diabetic crises
TRANSCRIPT
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Diabetic Emergencies: Diabetic Ketoacidosisand Hyperglycemic Hyperosmolar SyndromeALISHA WORTHNCSU CVM C/O 2015
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Diabetes Mellitus Overview
Impaired carbohydrate metabolism due to inadequate insulin Pancreas: exocrine and endocrine function
Exocrine: digestive enzymes Glucagon: ↑ [glucose]: glycogenolysis, gluconeogenesis Insulin: ↓ [glucose]: promotes glycogen formation;
glucose uptake into cells
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Diabetes Mellitus Types
Type I: Insulin-Dependent Diabetes Mellitus (IDDM) Immune-mediated destruction of beta cells
Genetic or chronic pancreatitis 50% of diabetic dogs Absolute insulin deficiency
Type II: Non Insulin-dependent Diabetes Mellitus (NIDDM) Insulin resistance, decreased insulin secretion
Obesity, inactivity, amyloid deposition in beta cells Most diabetic cats Relative insulin deficiency
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Quick Review: Normal Cellular Respiration
• ATP: currency of life!• From breakdown of
glucose• From Kreb’s cycle• From electron
transport chain
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Glucose Behaving Badly: Cellular Metabolic Derangements
Too much of a good thing↑ glucose + ↑ fatty acids = too much acetyl coA
Kreb’s cycle says “I can’t handle this!”
Acetyl coA says “Well, I have to go somewhere!”
Liver says “I got your back bro, let me convert you into ketone bodies for an alternative source of energy!”
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DKA Pathophysiology, Redux
↓ insulin and ↑ glucagon
↑ lipolysis for energy → ↑ free fatty acids ↑ glucose release from liver: glycogenolysis, gluconeogenesis
Mitochondrial B oxidation of FA → acetyl- CoA
Accumulation of acetyl- CoA
acetyl- CoA → ketones: B-hydroxybutyrate, acetoacetate, acetone
Dissociation of these anions → ↑ [H+] → ketotic acidosis
↑ [glucose] in blood
Glucose spillover into urineKitties: 250 mg/dL [RR: 60-125 mg/dL]Dogs: 200 mg/dL [RR: 60-125 mg/dL]
Osmotic diuresis → dehydration, urinary electrolyte losses: Na, Cl, K, Phos
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Clinical Pathology of DKA
Metabolic acidosis with a increased anion gapBonus NAVLE review time: Anion Gap! Body fluids are electrically neutral, aka equal amounts of anions and
cations. Commonly measured cations: Na+, K+ Commonly measured anions: Cl-, HCO3- Sum of the commonly measured cations < sum of commonly measured anions.
Aka, there are more unmeasured anions (UA) than unmeasured cations (UC) anion gap!
Anion gap = (Na+ + K+) – (Cl- + HCO3-) = UA –UC Ketoacids are anions; ↑ ketoacid levels ↑ the anion gap! Other causes of ↑ AG: lactic acidosis, uremic acidosis, toxins: ethylene
glycol, ethanol, aspirin
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Clinical Pathology of DKA: Chemistry
High serum osmolality. Due to hyperglycemia, azotemia, ketones.Bonus NAVLE Review time: Osmolality! Osmolality = osmoles per kg of solvent. Vs. Osmolarity = osmoles per L of
solution. Osmole = something that draws H2O toward it: Alcohols, sugars, lipids, proteins. Effective osmole = something that generates osmotic pressure b/c it draws and keeps
H2O on its side of a semipermeable membrane. Osmolality is both measured (osmometer), and calculated. The difference between
these two is the osmol gap, which is normally < 10 mOsm/kg. Calculated Osmlality = 2 (Na+ + K+) + BUN/2.8 + Glucose/18
Why do I care about this? If you have a high osmolal gap, this raises your suspicion for unsuspected osmols in the
serum (MAE DIE), because you didn’t account for them in your calculated osmol gap. Reference Values: Dogs: 308-335 mOsm/kg. Cats: 290-310 mOsm/kg.
Osmole MnemonicMethanolAcetoneEthanolDiuretics (mannitol, sorbitol)IsopropanolEthylene glycol
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Clinical Pathology of DKA: Chemistry
Hyponatremia True hyponatremia: urinary loss. Pseudohyponatremia: due to hyperglycemia. Correct for this below:
Corrected Na: Measured Na + 0.016 x (serum glucose – 100) Corrected Na if glucose > 600 mg/dL: Measured Na + 0.024 x (serum glucose – 100)
Potassium Low: urinary loss, vomiting, anorexia, or binding to ketoacids. High: due to intracellular to extracellular shifting to correct for acidemia: H+ in,
K+ out.
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Clinical Pathology of DKA: Chemistry
Hypophosphatemia: urinary loss, hemolysis (in cats: Heinz body anemia) Other Electrolytes: Hypochloremia, Hypomagnesemia, Hypocalcemia Hyperlactatemia: poor tissue perfusion 2o to hypovolemia from dehydration Azotemia: dehydration ↑ ALT, ALP, GGT, tibili (hepatocellular damage d/t altered metabolism; hepatic lipid
infilitration and 2o cholestasis or hemolysis of Heinz bodies) Hyperlipidemia ↑ amylase and lipase (pancreatitis)
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Clinical Pathology of DKA: CBC, UA CBC:
Stress or an inflammatory leukogram ↑ HCT/PCV and TS (dehydration) Heinz bodies in kitty RBCs anemia (Heinz body formation associated with B-
hydroxybutyrate formation) Urine
Ketonuria and glucosuria Pyuria, proteinuria, hematuria (diabetic animals are prone to UTIs) Low USG (medullary washout 2o to osmotic diuresis)
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Clinical Signs: What DKA looks like!
Runs the gamut: from BAR to severe Mentally dull Dehydrated (gums, skin tent, eyes) Vomiting/Anorexia Body condition: under or overweight Cranial organolmegaly Remember, this might be the first presentation for a previously
unknown diabetic animal.
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Diabetes Comorbidities and DDX
Dogs: Hyperadrenocorticism Acute pancreatitis Urinary tract infections Cataracts
Cats: Hepatic lipidosis Chronic renal failure Acute pancreatitis Bacterial/viral infections neoplasia
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DKA Treatment: Fluids and Elytes
Fluid TherapyReplacement fluids Consider a buffered solution like LRS or Normosol-R; fine to use 0.9% NaCl, too
Lactate converted into bicarbonate in the liver. How handy! Time over which to replace? Look at your patient!Maintenance Fluids: 0.45% NaCl +/- 2.5% or 5% dextrose once BG ~250 mg/dLElectrolyte Abnormality CorrectionsPotassium: If low, supplement with a potassium CRI, not to exceed 0.5 mEq/kg/hr. Hyperkalemia will often resolve as the acidemia improves with rehydration and insulin.Phosphorus: potassium phosphate CRI (has 4.4 mEq of K and 3 mM/ml of Phos)Magnesium: magnesium sulfate CRI 0.5-1 mEq/kg q24h
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DKA: Insulin TherapyInsulin Therapy Why: stops ketogenesis, ↑ utilization of ketones, ↓ gluconeogenesis, ↑ glucose
utilization. Most effective if tissue perfusion has been restored
When: 1-4 hours after you start your rehydration; wait longer (4-8 hours) if patient was hypokalemic. Supplement your fluids with potassium.
What: Regular insulin CRI, initially @ 10 ml/hr, in a separate line from fluids. Dogs: 2.2 U/kg of regular insulin added to a 250 ml bag of 0.9% NaCl Cats: 1.1 U/kg of regular insulin added to a 250 ml bag of 0.9% NaCl Recheck BG q2h; when <250, switch fluid to 0.45% NaCl + 2.5% dextrose and slow your
insulin rate to 7 ml/hr; see next slide. Run 50 ml of the insulin solution through the administration set first (insulin can adhere to the
plastic).
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Handy Insulin CRI Protcol courtesy of Dibartola
Blood Glucose Conc (mg/dL)
Intravenous Fluid Solution
IV Insulin Solution Rate
250 0.9% saline 10200-250 0.9% saline, 2.5%
dextrose7
150-200 0.9% saline, 2.5% dextrose
5
100-150 0.9% saline, 5% dextrose
5
<100 0.9% saline, 5% dextrose
Stop the insulin
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DKA Therapy Monitoring
Monitoring plan BG q2h-4h Blood pressure Electrolytes q8-12h PCV/TS q8-12h: assess rehydration Body weight q24h: is your hydration plan working? mentation
Other therapies: NUTRITION! We want these guys eating on their own again. Anti-emetics Heat support
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Hyperglycemic, Hyperosmolar State
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What makes a patient HHS?
Extreme hyperglycemia: >600 mg/dl
Serum osmolality: > 350 mOsm/kg
Little or no ketonuria
Decreased GFR severe dehydration
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Pathophysiology of HHS
Similar to DKA: ↓ insulin; ↑ glucagon, cortisol, growth hormone Small amounts of insulin help prevent ketone formation
HyperglycemiaAnd
hyperosmolality
Osmotic diuresis
dehydration
Reduced GFR
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HHS Therapy and Monitoring
Similar to DKA Therapy: Treat hypovolemic shock: 20 ml/kg bolus for cats; 30 ml/kg bolus for dogs of an
isotonic fluid Decrease sodium slowly to avoid cerebral edema: 1 mEq/L/hr or less! Nutrition Anti-emetics
Monitoring, as before for DKA: BG q2h-4h Blood pressure Electrolytes q8-12h PCV/TS q8-12h: assess rehydration Body weight q24h: is your hydration plan working? mentation
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Prognostic Information
DKA: 70% of dogs and cats survive until discharge Median time in hospital 6 days dogs; 5 days cats
7% of dogs have a recurrence of DKA 40% of cats have a recurrence of DKA
HHS: Very little data in veterinary patients One study in cats: 64% mortality in hospital; 38% in dogs Human children: 72% mortality
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References
Ettinger, SJ & Feldman, EC. (2009). Textbook of Veterinary Internal Medicine, vol 7. St. Louis, MO: Saunders Elsevier.
Hopper, K & Silverstein D. (2015). Small Animal Critical Care Medicine. St. Louis, MO: Elsevier Saunders.