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36 Cards in this Set
- Front
- Back
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Definition of DKA
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Blood glucose level greater than 250 mg/dL
Bicarbonate less than 15 mEq/L (low) Arterial pH less than 7.3 (low) Moderate ketoemia |
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DKA - Epidemiology
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1/4 of hospital admissions for DM
Occurs predominantly in type 1 though may occur type 2 Annual incidence: 8/1000 pts with DM (common) 20-30% of cases occur in new-onset DM Mortality less than 5% Mortality higher in elderly due to underlying renal disease or coexisting infection |
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Causes of DKA
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25% have no precipitating causes found
Errors in insulin use, esp in younger population Omission of daily insulin injections Stressful events (infection, MI, steroids) |
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Pathophysiology of DKA - Glucose
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Lack of insulin triggers gluconeogenesis, glycogenolysis (spilting up glycogen to increase glucose levels) and decrease hepatic glucose uptake. As a result, there is an increase circulating levels of glucose in the serum and decrease in intracellular glucose. This leads to increase cortisol, increase epi, increase GI and increase glucagon. In the end, there is profound hypoglycemia.
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Pathophysiology of DKA - Glucose levels increase above renal threshold
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Above 180 mg/dL
Osmotic diuresis with loss of H2O, Na+, K +, PO4, and Mg. Hyperosmolarity (>280 mOsm) causes intracellular ions (H2O, K, PO4) to move to extracellular space and face diuresis via the kidneys. |
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Pathophysiology of DKA - Fat Metabolism
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Lack of insulin causes TG to go through lipolysis to breakdown to FFA. In states of low insulin and high glucagon, FFA accumulates. This leads to production of B-OH BA (Hydroxybutyric acid), acetoacetic acid (diabetic acid) and acetone. These are all forms of ketone bodies and will lead to metabolic acidosis.
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Pathophysiology of DKA - Metabolic Acidosis
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Metabolic acidosis stimulates medullary chemoreceptors in the CNS to trigger tachypnea and hyperpnea (respiratory compensation) to blow off CO2 (decrease CO2). Eventually the buffer system is overwhelmed (also due to the presence of metabolic acids) and the patient will have DKA.
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DKA - Potassium Levels
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Total body potassium is depleted by renal loses
Measured levels usually normal or elevated - due to 1. Intracellular exchange of potassium for hydrogen ions during acidosis 2. Total body fluid deficit 3. Diminished renal function 4. Initial hypokalemia indicates severe total-body potassium depletion and requires large amounts of potassium within first 24-36 hours |
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Why do serum [K+] decrease with treatment? Why is this important?
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1. GIK (Glucose Insulin potassium) - glucose and insulin will drive K+ intracellularly
2. Reversal of acidosis 3. Dilution of extracellular fluid 4. Increased K+ excretion with increased GFR (urinary loss) |
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DKA - Sodium Levels
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Osmotic diuresis leads to excessive renal losses of NaCl in urine.
Hyperglycemia artificially lowers the serum sodium levels. These pts are managed with NS in fluid mgmt to help replace sodium stores. |
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DKA - Electrolyte Loss
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Osmotic diuresis contributes to urinary losses and total body depletion of: phosphorous, calcium and magnesium. Sometimes these are replaced but not to the extent of K+ replacement.
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DKA - Clinical Features
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Hyperglycemia
Increased osmotic load (>340 mOsm/L renal loss of Na, Cl, K, phos, Ca and Mg) --> Mental confusion Major signs: polyuria and polydipsia Increased ventilation Peripheral vasodilation (in response to prostaglandins and acidosis)- may cause N/V and abdominal pain Abnormal vital signs Tachycardia with orthostasis or hypotension Poor skin turgor Kussmaul respirations with severe acidemia Acetone presents with odor in some pts Hypothermia Abdominal pain and tenderness |
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Clinical Suspicion of DKA - Check immediately
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Blood glucose
Urine dipstick (glucose and ketones) ECG Venous blood gas Normal Saline IV drip (Almost all patients with DKA have glucose greater than 300 mg/dL) |
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Causes of Wide Anion Gap (Mud-Pies)
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Methanol toxicity
Uremia DKA Propylene glycol Infection Lactic acidosis Ethylene glycol Rhadomyolysis |
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Calculate Anion Gap
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Anion Gap = [Na+] − ([Cl-] + [HCO3−]
Normal (7-16) Anion gap at discharge should be less than 20 |
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DKA- Treatment Goals
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Volume depletion - order of therapeutic priorities is volume first, then insulin and/or potassium, magnesium and bicarbonate.
Close monitoring (glucose, electrolytes, anion gap) Resolving hyperglycemia alone is not the end point of therapy. |
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DKA - Fluid Administration
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Rapid administration is the single most impt step in treatment
Restores intravascular volume, normal tonicity and perfusion of vital organs. Improve GFR. Lower serum glucose and ketone levels Normal saline is most frequently recommended fluid for initial volume repletion. |
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DKA - Avg Adult Water and Sodium Deficit
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5-10 L water deficit
7-10 mEq/kg sodium deficit |
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DKA - Recommended Regimen for Fluid Administration
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First L of NS within first 30 mins of presentation.
Second L within the first 2 hours. Second 2 L of NS at 2-6 hours Third 2 L of NS at 6-12 hours. Above replaces 50% of water deficit within first 12 hours with remaining 50% over next 12 hours Glucose and ketone concentrations begin to fall with fluids alone |
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DKA - When do you add D5 to solution?
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When glucose level is between 250-300 mg/dL
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DKA and HHS- When do you change to hypotonic 1/2 NS or D51/2?
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When glucose is below 300 mg/dL after using NS
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DKA and HHS- Insulin Recommended Dose
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0.1unit/kg/hr
Effect begins almost immediately Loading dose not recommended in peds. It is recommended in adults - 0.15 units/kg. |
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DKA - When should K+ be added to IV?
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When K+ level drops below 5.5 mEq/L.
20-30 mEq K+ in each L of IVF |
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DKA - When should phosphate be treated?
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Level less than 1 mg/dL (normal 2.5 - 4.5)
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What are the main contributors to complications and mortality of DKA?
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MI and infection
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How to prevent DKA?
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1. Education - pts should not stop taking insulin (sick day rules - pt may need more insulin)
2. SMBG and when >250 mg/dL --> check for ketones 3. Corrective insulin doses 4. Contact provider with N/V, fever, persistent hyperglycemia or ketones. |
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HHS - Epidemiology
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HHS is much less frequent than DKA
Mortality rate higher in HHS (15-30%) |
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HHS -Definition
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Severe hyperglycemia (>600 mg/dL)
Elevated plasma osmolality (>315 mOsm/kg) Serum bicarbonate >15 pH > 7.3 Serum ketones that are negative to mildly positive |
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Pathophysiology of HHS - Three main factors
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1. Decreased utilization of insulin
2. Increased hepatic gluconeogenesis and glycogenolysis 3. Impaired renal excretion of glucose |
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What is the fundamental risk factor for developing HHS?
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Impaired access to water
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HHS - Avg Adult Water Deficit
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8-12 L (in a 70 kg person)
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Why is there a lack of ketoacidosis in HHS?
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1. Lower levels of counter regulatory hormones
2. Higher levels of endogenous insulin that strongly inhibits lipolysis 3. Inhibition of lipolysis by the hyperosmolar state |
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HHS - Precipitating Risk Factors
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Poorly controlled T2DM
Acute illness - Pneumonia and UTIs (30-50% of cases) Non-compliance with or under dosing of insulin |
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What are commonly prescribed drugs that may predispose to hyperglycemia, volume depletion or other effects leading to HHNS?
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Diuretics
Corticosteroids |
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HHS - Physical findings
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Non-specifc
Clinical signs of volume depletion, hyperglycemia and hyperosmolality (lethargy or coma) and duration of physiologic imbalance Normothermia or hypothermia Seizures CNS symptoms (tremor, clonus, hyperreflexia, hyporeflexia, positive Brudzinkis sign) |
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Osmolarity
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Serum osmolarity has been shown to correlate with severity of disease as well as neurologic impairment and coma.
Normal 275 - 295 mOsm/kg Hyperosmolarity >300 mOsm/kg Alterations of cognitive function >320 mOsm/kg |
