Question 24

College answer

a)

• The first priority is to prevent intubation. Induction will reduce minute ventilation and  worsen acidosis with a probably fatal result. Many ED ventilators would struggle to provide 40 Lpm ventilation and the PPV in a severely hypovolaemic patient may cause  haemodynamic collapse. Avoid sedation. Acidosis should resolve rapidly with fluid resuscitation and insulin.
• IV line and fluids – preferably HCO3- containing to minimise hyperchloraemic acidosis (note CVC is optional) e.g. CSL. Water deficit around 4L for 70 kg man
• IV insulin infusion (suggest 2-5 U/hr) with hourly glucose monitoring. Institute IV glucose once BGL < 12, and continue insulin until ketones cleared and beyond
• Hourly K+ and early replacement – watch for massive drop as pH rises
• Replace other electrolytes as needed (Mg, PO4)
• Check for precipitants esp. intoxication and infection
• Investigate cause of anaemia
• Disposition to appropriate high-care area (HDU/ICU/other)

b)

• Younger age (especially under 5’s)
• Newly diagnosed diabetes
• Severity of acidosis & hyperglycaemia
• Severity of dehydration
• Change in corrected [Na]
• Speed of rehydration & correction of hyperglycaemia
• Administration of bicarbonate

Additional Examiner Comments:
Many candidates stated they would intubate the patient; this would likely have precipitated a cardiac arrest due to acute rise in CO2 and worsening acidosis.

Discussion

a)

The ED registrar is unimpressed with the agitated patient's behaviour, and would prefer to intubate them to improve their manners. The college wisely cautions against this, as it might precipitate cardiac arrest from acidosis. This is likely correct. A CO₂ of 9 likely represents the physiological limits of hyperventilation. An important early goal would be to correct this acidosis, bringing the patient closer to the possibility of safe airway control. The story of "found collapsed" is going to score a head CT, and judging by the way the situation is evolving this guy will not hold still for it, so an intubation is still on the cards at some stage.

The college suggested insulin. This is rarely required in pure HHS; fluid resuscitation alone is often enough because the hyperosmolar state is frequently associated with an abnormally elevated insulin level in a Type 2 diabetic. However, in this scenario the patient is a Type 1 diabetic, and is probably more DKA than HHS (he clearly has high ketones; the anion gap is around 26.6, and only 4.0 mmol/L of this is explaied by lactate). So some insulin would be required (but probably not the 0.1u/kg/hr recommended by the usual DKA protocols, as you do not want to drop the BSL too quickly)

Thus, a standard approach to DKA is described below.

1. Assess airway patency. Intubate to protect the airway if comatose.
2. Ventilate with mandatory mode initially; aim for normocapnea if the metabolic acidosis is not particularly severe. 
3. Insert arterial line for frequent sampling and haemodynamic monitoring.
   Insert central line to manage electrolyte and fluid infusions.
   Expect a 200ml/kg total water deficit
   Commence fluid resuscitation:
   1. 15-20ml/kg in the first hour (and use colloid if they are shocked)
   2. 4-14ml/kg in the second hour (of 0.45% NaCl)
   3. 4-14ml/kg again in the third hour (use 0.9% NaCl if the sodium is low)
   4. When glucose is under 15mmol/L, Oh's Manual recommends to start 5% dextrose 100-250ml/hr, as well as some other sort of sodium-containing fluid to prevent hyponatremia 
4. May require benzodiazepines or anticonvulsants if the presentation history included seizures.
   May require a head CT venogram to rule out dural sinus thrombosis / venous infarction
5. Watch for a precipitous drop in serum osmolality.
   A safe drop is 3–8 mOsm/kg/h
   Correct electrolyte deficit:
   1. Sodium deficit: 5-13mmol/kg
   2. Potassium deficit: 5-15mmol/kg
   3. Chloride deficit: 3-7mmol/kg
   4. Phosphate deficit: 1-2mmol/kg
   5. Magneisum deficit: 1-1.5mmol/Kg
   6. Calcium deficit: 1-2mmol/Kg
6. Monitor renal function and consider dialysis
7. May require anticoagulation for dural sinus thrombosis.
8. May require antibiotics, given that infection is a common precipitant.
   A septic screen should be sent.

Key issues of "specific therapy:

• Fluid resuscitation
• Electrolyte replacement
• Careful slow reduction of serum osmolality
• Careful introduction of insulin
• Investigation for complications:
  • Myocardial infarction
  • Stroke
  • Cerebral oedema and brain injury
  • Venous thrombosis
• Management of other possible precipitating causes:
  • Infection, systemic inflammatory response
  • Intracranial haemorrhage
  • Hepatic encephalopathy
  • Drugs, including illicit substances, steroids, phenytoin, diuretics, TPN, lithium

b) This list of risk factors from the college seems to come from multiple references (see the list from the HHS chapter) and may be mainly paediatric in origin, as it appears this complication is much less common among adult patients  (Matz, 1999).

A complete list of risk factors from around the literature would look like this: