Transcript Endocrine Emergencies - UHCW Medical Education

Endocrine
Emergencies
Christian Hariman
Objectives
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Diabetic Emergencies
• Recognise and participate in the management of diabetic
ketoacidosis
• Recognise and participate in the initial management of honk
• Recognise and manage hypoglycaemia
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Other Metabolic Disorders
• Recognise the symptoms and signs of thyrotoxicosis
• Manage thyrotoxicosis using medical therapy
• Recognise and initiate the immediate management of
Addisonian crisis
• Initiate investigation of hypo and hyper natraemia and hypo
and hyperkalaemia initiate management of these conditions
• Recognise the circumstances when hypercalcaemia may occur
and initiate the management of hypercalcaemia
Diabetes Emergencies
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Diabetes Ketoacidosis
Hyperosmolar Non Ketosis (Hyperosmolar
Hyperglycaemic state)
Hypoglycaemia
Case
Rose Smith
Diabetic Ketoacidosis
(DKA)
Loss of Beta cell function in pancreas
Loss of beta cell
function is gradual
over time
“Honeymoon period”
alpha-cell
beta-cell
Symptoms and signs
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Nausea
Vomiting
Abdominal pain
Often preceding polyuria, polydipsia, weight loss
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Drowsiness/confusion/coma (severe)
Kussmaul respiration - hyperventilation
‘Pear drops’ breath
Sign of associated systemic illness (MI, infection,
etc)
Diabetic
Ketoacidosis:Pathophysiology
Normal – glucose in
blood
Diabetic
Ketoacidosis:Pathophysiology
Normal Mechanism
Diabetic
Ketoacidosis:Pathophysiology
1.
Insulin deficiency
*lack of glucose in muscle
2.
glucagon excess
*increase in gluconeogenesis
Diabetic
Ketoacidosis:Pathophysiology
3. Rapid lipolysis into free fatty acids
and ketone bodies
release of Beta-hydroxybutyrate
ketones makes you sick
Diabetic
Ketoacidosis:Pathophysiology
4. Hypovolaemia – vomitting + osmotic
diuresis
Increases concentration of ketones
+ glucose
How do I diagnose DKA?
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Diagnosis requires all 3 of the following:
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High blood sugar (i.e diabetes) Glucose > 11 mmol
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*Finger-prick blood glucose can be normal*
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Ketones (blood or urine ≥ +++)
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Acidosis (pH<7.30 or HCO3<15mmol)
How do I Manage DKA?
1.
2.
3.
4.
5.
6.
7.
ABC – if impaired – consider early ITU input /
central venous access
Replace fluids
Resolution of ketonaemia / insulin
Replace electrolytes
Look for cause
Close monitoring
Consider Low molecular weight heparin
Replacing fluids
Initial management
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1L 0.9% NaCl
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30 mins*
1hr
2hr
4 hr
Then continue NaCl
0.9% as dictated by fluid
status
*beware of elderly patients
Later
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Once blood glucose <14
mmol/L – give 10%
dextrose alongside 0.9%
Normal Saline at 125ml
/ hour
Resolution of ketonaemia
Insulin infusion
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Insulin infusion
50units actrapid made to 50ml with NaCl 0.9%
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Rate: 0.1 units/kg/hour
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E.g 70kg = 7 units/hour
Aim for fall in serum ketone of 0.5 mmol/L per hour
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OR rise in serum HCO3- by 3 mmol/hr or reduction of Blood glucose
by 3 mmol/hr
Increase rate of insulin by 1 unit per hour if above not achieved
Continue infusion until blood ketones <0.3, venous pH >7.3 and/or
HCO3- >18
Replace electrolytes
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K+ is most important
Insulin shifts K+ into cells therefore K+ will fall as rehydrate
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Serum K+ ≥ 5.5
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Serum K+ 3.5 - 5.4
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Add 20mmol per litre
Serum K+ <3.5
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No potassium supplement
Add 40mmol per litre
Hyponatraemia may occur due to osmotic effect of glucose - it will
correct with treatment of DKA
Monitoring
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Monitor urine output and vital signs closely
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catheterize
Repeat U&E, glucose, VENOUS bicarbonate – ABG
PAINFUL
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2 – 4 hours, 6 - 8 hours, 12 hours, 24 hours
Repeat ABG at 2 hours if not improving
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? Alternative cause for acidosis e.g. lactate
Case
Nicholas Brown
Hyperosmolar
Hyperglycaemic State
(HHS)
(the artist formerly known as
Hyperosmolar Non Ketotic – HONK)
Features of HHS
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Possibly osmotic symptoms
Dehydration around 10L deficit
Decreased level of conciousness
Signs of underlying infection in up to 50%
+/- thrombo-embolism in up to 30%
2/3 cases previously undiagnosed
As high as 50% mortality – higher than DKA
HHS: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
Diagnosis
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Diagnosis requires ALL of the following:
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Raised blood glucose (usually >30mmol)
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Absence of ketones (or + or ++ only)
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Serum osmolality >350mmol
Is the treatment the same as DKA?
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Fluid replacement – SLOWER (may be a
marker of population not pathology)
Electrolyte replacement
(pseudohyponatraemia)
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Insulin – ‘slower’ scale – normally very
responsive to IV insulin
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Search for cause
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ANTICOAGULATION
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Monitor
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1L 0.9% NaCl
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1 hr*
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2 hr
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4 hr
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8 hr
Then continue NaCl 0.9% as dictated
by fluid status
*half the rate of DKA
Insulin
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50units actrapid made to 50ml with NaCl 0.9%
Rate: 0.1 units/kg/hour
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More insulin sensitive
Reduce rate if Blood glucose falls >10 mmol / hour
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70kg = 7 units/hour
Consider halving the rate within the first 1-2 hours
Stop when patient is recovered
Case
Daniel Walters
Hypoglycaemia
Causes
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Insulin / medications
Liver disease
Insulinoma
Features of Hypoglycaemia
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Autonomic:
 sweating, palpitations, tremor, hunger
Neuroglycopenic
 confusion, clumsiness, behavioural changes, seizures
Non-specific
 nausea, headache, tiredness
Symptoms may not present at the same level of blood
glucose
Diagnosis with serum/capillary glucose (<3.0)
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*beware may not be accurate*
Treatment of hypoglycaemia
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If able to eat
 glucose: e.g 3 dextrosol tabs / 200mls of orange juice/ sugar
drinks
 followed by long acting carbohydrate eg toast/ sandwich
In the community: 1mg glucagon im and long acting
carbohydrate on recovery
Hospital options I.M. glucagon 1mg
 I.V. 20ml of 50% dextrose*
 Other: hypostop
Other Metabolic Disorders
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Thyrotoxicosis
Addisonian Crisis
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Initiate investigation of hypo and hyper natraemia and hypo and
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hyperkalaemia initiate management of these conditions
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Recognise the circumstances when hypercalcaemia may occur
and initiate the management of hypercalcaemia
Case
Joanna Webbley
Thyrotoxicosis
Thyrotoxicosis
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Sweating
Tachycardia with or without AF
Nausea, vomiting and diarrhea
Tremulousness and delirium, occasionally
apathetic
Diarrhoea
Exopthalmos (only in graves disease)
Hyperpyrexia ( >40 0C )
Causes
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Graves Disease
Thyroiditis (Hashimoto’s, de Quervain’s, etc)
Primary hyperthyroid (multinodular goitre,
single nodule, etc)
Exogenous thyroid
Diagnosis
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Free T4, Free T3 elevated
TSH suppressed
Thyroid antibodies (if autoimmune) present
Treatment
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Anti-thyroid medication
Carbimazole (CMZ), Propylthiouracil (PTU)
 Beware of CMZ in pregnancy
 Beware of aggranulocytosis
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Beta blocker
CMZ / PTU takes 2 weeks
 Beta blockade patient if symptomatic for 2-3 weeks
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Thyroid Storm
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rare
A-E of resuscitation, treat hyperthermia
Call senior help / ITU
May require parentral beta blockade and antithyroid medications
Can give lugol iodine to block thyroid release
Case
Brian Walker
Addison’s Disease
& Crisis
Hypothalamus-pituitary-adrenal axis
Hypothalamus
CRH
Pituitary
ACTH
Adrenals
Negative feedback
Glucocorticoids
Features
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rare
Lack of cortisol
Orthostatic hypotension, lethargy, faintings
If autoimmune – dark/pigmented skin
Causes:
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Iatrogenic : Adrenelectomy, sudden stop of long term
glucocorticoids
Autoimmune
Hypothalamic disease, pituitary disease, adrenal disease
Diagnosis
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Low random cortisol (not accurate)
Short Synachten test
Cortisol time 0
 Synacthen (artificial ACTH) Intramuscular
 Cortisol time 30 mins
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Interpretation
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Normal: increment of >200 nmol/L and 30min test
>600 nmol/L
Treatment
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Give Cortisol
Intravenous 200 mg Hydrocotisone
Oral Hydrocortisone
10mg – 10/5mg – 5mg routine
 Normal adult required 20-30mg HC daily
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Remember:
Sick patients require more cortisol
 5mg Prednisolone = 20mg Hydrocortisone
 STEROID CARD
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Hyperkalaemia
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Normal range 3.5 – 4.5
Danger of atrial / ventricular fibrillation
Assess patient (A-E of resus)
Re-check the Potassium levels (lab + blood gas)
Stop offending drugs (spironolactone, amiloride)
Hyperkalaemia treatment
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Urgent
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ECG – tall t waves / widening QRS
Cardiac compromise or impending
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Emergency call if cardiac compromise
10mL Calcium gluconate (10%) over 2 min
50mL of 50% dextrose + 10 units Actrapid over 20-30 mins
Consider dialysis / filtration
Non urgent
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Nebulised Salbutamol
Calcium resonium
50mL of 50% dextrose + 10 units Actrapid over 20-30 mins
Hyper + Hypo natraemia
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Assess patient’s fluid status
Hypovolaemia, euvolaemia, hypervolaemia
Hypernatraemia
 Hyponatraemia
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Beware of acute vs chronic
hyper/hyponatraemia
Hyponatraemia
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Common in elderly
If asymptomatic + chronic – may not need treatment
Investigate cause: Addisons, SIADH
Consider stopping the offending drug
ACE-i, diuretics, omeprazole
Main treatment:
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Fluid restrict if euvolaemia / hypervolaemia
If unable to tolerate – consider V2 receptor antagonist
If hypovolaemia– slow fluid resuscitation
BEWARE – too quick replacement can cause Central
Pontine Myelinolysis
Hypernatraemia
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Assess fluid status
Commonest cause is pure water loss
Chronic vs acute
Investigate cause: Conn’s, Diabetes insipidus
Fluid replacement – slowly if chronic
Hypercalcaemia
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Behavioural change, tetany, seizures
Investigate cause – Primary hyperPTH,
malignancy, recent bone radiotherapy, Familial
Hypercalcaemia hypocalciuria
Beware of true calcium levels in
hypoalbuminaemia
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Corrected Ca = measured Ca + 0.02 x (40-albumin)
Hypercalcaemia
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Treat underlying cause if possible
ABC of resus
IV fluids
Correct hypomagnasaemia / hypokalaemia
Consider diuretics once rehydrated
Bisphosphonates – takes 2-3 days, max 1 week
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Inhibits osteoclast + bone resorption
Thank you
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