Renal,Endocrine & metabolic emergencies Flashcards
(32 cards)
What are the causes of Metabolic alkalosis
- GIT excess acid loss
* Vomit (and pyloric stenosis)
* NGT drainage
* Diarrhoea
* Ileostomy
* Dehydration - Renal excess acid loss
* Bartter syndrome
* Gitelman syndrome
* Diuretics (Loss of H+, K+, Cl-) - Overdose of base
* Antacid OD, Laxative, Milk-alkali syndrome
* Massive Hartmann’s transfusion
* Iatrogenic use of HCO3 - Endocrine
* Cushing syndrome
* Steroid excess
* Hyperaldosteronism
What 5 clinical and lab features are key in diagnosing hyper-osmolar hyperglycaemic state
- Hypovolaemia
- Marked hyperglycaemia (30 mmol/L or more) without *significant hyperketonaemia or ketonuria
- Absence of academia (7.3, bicarbonate >15 mmol/L)
- Osmolality usually 320 mosmol/kg or more
what 3 medical treatment options would you consider in treatment of HHS?
- IV fluid = 0.9% normal saline 3-8 litres in th 1st 24 hours
- Insulin low dose fixed rate ( 0.05units/kg/hr )
- thromboprophylaxis ( due to
What important potential complications would you look for when treating HHS?
- electrolyte abnormalities- du to rapid correction of hyperglycaemia - can develop hypoglycaemia, hypokalaemia, hyponatraemia therefore cerebral oedema
- The severe dehydration results in increased blood viscosity and potential thromboembolic disease:
give 3 complications of over - aggressive treatment of HHS?
- fluid overload - cardiac failure
- cerebral oedema
- central pontine demyelination syndrome
A patient presents with a tonic-clonic seizure - Biochemistry shows hyponatraemia 108mmol/L - how will you treat this patient in the ED?
give 150 ML of 3% hypertonic saline by IV infusion over 20 minutes.
then check plasma soidum and you can repeat the bolus 1-2 times untill rise of 5mmol.l plasma sodium ( no more )
What are the causes of SIADH?
Neuro- tumour, trauma, SAG, CNS infection
Endo- addison’s , hypothyroidism
Drugs - lithium,haloperidol, opiates, carbamazepine
Pulmonary - Pneumonia, TB
What are the NICE 2015 recomendations for acute admission of a patient with renal colic?
- The person is in shock or has fever or other signs of systemic infection.
- The person is at increased risk of acute kidney injury, ( if there is a solitary or transplanted kidney, pre-existing chronic kidney disease, or bilateral obstructing stones are suspected. )
- The person is pregnant.
- The person is dehydrated and cannot take oral fluids due to vomiting.
- There is uncertainty about the diagnosis.
- There is no response to symptomatic treatment within 1 hour (or sooner depending on clinical judgement), or there is a rapid recurrence of severe pain.
What are the main causes of hypercalcaemia?
Resource:
https://www.rcem.ac.uk/docs/External%20Guidance/
10R.%20Acute%20Hypercalcaemia%20-%20Emergency%20Guidance%20
(Society%20for%20Endocrinology,%20Jan%202014).pdf
90% of the time it is caused by :
- malignancy
- primary hyperparathyroidism
other causes:
- tertiary hyperparathyroidism
- thyrotoxicosis
- therapies i.e. thiazides, lithium,
- renal failure
- acute adrenal failure ( adrenal insufficiency )
- hypervitaminosis A
- hypervitaminosis D
- milk alkali syndrome
- myeloma
Treatment options for hypercalcaemia?
1st Rehydration:
- Intravenous 0.9% saline 4-6 litres in 24h
After Rehydration IV Biphosphonates
- Zoledronic acid 4mg over 15 mins
Second Line Options:
- Glucocorticosteroids
Other considerations:
Parathyroidectomy
What are the complications of hyperthyroidism?
as per CKS NICE
1. Grave's orbitopathy ( 5% have risk of visual
impairment )
2. thyrotoxic crisis
3. atrial fibrillation
4. heart failure
5. reduced bone mineral density
6. anxiety and depressionIn a thyrotoxic crisis.
Name the 3 drugs that can be used and briefly explain their mechanism of action?
- beta- blocker : propanolol 80 mg po
( symptomatic treatment of adrenergic symptoms i.e. tremor and palpitations) - high dose carbimazole: 45-60mg/day
( decreases thyroid hormone synthesis ) - potassium iodide 200mg IV over 1 hour
( blocks the release of thyroid hormone ) - propylthiouracil
What are the signs of hypothyroidism ?
- puffy facial appearance
- apathetic facial appearance
- facial pallor
- dry skin
- thinning of the har
- loos of the outer 1/3 of eyebrows
what are the biochemical features of addisonian crisis?
- hyponatraemia
- hypoglycaemia
- low PH - metabolic acidosis
- hyperkalaemia
- hypercalcaemia
- increased urea
- Increased ACTH
Can you please EXPLAIN the causes of hypoglycaemia?
EXPLAIN pneumonic
EX - Exogenous drugs ( alcohol, insulin )
P - Pituitary insufficiency
L - Liver Failure
A - Addison’s disease
I - Infection ( malaria, sepsis ) Insulinoma’s
N - Non- pancreatic tumours ( as some release insulin
like peptides )
- What is the commonest cause of hyperthyroidism?
- and what is the commonest cause of Addison’s disease?
- What is the commonest cause of hypothyroidism?
- Autoimmune thyroiditis
- Autoimmune adrenalitis
- Hashimoto’s thyroiditis
WHat 3 blood tests would you perform if you suspect addiosnian crisis?
- synacthen test ( cortisol will be low )
- Plasma ACTH ( which will be raised )
- Plasma renin levels
What 2 clinical signs are specific for Grave’s Thyroid disease?
- pretibial myxoedema
2. exopthalmos
What are the features of HHS that would make you consider it as the diagnosis?
- hypovolaemia
- marked hyperglycaemia ( > 30mmol/L ) WITHOUT
significant ketonaemia < 3 mmol/L OR acidosis
PH >7.3 or HCO3 >15mmol/L - high serum osmolality > 320mOSmol/kg
What are the complications of HHS ?
VTE stroke seizures cerebral oedema CPM ( central pontine myelenosis myocardial infarction Dehydration AKI
What are the causes of a raised Osmolar gap?
- HHS
- alcohols: ethanol, methanol, ethylene glycol
- Manitol
- lorazepam infusion
What would you check for in DKA to ascertain resolution of DKA?
monitor hourly glucose and ketones and check that the concentrations fall by
3mmol/L/Hour - for glucose AND
0.5mmol/L/Hour - for ketones
According to the JBDS IP Group 2013 guidelines on managing DKA in adults -
what are the markers for severe DKA?
The presence of one or more of the following may indicate severe DKA.
- Blood ketones over 6mmol/L
- Bicarbonate level below 5mmol/L
- Venous/arterial pH below 7.0
- Hypokalaemia on admission (under 3.5mmol/L)
- GCS less than 12 or abnormal AVPU scale
- Oxygen saturation below 92% on air (assuming normal baseline respiratory function)
- Systolic BP below 90mmHg
- Pulse over 100 or below 60bpm
- Anion gap above 16 [Anion Gap = (Na+ + K+) – (Cl- + HCO3-) ]
What are the metabolic treatment targets in DKA?
The recommended targets are:
• Reduction of the blood ketone concentration by
0.5mmol/L/hour
• Increase the venous bicarbonate by 3.0mmol/L/hour
• Reduce capillary blood glucose by 3.0mmol/L/hour
• Maintain potassium between 4.0 and 5.5mmol/L
