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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



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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



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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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