Hyperglycemic Hyperosmolar State

Question 1

What is Hyperglycemic Hyperosmolar Non-ketosis state?

Answer 1

• Unlike DKA, the criteria for diagnosis of is not well defined.
• Normally occurs in Type II DM patients
• Unique distinguishing factor in HHNK is the absence of ketones or a low ketone production despite an insulinopenic state (unable to produce insulin or low insulin production due to Beta-cell exhaustion)
• Patients with HHNK present with severe dehydration due to the chronic nature of hyperglycemia with blood glucoses ranging above 600mg/dL
• Course of HHNK occurs over several days to weeks with the most common presentation being altered mental status.
• Associated with MI, stroke, and peripheral arterial thrombosis more frequently than DKA

Question 2

Describe the pathophysiology associated with HHNKS

Answer 2

• Decreased activity of insulin leads to increased serum glucose via gluconeogenesis, glycogenolysis and decreased cellular glucose uptake
• Resultant hyperglycemia leads to a fluid shift from intracellular to extracellular space
• Increased circulating glucose spills into urine resulting in osmotic diuresis
• Decreased circulating volume leads to a reduction in GFR and hypotonic urine
• Hypotonic diuresis produced dehydration and creates a cycle of hyperglycemia, hypernatremia and increased osmolality

Question 3

What are the goals of care when treating a patient with HHNKS?

Answer 3

1. Monitoring the response to treatment

• Measuring or calculating the serum osmolality regularly to monitor response to treatment
• Aim to reduce osmolality by 3-8 mOsm/kg/hour

2. Fluid and insulin administration

• Use 0.9NS as the principal fluid to restore circulating volume and reverse dehydration
• Fluid replacement along will cause a fall in blood glucose levels
• Withhold insulin until the blood glucose is no longer falling with IV fluids alone (unless mildly ketonemic)
• An initial rise in sodium level is expected and is not itself an indication for hypotonic fluids and
• Early use of insulin (before fluids) may be detrimental

3. Delivery of care

Consult endocrinology/critical care

Question 4

What can cause patients to get HHNKS?

Answer 4

• DM II
• Receiving TPN or high-calorie feedings
• Neurologic changes- often first presenting sign
• Illness, trauma, stress
• Pancreatitis
• Diabetic patients of advanced age
• Nonadherence to treatment in diabetic patients
• Comorbidities: CHF and chronic renal insufficiency- patients may not tolerate large amounts of fluid

Question 5

What labs/diagnostic tests are done for patients with HHnkS?

Answer 5

BMP & ABG

• Serum glucose levels > 600mg/dL
• Elevated serum osmolality > 350 mOsm/L (normal 275-295 mOsm/L)
• Elevated BUN and creatinine
  
  • Elevated BUN:Cr ratio common indicating pre-renal causes
  • Acute kidney injury (AKI) from hypo perfusion will often exist
• Hypo, normal or elevated serum sodium
• The measures serum Na concentration in uncontrolled DM is variable because of the interaction of multiple factors, some that lower Na concentration and some that raise it. The increase in plasma osmolality created by hyperglycemia pulls water out of the cells and this reduces the plasma Na concentration. MOST patients will be mildly hyponatremic which will correct itself with hydration.
• Profound hypokalemia secondary to osmotic diuresis
• Phosphate and magnesium levels commonly low
• Normal pH (> 7.3 mol/L)
• Normal sodium bicarbonate level (> 15 mEq/L) (non-ketotic)
• Anion gap is normal
• If C-peptides are present, indication that there is some insulin production still.

Question 6

How do you manage a patient with HHNKS?

Answer 6

• Critical care monitoring with frequent cardiac and lung re-assessments
• Massive fluid replacement- Isotonic fluids (0.9NS) until hemodynamically stable
• If no hypotension is present, once sodium reaches 145mEq/L, change to hypotonic solutions (0.45NS)
• Fluid volume deficit may be 6-10liters
• Monitor for complications, such as cerebral edema, heart failure, seizures
• Less insulin is required to control HHNK than is required to control DKA
• Patients with HHS will typically have adequate basal insulin levels and additional insulin may not be necessary
  
  • Convert to SQ insulin once patient is able to eat and serum glucose falls < 250-300mg/dL
  • Continuous monitoring of electrolytes with replacement prn
• Potassium: aggressive replacement frequently necessary
  
  • KCL 10-40mEq in each liter of fluid (CAUTION: infusion of > 10mEq KCL/hour will cause burning in peripheral IVs)
• Magnesium: Hypo K = Hypo Mg
  
  • Both electrolytes lost during osmotic diuresis
  • Cannot replace intracellular potassium without magnesium
  • Serum magnesium level may not correlate with total body stores
  • Dose: 1-2 gms MgSO4 IV
• Phosphorous:
  
  • If PO4 < 10 mEq, consider replacement with KPO4
• Cardiac monitoring for dysrhythmias
• Continuous monitoring of glucose levels

Question 7

When is HHNKS resolved?

Answer 7

The hyperglycemic crisis is considered resolved when the following goals are reached:

• Patient is mentally alert
• Plasma osmolality is < 315 mOsmol/kg