Renal,Endocrine & metabolic emergencies Flashcards
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 depression
In 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
What can trigger a thyroid storm?
- trauma
- infection
- surgery
- stroke
What are the complications of hyperthyroidism?
CKS NICE
- Graves orbitopathy
- thyroid storm
- atrial fibrillation
- heart failure
- anxiety/depression
What are the clinical feeatures of a thyrotoxic storm?
tachycardia, fever, atrial fibrillation, heart failure, fever, diarrhoea, vomiting, dehydration, jaundice, agitation, delirium, and coma
What are the endocrine causes of hypertension?
- Conn’s syndrome
- Cushing’s syndrome
- Pheochromocytoma
- Acromegaly
- Hyperthyroidism
What is a pheochromocytoma?
A rare tumour of the adrneal medulla that secretes catecholamines
What are the clinical features of pheochromocytoma?
paroxysmal clinical features of:
headache profuse sweating palipations tremor flushing hypertension postural hypotension hyperglycaemia
WHat drug can you prescribe in the short term management for treating pheochromocytoma while the patient is awaiting definitive surgical management?
Phentolamine which is a short acting alpha blocker
In a patient with hypercalcaemia:
What blood tests will you request to differentiate from the causes of primary hyperparathyroidism ( or tertiary )
vs
malignancy or other causes of hypercalcaemia?
High calcium and high PTH = primary or tertiary hyperparathyroidism
High calcium and low PTH = malignancy or other rarer causes