Hyperosmolar hyperglycemic syndrome ( HHS )
HYPEROSMOLAR HYPERGLYCEMIC SYNDROME ( HHS ) complication of diabetes ( type 2 diabetes in 90 % to 95 % of cases ) previously know by other names as non-ketotic hyperglycemic coma , hyperosmolar hyperglycemic non ketotic syndrome and hyperosmolar non-ketotic coma ( HONK ) Main features related to HHS are severe hyperglycemia ( e.g bl glucose > 30 mmol / L ) , high serum osmolality and extreme dehydration in the absence of ketoacidosis
Presentation – usually has a slower onset than DKA , develops over several days or weeks can be precipitated by infectious diseases , disorders of the respiratory , circulatory and genitourinary systems presentation can be with fatigue ( glucose cannot be utilized for energy ) , polyuria , polydipsia , weakness , blurred vision altered level of consciousness to confused , lethargic or comatose usually develops in the elderly mortality rates of 8 % to 20 % ( about 10 times higher than DKA patients )
Enquire – ask about insulin regimen ,compliance , missed doses infection is the most common precipitant ( particularly pneumonia & UTI ) over consumption of carbohydrate rich food chest pain , tightness , headache , dizziness , palpitations conditions as stroke , MI , trauma –> lead to counterregulatory hormone secretion and limit access to water bed ridden patient ( cannot access water , altered thirst response ) use of medications as glucocorticoid , thiazide diuretics , phenytoin , beta blockers , atypical antipsychotics
Check – raised blood sugar ( check capillary blood glucose & urinary ketones ) BP , pulse , respiratory rate signs/ symptoms of dehydration capillary refill , skin turgor, tenting sign ( pinch the skin & it stands like a tent ) urine output fever ( if infection present ) mental state ( confused , altered )
Insulin deficiency- reduced glucose utilization by peripheral tissue leading to hyperglycemia
Peripheral tissue enters in starvation state.
Release of counterregulatory hormones like glucagon , growth hormone , cortisol and catecholamines -leads to gluconeogenesis & glycogenolysis
Increased glucose levels ( due to increased gluconeogenesis , glycogenolysis & reduced use ) cause serum osmolarity to rise , glucose cannot be used for energy (fatigue , wt loss )
Water follows glucose ( glucose is an osmotically active solute ) ie free water is drawn out of the extravascular space due to increased osmotic gradient
Kidneys cannot handle the glucose load hence free water with electrolytes are lost via urinary excretion -glycosuria , leading to dehydration ( osmotic diuresis )
Causes further concentration of solutes and intense thirst ( polydipsia )
Due to higher levels of insulin still being produced by beta cells ( type 2 diabetes ) ie higher ratio of insulin/ glucagon -the generation of ketone bodies is minimal ( no ketogenesis )
REFERENCES
- Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients doi:10.1136/bmj.l1114 Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients | The BMJ
- Adeyinka A, Kondamudi NP. Hyperosmolar Hyperglycemic Nonketotic Coma. [Updated 2021 Nov 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482142/
- Pasquel, Francisco J, and Guillermo E Umpierrez. “Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment.” Diabetes care vol. 37,11 (2014): 3124-31. doi:10.2337/dc14-0984 Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment (nih.gov)
