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                               Thomas Repas D.O.
 Diabetes, Endocrinology and Nutrition Center, Affinity Medical Group, Neenah, Wisconsin
Member, Inpatient Diabetes Management Committee, St. Elizabeth’s Hospital, Appleton, WI
 Member, Diabetes Advisory Group, Wisconsin Diabetes Prevention and Control Program

                  Website: www.endocrinology-online.com
U.S. Total Costs of Diabetes, 2002

               Diabetes Care 26(3):917-932, 2003
Acute Complications of Diabetes

• Acute
  –   Poor wound healing
  –   Infections
  –   Vascular insufficiency
  –   Other
• Hyperglycemic Emergencies
  – Diabetic Ketoacidosis (DKA)
  – Hyperosmolar Hyperglycemic Syndrome (HHS)
Consequences of Poor Hospital Glycemic Control

•   Several studies show diabetes increases morbidity and mortality for myocardial
    infarction, coronary bypass surgery, and stroke. More specifically, when
    glucoses are elevated there may be:

•   Fluid and electrolyte abnormalities secondary to osmotic diuresis
•   Decreased WBC function
•   Delayed gastric emptying
•   Increased surgical complications including:
     – Relative risk for "serious" postoperative nosocomial infections increased by a factor of
       5.7 when glucose >220 mg/dl
     – Relative odds of wound infection increased to 1.17 with glucoses were 207-227 and
       1.78-1.86 when glucoses were >253.
•   Delayed hospital discharge
•   Double the mortality risk in patients admitted with a stroke
Intervention Studies: Evidence That Improving
Glucose Control Improves Outcome

•   Improved WBC function
     – Perioperative insulin infusion improves neutrophil phagocytic activity to 75% of
       baseline activity compared to only 47% in a control group
•   Decreased postoperative mortality
     – Diabetes team followed patients and controlled glucoses using perioperative IV insulin
       infusion and algorithm based SQ premeal insulin. Mortality of diabetic patients
       undergoing CABG in 1993-1996 was reduced to level of nondiabetics. Nationally,
       diabetic patients had 50% higher mortality
•   Decreased infections
     – Perioperative intravenous insulin infusion designed to keep glucoses <200 mg/dl
       reduces the risk of wound infection in diabetics after open heart operations. Incidence
       of Deep Wound Infections decreased from 2.4 to 1.5%
•   Decreased length of stay
     – Use of an inpatient diabetes consultation service decreased length of stay by 56%
  Importance of Excellent Glycemic Control

                                                                                                 •      In a surgical ICU, 1548 patients were
                                                                                                        randomized to intensive vs.
                                                                                                        conventional therapy
                                                                                                          – Intensive = IV insulin to maintain
                                                                                                            BG 80 – 110 mg/dl
                                                                                                          – Conventional = begin IV insulin if
                                                                                                            BG > 215 with goal of 180 – 200
                                                                                                 •      Risk reduction in ICU mortality was
                                                                                                 •      Overall in hospital mortality reduced
                                                                                                 •      Greatest benefits were seen in
                                                                                                        patients with multiorgan failure and
                                                                                                 •      Also reduced duration of mechanical
                                                                                                        ventilation, acute renal failure, and
                                                                                                        need for transfusion

Van de Berghe G, et al. Intensive Insulin Therapy in Critically ill Patients. N Engl J Med. 2001;345:1359-1367.
Cardiovascular Risk
Mortality After MI Reduced by Insulin Therapy in the DIGAMI Study

                                        Standard treatment
                                        IV Insulin 48 hours, then 4 injections daily

   .7       All Subjects                              .7       Low-risk and Not Previously on Insulin
   .6       (N = 620)                                 .6       (N = 272)
            Risk reduction (28%)                               Risk reduction (51%)
   .5       P = .011                                  .5       P = .0004
   .4                                                 .4
   .3                                                 .3
   .2                                                 .2
   .1                                                 .1
    0                                                  0
        0      1       2       3      4        5           0        1      2        3      4   5
                   Years of Follow-up                                   Years of Follow-up

Malmberg, et al. BMJ. 1997;314:1512-1515.

Common Errors in Inpatient Diabetes Management

 •   Admission orders
 •   Overly high glycemic targets
 •   Lack of therapeutic adjustment
 •   Overutilization of “sliding scales”
 •   Underutilization of IV insulin
Hyperglycemic Emergencies
Hyperglycemic Emergencies

• Diabetic Ketoacidosis (DKA)
   –   Occurs in type 1’s
   –   May or may not occur with other illness
   –   Typically younger patients
   –   Mortality <5 % under optimal management
• Hyperosmolar Hyperglycemic Syndrome (HHS)
   –   Occurs in type 2’s
   –   Often occurs with other concurrent illness
   –   Typically older patients
   –   Mortality ~ 15%
Precipitating Factors

•   Infection (Pneumonia and UTI most common)
•   Previously undiagnosed diabetes
•   Inadequate insulin treatment
•   Noncompliance with therapy
•   Unknown or other causes
Symptoms and Clinical Findings

• Diabetic Ketoacidosis: can present rapidly (<24hrs)
   –   nausea & vomiting (most common symptom)
   –   fruity (acetone) breath odor
   –   abdominal pain (but always rule out other pathology also)
   –   Kussmaul breathing (rapid and deep inspiration)
• HHS: often more insidious in presentation (develops over several
   – May have polyuria, polydipsia, and weight loss for days before diagnosis.
   – More likely to have mental status changes or even coma, and/or
     seizures or other focal neurologic findings.
• Both DKA & HHS can have evidence of dehydration such as poor
  skin turgor, dry oral mucosa, hypotension
Diagnostic Criteria

                   DKA        HHS
Plasma Glucose     >250       >600
Arterial pH        <7.3       >7.3
Serum Bicarb       <15        >15
Ketones            Positive   None or small
Serum Osmolality   Varies     >320
Anion Gap          >10        <12
Mental Status      Varies     Stupor/coma
    Anion Gap
A.G.=(Na+) - (Cl- + HCO3-)
  Normal= 7 to 9 mEq/l
  Serum osmolality
2[measured Na] + glucose/18
    Corrected Sodium
For each 100 mg/dl glucose >100 mg/dl, add 1.6
     mEq to sodium value for corrected serum
                 sodium value
Other Causes of Metabolic Acidosis

•   Alcoholic Ketoacidosis
•   Starvation Ketoacidosis
•   Lactic Acidosis
•   Chronic Renal Failure
•   Drug induced
    – Salicylate, Methanol, Ethylene Glycol, Paraldehyde
Therapeutic Goals

1.   Improving circulatory volume and tissue perfusion
2.   Decreasing serum glucose and plasma osmolality
     towards normal
3.   Clearing of urine and serum of ketones at a steady
4.   Correcting electrolyte imbalances
5.   Identifying and treating precipitating factors
Patient Outcomes: Neurologic status
•       Hyperosmolarity can be associated with mental status changes,
        stupor or coma
•       The presence of such mental status changes without
        hyperosmolarity requires consideration of other causes
•       Cerebral edema is a rare, but serious complication with high
        mortality (>70%).
•       Consider cerebral edema when:
    –      Lethargy with deterioration of mental status
    –      Decrease in arousal
    –      Headache
    –      Seizures
    –      Other: Incontinence, pupillary changes, bradycardia, respiratory arrest
Patient Outcomes: Fluid & electrolyte

• During therapy for DKA or HHS, blood should be drawn every
  2–4 h for determination of serum electrolytes, blood urea
  nitrogen, creatinine, osmolality, and venous pH (for DKA).
• Frequently, repeat arterial blood gases are unnecessary;
  venous pH (which is usually 0.03 units lower than arterial pH)
  and/or anion gap can be followed to monitor resolution of
Patient Outcomes: Fluid & electrolyte

• Fluid replacement should correct estimated deficits within the
  first 24 h.
• The induced change in serum osmolality should not exceed
  3 mOsm · kg–1 H2O · h–1
• In patients with renal or cardiac compromise, monitoring of
  serum osmolality and frequent assessment of cardiac, renal,
  and mental status must be performed during fluid
  resuscitation to avoid iatrogenic fluid overload.
    Calculating Fluid
BWD (L) = 0.6 (weight kg) ([measured Na] – 140)
Patient Outcomes:
Blood Glucose

•   Blood Glucose must be monitored every 1 to 2
    hours during treatment
•   Goal is to decrease plasma glucose concentration
    at a rate of 50–75 mg · dl–1 · h–1
Patient Outcomes:

• Ketonemia typically takes longer to clear than hyperglycemia.
• Direct measurement of ß-OHB in the blood is the preferred method
  for monitoring DKA. The nitroprusside method only measures
  acetoacetic acid and acetone.
• However, ß-OHB, the strongest and most prevalent acid in DKA, is
  not measured by the nitroprusside method.
• During therapy, ß-OHB is converted to acetoacetic acid, which may
  lead the clinician to believe that ketosis has worsened.
• Therefore, assessments of urinary or serum ketone levels by the
  nitroprusside method should not be used as an indicator of response
  to therapy.
Patient Outcomes:
Hemodynamic status

• Successful progress with fluid replacement is judged
  by hemodynamic monitoring (improvement in blood
  pressure), measurement of fluid input/output, and
  clinical examination.
Patient Outcomes: Identifying and treating
precipitating factors

•    It is essential to identify and treat precipitating
•    Chest x-rays, urinalysis, blood cultures and other
     studies should be obtained where appropriate
Therapeutic Interventions

•   Replacement of Fluids and electrolytes
•   Insulin Therapy
•   Potassium
•   Phosphate
•   Bicarbonate
Replacement of Fluids and electrolytes

• Initial fluid therapy is directed toward expansion of the intravascular
  and extravascular volume and restoration of renal perfusion.
• In the absence of cardiac compromise, isotonic saline (0.9% NaCl) is
  infused at a rate of 15–20 ml · kg–1 body wt · h–1 or greater during
  the 1st hour ( 1–1.5 l in the average adult).
• Subsequent choice for fluid replacement depends on the state of
  hydration, serum electrolyte levels, and urinary output.
• In general, 0.45% NaCl infused at 4–14 ml · kg–1 · h–1 is
  appropriate if the corrected serum sodium is normal or elevated;
  0.9% NaCl at a similar rate is appropriate if corrected serum sodium
  is low.
Insulin Therapy

• Unless the episode of DKA is mild, regular insulin by
  continuous intravenous infusion is the treatment of choice.
• In adult patients an intravenous bolus of regular insulin at
  0.15 units/kg body wt, followed by a continuous infusion of
  regular insulin at a dose of 0.1 unit · kg–1 · h–1 (5–7 units/h in
  adults), should be administered.
• An initial insulin bolus is not recommended in pediatric
  patients; a continuous insulin infusion of regular insulin at a
  dose of 0.1 unit · kg–1 · h–1 may be started in these patients.
Insulin Therapy

• If plasma glucose does not fall by 50 mg/dl from the initial value in
  the 1st hour, check hydration status; if acceptable, the insulin
  infusion may be doubled every hour until a steady glucose decline
  between 50 and 75 mg/h is achieved.
• When the plasma glucose reaches 250 mg/dl in DKA or 300 mg/dl in
  HHS, it may be possible to decrease the insulin infusion rate to 0.05–
  0.1 unit · kg–1 · h–1 (3–6 units/h), and dextrose (5–10%) may be
  added to the intravenous fluids.
• Thereafter, the rate of insulin administration or the concentration of
  dextrose may need to be adjusted to maintain the above glucose
  values until acidosis in DKA or mental obtundation and
  hyperosmolarity in HHS are resolved.

• Despite total-body potassium depletion, mild to moderate
  hyperkalemia is not uncommon in patients with hyperglycemic crises.
• To prevent hypokalemia, potassium replacement is initiated after
  serum levels fall below 5.5 mEq/l, assuming the presence of adequate
  urine output.
• Generally, 20–30 mEq potassium (2/3 KCl and 1/3 KPO4) in each liter
  of infusion fluid is sufficient to maintain a serum potassium
  concentration within the normal range of 4–5 mEq/l.
• Rarely, DKA patients may present with hypokalemia. In such cases,
  potassium replacement should begin with fluid therapy, and insulin
  treatment should be delayed until potassium concentration is restored
  to >3.3 mEq/l to avoid arrhythmias or cardiac arrest and respiratory
  muscle weakness.

• Despite whole-body phosphate deficits in DKA, serum phosphate is
  often normal or increased at presentation.
• Phosphate concentration decreases with insulin therapy.
• Studies have failed to show any beneficial effect of phosphate
  replacement on the outcome in DKA and overzealous phosphate
  therapy can cause severe hypocalcemia.
• However, to avoid complications, careful phosphate replacement
  may sometimes be indicated in patients with cardiac dysfunction,
  anemia, or respiratory depression and in those with serum
  phosphate concentration <1.0 mg/dl.
• When needed, 20–30 mEq/l potassium phosphate can be added to
  replacement fluids.

• Bicarbonate use in DKA remains controversial
• At a pH >7.0, reestablishing insulin activity blocks lipolysis and
  resolves ketoacidosis without any added bicarbonate.
• Studies have failed to show either beneficial or deleterious
  changes in morbidity or mortality with bicarbonate therapy in
  DKA patients with pH between 6.9 and 7.1
• No studies concerning the use of bicarbonate in DKA with pH
  values <6.9 have been reported.

• Because severe acidosis may cause adverse vascular
  complications, it is a consensus for adult patients with a pH
  <6.9, 100 mmol sodium bicarbonate be added to 400 ml sterile
  water and given at a rate of 200 ml/h.
• In patients with a pH of 6.9–7.0, 50 mmol sodium bicarbonate
  is diluted in 200 ml sterile water and infused at a rate of 200
• Thereafter, pH should be assessed every 2 h until the pH rises
  to 7.0, and treatment should be repeated every 2 h if
• No bicarbonate is necessary if pH is >7.0.

• In the pediatric patient, there are no well designed
  studies in patients with pH <6.9.
• If the pH remains <7.0 after the initial hour of
  hydration, it seems prudent to administer 1–2
  mEq/kg sodium bicarbonate over the course of 1 h.
• No bicarbonate therapy is required if pH is 7.0
Complications of Therapy

•   Hypoglycemia
•   Hypokalemia
•   Cerebral Edema
•   Acute Respiratory Distress Syndrome
•   Hyperchloremic metabolic acidosis

• Before of the advent or low dose insulin protocols,
  this occurred in as many as 25% of patients
• Close monitoring of BG’s, decreasing IV insulin rate
  when BG improves and adding dextrose to IV fluids
  when BG < 250 all can reduce risks of hypoglycemia

• Insulin therapy, correction of acidosis, and volume
  expansion decrease serum potassium concentration.
• Labs should be ordered every 2 to 4 hours to closely
  monitor this.
• To prevent hypokalemia, potassium replacement is
  initiated after serum levels fall below 5.5 mEq/l,
Cerebral Edema

• Cerebral edema is a rare, but serious complication with high
  mortality (>70%).
• It is more common in children, especially those with newly
  diagnosed diabetes
• Consider cerebral edema when:
   –   Lethargy with deterioration of mental status
   –   Decrease in arousal
   –   Headache
   –   Seizures
   –   Other: Incontinence, pupillary changes, bradycardia, respiratory arrest
• Prevention measures include:
   – gradual replacement of sodium and water deficits in patients who are
   – addition of dextrose to the hydrating solution once blood glucose
     reaches 250 mg/dl.
Prevention of DKA & HHS

• Hyperglycemic emergencies are often preventable through better
  access to medical care, proper education, and effective
• Sick day management should be reviewed with all patients
  periodically, including:
   –   When to call health care provider
   –   BG goals and when/how to use additional short acting insulin
   –   Means to address fever & treat infection
   –   Initiating easily digestible liquid diet with carbs and electrolytes
   –   Advise to never stop insulin
   –   Instruction for family members and caregivers
• Consultation by a dedicated diabetic education team prior to
  discharge from hospital are useful for instruction of self management

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