CASE PRESENTATION

Presented by
Capt Imran Haider
Khan
House Officer
CMH Bwp

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 HISTORY OFOF
HISTORY PRESENTING ILLNESS
PRESENTING ILLNESS

 Name : XYZ
 Age: 15yrs
 Student

The patient is a known case of T1DM from last

07 years who is on regular insulin

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 HISTORY CONT..

PAST MED/SURG/DRUG HX
T1DM from last 07 years

FAMILY HX
Non-significant

PERSONAL HX
Non-significant

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 GENERAL PHYSICAL EXAMINATION

VITALS

BP 108/58mmHG

PULSE 147/min

TEMP 98’F

R/R 30/min

SP02 98%

BSR 523mg/dl

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 SYSTEMIC REVIEW
GPE CVS
• Tachypnea S1 + S2 + 0
• Unconscious
• Acidotic breathing CNS
Plantars
ABDOMEN
• Soft + Tenderness on deep
palpation, No visceromegaly.

CHEST
• B/L Air entry
• B/L Vesicular breathingeathing
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 INVESTIGATIONS

 Diabetic Profile  RFTs

• BSR=37.8 mmol/l Serum Potassium= 7.1 mmol/l
 ABGs Serum Sodium= 127 mmol/l
Serum urea= 9.7 mmol/l
• pH= 6.68
Serum creatinine= 129 mmol/l
pCO2= 15.6 mmHg
HCO3= 1.8 mmol/l
 URINE RE
• Glucose Present (+++)
Urine for Ketone Bodies Present (+++)

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INVESTIGATIONS

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8
 DIAGNOSIS

DIABETIC KETOACIDOSIS

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 IMMEDIATE MANAGEMENT

• ABC Approach and 2 Wide-bore Cannula

• Fluids
• Insulin IV Infusion (FRII)
• Avoid Hypoglycemia
• LMWH
• Frequent Monitoring of ABGs, Ketones, Serum K,
and Urine Output
• Aggressive monitoring of vital signs

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SEQUENCE OF EVENTS

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SEQUENCE OF EVENTS
SEQUENCE OF EVENTS

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DIABETIC KETOACIDOSIS

CASE DISCUSSION

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 INTRODUCTION

• Diabetic Ketoacidosis is an acute, major, life-threatening

complication of Diabetes.
• It mainly occurs in patients with Type 1 Diabetes but it
is not uncommon in some patients with Type 2
diabetes.
• It is a state of absolute or relative insulin deficiency
aggravated by ensuing hyperglycemia, dehydration
and acidosis-producing derangements in
intermediary metabolism.

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 EPIDEMIOLOGY

• DKA accounts for 14% of all hospital admissions of patients

with diabetes and 16% of all diabetes-related fatalities.
• DKA is frequently observed in diagnosis of type 1 diabetes and
often indicates this diagnosis (3%).
• The overall mortality rate for DKA is 0.2-2%, being at the highest
in developing countries.
• The incidence of DKA in developing countries is higher.
• It is far more common in young patients.

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 ETIOLOGY

• Inadequate insulin treatment or • Drugs

noncompliance. • Clozapine or olanzapine
• New onset diabetes (20-25%) • Cocaine
• Acute illness • Lithium
• Infection (30 to 40%) • SGLT2 inhibitors
• CVA • Terbutaline
• Acute Myocardial Infarction
• Acute Pancreatitis
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 PATHOPHYSIOLOGY

• DKA is a complex disordered metabolic state

characterized by hyperglycemia, ketoacidosis and
ketonuria.
• It usually occurs as a consequence of absolute or relative insulin
deficiency that is accompanied by an increase in counter-
regulatory hormones (i.e, glucagon, cortisol, growth hormone,
epinephrine).
• This imbalance enhances hepatic gluconeogenesis,
glycogenolysis, lipolysis and ketogenesis.

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 CLINICAL PRESENTATION

• DKA usually evolves rapidly, over a 24 hour period.

• Earliest symptoms are polyuria, polydipsia and weight loss.
• Nausea, vomiting and abdominal pain are usually present.
• Malaise, generalized weakness and fatigability.
• As the duration of hyperglycemia progresses, neurologic
symptoms, including lethargy, focal signs, and obtundation can
develop. Frank coma is uncommon in DKA.

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 SIGNS

• Ill appearance. • Hypotension

• Labored respiration (Kussmaul). • Tachypnea
• Dry mucous membranes, dry • Hypothermia/ Fever (if infection
skin and decreased skin turgor. is present)
• Decreased reflexes. • Confusion
• Characterstic ketotic breath • Coma
odor. • Abdominal tenderness
• Tachycardia

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 DIAGNOSIS

• Triad of hyperglycemia, high anion gap metabolic acidosis and

ketonemia.

BSPED Guidelines
• Capillary blood glucose above 11 mmol/L
• Capillary ketones above 3 mmol/L or Urine ketones ++ or more
• Venous PH less than 7.3 and/or bicarbonate <15 mmol/L

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 LABORATORY EVALUATION

• Anion gap • Urine dipstick test

• Blood test for glucose every 1-2 (acetoacetate)
hour • CBC
• ABG/ VBG • Osmolarity
• Serum electrolytes (includes • Cultures
phosphate) • Amylase
• Renal function test  Repeat lab investigations are
• Serum ketones (3- key!
hydroxybetabutyrate)

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 SEVERITY OF DKA

PARAMETERS MILD MODERATE SEVERE

Arterial pH 7.25 – 7.30 7.0 – 7.24 < 7.0

Serum Bicarbonate 15 – 18 10 -15 < 10

Mental Obtundation Alert Alert / Drowsy Stupor/ Coma

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 MANAGEMENT

• Correction of fluid loss with intravenous fluids.

• Correction of hyperglycemia with insulin.
• Correction of electrolyte disturbances, particularly potassium
loss.
• Correction of acid-base balance.
• Treatment of concurrent infection, if present.

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INITIAL FLUID REPLACEMENT

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0 TO 60 MINUTES

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60 MINUTES TO 06 HOURS

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6 TO 12 HOURS

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12 TO 24 HOURS

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 RESOLUTION OF DKA
 Resolution is defined as ketones <0.3 mmol/L and venous
PH >7.3
 Patient should be eating,drinking and back to normal
insulin

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 CORRECTION OF FLUID LOSS
• It is a critical part of treating patients with DKA.
• Use of isotonic saline.
• 15-20mL/kg/hour for the first few hours.
• Recommended schedule:
• Administer 1-3 L during first hour.
• Administer 1 L during second hour.
• Administer 1 L during the following 2 hours.
• Administer 1 L every 4 hours, depending on the degree of dehydration
and CVP.
• When patient becomes euvolemic, switch to 0.45%
saline is recommended, particularly if hypernatremia
exists. 31
 INSULIN TH ERAPY

• Insulin therapy to be initiated only if potassium levels are above 3.3

mEq/L.
• Intravenous regular insulin preferred.
• Initiated with IV bolus of regular insulin (0.1 units/kg) followed by continuous
infusion of regular insulin of 0.1 units/kg/hour.
• SC route may be taken in uncomplicated DKA (0.3 U/kg then 0.2 U/kg one
hour later).
• When serum glucose reaches 250 mg/dl, reduce insulin infusion to 0.02-
0.03
U/kg/hour and switch the IV saline solution to dextrose in saline.
• Revert to SC insulin, after patient begins to eat (continue IV infusion
simultaneously for 1 to 2 hours). 32
 POTASSIUM
REPLACEMENT

• If the initial serum potassium is below 3.3 mEq/L, IV potassium

chloride is started with saline (20 to 40 mEq/hour).
• If the initial serum potassium is between 3.3 and 5.3 mEq/L, IV
KCl (20 to 30 mEq) is added to each liter of IV replacement fluid
and continued until the serum potassium concentration has
increased to the 4.0 to 5.0 mEq/L range.
• If the serum potassium is initially greater than 5.3 mEq/L,
then potassium replacement should be delayed.

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 COMPLICATIONS
• CVT
• Myocardial Infarction
• DVT
• Acute gastric dilatation
• Erosive gastritis
• Late hypoglycemia
• Respiratory distress
• Infection (UTI)
• Hypophosphatemia
• Mucormycosis
• CVA
• Cerebral edema (rare in adults)
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 REFERENCES

• Harrison’s Principles of Internal

Medicine
• British Medical Journal
• www.diabetes.org
• www.uptodate.com
• www.medscape.com
• www.rebelem.com
• www.ncbi.nlm.nih.gov

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THANK YOU

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Thank you