HHS

• Hyperosmolar hyperglycemic state (HHS) is a rare but potentially fatal complication of type 2 diabetes. It is characterised by hyperosmolality (water loss leads to very concentrated blood), high sugar levels (hyperglycaemia) and the absence of ketones, distinguishing it from ketoacidosis.
• Symptoms:

  • Polydipsia
  • Polyuria
  • Nausea and vomiting
  • Muscle cramps
  • Weakness
  • Altered mental status
  • Seizures
  • Coma
• HSS can develop over a course of week through combination of illness and dehydration
• Serum osmolarity is over 320 mmol/kg
• Management:

  • Most important is IV fluids
  • Electrolyte/potassium replacement
  • Only start insulin if ketones also present
  • Prophylactic LMWH
• The hyperosmolar state of the condition leads to hyperviscosity that increases the risk of arterial and venous thrombosis (e.g. stroke, DVT).
• Pathophysiology:

  • Relative lack of insulin is couples with a rise in counter-regulatory hormones (e.g. cortisol) that leads to a profound rise in glucose
  • Retain a certain level of insulin which prevents the development of ketosis
  • Excess glucose leads to massive osmotic diuresis within the kidneys with the loss of sodium and potassium
  • Proximal tubules only have a certain capacity for reabsorption of glucose - once this is reached the remaining glucose is passes through the renal nephrons causing diuresis
• Common precipitants of HHS include:

  • Infection
  • High-dose steroids
  • Myocardial infarction
  • Vomiting
  • Stroke
  • Poor treatment concordance
• The average age of presentation is 60 years old and it is associated with a 15-20% mortality. 
• Signs:

  • Dehydration
  • Hypotension
  • Decreased urine output
  • Decreased conscious level
  • Coma
  • Focal neurology signs
  • Features of precipitating cause e.g. infection
• Immediate investigations to establish diagnosis of HHS:

  • Laboratory glucose: > 30 mmol/L
  • Serum osmolality: > 320 mOsm/kg
  • Ketones:
  • Urine: 1+, trace, negative OR
  • Blood: < 3 mmol/L
• Only start a fixed rate insulin infusion once fluid replacement is adequate and glucose levels have plateaued - giving insulin straight away might cause a rapid drop in serum glucose levels leading to cerebral oedema
• You can expect sodium levels to increase when osmolality is declining - may need to change to 0.45% normal saline
• Insulin should only form part of initial management if there are features of DKA - pH < 7.3, bicarbonate < 18, or ketones > 3

  Insulin given at half the dose used in DKA - 0.5 units/kg/hr
• Continuing care:

  • Prophylactic LMWH
  • Regular foot assessments for ulceration
• Complications:

  • MI
  • Thrombotic - hyper viscosity state and hypovolaemia predisposes patients to clots
  • Cerebral oedema - rapid correction of hyperglycaemia with a resulting rapid drop in plasma osmolarity - headache and reduced GCS