CLINICAL PATHOPHYSIOLOGY CASE 4

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CLINICAL PATHOPHYSIOLOGYCASE 4

• Janet Lin, MD, MPH
• Assistant Professor
• Department of Emergency Medicine

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Emergency Department Presentation

• 22 y.o. female
• Vomiting
• Multiple episodes
• 2 days duration
• Lethargic, but arousable
• Abdominal pain
• Generalized

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HISTORY OF PRESENT ILLNESS

• No fever
• No chills
• No prior similar episodes
• Other

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PAST MEDICAL HISTORY

• None
• No medications

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VITAL SIGNS

• Pulse 120
• Respirations 36
• Blood pressure 100/60
• Temperature 980F
• Oxygen saturation 100
• Pain none

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PHYSICAL EXAMINATION

• Skin pale dry
• Mucous membranes dry cracked
• Heart normal with tachycardia
• Lungs clear with tachypnea

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PHYSICAL EXAMINATION

• Abdomen soft, minimally tender
• Neuro no focal findings
• No evidence of trauma

Conclusions?
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DIFFERENTIAL DIAGNOSIS

• 1.
• 2.
• 3.
• 4.
• 5.
• 6.

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DIAGNOSTIC TESTS

• Blood tests
• Urine tests
• Radiology tests
• Special tests

Why is each test ordered?
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BEDSIDE GLUCOSE TESTING

• Glucose oxidase reagent strip
• Light meter increases sensitivity
• Sensitive to light, heat, moisture
• More accurate in the low range

Accucheck 180-240 mg/dL
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DIAGNOSTIC TESTSElectrocardiogram (ECG)

• Normal sinus rhythm
• Normal T-waves
• No ST changes

Look for evidence of hyperkalemia!
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BEDSIDE DIAGNOSTIC TESTS

• Urine glucose and acetone
• Clinitest
• Acetest
• Chemstrips bG

Glucose 4 Ketones 2
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DIAGNOSTIC TESTS

• Blood tests
• Serum Electrolytes

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CORRECTION FOR SERUM SODIUM

• The sodium level is reduced by 1.6 mEq/L for
  every 100 mg/dL the glucose level is over 100
  mg/dL
• 540 mg/dL 100 mg/dL 440 mg/dL
• 1.6 X 4.4 7.04
• Corrected Sodium 130 7 137 mEq/L

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Estimation of Serum Potassium if pH were Normal

• Serum potassium will fall by 0.6 mEq/L for each
  0.1 increase in pH
• pH 7.4 7.2 0.2
• 0.2 x 0.6 mEq/L 1.2 mEq/L
• 4.0 mEq/L 1.2 mEq/L 2.8 mEq/L
• The expected serum potassium level when pH is
  corrected will be dangerously low

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DIAGNOSTIC TESTS

• Arterial blood gases
• pH 7.20
• PO2 105 mmHg
• PCO2 20 mmHg
• HCO3- 12 mEq/L

Metabolic Acidosis with Respiratory Compensation
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DIAGNOSTIC TESTS

• Serum acetone _at_ 18 dilution

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SERUM OSMOLALITY

• Correlates to mental status
• Measured by freezing point depression
• Calculated from clinical chemistries
• OSM 2(Na) Glu/18 BUN/3
• OSM 2(130) 540/18 30/3
• OSM 300 mOSM/L
• Normal OSM 285 295 mOSM/L

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DIABETES MELLITUS

• First described in Egypt 3000 years ago
• Estimated true prevalence 18.2 million Americans
• Annual cost 132 billion
• Initial presentation is diabetic ketoacidosis
  (DKA) in 10 of cases

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DIABETIC KETOACIDOSIS (DKA)

• State of endocrinologic imbalance
• Insulin deficiency
• Counter-regulatory hormone excess

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DIABETIC KETOACIDOSIS (DKA)Biochemical
Characteristics

• Hyperglycemia
• Blood sugar gt 300 mg/dL
• Ketonemia
• Serum ketones positive at gt 12 dilution (sodium
  nitroprusside test)
• Acidosis
• pH lt 7.30
• HCO3- lt 15 mEq/L

Hyperglycemia
DKA
Ketonemia
Acidosis
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Factors Predisposing to the Development of DKA

• Lack of adequate knowledge of the disease (2/3)
• Psychological problems
• Financial difficulties
• Intercurrent illness (gt 80)
• Infection (30-40)
• Vomiting
• Myocardial infarction
• CVA
• Pregnancy
• Other stressors

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PATHOPHYSIOLOGY OF DKA
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INSULIN DEFICIENCY

• Relative or absolute
• Prevents glucose from entering cells
• Intracellular starvation

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COUNTER-REGULATORY HORMONES

• Stress and intracellular starvation cause release
  of
• Catecholamines
• Glucagon
• Cortisol
• Growth hormone

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COUNTER-REGULATORY HORMONE EFFECTS

• Gluconeogenesis
• Breakdown of proteins and conversion of amino
  acids into glucose
• Glycogenolysis
• Breakdown of liver glycogen into glucose
• Lipolysis
• Breakdown of adipose tissue into non-esterified
  fatty acids (NEFA)

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PATHOPHYSIOLOGY OF DKA

• Hyperglycemia results from
• Blockage of intracellular glucose transport
• Counter-regulatory hormone effects

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Effects of Hyperglycemia in DKA
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Effects of Hyperglycemia in DKA
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Effects of Hyperglycemia in DKA
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PATHOPHYSIOLOGY OF DKA
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PATHOPHYSIOLOGY OF DKA
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CLINICAL PRESENTATIONEarly Symptoms

• Due to hyperglycemia
• Polyuria
• Polydipsia
• Polyphagia
• Visual disturbances
• Due to muscle breakdown and dehydration
• Weight loss
• Weakness

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CLINICAL PRESENTATIONLater Symptoms

• Due to ketonemia
• Anorexia
• Nausea
• Vomiting
• Fruity acetone breath
• Due to acidosis
• Abdominal pain
• Kussmaul respirations (deep, regular, sighing)

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CLINICAL PRESENTATIONLater Symptoms

• Due to hyperosmolarity
• Altered level of consciousness
• Alert patients have OSM lt 330 mOSM/kg
• 20 of patients are alert
• 10 of patients are comatose

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CLINICAL PRESENTATIONLater Symptoms

• Due to hypokalemia
• Gastric stasis and ileus
• Muscle cramps
• Cardiac dysrhythmias

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CLINICAL PRESENTATIONDKA Pearls

• Vague symptoms
• Hyperpyrexia rare
• Severe in cases in those who cannot communicate
• Signs Symptoms ? Biochemical Abnormality
• Dehydrated patient who is still voiding DKA

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DIABETIC KETOACIDOSIS Differential Diagnosis

• Hypoglycemia
• Meningitis
• Acute abdomen
• Gastroenteritis
• Respiratory infection
• Toxic ingestion

• CVA
• Brainstem hemorrhage
• Uremia
• Alcoholic ketoacidosis
• Starvation ketosis

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DKA MANAGEMENT

• INTRAVENOUS FLUID ADMINISTRATION
• INSULIN THERAPY
• ELECTROLYTES
• MONITOR USING A FLOW SHEET
• (BICARBONATE THERAPY)

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DKA MANAGEMENT

• INTRAVENOUS FLUID ADMINISTRATION
• Lowers blood glucose by as much as 18
• Normalizes pH
• Normal saline, 1 L over 30 min
• Then, Normal saline, 1 L over 1-2 h
• Then, 0.5 NS _at_ 300-500 mL/h, guided by urine
  output

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DKA MANAGEMENTElectrolytes

• Potassium
• Level will fall precipitously with treatment
• Hold only if peaked T-waves on ECG
• 20-40 mEq in the first liter of fluid
• ½ as chloride
• ½ as phosphate
• Monitor hourly

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DKA MANAGEMENTFlow Sheet

• Hourly Observations
• Electrolytes
• Glucose
• Osmolality
• Blood gases
• Output
• Vital signs
• Mental status

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DKA MANAGEMENTInsulin Therapy

• Route of Administration
• IM delayed absorption
• SQ
• High doses
• Rapid fluctuations
• IV continuous infusion
• Low dose
• Linear decline
• Less hypoglycemia
• Less hypokalemia
• Adjustments easy

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DKA MANAGEMENTInsulin Therapy

• IV continuous infusion
• 0.1 unit/kg/h
• Loading dose of 0.1 unit/kg used by some
• For BSgt1000 0.05 units/kg/h
• When BS reaches 300, reduce to 0.05 units/kg/h
  add glucose to the fluid
• Continue until acidosis corrected, BS controlled
  ketonemia resolved.

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DKA MANAGEMENTBicarbonate Therapy

• Complications
• Shift of oxyhemoglobin dissociation curve to the
  left
• Hypokalemia hypomagnesemia
• Overcorrection alkalosis
• Paradoxical CSF acidosis
• Cerebral edema
• Evidence for effectiveness lacking

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DKA MANAGEMENTBicarbonate Therapy

• Consider only if pH lt 7.0
• If used, DO NOT PUSH!
• Administer as 1-2 mEq/kg over 2 h

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DKA DISPOSITION

• ICU
• Age lt 2 years or gt 60 years
• pH lt 7.0
• Serious concurrent illness
• (Blood sugar gt 1000)
• Outpatient Management
• Alert
• No persistent vomiting
• Mild acidosis, ketonemia dehydration

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DKA SUMMARY

• DKA may be the presenting complaint in new
  diabetics, up to 10 of the time
• DKA is a state of endocrinological imbalance
  involving insulin AND counter-regulatory hormones
• DKA is characterized by the presence of
  hyperglycemia, acidosis and ketonemia.

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DKA SUMMARY

• Laboratory evaluation of the DKA patient is
  complex and must be repeated on an hourly basis
  until the patient is stable
• The most important components of the management
  of the DKA patient are fluid and electrolyte
  management.
• Insulin is an essential but secondary component
  of management.
• Bicarbonate therapy is rarely indicated.