Diabetic Emergencies

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Diabetic Emergencies

• Emergency Block

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Diabetic Emergencies

• Diabetes Ketoacidosis (DKA)
• Hyperosmolar Non Ketotic (HONK)
• Hypoglycaemia

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Objectives

• Recognise diabetic ketoacidosis.
• Participate in the management of diabetic
  ketoacidosis.
• Recognise Hyperosmolar Non ketotic state
• Recognise and manage hypoglycaemia.

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Diabetic KetoacidosisPathophysiology

• Severe insulin deficiency leads to uncontrolled
  catabolism.
• Increased hepatic glucose production, decreased
  peripheral uptake of glucose increased blood
  glucose leading to osmotic diuresis.
• Rapid lipolysis leads to ketone body formation
  metabolic acidosis.

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Pathophysiology

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Who gets DKA?

• Hallmark of type 1 diabetes (insulin
  insufficiency)
• Previously undiagnosed DM (about 25 30)
• Interruption to normal insulin regime
• Intercurrent illness - usually infection

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Symptoms and signs

• Nausea
• Vomiting
• Abdominal pain
• Often preceding polyuria, polydipsia, weight loss
• Drowsiness/confusion/coma (severe)
• Kussmaul respiration - hyperventilation
• Pear drops breath
• Sign of associated systemic illness (MI,
  infection, etc)

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How do I diagnose DKA?

• Diagnosis requires all 3 of the following
• High blood sugar (i.e diabetes) Glucose gt 11 mmol
• Finger-prick blood glucose can be normal
• Ketones (blood or urine )
• Acidosis (pHlt7.30 or HCO3lt15mmol)

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Investigations

• Bloods
• FBC, UE, HCO3, LFT, CRP, glucose, blood
  cultures, amylase, cardiac enzymes.
• Urine
• Ketones, MSU
• ABG
• Initially only (lab HCO3 after)
• CXR (if you suspect chest infection)
• ECG

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Example ABG

• Patient 1
• pH 7.35
• pCO2 3.2
• pO2 16.0
• HCO3 16.1

• Patient 2
• 7.1
• 2.1
• 9.1
• 11.2

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Treatment priorities

• ABC if impaired consider early ITU input /
  central venous access
• Resolution of ketonaemia
• Replace fluids
• Replace electrolytes
• Replace insulin
• Look for cause
• Close monitoring
• Consider Low molecular weight heparin

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Replacing fluids

• Initial management
• 1L 0.9 NaCl
• 30 mins
• 1hr
• 2hr
• 4 hr
• Then continue NaCl 0.9 as dictated by fluid
  status
• beware of elderly patients

• Later
• Once blood glucose lt14 mmol/L give 10 dextrose
  alongside 0.9 Normal Saline at 125ml / hour

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Replace electrolytes

• K is most important
• Insulin shifts K into cells therefore K will
  fall as rehydrate
• Serum K 5.5
• No potassium supplement
• Serum K 3.5 - 5.4
• Add 20mmol per litre
• Serum K lt3.5
• Add 40mmol per litre
• Hyponatraemia may occur due to osmotic effect of
  glucose - it will correct with treatment of DKA

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Insulin infusion

• 50units actrapid made to 50ml with NaCl 0.9
• Rate 0.1 units/kg/hour
• 70kg 7 units/hour
• Aim for fall in serum ketone of 0.5 mmol/L per
  hour
• OR rise in serum HCO3- by 3 mmol/hr or reduction
  of Blood glucose by 3 mmol/hr
• Increase rate of insulin by 1 unit per hour if
  above not achieved
• Continue infusion until blood ketones lt0.3,
  venous pH gt7.3 and/or HCO3- gt18

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Cause of Vomiting and Abdominal Pain

• Vomiting
• Excess ketone bodies causes vomiting
• Gastric atony due to electrolyte imbalance
• Abdominal pain
• Peritoneal dehydration
• Pancreatitits

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Monitoring

• Monitor urine output and vital signs closely
• catheterize
• Repeat UE, glucose, VENOUS bicarbonate ABG
  PAINFUL
• 2 4 hours, 6 - 8 hours, 12 hours, 24 hours
• Repeat ABG at 2 hours if not improving
• ? Alternative cause for acidosis e.g. lactate

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Pitfalls

• Does a high wcc mean infection?
• No, not necessarily!
• Give antibiotics as guided by findings
• Absence of fever doesnt mean absence of
  infection
• Consider alternative cause for acidosis if
  glucose and acidosis markedly out of proportion
• Non specific abdo pain and raised amylase doesnt
  always mean pancreatitis
• Do not stop insulin even if the blood glucose is
  normal or below 4

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Discharge, Prognosis and Prevention

• How do you stop a sliding scale?
• Overlap with normal insulin (breakfast) and keep
  in for an other 24 hours to monitor BMs
• Prevention
• Diabetic nurse docs can use opportunity for
  patient education about insulin regime etc.
• Mortality is lt 5
• Patients with frequent episodes are at increased
  risk of dying and diabetic complications

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HONK Hyperosmolar hyperglycaemic state (HHS)

• Hallmark of type 2 DM
• May occur in
• New diagnosis
• Poor compliance with treatment
• Intercurrent illness especially MI, Infection,
  CVA
• Drugs- Steroids
• Sugary drinks

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Why is it different from DKA?

• Insulin production markedly reduced but NOT
  absent.
• No switch to fat metabolism and therefore no
  ketones or acidosis
• Mortality markedly higher
• Co-morbidities, longer time to diagnosis,
  electrolyte disturbances
• Cerebral oedema and Pulmonary Embolism more common

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How do I recognise it?

• Diagnosis requires ALL of the following
• Raised blood glucose (usually gt30mmol)
• Absence of ketones (or or only)
• Serum osmolality gt350mmol

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How do you calculate osmolality?

• 2(NaK) urea glucose
• Or
• Ask for a serum osmolality level (U and E bottle,
  biochemistry)

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Clinical Presentation

• Possibly osmotic symptoms
• Dehydration around 10L deficit
• Decreased level of conciousness
• Signs of underlying infection in up to 50
• /- thrombo-embolism in up to 30
• 2/3 cases previously undiagnosed
• As high as 50 mortality

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Is the treatment the same as DKA?

• Fluid replacement SLOWER (may be a marker of
  population not pathology)
• Electrolyte replacement (pseudohyponatraemia)
• Insulin slower scale normally very
  responsive to IV insulin
• Search for cause
• ANTICOAGULATION
• Monitor

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Hypoglycaemia

• In diabetes blood sugar lt 4 mmol/l
• Whipples triad symptoms of hypoglycaemia, low
  blood sugar, resolution of symptoms on correction
  of low blood sugar
• Symptoms may not present at the same level of
  blood glucose

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Symptoms

• Autonomic
• sweating, palpitations, tremor, hunger
• Neuroglycopenic
• confusion, clumsiness, behavioural changes,
  seizures
• Non-specific
• nausea, headache, tiredness

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Aetiology

• Reactive Hypoglycaemia
• Post prandial
• gastric surgery
• Drug Induced
• insulin
• sulphonylureas
• alcohol

• Fasting
• P- pituitary failure
• L- liver disease
• A- Addison
• I - Islet cell tumours
• N- neoplasm- retroperitoneal fibro sarcomas

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Treatment of hypoglycaemia

• If able to eat
• glucose e.g 3 dextrosol tabs / 200mls of orange
  juice/ coca cola
• followed by long acting carbohydrate eg toast/
  sandwich
• In a semi-conscious patient
• In the community 1mg glucagon im and long acting
  carbohydrate on recovery

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Severe Hypoglycaemia

• Consider in any unconscious patient, those with
  CVA or odd behaviour
• Hospital options-
• I.M. glucagon 1mg
• I.V. 20ml of 50 dextrose
• Other options- Hypostop gel
• Look for precipitants/causes and avoid
• Psychological consequences
• Review oral hypoglycaemic drugs
• Driving precautions and regaining awareness

Extravasation of 50 dextrose can cause severe
tissue loss 20 preferable
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• Any questions about diabetic emergencies?

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Summary

• You should be able to
• Recognise diabetic ketoacidosis.
• Participate in the management of diabetic
  ketoacidosis.
• Recognise Hyperosmolar Non ketotic state
• Recognise and manage hypoglycaemia.