Diabetic Emergencies

18/07/2013 by admin | Endocrine

Diabetic ketoacidosis (DKA):

  1. Absolute insulin deficiency – occurs in DM T1 but NOT T2!
  2. Lack of insulin = hyperglycaemia (=osmotic diuresis and dehydration) = raised ketone levels = metabolic acidosis
  3. Precipitants: infection, missed insulin dose (hospital stay/psychological reasons), MI, trauma, undiagnosied DM T1
  4. p/c: thirst, polyuria, dehydration ( – even hypovolaemic shock), vomiting, abdo pain, tachycardic, tachypnoea and Kussmaul’s respirations (due to acidosis), decreased consciousness (normaltiredcoma), ketotic (peardrop) fetor on breath.
  5. Ix: BMs typically >20mmol/L, ketonuria, high urine potassium due to acidosis – but low body potassium, acidotic (= pH 7.0-7.2), decrease in bicarbonate (=due to acidosis usage) and dcrease in PCO2 as a result of hyperventilation
  6. Ix precipitant:microbiology, CXR, ECG, FBC, cardiac enzymes…
  7. Mx: fluid (3-5L in <6h), IV insulin (6 units), potassium replacement (10-20mmol/h) after initial insulin and fluid replacement (must be AFTER as risk of hypokalaemia – as insulin drives potassium into cells). May need bicarbonate, nasogastric tube inserted for gastoparesis. Tx underlying cause.
  8. Prognosis: need insulin longterm. Risk of mortality <5%

Hyperosmolar non-ketotic coma (HONK):

  1. Found in DM T2 but NOT T1!
  2. Insulin elevels are sufficient to prevent ketosis but insufficient to prevent hyperglycaemia
  3. Precipitants: infection, MI, sugary drinks
  4. p/c: thirst and polyuria – leading to progressive dehydration, impaired concentration levelscoma, hyperviscosity (=thrombotic complications=DVT/stroke)
  5. Ix: glucose often very high >50mmol/L, sodium often >160mmol/L, plasma osmolality is increased, acidosis is absent/mild. Urine = no ketones, but high glucose
  6. Ix of precipitant: ECG, cardiac enzymes, microbiology
  7. Mx: central venous monitoring in elderly/cardiac disease patients, IV fluids +/- potassium replacement. IV insulin 3units/h, anticoagulation.
  8. Prognosis:mortality is very high 20-40%. If they survive, can be managed in the future with their normal hypoglycaemic agents

 

Lactic acidosis:

  1. Rare complication of metformin treatment
  2. p/c: similar to acidaemia = malaise, anorexia, vomiting, hyperventilation (Kussmaul’s resps), normal glucose levels, no ketones in urine, an ABG shows profound acidosis with high base excess. Increased anion gap.
  3. Tx: supportive and withdraw metformin!

 

Hyperprolactinaemia:

  1. More obvious in women than men
  2. Women p/c: menstrual disturbance or infertility, galactorrhoea (in 30-80%)
  3. Men p/c: galactorrhoea (<30%), erectile dysfunction, infertility, features of macroadenoma and mass effect
  4. Ix:
    1. o Prolactin levels can be very high.
    2. o If pathology is microadenoma – full assessment of anterior pituitary function is needed

 

Microprolactinoma:

  1. Women tend to present earlier due to clearer symptoms – due to earlier presentation – women are more likely to have microprolactinoma (caused by stress, renal failure, hypothyroidism, PCOS, pregnancy, lactation, seizures – rule these causes out early).
  2. Mx of prolactinomas:
  3. Drugs: dopamine agonists (=bromocriptine, cabergoline) inhibit prolactin secretion and cause tumour shrinkage. s/e: N&V, postural hypotension
  4. Surgery: trans-sphenoidal removal if drug intolerance – or if failure to shrink with dopamine agonists
  5. RT: prevent re-growth after drug or surgical tx.

 

Acromegally:

  1. Prolonged excessive GH secretion in adults (excessive GH in children = gigantism)!
  2. Extremely rare: 5/mil. M=F. 40-60yo.
  3. Underlying pathologies include:
    1. o Benign pituitary tumour (macroadenomas more common than microadenomas)
    2. o Pituitary carcinoma (v rare)!
    3. o GH-releasing hormone (GHRH) secreting carcinoid tumour (v rare)!
  1. Pathophysiology: results from insulin-like growth factor (IGF-1) which mediates the effects of GH = increased sweating, headache, tiredness, lethargy, joint pains, pituitary fossa mass effects (=visual field defects, hypopituitarism).
  2. O/E: characteristic facial appearance (=course, frontal bossing, large sinuses, large tongue, prognathism, separation of teeth), deep voice, carpal tunnel syndrome, hand and foot enlargement and organomegally (=goitre, HSM).

 

  1. Complications: CVD and mortality from HTN, impaired glucose tolerance and DM (in 10%). Cardiac failure, IHD, CVA, obstructive sleep apnoea, colonic polyps, carcinoma, osteoporosis, joint disease (in 50%)
  2. Ix:
    1. o Lab: IGF-1 is high, GH is not supressed by oral glucose
    2. o MRI scan of pituitary and visual field assessment
  3. Tx: aim is to normlaise GH and reduce associated high mortality
    1. o Surgery:
    2. Trans-sphenoidal adenomectomy or craniotomy for very large tumours
    3. Pituitary RT: if tumour not fully removed – useful to reduce growth
    4. o Drugs:
    5. Somatostatin analogues (=octreotide, lanreotide) suppress GH in 60%
    6. Dopamine agonists (=bromocriptine, cabergoline) lower but rarely normalise GH 
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