Case Presentation
CAPT. MUHAMMAD IMRAN HAIDER
HOUSE OFFICER
CMH BAHAWALPUR
SUPERVISOR: BRIG.FAHEEM-UR-REHMAN KHAN
HOD MEDICINE DEPT. CMH BWP
Case: A 15 years old female patient was
brought to ER with acute loss of
consciousness, abdominal pain and shortness
of breath from last 02 hours.
Name : XYZ
Age: 15yrs
Occupation: student
HOPI
MY PT. IS A KNOWN CASE OF T1DM
FROM LAST 07 YEARS WHO IS ON
INSULIN
THERAPY…
SEQUENCE
• CASE HISTORY
• SEQUENCE OF EVENTS
• CASE DISCUSSION
PAST MED/SURG/DRUG HX
T1DM from last 07 years
FAMILY HX
Non-significant
PERSONAL HX
Non-significant
GENERAL PHYSICAL EXAMINATION
VITALS • Tachypnea
• Unconscious
BP 108/58mmHG • Acidotic breathing
PULSE 147/min
TEMP 98’F
CVS
S1 + S2 + 0
R/R 30/min
SP02 98%
CNS
Plantars
BSR 523mg/dl
SYSTEMIC REVIEW
GPE CVS
• Tachypnea S1 + S2 + 0
• Unconscious
• Acidotic breathing
CNS
ABDOMEN Plantars
• Soft + Tenderness on deep
palpation, No visceromegaly.
CHEST
• B/L Air entry
• B/L Vesicular Breathing
INVESTIGATIONS
Diabetic Profile RFTs
BSR=37.8 mmol/l Serum Potassium= 7.1 mmol/l
Serum Sodium= 127 mmol/l
ABGs 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 (+++)
DIAGNOSIS
DIABETIC KETOACIDOSIS
IMMEDIATE MANAGEMENT
• ABC Approach and 2 Wide-bore Cannula
• Fluids
• Insulin IV Infusion (FRII)
• Avoid Hypoglycemia
• LMWH
• Frequent Monitoring of CBG, Ketones, Serum K,
ABGs, and Urine Output
• Initiation of Insulin N and R administration
SEQUENCE OF EVENTS
1-CARDIAC ARREST AND REVIVAL OF PATIENT.
STAGE OF ACUTE KIDNEY INJURY
CASE DISCUSSION
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.
EPIDEM
IOLOY
• 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.
ETIOLOGY
• Inadequate insulin treatment or
noncompliance.
• New onset diabetes (20-25%)
• Acute illness
• Infection (30 to 40%)
• CVA
• Acute Myocardial Infarction
• Acute Pancreatitis
• Drugs
• Clozapine or olanzapine
• Cocaine
• Lithium
• SGLT2 inhibitors
• Terbutaline
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.
CLINICAL PRESENTATION : SYMPTOMS
• 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.
CLINICAL PRESENTATION SIGNS
• Ill appearance.
• Labored respiration (Kussmaul).
• Dry mucous membranes, dry skin and decreased skin
turgor.
• Decreased reflexes.
• Characterstic ketotic breath odor.
• Tachycardia
• Hypotension
• Tachypnea
• Hypothermia/ Fever (if infection is present)
• Confusion
• Coma
• Abdominal tenderness.
DIAGNOSI
S
• Triad of hyperglycemia, high anion gap metabolic
acidosis and ketonemia.
ADA (2009)
• Glucose> 13.9 mmol/L (250 mg/dl).
• Bicarbonate< 18mmol/L; pH< 7.3.
• Ketones positive result for urine or serum ketones by
nitroprusside reaction.
LABORATORY EVALUATION
• Blood test for glucose every 1-2 hour.
• ABG/ VBG.
• Serum electrolytes (includes
phosphate)
• Renal function test.
• Urine dipstick test (acetoacetate).
• Serum ketones (3-
hydroxybetabutyrate).
• CBC.
• Anion gap.
• Osmolarity.
• Cultures.
• Amylase.
Repeat lab investigations are key!
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
MANAGEME
NT
• 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.
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.
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).
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.
CORRECTION OF
ACIDOSIS
• Bicarbonate therapy is a bone of contention among physicians
and still remains a controversial subject, as clear evidence of
benefit is lacking.
• Bicarbonate therapy is only administered if the arterial pH is
less than 6.9.
• 100 mEq of sodium bicarbonate in 400 mL sterile water is
administered over two hours. Repeat doses until pH rises above
7.0.
• Bicarbonate therapy has several potential harmful effects.
COMPLICATION
S
• CVT
• Myocardial Infarction
• DVT
• Acute gastric dilatation
• Erosive gastritis
• Late hypoglycemia
• Respiratory distress
• Infection (UTI)
• Hypophosphatemia
• Mucormycosis
• CVA
• Cerebral edema (rare in
adults)
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
Thank you
