Appendix B
Full handout given to participants
SIMULATION OF DKA FOR CMBMP
Cellular and Molecular Basics of Medical Practice
January 29 - February 2, 2007
Facilitators’ Guide for DKA Simulation “Tiffany: The Soccer Player”
Simulation Development and Cognitive Science Laboratory
DEPARTMENT OF MEDICAL EDUCATION
FACULTY:
Developers: Department of Anesthesiology, Department of Physiology:
Instructors:
Technical Assistance:
Help with Original Development:
Learning Objectives: overall:
Based on the lecture material and upon completion of the simulation, students should be
able to:
1.
Describe the major causative factors of diabetic ketoacidosis (DKA)
2.
Outline clinical signs and symptoms of DKA leading to diagnosis
3.
Describe the major metabolic changes in DKA
4.
Understand the fluid and electrolyte changes in DKA
5.
Discuss the major objectives of medical management of DKA
6.
Provide strategies for prevention of DKA
Learning Objectives: Simulation Lab Practicum
1. Recognize the clinical signs and symptoms of diabetic ketoacidosis (DKA)
2. Describe the changes in vital signs caused by diabetic ketoacidosis
3. Implement therapy in a simulated environment
4. Describe how the bio-chemical abnormalities lead to clinical signs and symptoms
TIMING:
First 15 minutes:
Second 15 min:
Third 15 min:
Fourth 15 minutes:
Welcome and introduction to Sim Lab and simulator
History and Physical examination
Initial therapy and diagnosis
Definitive therapy based on underlying biochemical abnormalities
First 15 minutes:
Welcome and introduction
Introduce the Sim Lab and the Simulator
Multi-disciplinary facility
Pulses, eyes blinking, pupils constrict, gas moves in and out of mouth (place hand
over mouth), lungs move up and down (demonstrate chest movement)
Introduce the monitor (normal values as per table below)
From top to bottom of screen – mention range of normal values
ECG leads II & V, arterial BP, CVP, SPO2, capnograph, respiratory rate,
Introduce the lesson plan (as on bottom of first page i.e. four 15 min intervals)
Heart rate
beats per min
Blood pressure
mmHg
systolic / diastolic (mean) BP
CVP
cmH2O
central venous pressure
SPO2
%
pulse Ox
EtCO2
mmHg
End-tidal carbon dioxide concentration
Respiratory rate
breaths per min
Normal
Values
DKA
After
Therapy
71
120/52 (80)
127
95/53 (71)
70
120/50 (80)
8
8
100
0
negative
inspiration
95
100
40
30
39
12
24
14
Work (top to bottom on the monitor screen) through the normal values on the table
Ask Simulator Operator for the next “State” – DKA
Give the history (on the next page), as the mathematical models “settle” to their new
values
Second 15 min:
Give the history:
-
History and Physical examination
Tiffany has just been taken to the Emergency Department from her soccer game.
She is a 25 year old female who was driven to the Emergency Department by her
boyfriend, Adam.
She had developed nausea, extreme fatigue, mild disorientation and blurred vision
toward the end of the soccer match.
Start the diabetic keto-acidosis “state” on the simulator
Ask the students to point out any changes on the simulator (clinical examination)
Feel pulses and count Tachycardic
120 bpm
Look at chest and count Tachypneic
34 breaths/min
(rapid deep respiration - Kussmaul breathing - with scent of acetone)
Chest
Breath sounds present bilaterally
Cardiac
S1 and S2 Within Normal Limits; no S3/S4 or murmurs
Lungs
Clear without wheezes or rhonchi
Abdomen
The abdominal examination revealed diffuse mild epigastric
tenderness to deep palpation, but not rebound tenderness nor guarding
(This is not an uncommon occurrence in DKA that appears to result from
gastric stasis and distention, and resolves with treatment.
The examination does not indicate acute appendicitis.
Extremities
No cyanosis, clubbing or edema; pulses equal
Ask the students to point out any changes in the vital signs (monitor parameters)
The students will have all these values in their hand-outs
Feel pulse and count
EKG
Hypotensive
CVP
Pulse Ox
Tachypneic
ETCO2
Temperature
Tachycardic
120 bpm
Normal EKG complexes
90/30 mmHg
low (0-2 cmH2O)
CVP is NOT a learning objective – do not get side tracked
95-97% Decreased for a young, healthy, non-smoker
34 breaths/min
digital number
21 – 25 mmHg
37.1 oC
(98.5 oF)
not on monitor
Ask one of the students to talk to the patient (in an attempt to elicit the following information):
Tiffany is currently lethargic and slightly confused, but can respond to questioning.
She
moans
and
asks
what’s
happening
to
her?
Despite her acknowledged nausea, she still claims to be extremely thirsty.
Patient also volunteers that she has diabetes (speeds up getting the history)
Possible questions:
we want to focus on diabetes, not on a full “coma” differential diagnosis.
Any history of diabetes or insulin therapy ?
Yes
40u
Have you had unexplained weight loss recently?
Yes
20 lbs
Have you experienced increased thirst, appetite, or urination recently?
Yes, multiple times per day and night
Are you taking any drugs?
No
Make the comment about: “First look at the patient, then read the monitors”
Third 15 min:
Initial therapy and diagnosis
Ask students what they would do next (based on vital signs) discuss in any sequence
Start intra-venous infusion (IV)
Give fluids for low blood pressure and tachycardia
Pass around the I/V equipment
I/V cannulae, infusion tubing, Ringer’s Lactate, Normal Saline
Do not get side tracked with R/L and saline differences – not a learning objective
Give oxygen by mask or nasal cannulae
Pass around the oxygen equipment
nasal cannulae for oxygen, oxygen masks
open the oxygen bottle – demonstrate the “hiss” - close the oxygen tank
Note to students:
some emergency therapies are given even before a diagnosis is made such as
oxygen therapy and IV fluids
Do a urine dipstick test - on simulated urine
Demonstrate the urine dipstix test
Pass around the Dipstix and color code on the Dipstix bottle
Do a blood glucose measurement - on simulated blood
Perform a glucose test on the simulated blood
Pass around the measuring equipment with the result
might be electronic device, might be labStix and the color coded bottle
Smell the “ketones” in the container
Plan A:
Sprinkle a few drops of fresh simulated ketones on the cotton wool in the container
Pass around the container with the cotton wool / gauze with the liquid on it
Plan B:
Tear open methyl alcohol and ketone (nail polish remover) swabs
Place in containers marked A and B (under the cotton wool)
Pass around for the “sniffing” test
Fourth 15 minutes:
5 min
Definitive therapy based on underlying biochemical abnormalities
- the students have actually done the background reading – this is refresher only – NOT an in-depth discussion
- the discussion should focus on the relationship between the biochemistry and the clinical signs and symptoms
e.g. hyperosmotic state leads to dehydration leads to hypotension and tachycardia
Ask the students for a diagnosis
Ask why Tiffany is dehydrated?
Results primarily from osmotic diuresis due to hyperglycemia
(exceeds Tmax for renal glucose reabsorption and secondarily from vomiting.)
The hyperglycemia also initially causes the movement of water out of cells, with subsequent intracellular
dehydration, extracellular fluid expansion and hyponatremia.
Hyperglycemia also leads to a diuresis in which water losses exceed sodium chloride losses.
Urinary losses then lead to progressive dehydration and volume depletion.
Ask what are other signs and symptoms of dehydration?
Depends upon degree of dehydration
do NOT focus on numbers and percentages
3% decrease in total body water [TBW]) - dehydration just clinically detectable
mild, 5%
- dry mucous membranes, reduced skin turgor
moderate, 7.5% - above with sunken eyes, poor capillary return
severe, 10%
- severely ill with poor perfusion, thready rapid pulse
Ask why the acidosis develops?
Due to ketonemia from overproduction of ketone bodies;
also if tissue perfusion is low, from the reduction in blood flow, then some of the acidosis may be due to
anaerobic production of lactate.
Ask why the respiration is rapid and deep (Kussmaul)?
Compensatory respiratory response to the metabolic acidosis;
this may also contribute to dehydration (insensible water loss)
Ask what is the rationale for inpatient treatment?
The need for IV fluids, insulin and K+.
(also ask why the K+ is decreased – can be asked here or earlier e.g. with dehydration)
5 min
Show recovery of the patient after fluid treatment
Demonstrate on simulator and monitor
(Students have the value on page 2 of their hand-out)
5 min
Summary and questionnaire completion:
Clinical manifestations and therapy are based on the underlying biochemical
abnormalities
(this is the message that the developers wanted to get across
– drawing a line from the sub-cellular states to the clinical manifestations)
Introduction to DKA:
(This is an extract from note from PBL session used by participants during the preceeding study
of this case.)
DKA is an acute (rapid onset), major, life-threatening complication of diabetes with a morality
rate of approximately 5%. DKA is always caused by insulin deficiency, either relative or
absolute (12-24 h of insulin deficiency can cause dehydration and electrolyte imbalances). DKA
occurs in patients with type 1 diabetes, but is not uncommon in some patients with type 2 diabetes
(90% and 10%, respectively). In an established patient, DKA usually results from failure to take
insulin (most common) or acute stress (e.g., trauma, febrile illness). DKA is defined clinically as
an acute state of severe uncontrolled diabetes that requires emergency treatment and intravenous
(IV) fluids. Biochemically, DKA is characterized as an increase in the serum concentration of
ketone bodies (beta-hydroxybutyrate and acetoacetate) and a blood glucose level of >200 mg/dL.
Because the ketones must be neutralized, the buffering capacity of the blood becomes exhausted
which results a reduction of blood pH (< 7.2) and serum bicarbonate (< 15 mEq/L). Additionally,
there is laboratory evidence of glucosuria and ketonuria.
Patient Values Upon Admission: (from original PBL session)
Arterial blood gases (ABGs)
Patients’ value
pH
pCO2 (mmHg)
pO2 (mmHg)
HCO3 meq/L
Plasma osmolality (mOsm/kg)
Serum glucose (mg/dL)
Na+ (mEq/L)
K+ (mEq/L)
Cl- (mEq/L)
BUN (mg/dL)
7.15
15
90
5
340
720
139
5.5
112
74
Normal value
7.35-7.45
35-40
75-100
22-25
280-296
74-106
136-145
3.5-5.0
96-107
8-25
Goal of treatment:
(because of time limitations this will not be covered, but is provided for background)
Correction of volume depletion, improved tissue perfusion, normalization of serum glucose,
reduction in serum ketones, and attention to electrolyte balance are the cornerstones of therapy.
Profound volume depletion is rule, not exception. A) Therefore the initial priority is restoration
of ECF volume by IV infusion of normal saline (rate and composition is not important). B)
Repletion of K should begin before insulin or at the same time as insulin infusion (because of
total body K depletion and insulin-stimulated K uptake by muscle). C) Administer insulin. Once
rehydration fluids and K are started, blood glucose will begin to fall. However, it is essential to
give insulin to switch off ketogenesis and reverse the acidosis. D) HCO3 therapy is generally not
recommended; the low serum bicarbonate will resolve with the decrease in ketone body
production and a decrease in compensatory hyperventilation.
Summary:
Clinical manifestations and therapy are based on the underlying biochemical abnormalities
End of hand-out for students