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    Lecture 3 - Acute Hyperglycemic Complications

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    CristinaGheorghe
    The document discusses hyperglycemic crises in diabetes patients, focusing on diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). [1] DKA is caused by low insulin levels and high counterregulatory hormones, leading to increased hepatic glucose output, decreased glucose uptake, and fat breakdown producing ketones which cause metabolic acidosis. [2] HHS involves high blood sugar and severe dehydration but minimal ketones due to partial insulin deficiency and increased glucagon/cortisol. [3] Both can be precipitated by infection, insulin issues, or medical illness and require fluid and electrolyte correction along with treating the underlying cause.

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    © All Rights Reserved
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    Lecture 3 - Acute Hyperglycemic Complications

    Uploaded by

    CristinaGheorghe
    8 views24 pages
    The document discusses hyperglycemic crises in diabetes patients, focusing on diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). [1] DKA is caused by low insulin levels and high counterregulatory hormones, leading to increased hepatic glucose output, decreased glucose uptake, and fat breakdown producing ketones which cause metabolic acidosis. [2] HHS involves high blood sugar and severe dehydration but minimal ketones due to partial insulin deficiency and increased glucagon/cortisol. [3] Both can be precipitated by infection, insulin issues, or medical illness and require fluid and electrolyte correction along with treating the underlying cause.

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    Lecture 3- Acute Hyperglycemic Complications

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    The document discusses hyperglycemic crises in diabetes patients, focusing on diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). [1] DKA is caused by low insulin levels and high counterregulatory hormones, leading to increased hepatic glucose output, decreased glucose uptake, and fat breakdown producing ketones which cause metabolic acidosis. [2] HHS involves high blood sugar and severe dehydration but minimal ketones due to partial insulin deficiency and increased glucagon/cortisol. [3] Both can be precipitated by infection, insulin issues, or medical illness and require fluid and electrolyte correction along with treating the underlying cause.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    8 views24 pages

    Lecture 3 - Acute Hyperglycemic Complications

    Uploaded by

    CristinaGheorghe
    The document discusses hyperglycemic crises in diabetes patients, focusing on diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). [1] DKA is caused by low insulin levels and high counterregulatory hormones, leading to increased hepatic glucose output, decreased glucose uptake, and fat breakdown producing ketones which cause metabolic acidosis. [2] HHS involves high blood sugar and severe dehydration but minimal ketones due to partial insulin deficiency and increased glucagon/cortisol. [3] Both can be precipitated by infection, insulin issues, or medical illness and require fluid and electrolyte correction along with treating the underlying cause.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 24

    Hyperglycemic crises in patients

    with diabetes

    As. Univ. Dr. Stegaru Daniela

    UMF “Carol Davila” Bucuresti


    DIABETIC KETOACIDOSIS (DKA)
    HYPERGLICEMIC HYPEROSMOLAR STATE (HHS)
    LACTIC ACIDOSIS
    DKA Pathogenesis

    DECREASED INSULIN LEVEL


    INCREASED LEVELS OF COUNTERREGULATORY HORMONES

    1.Increased hepatic glucose output

    2. Decreased peripheral glucose uptake

    3. Increased lipolysis with FFA release – substrate for ketone


    production (acetoacetate, β-hidroxibutirate, acetone)

    KETONEMIA/KETONURIA – METABOLIC ACIDOSIS


    DKA Pathogenesis

     FFA ↑ = substrate for the production of ketones

     FFA β oxidation → ketones


     β hidroxibutirate/ acetoacetate = 10:1

    KETONEMIA /ACIDOSIS
    - inotrope negative effect
    - Hypotension secondary to peripheral vasodilatation
    - ↑ arrhythmia risk
    - Respiratory distress
    DKA/HHS pathogenesis

    Pathogenesis of DKA and HHS: stress, infection, or insufficient insulin.

    Abbas E. Kitabchi et al. Dia Care 2009;32:1335-1343


    Epidemiology

    Annual frequency of DKA 0,5-0,8%


    Mortality rates 2-5%
    Tendency of decreased mortality in the last decades !
    PRECIPITATING FACTORS

    INFECTION (30-50%)

    INSULIN TREATMENT CESSATION


    (INADEQUATE TREATMENT)

    TYPE 1 DIABETES at onset

    ACUTE SEVERE MEDICAL DISEASES


    STROKE
    MYOCARDIAL INFARCTION
    SEVERE TRAUMA
    PANCREATITIS

    ALCOHOL AND DRUG ABUSE


    DKA -
    CLinical
    SYMPTOMS:
    Intense thirst, polyuria, polyfagia, adynamia,
    Vomiting, abdominal pain, false surgical abdomen
    Meteorism, sometimes no transit (adynamic ileus),
    Polypnea, ketone smell of breathing (“rotten apples”)
    Altered sensorium and, finally, coma

    PHYSICAL EXAMINATION:
    Dehydration – Dry tongue, decreased skin elasticity,
    hypotonic eye bulbs
    Acidotic breathing - Kussmaul, deep, noisy
    pH < 7,2
    Cardiovascular –Tachycardia; Hypotension;
    Neurologic - Obnubilation, Coma;

    Hypotermia (peripheral vasodillatation);


    DKA – Clinical
    Picture
    Clinical/biological parameters
    Parameter Rhytm

    Vitals, neurologic status, Fluid intake / Fluid loss 1h

    Capillary blood glucose 1h

    Glycemia, ionogram (Na, K, Cl, Ca, P) 2h

    pH, Bicarbonate, pCO2 2h

    Anionic gap: Na – (HCO3 + Cl); Normal: 10-12 mEq/L 2h

    Effective Osmolarity : 2x(Na + K) + Gliycemia (mmol/L) 2h

    Uree, Creatinin, Blood count 24 h

    Urine, Blood cultures

    Pulmonary Rx
    LABORATORY DATA

    GLYCEMIA ↑
    Ph ↓
    SERUM BICARBONATE ↓
    Osmolarity N ; ↑
    Glycosuria, urinary ketones+
    Lipids ↑
    Leukocytosis
    Natremia ↓↓ , N , ↑
    Kalemia ↑↑ , N , ↓
    ± creatinin ↑
    DKA Diagnostic Criteria

    MILD MODERATE SEVERE


    Glycemia >250 mg/dl >250 mg/dl >250 mg/dl

    PH 7,25-7,30 7-7,25 <7

    Serum HCO3- (mEq/i) 15-18 10-15 < 10

    Urine ketones positive positive positive


    Serum ketones positive positive positive

    Osmolarity. variable variable variable

    Anionic Gap >10 >12 >12

    Neurologic Status vigile vigile/confusion stupor/coma


    Treatment Objectives

    Correction of fluid deficit (dehydration)


    Correction of acidosis / ketosis remission
    Correction of hyperglycemia
    Complication Prevention
    Hypoglycemia
    Hypokalemia
    Cerebral Edema

    Identification/Treatment of trigger factor


    Abbas E. Kitabchi et al. Dia Care 2009;32:1335-1343
    Hyperglicemic Hyperosmolar State (HHS)
    (Hyperosmolar Coma)
    Definition – biochemical features

    • Marked Hyperglicemia
    • Severe Dehydration
    • Hyperosmolarity (Glucose + Na)
    • Usually in elderly subjects (altered thirst
    sensation)

    Presence of a minimal insulin secretion


    prevents lipolysis in adipose tissue –
    Ketones and metabolic acidosis are absent !
    Pathogenesis

    Partial / relative insulin deficit

    Increased
    Decreased perihperal glucose uptake
    glucagon + cortisole
    (muscle, adipose tissue, liver)
    Increased hepatic
    glucose output

    Hyperglicemia
    Glycosuria
    Osmotic diuresis
    Polyuria
    Dehydration
    Pathogenesis

    • If adequate fluid intake cannot be provided (loss of


    thirst sensation in elderly patients) or in the presence of
    excessive fluid loss (fever, vomiting, diarheea, burns)
    marked dehydration
    Prerenal renal failure

    Glycemia + Na = increased osmolarity

    Osm > 320-330 mOsm/L


    OBNUBILATION / COMĂ
    Diagnostic Criteria
    Clinical features
     Sypmtoms onset is insidious – days or even
    weeks !
     Severe Dehydration – Hypotension
     Oliguria
     Astenia, letargy
     Absence of acidotic breathing (Kusmaul)
     Different degrees of neurologic impairment, up
    to deep coma
     ± focal neurologic signs – Stroke should be rulled
    out (CT scan)
    Precipitating Factors

     Infection (Respiratory / urinary)


     AMI, Stroke, Pulmonary Embolia, Acute Pancreatitis
     Burns / Recent surgery
     Politrauma
     Acute Renal Failure

    • Drugs

     diuretics - increase dehydration, K loss


     glucocorticoids (prednisone, hydrocortisone,
    dexamethasone, methylprednisolone)
    Evaluation and treatment

    Abbas E. Kitabchi et al. Dia Care 2009;32:1335-1343


    Complication / Prognosis

     Poor prognosis

     Renal injury – Sometimes requiring dyalisis

     Rabdomiolysis with increased CK (> 1000U/l) in the


    absence of AMI

     Mortality rates higher (10 x) compared to DKA (elderly,


    frail patients, preexistent CV disease or other severe
    medical conditions)

     Usually prognosis is determined by the medical condition


    that induced HHS
    Diferential Diagnosis DKA = Hypoglycemia
    Criterion Severe hypooglycemia DKA
    Causes Decreased food intake Infection
    Increased exercise Skipped insulin shots
    Insulin overdosing Vomiting
    Alcohol intake Stress
    Onset Relatively abrupt (30 min) Slow, hours or days
    or very rapid (minutes)
    Clinical
    - Breathing Normal sau stertorous Acidotic, Kussmaul
    - Halenă Not significant Acetone
    - Skin Moist, pale Dry
    - Tongue Moist Dry, burned
    - Pupila Midriasis (large) Normal
    - Eye globes Normal Tonus Decreased Tonus
    -Muscle tone Increased, contractions, convulsions Hypotonia
    - BP Mildly increased, Normal Mildly decreased, Normal
    - Pulse Strong, normal Decreased

    Biochemistry
    - Glycosuria Absent or weekly positive Intense positive
    - Ketonuria Absent or weekly positive Intense positive
    - BG Decreased Increased
    - pH Normal Decreased
    - Leukocytosis Absent Present / Severe
    Atitute in front of a comatous
    diabetic subject ?
     If no laboratory / glucometer data are available and
    if the clinical picture is non relevant …

    Give glucose !!!

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