Endocrine emergencies Flashcards
(24 cards)
What are the definitions of hypoglycaemia in different age groups?
Adults BGL <3.9mmol/L
Paediatrics <3.3mmol/L
Infants <2.6mmol/L
What are the main causes of Hypokalaemic periodic paralysis?
Acquired is almost always due to hyperthyroidism
Congenital is the most common, 1:100,000 people have it with variable penetrance, autosomal dominant
What provokes attacks of hypokalaemic periodic paralysis?
High carbohydrate meals (insulin release)
Significant exercise (catecholamine release)
Exogenous insulin, catecholamines or other K+ lowering agents
What is the treatment for hypokalaemic period paralysis?
Unless a very severe attack it is usually treated with oral potassium chloride (600-1200mg Q30mins) due to the risk of rebound hyperkalaemia (relative not absolute hypokalaemia due to shifting of K+ into cells)
Very rarely patients have hyperkalaemic periodic paralysis so K+ should always be checked
What preventative medications are used for hypokalaemic periodic paralysis?
Carbonic anhydrase inhibitors such as acetazolamide (mechanism not known)
Potassium sparing diuretics such as spirinolactone
What medications are used in the acute treatment of hyperthyroidism aka thyrotoxicosis?
- Lugols iodine 10drops/0.5mls TDS (blocks release of thyroid hormone)
- Hydrocortisone 100 TDS (prevents conversion of T4 to T3)
- Propothiouracil 1gm load then 250mg PO TDS for mild or Q4hr for thyrotoxicosis (decreases T4 >T3 and reduces gland acitivty)
- Carbimazole PO 20mg (same PTU)
- Propranolol 40-60mg QID PO or 1mg aliquots IV (lower BP/HR, prevents T4 >T3)
What differentiates HHS and DKA?
- DKA defined by ketoacidosis, may have minimal to no hyperglycaemia (especially if on SGLT-2 inhibitors with euglycaemic DKA) and usually have normal plasma osmolality
- HHS may have minimal to no ketoacidosis but will have significant hyperglycaemia (usually >50mmol/L) and raised osmolality
- DKA more common in Type 1s and HHS in type 2’s
- Can have overlap between the two with significant hyperglycaemia and raised osmolality complicating ketoacidosis
What is the treatment for HHS?
Fluids
- IV Normal Saline either bolus or 1L/hr for 2-3hrs as patients usually hypovolaemic
- Reassess fluids after 1st 2-3L
- May need to replace deficit with 0.45% saline if very hypernatraemic when corrected for glucose
- Try to replace half of deficit over 24hrs, deficit = 0.6 x Kg x (1 - 140/ corrected Na+)
Insulin
- IV insulin infusion 0.05-0.1units/kg bolus followed by 0.05units/kg/hr, ie 80kg man gets 8unit bolus then 4/hr
- usual upper limit is 3units/hr as aiming for slow BSL drop
- Fast drop can precipitate myelinolysis
Electrolytes
- IV potassium replacement aiming K 4-5, if K <3.3 then stop insulin infusion and replace K
- Replace Mg+ as well
- Aim not to drop Na+ more than 10mmols in 24hrs
Other
- VTE prophylaxis
- Treat underlying cause
Why is fluid replacement important in DKA and HHS?
- Patients often somewhat to severely dehydrated
- IV fluids will correct hypovolaemia, improve perfusion, reduce plasma osmolality through dilution and improve insulin responsiveness
- Patients with HHS/DKA who are fluid overloaded have very poor outcomes
What is a simple way of estimating the corrected Na+ in hyperglycaemia?
For every 5.5mmol of sugar above normal (5.5mmol) add 2 mmol of Na+
Ie Na+ 140, BSL 5.5 = Na+ 140
BSL 11 = Na+ 142
BSL 22 = 146
How is effective serum osmolality (osmolarity) measured?
(2 x Na+) + BSL + Urea + (ETOH x 1.25)
The sodium value used is the measured sodium and not the corrected sodium
Na+ 145, BSL 30, Urea 10, ETOH 0
(2 x 145) + 30 +10 = 290 + 40 = 320
In clinical terms what is the difference between osmolality and osmolarity? What is the osmolar gap
Osmolality measures the number of moles of particles dissolved per Kg of solvent, whereas osmolarity is per litre of solvent
Biochem machines will measure osmolality, whereas the calculated serum osmolality is actually osmolarity, however the terms are used interchangeably so it is often referred to as osmolality
The osmolar gap is the measured osmolality - calculated osmolarity
An osmolar gap is present if the gap is > 10 mOsmol/Kg
What is the importance of and what are the causes of a raised osmolar gap?
An osmolar gap suggests the presence an unaccounted for solute present at a high concentration
- Ethanol (most common cause), although this can be accounted for by altering the equation to (2xNa+) + BSL + Urea + (1.25 x ethanol in mmol/L)
- Toxic alcohols
- Mannitol (ie for cerebral oedema)
- Glycine or Sorbitol (TURP syndrome)
- Pseudohyponatraemia (severe hyperproteinaemia and hyperlipidaemia)
- A complication of IVIG administration (10% Mannitol solution, poor excretion with renal failure)
- Sick cell syndrome in MOF
What is the treatment for paediatric CAH with adrenal crisis?
IV 50mg/m2 Hydrocortisone
IV bolus with 0.9% saline
Treat hypoglycaemia
Consider treatment for hyperkalaemia but often resolves
What is the classid triad in adrenal crisis?
Hyperkalaemia
Hyponatraemia
Hypoglycaemia
Also metabolic acidosis and hypochloraemia
What is a simplified management of thyroid storm?
What are the factors contributing to osmotic myelinolysis?
Risk factors
- Alcoholics
- Malnourished
- Burns victims
- Hypokalaemia
Clinical
- Usually manifests as dysarthria, mutism and affective changes which can be mistaken for mental illness
- Prominent Pons involvement has rapidly progressive spastic quadraparesis, coma and death
What are the main physiological and biochemical differences between DKA and HHS?
What are the symptoms and signs of severe hypocalcaemia?
Neurological
- Hyperreflexia, seizures, delerium
- Peri-oral and digital paraesthesia
MSK
- Chvostek sign, Trousseau sign
- Muscle cramps, tetany
- Laryngospasm
Cardiac
- Long QT, TdP, heart block, arrest
Treatment
- IV 60mls of calcium gluconate or 20mmols calcium chloride (13.2mmols)
What is the treatment for symptomatic (ie seizures) hyponatraemia?
- Hypertonic saline 3-5mls/kg (ie 100-150mls) with repeat Q10mins to max 300mls total 3% saline
- Aiming to increase sodium by 4-6mmols rapidly, will usually resolve symptoms
- any more than this has no proven benefit and may cause harm
- Not to exceed 8-10mmol rise in 24hrs (osmotic demyelinosis)
What is the treatment of acute hypercalcaemia? What are the causes?
Causes
- Malignancy (bone mets, MM, paraneoplastic syndromes ie NSCLC)
- Hyperparathyroidism
- Drugs (Thiazides, lithium)
- Hyperthyroidism, phaeo
- Acromegaly, pagets disease
- Milk-alkali syndrome
- Long term immoblisation
Treatment
- IV fluids 0.9% saline, titrated to normovolaemia + 0.5-1ml/kg/kr UO
- Bisphosphonate (IV Pamidronate 60- 90mg)
- Calcitonin 4 international units/kg
- IV hydrocortisone 100mg QID
- Withhold meds that cause hypercalc (ie thiazides)
- Haemodialysis if other treatments are refractory
What are the clinical features and treatment of Hypothyroid myxedema?
Causes
- Hypothyroidism of any cause
- Exacerbated by infection. MI, cold exposure, surgery, trauma, opioids and new medication changes
Clinical
- Hallmark is AMS + hypothermia
- Myxedema (face, tongue, hands, legs etc, non-pitting from mucin deposition)
- AMS may include psychosis and retardation»_space; coma
- Focal/generalised seizures
- bradycardia, hypotension signs of pericardial effusion
Blood tests
- Hyponatraemia
- Hypoglycaemia
- low T4, high TSH
Treatment
- Hydrocortisone 100mg IV QID
- T4 replacement (levothyroxine) 200mcg bolus IV then 100mcg PO daily
- T3 replacement (Liothyronine) 10mcg IV then 5mcg IV TDS
- Supportive care
What are the principles of managing HHS? What rate should the osmolarity and hypernatraemia be corrected at?
Osmolarity
- aiming for osmolarity of approx 300
- Correct at a rate of 3-8 mOsm/kg/hr
Hypernatraemia
- Aiming for normotraemia (<145)
- Aim to correct 10mmol/24hrs
