Welcome Interpreting and Managing Blood Results A Masterclass Dr Karen McEwan Dr Sayee Chirputkar amp Dr Gill Burrows Good Afternoon and welcome to this session It is due to start at 1230 ID: 935366
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Slide1
Title of Presentation goes here
Welcome
Interpreting and Managing Blood Results – A Masterclass
Dr Karen McEwan,
Dr
Sayee Chirputkar & Dr Gill Burrows
Good Afternoon and welcome to this session. It is due to start at 12:30.
Slide2Interpretation of haematology resultsDr Sayee Chirputkar
12/01/2021
Slide3AgendaSerum protein electrophooresisNeutropeniaB12 Iron studies
Slide4Serum Protein ElectrophoresisWhat we are trying to measure- presence of a paraprotein
Associated bloods- total proteins and globulins(part of LFTs), immunoglobulins (checked reflexly when we request serum protein electrophoresis), Urinary bence jones protein and serum free light chains.SPE may be requested by you or added on by the lab if globulins are raised.
Slide5SPE report Worded as-
SPE shows band in gamma region. band too faint to quantify or band measures x g/dl band typed as (or previously typed as) Ig G lamda ( as an example)2. SPE shows polyclonal rise in gamma globulins
Slide6Polyclonal vs MonoclonalPolyclonal rise – This means there is no paraprotein, the rise in gamma globulins is due to an inflammatory process and THIS inflammatory process is what needs investigation. Could be due to infection, autoimmune process or malignancy.
Monoclonal band – this is the paraprotein band ie evidence of MONOCLONAL cells secreting immunoglobulins.Monoclonal bands are of any of the heavy chain subtypes ie IgG, IgM, IgA, Ig D and Ig E- in that order of frequency and with a light chain type of either Kappa or Lambda for each.
Slide7ParaproteinsQuantity does matter- too faint to quantify vs 1-9g/l vs higher amounts
IgG of 30 g/l or IgA of 20g/l or higher- diagnostic of myeloma, lesser amounts may be MGUS or myeloma- need further investigation. Very small amounts are unlikely to be myeloma, but can rarely be due to light chain myeloma or non secretory myeloma.IgM is usually associated with lymphoplasmacytic lymphoma (aka Waldenstrom’s Macroglobulinaemia) and sometimes other lymphomas. Rarely may be associated with myeloma.Bence Jones Protein- indicator or urinary light chains and should prompt measurement of serum free light chains. BUT presence of absence of BJP does not indicate whether this is MGUS or not.
Slide8When to refer with a paraproteinParaprotein Ig G of more than 30 or IgA more than 20g/l refer on 2 week wait.
Smaller paraproteins- review ca, u and e, h/o bone pain, anaemia and refer on 2 week wait if any present. Paraprotein in single digits and no other biochemical abnormality- MGUS, can be referred or reviewed locally. Higher paraprotein – refer.Ig M- review for symptoms of lymphoma and symptoms of hyperviscosity. If either present- refer as 2 week wait. If none present – can be referred routinely.Very happy to be contacted about any paraprotein on advice and guidance! If in doubt, please ask.
Slide9Serum free light chainsWill be checked if Bence Jones positiveLevels for free kappa and lambda and ratio
If ratio is abnormal, please get advice on A and GNo specific level is of significance, other blood results including SPE are important for context. Does not automatically imply this is myeloma.
Slide10MGUS- what is it?Small amount of paraprotein with or without positive BJP/abnormal serum free light chains
ABSENCE of end organ damage (normal calcium, no renal impairment/anaemia/ bone lesions attributed to the paraprotein.If bone marrow is done- shows plasma cells less than 10% of all nucleated cells.Premalignant condition- for routine monitoring
Slide11MGUSFor haematology review in the first instance. Once MGUS diagnosed- for further review in 3 months. If stable discharged to primary care
Patient hand held leaflet re MGUS given to patient. We are not yet in the process of making this digital. The leaflet is to be populated with results at each visit, blank copy also available on CCG websiteGives information re what is MGUS, symptoms, when to seek help. What bloods to do and at what frequency and when to refer back to haematology.The bloods for monitoring are- SPE, ca, creatinine and eGFR, full blood count.Monoitoring done every 6 months for a year and if stable, yearly.
Slide12When to re-refer to haematologyRe- referral if Hb<100 g/l (unexplained)platelets
<100bone pain, hypercalcaemiarenal impairmentrise in paraprotein >25% (absolute rise must be at least 5 g/l)
Slide13NeutropeniaNormal limits – 1.7 to 4 x 10^9/ LWhen to get excited? Neutrophils <1.0 x 10^9/L
When to refer urgently- (call haematologist on call)-unexpected count of neutrophils < 0.5 x10^9/L
Slide14Common CausesPost viralMedicationAutoimmune
Benign and cyclicalHIV/Hep B / Hep CB12/ folate deficiencyHaematological causes- leukaemia, MDS, myelofibrosisInfiltration by other maliganat processes
Slide15How to approach?History- review all medication, especially those started within the last 6 months.
Review for viral symptoms including COVIDInvestigation- B12/folate/ferritinRheumatoid factor/ANAHep B, Hep C, HIV
Slide16Neutrophils >/= 1.0- recheck in the first instance. History and investigations as above.
Neutrophils <1.0 but greater than 0.5- (no cause found) history, investigate and refer urgently to haematology if no cause is evident. Ensure FBC is rechecked in 2-3 weeks.Neutrophils <0.5- call haematology and potentially refer as 2 week wait.Neutrophils <1.0- advise re high temperature (over 37.5 degC)) if temp goes up- to present to A and E.
Slide17B12 deficiency- causesVegetarians, particularly vegans.Food cobalamin malabsorbtion.Achlorhydria- also medication induced.
Pernicious anaemia.Subtotal gastrectomy, ileal resection, anastomoses.Pancreatic insufficiency.Blind loop, bacterial overgrowth.Extensive inflamatory bowel disease ( affecting ileum)
Slide18Pernicious AnaemiaOne specific cause of B12 deficiency- commonest cause of profound deficiency
Autoimmune condition due to antibodies to intrinsic factor.Runs in families.Other autoimmune problems- thyroid, vitiligo often coexist.Small increase in risk of gastric cancer- esp in men.
Slide19Signs and symptomsMacrocytosis
Anaemia, thrombocytopenia, neutropenia, hypersegmented neutrophils.Neurological signs- parasthesias, loss of position and vibration sense, motor deficit- subacute combined degeneration of the cord.Dementia
Slide20Who should we test?Unexplained macrocytosis
.Anaemia/pancytopenia work up.Neurological signs.Investigating dementia (early)
Slide21How to test?There is NO GOLD STANDARD.Routinely tested for by serum B12 (cobalamin)
Slide22Serum CobalaminWide variations in ‘Normal limits’ between institutions, depending on exact assay used.
Variations between individuals- some with normal levels may have a clinical deficiency, others with low levels are not clinically deficient.Variations within individuals at different times.False low levels in pregnancy, COCP use, folate deficiency.False high levels with high haptocorrin- eg in CML, in damage to hepatocytes
Slide23Yet, is the first- line investigation as it is widely available, relatively cheap.Clearly there are limitations, so needs to be interpreted in view of clinical context.
If clearly low- by more than 25% lower than lower limit- clearly deficient. If >/= 25% over lower limit of normal- likely OK. But large ‘grey area’There are confirmatory tests available- but..
Slide24Confirmatory tests for B12 deficiency
Methyl malonic acid levels. These go up with B12 deficiency.Serum Homocystine levels- also go up with B12 deficiencySerum Holocobalamin- measures cobalamin bound to transcobalamin IIAll 3 are not routinely available and have cost implications. 1 and 2 may go up due to a variety of other resons, not just with B12 deficiency.
Slide25Tests for cause of low B12
Clinical history- diet, medication, operations, malabsorbtion symptoms.Family history of pernicious anaemiaOther autoimmune problems.Intrinsic factor antibodies- very specific- their presence means pernicious anaemia, but only seen in 60- 70% of patients with PA.Gastric parietal cell antibodies, serum gastrin levels- non specific, variable degrees of sensitivity.Schilling test- brilliant, but oh so cumbersome, not routinely available now.
Slide26So, whats a practical way forward?
Choose who we test.- macrocytosis, early demetia, neurological symtoms and signs. Not for fatigue, tired all the time, body ache…Our normal limits- 180-910. If level less than 140- definitely deficient- needs replacement. If dietary deficiency ruled out by history, replace parenterally. Check IF antibodies, but if negative, can’t write off PA- ie they will all need lifelong replacement.
Slide27If not clearly deficient- see clinical context.If we have chosen whom to test- much easier.
If clinical signs of deficiency- give a trial of parenteral replacement for 3 months.If this works- needs lifelong replacement.If it doesn’t work- stop.
Slide28IF antibodies- can be done, if positive, then need lifelong parenteral replacement.
If negative- see clinical history .If clear intestinal or surgical cause of deficiency, will again need lifelong parenteral replacement.If not, i.e. suspicion of food-cobalamin malabsorbtion, can consider oral B12 replacement. Parenteral ends up being a lot more cost effective- 61 p a shot (3 monthly for maintenance); cyanocobalamin tabs- 50 mcg cost £6.24 for a pack of 50- 1-3 tablets a day.
Slide29Pregnancy
This causes low B12 levels( without clinical deficiency) may also cause a macrocytosis, which is due to pregnancy per say.Can also cause paresthesias so its getting increasingly complicated…IF antibodies may take a while to be back, if negative, we are no further forward.Again, practical solution is treat to avoid problems with babe.Test If antibodies, if pos- lifelong treatment, if neg, can give a trial off B12post partum, recheck in 6 -8 months, depending on levels.
Slide30Making sense of anaemias/iron studiesMicrocytic anaemias, with new onset microcytosis are iron deficiency anaemia unless proven otherwise.Good practice to check ferritin neverthelessIf ferritin is LOW- this is clear cut iron deficiency.
This needs GI investigations/ gynaecology referral. Does not need haematology referral.
Slide31CausesPoor intake of iron- diet poor in iron, high amounts of phytates that bind iron, malnutritionPoor absorbtion of iron- GI bacterial overgrowth, antacids/ PPIs, Poor secretion of HCL, partial gastrectomy/ banding, coeliac disease,
Crohns/UCIncreased loss of iron through bleeding- overt or not overt- GI, menstrual, nosebleeds etc.RARE AS HENS TEETH-
Slide32IRON studiesSerum iron, transferrin, transferrin saturations
Both should be done, even in the context of acute infection/ rheumatological conditions/ inflammation etc.Ferritin may be done on its own and if that does not get all the answers- iron studies can be done to clarify.
Slide33Iron studies
Anaemia typeFerritinSerum ironTransferrinTransferrin satsIron deficiencyLowLowHighLow
Anaemia of chronic diseaseHighLowLowLow
Both coexistingHigh or normal(usually <100)Low
Low/normal
Low
Slide34Anaemia of chronic disease Iron utilisation defectAdequate storage ironMay be treated with IV iron - if ferritin less than 100.Ferritin over 100mg/dl is a relative contraindication for treating with IV iron
(oral causes less harm but is not effective!)Based off renal guidance.
Slide35Thanks Folks!Any questions?Any other topics you’d like me to send a PP presentation on?
Slide36HaematologyDr S. Chirputkar
Slide37Case 1Urology Specialist nurse phone call69 year old gentleman with new onset haematurea, awaits cystoscopy.Blood count has shown – Hb
110, WCC 12.1, platelets 64.Otherwise fit and well.What next?
Slide38Investigations for a low platelet countDrug historyAlcohol historyBleeding historyBlood filmCoagulation ‘screen’
U and ELFTsHep C and HIV screenMay consider checking for autoantibodies
Slide39Case 1 continuedNormal U and E, LFTs. Not a drinker.Blood film- low platelet count confirmed but nil else of significancePt 15 sec, APTT 39sec.What next?
Slide40Fibrinogen- 0.9D dimers > 2000What does this indicate? What investigations would you do next?
Slide41Metastatic ca prostrate on CTDIC in malignancy is usually a chronic process as opposed to acute DIC seen in most other conditionsTreatment is supportive- blood products including FFP, platelets and cryoprecipitate as needed in the presence of bleeding.
Slide42Case 2Also a urology referral, 62 yr old manKnown to have end-stage Ca prostrate, palliative treatment only.Had a nephrostomy in situ for obstructive nephropathy. Despite this, renal function was deteriorating
Falling platelet count- from normal ( in 200s) to 11 in 3 days
Slide43InvestigationsNormal Pt and APTT. Fibrinogen 5, in keeping with acute phase responseWhat next?
Slide44Blood film
Slide45Thrombotic thrombocytopenic purpuraPro-thrombotic condition, despite low platelet countVarious causative factors- drugs, autoimmune disorders, pregnancy, malignancy, post transplant.Platelet infusions are ( relatively) contraindicated
Treatment is with plasma exchange and aspirin once pl>50, steroids
Slide46Malignancy associated TTPUniversally poor prognosisDoes not respond to steroids, P Ex, FFP infusionUsually a terminal event
Slide47Case 3Also a urology referral! 65 yr old gentleman, haematurea, known ca prostrate. Hormonal treatment.Urology
sp nurse phone call- platelets 23, hb 90, WCC 21. Clotting normalU and E- deranged, longstanding.LFTs normal
Slide48film
Slide49Case 4Urology patient again. With ca prostrate, on hormonal treatment, recent DVT- 2 months agoOn warfarin. Had haematurea so warfarin witheld and
clexane startedPlatelets crashed from 210 to 30 within a day.Haematurea had settled by then
Slide50U and E- normalLFTs- normalHb, WCC, neutros- all normalCoag screen-
prologed APTT to 39 sec, normal PT.Fibrinogen- normal (4)Blood film- low platelets, nil elseWhat next?
Slide51Heparin Induced thrombocytopeniaHIT is caused by the development of IgG antibodies directed against a complex of platelet factor 4 (PF4) and heparin.
The antibodies primarily recognize a heparin induced conformational change in the PF4 tetramer( dependent on degree of sulphation of the heparin, hence each heparin has different antigenicity)4 Ts- Thrombocytopenia with nadir 20-50, Thrombosis, timing (5-14 days post heparin OR within24 hrs if previous exposure to heparin in 100 days) oTher causes of thrombocytopenia
Slide52What to do?Stop heparinSwitch to fondaparinux( pentamer- too small to react with the antibody- PF4 complex)can also give DOACs
Start anticoagulation with warfarin in the event of thrombosisHIT antibodies by ELISA, send Heparin sample to confirmEnsure patient has NO FURTHER HEPARIN EVER
Slide53Last one!Urology patient with ca prostrateAdmitted electively for TURBTPre-op FBC showed a platelet count of 22No bleedingCoag, U and E, LFTs, rest of the blood count- all normal
Slide54Film
Slide55PsuedothrombocytopeniaPlatelet aggregation due to EDTA anticoagulationSeen on filmRecheck count with Li Hep or citrate sample- normal countCan sometimes happen due to ‘platelet satellitism
’
Slide56filmSeen in infection sometimes- activated neutrophils cause aggregation of platelets on the surface- in vitro phenomenon
Slide57Low PlateletsSystematic approachDetailed history- can this be congenital? Is there bleeding? Is there thrombosis despite low counts? Any previous counts? Drug history, alcohol history.Rest of the count- is it normal?Caog
screen including fibrinogen (Clauss)U and E, LFTsNever underestimate the power of the blood film!If no cause obvious- ANA, Hep C, HIVITP is a diagnosis of exclusion
Slide58Any questions?
Slide59Interpreting blood resultsGill Burrows
Slide60TopicsAbnormal LFTsDyslipidaemiaHypomagnesaemiaHyper/hyponatraemiaVitamin DRequests
Slide61Abnormal LFTsLFP (liver function profile)Total BilirubinALTTotal proteinAlbuminGlobulin
ALP
Slide62PitfallsLFTs are markers of liver injury not liver functionAbnormal tests found in 1-9% of asymptomatic populationPeople with chronic liver disease/cirrhosis may have normal LFTsLack of specificity:
AST (muscle; brain; heart; red cells)ALP (bone; pregnancy)
Slide63BilirubinIsolated hyperbilirubinaemiaGilbert’shaemolysis
Slide64TransaminasesPredominantly raised ALTHepatocellular diseaseMixed (infiltrative)
Slide65Alkaline phosphatasePredominantly raised in:Cholestatic diseaseMixed (infiltrative)
Slide66AetiologyToxin:MedicationSubstance related (alcohol)MetabolicInfectious
Benign obstructionMalignancyAutoimmuneHereditaryCardiovascularPregnancy related
Slide67ToxinAlcohol; raised GGT; ALT; MCV; TGsDrugs:Raised ALT:Paracetamol; HIV Rx; statins; NSAIDs; amiodarone; OCP; antibiotics/antiviralsRaised GGT:
Anticonvulsants; warfarin
Slide68MetabolicNon alcoholic fatty liver diseaseAdditional risk factors:DiabetesHypertensionHypercholesterolaemia
Estimated prevalence in US is 20-30%Raised ALT (raised glucose; IGT; raised TGs/cholesterol)
Slide69NAFLDNAFLD score:AgeBMIIFGAST:ALT ratio
PlateletsAlbuminThe score is interpreted as follows. <-1.455 is low risk absence of fibrosis F0-F2>-1.454 to 0.675 borderline /indeterminate score>0.675 high risk suggests F3-F4 fibrosis
Slide70NAFLD commentsResult suggests absence of fibrosis with 90% accuracy. These patients can be managed in Primary CareBorderline score. Suggest refer to Secondary Care for fibrosis assessmentResult suggests increased fibrosis risk with 85% accuracy. Suggest refer to secondary care for fibrosis assessment.
Slide71Other metabolic/hereditaryHaemochromatosis:Genetic prevalence 1:227; but clinical disease less commonCheck transferrin saturationIf family history check genetics
Alpha-1-antitrypsin deficiencyGenetic prevalence 1:1800-2000; clinical disease in 10%Check A1AT concentrationWilson’s diseaseRare; usually diagnosed in children/young adults
Slide72InfectiousViral hepatitis:A, B, CD – requires hep B surface antigen – therefore only occurs in HBsAg carriers
E – increasing prevalence in developing world; causes acute infection; mild diseaseCMVEBVHSVHIVTBsepsis
Slide73ImmunologicalAutoimmune hepatitis Prevalence 10-17 per 100,0004:1 F:MPredominantly raised ALT
Check smooth muscle cell antibodiesPrimary biliary cholangitis9:1 F:MPredominantly raised ALP/GGTCheck antimitochondrial antibodyPrimary sclerosing cholangitisOften associated with IBD (especially UC)Predominantly raised ALP/GGT
Slide74UrgentPregnancy related:Intrahepatic cholestasis of pregnancy Acute fatty liver of pregnancyHELLP (haemolysis, elevated liver enzymes, low platelets) – late pregnancy; can occur in pre-eclampsia; can cause acute liver failure
Acute liver failureJaundiceHepatic encephalopathycoagulopathy
Slide75DysplidaemiaHypercholesterolaemiaMixed dyslipidaemiaHypertriglyceridaemia
Slide76Hypercholesterolaemia
Slide77Q-risk 3
Slide78Slide79Lipid modification RxNon fasting lipid profileExclude secondary causesConsider FHUrgent specialist review if TGs > 20
mmol/L
Slide80Lifestyle modificationsCardioprotective dietPhysical activityWeight managementAlcohol restriction
Smoking cessationPlant sterols/stannolsNot if on RxNot if CKD or diabetes
Slide81Lipid modification RxPrimary preventionDiscuss benefits of lifestyleOffer further CVD risk assessment after lifestyle improvements
Offer atorvastatin 20 mg od for people with CVD 10 year risk of ≥ 10%In Type 1 diabetesConsider statin Rx in all patients with Type 1Offer Rx if > 40 years; diabetes for > 10 years; nephropathy; other CVD risk factorsUse atorvastatin 20 mg od
Slide82Lipid modification RxSecondary prevention:Start atorvastatin 80 mg in people with CVD
Offer atorvastatin 20 mg od for people with CKD
Slide83Mixed dyslipidaemia (raised TC and TGs)Causes:Poorly controlled DM
Alcohol XSGenetic causes/lifestyle causesRisks:Premature CV diseasePancreatitis
Slide84ManagementTreat underlying causeConsider 12/7 alcohol abstinenceDietary management
Slide85Heart UK dietary recommendations for TG reduction• Achieve and maintain a healthy body weight.
• Drink alcohol moderately, if at all. • Reduce consumption of high-sugar food and drinks.• Try to follow a diet low in saturated fat and total fat, with less than 30% of daily calories from total fat.• Enjoy several meals of oil-rich fish per week
Slide86StatinsFibratesOmega 3 fatty acids
Slide87Pure hypertriglyceridaemiaCauses:
Usually geneticOccasionally alcoholRisks:Premature CV diseasePancreatitisManagement – as for mixed dyslipidaemia
Slide88PCSK9 inhibitorsPCSK9 is a protein expressed by the liver which binds to LDL receptors and targets them for degredationInhibitor is a monoclonal AB which binds circulating PCSK9
Injectable; one dose per 2 weeksNICE TAs support use in specific patients
Slide89When to use PCSK9 inhibitors (NICE)
Without cardiovascular diseaseWith cardiovascular disease High risk of cardiovascular disease1Very high risk of cardiovascular disease2Non-familial hypercholesterolaemia or mixed dyslipidaemia
Not recommended at any LDL-C concentrationRecommended only if LDL‑C concentration is persistently above 4.0 mmol/litre
Recommended only if LDL‑C concentration is persistently above 3.5 mmol/litre
Heterozygous-familial hypercholesterolaemia
Recommended only if LDL‑C concentration is persistently above 5.0 mmol/litreRecommended only if LDL‑C concentration is persistently above 3.5 mmol/litre
Slide90Local agreementAdverse statin event:CK > 5x ULNALT > 3x ULN
‘Persistent’ – 2 samples > 3/12 apartHigh riskACS OR ischaemic CVA OR PVDVery high riskCV event > 1 site
Slide91HypomagnesaemiaReference range 0.7 – 1.0 mmol/LMild-moderate hypomagnesaemia
0.5-0.7 mmol/LSevere hypomagnesaemia<0.5 mmol/L. Usually associated with symptoms:Neuropsychiatric symptoms include: agitation, irritability, confusion, delirium, hallucinations and seizures. Neuromuscular symptoms include: tetany, tremor, small muscle contractions, cramps, paraesthesia and weakness. Cardiovascular signs: ECG changes, ventricular arrhythmias. Often associated with multiple biochemical abnormalities such as hypokalaemia, hypocalcaemia and metabolic alkalosis.
Slide92AetiologyNutritionalEsp patients with alcohol excess; post opToxic/iatrogenic
PPIsDiureticsSome antibiotics; cyclosporine; insulinGastrointestinalEndocrineHypoparathyroidismHyperthyroidismDKAHyperaldosteronismHungry bone syndromeRenal
Slide93GISecretory diarrhoeaMalabsorptionPancreatitisRenalRecovery from ATN
RTAPost obstructive diuresis
Slide94InvestigationExclude drugs, esp PPIs; diureticsAlcohol historyExclude diarrhoea; evidence of poor diet/malabsorptionCheck serum calcium; potassium; sodium
Check urine Mg (not on Rx)24 hour urine Mg orFractional excretion of Mg (FEMg = [(UMg x PCr) / (PMg x UCr x 0.7)] x 100). If <0.03 suggests extrarenal loss
Slide95TreatmentOral replacement (preferred)Magnesium aspartate sachets (10 mmol per sachet), one sachet twice a day2,3 Monitor
levels daily Reduced absorption if given within 2 hours of bisphosphonates and tetracycline antibiotics
Slide96Severe/symptomatic hypomagnesaemia; or concomitant hypocalcaemia; or oral not appropriateIntravenous replacement Magnesium sulphate 20 mmol in 100 mL sodium chloride 0.9 % Administer
over 2 to 5 hours Recommended starting rate 4 mmol/hour 5,6,7 Centrally or peripherally via infusion pump Monitor daily and repeat doses if needed- up to 5 days Higher doses and faster rates of infusion can be used on intensive care
Slide97Sodium concentration Usually ~ 140 mmol/L (133-146 mmol/L)Mainly dependent on water; not sodium Controlled by ADH (AVP) acting on collecting ducts
Hyponatraemia (usually excess water)Hypernatraemia
Slide98HyponatraemiaClinical effects:ConfusionNausea and vomitingHeadacheFatigueSeizures
Coma
Slide99CausesDrugsPseudohyponatraemiaSIADGI lossRenal loss including Addisons
Slide100HyponatraemiaConsider drugs:Known offenders include acetazolamide, amiloride, amphotericin,
aripiprazole, atovaquone, thiazide diuretics, amiodarone, basiliximab, angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, bromocriptine, carbamazepine, carboplatin, carvedilol, celecoxib, cyclophosphamide, clofibrate, desmopressin, donepezil, duloxetine, eplerenone, gabapentin, haloperidol, heparin, hydroxyurea, indapamide, indomethacin, ketorolac, levetiracetam, loop diuretics, lorcainide, mirtazapine, mitoxantrone, nimodipine, oxcarbazepine, opiates, oxytocin, pimozide
, propafenone, proton pump inhibitors, quetiapine, sirolimus, ticlopidine, tolterodine, vincristine, selective serotonin reuptake inhibitors
, sulfonylureas, trazodone, tolbutamide, venlafaxine, zalcitabine, and zonisamide
Slide101Investigation/ManagementStop medicationTreat underlying causeSerum/urine osmolalitiesUrea/creatinine
TFTsConsider short Synacthen testConsider fluid restriction?? demeclocycline
Slide102Hyponatraemia
Slide103Hypernatraemia
Slide104HypernatraemiaClinical effects:ConfusionWeakness; lethargycoma
Slide105CausesDehydrationGlucocorticoid excessPrimary hyperaldosteronismDiabetes insipidusOthers
Slide106Investigation/managementFluid intakeSerum/urine osmolalityEmu urine osmolalityRenin/aldosterone24 hr UFC/dexamethasone suppression test
Slide107Hypernatraemia
Clinical assessment of patientSerum [Na] > 160 mmol/L
? underlying cause of sodium load
Consider
Cushings
syndrome
Conns syndrome
Non ketotic
hyperglycaemia
? likely to be due to inadequate fluid intake
? known to be near the end of life e.g terminal illness, end stage dementia
Yes
No
Individualised EOL Care Plan
Aggressive fluid replacement
Review clinical state and serum [Na] at 24 and 48 hrs
If no significant
improvement by 48 hrs, ? near end of life
Significant improvement
Identify and correct reason for inadequate intake
Slide108Vitamin DGMMG guidelines 2016:Serum 25OHD measurement is recommended for: Patients with bone diseases that may be improved with vitamin D treatment e.g. those with
osteomalacia or osteoporosis or other bone diseases where correcting vitamin D deficiency before drug treatment is recommended Patients with musculoskeletal symptoms that could be attributed to vitamin D deficiency. Routine vitamin D testing may be unnecessary in patients with osteoporosis or fragility fracture, who may be co-prescribed vitamin D supplementation with an oral antiresorptive treatment. Although vitamin D deficiency is highly prevalent, universal screening of asymptomatic populations is not recommended.
Slide109The following vitamin D thresholds have been adopted in respect to bone health in Greater Manchester: serum 25OHD < 30 nmol/L [12ng/ml] is deficient. Treatment is recommended serum
25OHD of 30–50 nmol/L [12–20ng/ml] may be inadequate in some people. Treatment is advised in the following groups: fragility fracture, documented osteoporosis or high fracture risk treatment with antiresorptive medication for bone disease symptoms suggestive of vitamin D deficiency increased risk of developing vitamin D deficiency in the future because of reduced exposure to sunlight, religious/cultural dress code, dark skin, etc. raised PTH medication with antiepileptic drugs or oral glucocorticoids conditions associated with malabsorption. serum 25OHD > 50 nmol/L [20ng/ml] is sufficient for almost the whole population. Provide reassurance and give advice on maintaining adequate vitamin D levels through safe sunlight exposure and diet.
Slide110Adults:Recommendations: All pregnant and breastfeeding women should take a daily supplement containing 10 μg (400 units) of vitamin D, to ensure the mother’s requirements for vitamin D are met and to build adequate foetal stores for early infancy. [Healthy Start Vitamins for pregnant and breastfeeding women should be considered]
People aged 65 years and over and people who are not exposed to much sun should also take a daily supplement containing 10 μg (400 units) of vitamin D.
Slide111Covid?NICE, PHE and SACN publish rapid COVID-19 guidance on vitamin D (Dec 2020)The expert panel supported current government advice for everyone to take the supplement throughout the autumn and winter, however the panel concluded that there is currently not enough evidence to support taking vitamin D solely to prevent or treat
COVID-19It is recommended that everyone should take a daily 10 microgram (400 international units) vitamin D supplement from October to early March. This dose is safe and effective at maintaining healthy vitamin D blood levels.
Slide112Questions