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Furtherreading
1. Wilkinson IB, Raine T, Wiles K, et al. (2017). Hypoglycaemia. In: Oxford Handbook of Clinical
Medicine, 10th ed (p. 214). Oxford: Oxford University Press. Available at:
https://doi.org/10.1093/med/9780199689903.003.0005
2. Diabetes UK. Insulin wall chart. Available at: https://www.diabetes.org.uk/resources-s3/2017-
11/wallchartinsulins.pdf
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Chapter22
Hyponatraemia
Guideline: Society for Endocrinology (Emergency management of severe
hyponatraemia in adult patients):
https://ec.bioscientifica.com/view/journals/ec/5/5/G4.xml
OUPdisclaimer:OxfordUniversity Press makesno representation, express
or implied, that the drugdosagesarecorrectand thatthe recommendations
are an exclusive or mandatory course of care. All health professionals
readingthistexthavearesponsibilitytoevaluateitsappropriatenessandtake
theindividualneedsofthepatientintoaccount.
Localtrustguidelines:pleaserefertoyourlocalguidelinesasnecessary.
Overview
Hyponatraemia is diagnosed when serum sodium is <135mmol/L. It may be acute or
chronicandhasavarietyofpossiblecauses(Box22.1).
Severehyponatraemiaispredominantlyaclinicaldiagnosis,madeonthebasisofsigns
andsymptomsandsupportedbythebiochemicalsodiummeasurement(<130mmol/L).If
diagnosed,severehyponatraemiaisamedicalemergencyandshouldbetreatedpromptly,
regardless of the cause. This approach differs to the management of non-severe
hyponatraemiawhichisdetailedattheendofthechapter.
Box22.1Commoncausesofhyponatraemia
Excessive bodily water, e.g. excessive oral intake, liver cirrhosis, heart failure, nephrotic
syndrome, syndrome of inappropriate secretion of antidiuretic hormone (SIADH), or
glucocorticoidinsufficiency
Sodiumloss,e.g.renaldisease,skinorGIlosses
Pseudohyponatraemia,e.g.lipaemiaorproteinaemia
Excessofsolute,e.g.glucose,mannitol,orethanol.
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Diagnosis
History
Onsetofsymptoms
Recentdiagnosesorothersymptoms,e.g.GIinfections,pancreatitis,malignancy
Recentdietandfluidintake
Past medical history, e.g. cardiac failure, liver failure, nephrotic syndrome, hypothyroidism,
hypoadrenalism
Drughistoryspecificallyaskingaboutdiuretics(particularlythiazides)
Recreationaldruguse,e.g.ecstasy.
The symptoms that distinguish severe hyponatraemia from non-severe hyponatraemia
include:
Vomiting
↓consciousness(GCSscore≤8)
Seizures
Cardiorespiratoryarrest.
Other symptoms thatcommonly develop in both severe and non-severe hyponatraemia
includenausea,confusion,andheadache.
Examination
Theclinicalsignsdependonthecauseofthehyponatraemiaandthespeedwithwhichit
developed. Different causes may result in signs of hypervolaemia (e.g. raised JVP,
oedema), hypovolaemia (e.g. dry mucous membranes, postural hypotension), or
euvolemia.
Thefollowingobservationsshouldbemeasured:
Temperature,respiratoryrate,oxygensaturation,andheartrate
Lyingandstandingbloodpressure
GCSscore.
Hyponatraemia can develop secondary to other conditions (see Fig. 22.2 later in the
chapter).Signsoftheseunderlyingconditionsmaybeevidentonexamination.
Investigations
Bedside
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ECG.
Bloods
FBC
U&E
LFT
Boneprofile
Serumglucose
TFT
Serumosmolality(Fig.22.1)
9amcortisol
Amylase(ifpancreatitisissuspected).
Other
Urineosmolality(Fig.22.1)
Urinesodium(Fig.22.1).
A serum sodiumshouldbecollectedatthe sametimeastheurineosmolality andsodiumso
thatthemeasurementsare‘paired’(Fig.22.1).
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Fig.22.1Interpretationofpairedosmolalitytestinganddifferentialdiagnosis.
If the patient has kidney disease or has been taking diuretics, all possible causes of
hyponatraemia should be considered as a possible underlying diagnosis, regardless of the
urineosmolalityandurinesodiumresults.
Managementofseverehyponatraemia
Acutemanagement
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Management steps are detailed in Fig. 22.2 and should be provided with senior
supervisionandwiththepatientconnectedtocardiactelemetry.
Fig.22.2Acutemanagementofseverehyponatraemia.*Orequivalentconcentration.
Treatmentafterstabilization
Targetsodiumlevel
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Theserumsodiumlevelshouldnotrisemorethan10mmol/Linthefirst24hours.From
then onwards, the daily increase should not exceed 8mmol/L until the level is
130mmol/L.
Requesthelpfromanendocrinologist,particularlyifthedailythresholdisexceeded.
Adailyriseinsodiumlevelbeyondthesethresholdsrisksthedevelopmentofcentralpontine
myelinolysis,whichcancauseneurologicaldamagewhichmaybepermanent.
Monitoringfrequency
Serum sodium should be measured 6 hours after treatment has been givenand then again at12
hours.Afterthis,serumsodiumshouldbecheckeddailyuntilstable.
Managementofnon-severehyponatraemia
Themanagementofnon-severehyponatraemiadependsontreatingtheunderlyingcause,
rather than activelyattemptingtocorrectthesodium. Adviceshould be soughtfroman
endocrinologistwherethereisdiagnosticdoubtordifficultytreating.
Furtherreading
1. EuropeanSociety of Endocrinology, EuropeanSociety of Intensive Care Medicine,European Renal
Association-European Dialysis and Transplant Association (2014). Clinical practice guideline on
diagnosis and treatment of hyponatraemia. Available at:
https://eje.bioscientifica.com/view/journals/eje/170/3/G1.xml
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Chapter23
Hypothyroidism
Guideline: NICE NG145 (Thyroid disease: assessment and management):
https://www.nice.org.uk/guidance/ng145
British Thyroid Association (UKguidelines for the use of thyroid function
tests): https://www.british-thyroid-
association.org/sandbox/bta2016/uk_guidelines_for_the_use_of_thyroid_function_tests.pdf
OUPdisclaimer:OxfordUniversity Press makesno representation, express
or implied, that the drugdosagesarecorrectand thatthe recommendations
are an exclusive or mandatory course of care. All health professionals
readingthistexthavearesponsibilitytoevaluateitsappropriatenessandtake
theindividualneedsofthepatientintoaccount.
Localtrustguidelines:pleaserefertoyourlocalguidelinesasnecessary.
Overview
Hypothyroidism is the clinical state that occurs as a result of impaired production of
thyroidhormones:T4andT3.
Hypothyroidism is common, affecting 1–2% of the population. Incidence increases
withincreasingage.Itdisproportionallyaffectsfemaleswitharatioof10:1.
Primaryhypothyroidism(95%):
Atrophicautoimmunethyroiditisorgoitrousautoimmunethyroiditis(Hashimoto’sdisease)—
mostcommon
Following destructive treatment to the thyroid or nearby tissue, e.g. radioiodine therapy,
thyroidectomy,externalbeamradiotherapy
Drugsincludingamiodarone,interferon,andlithium
Congenitalhypothyroidism(rare)
Secondaryhypothyroidism(5%):
TheresultofpituitarydiseaseordamagecausingreducedTSHproduction
Subclinicalhypothyroidism—astatewhereTSHiselevated,butT4isnormal.Symptomsmayor
maynotbepresent.
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Diagnosis
History
Symptoms can be vague and their onset insidious. Have a low threshold for checking
TFTinpatientspresentingwithnon-specificsymptoms.
Symptoms
Lowmoodorcognitiveimpairment
Hoarsevoice
Thinninghair
Fatigue/lethargy
Coldintolerance
Dryorthinningskin
Constipation
Weightgain
Irregularmenstruation.
Examination
Forclinicalsignsremember‘BRADYCARDIC’:
Bradycardia
Reflexesrelaxslowly
Ataxia
Dry,thinhairandskin
Yawning/drowsy/coma
Coldhands
Ascites±non-pittingoedema
Round,puffyface
Defeateddemeanour
Immobile±ileus
Congestivecardiacfailure.
Neuropathy,myopathy,andgoitremayalsobepresent.
Investigations
Bloods
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TFT:
WhenTSHis≥10mU/LandT4isbelowthereferencerange,thisisoverthypothyroidismand
shouldbetreated
SeeTable23.1forinterpretation
FBC
Cholesterol/lipidprofile
HbA1c/fastingbloodglucose
VitaminD
Calcium.
Table23.1Interpretationofthyroidfunctiontestsinhypothyroidism
TFTresults Interpretation
TSH↑(≥10mU/L)
T4↓
Primaryhypothyroidism
TSH↑
T4↔
Subclinicalhypothyroidism
TSH↓
T4↓
Secondary(central)hypothyroidism—rare
Source:datafromUKGuidelinesfortheUseofThyroidFunctionTests.July2006.BritishThyroid
Association.
Antithyroidperoxidaseantibodiesmaybetestedtoinvestigateforautoimmunecausesof
primary hypothyroidism. Although the results might not change the treatment, there is
evidencetosuggestthatwhenpatientsunderstandthecauseoftheircondition,thisleads
toincreasedtreatmentcompliance.
Management
ManagementofovertandsubclinicalhypothyroidismiscoveredinFig.23.1.
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