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Acute complications of diabetes

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Title: Acute complications of diabetes


1
Acute complications of diabetes
2
  • Glucose homeostasis refloects a precise balance
    between hepatic glucose production and
    periphereal glucose uptake and utilization.
  • Insulin is thye most important regulator of the
    metabolic equilibrium.

3
In the fasting state
  • Low insulin levels promote hepatic
    gluconeogenesis and glycogenolysis to prevent
    hypoglicemia

4
Postprandially
  • A large glucose load elicits a rise in insulin
    and fall in glucagon.

5
Diabetes Mellitus
6
DM
  • Comprises a group of common metabolic disorders
    that share the phenotype of hyperglycemia.

7
  • In the US, DM is the leading cause of
  • End-stage renal disease
  • Nontraumatic lower extremity amputations.
  • Adult blindness.

8
Clasification
9
Epidemiology
  • In 1998, approximately 16 million individuals in
    the US met the diagnoistic criteria for DM (6 of
    the population)
  • The vast majority of these gt90 have type 2

10
  • Incidence
  • 1.5 (20 to 39 years)
  • 20 (gt75 years)

11
Diagnosis
12
Acute complications of diabetes
13
  • Diabetic ketoacidosis (DKA) and hyperglicemic
    hyperosmolar nonketotic syndrome (HHNS) are life
    threatening acute metabolic complications of
    diabetes mellitus.

14
  • These complications can be seen in type 1 and
    type 2 diabetes.
  • DKA is usually seen in patients with type 1
    diabetes.
  • HHNS in patients with type 2 disease.

15
  • Both disorders are associated with
  • Absolute or relative insulin deficiency
  • Volume depletion
  • And altered mental status.
  • Potentially serious complications if not promptly
    diagnosed and treated.

16
Diabetic ketoacidosis
17
  • DKA is a complex disordered metabolic state
    characterized by hyperglycemia, acidosis, and
    ketonuria.

18
  • DKA still accounts for 50 of diabetes-related
    admissions in young persons
  • And 1-2 of all primary diabetes-related
    admissions.

19
Incidence
  • Exact incidence is not known, but it is estimated
    to be 1 out of 2000.

20
  • Race Incidence of DKA is higher in whites
    because of the higher incidence of type 1
    diabetes in this racial group.

21
  • Sex Incidence of DKA is slightly more common in
    females than in males for reasons that are
    unclear.

22
  • Age DKA is much more common in young children
    and adolescents

23
Pathophysiology
  • DKA usually occurs as a consequence of absolute
    or relative insulin deficiency that is
    accompanied by an increase in counter-regulatory
    hormones

24
  • Counter-regulatory hormones (ie, glucagon,
    cortisol, growth hormone, epinephrine).
  • This type of hormonal imbalance enhances hepatic
    gluconeogenesis, glycogenolysis, and lipolysis

25
  • Hepatic gluconeogenesis, glycogenolysis secondary
    to insulin deficiency, and counter-regulatory
    hormone excess result in severe hyperglycemia,
    while lipolysis increases serum free fatty acids.

26
  • Hepatic metabolism of free fatty acids as an
    alternative energy source (ie, ketogenesis)
    results in accumulation of acidic intermediate
    and end metabolites (ie, ketones, ketoacids).
  • Ketones include acetone, beta hydroxybutyrate,
    and acetoacetate.

27
  • Progressive rise of blood concentration of these
    acidic organic substances initially leads to a
    state of ketonemia.
  • Natural body buffers can buffer ketonemia in its
    early stages.

28
  • When the accumulated ketones exceed the body's
    capacity of extracting them, they overflow into
    urine (ie, ketonuria).

29
  • If the situation is not treated promptly, more
    accumulation of organic acids leads to frank
    clinical metabolic acidosis (ie, ketoacidosis),
    with a drop in pH and bicarbonate serum levels.

30
  • Respiratory compensation of this acidotic
    condition results in rapid shallow breathing
    (Kussmaul respirations).

31
  • Ketones, in particular beta hydroxybutyrate,
    induce nausea and vomiting that consequently
    aggravate fluid and electrolyte loss already
    existing in DKA.

32
  • Acetone produces the characteristic fruity breath
    odor of ketotic patients.

33
  • Hyperglycemia usually exceeds the renal threshold
    of glucose absorption and results in significant
    glycosuria.
  • Consequently, water loss in the urine is
    increased due to osmotic diuresis induced by
    glycosuria.
  • This incidence of increased water loss results in
    severe dehydration, thirst, tissue hypoperfusion,
    and lactic acidosis.

34
  • Typical free water loss in DKA is approximately 6
    liters or nearly 100 mL/kg of body weight.
  • The initial half of this amount is derived from
    intracellular fluid and precedes signs of
    dehydration.
  • The other half is from extracellular fluid and is
    responsible for signs of dehydration.

35
  • Hyperglycemia, osmotic diuresis, serum
    hyperosmolarity, and metabolic acidosis result in
    severe electrolyte disturbances.

36
  • The most characteristic disturbance is total body
    potassium loss.
  • This loss is not mirrored in serum potassium
    levels, which may be low, within the reference
    range, or even high.

37
  • Potassium loss is caused by a shift of potassium
    from the intracellular to the extracellular space
    in an exchange with hydrogen ions that accumulate
    extracellularly in acidosis.

38
  • A large part of the shifted extracellular
    potassium is lost in urine because of osmotic
    diuresis

39
  • Patients with initial hypokalemia are considered
    to have severe and serious total body potassium
    depletion.

40
  • High serum osmolarity also drives water from
    intracellular to extracellular space, causing
    dilutional hyponatremia.
  • Sodium also is lost in the urine during the
    osmotic diuresis.

41
  • Typical overall electrolyte loss includes
  • 200-500 mEq/L of potassium
  • 300-700 mEq/L of sodium
  • 350-500 mEq/L of chloride.

42
  • The combined effects of serum hyperosmolarity,
    dehydration, and acidosis result in increased
    osmolarity in brain cells that clinically
    manifests as an alteration in the level of
    consciousness.

43
Pathogenesis of DKA
Type 1 diabetes
Initiatig event
Insulin Glucagon
Lypolisis
Protein catabolism
Glycerol
FFAs
Amino acids
Ketogenesis
Hyperglicemia
Gluconeogenesis
Ketonemia
Ketonuria
Osmotic diuresis
Volumen depletion Dehydration
Acidosis
Electrolite depletion
44
Lipolysis
45
Causes
  • Patients with type 1 diabetes
  • DKA present at diagnosis of type 1 diabetes.
  • Omission of insulin injections.
  • Intercurrent illness (eg, UTI, vomiting)
  • Medical, surgical, or emotional stress
  • Idiopathic (no identifiable cause)
  • Insulin infusion catheter blockage
  • Mechanical failure of insulin infusion pump
  • Patients with type 2 diabetes
  • Intercurrent illness (eg, myocardial infarction,
    pneumonia, prostatitis, UTI)
  • Medication (eg, corticosteroids, pentamidine,
    clozapine)IFFERENTIALS

46
Syntoms
  • Polydipsia
  • Polyuria
  • Nausea
  • Vomiting
  • Diffuse abdominal pain.
  • Generalized weakness
  • Fatigability
  • Altered consciousness (frank coma is uncommon)

47
Physical Finding
  • Dehydration
  • Rapid pulse
  • Dry tongue and skin
  • Hypotension
  • Increased capillary refill time
  • Patient odor - Characteristic acetone odor
  • Signs of acidosis..

48
  • Signs of acidosis
  • Shallow rapid breathing (Kussmaul respiration).
  • Abdominal tenderness.
  • Disturbance of consciousness

49
  • Although these signs are not usual in all cases
    of DKA, their presence signifies a severe form of
    DKA

50
Laboratory Criteria DKA
  • Glucose 300 600
  • Arterial pH lt 7.3
  • HCO3 lt15
  • BUN lt 25
  • Osmolality lt320
  • Ketones

51
Hyperglycemic hyperosmolar nonketotic syndrome
  • HHNS

52
Definition
  • State of extreme hyperglycemia, marked
    dehydration, serum hyperosmolarity, altered
    mental status, and absence of sever ketoacidosis

53
  • Progression from poor glucose control to overt
    HHNS requires profound hyperglycemia for a
    significant period of time (2 days to 2 weeks),
    which allows an extreme of hyperosmolality an
    dehydration to develop.

54
  • Occurs in non insulin dependent diabetics and
    in patients deprived of fluid intake.
  • Typical patient is usually an elderly, or
    bed-confined diabetic with impaired or no ability
    to communicate thirst.

55
  • Patients who do not monitor their blood sugar may
    be at increased risk for HHNS

56
Clinical Features
  • Polyuria
  • Orthostatic hypotension
  • Neurologic symptoms
  • Altered mental status
  • Lethargy
  • Obtundation
  • Seizure
  • coma.

57
  • Absent of nausea, vomiting and abdominal pain,
    and the kussmaul respiration.

58
Phathogenesis.
  • In HHNS, basal insulin secretion is maintained.
  • Insulin levels are adequate to prevent peripheral
    lipolysis in adipose tissue.
  • But are not sufficient to allow adequate
    periphereal uptake of glucose or to prevent
    hepatic overproduction of glucose.

59
  • In patients with HHNS
  • Insulin is the major factor suppresing hepatic
    ketogenesis.
  • Levels of insulin are not adequete to prevent
    glucagon-induced hepatic gluconeogenesis.

60
  • HHNS water-deprived, have a subnormal
    osmorregulated thirst and fluid intake.
  • As hyperglicemia worsens, hyperosmolality
    develops, and alteration in mental status occur.

61
  • A depressed level of consciousness leads to a
    decrease in fluid intake, worsening
    hyperglicemia, and hyperosmolality.
  • With eventual development of lethargy or coma.

62
  • In HHNS, the degree of mental status change is
    associated with the degree of hyperosmolality and
    dehydration.

63
Pathogenesis of HHNS
Type 2 diabetes
Initiatig event
Insulin Glucagon
Pre Renal Azotemia
Hyperglicemia Hyperosmolality
Glucose uptake
Osmotic diuresis
Thirst
Volumen depletion Dehydration
Electrolyte depletion
64
Precipitating factors
  • Diabetes
  • Acute illness
  • Medication
  • Substance abuse

65
  • Diabetes
  • New onset
  • Poorly controlled
  • Cessation of therapy
  • Omission of insulin/medication
  • CSII (pump) failure.
  • Fear of hypoglycemia or a poor understanding of
    diabetes and insulin kinetics may be compained by
    omission or a significant reduction of an insulin
    dose.

66
  • Acute illness
  • Infection (pneumonia, UTI, gastroenteritis,
    sepsis)
  • Infarction (cerebral, coronary, mesenteric,
    periphereal)
  • Acute pancreatitis
  • Sever burns
  • Renal Failure
  • Myocardial infarction may be symptomatically
    silent in patients with long standing
    diabetes.

67
  • Medications
  • Thiazides
  • Beta blockers
  • Phenytoin
  • Glucocorticoids
  • Didanosine
  • Somatostatin
  • Hyperalimentation

68
  • Substance abuse
  • Alcohol
  • Cocaine
  • Alcohol and cocaine use were associated with HHNS
    in 44 and 9 of an urban population.

69
Syntoms
  • Several days of deteriorating glycemic control,
    polyuria, and plydipsia are followed by
    increasing lethargy.
  • Alteration in mental status (mild confusion to
    lethargy, stupor, generalized or partial complex
    seizures, myoclonic jerks, chorea, aphasia,
    cerebrovascular accident or coma)

70
Physical findings
  • Hypotension
  • Tachycardia
  • Tachypnea
  • Fever
  • Extreme dehydration
  • Shock with periphereal hypoperfusion
  • Altered mental status (varying degrees)
  • CNS changes in HHNS may mimic a focal neurologic
    event.

71
Laboratory Criteria HHNS
  • Glucose gt600
  • Arterial pH gt 7.3
  • HCO3 gt20
  • BUN gt30
  • Osmolality gt330
  • Ketones or small

72
Clinical evaluation
  • History
  • Physical examination
  • Evaluation of volume and hydration status should
    proceed immediately.
  • Laboratory studies
  • Treatment with insulin can begin before the
    results of laboratory studies have been obtained.

73
Routinely
  • Laboratory studies
  • Glucose
  • Electrolytes Na, K, CO2, CL
  • BUN
  • Cr.
  • pH
  • Anion gap calculated

74
Routinely
  • Chest radiographs
  • Electrocardiograms
  • Cultures of blood, urine and sputum
  • Cardiac enzymes
  • Amylase

75
Laboratory results
  • Hyperglycemia gt 600
  • Hyperosmolarity gt330
  • Electrolytes
  • Na low, normal, or high
  • K low, normal, or high (loss is approximately 5
    to 15 mEq)
  • Ca low
  • Mg low
  • P low
  • BUN high (azotemia prerenal)

76
Formulas
  • Calculation of the anion gap.
  • AG (Na) (Cl HCO3)
  • Calculation effective serum osmolality
  • Efective S osm 2x Na K gl /18
  • Correction of serum sodium
  • Correction Na Na 1.6 x gluc 100
  • 100

( )
( )
( )
77
Terapy
  • Replacement of fluid losses
  • Correction of hyperglycemia and in DKA of
    metabolic acidosis.
  • Replacement of electrolyte losses
  • Detection and treatment of precipitating causes
    and complications.
  • Conversion to a durable diabetes management
    regimen following the correction of DKA or HHNS
  • Prevention of recurrence

78
  • DKA and HHNS require treatment in an intensive
    care (during the first 24-48 hours).
  • Close monitoring is essential
  • Successful treatment requires frequent monitoring
    of the patiens condition and response to
    interventions.

79
  • Points that must be considered and closely
    monitored include
  • Correction of fluid loss with IV fluids.
  • Correction of hyperglycemia with insulin.
  • Correction of electrolyte disturbances,
    particularly potassium loss.
  • Correction of acid-base balance.
  • Treatment of concurrent infection if present.

80
Replacement fluid
  • Infuse 1000 to 1500 ml/hr for the initial the
    first 2 hours
  • Then decrease the rate of infusion to 500 ml/hr
    the following 2 hours
  • Administer 1 liter every 4 hours, depending on
    the degree of dehydration and central venous
    pressure (CVP) readings.

81
  • Initial correction of fluid loss is either by
    isotonic sodium chloride solution or by lactated
    Ringer solution.
  • When the patient becomes euvolemic, the physician
    may switch to half the isotonic sodium chloride
    solution, particularly if hypernatremia exists.

82
  • When blood sugar decreases to less than 180
    mg/dL, isotonic sodium chloride solution is
    replaced with 5 dextrose

83
Correct hyperglycemia
  • IV hydration decrease glucose 80 mg/dl/per hour
  • Insulin infusion 5 to 10 U/hr
  • Optimal rate of glucose decline is 75 to 100
    mg/dl/per hour.

84
  • Blood tests for glucose should be performed
    hourly (until patient is stable, then every 6 h).

85
Insulin
  • The initial insulin dose is a continuous IV
    insulin infusion using an infusion pump, if
    available, at a rate of 0.1 U/kg/h.
  • A mix of 25 units of regular insulin in 250 cc of
    isotonic sodium chloride solution usually is
    infused at a rate of 1 microdrip/Kg/min
  • 70 kg 7 U/h 7 microdrip/min

86
  • The blood sugar drops to less than 180 mg/dL,
    then the rate of infusion decreases to 2-3 U/h
    until the ketoacidotic state abates.

87
  • Do not allow the blood glucose level to fall
    below 200 mg/dL during the first 4-5 hours of
    treatment.
  • Hypoglycemia may develop rapidly with correction
    of ketoacidosis.
  • Rapid correction of hyperglycemia and
    hyperosmolarity may shift water rapidly to the
    hyperosmolar intracellular space and may induce
    cerebral edema.

88
Replace electrolytes
  • Serum electrolyte determinations should be
    obtained hourly (until patient is stable, then
    every 6 h).

89
Replace electrolytes
90
  • The infusion must stop if the potassium level is
    greater than 5 mEq/L.
  • Monitoring of serum potassium must continue even
    after potassium infusion is stopped in the case
    of (expected) recurrence of hypokalemia.

91
  • In severe hypokalemia, not to starting insulin
    therapy is advisable unless potassium replacement
    is underway in order to avoid potentially serious
    cardiac dysrhythmia that may result from
    hypokalemia

92
Acid base balance
  • Sodium bicarbonate only is infused if
    decompensated acidosis starts to threaten the
    patients life, especially when associated with
    either sepsis or lactic acidosis.
  • (EB x 0.3) (Kg) / 3

93
  • Rapid and early correction of acidosis with
    sodium bicarbonate may worsen hypokalemia and
    cause paradoxical cellular acidosis.

94
Treatment of concurrent infection
  • In the presence of infection, administer proper
    antibiotics guided by the results of culture and
    sensitivity studies.
  • Starting empiric antibiotics on suspicion of
    infection until culture results are available may
    be advisable.

95
Mixed syndrome
  • DKA and HHNS should be suspected if
  • pH lt 7.3
  • Ketones are present in the serum
  • Osmolarity is greater than 320 mOsm/L

96
Mortality
  • Even with proper treatment, HHNS has a
    substantially higher mortality than DKA.
  • Up to 50 in some clinical series.
  • 1 10 of all DKA admissions.
  • Better understanding of the pathophysiology of
    DKA and HHNS has resulted in significant
    reduction in the mortality.
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