Oh sugar!

Labs and Lytes 031

Author: David Humphreys
Reviewer: Sarah Yong

A 66-year-old man was found by a neighbour lying face down on the grass outside his home. He was in a confused and disoriented state. An ambulance was called.

On presentation to the emergency department these biochemistry results were obtained from a venous sample:

Sodium (mmol/L) 142 (135-145)
Potassium (mmol/L) 7.4 (3.5-5.2)
Chloride (mmol/L) 101 (95-110)
Bicarbonate (mmol/L) 11 (22-32)
Urea (mmol/L) 34.9 (4-9)
Creatinine (umol/L) 390 (60-110)
Glucose (mmol/L) 71.3 (3.5-7.7)

NB. reference ranges also shown in brackets in the right-hand column.

Q1. Are you happy with this patient’s serum sodium concentration?


Serum sodium is likely significantly elevated (beyond the reported value) but masked by the osmotic effect of the severe hyperglycaemia.

Due to the water shift provoked by severe hyperglycaemia, serum sodium does not initially appear as high as would be expected for the actual degree of total body dehydration (i.e. dilutional or pseudo-hyponatraemia).

Q2. What is the ‘corrected’ sodium concentration?

Approximately 166 mmol/L.

An appreciation of the serum sodium concentration that would be present but for the hyperglycaemia-driven fluid shift can be estimated using this formula:

Measured serum sodium + 1/3 x blood glucose (mmol/L)

Therefore in this patient:

142 + (1/3 x 71) = 142 + 23.7 = 165.7

In addition, the patient’s initial serum osmolality was measured at 427 mosm/kg (ref. 275-300).

Q3. What is the diagnosis and its pathophysiology?

Hyperosmolar hyperglycaemic state (HHS), due to relative insulin deficiency.

Hyperosmolar hyperglycaemic state (HHS) is one of the most severe acute metabolic complications of diabetes. Mortality rates have been reported at 5-20%. HHS is typically characterised by severe hyperglycaemia, hyperosmolarity, dehydration (due to osmotic diuresis) and change in mental state, in the absence of significant ketoacidosis.

In HHS there is a relative insulin deficiency, limiting peripheral glucose uptake, but sufficient to prevent lipolysis and subsequent ketone production.

You could argue, though, that HHS isn’t really a diagnosis — we still need to go looking for the underlying cause!

Q4. What are likely precipitants of this condition?

Underlying precipitating events should be always be considered, including:

  • Acute infection (e.g. LRTI, UTI)
  • Other acute illness (AMI, CVA, pancreatitis, etc)
  • Discontinuation of or inadequate insulin therapy
  • Compromised fluid intake due to underlying medical conditions
  • Excessive fluid losses resulting in dehydration (e.g. gastroenteritis)
  • Drugs that affect carbohydrate metabolism (e.g. glucocorticoids, higher dose thiazide diuretics)
  • Psychological or psychiatric illness (including dementia)

Consideration of ‘unmeasured osmoles’ should also be included here, if there is a significant gap between the measured osmolality and estimated osmolarity.

Q5. What principles will guide your treatment of this patient?

The principles of HHS treatment are:

  1. Rehydration: replacement of fluid losses
  2. Lowering serum glucose
  3. Monitoring and correcting  sodium
  4. Monitoring and correcting potassium
  5. Avoiding potential complications
  6. Investigation and management of precipitating factors

Management of HHS should proceed more slowly than is typical for diabetic ketoacidosis (DKA), aiming to restore volume state and establish normoglycaemia over days rather than hours. Serial clinical evaluation and monitoring of pH, UECs, glucose, and calculated omsolality is critical.

1. Rehydration

  • Fluid losses can be profound, from 100-220 mL/kg (6-13 litres in a 60kg patient)
  • Aim to replace 50% of the estimated deficit within the first 12 hours, and the remainder over the ensuing 36 hours (NB. local protocols may vary)
  • Rapid complete saline rehydration should be avoided as this can provoke hypo-osmolality and cerebral oedema

2. Lowering serum glucose

  • Most of the initial fall in blood glucose is due to rehydration, not insulin action, and relates to the shift of water back into the interstitial space
  • Commence insulin therapy after fluid resuscitation is underway and serum potassium is above 3.5 mmol/L, as serum potassium is likely to decrease
  • Commence dextrose when serum glucose decrease to 15mmol/L, to continue replenishment of total body water whilst preventing hypoglycaemia

3. Monitoring and correcting sodium

  • An initial (rebound) rise in serum sodium concentration can be expected during treatment as blood glucose falls
  • The rate of decrease in serum sodium concentration should generally not exceed 10 mmol/L in 24 hours to prevent osmotic demyelination as a complication

4. Monitoring and correcting potassium

  • Total potassium deficit is common due to increased urinary losses (due to glucose osmotic diuresis) and the effects of insulin and fluid therapy
  • Careful monitoring including telemetry, and timely administration of potassium replacement is essential

5. Avoiding potential complications, including:

  • Cardiovascular instability due to volume depletion
  • Thromboembolic complications due to low circulating and viscous blood flow (e.g. stroke, myocardial infarction, and venous thromboembolism)
  • Non-cardiogenic pulmonary oedema may occur, due to excessive fluid resuscitation (especially older patients)
  • Osmotic demyelination from rapid correction of serum sodium

6. Investigation and management of precipitating factors

  • As above


  • UpToDate Online: Kitabchi AE et al. Diabetic ketoacidosis and hyperosmolar hyperglycaemic state in adults: clinical features, evaluation, and diagnosis. July 2014. [Accessed online February 2016]
  • UpToDate Online: Kitabchi AE et al. Diabetic ketoacidosis and hyperosmolar hyperglycaemic state in adults: treatment. December 2015. [Accessed online February 2016]
  • Local guidelines, e.g.: Wyatt S et al. Alfred Health guideline: Management of hyperosmolar hyperglycaemic state in adults. Alfred Health intranet. June 2014. [Accessed online February 2016]
  • LITFL: Hyperosmotic Hyperglycaemic Syndrome (HHS), see: https://lifeinthefastlane.com/ccc/hyperosmotic-hyperglycaemic-syndrome-hhs/
  • LITFL: Treatment of HHS/DKA, see: https://lifeinthefastlane.com/treatment-of-hhs-dka/

All case-based scenarios on INTENSIVE are fictional. They may include realistic non-identifiable clinical data and are derived from learning points taken from clinical practice. Clinical details are not those of any particular person; they are created to add educational value to the scenarios.

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RescueICP and Decompressive Craniectomy by Dash Gantner and Jamie Cooper

The INTENSIVE Podcast Episode 5

Dr Dash Gantner and Prof Jamie Cooper team up to critically appraise the RescueICP trial and the role of decompressive craniectomy in the management of severe traumatic brain injury (TBI).

These talks were  presented at the regular interdisciplinary neurocritical care meeting held at the Alfred Hospital in Melbourne. The target audience is health professionals in the intensive care, trauma, neurosurgical fields.


  • Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. NEJM. 2011; 364(16):1493-502. [pubmed]
  • Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. NEJM. 2016; 375(12):1119-30. [pubmed]

Learn more here:

Subscribe to the podcast: iTunes | RSS

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Amazing And Awesome ‘Hot’ Debriefs for Critical Incidents

Amazing and Awesome 1
Author: Chris Nickson
Peer reviewer: Judit Orosz

The Alfred ICU now has an ‘Amazing And Awesome’ project so that we can learn from the excellence that takes place every day in the workplace.

We even have a very ‘bling’ AAA slip collection box in the tea room:

Recently, three of our ICU nurses — Jayne Sheldrake, Chris Broadfoot, and Bridgina Mackay — helped facilitate and lead a ‘hot debrief’ after a crisis event. It was both ‘amazing’ and ‘awesome’ :-). Such debriefs seem to have a big impact, as they help us all understand what happened and why, help us support each other, and provide us all with an opportunity to reflect and start thinking about how we can do things even better.

So, how can we do a ‘hot debrief’ effectively?

Firstly, after a critical event, I like to make sure “all the loose ends are TIED up”…

  • Team check (is everyone OK?)
  • Ingest and imbibe (if possible, take a break to eat, drink, and recharge)
  • Equipment resupply (be ready the next emergency)
  • Debrief (soon after the event)

As for the debrief, our unit doesn’t (yet) have a specific protocolised approach to critical incident debriefing, so here’s what I try to do in 3 steps:

Step 1. Plan the debrief and give a prebrief

  • TIE up the loose ends first and attend to patient care requirements
  • Choose a facilitator (can be a doctor or a nurse, ideally with debriefing/ facilitation skills)
  • Gather the team in a quiet and confidential space
  • Establish the ground rules:
    • We all worked hard and did our best, and we all want to do even better
    • We want to understand what happened and why, support each other, and see what we can change for next time
    • Everyone’s voice matters
    • Everything discussed is confidential (the Chatham House rule applies)
  • Explain who to contact if anyone needs more support or doesn’t feel comfortable speaking in front of everyone

Step 2. Have a “FAST” discussion (feelings/ facts, analysis, summary, take homes)

  • Check initial reactions to how everyone is feeling.
  • Go over the “facts” of the event (explain what happened and check that everyone is on the same page)
  • Analyse any issues – often time is limited so a ‘learner-self assessment’ approach like ‘Plus-Delta’ is often suitable:
    • “What aspects of the case went well?
    • “What aspects of the case would we want to change?”
  • Check if there are any outstanding issues after exploring these and ensure everyone has had an opportunity to have their say.
  • Summarise the discussion
  • Ask for take homes from the group

Step 3. “Close the loop”

  • identify (and assign) any actions that need to be taken
  • this may include things like checking in on people affected by the event, following up a patient’s outcome, reporting a sentinel event, instigating a guideline change, or filling out an ‘Amazing and Awesome’ slip and putting in the collection box…

All this should take only 10-15 minutes. There are non-trivial barriers to doing an effective ‘hot debrief’ (time, finding the right place to do it, getting everyone together, and having skilled facilitators) but we think it is important. It fits with our unit’s culture of supporting each other to take the best possible care of our patients, and to keep striving to get better. This is what post-event debriefing is all about.

Finding ways to improve clinical debriefing during our day-to-day work in the ICU will make for an exciting project… 😉

References and Resources

Journal articles

  • Couper K, Perkins GD. Debriefing after resuscitation. Current opinion in critical care. 2013; 19(3):188-94. [pubmed]
  • Kessler DO, Cheng A, Mullan PC. Debriefing in the emergency department after clinical events: a practical guide. Annals of emergency medicine. 2015; 65(6):690-8. [pubmed]
  • Mullan P, Kessler D, Cheng A. Educational opportunities with postevent debriefing. JAMA. 2014;312(22):2333-2334. [pubmed]

FOAM and online resources

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