Hyperglcemic Crises

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Transcript of Hyperglcemic Crises

  • DIABETIC KETOACIDOSISHYPEROSMOLAR HYPERGLYCEMIC STATELACTIC ACIDOSIS

    HYPERGLYCEMIC CRISES

  • Pathogenesis of DKA

    REDUCTION OF CIRCULATING INSULIN

    ELEVATION OF COUNTERREGULATORYHORMONES(glucagon, catecholamines, cortisol,growth hormone)

  • Pathogenesis of DKAREDUCTION OF CIRCULATING INSULINELEVATION OF COUNTERREGULATORYHORMONES

    1.increased hepatic glucose production HYPERGLYCEMIA2. impaired glucose utilization in peripheral tissues3.lipolysis - release of free fatty acids into the circulationand to unrestrained hepatic fatty acid oxidation to ketone bodies(acetoacetat, -hydroxibutyrat)KETONEMIA( METABOLIC ACIDOSIS)

  • HyperglycemiaGlycozuria osmotic diuresisLoss of water+electrolytesPathogenesis of DKA

  • Epidemiology

    Annual incidence of DKA 0,5-0,8%Two-third of DKA patients were considered to have type1 diabetes Mortality rate 2-5%Death is rarely due to the metabolic complications ofhyperglycemia or ketoacidosis but relates to theunderlying precipitating illness.

  • INFECTION(30-50%)

    DISCONTINUATION OF INSULIN(inadequate insulin)NEW-ONSET TYPE 1 DIABETES

    CEREBROVASCULAR ACCIDENTMYOCARDIAL INFARCTIONSEVERE TRAUMA PANCREATITISALCOHOL ABUSEDRUGS( ex.corticosteroids )

    Precipitating Factors

  • DKA clinical picture:

    The metabolic alterations typical of DKA- usually evolve within a short time frame, < 24 h.

    SYMPTOMS:Polyuria, polydipsia, weight loss, weakness, Nausea,vomiting( emesis which may be ,,cofee- ground), diffuse abdominal pain.

    Polypnea;the breath has an acetone odor.Clouding of sensoria and finally coma.

  • DKA clinical picture:

    PHYSICAL FINDINGS:Dehydration- poor skin turgor, dry mouth

    Kussmaul respiration, deep, noisy pH < 7,2Cardiovas.- Tachycardia; Hypotension or normal BP;Neuro. mental status can vary from full alertness to profound lethargy or coma Hypotermia ( peripheral vasodilation );

  • LABORATORY FINDINGS

    Glucose(mg/dl)PH Bicarbonate(mEq/l) OsmolalityKetonemia/Ketonuria Na(mEq/l), K(mEq/l)Anion gap = [Na+] - [Cl- + HCO3-] BUN, creatinine,complete blood count, ECG, chest X-rayUrine or blood cultures,etc.

  • DKA....Laboratory

    Hyperglycemia is a key diagnostic criterion of DKA, however, a wide range of plasma glucose can be present on admision. ~10% of DKA presents glucose levels 250mg/dl due to antecedent food restriction, inhibition of gluconeogenesis or insulin injection en route to the hospital.Leukocytosis (10000-15000mm) is the rule in DKA and may not be indicative of an infectious process.

  • DKA....LaboratoryHyperamylasemia has been reported but there is little correlation with the presence of gastrointestinal symptoms

    Na+ = N or ( usually low because of the osmotic flux of water from intracellular to extracellular space) K+ = , N or ( usually elevated because of an extracellular shift of potassium caused by acidemia )

  • DKA....Laboratory

    Accumulation of ketoacids results in pH 7,30and an increased anion gap metabolic acidosisDKA intensity pH, HCO3-

    AG = [Na+] - [Cl- + HCO3-] AG > 10-12 mmol/l indicate the presence of increased anion gap metabolic acidosis. Severe DKA AG = 25 35mmol/lKetonuria not correlate with the intensity of acidosis

  • Diagnostic criteria for DKA

    MILDE MODERATE SEVERE Plasma glucose >250 mg/dl >250 mg/dl >250 mg/dl

    Arterial pH 7,25-7,30 7-7,25 < 7

    SerumHCO3-(mEq/i) 15-18 10-15 < 10

    Urine ketone pozitive pozitive pozitiveSerum ketone pozitive pozitive pozitiei

    Serum osmolality. variable variable variable

    Anion gap >10 >12 >12

    Mental status alert alert/drowsy stupor/coma

  • ALCOHOLIC KETOACIDOSIS

    STARVATION KETOSIS

    Other METABOLIC ACIDOSIS(lactic acidosis, ingestion of salicylate ,methanol,ethylenglycol,paraldehyde)

    GASTROINTESTINAL SYMPTOMS(ex. serum lipase determination may be beneficial in the dif.diag.of pancreatitis)

    COMA

    DIFFERENTIAL DIAGNOSIS

  • Corection of:

    Dehydration

    Hyperglycemia

    Electrolyte imbalances

    use of bicarbonate

    Treatment of comorbid precipitating events

    TREATMENT OF DKA

  • Frequent patient monitoring !!!!

    2 h. control glycemia electrolytes physical examination

  • Fluid therapy

    Isotonic saline (0,9% NaCl) is infused at a rate of 15-20 ml/kc body w./h or 1l during first hour

    Subsequent choice for fluid replacement depends on hemodynamics,the state of hydration, serum electrolyte levels and urinary output.

    5% dextrose should be added when plasma glucose is 250 mg/dl.

  • !!! REGULAR INSULIN !!!

    The administration of continuous intravenous infusion of regular insulin is the preferred route

    Treatment algorithms recommended the adm. of an initial intravenous dose of regular insulin 0,1u/kgCfollowed by the infusion of 0,1u/kg/h

    If serum glucose does not fall by 10% in first hour(50- 70mg/dl/h) the insulin infusion shoud be increasedevery hour.

    INSULIN therapy

  • POTASSIUM < 3,3 mEq/l + 40 mEq K 3,3 5 mEq/l + 20-30 mEq K 5,0 mEq/l NO

    Insulin therapy,correction of acidosis and volume expansiondecrease serum potassium concentration!

    To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5mEq/l

    ELECTROLYTE replacement

  • PH < 6,9NaHCO3 100 mmol in 400ml steril water

    PH > 7,0No

    BICARBONATE therapy

  • HYPOPOTASEMIA

    HYPOGLYCEMIAare two common complications

    CEREBRAL EDEMA prevention might includeavoidance of excessive hydration anda gradual decrease in serum glucosePULMONARY EDEMA HYPERCHLOREMIC ACIDOSIS DEATH

    COMPLICATIONS

  • PREVENTION

    Many cases of DKA and HHS can be prevented by :

    better access to medical care,proper patient education, andeffective communication with a health care providerduring an intercurent illness.

  • HYPEROSMOLAR HYPERGLICEMIC STATE

    Definition:Hyperosmolarity(Osm > 320-330 mosm/kg) Hyperglycemia Dehydration Occurs in middle-aged and older adults with type 2 diabetes In most patients with HHS, restricted water intake is due to patient being bedridden and is exacerbated by the altered thirst response of the elderly.Ketonuria and acidosis are missing!

  • HyperglycemiaGlycozuria osmotic diuresisLoss of water+electrolytesPathogenesis of DKA

  • Pathogenesis of HHS

    Insulin levels in HHS are inadequate to facilitate glucose utilization by insulinsensitive tissues but adequate to prevent lipolysis and subsequent ketogenesis!

  • HHS clinical picture:

    The process of HHS usually evolves over several days to week ! intense thirstpolyuriaweaknessmental status can vary but coma is more frequent. focal neurologic signs(hemianopsia, hemiparesis) and seizures(focal or generalized) may also be features of HHS (exam. CT)

  • HHS clinical picture:

    Physical examination

    Severe dehydration (hypoT, tahycardia shock)stupor / comaOliguria suggests Acute renal failure due to dehydration (prerenal azotemia or preexisting chronic renal failure)

  • DIAGNOSIS

  • Precipitating Factors

    Infection- particulary pneumonia or gram-negative sepsis, is the most common initiating event.Myocardial infarction, cerebrovascular accident, TE, PancreatitisBurns / Severe traumaDrugs diuretics - enhances dehydration, corticosteroids PhenytoinAntipsychotic drugs

  • HHS....Laboratory

    Severe hyperglycemia (800.2400 mg/dl)Hyperosmolarity - (320 -440 mOsm/kg) Na+ = , N or Osm pl = 2 x (Na +glu / 18) N = 290-310 mOsm/kg

  • Treatment of HHS

  • COMPLICATIONS / PrognosticRhabdomyolysis(non-traumatic.)CreatinKinase (> 1000U/l) One of the dreaded complications of R. is Kidney failure. Pulmonary thromboembolism;Peripheral venous thrombosis- Mortality attributed to HHS is considerably higher than that attributed to DKA(10 times)- The prognostic is substantially worsend at the extremes of age in the presence of coma, hypotension and severe comorbidities.

  • Lactic Acidosis

    LA may develop in any state of:Diminished tissue oxygenation(eg.vascular shock)- excessive lactat production. Hepatic dysfunction (and diminished conversion of lactat to glucose)LA is characterized by low pH acompanied by the buildup of lactat.Abnormal anion gap + Lactat level > 7 mmol/l

  • Causes of LA

    ShockSepsisEthanol toxicityHepatic diseaseDiabetic ketoacidosisDrugs: metformin/ phenforminInborn error of metabolism

  • Symptoms

    Nousea, vomiting, abdominal painHyperventilation (to remove CO2)Severe anemiaHypotension Irregular heart rateTachycardia Anxiety/ lethargy

  • Treatment of LA

    1.Sodium