Endocrine & Electrolytes Flashcards
Endocrine Emergency - Thyroid Storm
2023.1 Case Based Discussion
Assessment and management of an unstable patient with an endocrine emergency
Interpret ECG
History:
- known thyroid disease
- non-compliance with medication
- overdose on thyroxine
-
Identify Precipitants
EM crit episode on thyroid storm
DIFFERENTIAL DIAGNOSES:
- Sepsis
- Heat stroke
CLINICAL FEATURES:
- hyperthyroidism
- fever
- altered mental state
- sympathetic surge (tachycardia, hypertension)
High output cardiac failure with acute cardiogenic shock
Precipitating Event:
- medication non-compliance
- pregnancy
- infection
- surgery
High mortality
EXAM FINDINDS:
Goitre
Thyroid scar
Tremor
Palmar erythema
Pretibial myxoedema
Fever
Tachycardia
AF
High output heart failure with pulmonary oedema
Ophthalmoplegia
Proptosis
Lid-lag
Altered mental status
Agitation, delirium, psychosis, Hyperreflexia
Clonus
PRIMARY CAUSES:
Graves disease (proptosis/exopthalmos)
Toxic multinodular goitre -
Toxic adenoma -
Hashimotos thyroiditis (tender thyroid)
Others:
drug induced - amiodarone
exogenous thyroxine
DIAGNOSIS:
Burch and Wartofsky’s Diagnostic Criteria:
- Temp
- CNS effects
- CVS dysfunction
- GI dysfunction
INVESTIGATIONS:
ECG - AF with RVR
TSH, T3, T4
Septic screen:
- Urinalysis
- CXR
MANAGEMENT:
OXYGEN - hypermetabolic state
FLUID RESUSCITATION
- Crystalloid 20ml/kg iv fluid bolus, repeat until intravascular volume repleted as per POCUS assessment of IVC
INHIBITION OF THYROID HORMONE SYNTHESIS:
Propylthiouracil 600mg loading then 200mg qid PO/PR (preferred because in high doses it also blocks conversion of T4 T3)
Carbimazole 20mg qid orally
both are used in pregnancy
INHIBITION OF THYROID HORMONE RELEASE:
Iodine 5% + potassium iodine 10% (Lugol solution) – 0.5ml tds
PREVENTING CONVERSION OF THYROXINE TO TRIIODOTHYRONINE:
coexisting adrenal insufficiency
Dexamethasone 4mg IV bd
CONTROL TACHYCARDIA AND PREVENT RATE-DEPENDENT HEART FAILURE:
Propranolol 40-80mg QID orally
(also blocks peripheral conversion of T4 to T3)
- Target HR 100
- Esmolol 500 mcg/kg IV Loading, followed by 50 mcg/kg/min infusion
- Metoprolol 5mg iv over 2min, repeat every 5min (max 15mg)
TEMPERATURE CONTROL:
- paracetamol and ice packs
TREAT AGITATION:
- diazepam 5-10mg QID/PRN
Seek and treat precipitant:
- infection, MI, DKA etc
DEFINATIVE THERAPY:
- Radioactive iodine ablation therapy or surgery may be necessary.
DISPOSITION:
- ICU with endocinology input
Endocrine Emergency - Hypothyroid Myxoedema
CLINICAL FEATURES:
- elderly women
- lethargy/decline
- hypoactive delirium
- non-pitting oedema
- bradycardia
- hypothermia
- macroglossia
- hair thinning
- leathery skin
PRECIPITANTS:
- Non-compliance with thyroxine
- Infection
- Surgery
- MI
- Stroke
- Iodine contrast (suppress thyroid)
- GI bleeding
- cold exposure
EXAMINATION:
Thyroidectomy scar
Non-pitting oedema - face
Macroglossia
Alopecia
POCUS - massive pericardial effusion (don’t often tamponde because they are chronic, they usually resolve with treatment of hypothyroidism)
INVESTIGATIONS:
ECG - bradycardia, prolonged QTc, low voltage complexes due to pericardial effusion
BSL - hypoglycemia
TSH high, T4
Electrolytes - hyponatremia
FBC - leukopenia
Sepsis is common precipitant - perform septic screen:
- Urinalysis
- CXR
MANAGEMENT:
co-existing adrenal insuficiency - give hydrocortisone first!
Hydrocortisone 100mg IV first!
Levothyroxine 300mcg IV over 30min
Add T3 (iiothyronine) 20mcg IV over 30min if no improvement in 24hrs
Fluid resuscitation:
Hartmanns 250ml IV boluses until intravascular volume repleted as per POCUS assessment of IVC
- hartmann’s is more isotonic to the patients serum which is appropriate in the setting of hyponatremia
Vasopressors:
Noradrenaline 10mcg/kg/hr
Target MAP 65-70
Rewarming:
- bair huggers
- warm blankets
- warmed IV fluids
- humidified oxygen
Treat hypoglycemia:
- 10% dextrose 2ml/kg IV over 20min
- 5% dextrose infusion 125ml/hr
Treat hyponatremia:
- NBM
- still need to fluid resuscitate patients
Pericardial effusion:
- chronic, don’t tend to tamponade
- will improve with treatment of hypothyroidsm
- prone to bleeding so pericardiocentesis is not advised
Treat Precipitant:
Infection is a common precipitant. Treat with broad spectrum antibiotics
Disposition:
ICU
Refractory Shock - Endocrine emergency
pan hypopituitarism - previous pituitary surgery for adenoma
pituitary tumours - compress optic chiasm and cause bitemporal hemianopsia
EM Board Bombs ep 220
Reference: Tintinalli’s
Adrenal Crisis/adrenal insuficiency
Primary:
- Addison’s (autoimmune)
- drugs (etomidate, ketaconazole)
- Infection (TB)
- Surgery (adrenalectomy)
- Tumours (metastatic disease)
- Hereditary (congenital adrenal hyperplasia)
Secondary:
“suppression of hypothalamus-pituitary-adrenal axis”
- prolonged glucocorticoid use
- brain tumours
- pituitary apoplexy (haemorrhage or necrosis)
- CNS infections/meningitis (TB, HIV)
Pathophysiology:
Adrenal cortex produces steroids:
- glucocorticoids (cortisol)
- mineralcorticoids (aldosterone)
- sex hormones
Adrenal medulla produces catecholamines:
- adrenaline
- noradrenaline
- dopamine
CLINICAL FEATURES:
hyperpigmentation due to high ACTH
Cortisol deficiency symptoms:
- hypotension refractory to vasopressors
- abdominal pain
- nausea and vomiting
- confusion, disorientation, lethargy
- weight loss
Mineralocorticoid (aldosterone) deficiency symptoms include:
- dehydration
- syncope
- salt craving
- hypotension (usually orthostatic).
Gonadocorticoid deficiency symptoms are observed more in women, who present with
- decreased axillary and pubic hair and decreased libido.
Differential Diagnoses for refractory shock:
- hypothyroid myxoedema
- B-blocker overdose
- calcium channel blocker overdose
- sepsis
- anaphylaxis
- hypocalcemia
- cardiogenic shock
- occult bleeding, severe
Lab findings:
- hypoglycemia
- hyponatremia
- hyperkalemia
- renal impairment
- NAGMA
- low bicarbonate
ECG findings are due to hyperkalemia
Management:
hydrocortisone 100mg IV, followed by hydrocortisone 50mg IV Q6h (eTG)
treat hypoglycemia 2mg/kg 10% dextrose, then infusion 5% dextrose 125ml/hr (target bsl <4mmol/L)
treat hyperkalemia
Hyponatremia –> status epilepticus
2022.1 VBG Teaching Station
21yr old male suffered a seizure at the night club
Interpret the VBG
pH = 7.04
pCO2 = 47
BE = -18
HCO3 = 13
Creatinine = 52
Lactate = 10.7
Na+ = 110
K+ = 2.6
Cl- = 73
Glu = 2.0
Medical Expertise: Assessment (40%)
* Correctly interprets the results of an investigation within the scenario
* Creates and explains a focused investigation plan that confirms or excludes time critical
diagnoses
* Formulates a provisional diagnosis to match the immediate issues.
Medical Expertise: Management (30%)
* Correctly chooses time critical interventions based on assessment
* Initiates treatments specific to identified abnormalities in airway and/or ventilation
* Initiates treatments specific to identified neurological pathologies
* Creates an appropriate ongoing reassessment and management plan.
Prioritisation and Decision Making (30%)
* Highlights high-risk features identified during initial patient assessment
* Prioritises chosen treatment options to create an appropriate escalating treatment plan
* Prioritises essential components of ongoing assessment of any patient in the emergency
department
* Provides a rationale to explain decisions about ongoing assessment, treatment and
disposition decisions.
Candidates were required to meet with a registrar and to:
* review the results of the VBG provided
* discuss the assessment and management of the patient
* answer any further questions from the registrar.
DIFFERENTIAL DIAGNOSES:
Metabolic:
- hypoglycemia
- hyponatremia
Toxins:
- TCA overdose
Withdrawal
- alcohol or drugs
Trauma:
- head injury
Intracranial haemorrhage
Infection:
- meningitis/encephalitis
Stroke:
- ischemic or haemorrhagic
Malignancy:
- brain tumour
ASSESSMENT:
History:
Examination:
Investigations:
MANAGEMENT:
Airway manouvres - chin lift + jaw thrust, OPA +/- NPA
High flow oxygen 15L NRBM
Treat hypoglycaemia with 2ml/kg 10% dextrose IV until BSL >4 mmol/L
TREAT HYPONATRAEMIA:
- 2ml/kg 3% NS IV (100ml IV over 10min)
serum Na+115-120 and seizure terminates
First line agents
- Midazolam5-10mg IM/IV (0.2mg/kg)
- Diazepam 10-20mg IV over 2-5 mins (0.1-0.3mg/kg)
Second line agents
- Sodium valproate 20mg/kg up to 3g followed by infusion (avoid in pregnancy)
- Levetiracetam 40mg/kg up to 4.5g over 15 min
- Phenytoin 20mg/kg IV over 20min– need cardiac and BP monitoring
Third line agents
- Phenobarbitone 20mg/kg IV
- RSI and intubate with thiopentone 5mg/kg and suxamethonium 1.5mg/kg
COMPLICATIONS:
- aspiration
- trauma (eg posterior shoulder dislocation)
- non cardiogenic pulmonary oedema
- rhabdomyolysis
- acidosis
- kidney failure
- hyperthermia
Hyponatraemia
2023.1 Teaching Station
In this station candidates were required to help a junior doctor interpret blood results,
provide a list of differential diagnoses, and outline an approach to further investigation and
management of this patient.
True hyponatremia?
- pseudohyponatremia
- hyperglycemia
Causes:
- hypervolemic
- euvolemic
- hypovolemic
Management:
Correct hypotension/replace intravascular volume
- hartmann’s solution (more isotonic to patients serum)
Treat neurological emergencies
- 3% hypertonic saline
- OR sodium bicarbonate
Prevent worsening hyponatremia
- fluid restriction
Prevent overcorrection/osmotic demyelination syndrome
- monitor Na+
- slow increase 6-8mmol/day
- monitor urine output, if >100ml/hr check urine osmolality and Na+. if urine osmolality <100 –> give vasopressin
Osmotic demyelination syndrome:
- presents 7 days after rapid overcorrection
- symptoms depend on brain structures affected
- most commonly affects pons, cerebellum, basal ganglia
- symptoms include ataxia, quadriplesia, cranial nerve palsies, ‘locked in syndrome’
IS THIS TRUE HYPONATREMIA?
Pseudohyponatremia if high triglycerides >17mmol/L
Low Na+ reading with hyperglycaemia due to shift of water out of cells. Think DKA/HHS.
Formula for corrected NA+:
= measure Na+ + (0.3 x glucose) - 5.5
HYPERVOLEMIA: “oedematous states)
- heart failure
- liver cirrhosis
- kidney failure
- nephritic syndrome
EUVOLEMIA:
SIADH - retain water, low serum osmolality
- Drugs (SSRI’s - sertraline, SNRI’s - venlefaxine, anticonvulsants - carbamazepine)
- cerebral pathology (stroke, malignancy, abscess)
- pulmonary pathology (pneumoniae, PE, malignancy)
- malignancy-associated (tumours produce ADH like hormone)
psychogenic polydipsia
hypothyroidism
HYPOVLEMIA: ‘water losing state’
- diarrhoea and vomiting
- diuretics (thiazides)
- adrenal insufficiency (addison’s disease)
Burns
Usually asymptomatic when mild.
Chronic hyponatraemia is usually better tolerated than acute hyponatraemia.
HISTORY:
Symptomatic hyponatremia:
- Confusion
- Irritability
- Unsteady on their feet
- Reduced level of consciousness/somnolence
- Seizures
Diarrhoea or vomiting
Drinking lots of water or alcohol
Symptoms of pulmonary pathology - cough, fever, SOB, chest pain
Symptoms of cerebral pathology - headaches, focal neurological deficits - weakness, parasthesia
Constitutional symptoms of malignancy - unintentional weight loss, night sweats
PMHx:
- nephrotic syndrome
- liver cirrhosis
- heart failure
- brain or lung malignancy
Medications:
- SSRI’s, anti-epileptics
- diuretics
- long term oral or inhaled steroids (adrenal insuficiency)
EXAMINATION
Perform assessment of FLUID STATUS to determine cause:
CLINICAL:
- tachycardia, hypotension, postural hypotension >20mmHg
- dry mucous membranes
- reduced skin tugor
- JVP
- sternal capillary refill
- displaced apex beat (over filled)
- 3rd heart sound (over filled)
- crackles in bases (pulmonary oedema in overload)
- peripheral oedema
- shifting dullness in ascites
POCUS:
IVC:
- a flat IVC <1.5cm that completely collapses during inspiration vs. plethoric or dilated IVC <2.5cm that does not collapse
LV - hyperdynamic
Eye - papilloedema, optic sheath diameter >5mm
Ascites
GCS and neurological exam - focal neurological defits
Cardiovascular examination
Respiratory examination
Abdominal examination
INVESTIGATIONS:
SIADH
- serum Na+ < 130 mmol/L
- serum osmolality < 275 mmol/kg
- urine osmolality > 100 mmol/kg
- urine sodium > 30 mmol/L.
Triglycerides - pseudohyponatremia
Glucose - hyperglycemia
UEC - renal failure, high K+ in adrenal insuficiency
LFTs - liver cirrhosis (albumin)
TSH - hypothyroidism
CXR - pneumoniae, malignancy
CT brain - suspect cerebral pathology (infarction, abscess, tumour), assess for cerebral oedema (sulcal effacement)
MANAGEMENT:
Treat immediate life threats:
- cerebral oedema
- coma
- brain herniation
- seizures
sodium chloride 3% 100 mL IV over 10 minutes. Repeat as needed up to a maximum of 3 infusions.
Alternative is sodium bicarbonate 1amp over 10min
Restore intravascular volume:
- the brain, kidneys and heart need to be perfused
- 250-500ml Hartmann’s IV (Hartmann’s is more isotonic to the patients serum than 0.9% NS)
Hartmann’s = Na+ 128mmol/L
0.9% NS = Na+ 154mmol/L
Avoid worsening hyponatraemia:
- fluid restriction or NBM
- stop inciting agents
- treat underlying pathology
Avoid over-correction of Na+:
- monitor Na+ and urine output
- aim 6mmol per day in those with minimal symptoms
- aim 6mmol in the the first 6hrs in those with severe symptoms
Correct hypokalemia
- this will improve Na+ correction
- 40mmol in 1L hartmann’s rate 50ml/hr
Rapid correction can cause central pontine myelinosis AKA osmotic demyelination syndrome (permanent neurological injury)
Disposition ICU
Euglycemic DKA
2022.2 Teaching VBG to junior doctor
Pt. has euglycaemic DKA
SGLT2 inhibitors - end in “flozin”
Renal Failure
2023.1 Data analysis: Renal function
Discuss with a junior doctor, the
interpretation of blood results showing renal failure in a patient with significant prior medical
history.
*Review and interpret the available blood results.
*Formulate a differential diagnosis.
*Outline your approach to ongoing management.
The indications for dialysis for rhabdomyolysis are the same as for any patient with AKI “AEIOU”
Acidemia – pH<7.1 despite medical management
Electrolyte abnormalities – hyperkalemia refractory to medical management
Ingestion – nephrotoxic drug ingestion amenable to dialysis
Overload – volume overload resulting in respiratory failure
Uremia with bleeding, pericarditis or encephalopathy
PRE-RENAL CAUSES: (90%)
- Hypovolemia
- diuretics
- vomiting/diarrhoea
- haemorrhage
- third spacing
- Shock
- cardiogenic shock
- septic shock
- Cardiorenal syndrome
- Hepatorenal syndrome
- Abdominal compartment syndrome
- Hypertensive emergency
- Thrombotic thrombocytopenic purpura & hemolytic
uremic syndrome
INTRINSIC CAUSES:
*Nephritic syndrome - “can’t miss” diagnosis is NEPHRITIC SYNDROME
nephritic syndrome presents with high cr, hypertension, haematuria and proteinuria
*Nephrotoxic medications
- ACEi & Angiotensin receptor blockers (ARBs)
- NSAIDs
- Gentamicin
- Amphotericin
*Acute Tubular Necrosis (ATN)
- rhabdomyolysis
- hemolysis
- tumor lysis syndrome
*Renal thrombosis
POST-RENAL CAUSES:
*BPH (most common)
*Bilateral renal calculi or renal calculi in solitary kidney
*Pelvic mass causing bilateral ureteric obstruction
EXAM:
Pulmonary oedema
Peripheral oedema
Fluid status assessment
Shocked state
POCUS:
- absence of ureteral jets entering the bladder
- hydronephrosis
- pulmonary oedema
- IVC assessment
INVESTIGATIONS:
VBG - hyperkalemia and metabolic acidosis
post void bladder scan - to check for obstructive nephropathy
Urinalysis - blood, protein (nephritis)
USS renal or CT KUB
- pelvic mass causing bilateral ureteric obstruction
MANAGEMENT:
Get a VBG to rule out the 2 immediate life-threats
*Hyperkalemia – get ECG
*Severe acidosis
Can trial fluids if:
- no blood or protein on urine dip
- no pulmonary oedema
- no peripheral oedema
Hartman’s is recommended over NS
- avoids hyperchloremia metabolic acidosis which worsens hyperkalemia
IDC to measure UO
Furosemide if pulmonary oedema or peripheral oedema
norepinephrine is the first line vasopressor in patients with AKI and septic shock.
Sodium bicarbonate for severe metabolic acidosis as a temporising measure until dialysis
Generally safe to delay dialysis for 1-2 days
INDICATIONS FOR DIALYSIS:
“AEIOU”
A - Acidosis pH <7.1
E - Electrolytes hyperkalemia + causing arrythmias, refractory to medical therapy
I - Intoxication with nephrotic medication amenable to dialysis
O - Overload Pulomonary oedema with respiratory failure
U - ureamia with pericardial effusion, encephalopathy, bleeding
HHS
Clinical features:
- T2DM
- Older
- medication non-compliance
- typically develops over days-weeks with polydipsia, polyuria and weight loss.
- altered mentation
- very high BSL >30
- pH normal
- ketones low or none
- serum osmolality >320
pH >7.3
HCO3 >18
Ketones <3
BSL >33
Serum osmolality >320
MANAGEMENT:
Hartmann’s 1L stat
250ml/hr
Replace K+ 20mmol in 1L over 2 hours
Start insulin infusion 0.05u/kg/hr once K+ 5
BSL <15 –> Start 5% dextrose 125ml/hr
IDC and monitor UO
DVT prophylaxis 40mg clexane sc
decrease bsl by 5mmol/hr
decrease osmolality by 3mosm/hr
Seek and treat precipitant
Common causes include “The 5 I’s”:
Infection:
- pneumonia
- UTI
- skin
- abdominal
Infraction
- MI
- stroke
- bowel infarction)
Infant on board (pregnancy)
Indiscretion (dietary nonadherence)
Insulin deficiency (insulin pump failure or nonadherence)
In addition, common drugs that can trigger DKA include glucocorticoids, diuretics and atypical antipsychotics.
Congenital Adrenal hyperplasia
18month old girl with hypoglycemia 1.4 and altered menation
MANAGEMENT:
oral glucose load 30g or 250mls sugar drink - soft drink or juice followed by sandwich or banana
glucagon IM
<25kg 0.5units (1/2 vial)
>25kg 1unit (1vial)
10% dextrose 2ml/kg IV
DIFFERENTIAL DIAGNOSIS
Congenital adrenal hyperplasia:
- hyperpigmentation
- ambiguous genitalia in females
- refractory shock
Infection - sepsis from any cause
Hyperinsulinism - islet cell adenoma
Non-accidental injury:
- Exogenous insulin - Münchausen by proxy
Toxicological - accidental ingestion of sulphonyurea (glipizide) or beta blocker
Hypothyroidism
Inborn errors of metabolisms
Decreased glucose supply:
- poor feeding
- malabsorption
- poor glycogen stores (liver disease)
Accelerated starvation ketosis
