endocrinology Flashcards
what are the causes of subclinical hypothyroidism
Chronic autoimmune disease (Hashimoto’s thyroiditis, atrophic thyroiditis)
Iatrogenic (due to treatment of hyperthyroidism with radioiodine, surgery, radiotherapy to neck)
Medications (e.g. lithium, amiodarone) Iodine deficiency (the commonest cause worldwide)
Infiltration of the thyroid (e.g. sarcoidosis, haemochromatosis)
what are the effects of therapy in subclinical hypothyroidism?
Prevention of progression to overt hypothyroidism
Improvement in total and LDL cholesterol
Improvement in symptoms, mood and cognition
what must you be aware of when treating hypothyroidism
The TSH should not fall below the normal range during treatment as this increases the risk of atrial fibrillation, osteoporosis and some neuropsychological symptoms
would you offer annual surveillance or thyroid testing at initial presentation for these at risk patients?
- AF
- T1DM
- T2DM
- downs/turners
- addisons
- postpartum depression
- osteoporosis
- on amiodarone/lithium
- history of postpartum thyroiditis
- subfertile
- hx of radio active iodine
- giotre
- previous neck radiation
- dyslipidaemia
- AF - initial
- T1DM - follow-up
- T2DM - initial
- downs/turners - follow-up
- addisons - follow-up
- postpartum depression -initial
- osteoporosis -initial
- on amiodarone/lithium -follow-up
- history of postpartum thyroiditis -follow-up
- subfertile -initial
- hx of radio active iodine - follow-up
- giotre - initial
- previous neck radiation - follow-up
- dyslipidaemia -initial
in women who are pregnant or planning pregnancy offer thyroid function testing at earliest opportunity if…
Goitre (also at 6 weeks postpartum/after miscarriage/termination)
Family history of thyroid disease; personal history of thyroid disease
History or thyroid lobectomy; history of other autoimmune disorders
Positive thyroid autoantibodies (also at 6 weeks postpartum/after miscarriage/termination)
History of postpartum thyroiditis
hyponatraemia what is acute classification clinical symps causes how to approach when bleeped mgmt worries with overcorrection
acute
<48hrs
classification
mild - 130-135 asymp, subtle changes in mental and physical function
mod - 125-130, non-specific symps (nausea + malaise)
severe - <125, progressive neurologic symps ranging from confusion to coma
clinical symps
diarrhoea/vomiting/polyuria - likely to be hypovolaemic
dizziness on standing - suggests postural hypotension
thirst
habitual drinking/alc (beer potomania)
recent surg or IV fluids cont.
resp symps - as can be assoc with pneumonia
stroke
any failures (cardiac/renal etc)
causes
ISOTONIC 280-295 - hyperproteinemia, hyperlipidaemia
HYPOTONIC <280:
- hypovolaemic -> dehydration, diarrhoea, vomiting, diuretics, ACEi, nephropathies, mineralcorticoid deficiencies
- euvolemic -> SIADH, post-op hyponat, hypothyroidism, psychogenic polydipsia, beer potomania, endurance exercise
- hypervolaemic - FAILURES - heart, liver, nephrotic, kidney
HYPERTONIC >295 - hyperglycaemia, mannitol, sorbitol, glycerol, maltose, radiocontrast agents
how to approach when bleeped
- EXAMINATION
- gen look + weight
- obs - pulse, BP, postural BP
- assessment of volume status + calc osmolality
- skin turgor and mucous membranes
- resp status
- cardio - JVP, pulm oedema
- full neuro - ?confusion/agitation/seizures/CVA
- review prev lab tests- sodium, cortisol, TFT, paired osmolalities
- ix to send now - U/E, FBC, LFT, Glc, TFT, 0900 cortisol, lipids, urine analysis, CXR, ?CT head, ECG
- ?SIADH - paired urine + plasma osmolality and urine sodium
mgmt
MILD CHRONIC - IV 0.9% nacl - repeat UE 12hrs then daily
MODERATE - stop drugs PPI/ACEi, liase with neuro/psych for carbamazepine/anti-dep, rx hypothyroid/ GC insuff, check for HF, liver failure, kidney failure
SEVERE - emergency, senior help, reduce brain oedema, avoid overcorrection/osmotic demyelination + HDU/ITU transfer, within 1hr 150ml hypertonic saline 3% over 20 min with close monitoring
NEVER INCREASE SODIUM QUICKLY
worries with overcorrection (central pontine myelinosis)
also happens in alcoholism, liver disease and malnutrition
- hyponatraemia can lower the seizure threshold
- neuro det 48-72 hrs
- variable
- confusion
- horizontal gaze paralysis
- spastic quadriplegia - increased tone, weakness, hyper-reflexia
- pseudobulbar palsy - demyelination
- c-sp and c-bul tracts in pons
basically it causes the brain tor shrink after it has been swollen from hyponatraemia
causes of pseudohyponatraemia
hyperglycaemia
SIADH def patho causes pres ix if euvolaemic types mgmt worries with management
def
Euvolaemic hypotonic hyponatremia with concentrated urine
hyponat <135mmol/L
patho
increased AVP release leads to impairment of free water excretion
AVP release mediated by osmotic pressure at hypothalamus
Decrease of osmolality by 1% rapidly suppresses AVP -> this is lost with below conditions
ADH works to stop you peeing to increase intravascular volume at collecting duct in kidney
causes
Pulmonary processes: pneumonia, lung cancer (esp small cell)
CNS disorders: infection, trauma, MS, haemorrhage, malignancy
Malignancy: lung, pancreas, prostate
Drugs: SSRIs, tricyclics, NSAIDs, SU, chemo drugs, rule out thiazide (most common hyponatraemia)
pres
Euvolaemic, confusion, nausea, irritability, nausea, vomiting
ix
assess volume and TFT, cortisol,
renal function - sodium <135 (wont be responsive to saline infusion)
request paired osmolalities - serum = <280 proportional to hyponatraemia, urine = >100Osm/kg - typically higher than plasma
spot urine na = hgih >30mmol/l
NORMAL renal + adrenal function
if euvolaemic - SIADH is diag of exclusion
subtypes
1-4
mgmt
Acute (<48) + severe (<125)
- IV hypertonic saline (3%) and check Na every 2 hours
- Aim to increase 1-2 per hour until neurological symptoms resolve
+ treat cause + furosemide if risk of fluid overload
Chronic + severe
- IV hypertonic saline
- Vasopressin receptor antagonist tolvaptan + cause + furosemide
- demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
Mild - mod (>125) + acute
- Treat cause + fluid restrict: 1-1.5l /day
Mild - mod + chronic
- Treat cause + vasopressin receptor antagonist
worries with management
central pontine myelinolysis
endocrine tests:
- what test for under secretion/deficiency
- over secretion/excess?
- acromeg
- cushings
- prolactinoma
- GH deficiency
under
- stimulation test
- eg short synacthen test
over secretion
- suppression test
- eg dexamethasone suppression test (cushings rule out)
acromeg - OGGT with GH profiles
cushings syndrome - Over Night Dexamethasone Suppression Test
prolactinoma - cannulated prolactin
Growth Hormone deficiency - Insulin Tolerance Test/glucagon
causes of adrenal insufficiency and aka + def
AAb
aka addisons, primary hypoaldosteronism
def Destruction of adrenal cortex and subsequent reduction in output of adrenal hormones: glucocorticoids (cortisol), and mineralocorticoids (aldosterone)
CAUSES primary - TB - addisons - autoimmune destruction - malignancy - infiltration - infection - vascular haemorrhage - infarction - iatrogenic - surgery
secondary
- pituitary/hypothalamic lesions
- exogenous steroids suppress axis
- CRH def
tertiary
- suppression from GC
- post treatment cushings disease
AAB - anti-21-hydroxylase -> causes loss of aldosterone and cortisol, but testosterone if fine
presentation of adrenal insufficiency
either acute (addinsonian crisis) or chronic
fatigue lack of energy weight loss tanned - due to increase of CRH and ACTH low BP postural dizziness hypotension (>20mmhg drop) hypovolaemic shock abso pain, tenderness, gaurding, vomiting fever confusion somnolence delirium coma cramps in back of legs primary - skin pigmentation, palmar creases, scars, oral mucosa secondary - pale skin, alabaster
adrenal insufficiency history key points
insidious onset - malig? check FH smoking - lung lesion and ACTH GI symps thyroid disease symps hypoglycaemia symps DH - inhalers, creams, steroid inject, alt meds reduced axillary/pubic hair
findings on examination in adrenal insufficiency
gen exam to rule out malig - breast, thyroid, colon
BP lying/standing
skin/hair - depp pig, fine wrinkles, pale skin of hypopituitarism, pallor of anaemia, myxoedema of hypothryoidism
body habitus and BMI - weight loss
muscle wasting
adrenal insuff ix
FBC
haematinics
U/E - low sodium, high potassium (due to low aldosterone, low ENaC and ROMK)
LFT
bone
glucose - low
0900 cortisol <350 probable insufficiency
random if unwell with paired ACTH - to diff primary (high)/secondary (low)
DIAGNOSTIC = Short Synacthen Test = take cortisol, give 250mcg synacthen IM, 30mins retake cortisol, if rises exclude addisons >500
TSH FT4
HBa1c
Aantibodies = anti 21-hydroxylase
lipids
renin and aldosterone - high r + low a = addisons
ABG - met acidosis
Bilateral CT adrenals
CXR
DEXA
vit D levels
adrenal insufficiency
mgmt and comps
screening
start treatment hydrocortisone
emergency immediate HC - 100mg IM, then 200mg infusion 24hrs
IV sline 1L over 1 hr followed by 4-6 L/24 hours
urgent endocrine input
maintenance dosing
counsel patient - sick day rules, provide emergency kit 100mg HC sodium succinate, medical emergency bracelet + steroid card, explain imp of not missing steroid doses
sick day rule 1 - double daily oral dose of glucocorticoids
sick day rule 2 - parenteral admin during prolonged vom or diarrhoea, prep colonoscopy, surgery
if not emergency = glucocorticoid replacement = hydrocortisone TDS highest dose at morning 15-30mg
mineralcorticoid = fludrocortisone 50-300mcg/day will correct postural hypotension and electrolyte balance
comps
over replacement = HTN, thin skin blah blah
screening
annual TFT, glucose + hba1c, coeliac
pituitary apoplexy
what is it
how to manage
Rapid enlargement due to bleed into tumour -> mass effect, CV collapse and acute hypopituitarism
emergency: ABCDE call senior valuate electrolytes, glucose, and pituitary hormones high dose corticosteroids
T1 diabetes what is it ix to differentiate from T2DM main comps assoc panc cells + their function insulin release + action when eat patho causes pres immediate comp ix diagnostic criteria ix for comp mgmt regimes + SE sick day rules
what is it
Autoimmune destruction of pancreatic beta cells in islet of langerhans leading to reduced insulin
ix to diff
C-peptide: low @ T1, high @ T2
released at the same time as insulin to distinguishes lack of insulin from resistance
main comps
Retinopathy, neuropathy, nephropathy, skin infection (low immunity), DKA, CVS risk, autonomic dysfunction
assoc
AI diseases
panc cells and their function
alpha - glucagon
beta - insulin
insulin release - Glucose -> beta cell. Enters via GLUT-2. Increases ATP. ATP closes K+ channels which depolarise cell. VgCa channels open Ca to cell. Insulin released.
insulin action - To peripheral muscle. Binds insulin receptor. Mobilises GLUT-4 to membrane. Glucose able to enter cell.
when eat -
Increase glucose -> increased insulin
Increase uptake liver (200g) and muscles (150g) as glycogen
Suppresses gluconeogenesis, lipolysis, proteolysis, ketogenesis
cause
Genetic predisposition and autoimmune process (insulin/islet cell autoantibodies)
Family history of other autoimmune conditions HLA DR3/4
pres
Polyuria, polydipsia (due to water being dragged out by glucose in urine), weight loss, lethargy, DKA problems… (dehydration, kussmauls breathing, abdo pain)
immediate comp
DKA
ix urine dip FPG RPG OGTT HbA1c - measures the amount of glycosylated haemoglobin and represents the average blood glucose over the past 2-3 months.
diagnostic criteria diabetes
1. symptoms + FPG >7 or RPG >11.1
2. asymp + 2x FPG or RPG
3. OGTT 75g glucose with 2hr glucose reading >11.1
4. HbA1c >48 or 6.5%
prediabetes
hba1c = 5.7-6.4%, FPG 5.6-7, OGTT 7.8-11.0
ix for comp
DKA - blood glucose, ketones, ABG
long-term = Urine dip for protein, BP for HTN, Fasting lipid for hyperlipidaemia
mgmt GEN 1. education 2. diet + exercise - low sug, low fat, high starchy carb 3. no smoking 4. maximal glucose control - test QDS, target 5-7 morning, 4-7 before meals MEDS insulin regimes: 1. twice daily - pre breaky/evening meal 2. basal-bolus - long or intermed at bedtime with rapid/short to cover meals 3. continuous subcut or insulin pump - if control very poor S/E - hypo (sweating, anxiety, blurred vision, confusion), lipodystrophy, weight gain NICE RECOMMENDS basal-bolus insulin regime: twice daily: - long acting eg detemir - rapid acting eg novorapid before meals ANNUAL REVIEW Educate + modifiable RFs Check BMI Check complications: hypos, DKA Assess CVS: BP, pulses, bruits Inspect injection sites - lipodystrophy Foot check - neuropathy and pulses Urine dip - protein, nitrites, ketones Check eyes - acuity and ophthalmoscopy -> refer opthalmology Ask erectile dysfunction Bloods: HbA1c every 3-6 months and home capillary monitoring results, random lipids
diabetic comps patho
NEUROPATHY -
Hyperglycaemia -> oxidative stress -> lipid peroxidation of myelin -> glove and stocking + loss of ankle jerks (loss of afferent arc of the tendon reflex)
mononeuropathy = single nerve trunk affected eg 3rd nerve palsy
mononeuropathy multiplex - more than one individual nerve trunk affected
diabetic fem neuropathy - sudden onset wasting and weakness of quads with loss of knee jerks
autonomic neuropathy
cerebrovascular disease
diabetic peripheral polyneuropathy - typically affects longest nerves first (length dependent neuropathy). loss of all modalities in glove + stocking. if small fibres affected presents as painful neuropathy. can cause tingling, numbness or ‘walking on cotton wool’.
causes: ABCDE
A - alcohol
B - B12 deficiency - as well as causing subacute combined degen of cord
C -CKD and carcinoma - para-neoplastic
D - diabetes + drugs eg nitrofurantoin, metronidazole, ethambutol, isoniazid
E - every vasculitis (RA, polyarteritis, sarcoid, scleroderma, wegener’s)
NEPHROPATHY
Hyperglycaemia -> mesangial expansion + thickening of glomerular BM
Narrowing of efferent renal artery -> increased pressure in glomerulus -> glomerular sclerosis + thickening BM -> increased gaps between podocytes (more permeable) = hyperfiltration
Proteinuria and loss of pericytes
Use photocoagulation
screen for microalbuminaemia - urinary albumin : creat ratio
ACE-i slows the progression of renal impairment
CVS RISK
MI/Stroke -> BP control + diet + smoking + statin -> QRISK
AUTONOMIC DYS
Erectile dysfunction, bladder retention, postural hypotension, tachycardia, diarrhoea
INFECTION
Hyperglycaemia -> reduced phagocytsis
Pneumococcal vaccine and annual influenza
sick day rules for diabetics + why
GEN 4 hourly monitoring be aware of DKA monitor ketones 3L fluids/24 hours cant eat? take sugary drinks
MEDS
continue metformin + insulin but with increased monitoring
if glucose goes above upper limit, increase insulin or seek help
WHY
Stress response to illness -> increased cortisol
Cortisol increases blood sugars and decreases insulin
diabetic foot RF for ulcers + PAD what is it pres synonym exam
RF
ulcers: PAD, peripheral neuropathy, callus
PAD: hypercholesterolaemia, HTN, smoking
what is it
neurovascular foot
secondary to:
Peripheral artery disease, neuropathy + charcot’s
Loss of protective sensation -> severe damage and disruption due to mechanical and vascular factors
large and small vessel injury
pres
Ulcers (neuropathic painless and punched out or arterial), loss of pulses
Bone and joint degeneration -> deformity, osteoporosis, fracture, acute inflammation
Hot, swollen foot after minor trauma
chronic:
- Rockerbottom sole, claw toes, loss of transverse arch
synonym
neuropathic joints
exam inspect heels palpate cap refill + pulses light touch - loss of sensation glove + stocking vibration ankle jerks
diabetes and ramadan
normally have type 2
they can be excused as they have a chronic condition
if choose to fast:
- try eat a long-acting carbohydrate before sunrise
- provide glucose monitor
- if taking metformin then split dose one-third before sunrise and two-thirds after sunset
- if on SU - take these after sunset if OD, if BD then larger proportion of dose taken after sunset
- no adjustment needed for pioglitazone
T2DM what is it ix to diff assoc who gets it RF pres ix mgmt
what is it
Hypersecretion of insulin by depleted beta cell mass. Increasing insulin resistance.
ix diff
c-peptide
assoc
metabolic syndrome
who
30+ obese, low physical activities
RFs obesity lack of activity PCOS metabolic synd fam hist south asian pre-diabetes
pres
Polyuria, polydipsia, lethargy, prolonged/frequent/recurrent infections (e.g. vaginal thrush)
ix
Urine dip, FPG, RPG, OGTT, HbA1c
as for T1DM
mgmt
gen stuff as T1DM
Lifestyle and diet - (6 weeks) + inform DVLA
Low GI, low dairy, control fats, limit sugar, aim 5-10% weight loss
MEDS
if can have metformin (aka are they FAT)
if >58 dual therapy:
+ gliptin or SU or pioglitazone
if still >58 with dual:
- Metformin + sulfonylurea + pioglitazone
- Metformin + sulfonylurea + gliptin
- Start insulin
if cant have metformin then start with one of others
diabetic eye problems which ones patho for retinopathy features ix classification mgmt emergency referral for
which probs
Cataracts, retinopathy, maculopathy, glaucoma
patho for retinopathy
Microvascular occlusion -> retinal ischaemia -> AV shunts + neovascularisation
Pericyte loss -> leakage -> haemorrhages or diffuse oedema
features
Painless, gradual reduction of central vision, sudden onset dark, painless floater
Microaneurysm - from physical weakness
Hard exudates - lipoproteins from leakage
Haemorrhages - rupture of weakened capillaries small dots, blots or flame (track along nerves in superficial retinal haemorrhages)
Cotton wool spots - build up of axonal debris
Neovascularisation
ix
slit lamp
classification
Background - one microaneurysm (dot haem), hard exudates, blot haemorrhages
Mod/maculopathy - microaneurysms, IR haem ± cotton wool spots, venous beading + IRMAs (intra-retinal micro vasular abnormalities)
Severe/pre-prolif - depends on number and quadrants, mainly same as above
Proliferative (non-high risk) new vessels on disc (or <1 diam) or NV everywhere
Proliferative/end-stage (high risk) large NVD or NVE
mgmt
Optimise glycaemic control
Blood pressure control
Lipid control
Laser photocoagulation: Or intravitreal steroids, Anti-VEGF
signs for referral - fall in correct visual acuity, single cotton wool spot, 3 blot haemorrhages, anything @ macula
emergency ref sudden LOV red eye retinal detachment new vessels
metformin type of oral hypoglycaemic MoA CI SE
type - Biguanide
MoA - Increases insulin sensitivity (GLUT 4), decreases gluconeogenesis
CI - CKD, eGFR < 30
SE - GI upset: nausea, anorexia, diarrhoea - 2e0% intolerabl
Gliptin
type
MoA
SE
type - DPP-4 inhibitors (DPP-4 destroys incretin)
MoA - Raised incretin -> produce more insulin when needed
SE - GI upset and flu-like symptoms
sulphonylurea type MoA CI SE
type - Oral hypoglycaemics
MoA - Increase panc insulin secretion
CI - Pregnancy
SE - Hypo, weight gain
Piaglitazone
MoA
SE
CI
MoA
Increases insulin sensitivity
SE
Weight gain, fluid retention and osteoporosis
CI
Heart failure and osteoporosis
DKA precipitants pres patho ix mgmt monitor
precipitants
Missed insulin, infection, intoxication, ischaemia, infarction
pres Abdominal pain + vomiting Polyuria, polydipsia, dehydration Kussmaul respiration (deep hyperventilation to correct acidosis) Acetone breath (pear drop)
patho
decreased insulin ->
1. increased protein catabolism -> hyperglycaemia, glycosuria, osmotic diuresis, K+ depletion (acidosis buffer) -> dehydration acidosis coma + death
2. decreased cell glucose uptake -> hyperglycaemia etc
3. increased lipolysis -> Increased plasma FFA to liver. Ketogenesis: ketonuria and ketonaemia (beta hydroxybutyrate and aceto- acetate) -> dehydration, acidosis, coma, death
ix Plasma glucose: high >11 or known DM Plasma ketones: high >3mmol/l ABG: metabolic acidosis pH < 7.3 Urine dip: ketones (++) and glucose
mgmt
ABCDE sats etc… + catheterise
Volume depletion: IV NaCl (1L stat, over 1hr, 2h, 4h, 8h)
*switch to 5% dex when glucose <12
Hyperglycaemia: IV insulin - will drop the potassium…
*Fixed rate IV infusion: 0.1U/kg/hr add glucose when drops
Hypokalaemia (as a result of fluids and insulin): K+in fluids
>5.5 = nil
3.5-5.5 = 40mmol/L infusion solution
<3.5 = senior review
Acidaemia: IV bicarbonate
if vomiting + decreased consciousness - gastric aspiration
MONITOR - electrolytes + ABG, fluid balance, glucose ECG hourly
hypoglycaemia
def
vital signs
neuro manifestations
def
FOUR IS THE FLOOR <4mmol/l
neuroglycopaenia <3mmol/l
vital signs THIS PATIENT LOOKS UNWELL normal RR/BP peripheral vasoconstriction (alpha 1) pale cold clammy sympth overdrive tachycardia (B1)
neurological mani
low GCS
seizure - tonic/clonic -> todds paralysis (hemi parasis post seizure)
brisk reflexes
bilateral upgoing plantars -> ddx pontine haemorrhage
in peripheral neuropathy which is more likely to be affected first motor or sensory, except when
sensory
except in acute segmental demyelination (GBS) where motor involvement is the main feature + hereditary sensory motor neuropathy eg charcot marie tooth disease
large fibre neuropathy
when
symps
eg b12 affecting large myelinated sensory nerves
neg symps - unsteady gait, walking on cotton wool as loss of discriminatory sensation
posi symps - pins and needles, band-like feeling around calf
small fibre neuropathy
when
symps
alcohol affecting small unmyelinated c fibres
neg symps - loss of pain and temp sensation
posi - painful dyasthesiae eg burning causalgia, hyperalgesia
mixed nerve fibre neuropathy
when
symps
diabetes
very variable - some have painful neuropathy others have no pain and profound loss of proprioception and unsteady gait
what sensation do large, medium and small nerve fibres carry
large - A alpha - proprioception
medium - A beta - touch
small - c fibre - pain/temp
testing for loss of protective sensation
screened using 10g monofilament over 3 toes, 3 points on ball of foot, 3 points near arch of heel
instruction should be ‘say yes when you feel it’
1-2 not felt = reduced sensation, ‘at risk’ foot
all not felt = absent sensation
charcot joint
what is it
patho
aspects of management
arthropathy is a progressive condition of the musculoskeletal system that is characterized by joint dislocations, pathologic fractures, and debilitating deformities
patho
1. loss of protective sensation = repeated microtrauma -> degen change, joint destruction, rubbery feel when moving MetoTarsoPharngeal joints, ulceration
- autonomic neuropathy = increased blood supply -> oedema, warmth, redness + increase in osteoclast activity = bone resorption
mgmt
vascular, infection control, pressure relief
hyperosmolar hyperglycaemic state who features precip patho criteria ix mgmt comp
who
T2DM + elderly
features
extreme dehydration (but may not look it as all the water in the intravascular space)
fatigue + n+v
altered mental state, headache +/- seizures +/- delirium
hyperviscosity = MI, stroke, peripheral arterial thrombosis
comes on over many days in comp to DKA which is hours
precip infection MI dehydration inability to take normla meds thiazides + loop poor control
mech
Hyperglycaemia -> osmotic diuresis = loss of na + k -> hyperosmolarity leading to fluid shift of water into intravascular compartment -> severe dehydration
No ketosis as enough insulin to suppress ketogenesis
criteria
1. Hypovolaemia
2. Marked hyperglycaemia (>30) without hyperketonaemia or acidosis
3. Osmolality > 320 mosmol/kg (concentration of blood)
Calc osmolarity = 2(Na + K) + gluc + urea
Plasma osmolality is a guide to intracellular osmolality -> if high will secrete ADH
ix Urinalysis: glycosuria +++. Ketonuria + Capillary glucose > 30 Serum osmolarity > 320mmol/L U+E -> AKI ABG -> normal Blood cultures -> rule out sepsis
mgmt
GRADUAL
Treat cause
Safely normalise osmolality - replace fluid and electrolytes
Normalise blood glucose
ABCDE
IV access, ECG, SaO2, BP
Calculate osmolality frequently (2Na + gluc + urea) and plot on graph
IV 0.9% NaCl -> aim for fall of Na by 10mmol/24 hours (if not switch to 0.45%), glucose 5mmol/hr
Aim for 3-6 litres +ve by 12 hours
IV insulin (0.05U/kg/hr) if glucose no longer falling + ketonuria + acidosis
RAPID DECLINE IS HARMFUL
Rising sodium is only a concern if the osmolality is NOT declining concurrently
comp
cerebral oedema
central pontine myelinosis
