Endocrine

Question 1

Hyperkalemia

Answer 1

ECG changes:
K+ 5.5-6.5
- Peaked T waves - narrow
K+ 6.5-7.5
- Loss of P waves (merge with QRS)
K+ 7-8
- Widening QRS complexes (no bundle branch block pattern)
K+ 8-10
- Heart block
- “sine wave” ECG
- Asystole

Management:

Stabilize myocardial cell membrane:
* Calcium chloride (10%): 6.8 mmol (10ml) over 2-5 minutes
* Calcium gluconate (10%) 2.2mmol (10ml)

Shift potassium into cells:
* Sodium bicarbonate: 50-100mmol/L, over 5 minutes
* 50ml of 50% dextrose with 10 units of Actrapid insulin
* Salbutamol: 2-4 ×salbutamol nebs (5mg each)

Promote potassium excretion:
* Frusemide 40 to 80 mg IV
* Cation-exchange resin - Resonium
* Dialysis is ultimately the most effective clearance mechanism

Question 2

Hypercalcemia

Answer 2

Causes:

Hyperparathyroidism
Malignancy
Vitamin D toxicity
Granulomatous conditions - sarcoidosis
Drugs - thiazide diuretics
Thyrotoxicosis

Investigations:
1. Albumin OR ionised calcium
2. PTH
3. Vitamin D
4. PTH related protein
5. Specific causes - CXR for malignancy or sarcoidosis, Thyroid function for severe hyperthyroidism

Management:

Dilute serum calcium and promote diuresis and renal excretion
- Rehydration with IV fluids (0.9% NS, not hartmann’s) 4-6L over 24hr

Decrease calcium resorption from bone - inhibits osteoclast activity
- Bisphosphonates
Zoledronic acid 4mg IV
Pamidronate 60-90mg over 4hrs
- Calcitonin
Salcalcitonin 100IU IM/IV TDS

Decrease calcium resorption from renal tubule (enhanced elimination)
- Loop diuretics/furosemide – out of favour
- Calcitonin

Decrease calcium absorption from the gut
- Corticosteroids – prednisone 30mg daily (in malignancy and sarcoidosis)

Forcibly remove excess calcium from the circulation
- Haemodialysis
- EDTA administration (as chelating agent)

Question 3

Renal Stones

Answer 3

RISK FACTORS FOR KIDNEY STONES:
- obesity
- excess dietary meat (purine)
- excess dietary Na+
- family history
- gout (not pseudogout)
- bowel resection
- inflammatory bowel disease
- hyperparathyroidism (hypercalciuria)
- medications (loop diuretics)
- prolonged immobilization (hypercalciuria)
- neurogenic bladder

IMAGING:
- CT KUB
Advantages:
- readily available
- no contrast induced nephropathy
- assess alternative diagnoses
- adequately assess stone size and location (important for definitive management)
- can assess complications - hydronephrosis and pyelonephritis

Disadvantages:
- radiation exposure
- stone size measured on CT is 88% of actual size

Renal US:
- preferred in pregnancy
- no contrast nephropathy
- no radiation
- can assess hydronephrosis and pyelonephritis

Disadvantages:
- less sensitive and specific than CT
- may miss smaller stones <5mm

AXR:
- poor sensitivity and specificity
- stone size is magnified 20% (appears bigger than actual size)
- may be used to follow stone passage (rather than repeating CT)

MOST COMMON SITES OF OBSTRUCTION:
- uretero-pelvic junction
- the pelvic brim where the ureter crosses the pelvis and iliac vessels
- ureterovesical junction

INDICATIONS FOR ADMISSION:
- intractable pain and vomiting
- urosepsis
- single or transplanted kidney
- renal failure
- hypercalcemic crisis
- stone unlikely to pass (large >5mm, proximal above pelvic rim)
- urinary extravasation on scan
- significant co-morbidities/advancing age

“during acute obstruction, most patients have normal creatinine because the other kidney functions at 185% of its baseline capacity”

Question 4

DKA

Answer 4

Diagnosis:

blood gas:
pH < 7.3
HCO3- <18
BSL
Ketones in urine and blood

a)
fluid resuscitation
20ml/kg hartmanns iv

insulin infusion
50units actrapid in 50mils 0.9% NS
0.05-0.1unit/kg/hr

targets:
ketones drop 0.5mmols per hour
glucose drops 1-2mmol/hr
HCO3- rise 1-2mmol per hour

K+ >5.5 - can start insulin
K+ 3.5-5.5 - start insulin with K+ replacement
K+<3.5 - give potassium before starting insulin infusion
aiming for bsl drop of 1-2mmol/L/hr

replace electrolytes
- replace K+ 10mmol/hr
replace Mg+, PO4- if very low

start 10% dextrose infusion 125ml/hr IV when bsl <15mmol/L

monitor
- VBG hourly
- ketones hourly
- mental status hourly (cerebral oedema)
- urine output
- fluid status

thromboprophylaxis LMW heparin

Treat precipitant - infection - UTI/pneumoniae, pancreatitis, PREGNANCY, MI, insulin non-compliance, psycho-social issues,

Admit ICU

Question 5

DKA and Cerebral Oedema

Answer 5

seen mainly in paediatrics

altered mental status, reduced level of consciousness, seizures

Management:
stop iv fluids
head of bed up 45degs
manitol 1g/kg iv
3% hypertonic saline 2.5-5ml/kg

Question 6

Acid-base calculations

Answer 6

AG = Na+ - (HCO3- + Cl-)
normal AG = 12

expected CO2 = 1.5 x HCO3- + 8 (+/-2)

• Delta ratio = (change in anion gap) / (change in bicarbonate)
• This can reveal any mixed acid-base disorders
• Less than 0.4 = pure normal anion gap acidosis
• 0.4-0.8 = mixed high and normal anion gap acidosis
• 0.8-2.0 = pure high anion gap acidosis
• More than 2.0= high anion gap acidosis and a pre-existing metabolic alkalosis

Question 7

Thyroid Storm

Answer 7

Ref: Tintinalli’s

1)
Examination findings:
Fever, tachycardia, AF, hypertension
Goitre
Tremor
Diaphoresis
Palmar erythema
Hyperreflexia
Peritibial myxoedema
Lid lag
Exophthalmos
Ophthalmoplegia

2)
Primary causes:
graves disease - proptosis/exopthalmos
toxic multinodular goitre -
toxic adenoma -
thyroiditis - tender thyroid
hashimotos thyroiditis

Others:
drug induced - amiodarone
ingestion of thyroxine
iodine
metastatic thyroid cancer

3)
Diagnosis:

Burch and Wartofsky’s Diagnostic Criteria

Score of ≥45: Highly suggestive of thyroid storm.

1. Thermoregulatory dysfunction
     Temperature °C (°F)
      37.2–37.7 (5)
      37.7–38.3 (10)
      38.3–38.8 (15)
      38.9–39.4 (20)
      39.4–39.9 (25)
   ≥40 (30)
2. CNS effects
      Absent 0
      Mild (agitation) 10
      Moderate (delirium, psychosis) 20
      Severe (seizures, coma) 30
3. GI-hepatic dysfunction
      Absent 0
      Moderate (diarrhoe, N&V abdominal pain) 10
      Severe (unexplained jaundice) 20
4. CV dysfunction
     Tachycardia (beats/min)
      90–109 (5)
      110–119 (10)
      120–129 (15)
      ≥140 (25)
    
5. Congestive heart failure
      Absent 0
      Mild (pedal edema) 5
      Moderate (bibasilar rales) 10
      Severe (pulmonary edema) 15
6. Atrial fibrillation
      Absent 0
      Present 10

Management:

Oxygen - hypermetabolic state

Treat fever - paracetamol and ice packs

Restoring hydration
- Crystalloid 20ml/kg iv fluid bolus

Providing sedation for agitation
- Diazepam 5-10mg qid/prn

Others - glucose, multivitamins, thiamine, folate (depleted due to hypermetabolic state)

Control tachycardia and prevent rate-dependent heart failure:

• Propranolol 40-80mg QID orally
• Metoprolol 5mg iv over 2min, repeat every 5min (max 15mg)
• esmolol 500 mcg/kg IV Loading, followed by 50 mcg/kg/min infusion

Inhibition 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 peripheral conversion of thyroxine to triiodothyronine

Dexamethasone 4mg IV bd

AVOID aspirin - causes free thyroid hormone (displaces T4 from binding proteins)

Seek and treat precipitant:
- infection, MI, DKA etc

Definitive therapy:
- Radioactive iodine ablation therapy or surgery may be necessary.

Question 8

DKA vs HHS

Answer 8

History:
DKA - Known type 1 DM; discontinuation of or inadequate insulin therapy in DKA

HHS – history of type 2 DM +/- non-compliance

Age – DKA usually younger, HHS usually older

Presentation:

DKA evolves rapidly (24 hours)
HHS typically days-weeks with polydipsia, polyuria and weight loss.

Abdominal pain in DKA
Altered mental state more common in HHS

Kussmaul respiration / hyperventilation and ketotic breath in DKA

Laboratory features:

Degree of hyperglycemia:
HHS typical higher, exceeding 56 mmol/l; DHA usually< 44 mmol/l)

Degree of acidosis:
severe in DKA, mild in HHS

Anion gap acidosis present in DKA; absent (or mild in case of concomitant lactic acidosis) in HHS

Ketones: HHS small ketonuria, absent to low ketonaemia

Hyperosmolality more severe in HHS, typically > 320 mosm/l

Complications during treatment of HHS:
Hypoglycaemia
Hypokalaemia
Hypophosphataemia
Hypo or Hypernatremia
Pulmonary oedema
DVT and PE
Hyperchloraemic acidosis (usually not clinically significant)

Question 9

Hyponatremia

Answer 9

a) Tintinalli’s table

3 hypovolemic
- diuretics
- adrenal insuficiency (mineralcorticoid insuficiency)
- diarrhoea and vomiting

3 euvolemic
Psychogenic polydipsia
Glucocorticoid deficiency
Drugs - SSRI’s
SIADH

3 oedematous
- CHF
- liver cirrhosis
- nephrotic syndrome

b)
2ml/kg 3% NS IV
serum Na+115-120 and seizure terminates

**** rapid correction of chronic hyponatraemia can cause “OSMOTIC DEMYELINATION SYNDROME”

Question 10

Rhabdomyolysis

Answer 10

a) Ref Tintinalli’s table

CAUSES:

Trauma - crush injury
Ischemic - compartment syndrome
Environmental - heat stroke
Excessive muscular activity - extreme exercise (xfit)
Drug induced - statins causing myositis
Genetic disorder - fatty acid oxidation disorders
Drugs of abuse - methamphetamines

COMPLICATIONS:

renal failure
hyperkalemia
DIC
Hypocalcemia
Hyperphosphatemia

MANAGEMENT

72hr aggressive fluid resuscitation with 0.9% NS 4 mL/kg/h, with the goal of maintaining a minimum urine output of 3 to 4 mL/kg/h

“No prospective controlled studies have identified ideal fluid choice or demonstrated benefit from alkalinization of the urine with sodium bicarbonate or forced diuresis with mannitol or loop diuretics”

Manage hyperkalemia with calcium resonium 15g QID
Insulin and dextrose, sodium bicarbonate

Avoid neprhotoxins - NSAIDs

Consider dialysis