Diabetic Ketoacidosis. Case presentation with Latest guidelines. Case from Pakistan

1. CASE PRESENTATION
DR MIQDAD HAIDER
PGR-I MEDICINE

2.  My Patient XYZ, 15 years old female, unmarried,
Resident of Gulberg (suburbs) Lahore.
Admitted in Fatima Memorial Hospital Lahore through
Emergency on 19th November, 2016.

3. Presented with
Vomiting 15-20 episodes …..09 hours
Loose stools 15-20 episodes …..09 hours

4.  My patient is a known case of Type 1 Diabetes Mellitus,
well 1 day ago.
 Since 5 am she started with sudden onset non projectile
vomiting initially with some undigested food, no peculiar
odor, total 15 to 20 episodes, with generalized abdominal
pain, preceded by nausea. It was not associated with food
intake.
 There was no blood in vomits, no heart burn, burning
micturition, fever or headache, no history of eating outside
or drug intake.

5.  Loose stools of sudden onset, 15-20 episodes in 09
hours, in large quantity with watery consistency, light
yellowish in colour with no mucus or blood in it, with
mild generalized abdominal pain, foul smelling odor.
 Urine Output diminished
 She has history of vaginal discharge, whitish in colour
since one month

6.  Lower middle class, unmarried, studied till 6th
grade.
 no specific hobbies
 no family history of DM, TB, IHD, HTN.
 Parents, 3 brother and one sister, healthy and
alive.

7. 1. Diagnosed to have Type 1 Diabetes Mellitus when she was 8
years old.
 Taking insulin regular + NPH (poor compliance, self
alteration of dosage)
 Glycemic control: Mother left monitoring BSL since 1 year.
No HbA1c done. No fundoscopy done. No regular follow ups
 Poor dietary compliance
 When she was diagnosed to have Diabetes Mellitus, she had
symptoms of weight loss, polyuria, polydipsia.
 No evidence of any other associated autoimmune diseases.
 No history of any psychiatric illness or previous hospital
admissions/emergency short stays.

8.  No history of herbal, hakeem, homeopathic or any
kind of medication usage or drug/food allergy

9.  Ill looking young thin and lean female with black hair, lying with agony
with rapid breathing, right hand placed on epigastric region with i.v line
placed, pale complexion, drowsy, not well oriented in time place and
person, slow to respond.
 Pallor present
 Jaundice ..No
 Thyroid not enlarged
 Cyanosis..not present
 Lymphnodes not palpable
 Pedal and sacral oedema not present
 Nails normal, hands normal, no leukonychia, clubbing, koilonychia
 Oral cavity: dry mucosa and tongue, lips, gums, teeth are normal
 Neck veins not distended

10.  Heart rate: 120/min, regular pulse, low volume, no radioradial
or radiofemoral delay.
 Blood pressure 90/60mmHg
 Temperature 97.5 F
 Respiratory rate 32/min
 Spo2 98% at room air

11.  Abdomen is not distended, skin normal with normal hair
distribution as per age.
 No scar mark, no distended veins, genital and perenial area
normal looking*, no visible mass

12.  There is generalized mild tenderness over deep
palpation of abdomen
 Upper border of the liver dullness is in the right 5th
intercostal space.
 Spleen not palpable
 Kidneys are bilaterally not ballotable
 No other mass palpable
 Bowel sounds: 4-5/min

13.  CNS……….. Patient drowsy but arousable, oriented in
time and place. Pupils B/L reactive
 RESP………… inspection: deep rapid breathing.
 CVS……unremarkable
 MUSKULOSKELETAL………. unremarkable
 GENITOURINARY………. unremarkable

14.  15 years old female known case of Type 1 DM, poor
compliance with insulin
 Sudden onset loose motions and vomiting
 Drowsiness, deep rapid breathing, abdominal pain
 H/O Vaginal Candidiasis

15. What could be the
Diagnosis …????

16.  Diabetic Ketoacidosis
 Acute Gastroenteritis
 Acute Pancreatitis
 Acute Cholecystitis
 Drug intake
 Psychiatric disorders (Anorexia nervosa)

17.  BSL in ER: 436 mg/dl
 URINARY KETONES: ++
 ABGs:
pH: 7.30 pCO2: 24 HCO3: 10
 Na: 135, HCO3: 10, Cl: 103
 “Metabolic Acidosis with high Anion Gap”

18. 19/11
1.30pm
19/11
7.30pm
20/11
02.30Am
20/11
08.00am
20/11
2.45pm
21/11
6.50am
22/11
8.50am
pH 7.30 7.428 7.423 7.426 7.385 7.393 7.488
pCO2 24 22.2 18.4 21 23.6 23.6 32.9
pO2 118 127.7 72.9 98.3 136.5 125.6 80.3
HCO3 10 14.3 11.8 13.5 13.8 14.1 24.4
BE -12 -7.7 -9.8 -8.3 -9.0 -8.6 1.7
O2 sat 98.9 98.9 94.4 97.6 98.9 98.7 96.8

19. 0
50
100
150
200
250
300
350
400
450
500
0 6 12 24 36 48
Series 1
Series 1

20. 19/11 20/11 21/11 22/11 – 23/11
URINARY
KETONES
++ + TRACES NIL..NIL..NIL
HB 14.3 12.1
TLC 17.4 10.46
NEUTR 88 72
LYMPH 09 23
PLT 437 309
T BILI 0.7
ALT 47
AST 40
ALK.PHOS 411
UREA 47
CREAT 1.1 0.7 0.6
U.A 8
S/AMYLASE,
LIPASE
35
83

21. 19/11 20/11 21/11 22/11
S/Mg 1.4 2.1
S/PO4 4.7
Calcium Total 9.3
Ca (IONIZED) 1.29 1.28 1.26 1.29
S/Na 135 133 131 134
S/K 5.2 3.7….3.2….4.1 3.3 3.4
HCO3 11 12 14 24
Cl 103 101 103.7 100
TSH 1.319
HbA1C 8.8
STOOL
ANALYSIS
-VE
VIT D < 3.00
HVS Staph aureus

23.  DIABETIC KETOACIDOSIS SECONDARY TO
 ACUTE GASTROENTERITIS
 POOR COMPLIANCE WITH INSULIN

24.  ADMISSION IN ICU
 FOLEY CATHETER PASSED
 I.V FLUIDS
1 LITER IN 1ST HOUR (Potassium not added in first liter)
1 LITER IN 2ND HOUR
1 LITER IN NEXT TWO HOURS
1 LITER IN NEXT TWO HOURS
1 LITER IN NEXT FOUR HOURS
1 LITER IN NEXT FOUR HOURS
1 LITER IN NEXT 6 HOURS
 INJ. INSULIN PUMP @ 4 U / HR (0.2U/KG/HR)
 INJ. GRAVINATE 50 MG I/V TDS
 ANTIBIOTICS: INJ CEFTRIAXONE 01 GM I/V BD
 INJ FLAGYL 500MG I/V TDS
 INJ. OMEPRAZOLE 40 MG I/V OD
 INTAKE / OUTPUT MONITORING
 ABGs, S/Electrolytes, BSL and urine Ketone monitoring.

26. DKA = 3 letters= triad of D K A
Diabetic
glucose >250 mg/dL (usually 500-800)
Keto
ketones produced
ketones – both in urine and in serum
acetoacetate, acetone, betahydroxybutyrate
fruity smell, not often encountered in real life
consider that if these criteria aren’t met, it may not be DKA
Acidosis
Increased anion gap, metabolic acidosis; HCO3- <15, pH<7.30

27. Hyperglycemia
Ketosis
Acidosis
*
27

28.  DKA is reported in 2-5% of known type 1 diabetic
patients in industrialized countries, while it occurs
in 35-40% of such patients in Africa.
 Higher incidence below 5 years
 Overall mortality rate ranges from 2-10%
 Higher in older patients

29. PRECIPITATING EVENTS
 Infection (Pneumonia / UTI / Gastroenteritis /
Sepsis)
 Inadequate insulin administration
 Drugs (steroids, cocaine)
 Pregnancy
 Stress
Harrison’s Principle of internal medicine 18th edition p2977

30. Insulin Deficiency
Glucose uptake
Proteolysis
Lipolysis
Amino Acids
Glycerol Free Fatty Acids
Gluconeogenesis
Glycogenolysis
Hyperglycemia Ketogenesis
Acidosis
Osmotic diuresis
Polyuria
Polydipsia
Fruity breath (acetone smell)
Kussmaul breathing (acidotic)
Mental status changes
Dehydration
Dry tongue Tachycardia Hypotension Abd pain
Electrolyte imbalance
PATHOPHYSIOLOGY

31. DKA can be the first
presentation.
Nausea/vomiting
Thirst/polyuria
Abdominal pain
Shortness of breath
Tachycardia
Dehydration/hypotension
Tachypnea/kussmaul
respirations/respiratory
distress
Fruity odour in breath.
Abdominal tenderness(may
resemble acute pancreatitis
or surgical abdomen)
Lethargy/obtundation/cere
bral edema/possibly coma.
SYMPTOMS PHYSICAL FINDINGS
Harrison’s Principle of internal medicine 18th edition p 2976

32. HHSDKA
More in elderlyMore in childrenAge
More in type IIMore in type IDM type
> 600> 250Glucose
+ or -+++++Ketonuria/emia
>7.3<7.3pH
>15<15HCO3
HyperosmolarityVariableS/osmolarity
Sensitive to small doseVariableSensitivity to insulin

33. NHS GUIDELINE FOR THE MANAGEMENT
OF DIABETIC KETOACIDOSIS*
Published: April, 2016
*http://www.rcht.nhs.uk/DocumentsLibrary/RoyalCornwallHospitalsTrust/Clinical
/EndocrineAndDiabetes/DiabeticKetoacidosis.pdf

34. Definition:
Severe uncontrolled known diabetes or new
presentation
1. Blood Glucose > 11mmol/L (200mg/dl) or known
diabetes mellitus
2. Bicarbonate (HCO3) < 15 mmol/L and /or blood
PH < 7.3
3. Significant ketonuria more than 2+ on standard
urine sticks or ketonaemia > 3.0mmol/L

35. SEVERE DKA:
The Presence of one or more of the following may indicate
severe DKA and require admission to the critical care unit
• Pregnancy
• Bicarbonate < 5 mmol/l
• pH < 7.0
• Hypokalaemia on admission < 3.5 mmol/l
• GCS < 12
• Oxygen saturation < 92 %
• Systolic BP below 90 mmHg, Pulse < 60 or > 100 bpm,
• Anion Gap > 16
• Blood ketones > 6mmol/L

36. STEP 1: 0-60 MINUTES
• I/V cannula
• Start 0.9% Normal saline 1000ml/h
• INITIAL INVESTIGATIONS:
• Abgs, S/Electrolytes, Urine C/E, BSL, Urine Ketones
• CBC, Blood cultures, Chest X-ray, ECG, Pulse oximeter,
Pregnancy test in women of child bearing age.
• START INSULIN (rapid acting): 6 units/ hr I/V
• OTHER INTERVENTIONS:
• GCS, Consider central line, consider cardiac monitoring, NG
tube if vomiting.

37. TYPICAL FLUID REPLACEMENT REGIMEN
FLUID VOLUME
0.9% Sodium chloride 500 ml stat
0.9% Sodium chloride 1000 ml over 1 hr
0.9% Sodium chloride with KCL 1000 ml over next 2 hrs
0.9% Sodium chloride with KCL 1000 ml over next 2 hrs
0.9% Sodium chloride with KCL 1000 ml over next 4 hrs
0.9% Sodium chloride with KCL 1000 ml over next 4 hrs
0.9% Sodium chloride with KCL 1000 ml over next 6 hrs
Under no circumstances should KCl be administered at a rate greater than 20
mmol/hour unless facilities for intensive monitoring are available.
Potassium < 3.5 mmolL gain senior medical review
POTASSIUM

38. STEP 2: 60 MINS – 6 HOURS
• Biochemical and Clinical monitoring
- Urine ketones, S/Electrolytes, ABGs, GCS 2 hourly
- Glucose monitoring hourly
• Fluids and electrolytes
-Continue I/V 0.9 % Sodium Chloride according to patient’s
volume requirement
- Use fluids with potassium

39. STEP 2: 60 MINS – 6 HOURS (cont.)
• Insulin and dextrose
-Infuse insulin at 6 units/hr if blood glucose is falling at less
than 5 mmol/L/hr (90mg/dl/hr)
- Reduce insulin infusion to 3 units/hr if blood glucose is
falling at more than 5 mmol/L/hr
-Infuse 10% dextrose at 100 ml/hour. If blood glucose <14
mmol/L (250mg/dl) at 125 ml/hr along side 0.9% sodium
chloride
• Other investigations as indicated
• Urinary Catheter if diuresis has not occurred

41. CEREBRAL EDEMA
• Children and adolescent at high risk.
• Risks increases if BSL falls at a rate > 5mmol/hr (90mg/dl)
• Presentation is with headache or declining GCS in a patient
who is otherwise biochemically improving. If cerebral
oedema is suspected refer to critical care

42. STEP 3: HOUR 6 - 12
• Biochemical and Clinical monitoring
- Urine C/E, S/Electrolytes, ABGs, GCS, Glucose monitoring
DKA resolved is defined as:
1. pH > 7.3,
2. bicarbonate > 15 mmolL
3. (Blood ketones < 0.6mmolL but local resolution is to use pH
and Bicarb)
 If DKA resolved go to Step 4
 If DKA not resolved return to Step 2

43. STEP 4: HOUR 12 - 24
• After 8 hours if no signs of sepsis or other remaining medical
precipitant of DKA patient can move out of a level 2 care
setting .
• If the patient is not eating and drinking
and there is no ketonuria change to a variable rate insulin
infusion (standard sliding scale insulin infusion)
• If the patient is eating and drinking convert back to an
appropriate subcutaneous insulin regimen.
• Recommence long acting background at least 6 hours prior to
discontinuing the intravenous insulin infusion at a meal time
• Transfer to endocrine ward

44. DISCHARGE PLAN
SPECIALIST REVIEW
To determine cause of episode and review diabetes education
DISCHARGE ONLY WHEN
- Biochemically stable
- Eating and drinking
- Established on subcutaneous insulin regimen
FOLLOW UP
- Outpatient Endocrinologist appointment

45.  Never omit insulin
 Cut long acting in half
 Prevent dehydration and hypoglycemia
 Monitor blood sugars frequently
 Monitor for ketosis
 Provide supplemental fast acting insulin
 Treat underlying triggers
 Maintain contact with medical team

46.  Clinical Guidleines for the management of Diabetic Ketoacidosis
in adults.
http://www.rcht.nhs.uk/DocumentsLibrary/RoyalCornwallHospi
talsTrust/Clinical/EndocrineAndDiabetes/DiabeticKetoacidosis.
pdf. Last accessed 22 November 2016
 Diabetes (type 1 and type 2) in children and young people:
diagnosis and management.
https://www.nice.org.uk/guidance/ng18. Last accessed 22
November 2016
 Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of
clinical and biochemical findings with diabetic ketoacidosis-
related cerebral edema in children using magnetic resonance
diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline].
 Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus
human insulin in the treatment of patients with diabetic
ketoacidosis: a randomized controlled trial. Diabetes Care. 2009
Jul. 32(7):1164-9. [Medline]. [Full Text].
 Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are
arterial and venous samples clinically equivalent for the
estimation of pH, serum bicarbonate and potassium
concentration in critically ill patients?. Diabet Med. 2012 Jan.
29(1):32-5. [Medline].
 Mrozik LT, Yung M. Hyperchloraemic metabolic acidosis slows
recovery in children with diabetic ketoacidosis: a retrospective
audit. Aust Crit Care. 2009 Jun 26. [Medline].
 Potenza M, Via MA, Yanagisawa RT. Excess thyroid hormone
and carbohydrate metabolism.Endocr Pract. 2009 May-Jun.
15(3):254-62. [Medline].
 Bowden SA, Duck MM, Hoffman RP. Young children (12 yr) with
type 1 diabetes mellitus have low rate of partial remission:
diabetic ketoacidosis is an important risk factor. Pediatr Diabetes.
2008 Jun. 9(3 Pt 1):197-201. [Medline].
 Zargar AH, Wani AI, Masoodi SR, et al. Causes of mortality in
diabetes mellitus: data from a tertiary teaching hospital in
India. Postgrad Med J. 2009 May. 85(1003):227-32. [Medline].
 National Patient Safety Agency. Potassium solutions: risks to
patients from errors occurring during intravenous
administration.http://www.nrls.npsa.nhs.uk/resources/?entryid4
5=59882. 2002. Last accessed 2nd September 2013
 Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA,
Courtney CH et al. Joint British Diabetes Societies guideline for
the management of diabetic ketoacidosis. Diabetic Med 2011;
28(5):508-515
 Wolfsdorf J, Craig ME, Daneman D, Dunger D, Edge J, Lee WR et
al. ISPAD Clinical Practice Consensus Guidelines 2009. Diabetic
ketoacidosis. Pediatr Diabetes 2009; 10(Suppl 12):118-133.
 Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic
crises in adult patients with diabetes. Diabetes Care 2009;
32(7):1335-1343

47.  GREATLY THANKFUL TO DR EJAZ ZEESHAN CHACHAR
AND DR. RIZWANA KITCHLEW FOR MANAGING THIS
PATIENT AND HELPING ME IN CASE PRESENTATION

48. THANKS FOR YOUR PATIENCE!