Endocrine Endocrine EmergenciesEmergencies

Christian HarimanChristian Hariman

ObjectivesObjectives Diabetic EmergenciesDiabetic Emergencies

• Recognise and participate in the management of diabetic • Recognise and participate in the management of diabetic ketoacidosis ketoacidosis • Recognise and participate in the initial management of • Recognise and participate in the initial management of honk honk • Recognise and manage hypoglycaemia• Recognise and manage hypoglycaemia

Other Metabolic DisordersOther Metabolic Disorders • Recognise the symptoms and signs of thyrotoxicosis • Recognise the symptoms and signs of thyrotoxicosis • Manage thyrotoxicosis using medical therapy• Manage thyrotoxicosis using medical therapy• Recognise and initiate the immediate management of • Recognise and initiate the immediate management of Addisonian crisisAddisonian crisis• Initiate investigation of hypo and hyper natraemia and hypo • Initiate investigation of hypo and hyper natraemia and hypo and hyperkalaemia initiate management of these conditions and hyperkalaemia initiate management of these conditions • Recognise the circumstances when hypercalcaemia may • Recognise the circumstances when hypercalcaemia may occur and initiate the management of hypercalcaemia occur and initiate the management of hypercalcaemia

Diabetes EmergenciesDiabetes Emergencies

Diabetes KetoacidosisDiabetes Ketoacidosis Hyperosmolar Non Ketosis Hyperosmolar Non Ketosis

(Hyperosmolar Hyperglycaemic (Hyperosmolar Hyperglycaemic state)state)

HypoglycaemiaHypoglycaemia

CaseCase

Rose SmithRose Smith

Diabetic Diabetic KetoacidosisKetoacidosis

(DKA)(DKA)

Loss of Beta cell function in Loss of Beta cell function in pancreaspancreas

beta-cell

alpha-cell

Loss of beta cell function is gradual over time

“Honeymoon period”

Symptoms and signsSymptoms and signs

NauseaNausea VomitingVomiting Abdominal painAbdominal pain Often preceding polyuria, polydipsia, Often preceding polyuria, polydipsia,

weight lossweight loss

Drowsiness/confusion/coma (severe)Drowsiness/confusion/coma (severe) Kussmaul respiration - hyperventilationKussmaul respiration - hyperventilation ‘‘Pear drops’ breathPear drops’ breath Sign of associated systemic illness (MI, Sign of associated systemic illness (MI,

infection, etc)infection, etc)

B L O O D

MUSCLE

Diabetic Diabetic Ketoacidosis:PathophysiKetoacidosis:Pathophysi

ologyology

Normal – glucose in blood

B L O O D

MUSCLEInsulin

Diabetic Diabetic Ketoacidosis:PathophysiKetoacidosis:Pathophysi

ologyology

Normal Mechanism

B L O O D

MUSCLE

1. Insulin deficiency

*lack of glucose in muscle

2. glucagon excess

*increase in gluconeogenesis

Diabetic Diabetic Ketoacidosis:PathophysiKetoacidosis:Pathophysi

ologyology

Insulin

Liver Glucagon

B L O O D

MUSCLEketones

Diabetic Diabetic Ketoacidosis:PathophysiKetoacidosis:Pathophysi

ologyology

3. Rapid lipolysis into free fatty acids and ketone bodies

release of Beta-hydroxybutyrate

ketones makes you sick

ketonesketones

ketones

B L O O D

MUSCLE

Diabetic Diabetic Ketoacidosis:PathophysiKetoacidosis:Pathophysi

ologyology

4. Hypovolaemia – vomitting + osmotic diuresis

Increases concentration of ketones + glucose

ketones

ketones

How do I diagnose DKA?How do I diagnose DKA?

Diagnosis requires all 3 of the Diagnosis requires all 3 of the following:following:

High blood sugar (i.e diabetes) Glucose > 11 High blood sugar (i.e diabetes) Glucose > 11 mmolmmol **Finger-prick blood glucose can be normalFinger-prick blood glucose can be normal**

Ketones (blood or urine ≥ +++)Ketones (blood or urine ≥ +++)

Acidosis (pH<7.30 or HCOAcidosis (pH<7.30 or HCO33<15mmol)<15mmol)

How do I Manage DKA?How do I Manage DKA?

1.1. ABC – if impaired – consider early ITU ABC – if impaired – consider early ITU input / central venous accessinput / central venous access

2.2. Replace fluids Replace fluids 3.3. Resolution of ketonaemia / insulinResolution of ketonaemia / insulin4.4. Replace electrolytesReplace electrolytes5.5. Look for causeLook for cause6.6. Close monitoringClose monitoring7.7. Consider Low molecular weight Consider Low molecular weight

heparinheparin

Replacing fluidsReplacing fluids

Initial managementInitial management

1L 0.9% NaCl 1L 0.9% NaCl 30 mins*30 mins* 1hr1hr 2hr2hr 4 hr4 hr

Then continue NaCl Then continue NaCl 0.9% as dictated by 0.9% as dictated by fluid statusfluid status

*beware of elderly *beware of elderly patientspatients

LaterLater

Once blood Once blood glucose <14 glucose <14 mmol/L – give 10% mmol/L – give 10% dextrose alongside dextrose alongside 0.9% Normal 0.9% Normal Saline at 125ml / Saline at 125ml / hourhour

Resolution of Resolution of ketonaemiaketonaemiaInsulin infusionInsulin infusion Insulin infusionInsulin infusion 50units actrapid made to 50ml with NaCl 50units actrapid made to 50ml with NaCl

0.9%0.9%

Rate: Rate: 0.1 units/kg/hour0.1 units/kg/hour E.g E.g 70kg = 7 units/hour70kg = 7 units/hour

Aim for fall in serum ketone of 0.5 mmol/L Aim for fall in serum ketone of 0.5 mmol/L per hourper hour OROR rise in serum HCO3- by 3 mmol/hr or reduction of rise in serum HCO3- by 3 mmol/hr or reduction of

Blood glucose by 3 mmol/hrBlood glucose by 3 mmol/hr Increase rate of insulin by 1 unit per hour if above not Increase rate of insulin by 1 unit per hour if above not

achievedachieved Continue infusion until blood ketones <0.3, venous pH Continue infusion until blood ketones <0.3, venous pH

>7.3 and/or HCO3- >18>7.3 and/or HCO3- >18

Replace electrolytesReplace electrolytes KK++ is most important is most important Insulin shifts KInsulin shifts K++ into cells therefore K into cells therefore K++ will fall as will fall as

rehydraterehydrate Serum K+ ≥ 5.5 Serum K+ ≥ 5.5

No potassium supplement No potassium supplement

Serum K+ 3.5 - 5.4 Serum K+ 3.5 - 5.4 Add 20mmol per litre Add 20mmol per litre

Serum K+ <3.5 Serum K+ <3.5 Add 40mmol per litre Add 40mmol per litre

Hyponatraemia may occur due to osmotic effect of Hyponatraemia may occur due to osmotic effect of glucose - it will correct with treatment of DKAglucose - it will correct with treatment of DKA

MonitoringMonitoring Monitor urine output and vital signs Monitor urine output and vital signs

closelyclosely catheterizecatheterize

Repeat U&E, glucose, Repeat U&E, glucose, VENOUSVENOUS bicarbonate – ABG PAINFULbicarbonate – ABG PAINFUL

2 – 4 hours, 6 - 8 hours, 12 hours, 24 hours2 – 4 hours, 6 - 8 hours, 12 hours, 24 hours

Repeat ABG at 2 hours if not improvingRepeat ABG at 2 hours if not improving ? Alternative cause for acidosis e.g. lactate? Alternative cause for acidosis e.g. lactate

CaseCase

Nicholas BrownNicholas Brown

Hyperosmolar Hyperosmolar Hyperglycaemic Hyperglycaemic

State (HHS)State (HHS)

(the artist formerly known as (the artist formerly known as Hyperosmolar Non Ketotic – Hyperosmolar Non Ketotic –

HONK)HONK)

Features of HHSFeatures of HHS

Possibly osmotic symptomsPossibly osmotic symptoms Dehydration around 10L deficitDehydration around 10L deficit Decreased level of conciousnessDecreased level of conciousness Signs of underlying infection in up to 50%Signs of underlying infection in up to 50% +/- thrombo-embolism in up to+/- thrombo-embolism in up to 30%30% 2/3 cases previously undiagnosed2/3 cases previously undiagnosed As high as 50% mortality – higher than DKAAs high as 50% mortality – higher than DKA

B L O O D

MUSCLEInsulin

HHS:PathophysiologyHHS:Pathophysiology

1. Insulin production markedly reduced but NOT absent.

No switch to fat metabolism and therefore no ketones or acidosis

2. Gluconeogenesis

3. Loss of intravascular volume

DiagnosisDiagnosis

Diagnosis requires ALL of the Diagnosis requires ALL of the following:following:

Raised blood glucose (usually >30mmol)Raised blood glucose (usually >30mmol)

Absence of ketones (or + or ++ only)Absence of ketones (or + or ++ only)

Serum osmolality >350mmolSerum osmolality >350mmol

Is the treatment the same as Is the treatment the same as DKA?DKA?

Fluid replacement – SLOWER Fluid replacement – SLOWER

(may be a marker of population (may be a marker of population

not pathology)not pathology) Electrolyte replacement Electrolyte replacement

(pseudohyponatraemia)(pseudohyponatraemia) Insulin – ‘slower’ scale – normally Insulin – ‘slower’ scale – normally

very responsive to IV insulinvery responsive to IV insulin Search for causeSearch for cause ANTICOAGULATION ANTICOAGULATION MonitorMonitor

1L 0.9% NaCl 1 hr*

2 hr

4 hr

8 hr

Then continue NaCl 0.9% as dictated by fluid status

*half the rate of DKA

InsulinInsulin 50units actrapid made to 50ml with 50units actrapid made to 50ml with

NaCl 0.9%NaCl 0.9% Rate: 0.1 units/kg/hourRate: 0.1 units/kg/hour

70kg = 7 units/hour70kg = 7 units/hour More insulin sensitiveMore insulin sensitive Reduce rate if Blood glucose falls >10 Reduce rate if Blood glucose falls >10

mmol / hourmmol / hour Consider halving the rate within the first 1-2 Consider halving the rate within the first 1-2

hourshours Stop when patient is recoveredStop when patient is recovered

CaseCase

Daniel WaltersDaniel Walters

HypoglycaemiaHypoglycaemia

Causes

Insulin / medications Liver disease Insulinoma

Features of Features of HypoglycaemiaHypoglycaemia

Autonomic: Autonomic: sweating, palpitations, tremor, hungersweating, palpitations, tremor, hunger

NeuroglycopenicNeuroglycopenic confusion, clumsiness, behavioural changes, confusion, clumsiness, behavioural changes,

seizuresseizures Non-specific Non-specific

nausea, headache, tirednessnausea, headache, tiredness

Symptoms may not present at the same level of Symptoms may not present at the same level of blood glucoseblood glucose

Diagnosis with serum/capillary glucose (<3.0) Diagnosis with serum/capillary glucose (<3.0) *beware may not be accurate**beware may not be accurate*

Treatment of Treatment of hypoglycaemiahypoglycaemia

If able to eatIf able to eat glucose: e.g 3 dextrosol tabs / 200mls of glucose: e.g 3 dextrosol tabs / 200mls of

orange juice/ sugar drinksorange juice/ sugar drinks followed by long acting carbohydrate eg followed by long acting carbohydrate eg

toast/ sandwichtoast/ sandwich In the community: In the community: 1mg glucagon im and 1mg glucagon im and

long acting carbohydrate on recoverylong acting carbohydrate on recovery Hospital options-Hospital options-

I.M. glucagon 1mgI.M. glucagon 1mg I.V. 20ml of 50% dextrose*I.V. 20ml of 50% dextrose* Other: hypostopOther: hypostop

Other Metabolic Other Metabolic DisordersDisorders

ThyrotoxicosisThyrotoxicosis Addisonian CrisisAddisonian Crisis

Initiate investigation of hypo and hyper Initiate investigation of hypo and hyper natraemia and hypo and hyperkalaemia initiate natraemia and hypo and hyperkalaemia initiate

management of these conditionsmanagement of these conditions Recognise the circumstances when Recognise the circumstances when

hypercalcaemia may occur and initiate the hypercalcaemia may occur and initiate the

management of hypercalcaemiamanagement of hypercalcaemia

CaseCase

Joanna WebbleyJoanna Webbley

ThyrotoxicosisThyrotoxicosis

ThyrotoxicosisThyrotoxicosis

SweatingSweating Tachycardia with or without AFTachycardia with or without AF Nausea, vomiting and diarrheaNausea, vomiting and diarrhea Tremulousness and delirium, Tremulousness and delirium,

occasionally apatheticoccasionally apathetic DiarrhoeaDiarrhoea Exopthalmos (only in graves disease) Exopthalmos (only in graves disease) Hyperpyrexia ( >40 Hyperpyrexia ( >40 00C )C )

CausesCauses

Graves DiseaseGraves Disease Thyroiditis (Hashimoto’s, de Thyroiditis (Hashimoto’s, de

Quervain’s, etc)Quervain’s, etc) Primary hyperthyroid (multinodular Primary hyperthyroid (multinodular

goitre, single nodule, etc)goitre, single nodule, etc) Exogenous thyroidExogenous thyroid

DiagnosisDiagnosis

Free T4, Free T3 elevatedFree T4, Free T3 elevated TSH suppressedTSH suppressed Thyroid antibodies (if autoimmune) Thyroid antibodies (if autoimmune)

presentpresent

TreatmentTreatment

Anti-thyroid medication Anti-thyroid medication Carbimazole (CMZ), Propylthiouracil Carbimazole (CMZ), Propylthiouracil

(PTU)(PTU) Beware of CMZ in pregnancyBeware of CMZ in pregnancy Beware of aggranulocytosisBeware of aggranulocytosis

Beta blockerBeta blocker CMZ / PTU takes 2 weeks CMZ / PTU takes 2 weeks Beta blockade patient if symptomatic Beta blockade patient if symptomatic

for 2-3 weeksfor 2-3 weeks

Thyroid StormThyroid Storm

rare rare A-E of resuscitation, treat A-E of resuscitation, treat

hyperthermiahyperthermia Call senior help / ITUCall senior help / ITU May require parentral beta blockade May require parentral beta blockade

and anti-thyroid medicationsand anti-thyroid medications Can give lugol iodine to block Can give lugol iodine to block

thyroid releasethyroid release

CaseCase

Brian WalkerBrian Walker

Addison’s Addison’s Disease Disease & Crisis& Crisis

Hypothalamus-pituitary-Hypothalamus-pituitary-adrenal axisadrenal axis

Hypothalamus

Pituitary

Adrenals

CRH

ACTH

Glucocorticoids

Negative feedback

FeaturesFeatures

rarerare Lack of cortisolLack of cortisol Orthostatic hypotension, lethargy, faintingsOrthostatic hypotension, lethargy, faintings If autoimmune – dark/pigmented skinIf autoimmune – dark/pigmented skin Causes:Causes:

Iatrogenic : Adrenelectomy, sudden stop of long Iatrogenic : Adrenelectomy, sudden stop of long term glucocorticoidsterm glucocorticoids

AutoimmuneAutoimmune Hypothalamic disease, pituitary disease, Hypothalamic disease, pituitary disease,

adrenal diseaseadrenal disease

DiagnosisDiagnosis

Low random cortisol (not accurate)Low random cortisol (not accurate) Short Synachten testShort Synachten test

Cortisol time 0Cortisol time 0 Synacthen (artificial ACTH) Synacthen (artificial ACTH)

IntramuscularIntramuscular Cortisol time 30 minsCortisol time 30 mins

Interpretation Interpretation Normal: increment of >200 nmol/L and Normal: increment of >200 nmol/L and

30min test >600 nmol/L30min test >600 nmol/L

TreatmentTreatment

Give CortisolGive Cortisol Intravenous 200 mg HydrocotisoneIntravenous 200 mg Hydrocotisone Oral Hydrocortisone Oral Hydrocortisone

10mg – 10/5mg – 5mg routine10mg – 10/5mg – 5mg routine Normal adult required 20-30mg HC dailyNormal adult required 20-30mg HC daily

Remember:Remember: Sick patients require more cortisolSick patients require more cortisol 5mg Prednisolone = 20mg Hydrocortisone5mg Prednisolone = 20mg Hydrocortisone STEROID CARDSTEROID CARD

HyperkalaemiaHyperkalaemia

Normal range 3.5 – 4.5Normal range 3.5 – 4.5 Danger of atrial / ventricular Danger of atrial / ventricular

fibrillationfibrillation Assess patient (A-E of resus)Assess patient (A-E of resus) Re-check the Potassium levels (lab + Re-check the Potassium levels (lab +

blood gas)blood gas) Stop offending drugs Stop offending drugs

(spironolactone, amiloride)(spironolactone, amiloride)

Hyperkalaemia Hyperkalaemia treatmenttreatment

UrgentUrgent ECG – tall t waves / widening QRSECG – tall t waves / widening QRS Cardiac compromise or impendingCardiac compromise or impending

Emergency call if cardiac compromiseEmergency call if cardiac compromise 10mL Calcium gluconate (10%) over 2 min10mL Calcium gluconate (10%) over 2 min 50mL of 50% dextrose + 10 units Actrapid over 20-50mL of 50% dextrose + 10 units Actrapid over 20-

30 mins30 mins Consider dialysis / filtrationConsider dialysis / filtration

Non urgentNon urgent Nebulised SalbutamolNebulised Salbutamol Calcium resoniumCalcium resonium 50mL of 50% dextrose + 10 units Actrapid over 20-50mL of 50% dextrose + 10 units Actrapid over 20-

30 mins30 mins

Hyper + Hypo natraemiaHyper + Hypo natraemia

Assess patient’s fluid statusAssess patient’s fluid status Hypovolaemia, euvolaemia, Hypovolaemia, euvolaemia,

hypervolaemiahypervolaemia HypernatraemiaHypernatraemia HyponatraemiaHyponatraemia

Beware of acute vs chronic Beware of acute vs chronic hyper/hyponatraemiahyper/hyponatraemia

HyponatraemiaHyponatraemia Common in elderlyCommon in elderly If asymptomatic + chronic – may not need If asymptomatic + chronic – may not need

treatmenttreatment Investigate cause: Addisons, SIADHInvestigate cause: Addisons, SIADH Consider stopping the offending drugConsider stopping the offending drug ACE-i, diuretics, omeprazoleACE-i, diuretics, omeprazole Main treatment:Main treatment:

Fluid restrict if euvolaemia / hypervolaemiaFluid restrict if euvolaemia / hypervolaemia If unable to tolerate – consider V2 receptor antagonistIf unable to tolerate – consider V2 receptor antagonist If hypovolaemia– slow fluid resuscitationIf hypovolaemia– slow fluid resuscitation BEWARE – too quick replacement can cause Central BEWARE – too quick replacement can cause Central

Pontine MyelinolysisPontine Myelinolysis

HypernatraemiaHypernatraemia

Assess fluid statusAssess fluid status Commonest cause is pure water lossCommonest cause is pure water loss Chronic vs acuteChronic vs acute Investigate cause: Conn’s, Diabetes Investigate cause: Conn’s, Diabetes

insipidusinsipidus Fluid replacement – slowly if chronicFluid replacement – slowly if chronic

HypercalcaemiaHypercalcaemia

Behavioural change, tetany, seizuresBehavioural change, tetany, seizures Investigate cause – Primary Investigate cause – Primary

hyperPTH, malignancy, recent bone hyperPTH, malignancy, recent bone radiotherapy, Familial radiotherapy, Familial Hypercalcaemia hypocalciuriaHypercalcaemia hypocalciuria

Beware of true calcium levels in Beware of true calcium levels in hypoalbuminaemiahypoalbuminaemia Corrected Ca = measured Ca + 0.02 x Corrected Ca = measured Ca + 0.02 x

(40-albumin)(40-albumin)

HypercalcaemiaHypercalcaemia

Treat underlying cause if possibleTreat underlying cause if possible ABC of resusABC of resus IV fluidsIV fluids Correct hypomagnasaemia / Correct hypomagnasaemia /

hypokalaemiahypokalaemia Consider diuretics once rehydratedConsider diuretics once rehydrated Bisphosphonates – takes 2-3 days, max Bisphosphonates – takes 2-3 days, max

1 week1 week Inhibits osteoclast + bone resorptionInhibits osteoclast + bone resorption

Thank youThank you

Christian.Hariman@uhcw.nhsChristian.Hariman@uhcw.nhs.uk.uk