acidosis (venous pH<7.3) and blood ketones \211 3mmol/l or ketonuria( \211 2+). Stabilize the patient as shown on b p324, then: Continue IV insulin infusion and fl uid rehydration (see box) \210\222 \200 Monitor veno us K+, pH and HCO 3 after 1h, 2h and then 2hrly using a venous sample on a gas analyzer for rapid testing Monitor venous glucose and ketones hourly aiming for blood ketones to fall by >0.5 mmol/l/h and glucose by >3mmol/l/h If patient uses long-acting insulin continue at normal dose/time \200 Continue insulin in fusion until ketones <0.3mmol/l and pH>7.3. At this point convert to regular SC insulin if eating and drinking normally, else use a slidin g scale (b p327). DKA \202 uids 0.9% saline is the most appropriate fl uid replacement. A guide in adults w ould be to prescribe 1l over 1h, 1l over 2h, 1l over 2h and 1l over 4h. If systolic BP <90m mHg on admission an initial 500 \200\2231000ml bolus must be carefully given under senior s upervision. Since excess fl uid replacement can lead to cerebral oedema, reassess frequentl y for signs of overload (b p380), and tailor to volume status and patient weight. Add 40mmo l/l KCl after the fi rst liter of fl uid if the plasma K+ is 3.5 \200\2235.5mmol/l. Omit ad di- tional KCl if K+ >5.5; if K+ <3.5 seek senior review. Adding a 10% glucose infusion at 125ml/h if glucose <14mmol/l but do not stop saline. Management tips in DKA/HONK These patients require close monitoring. If severely ill, cathe terise, consider admission to HDU or ICU and an arterial and/or central line. If obtunded o r persistent vomiting, keep NBM and pass NG tube. Dehydration and dGCS predispose to thromb oembolism: give pro- phylactic LMWH (b p406). Consider likely precipitants: poor compli- an ce/incorrect insulin dose, alcohol, infections (may be asymptomatic \200\223 check blood c ultures, MSU and CXR; low threshold for starting anti- biotics), MI (check an ECG), CVA, su rgery. Hyperosmolar non-ketotic state (HONK) (OHAM3 b p524) Severe, uncorrected hyperglycaemia lea ds to dehydration, but in the presence of residual insulin production in T2DM, ketoacidosis does not develop. Also referred to as hyperosmolar hyperglycaemic state (HHS). Diagnose ba sed upon raised plasma osmolality2 (typically >340 mOsmol/kg) with high glucose (typically >30mmol/l). \200 Stabilize the patient as shown on the treatment plan, b p324, then: \200 Continue IV fl uid replacement (eg at half the rate used in DKA) \200 Monitor U+E, glucose and osmolality every 2h. Be aware that hyperglycaemia will drive redistribution of water into the extracellular fl uid, lowering s erum Na+ concentrations ( \200\230spurious hyponatraemia \200\231) Convert to insulin/oral hypoglycaemics when glucose <12mmol/l. 1 Joint British Diabetes Soc ieties guidelines at (cid:27)www.diabetologists-abcd.org.uk/JBDS_DKA_ Management.pdf 2 Plasma osmolality may be estimated as 2x([Na+] + [K+])+ urea + glucose whilst awaiting a formal lab measurement. OHFP.indb 326 OHFP.indb 326 30/05/2014 16:18 30/05/2014 16:18 327 SLIDING SCALES Sliding scales These give strict monitoring and control of blood glucose levels. They are u sed in the treatment of HONK, for diabetic patients requiring insulin whose oral intake is signifi cantly disrupted (eg NBM, severe vomiting or serious illness), and in critical illn ess, where good gly- caemic control improves outcomes, eg post-MI or on ICU. You need to pr escribe both the insulin infusion and appropriate IV main- tenance fl uids on the infusions section of the drug card (Fig. 10.1). Use 0.9% saline or 5% glucose (with KCl as necessary ), according to the blood glucose (use 0.9% saline if the glucose is running >11mmol/l). Date Route Fluid Additives Vol Rate Signature 18.8.14 IV 0.9% saline 50units Actrapid 50ml Sliding Scale P Roluos 18.8.14 IV 5% glucose 20mmol KCl 1l 8h P Roluos Fig. 10.1 Prescribing insulin and fl uids for a sliding scale. Insulin Date Start time Blood glucose (mmol/l) <4 4 \200\2237 7.1 \200\22311 11.1 \200\22320 >20 Rate (ml/h) Actrapid Dose 1unit/ml 18.8.14 Route IV 13:45 Stop \200\223 call doctor 1 2 4 7 \200\223 call doctor Signature S Dixon Fig. 10.2 Example of sliding scale regimen (check local guidelines). If the patient remains hyperglycaemic despite the sliding scale (Fig. 10.2) then check the infusion pump and cann ula; if no problems found, pre- scribe a STAT bolus of short-acting insulin eg Actrapid 4 \200\2236 units SC. If control still poor, increase infusion rates by 1.5 \200\2232-fold, and check venous pH (T1DM) or osmolality (T2DM). If the capillary blood glucose is <4mmol/l check that there is 5% glucose running, increase the fl uid rate and/or glucose concentrat ion (up to 10%); recheck glucose in 30min. If persistently <4mmol/l stop the sliding scale, and restart the infusion at half the doses once blood glucose >6mmol/l. If glucose <2, see b p322. Stop a sliding scale once a patient is eating normally and able to resume normal d iabetes medication. Give normal dose of SC insulin 30mins before stopping the scale, unless rapid acting (eg Novorapid , Humalog ) in which case give at same time as stopping the s cale. Prescribing insulin Most hospitals have separate drug cards for prescribing insulin. Always specify the insulin formulation, and avoid using the abbreviation \200\230U \200\231 for units (since this can be misread as a number). See Fig. 10.3 for an example. Breakfast Insulin Novomix 30 Dose (units) Route Start 18 SC 18.8.14 Night Insulin Novomix 30 Dose (units) Route Start 10 SC 18.8.14 Fig. 10.3 Prescribing subcutaneous insulins. _OHFP.indb 327 _OHFP.indb 327 30/05/2014 16:18 30/05/2014 16:18 328 CHAPTER 10 Endocrinology Diabetes mellitus Fasting plasma glucose \211 7.0mmol/l, or \211 11.1mmol/l 2h after a 75 g oral glucose load (given in 300ml water as oral glucose tolerance test \200\223 OGTT).1 \200 Type 1 autoimmune pancreatic B cell destruction, resulting in dependence on exogenous insulin; typically presents in children or young adults Type 2 relative insulin hyposecretion or resistance to eff ects, requiring drugs to potenti ate insulin secretion or eff ects, or exogenous insulin; typically occurs in adults, especi ally if overweight \200 Impaired glucose tolerance (IGT) plasma glucose \211 7.8mmol/l a fter OGTT, but <11.1mmol/l; 20 \200\22350% progress to T2DM in 10yr Impaired fasting glucose (IFG) plasma glucose \211 6.1mmol/l after an overnight fast, but <7.0mmol/l; lower risk of developing T2DM \200 Gestational any degree of glucose intolerance fi rst detected during pregnancy (b p505); around 30% will progress to T2DM within 5yr. Type 1 DM (OHCM9 b p198) Symptoms tiredness, weight loss, thirst, polyuria, abdo pain, vomi ting. Signs sweet-smelling breath, shock, abdominal pain (all suggest DKA). \210\222 Investigations Glucose testing as above. Check venous HCO 3 and pH and urine (ket ones) to exclude DKA. If uncertainty about type of dia- betes, positive islet cell or gluta mic acid decarboxylase antibodies, or low C-peptide levels all suggest T1DM. Check HbA1C (s ee box). Treatment resuscitate and investigate for DKA; in the absence of DKA, a new diagnosis of T1 DM does not necessitate admission, but the patient should be started on a suitable insulin regimen by an appropriately experi- enced individual (eg endocrine registrar or diabetes nu rse specialist) with regular fi nger-prick glucose monitoring and prompt out-patient follow -up. For properties of some commonly used insulins, see b p203. Chronic management \200 \223 see b p330. HbA1c HbA1c refl ects non-enzymatic glycosylation of hemoglobin at a rate proportional to p lasma glucose. Since erythrocytes (and hence hemoglobin) undergo slow but constant turnover , HbA1c refl ects plasma glucose control over the preceding 1 \200\2233 months and is a rel i- able predictor of diabetes complications. Target HbA1c levels should be set with patient involvement, taking into account an individual \200\231s risk profi le, as well as tolerab ility of therapy. In T2DM targets are gener- ally around 48mmol/mol, whilst for T1DM <59mmo l/mol is a better target given risks of recurrent hypoglycaemia.2 2 ie \211\2107.5% (T2DM) or <6.5% (T1DM). Since 2009 HbA1c levels have been reported as mmol per mol (of hemoglobin without glucose attached) but previous units of % were reported in key trials, used in gui delines and permeate the consciousness of patients and clinicians alike. 1 In the presence of diabetes symptoms, a random plasma glucose \211 11.1mmol/l may be con - sidered diagnostic; in the absence of symptoms, all tests should be repeated on a separat e occasion. OHFP.indb 328 OHFP.indb 328 30/05/2014 16:18 30/05/2014 16:18 329 DIABETES MELLITUS Type 2 DM (OHCM9 b p198) Symptoms as for type 1, but can also present with diabetic complic ations, eg visual problems, neuropathy, CRF, MI, CVA, claudication. Signs foot ulcers, infe ctions, peripheral neuropathy, poor visual acuity and retinopathy, evidence of cardiovascul ar disease. Investigations blds confi rm diagnosis based upon plasma glucose testing OGTT (b p328), HbA1c (see \200\230HbA1c \200\231 box), U+E, lipid profi le; ECG Treatment T2DM may initially be controlled by a healthy diet with minimal rapid-release carbohydrates (as found in sugary drinks or sweets) and weight loss. If medication required, uptitrate pharm acological agents before adding in insulin therapy (see Table 10.1). Chronic management \200\223 see b p330. Table 10.1 Medications for glycaemic control in T2DM1 Class Examples Comment Metformin 1st line for obese; iglucose uptake and Biguanides dappetite; avoid if any renal failure Sulphonylureas Gliclazide Add to metformin (1st line if metformin not suitable); iinsulin secretion, but causes weight gain Added if metformin+sulphonylurea insu ffi cient, but add 2nd line agents instead if insulin unacceptable Thiazolidinediones Piogl itazone 2nd line if other drugs not tolerated or eff ective; Insulin Isophane (given SC) dinsulin resistance; avoid in heart failure 2nd line if other drugs not tolerated or eff ec tive; iinsulin and dglucagon secretion 2nd line if other drugs not tolerated or eff ective, especially if iBMI; iinsulin and dglucagon secretion 3rd line where other oral drugs not t olerated; dcarbohydrate absorption; causes fl atulence DPP-4 inhibitors Sitagliptin, dapaglifl ozin GLP-1 activators (given SC) A-glucosidase inhibitors Exenatide, liraglutide Acarbose 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG87 Sick day rules Educate diabetic patients what to do if they are feeling unwell: \200 Drin k plenty of fl uids \200 If not eating try milk, soup, fruit juice or fi zzy drinks inste ad \200 Increase frequency of blood glucose monitoring to at least 4 times/day \200 See k medical attention if you cannot keep fl uids down, becoming drowsy or confused, blood glu cose <4mmol/l or persistently >20mmol/l If on insulin: this should never be stopped; hyperglycaemia can arise from intercurrent illness, regardless of calorie intake. Consider increasing insulin dose i f blood glucose >13mmol/l even if unable to eat. Dipstick urine for ketones at least daily and seek medical attention if +ve \200 If on tablets: continue regular diabetic medicatio ns providing calorie intake continues. Metformin may need to be stopped if becoming dehydra ted: seek medical advice. _OHFP.indb 329 _OHFP.indb 329 30/05/2014 16:18 30/05/2014 16:18 330 CHAPTER 10 Endocrinology Long-term management of diabetes mellitus1,2 Diabetes mellitus is associated with macrovasc ular (IHD, CVA, PVD) and microvascular (CRF, nephropathy, neuropathy, retinopathy) complica tions. Large, long-term studies show reductions in complications with control of risk facto rs; these should be assessed at least annually in a formal review. Education and lifestyle ensure understanding and motivation for gly- caemic control (including self-monitoring, med ication compliance, and diet), vascular risk factors and complications (physical activity, smoking cessation, foot care). Glycaemic control measure HbA1c (every 2 \200\2236mth)and ad just therapy accordingly (see box, b p328); consider revising target if tight control unacc eptable to patient based upon individual risk profi le. BP aim for BP <140/80 (uncomplicate d T2DM) or <135/80 (uncompli- cated T1DM); if end-organ damage aim for BP <130/80 (b p263). Use an ACEi as 1st line in T2DM (plus diuretic or Ca2+ channel blocker if African- Caribbe an descent); use a thiazide diuretic in T1DM (ACEi if nephropathy). Lipids measure lipid pr ofi le and consider cardiovascular risk factors; in all T2DM age >40yr (except those judged to be very low risk) initiate statin therapy and assess response; in T1DM consider statin therapy in those with microalbuminuria, family history, age>35yr, or other high-risk featur es. Nephropathy test early morning urine albumin:creatinine ratio; if \211 2 repeated meas urements show microalbuminuria (4: >2.5mg/mmol, 5: >3.5mg/mmol), tighten BP control, initia te ACEi and consider renal referral. Retinopathy arrange annual retinal photography and rev iew by appropriately trained staff ; sudden loss of vision, rubeosis iridis, pre-retinal or vitreous hemorrhage, or retinal detachment require emergency ophthalmology review; new ves sel formation requires urgent referral; pre-proliferative retinopathy, signifi cant maculop athy, or unexplained change in visual acuity require routine referral. Footcare3 assess for ulcers, peripheral pulses, sensory function, and foot deformity. If ulcers present, refer urgently to a specialist diabetic footcare team. Those with previous ulcers, absent pulses or impaired sensation require referral to a footcare team for frequent review. Neuropathy a ssess for autonomic neuropathy in the form of unexplained vomiting (gastroparesis \200\223 consider trial of prokinetic agents, eg metoclopra- mide), erectile dysfunction (off er ph osphodiesterase-5 inhibitor, eg sildenafi l), nocturnal diarrhea, bladder voiding problems, or orthostatic hypotension. Neuropathic pain4 requires oral duloxetine as 1st line; if thi s fails, switch to or combine with pregabalin, or switch to amitriptyline. Refractory or se vere pain may require opioid analgesia and specialist pain service referral. Aspirin is use d,5 but not licensed, for primary prevention of vascular events. Risk of GI bleeding needs to be balanced against vascular risk. Consider aspirin in T1DM if on a statin, or in T2DM i f age \211 50 (provided BP con- trolled to <145/90) or age<50 and signifi cant cardiovascu lar risk factors. Pneumovax and yearly \202 u vaccines should be off ered to all patien ts. 1 For NICE guidelines on management of T1DM see (cid:27)guidance.nice.org.uk/CG15 2 For NIC E guidelines on management of T2DM, see (cid:27)guidance.nice.org.uk/CG87 3 For NICE guidel ines on footcare in T2DM, see (cid:27)guidance.nice.org.uk/CG10 4 For NICE guidelines on ne uropathic pain, see (cid:27)guidance.nice.org.uk/CG173 5 Evidence and recommendations confl icting, see (cid:27)www.ncbi.nlm.nih.gov/pmc/articles/PMC3513879 OHFP.indb 330 OHFP.indb 330 30/05/2014 16:18 30/05/2014 16:18 331 PITUITARY AXIS Pituitary axis Hypopituitarism Failure of secretion may aff ect one or more anterior pituit ary hormones. Causes damage to the hypothalamic \200\223pituitary axis after surgery, irrad iation, tumors, ischaemia, infection (eg meningitis) or infi ltration (eg amyloidosis). Sym ptoms and signs are specifi c to each hormone lost, eg growth hormone (GH) loss: weakness, malaise, dcardiac output, hypoglycaemia; gonadotro- phin (LH, FSH) loss: amenorrhoea, dlibi do, erectile dysfunction; TSH loss: hypo thyroidism (b p334); ACTH loss: adrenal insuffi ci ency (b p332). Investigations tests of pituitary function include LH, FSH, TSH, paired with target organ hormones: testosterone/oestradiol, T4, cortisol and insulin-like growth facto r-1 (IGF-1, a marker of growth hormone secretion). Dynamic testing (eg short Synacthen te st, b p571) is also informative. Generally testing of pituitary function should be undertak en and interpreted with specialist advice. Treatment identify and treat underlying cause; a ppropriate hormone replace- ment may be required eg hydrocortisone (b p202) or thyroxine (b p205). 3On the ward, the most important point is to ensure any patient with pan- hypopitui tarism gets regular steroids (increased in acute illness and given IV if necessary) with ea rly endocrinologist involvement (b p332). Diabetes insipidus Failure of urine concentration due to loss of either ADH secretion (neu- rogenic) or renal response (nephrogenic). Causes neurogenic idiopathic, brain tumor or metastases, head trauma, cranial surgery; nephrogeni c drugs (eg lithium), CRF, post- obstructive uropathy, iCa2+, dK+. Symptoms polyuria, thirs t (may be extreme). Signs dilute urine, clinically dehydrated (b p380). Investigations duri ne osmolality (<400mOsmol/kg), iplasma osmolality and iNa+. In the water deprivation test ( fl uid balance, weight, urine and plasma osmolality recorded over 8h without fl uids) \200 \223 failure to concentrate urine (>600mOsmol/kg) confi rms DI. Desmopressin (an ADH analog ) is then given \200\223 the production of a concentrated urine at this point implies neur o- genic DI; failure to concentrate implies nephrogenic DI. Treatment identify and treat th e cause. In neurogenic DI, intranasal desmopressin may be used regularly. In nephrogenic DI , bendrofl ume- thiazide or NSAIDs may be used. Acromegaly Hypersecretion of GH from a pituitary tumor drives soft-tissue and skeletal grow th resulting in characteristic facial and body features. Symptoms and signs enlarged hands and feet, coarse facial features, prog- nathism, macroglossia; headache bitemporal hemian opia. Sweating, hypertension and hyperglycaemia are markers of disease activity. Investigat ions IGF-1 levels refl ect GH secretion; OGTT and other tests of pituitary function under s pecialist guidance; pituitary MRI. Treatment Transsphenoidal resection of pituitary tumor w here pos- sible; medical therapy includes somastostatin analogs (eg octreotide). _OHFP.indb 331 _OHFP.indb 331 30/05/2014 16:18 30/05/2014 16:18 332 CHAPTER 10 Endocrinology Adrenal disease Cushing \200\231s syndrome (OHCM9 b p216) Excess of glucocorticoids (eg cor tisol); \200\230Cushing \200\231s disease \200\231 when due to an ACTH-producing pituitary tumor. ACTH may also be produced ectopically, eg by small-cell lung cancers. Adrenal adeno mas or carcinomas are ACTH- independent causes (and will suppress ACTH). A patient on stero ids may become \200\230Cushingoid \200\231. Symptoms weight gain, depression, psychosis, t iredness, weakness, oligo- or amenorrhoea, hirsutism, impotence, infections, DM. Signs cent ral obesity (buff alo hump), moon-face, water retention, iBP, thin skin, striae, bruising, peripheral wasting; hyperpigmentation only in Cushing \200\231s disease or ectopic ACTH pro duction. Investigations iglucose, i24h urinary cortisol, plasma ACTH and 8am cortisol, dexa methasone suppression tests (OHCM9 b p217); imaging tests are problematic due to high rates of \200\230incidentalomas \200\231 on adrenal CT or pituitary MRI. Treatment localize and remove source of cortisol, eg transsphenoidal resec- tion of pituitary adenoma, adrenalect omy for adrenal adenoma. If surgical treatment fails or unsuitable (eg ectopic ACTH from me tastatic lung cancer), suppress steroidogenesis, eg with ketoconazole or metyrapone. If iat rogenic cause, try to taper steroid dose (b p177). Consider bone protection with bisphospho nate and vitamin D; monitor for iglucose. Complications osteoporosis, DM, infection, poor h ealing, infertility. Adrenal insuffi ciency (OHCM9 b p218) Adrenal defi ciency, typically s een upon abrupt withdrawal of long-term steroid therapy; p adrenal (Addison \200\231s) dise ase includes autoimmune (commonest in UK), TB (commonest worldwide), metastases (eg lung, b reast), Waterhouse \200\223Friederichsen syndrome (sepsis and adrenal hemorrhage). Symptoms tiredness, lethargy, weight loss, weakness, dizziness, depression, abdo pain, diarrhea or constipation, vomiting, myalgia. Signs vitiligo, postural hypotension, hyperpigmentation of creases, scars and mouth (buccal). Investigations dNa+, iK+, iurea, may have abnormal FBC and LFT. If sus- pected perform short Synacthen test: order 250micrograms Synacthen fro m drugstore, once this arrives send a blood sample for cortisol and ACTH levels, give the S ynacthen IM/IV (b p524); repeat cortisol levels in 30min. Addison \200\231s is excluded i f initial, or 30min cortisol are >550nmol/l. Treatment hydrocortisone 20mg PO OM and 10mg P O ON, may also need fl udrocortisone (50 \200\223200micrograms PO OD) if electrolytes deran ged or postural hypotension. If unwell, trauma or post-op double all steroid doses for at l east 1wk. If vomiting, replace oral dose with hydrocortisone 100mg IM/IV and seek specialis t advice. Addisonian crisis shock, dGCS or hypoglycaemia in a patient with Addison \200\231 s disease or stopping long-term steroid therapy. Resuscitate according to b p472, send bloo ds for cortisol levels and give hydrocortisone (200mg IV STAT, then 100mg IV/8h) with broad -spectrum antibiotics (eg Tazocin 4.5g IV); seek urgent endocrinologist advice. OHFP.indb 332 OHFP.indb 332 30/05/2014 16:18 30/05/2014 16:18 333 ADRENAL DISEASE Hyperaldersteronism (OHCM9 b p220) Excess aldosterone secretion, resulting in Na+ and water retention; typically from an adrenal adenoma (Conn \200\231s syndrome), or adrenal hyperpl asia. Symptoms thirst, polyuria, weakness, muscle spasms, headaches. Signs hypertension (especially if refractory to multiple antihypertensive agents or young a ge of onset). Investigations dK+, normal or iNa+, metabolic alkalosis; measure plasma renin and aldosterone together after 2h in sitting position (postural changes aff ect renin secr etion). Ideally the patient should be off all antihypertensives apart from A-blockers. iAld osterone with drenin supports the diagnosis; consider CT abdo (but beware \200\230incident alomas \200\231: abnormal CT fi ndings, such as a small adrenal mass of no clinical signifi cance). Treatment spironolactone 200 \200\223300mg/24h PO; if adenoma, surgical resection may be at tempted after 4wk medical therapy once electrolytes and BP controlled. Secondary hyperaldosteronism occurs when renal perfusion is decreased, leading to high reni n secretion. Common causes include diuretics, heart failure, liver failure and renal artery stenosis. Features are similar, but aldosterone:renin ratio will not be high. Manage with spironolactone or ACEi. Phaeochromocytoma (OHCM9 b p220) Catecholamine (eg noradrenaline) p roduction from tumors within the adrenal medulla, or more rarely extra-adrenal source. Cons ider in those with drug-resistant or young onset hypertension, or typical symptoms. Symptoms episodic anxiety, sweating, facial fl ushing, chest tightness, breathlessness, tre mor, palpitations, headaches, abdo pain, vomiting or diarrhea. Signs episodic hypertension. Investigations glycosuria during attack; plasma metanephrine testing has high sensitivity, but lower specifi city (hence useful in high-risk patients); in all others, 24h urine colle ction for creatinine, total catecholamines, vanillylman- delic acid (VMA), and metanephrine s has a high specifi city and acceptable sensitivity; CT abdomen to evaluate for tumor. Treatment surgical resection of tumor can safely be performed only after adrenoreceptor blo ckade. A-blockers (eg phenoxybenzamine), are used before B-blockers (eg propranolol) to avo id hypertensive crisis of unopposed A-adrenoreceptor stimulation. _OHFP.indb 333 _OHFP.indb 333 30/05/2014 16:18 30/05/2014 16:18 334 CHAPTER 10 Endocrinology Thyroid disease Hyperthyroidism Hypermetabolic state driven by excess thyroxine. Causes Gra ves \200\231 disease (50 \200\22360%; agonistic autoantibodies to TSH receptor), toxic mult inodular goiter (15 \200\22320%), subacute thyroiditis (15%; self-limiting, with painful gr anulomatous infi ltrates as de Quervain \200\231s thyroiditis, or painless lymphocytic infi ltrates), toxic adenoma (5%), excess exogenous replacement, metastatic thyroid carcinoma, struma ovarii. Symptoms weight loss, agitation, anxiety, psychosis, sweating, heat intol- e rance, diarrhea, tremor, oligomenorrhoea. Signs thin, iHR, irregular pulse, warm hands, tre mor, goiter nodules, lid lag, lid retraction, muscle weakness; speci \201 c to Graves \200\231 disease: exoph- thalmos, ophthalmoplegia, pretibial myxoedema, thyroid acropachy. Investigations TSH used as screening test \200\223 if d then measure fT4 (free thyroxine, ie active, not bound to plasma proteins); antithyroid peroxi- dase (TPO) antibodies positiv e in Graves \200\231 and other forms of thyroiditis (TSH receptor antibodies more specifi c for Graves \200\231 but not routinely measured); ECG to exclude AF; USS thyroid, or nuclea r scintigraphy may help localize lesion and assess uptake. Treatment symptom relief with pr opranolol 40mg/6h (or rate limiting calcium-channel blocker if asthmatic); suppress thyroid function using car- bimazole in dose titrated to TFTs, or with thyroxine in \200\230block and replace \200\231 approach. Other options include radioiodine ablation or surgical rese ction. Complications CCF, AF, ophthalmopathy, osteoporosis. 3Thyrotoxic storm Caused by inf ection, severe illness, recent thyroid surgery or radioiodine. Tachycardia, AF, agitation , confusion or coma with ifT4 or iT3. Resuscitate as required (b p472) and get senior help. Propranolol (suppresses sympathetic response, blocks T4 to T3 conversion and alleviates sy mptoms), propylthiouracil (inhibits T3/T4 production and T4 to T3 conversion and hydrocorti sone (reduces iodine uptake and inhibits T4 to T3 conversion) are the main treatments. Carb imazole (inhibits T3/T4 production) has a slower onset of action but may be preferred to pr opylthi- ouracil since it has a longer duration of action and is less hepatotoxic. Hypothyroidism Common and insidious; characterized by insuffi cient thyroxine release. Caus es Hashimoto \200\231s thyroiditis (autoimmune destruction), resolution stage of subacute t hyroiditis, drugs (eg amiodarone, lithium), iatrogenic (post surgery or radioiodine), iodin e defi ciency (commonest worldwide). Symptoms fatigue, lethargy, weight gain, hair loss, de pression, confusion, dementia, cold intolerance, constipation, menorrhagia, infertility. Si gns obese, bradycardia, dtemp, cold/dry hands, macroglossia, jaundice, pitting oedema, goit er, peripheral neuropathy, slow relaxing refl exes. Investigations iTSH, dfT4; +ve thyroid autoantibodies. Treatment levothyroxine (T4): 50micrograms/24h PO, gradually titrated up in to range 50 \200\223150micrograms/24h based upon monthly TFTs until TSH in normal range; ye arly TFT once stable. Beware of worsening underlying ischaemic heart disease: Consider prop ranolol 40mg/6h PO to prevent iHR. Complications angina from treatment, myxoedema coma. OHFP.indb 334 OHFP.indb 334 30/05/2014 16:18 30/05/2014 16:18 335 THYROID DISEASE Subclinical thyroid disease Patients with normal fT4 and T3 but iordTSH have subclinical th yroid disease. Although some will progress to frank hypo/hyperthyroidism, there is no manag ement consensus. Recheck TFTs after 3mth; if TSH grossly iord (eg >10 or <0.1mU/l) then con sider thyroxine/ carbimazole or surveillance. dTSH and dfT4 suggests \200\230sick euthy- r oidism \200\231 in systemic illness \200\223 recheck after recovery. Parathyroid disease \200\223 see b p389. _OHFP.indb 335 _OHFP.indb 335 30/05/2014 16:18 30/05/2014 16:18 This page intentionally left blank Chapter 11 Neurology and psychiatry 337 Coma and reduced GCS emergency 338 Coma and reduced GCS 340 Acute confusion 341 Dementia 34 2 Adult seizures emergency 344 Pediatric seizures emergency 345 Seizures 346 Neurodegenerat ive disorders 349 Stroke/CVA/TIA emergency 350 Stroke 351 Focal neurology 353 Back pain 356 Headache 358 Dizziness 362 Aggressive behavior emergency 364 Mood disturbance/psychosis 36 5 _OHFP.indb 337 _OHFP.indb 337 30/05/2014 16:18 30/05/2014 16:18 338 CHAPTER 11 Neurology and psychiatry Coma and reduced GCS emergency Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM Airway Breathing If no palpable pulse \200\223 CALL ARREST TEAM Circulation If GCS \211 8 \200\223 CALL anesthetist Disability 3Call for senior help early if patient unwell or deteriorating. Airway and C-spine \200 S tabilize cervical spine if there is any risk of injury (eg fall) \200 Look inside the mou th, remove obvious objects/dentures \200 Wide-bore suction under direct vision if secreti ons present \200 Jaw thrust/chin lift; oro/nasopharyngeal airway if tolerated. Breathing \200 15l/min O2 if SOB or sats <94%; beware if known COPD/CO2 retainer If hypoxic see b p270 \200 Monitor O2 sats and RR \200 Bag and mask ventilation if poor /absent respiratory eff ort. Circulation \200 Venous access, take bloods: FBC, U+E, LFT, glucose, Ca2+, cardiac markers, clotting, G+S, bld cultures, paracetamol, salicylate and alcohol levels \200 ECG and treat arrhythmias (tach y b p248, brady b p256) \200 Start IV \202 uids if shocked \200 Monitor HR, cardiac t race and BP. Disability \200 Check blood glucose \200 Check drug card especially for op ioids and benzodiazepines \200 Control seizures (b p344) \200 Check GCS, pupil refl exe s, limb tone, plantar responses Look for brainstem, lateralising or meningeal signs (see Table 11.1) Call anesthetist for airway support if GCS \211 8. Exposure \200 Check temp \200 Look over whole body for evidence of injury or rashes \200 Ask ward staff for a brief history or check notes \200 Examine patient brief RS, CVS, abdo and neuro exam \200 ABG, but do n \200\231t leave the patient alone \200 Request urgent portable CXR \200 Stabilize and treat, see following sections \200 Call for senior help \200 Reassess, starting with A , B, C \200 OHFP.indb 338 OHFP.indb 338 30/05/2014 16:18 30/05/2014 16:18 339 COMA AND REDUCED GCS EMERGENCY Stabilization \200 Get senior help \200 Treat hypoxia with O2, airway aids, ventilat ion \200 Treat arrhythmias and hypotension urgently \200 Start broad-spectrum antibioti cs if sepsis suspected (?meningitis) \200 Treat simple metabolic/intoxication abnormaliti es: glucose <3.5mmol/l, give 100ml of 20% glucose STAT \200 glucose >20mmol/l, 0.9% saline 1l IV STAT (consider DKA/HONK) \200 opioids (pinpoint pupils and dRR), naloxone 0.4mg IV/IM STAT \200 history of chronic alcohol excess, Pabrinex 2 pairs IV over 10min \200 ben zodiazepine overdose alone, fl umazenil 200micrograms IV. b p271 b p473 b p263 b p250 b p258 b p360 b p323 b p325 b p313 b p385 b p482 b p493 Hypoxia Hypotension Hypertension Tachyarrhythmia Bradyarrhythmia Meningitis Hypoglycaemia Hyperglycaemia Liver failure Metabolic Pyrexia Overdose Further management \200 Check brainstem function (see Table 11.1): normal stabilize the patient and get an urgent CT head \200 gradual onset dysfunction con sider mannitol and urgent CT head \200 rapid onset dysfunction give mannitol, normalize P aCO2 with ventilator and contact a neurosurgeon urgently; the patient \200\231s brain is probably her niating due to iintracranial pressure \200 If CT normal consider LP to test for meningiti s or encephalitis \200 If CT and LP normal the cause is probably metabolic or intoxicatio n. Table 11.1 Common causes of reduced GCS Cause Signs Intoxication May have shallow, slow breathing, pinpoint pupils suggests opioids, iiRR suggests salicylates Eyes dilated or slow reacting pupil (unilateral or bilat eral), absent corneal refl ex, eyes looking in diff erent directions (III, IV, VI lesion), eyes fi xed: doll \200\231s head movements (not drifting back to forwards gaze when neck ro tated) Swallow water not swallowed spontaneously/no gag refl ex Respiration apnoeas, gaspin g, irregular or Cheyne \200\223Stokes breathing (alternating rapid breathing and apnoeas) B ody increased tone and upgoing plantars unilaterally/ bilaterally/crossed Facial asymmetry, asymmetrical tone and plantar responses Brainstem dysfunction Lateralising (cerebral dysfunction) Meningism Neck stiff ness, photophobia, Kernig \200\231s sign, Brudzinski \200\231s sign, straight le g raise (b p132) _OHFP.indb 339 _OHFP.indb 339 30/05/2014 16:18 30/05/2014 16:18 340 CHAPTER 11 Neurology and psychiatry Coma and reduced GCS Think about \200 No focal neurology dO2, iCO2, hypotension, metabolic (i/dglucose, Na+, C a2+, K+; acidosis, alkalosis, renal failure, liver failure), overdose (alcohol, opioids, tr icyclics, benzodiazepines), epilepsy/post-ictal, hypothermia, pyrexia, hypothyroid, maligna nt hypertension Brainstem dysfunction or lateralising signs CVA, tumor, abscess, haematoma, hypoglycaemia o r rarely other metabolic abnormalities Meningism meningitis, encephalitis, subarachnoid hemorrhage. Ask about (notes, relatives, n urses) speed of onset, headache, chest pain, palpitations, vomiting, seizures, weight loss; PMH cardiac, respira- tory, DM, kidney, liver, psychiatric, stroke/TIA, seizures; DH elici t past medical history from medications, consider the possibility of overdose; SH alcohol, recreational drugs (overdose or withdrawal). Obs GCS (Table 11.2), temp, BP, HR, O2 sats, O2 requirements, RR, pupil size. Neuro obs GCS, limb movements, pupil size and reactivity, HR, BP, RR, temp. Look for respiration rate, depth, distress, added sounds, air entry on both sides; pulse ra te and rhythm; abdomen rigidity, pulsatile mass, organomegaly; neuro pupil responses, papil loedema (late sign), limb tone, plantar refl exes; skin rashes, injection marks or trauma. Investigations blds FBC, U+E, LFT, Ca2+, glucose, cardiac markers, CRP, clotting, bld cultu res, toxicology screen (paracetamol, salicylate, alcohol); ABG pH, dO2 or diCO2; ECG arrhyt hmias; CXR evidence of aspiration; CT if the patient has focal neurology or there is no cle ar diagnosis then an urgent CT head is required, the patient may need to be intubated fi rs t; LP after a CT scan if CT normal. Table 11.2 GCS scoring (3/15 minimum) Eyes Open spontaneously 4 Motor Obeys commands 3 2 1 6 Localizes pain 5 Flexes/withdraws to pain 4 3 Abnormal fl exion to pain 2 Extension to pa in 1 No movement Open to command Open to pain No response Voice Talking and orientated 5 4 Confused/disorientated Inappropriate words 3 Incomprehensible sounds 2 1 No vocalizatio ns Originally described in 1974 as a 14-point scale (omitting \200\230abnormal fl exion \200 \231) by neurosurgeons at the University of Glasgow for use in patients with head injuries, this revised scale is now widely used in acute medicine and trauma. OHFP.indb 340 OHFP.indb 340 30/05/2014 16:18 30/05/2014 16:18 341 ACUTE CONFUSION Acute confusion 1 Delirium or acute confusional state is a common but easily missed diag- n osis associated with increased morbidity and mortality. Delirium can aff ect any patient bu t is especially common in the hospitalized elderly, where it may be misdiagnosed as dementi a (with which it may co-exist). Unlike dementia, delirium is often fl uctuating, worse at c ertain times of day.2 uctuat g, wo se at ce ta t es o ay. e u CAM: Confusion assessment met hod3 This validated aid to the recognition of delirium requires the presence of: \200 Acu te onset + fl uctuating course and \200 Inattention (easily distractible) Both of the abo ve must be present, together with either of: or s o te Disorganized thinking Altered level of consciousness Think about emergencies dO2, iCO2, MI, CVA, intracranial bleed, men- ingitis, encephalitis; common sepsis, metabolic (dglucose, dNa+), drug tox- icity (opioids, benzodiazepines, post -GA), heart failure, head injury, alcohol withdrawal or intoxication, post-ictal, urinary r etention, constipation, pain. Ask about use direct questions to assess eg for pain; further history from the ward staff , relatives, notes or residential/nursing home: speed of onset , chest pain, cough, sputum, dysuria, frequency, incontinence, head injury, headache, photo phobia, vomiting, dizziness; PMH DM, heart, lung, liver or kidney problems, epilepsy, demen tia, psychiatric illness; DH ben- zodiazepines, antidepressants, opioids, steroids, NSAIDs, antiparkinsonian drugs; SH alcohol, recreational drugs, baseline mobility and state. Obs G CS (Table 11.2), temp, HR, BP, RR, O2 sats. Look for respiration rate, depth, added sounds, cyanosis; pulse rate and rhythm; abdomen rigidity, palpable bladder; PR fecal impaction; n euro signs of head injury, pupil responses, neck stiff ness, photophobia, focal neurology, plantar responses; AMT score (see Table 11.3). Investigations urine dipstick, M,C+S; blds F BC, U+E, LFT, CRP, glucose, Ca2+, consider cardiac markers, blood cultures, amylase, TFT, B 12, folate; ABG dO2 diCO2; ECG arrhythmias; CXR infection or aspiration; CT if focal neur ology, head injury or non-resolving confusion; LP if CT normal. Table 11.3 Abbreviated Mental Test (AMT) score ( \211 8 is normal for an elderly patient) 1 Age 1 Date of birth Current year 1 Time (nearest hour) 1 1 Name of hospital Recognize two people (eg Dr, nurse) Year World War Two ended (1945) Who is on the throne (E lizabeth II) Recall address: \200\23042 West Street \200\231 Count backwards from 20 to 1 1 1 1 1 1 Management \200 Nurse in a quiet, appropriately lit environment with close, supportive observation (relatives, \200\230special \200\231 nurse); avoid restraints Investigate and treat the cause; pain and infection are the most common \200 Sedate only if patient or staff safety threatened; use oral route where possible (eg haloperidol 0.5 \200\2231mg PO/1 \200\2232mg IM every 1 \200\2232h, max 5mg/24h; if PMH Lewy body dementia, alcohol excess or Parkinson \200\231s, lorazepam 0.5 \200\2231mg PO/IM every 1 \200\2232h, max 3mg/24h). 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG103 2 Typically \200\230out- of-hours \200\231, when you may be asked to review whilst on-call. 3 Inouye, S.K. et al. An n Intern Med. 1990 113:941 (requires subscription) _OHFP.indb 341 _OHFP.indb 341 30/05/2014 16:18 30/05/2014 16:18 342 CHAPTER 11 Neurology and psychiatry Dementia 1 Progressive global cognitive impairment with normal consciousness. Worrying features rapid progression, <65yr. Think about common Alzheimer \200\231s, Lewy body disease, frontotemporal dementia (Pick \200\231s), vascular dementia, Parkinson \200\231s (late), normal pressure hydrocephalus, d epression (pseudodementia), chronic subdural haema- toma, Korsakoff \200\231s syndrome; ra re HIV, CJD, syphilis, space-occupying lesions, hypothyroid, B12 defi ciency, malnutrition. Ask about age of onset, progression, memory (short and long term), personality, thinking, planning, judgment, language, visuospatial skills, concentration, social behavior, confusio n, wandering, falls, head injury, tremor, mood, sleep quality, delusions, hallucinations, h earing, sight; PMH seizures, CVA/TIA; DH regular medications, sleeping tablets, anticholine rgics; FH dementia, neurological problems; SH eff ect on work, relationships and social abi lities; independence with activities of daily living (ADLs \200\223 food, cleaning, washin g, dressing, toilet); ability to manage fi nances; alcohol intake; try to build a picture o f the domestic environment: Who is at home and what local support is available?