperkalaemia May present wit h neuromuscular symptoms (eg muscle spasms, weakness, paralysis, paraesthesiae) or arrhythm ias, including cardiac arrest. Standard treatment ( b p.162) can buy time while emergency d ialysis is arranged. When giving glucose/insulin, give 6U of insulin at most (there is a ri sk of late hypoglycaemia, since insulin half-life will be i ). Complications of vascular ac cess Arteriovenous \201 stulae are a dialysis patient \200\231s lifeline \200\224 never occlude limb with BP cuffs or tourniquets. Do not use for vascular access unless life-threa tening emergency. Acute shunt thrombosis (loss of palpable thrill, often local pain/redness ) is a vascular emergency. Arteriovenous \201 stulae and central lines are common infecti on sources (usually staphylococcal), often with no overt external abnormality, but presenti ng with acute \200\230viral illness \200\231 symptoms. Continuous ambulatory peritoneal dialysis Bacterial peritonitis Occurs every 12 \200\22318 patient-months. Features are cloudy drained dialysate bags, abdominal pain, and peritonism. Systemic sepsis is usually absent or minimal. Staphylococci are most common organisms. Sus pect underlying surgical cause (most often diverticular abscess) if Gram \200\223ve organi sms or anaerobes present in drainage \202 uid, and particularly if > 1 type of organism i s found on microscopy or culture. Diabetic patients on continuous ambulatory peritoneal dialysis can develop acute severe (us ually non-ketotic) hyperglycaemia , related to high dialysate glucose concentrations (80 \200\223140mmol/L). Hernias of all types, leakage of dialysate into the abdominal wall or the pleural cavity, a nd scrotal swelling (open processus vaginalis) may occur. Transplant patients Contact the transplant team whenever any transplant patient presents to the ED. They will know the patient well and will advise about drug therapy, intercurrent p roblems, and help with follow-up. Acute rejection Signs include pain, tenderness, and swelling over graft, d urine output, fe ver, systemic upset, biochemical deterioration. Often indistinguis\hable from acute bacteri al infection: if in doubt treat for both, pending results of further testing by specialists (renal biopsy, blood, and urine cultures). Infections May be opportunist, whilst \200\230conventional \200\231 infections are unduly severe, with response modulated by steroids. Poor wound healing, avascular necrosis and pathological fractures May be caused by steroids . 162 CHAPTER 3 Medicine Hyperkalaemia Hyperkalaemia is classi \201 ed as mild (K + 5.5 \200\2236.0mmol/L), moderat e (K + 6.1 \200\2236.9mmol/L) or severe (K + > 7.0mmol/L).