Hyperosmolar hyperglycemic state
(Redirected from Hyperosmotic Coma)
Background
- Prototypical patient is elderly with uncontrolled type II DM without adequate access to H2O
- Occurs due to 3 factors:
- Insulin resistance or deficiency
- Increased hepatic gluconeogenesis and glycogenolysis
- Osmotic diuresis and dehydration followed by impaired renal excretion of glucose
- May result in TBW losses of 8-12L
- Ketosis usually absent (may be mild)
- Cerebral edema is uncommon complication (case reports)
- Estimated mortality 10-20%, usually due to underlying precipitant[1]
- In contrast to DKA, in which mortality is 1-5%
- Incidence of HHS < 1% of hospital admissions of patients with diabetes
Precipitants
- Pneumonia (Main)
- Urinary tract infection
- Medication non-adherence
- Cocaine intoxication
- Meds: Beta-blockers, diuretics
- GI bleed
- Pancreatitis
- Heat related emergencies
- Acute coronary syndrome
- Stroke
Clinical Features
- Dehydration
- Seizure (15% of patients)
- Altered mental status
- Lethargy/coma
Differential Diagnosis
Hyperglycemia
Diabetic Emergencies
- Diabetic ketoacidosis (DKA)
- Diabetic ketoacidosis (peds)
- Hyperosmolar hyperglycemic state (HHS)
- Nonketotic hyperglycemia
- Euglycemic DKA (SGLT-2 inhibitors, pregnancy, fasting)
Diabetes Mellitus (New or Known)
- Type 1 diabetes mellitus (new-onset or uncontrolled)
- Type 2 diabetes mellitus (new-onset or uncontrolled)
- Medication noncompliance or insulin pump malfunction
- Gestational diabetes
- Latent autoimmune diabetes of adults (LADA)
Medication/Drug-Induced
- Corticosteroids (most common drug-induced cause)
- Thiazide diuretics
- Atypical antipsychotics (olanzapine, clozapine, quetiapine)
- Beta-blockers (especially non-selective)
- Phenytoin
- Tacrolimus, cyclosporine (transplant patients)
- Protease inhibitors (HIV antiretrovirals)
- Catecholamines (epinephrine, norepinephrine infusions)
- SGLT-2 inhibitors (paradoxical DKA with euglycemia)
- Total parenteral nutrition (TPN)
- Dextrose-containing IV fluids (iatrogenic)
- Niacin
- Pentamidine (initially hyperglycemia, then hypoglycemia from beta-cell destruction)
Physiologic Stress Response
- Sepsis / critical illness (stress hyperglycemia — very common in the ED)
- Trauma / major surgery / burns
- Acute coronary syndrome / myocardial infarction
- Stroke (especially hemorrhagic)
- Pancreatitis (both a cause and consequence)
- Shock (any etiology)
- Pain (catecholamine surge)
- Seizure (postictal)
- Physiologic stress alone rarely causes glucose >200 mg/dL in non-diabetics; glucose >200 in a "stress response" should prompt evaluation for undiagnosed diabetes or prediabetes
Endocrine
- Cushing syndrome / Cushing disease (cortisol excess)
- Pheochromocytoma (catecholamine excess)
- Hyperthyroidism / thyroid storm
- Acromegaly (growth hormone excess)
- Glucagonoma (rare)
- Somatostatinoma (rare)
Pancreatic
- Pancreatitis (acute or chronic — destruction of islet cells)
- Pancreatic malignancy (adenocarcinoma, neuroendocrine tumors)
- Post-pancreatectomy
- Cystic fibrosis-related diabetes
- Hemochromatosis (iron deposition in pancreas — "bronze diabetes")
Toxic/Overdose
- Iron toxicity (hepatic injury → impaired glucose regulation)
- Salicylate toxicity (can cause both hyper- and hypoglycemia)
- Sympathomimetic toxicity (cocaine, methamphetamine)
- Calcium channel blocker toxicity (impairs insulin secretion)
- Carbon monoxide toxicity (stress response)
Other
- Renal failure (chronic kidney disease, acute kidney injury — impaired insulin clearance AND insulin resistance)
- Cirrhosis / hepatic failure (impaired glycogenolysis regulation)
- Pregnancy (gestational diabetes, steroid administration for fetal lung maturity)
- Parenteral nutrition (TPN, dextrose-containing fluids)
- Post-transplant diabetes (immunosuppressants)
Complications of Diabetes (Not Causes of Hyperglycemia)
These are associated conditions that may be present alongside hyperglycemia but do not themselves cause elevated glucose:
- Diabetic foot infection
- Diabetic peripheral neuropathy
- Cerebral edema in DKA
- Diabetic retinopathy
- Diabetic nephropathy
Evaluation
Work Up
- Chemistry
- Serum osm
- Lactate
- Serum ketones
- CBC
- Also consider:
Diagnosis
- Glucose >600
- Osm >320
- Bicarb >15
- pH >7.3
- Serum ketones negative or mildly positive
- Neurologic abnormalities frequently present (coma in 25-50% of cases)
Management
- Fluid replacement
- Average fluid deficit is 8-12L
- 50% should be replaced over the initial 12hr
- May have to replace slower if patient has cardiac/renal impairment
- Aggressiveness of fluid replacement must be weighed against the risk of cerebral edema, which increases with younger age[2]
- Average fluid deficit is 8-12L
- Hypokalemia
- Must treat aggressively
- Once adequate urinary output has been established K+ replacement should begin
- Hyperglycemia
- Do not start insulin until K > 3.3 and adequate urinary output has been established
- Hypomagnesemia
- Repletion will help correct hypokalemia
- Hypophosphatemia
- Routine correction unnecessary unless phos <1.0
Disposition
- Most patients require ICU admission
See Also
References
- ↑ Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care. 2014; 37(11):3124-31.
- ↑ Stoner GD. Hyperosmolar Hyperglycemic State. Am Fam Physician. 2005 May 1;71(9):1723-1730. http://www.aafp.org/afp/2005/0501/p1723.html

