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Diabetes Emergencies - Hyperosmolar Hyperglycemic State (HHS) [for Residents]

Writer's picture: Rhea ChatterjeaRhea Chatterjea

Many residents get jittery the moment they know they have a diabetic crisis to manage on their shift. This post aims to put those feeling of dread at bay and give you some guidance on how to effectively and safely manage a patient who has HHS. Not only is this a resource for learning and exam prep, but also a quick guide you can pull up whenever you are faced with a patient who has HHS.


What are the key features of HHS?

Hyperosmolar hyperglycaemic state or HHS is a diabetes emergency that needs urgent attention. The key features that characterise HHS are:

  • Uncontrolled hyperglycaemia (a blood glucose level of > 33.3mmol/L)

  • Hyperosmolality (>320mosm/kg)

  • Dehydration

  • Absence of significant ketosis

pH is usually normal (>7.3) and bicarbonate levels should be > 15mmol/L unless there are other contributing factors like DKA-HHS overlap syndrome. Mortality in HHS can be between 5-20% and the patient should be urgently attended to to avoid deterioration.


Physical examination:

  • Fluid status: Skin turgor, mucous membranes, jugular venous pressure (JVP)

  • Auscultate lungs and examine abdomen looking for localising signs of infection

  • Body Mass Index (BMI should give you an idea of the type of underlying diabetes the patient may have if that is as yet unclear)

  • Features of insulin resistance: acanthosis nigricans and skin tags - again, this will give you a better idea of the underlying diabetes subtype

  • Look out for features of secondary causes of diabetes such as cushing's syndrome and acromegaly

  • Look out for a goitre and the thyroid status: consider that hyperthyroidism and thyroid storm can also trigger a hyperglycaemic crisis

Treatment:

Key principles:

  • Hydration/fluid therapy

  • Insulin

  • Electrolyte replacement

  • Treat the underlying cause


Fluid therapy:

  • Monitor input and output strictly

  • If not in shock: Isotonic 0.9% normal saline at 15-20ml/kg/hr for the first hour

  • If in shock: Isotonic 0.9% normal saline at 20-30ml/kg/hr

  • Subsequently assess haemodynamics, hydration status, serum electrolytes and urine output

  • If serum sodium is normal or elevated, use 0.45% NaCl at 250-500ml/hour

  • If serum sodium is low use normal saline at 250-500ml/hour

  • Be careful to avoid fluid overload in patients with heart failure or CKD/ESRF

  • Once serum glucose is < 16.0mmol/L, a dextrose drip 5% should be added to allow continued insulin administration until hyperosmolarity and mentation resolves without causing hypoglycaemia (and the IV insulin rate should be halved, see below)

  • Hyperglycaemia usually takes 6 hours to resolve, hyperosmolality may take longer


Insulin therapy:

  • Either continuous IV insulin OR regular frequent SC/IM insulin injections

  • IV insulin is preferred due to the short half life and easy titration whereas SC and IM insulin has a delayed onset of action with a prolonged half life

  • Options include 0.1unit/kg bolus followed by 0.1unit/kg/hr infusion OR

  • 0.14units/kg/hr continuous infusion WITHOUT initial bolus

  • Aim for a 3-4mmol/hour reduction in plasma glucose

  • When glucose levels reach 16mmol/L, consider decreasing the insulin infusion rate to 0.02-0.05units/kg/hr and adding the dextrose drip component

  • Maintain the plasma glucose between 14-16mmol/L for HHS

Electrolytes:

Potassium:

  • Because volume expansion, insulin therapy and correction of acidaemia will lower serum potassium, it is important to replace potassium once the serum potassium is in the normal range

  • Infuse 20-30mmol/L of potassium per litre of IV fluids administered (in reality, infuse one to two cycles of 10mmol potassium chloride premix solution for every pint of IV fluids administered)

  • If there is hypokalaemia, delay insulin administration until K > 3.3mmol/L (in reality, consider inserting a central line for more rapid potassium replacement, and reducing the IV insulin rate until potassium is > 3.3mmol/L)

Phosphate:

  • Regular phosphate replacement has not been shown to have significant benefits

  • Aim for normal phosphate, slow replacement if required

Criteria for resolution:

  • Normal osmolality

  • Regain of normal mental status


Common exam questions to consider:

What is the calculated free water deficit?

  • Total body water

    • 0.6 x body weight for men

    • 0.5 x body weight for women

    • 0.5 x body weight for elderly men

    • 0.45x body weight for elderly women

  • Free water deficit = Total body water x (1- (140/serum Na))

  • Estimated fluid losses in HHS are 100 – 220 ml/kg (JBDS 2022)

As you institute resuscitation measures, how would you expect the sodium level to behave? Will it go down or go up and why?

Initially, as insulin allows glucose to be taken up into cells, water will follow the glucose and concentrate the sodium in the blood, leading to unmasking of the hypernatraemia. Subsequently as fluid resuscitation continues, serum sodium should start to fall again and slowly normalise.


What are the possible triggers for HHS?

Common triggers include infections, dehydration, MI, stroke, medications such as steroids, and medication non adherence.

Compare and contrast the ADA 2009 and JBDS 2022 HHS treatment guidelines

Topic

ADA Guidelines 2009

JBDS Guidelines Feb 2022

Definition of HHS

Blood glucose >600 mg/dL (>33.33mmol/L), serum osmolality >320 mOsm/kg, and absence of ketosis

Blood glucose >30 mmol/L, serum osmolality >320 mOsm/kg, and absence of ketosis (Ketones ≤3.0mmol/L)

Fluid replacement

Initial bolus of 1-1.5 L normal saline over 1 hour, then 250-500 mL/hour. Subsequently, 0.45% NaCl infused at 250 –500 ml/h is appropriate if the corrected serum sodium is normal or elevated.

Initial bolus of 1L normal saline over 1 hour, then 250-500 mL/hour. Only switch to 0.45% sodium chloride solution if the osmolality is not declining despite adequate positive fluid balance


Insulin therapy

Regular insulin infusion of 0.1U/kg bolus followed by 0.1 U/kg/hour, with hourly glucose monitoring

No bolus. Start IV insulin AFTER adequate fluid replacement and serum glucose has plateaued. Rapid-acting insulin analog infusion of 0.05-0.1 U/kg/hour

Glucose levels

Hourly glucose monitoring aiming to maintain glucose values between 250 and 300 mg/dl. Once glucose is <200 mg/dl, 5% dextrose should be added.

Hourly glucose monitoring aiming for reduction of not more than 5mmol/hour. Aim to maintain glucose at 10-15mmol/L. If glucose falls<14mmol/L start an additional 5-10% dextrose drip if required at 125ml/hour

Potassium replacement

Start potassium replacement of 20-30mmol/L of replacement fluids if potassium is below the upper limit of the local reference range.

Start potassium replacement after serum potassium is checked and confirmed to be <5.5 mmol/L

Monitoring and treatment of complications

Frequent monitoring of electrolytes, glucose, and acid-base status. Treat hypoglycemia, hypokalemia, and cerebral edema promptly.

Monitoring of electrolytes, glucose, and acid-base status every 1-2 hours until stable. Treat hypoglycemia, hypokalemia, and cerebral edema promptly. Start LMWH as HHS is a hyper coagulable state. Use heel protectors to reduce risk of ulceration while patient is obtunded

Transition to subcutaneous insulin

After resolution of hyperosmolarity and return of normal mental status, transition with overlap of 1-2 hours

When serum osmolality is <300 mOsm/kg, urine output ≥0.5 ml/kg/hr), mental status has returned to normal and blood glucose is <15 mmol/L, transition to SC insulin within 2 hours

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