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Dr. Hammad HasanMedical Unit 2
Holy Family Hospital
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Define diagnostic criteriafor diabetic ketoacidosis
Define diagnostic criteriafor hyperosmolarhyperglyemia
Understand the five keycomponents to thetreatment algorithm
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Earliest known record of diabetesmentioned on 3rd Dynasty Egyptian
papyrus by physician Hesy-Ra: mentionspolyuria as a symptom.
250 BC, Apollonius of Memphis coined
the name "diabetes meaning "to gothrough" or siphon. He understood thatthe disease drained more fluid than aperson could consume.
.
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Gradually the Latin word for honey,"mellitus," was added to diabetes because
it made the urine sweet.
Up to 11th
century diabetes wascommonly diagnosed by water tasterswho drank the urine of those suspected ofhaving diabetes, as it was sweet-tasting.
.
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In the 1869, Paul Langerhans, aGerman medical studentannounced in a dissertation, that
the pancreas contains two systemsof cells.
1889 Oskar Minkowski and Josephvon Mering in France, removed the
pancreas from a dog to determinethe effect of an absent pancreas ondigestion
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Boss leaves on vacationMay 1921
Banting and his
assistant Best isolateinsulin from dogs, andgive it to diabetic dogs.
Boss returns and is
skeptical that insulinworks
Try extract onthemselves, then on:
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The first patient to receive injections ofpancreatic extract on January 11, 1922. He was14. The young Toronto resident had been
diabetic since 1919. He weighed only 65pounds and was about to slip into a coma anddie. At first he received Dr, F. Bantings andDr. Charles Bests extract. Two weeks later heused the purified extract of Dr. J.B. Collip andThompson's symptoms began to disappear; hisblood sugar returned to normal and he wasbrighter and stronger. Thompson livedanother 13 years with the insulin. He died atthe age of 27 due to pneumonia, acomplication of his diabetes
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Pancreas
Normal Insulin Sensitivity
Liver
Euglycemia
IsletF-Cell Degranulation;
Insulin Released in Response to
Elevated Plasma GlucoseMuscle Adipose Tissue
Increased Glucose
Transport
Decreased
ipolysis
GlucoseProduction
GlucoseUptake
Normal Physiologic
Plasma Insulin
Decreased Glucose Output
NormalF-Cell Function
DecreasedPlasma FFA
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Features of type 2 diabetes Usually presents in over-30s (but
also seen increasingly inyounger people)
Associated with
overweight/obesity Onset is gradual and diagnosis
often missed (up to 50% of cases) Not associated with
ketoacidosis, though ketosis canoccur
Immune markers in only 10% Family history is often positive
with almost 100% concordancein identical twins
Features oftype 1 diabetes
Onset inchildhood/ dolescence
Le n body h bitus
Acute onset of osmoticsym toms
Ketosis- rone
High levels of isletuto ntibodies
High rev lence of geneticsusce tibility
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Schematic of the pathogenesis of diabetic ketoacidosis(DKA) and the hyperglycemic hyperosmolar state (HHS)
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Islets of
Langerhans
F-cell destruction Insulin Deficiency
Adi o-
cytes
Muscle
Liver
Decreased Glucose tilizationIncreased Production
GlucagoIncreased
ProteinCatabolism Increased
Ketogenesis
Gluconeogenesis,
GlycogenolysisIncreased ipolysis
Hyperglycemia
Ketoacidosis
HyperTG
Polyuria
olume Depletion
Ketonuria
Amino
Acids
FattyAcids
Stress
Threshold
180 mg/dl
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Pancreas
Insulin Resistance
Li er
Hyperglycemia
IsletF-Cell Degranulation;
Reduced Insulin Content
Muscle Adipose Tissue
Decreased Glucose
Transport & Activity
(expression)
of GLUT4
Increased
ipolysis
GlucoseProduction
Glucose
Uptake
Reduced
Plasma Insulin
Increased Glucose Output
F-Cell Dysfunction
ElevatedPlasma FFA
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Autoimmune destruction
Diabetes threshold
Honeymoon
100% Islet loss
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Insulin
Glucagon
E ine hrine
CortisolGrowth Hormone
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Dec Glucose tilization
Li olysis
Insulin
Glucagon
E ine hrine
CortisolGrowth Hormone
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Relative Insulin Deficiency Glycogenolysis &
gluconeogenesis restrained
Peripheral glucoseuptake
Elevates
blood glucose
Decreased tilization ost- r andial
andStress-Induced
hy erglycemia
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Gluconeogenesis
Glycogenolysis
Li olysis
Ketogenesis
Insulin
Glucagon
Epinephrine
CortisolGrowth Hormone
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Insulin DeficiencyGlycogenolysisGluconeogenesisHepatic glucose output
Peripheral glucoseuptake
Elevates blood glucoseLipolysis
Release FFA -> liverVLDL & ketonesKetonemiaand hyperTG Acidosis & Diuresis
Increased Production &
Decrea
sed tilization Fasting
hy erglycemia
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Glucose > 250
Arterial pH 7.25-7.30 Serum bicarb 15-18 mEq Urine and Serum ketones B-hydroxybutyrate- high Anion gap >10 Patient is alert
22Trachtenbarg David, Diabetic Ketoacidosis,American Family Physician,2005;71:1705-1714
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Glucose > 250
Arterial pH 7.00-7.24 Serum bicarb 10 to 12 Patient is alert/drowsy
23Trachtenbarg David, Diabetic Ketoacidosis,American Family Physician,2005;71:1705-1714
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Glucose > 250
Arterial pH
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Anion gap acidosis DKA
Lactic acidosis Alcoholic ketoacidosis
Renal failure
Certain poisonings (ethylene glycol, methylalcohol, paraldehyde, methanol, salicylates)
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Glucose > 600
Arterial pH
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HHNS DKA
Epidemiology 17.5 cases per 100,000 person-years; 1 in 1000 diabetic hospitaladmissions. Mortality as high as12% to 46%. Increasing ageand higher S/Sx correspond withincreased mortality.
4.6 8 per 1000 diabetic patients; 2%to 8% of all diabetic hospitaladmissions. Mortality 1-2% (usuallyNOT from DKA itself but rather theprecipitant, e.g., MI, sepsis,pancreatitis) OR complications oftreatment.
Presentation poor glycemic control, polyuria,polydipsia, lethargy, AMS (mildconfusion to lethargy), seizures,
coma
vomiting, thirst, polyuria, altered,weakness, fatigue, abdominal pain
Onset Insidious (days to weeks) Short (hours to days)
Precipitants new diabetes OR existing diabetes AND: med noncompliance, acuteillness (infection, MI, pancreatitis, CVA, burns, GI bleed, PE, trauma,renal failure), meds (thiazides, beta-blockers, phenytoin, steroids,cisplatinum), substance abuse (EtOH, cocaine). Precipitant not alwaysclear but try to identify one whenever possible.
Blood Glucose > 600 > 250Arterial pH > 7.3 < 7.3Serum bicarbonate > 20 < 15BUN >30 330
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Symptoms
Nausea and vomiting
Abdominal pain Thirst and polyuria
Visual disturbances
Weakness and/or anorexia
Somnolence
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Signs Tachycardia
Weight loss
Hypotension
Warm, dry skin
Hyperpnea or Kussmauls
Impaired consciousness, respiration and/or coma
Fruity breath (odor of ketones)
Dehydration
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1. Hyperglycemia2. Glycosuria
3. Non-respiratory Acidosis
4. Ketonemia
5. Uremia
6. Hyperkalemia
7. Hypertriglyceridemia
8. Hemoconcentration
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DKA can be resent with BS
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Manage symptoms
Prevent acute and late complications Improve quality of life
Avoid premature diabetes-associated death
An individualized approach
Management
Glycemic
control
BP
Li ids
Pa
tienteducation
Lifestyle
(e.g. diet & exercise)
Foot care
Eye careMicroalbuminuria
& kidneys
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Treatment involves 5 key components:
1. Monitoring
2. Fluid resuscitation
3. Insulin and dextrose infusion
4. Electrolyte repletion5. Treating underlying cause
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ICU
2 IVs, Oxygen, cardiac monitor,continuous vitals, pulse ox
Foley to monitor I &O
Initially blood work every 1-2 hours
If pH is less that 6.9 be frightened
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Glucose, lytes with calculated anion gap, Mag Bun & creatinine, calculateGFR
Beta-hydroxybutyrate or serum ketones UA CBC EKG
Infection-cultures,chest xray Cardiac status-cardiac enzymes
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HHNS
Resuscitate with isotonic saline(NS) initially followed by
hypotonic saline (1/2NS). InHHNS water losses usuallyexceed sodium losses resulting inhypertonic dehydration.
If severely hyperosmolar(>330) begin with hypotonicfluids (1/2 NS).
Replace at a rate of 1 2L/hr for first 1 to 2 hoursfollowed by 1 L/hr for 3 to 4hour.
Goal is to replace half ofTBW deficit over first 12 hours
and remainder in the next 24hours. 42
DKA
Initial goal is to correct intravascular
volume beginning with isotonic saline
(NS), then correct total body water deficitin the following 24 to 48 hours with
hy otonic saline (1/2NS or D5-1/2NS).
If initial corrected serum sodium is >
150 or when calculated serum Osm >320
may begin with hy otonic saline.
Begin initial re lacement with NS at
1-2L/hr for first 1-2 hours followed by
250/hr.
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Sodium
Potassium Ketones
WBC
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Na+ depressed 1.6 mEq/L per 100 mg% glucose
Corrected Na+
= measured Na +1.6 meq/L x (glucose-100)/100))
Example:
Na+ = 123 meq/L and Glucose = 1,250 mg/dl
1,250 100 = 1,150 / 100 = 11.5 x 1.6 = 18 meq/L
Corrected Na+ = 123 + 18 = 141 meq/L
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Triglycerides also artificially lower Na
Li id Li idNa Na NaNa Na Na
Na Na Na
Na NaGluc Na
Na Gluc
Serum
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Acidosis leads to flux of K+ out of cells as H+
enters cells to buffer
Dehydration and volume depletion
Aldosterone Na reabsorption andK+ wasting
Serum K+ usually normal or high, but total bodyK+ is low
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With insulin therapy
K+
moves into cells (1 meq/L / 0.1 unit pH ) Even with K+ you must
Give large doses (40 meq/L) K+
Monitor K+ levels and EKG
High K - tall peaked T, long PR, wide QRS Low K - depressed ST, diphasic T, Prom U-wave
Cardiac dysrythmia
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Acetyl-CoA condenses to acetoacetate Insulin revents utilization ofacetoacetate so levels and shunt to -hydroxybutyrate and aceton
In the absence ofinsulin, FFA go to the
liver, and intomitochondria viacarnitine
-oxidation excessacetylCoA
Nitro russid
reaction
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Urine Dip stick vs. anion gap/serum bicarb
Sensitivity Specificity
DKA 99 % 69 %
Diabetic with minor signs and symptoms andnegative urine ketone dip stick is unlikely tohave acidosis= high negative predictive value forexcluding DKA
Am J Emer Med 34:199
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Initially 10 units R Insulin IV,
.15 units/kg
Insulin drip, most protocols 5-7units per hour, .1 units/kg/hr
Patient to ICU
Stop insulin drip when sugar isless than 250
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HHNS Begin with hydration alone
glucose concentration may fall by 80to 200 per hour with hydrationalone. Manage HHNS using drip orSQ insulin. Because the primaryproblem is one of dehydration,
mainstay of therapy should berehydration.
Insulin drip may be used butremember that hydration comes firstin HHNS. Subcutaneous insulin isusually sufficient and is notaccompanied by the risks of
hypoglycemia that one has withinsulin drips. Frequent assessmentof the patients clinical status andlabs followed by judicious use ofinsulin is preferable to simply usingan insulin sliding scale.
DKALOADING DOSE OF INSULIN: 0.1 to 0.2U/kg IV
INITIATE INSULIN DRIP (5-10 U/hr) torestore euglycemia and correct acidosis whilelimiting rapid changes in serum osmolality.
Follow blood glucose hourly x 4 8 hours.
Goal of decrease of 75 100 of serumglucose/hr.
CHANGE IVF TO D5-1/2NS when plasmaglucose reaches 250 (to avoid hypoglycemiaand excessive decline in Sosm that might
precipitate cerebral edema) with the goal ofcontinuing the insulin infusion and resolvingthe acidosis (close anion gap).
Decrease insulin drip to Regular Insulin 1u perhour for every 100cc hr of D5-1/2NS in IVFs.
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Whole body potassium deficits exist. (3-5mmol/kg)
Acidosis increases K Glucose + Insulin lowers K Start K with K less than 5 mmol and adequate
urine output If initial K less than 3.3 mmol
replete, and then start insulin when K above 3.3mmol/L
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Commonly under repleted
Resident mistakenly uses the replacement ofpotassium protocol, which vastly underrepletes potassium
Watch like a hawk!!!! Replace/repete/replace/repete
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Potassium: regardless of measured K, there is always total body Kdepletion (3 to 5 in DKA and 5 to 10 in HHNS). If initial measured K isnormal or low there is severe K deficit. Hypertonicity, insulin deficiency,and acidosis can cause shift of K out of the intracellular space which inthe setting of diuresis causes significant urinary loss of K. As rehydrationand correction of hyperglycemia occurs, K reenters the cell causing
further decrease of serum K. If patient has normal renal function, for thefirst 3 to 4 hours, add K to IVFs as follows: K < 3.5 give >40meq/L, K 3.5-4.0 give 40/L, K=4.0-4.5 give at 30/L, K=4.5-5.0 give at 20/L, K=5.0-5.3give at 10/L. Follow K closely!
Phosphate: Like K, there is often total body phosphate deficit in bothDKA and HHNS. Actual repletion of phosphate is rarely required unlessit is severe (i.e., less than 1.0). Always follow serum calcium becauserapid phosphate repletion can cause hypocalcemia.
Magnesium: Caution in renal failure, replace only if severe (
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1. Hypoglycemia:
Severe hypoglycemia can be a life-threatening complication. Sweating,tremors, and palpitations may occur with mild hypoglycemia; loss ofconsciousness and convulsions can occur with severe hypoglycemia.
Patients should receive hourly monitoring of plasma glucose initially andafter adjustments in intravenous insulin or administered carbohydrates todetect a rapidly decreasing blood glucose level and to prevent the
development of hypoglycemia
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2. Hypokalemia
Potentially life-threatening if potassium replacement is delayed or
inadequate.
Hypokalemia usually occurs after the initiation of insulin therapy,secondary to the intracellular movement of potassium
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3. Hyperchloremia:
Hyperchloremic normal anion gap metabolic acidosis, is present in ~10%
of patients admitted with DKA and is common in patients recoveringfrom DKA.24 It is usually caused by an excessive use of saline
for fluid and electrolyte replacement during treatment.
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4. Thromboembolic events:
May cause death in adults with DKA. Prolonged stasis, immobility, andhemoconcentrationare major precipitating factors of a thromboembolic
event.19 Antithrombotic therapy in the form of external compressiondevices or subcutaneous heparin is warranted in more severe orprolonged cases.
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5. Congestive heart failure
Can develop with fluid replacement therapy,
especially if an acute myocardial infarction or anunderlying diabetic cardiomyopathy is missed
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6. Cerebral edema:
It is a rare, often fatal complication thatusually occurs within the first 4 to 24 hours after the
initiation of therapy. It is more common in children,especially those younger than 4 to 5 years of age withDKA and new-onset diabetes. There are no establishedwarning signs or clinical predictors. Frequent ongoingneurologic assessments of the patient are critical during
fluid replacement and insulin therapy. Signs andsymptoms may include headache, lethargy, abnormalpupil response, behavioral changes, seizures, bradycardia,papilledema, or unconsciousness.
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Cerebral edema is an extremely
serious, although rare, complication of DKA and occurs more often in
children than adults.
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7. Respiratory distress syndrome:
It is a form of acute lung injury that may occur as aresult of various insults. This may lead to decreased
intravascular osmotic pressure and fluid shiftsresulting in pulmonary edema. Sepsis is thepredominant risk factor.Other predisposing conditionsinclude multiple transfusions, severe nonthoracictrauma, pulmonary contusion, aspiration of gastriccontents, multiple fractures, drug overdose, and
pneumonia. Caution in the rate of replacement ofintravenous fluids should be exercised in patients withhypoxia and with suspected intrapulmonary orsystemic infection.
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The A.D.A. suggests that i.v. insulin can be tapered
and s/c insulin can be started in patients who meetthe following diagnostic criteria:
1.Serum glucose 7.3
(The last three criteria apply only to DKA)
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In newly diagnosed diabetic, give 0.15-0.3 U/kg regular insulin AC orQ 4-6 hours; give less when not eating full meal (i.e. bedtime, or stillnauseous.) BE SURE TO STOP GLUCOSE INFUSION WHENSTOPPING INSULIN DRIP.
OR
b. Can give 0.5-1 U/kg/d and divide dose into 2/3 in AM (1/3 to beregular or humalog, the remainder NPH) and 1/3 before dinner (1/3 to1/2 regular or humalog, the remainder NPH)
OR
c. Lantus (glargine) or Detemir and Novlog or Humalog give 0.5 to 1.0units/kg/day total with 50% long-acting and 50% short acting (splitbetween 3 meals). Check QAC, 3 hour post-prandial, QHS and 0200 d-sticks to optimize dose.
d. NOTE: **Small children may only need long-acting insulin**
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Protocols- but use
Common sensewhich
is not common
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