Transcript CLINICAL PATHOPHYSIOLOGY CASE 4

CLINICAL PATHOPHYSIOLOGY
CASE 4
Janet Lin, MD, MPH
Assistant Professor
Department of Emergency Medicine
Emergency Department
Presentation
• 22 y.o. female
• Vomiting
– Multiple episodes
– 2 days duration
• Lethargic, but
•
arousable
Abdominal pain
– Generalized
HISTORY OF PRESENT ILLNESS
• No fever
• No chills
• No prior similar episodes
• Other
PAST MEDICAL HISTORY
• None
• No medications
VITAL SIGNS
• Pulse 120
• Respirations 36
• Blood pressure
•
•
•
100/60
Temperature 980F
Oxygen saturation
100%
Pain: none
PHYSICAL EXAMINATION
• Skin: pale & dry
• Mucous membranes:
•
•
dry & cracked
Heart: normal with
tachycardia
Lungs: clear with
tachypnea
PHYSICAL EXAMINATION
• Abdomen: soft,
•
•
minimally tender
Neuro: no focal
findings
No evidence of
trauma
Conclusions?
DIFFERENTIAL DIAGNOSIS
• 1.
• 2.
• 3.
• 4.
• 5.
• 6.
DIAGNOSTIC TESTS
•
•
•
•
Blood tests
Urine tests
Radiology tests
Special tests
Why is each test ordered?
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
DIAGNOSTIC TESTS
Electrocardiogram (ECG)
• Normal sinus rhythm
• Normal T-waves
• No ST changes
Look for evidence of hyperkalemia!
BEDSIDE DIAGNOSTIC TESTS
• Urine glucose and
acetone
– Clinitest
– Acetest
– Chemstrips bG
Glucose: 4+
Ketones: 2+
DIAGNOSTIC TESTS
• Blood tests
– Serum Electrolytes
Na
Cl
BUN
Glu
K
CO2
Cr
130
100
30
540
4.0
12
1.8
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
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
DIAGNOSTIC TESTS
• Arterial blood gases:
– pH: 7.20
– PO2: 105 mmHg
– PCO2 : 20 mmHg
– HCO3-: 12 mEq/L
Metabolic Acidosis with Respiratory Compensation
DIAGNOSTIC TESTS
• Serum acetone: + @ 1:8 dilution
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
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
DIABETIC KETOACIDOSIS (DKA)
• State of
endocrinologic
imbalance
– Insulin deficiency
– Counter-regulatory
hormone excess
DIABETIC KETOACIDOSIS (DKA)
Biochemical Characteristics
• Hyperglycemia
– Blood sugar > 300 mg/dL
• Ketonemia
– Serum ketones positive at
> 1:2 dilution (sodium
nitroprusside test)
• Acidosis
– pH < 7.30
– HCO3- < 15 mEq/L
Hyperglycemia
DKA
Ketonemia
Acidosis
Factors Predisposing to the
Development of DKA
•
•
•
•
Lack of adequate knowledge of the disease (2/3)
Psychological problems
Financial difficulties
Intercurrent illness (> 80%)
–
–
–
–
–
–
Infection (30-40%)
Vomiting
Myocardial infarction
CVA
Pregnancy
Other stressors
PATHOPHYSIOLOGY OF DKA
DKA
COUNTER-REGULATORY
HORMONE EXCESS
INSULIN DEFICIENCY
INSULIN DEFICIENCY
• Relative or absolute
• Prevents glucose from
•
entering cells
Intracellular
“starvation”
COUNTER-REGULATORY
HORMONES
• Stress and intracellular starvation cause
release of:
– Catecholamines
– Glucagon
– Cortisol
– Growth hormone
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)
PATHOPHYSIOLOGY OF DKA
• Hyperglycemia results
from:
– Blockage of
intracellular glucose
transport
– Counter-regulatory
hormone effects
CRH
Excess
Insulin
Deficiency
Hyperglycemia
Effects of Hyperglycemia in DKA
HYPERGLYCEMIA
HYPEROSMOLARITY
Mental Status
Changes
GLUCOSURIA
Effects of Hyperglycemia in DKA
GLUCOSURIA
OSMOTIC DIURESIS
DEHYDRATION
Effects of Hyperglycemia in DKA
KETOACIDS
HYDROGEN IONS
ACIDOSIS
PATHOPHYSIOLOGY OF DKA
ELECTROLYTE
IMBALANCE
ACIDOSIS
DEHYDRATION
DIAPHORESIS
TACHYPNEA
PATHOPHYSIOLOGY OF DKA
DEHYDRATION
SHOCK
INCREASED
ACIDOSIS
DECREASED
GFR
ACUTE TUBULAR
NECROSIS
INCREASED
HYPERGLYCEMIA
CLINICAL PRESENTATION
Early Symptoms
• Due to hyperglycemia
–
–
–
–
Polyuria
Polydipsia
Polyphagia
Visual disturbances
• Due to muscle breakdown and dehydration
– Weight loss
– Weakness
CLINICAL PRESENTATION
Later Symptoms
• Due to ketonemia
– Anorexia
– Nausea
– Vomiting
– Fruity acetone breath
• Due to acidosis
– Abdominal pain
– Kussmaul respirations (deep, regular, sighing)
CLINICAL PRESENTATION
Later Symptoms
• Due to hyperosmolarity
– Altered level of consciousness
• Alert patients have OSM < 330 mOSM/kg
• 20% of patients are alert
• 10% of patients are comatose
CLINICAL PRESENTATION
Later Symptoms
• Due to hypokalemia
– Gastric stasis and ileus
– Muscle cramps
– Cardiac dysrhythmias
CLINICAL PRESENTATION
DKA Pearls
• Vague symptoms
• Hyperpyrexia rare
• Severe in cases in those
•
•
who cannot communicate
Signs & Symptoms ≠
Biochemical Abnormality
Dehydrated patient who
is still voiding = DKA
DIABETIC KETOACIDOSIS
Differential Diagnosis
•
•
•
•
•
•
Hypoglycemia
Meningitis
Acute abdomen
Gastroenteritis
Respiratory infection
Toxic ingestion
• CVA
• Brainstem
•
•
•
hemorrhage
Uremia
Alcoholic ketoacidosis
Starvation ketosis
DKA MANAGEMENT
• INTRAVENOUS FLUID ADMINISTRATION
• INSULIN THERAPY
• ELECTROLYTES
• MONITOR USING A FLOW SHEET
• (BICARBONATE THERAPY)
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 @ 300-500 mL/h, guided by
urine output
DKA MANAGEMENT
Electrolytes
• 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
DKA MANAGEMENT
Flow Sheet
• Hourly Observations
–
–
–
–
–
–
–
Electrolytes
Glucose
Osmolality
Blood gases
Output
Vital signs
Mental status
DKA MANAGEMENT
Insulin 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
DKA MANAGEMENT
Insulin Therapy
• IV continuous infusion
• 0.1 unit/kg/h
• Loading dose of 0.1
unit/kg used by some
• For BS>1000; 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.
DKA MANAGEMENT
Bicarbonate Therapy
• Complications
– Shift of oxyhemoglobin dissociation curve to
the left
– Hypokalemia & hypomagnesemia
– Overcorrection alkalosis
– Paradoxical CSF acidosis
– Cerebral edema
• Evidence for effectiveness: lacking
DKA MANAGEMENT
Bicarbonate Therapy
• Consider only if pH < 7.0
• If used, DO NOT PUSH!
– Administer as 1-2 mEq/kg over 2 h
DKA DISPOSITION
• ICU
–
–
–
–
Age < 2 years or > 60 years
pH < 7.0
Serious concurrent illness
(Blood sugar > 1000)
• Outpatient Management
– Alert
– No persistent vomiting
– Mild acidosis, ketonemia & dehydration
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 counterregulatory hormones
• DKA is characterized by the presence of
hyperglycemia, acidosis and ketonemia.
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.