Hyperosmolar hyperglycaemic state Flashcards
What is HHS? Who does it occur in?
Complication of DM
Unwell patient with T2DM, can in T1
Marked dehydration and blood glucose over 30mmol/L
Results in high osmolarity without ketoacidosis
What are the diagnostic features of HHS?
Hypovoalemia BM > 30mmol/L without hyperketonaemia (<3mmol/L Osmolarity > 320mOsm/kg pH>7.3 HCO3 > 15
What are the symptoms of HHS? Ddx?
Signs of dehydration (thirst, headaches reduced urine output, confusion, tiredness, seizure) Increased urination due to glycosuria Weakness Leg cramps Trouble seeing Altered level of consciousness Orthostatic hypotension
Diabetic ketosacidosis
What is the onset in HHS?
Days to weeks
What are complications of HHS?
Seizrues Disseminated intravascular coagulopathy Mesenteric artery occlusion Leg ischamemia Rhabdomyolysis
What are triggers for HHS?
Infection
Stroke
Trauma
Heart attack
What is immediate management?
Rehydrate slowly with 0.9% saline IV infusion over 48 hours
Replace K when urine starts to flow
LMWH to decrease risk of clotting unless contraindicated (bleeding disorder, platelets low, precious heparin induced thrombocytopenia, peptic ulcer, cerebral haemorrhage, severe HTN
IV insulin if blood glucose not falling by 5mmol/L/h with dehydration or if ketonsemia
Antibiotics if required
Investigate cause
Why should you keep blood glucose high initially and not decrease it too quickly?
Risk of cerebral oedema
Rapidly lowering blood glucose, rapidly drops plasma osmolarity
Brain cells which trap osmotically active particles, absorb water and swell during rapid rehydration.
Cerebral oedema follows which can result in raised ICP and herniation
When should you start insulin infusion
If significant kaetonaemia is present
This indicates hypoinsulinaemia and insulin should be started
Fixed rate intravenous insulin infusion
What investigations for HHS?
Bedside:
ECG - possible MI
Urinalysis - possible UTI
Bloods: Coagulation screen - to check CI for anticoagulation FBC - platelet count for heparin CRP - for infective marker Blood culture - for infection Serum lactate
Micro:
Stool culture
Sputum culture
Goals of treatment in HHS? How can you assess patients response to treatment?
Normalise osmolarity
Replace fluid and electrolyte
Normalise blood glucose
Assess U&E and blood glucose and BP
As the blood glucose falls and electrolytes return to normal.
How would you alter diabetic medication after discharge?
IV insulin can usually be discontinued once they are eating and drinking but IV fluids may be required for longer if intake is inadequate.
Most patients should be transferred to subcutaneous insulin (the regime being determined by their circumstances). For patients with previously undiagnosed diabetes or well controlled on oral agents, switching from insulin to the appropriate oral hypoglycaemic agent should be considered after a period of stability (weeks or months).
All patients will require diabetes education to reduce the risk of recurrence and prevent long-term complications.
Why does HHS happen? Why is ketosis absent?
HHS is usually precipitated by an infection, myocardial infarction, stroke or another acute illness.
A relative insulin deficiency leads to a serum glucose that is usually higher than 33 mmol/L (600 mg/dL), and a resulting serum osmolarity that is greater than 320 mOsm.
This leads to excessive urination (more specifically an osmotic diuresis), which, in turn, leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level.
Ketosis is absent because the presence of some insulin inhibits hormone-sensitive lipase mediated fat tissue breakdown.
What is the difference between DKA and HHS?
Serum glucose is extremely high in HHS compared with DKA and there is no ketosis - ketosis in DKA due to breakdown of fat for energy
Metabolic acidosis is absent or mild in HHS.
HHS tends to affect older T2DM while DKA younger T1DM
DKA may have fruity breath and rapid deep breathing.
DKA rapid onset, HHS gradual over few days.
