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CASE PRESENTATION

Presented by
Capt Imran Haider Supervised by
Khan Brig Faheem ur Rehman
Cl Med Spec,
House Officer Head Of Dept Medicine CMH
Bwp
CMH Bwp

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CASE ILLNESS
HISTORY OF PRESENTING

A 15 years old female patient was brought to ER with acute loss of


consciousness, abdominal
A 15 pain and
years old female shortness
patient of breath from last
was brought
02 hours to ER with acute loss of consciousness,
abdominal pain and shortness of breath
from last 02 hours.

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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
E1V1M2
ABDOMEN Plantars
• Soft + Tenderness on deep Neck Supple
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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DIAGNOSIS

???

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DIAGNOSIS

DIABETIC KETOACIDOSIS

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IMMEDIATE MANAGEMENT

• ABC Approach and 2 Wide-bore Cannula


• Fluids
• Insulin IV Infusion (FRII)
• Emperic Antibiotic therapy was started
• 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 Life threatening complication


• Mostly occurs in Type 1 Diabetics
• 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 the first presentation of type 1 diabetics (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

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CLINICAL PRESENTATION

 Polyuria  Malaise
 Polydypsia  Weakness
 Weight loss  Lethargy
 Nausea
 Obtundation
 Vomiting
 Abdominal Pain

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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.

NHS 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(acetoacetate)


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

• CVT • Respiratory distress


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

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REFERENCES

• Harrison’s Principles of Internal


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

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TAKE HOME MESSAGE

 Counselling
 Correct Dosage and administration
 Compliance to treatment

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THANK YOU

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