Diabetic Emergencies

Definition/Etiology:

DKA:
results from an inadequate amount of available insulin and is characterized by profound dehydration, electrolyte losses, ketonuria, and you guessed it, acidosis.
Classic findings of DKA include:

• BG over 250
• pH less than 7.3
• Serum HCO3 less than 15-20
• Ketonemia

Causes of DKA can include:

• New onset DM
• Poor insulin dosing
• Illness or infection in known diabetic (most common)
• Alcohol or drug use
• MI
• Pancreatitis and abd disorders

HHS:

• Hyperosmolar Hyperglycaemic State (HHS) occurs in people with type 2 diabetes who experience very high blood glucose levels (often over 40mmol/l). It can develop over a course of weeks through a combination of illness (e.g.infection) and dehydration.
• Many patients who suffer from HHS have a precipitant medical or surgical condition such as an infection, AMI, or stroke. Meds such as thiazide diuretics, steroids, dilantin, inderal, tagamet can causes.

Pathophysiology:

DKA – when insulin is unavailable to transport glucose into the cells, the liver metabolizes fatty acids into ketone bodies. This accumulation of ketones produces metabolic acidosis.

HHS: Elevated levels of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone) initiate HHS by stimulating hepatic glucose production through glycogenolysis and gluconeogenesis, leading to hyperglycemia, intracellular water depletion, and subsequent osmotic diuresis

Clinical Presentation:

Differences in presentation-

DKA:

• Usually <40 years old
• Symptoms usually <2 days
• Glucose <600
• Sodium normal or low
• Bicarb Low
• Ketones at least 4+
• pH usually low <7.3
• Prognosis – 3-10% mortality
• Subsequent course – ongoing insulin therapy
• Most commonly seen with Type 1 DM

S&S:

• Tachycardia, Hypotension
• Dry skin, poor skin turgor
• Fatigue
• Changes in LOC
• Kussmaul respirations (rapid deep breathing) – body trying to blow off CO2
  • Upon exhalation, breath may smell like fruity nail polish remover
• Abd pain without rebound tenderness

HHS:

• Usually, >60 years old
• Symptoms usually >5 days
• Glucose >600
• Sodium normal or high
• Bicarb normal
• Ketones at least <2+
• pH Normal
• Prognosis – 20-60% mortality
• Subsequent course – insulin therapy not often required

S&S:

• Weakness
• Polyuria, polydipsia
• Dry mucosa, dry skin
• Orthostatic hypotension
• N/V
• Acute changes in LOC
• Seizures

Collaborative Management:

DKA-

• Obviously – get a finger stick to start but confirm with a serum glucose level
• Test for glucose and ketones in urine
• UA
• CBC, CMP (BUNm Cr Phosphate, Amylase)
• ABG
• Chest x-ray, 12-lead

Interventions:

• Fluid replacement – OK so more and more facilities are developing protocols for fluid replacement with DKA, so check your own policies. That being said, commonly we start with NS and change to ½ ns if hypovolemia reverses, or the sodium stays high.
• IV insulin – Treatment of choice
• Measure serum glucose hourly and titrate the infusion according to your protocols.
• Replace electrolytes:
• Potassium, phosphate, bicarb

HHS-

The main difference between DKA and HHS is that HHS is indicated by a more elevated serum glucose and the absence of ketoacidosis.

Labs: Serum glucose, UA, Bicarb, ABG

Treatment:

• Similar to DKA though we need less insulin
• Replace fluids – NS
• Monitor I&O – Foley
• Admin insulin
• Replace electrolytes – specifically watch the potassium.

Evaluation | Patient Monitoring | Education:

• Evaluation of DKA involves repeated lab work. Is there a reduction in glucose, are we correcting the anion gap, are the electrolytes returning to normal levels, and of course, how is our patient. Neuro status and hemodynamics are constantly monitored throughout treatment.

• Eval of HHS is similar to DKA. Is the glucose normalizing? Are the electrolytes normalizing? And is our patient showing less symptoms.

Linchpins: (Key Points)

• Early identification
• Fluids
• Insulin