 DEFINITION

 EPIDEMIOLOGY
 MECHANISM
 PATHOPHYSIOLOGY
 INITIATING FACTORS
 SIGN AND SYMPTOMS
 DIAGNOSIS
 TREATMENT
 CASE REPORT
 It is a state of absolute or relative insulin
deficiency aggravated by ensuing
hyperglycemia,dehydration & acidosis
producing derangements in
intermediatory metabolism.
 DKA is far more characteristic feature of
type 1 Diabetes mellitus than of type 2
Diabetes mellitus.
Blood glucose level > 250 mg/dl
Blood pH < 7.3
Ketones in serum > 5 m.eq/L
 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.
 DKA at the time of first diagnosis of diabetes
mellitus is reported in only 2-3% in western
Europe, but is seen in 95% of diabetic
children in Sudan. Similar results were
reported from other African countries
 A; The basic underlying mechanisms are:
 Absolute deficiency of circulating insulin.
 secretion of insulin counterregulatory
hormones; glucagon, adrenaline, cortisol and
growth hormone.
 B-This leads to disturbances in the following
physiological processes:
 -glucose utilization (hyperglycemia).
 - proteolysis ( amino acids, glutamine and
alanine).
 - lipolysis ( glycerol and FFAs).
 - glycogenolysis (breakdown of muscle
glycogen lactate).
 - gluconeogensis (glutamine & alanine &
glycerol & lactate are the precursors).
 1:HYPERGLYCEMIA:
Serum osmolality → insulin resistance
increases → hyperglycemia worsens.
 2:ACIDOSIS:
Decrease insulin → increase lipolysis →
ketone bodies → ketonemia → ketone
anions→ depletes alkali reserves →
kussmaul respiration.

 3:DEHYDRATION:
 Hyperglycemia → hyperosmolality →
increase urination
 Nausea and vomiting → further water
loss
 Decrease renal blood flow → GFR decrease
 Hypovolumic shock
 4:ELECTROLYTE IMBALANCE
 Loss of potassium
 Blood urea nitrogen
 Infection
Pneumonia & UTI most commonly
 Inadequate use of insulin
Not taking insulin.
 Emotional stress
 Drugs:
Corticosteroids
Antihistamines
Thiazide Diuretics
 Pancreatitis
 A-Symptoms of DKA:
 1-Classic symptoms of hyperglycemia: short
period of time:
 Polyuria, polydipsia, weight loss and thirst.
 2-Other symptoms:
 - General weakness, malaise and lethargy.
 -Nausea, vomiting and abdominal pain.
 - Perspiration.
 - Disturbed consciousness and confusion.
 3-Symptoms of underlying infections or other
conditions; fever, abdominal pain, dysuria, chest
pain…etc
 a-General signs: Ill appearance and disturbed
consciousness.
 b-Signs of dehydration:
 -Skin: Dry, hot, flushed, and loss of skin turgor.
 -Tongue: Dry (sometimes woody tongue).
 -Eyes: Sunken eyes and dark circles under the eyes.
 c-Vital signs:
 -Tachycardia, hypotension and tachypnea.
 d-Specific signs:
 -Ketotic breath: A strong, fruity breath odour (similar
to nail polish remover or acetone).
 -Acidotic breath (Kussmaul's respiration): deep and
rapid.
 -Abdominal tenderness.
 You should suspect DKA if a diabetic patient
presents with:
 Dehydration.
 Acidotic (Kussmaul’s) breathing, with a fruity
smell (acetone).
 Abdominal pain &\or distension.
 Vomiting.
 An altered mental status ranging from
disorientation to coma.
 High WCC: may be seen in the absence of
infections.
 BUN: may be elevated with prerenal
azotemia secondary to dehydration.
 Creatinine: some assays may cross-react
with ketone bodies, so it may not reflect true
renal function.
 Serum Amylase: is often raised, & when
there is abdominal pain, a diagnosis of
pancreatitis may mistakenly be made
 The main lines of management include:

 A-Primary assessment:
 -Volume status and degree of dehydration.
 -Blood pressure and cardiac condition.
 -Degree of consciousness.
 -Degree of acidosis.
 -Precipitating disease
 -Blood glucose (using glucometers) every
hour.
 -Electrolytes and pH every 4 hours.
 -Urine for glucose and ketones every 4
hours
 1-General measures:
 -Airway and O2 inhalation if needed.
 -IV line.
 -Urinary Foley's catheter (if in shock).
 -NGT (Nasogastric Tube): to avoid gastric
dilatation and protection from aspiration .
 -Thrombosis prophylaxis: 5000 units of heparin
SC/12 hours.
 -Empiric use of 3rd generation cephalosporin
antibiotics.

 2-Specific measures:
 Successful therapy of hyperglycemic crises requires
the administration of:
 a-Fluids:
 1- Correct volume deficit and hypotension.
 2- Improve tissue perfusion.
 3-Improve insulin sensitivity ( insulin
counterregulatory hormones).
 4-Improve glomerular filtration rate:
 i-↑ excretion of large amount of glucose in urine.
 ii-Clears hyperketonemia.
 5- Correct metabolic acidosis.
 b-Insulin: Reversal of metabolic abnormalities
:
 i-Corrects hyperglycemia.
 ii-Inhibits ketogenesis.

 c-Potassium: Prevents complications
associated with hypokalemia.
 The expected volume deficits calculated as:
 5-10% of body wt in DKA (3-6 liters).
 15 % of body wt in NKHH (9 liters).
 Replacement therapy should be given within 24 hours
after admission:
 50% of the deficit in the first 4 hours.
 50% of the deficit in the next time for up to 24
hours, guided by ongoing clinical evaluation.
 For children and adolescents (less than 20 years):
 Fluids are given as 10-20 ml/kg/hour in the first four
hours.
 Then given guided by clinical evaluation
 1-Normal saline (0.9% sodium chloride).
 Advantages:
 -Available all the time.
 -Rapid expansion of extracellular compartment.
 -Slow decline of extracellular osmolarity.
 -Slow rate of cerebral edema evolution.
 Disadvantages: May accentuate hypernatrimia if
present.
 Indications:
 -All cases of DKA.
 -Initial (1st 2 liters) in NKHH state.

 Standard low dose insulin regimen: This regimen
is the only effective therapy in DKA & NKHH
state:
 1-Inhibits ketogenesis and gluconeogenesis.
 2- Presence of insulin resistance state
secondary to:
 a- Stress insulin counterregulatory hormones.
 b- Ketone bodies & FFAs.
 c- Hemoconcentration and electrolytes
imbalance. d- Hyperosmolarity.
 e- Infection.
 Type of insulin : Regular : Rapid or short
acting insulin U-40 & U-100.

 Regimen:
 Initial bolus: 0.1 U/kg body wt given IV.
 Maintenance: 0.1 U/kg/body wt /hour:
 a- IV Infusion set: Add 100 units of regular
insulin +500 ml saline i.e. every 5 cc fluid
contains 1 unit of insulin
 b-IV infusion set is not available:IM route.
 Initially: Mild to moderate hypokalemia occur
in patients with DKA.
 Later on: After initiation of Insulin therapy
Correction of acidosis lead to hypokalemia.
 Volume expansion & hydration
Monitoring:
 Blood glucose by glucometer every hour.
 Urine analysis for glucose and ketones every 4 hours.
 Order IV glucose 5% (second line) once blood glucose
reaches:
 < 250 mg/ dl in DKA.
 < 300 mg/ dl in NKHH state.
 Re-evaluate parameters of rehydration
establishment:
 Stable blood pressure.
 Normal urine output.
 Clinical signs of rehydration.
Evaluate the criteria for stopping hourly insulin
regimen (resolving DKA):
 Acidosis corrected clinically and by pH.
 Negative ketoneuria.
 Eating.
 Patient looks good and feels good.
 1-Complications of associated illnesses e.g.
sepsis or MI.
 2-Adult respiratory distress syndrome.
 3-Thromboembolism (elderly).
 4-Complications of treatment:
 a-Hypokalemia: Which may lead to:
 -Cardiac arrhythmias.
 -Cardiac arrest.
 -Respiratory muscle weakness.
 b-Hypoglycemia.

 c-Overhydration and acute pulmonary edema:

particularly in:
 -Treating children with DKA.
 -Adults with compromised renal or cardiac
function.
 -Elderly with incipient CHF.
 A female patient lal mai was admitted to the
medical ward 4 of BVH and was suffering
from pain in right hypochondrium and
diabetic ketoacidosis.
 Age:80yrs
 Weight:60kg
 Family history:Insignificant
 Socioeconomic:Poor
 Vital Signs:
 B.P:130/90mmhg
 Temperature:101F
 Pulse:110 per min
DRUG DOSE ROUTE FORM FREQUENCY
Omeprazole 40mg/100m IV INJ. NOT
Qzone 1.0gm IV INJ. MENTIONED
Maxolon 10mg/2ml IV INJ.
Avil 25mg/2ml IV INJ.
lasix 20mg/2ml IV INJ.
PARTIAL DIFFERENTIAL
Pain in right hypochondrium Diabetic ketoacidosis
UNTREATED IMPROPER DRUG SBTHERAPEUTIC FAILURE TO
INDICATION SELECTION DOSE RECEIVE DRUGS
Ketoacidosis is improper drug No drug Nursing staff was
untreated selection available all the
indication time

OVER DOSE ADVERSE DRUG DRUG DRUG USE

EVENTS INTERACTIONS WITHOUT
INDICATION

No drug Headache rash No clinically Lasix was

dizziness diarrhea significant drug prescribed without
insomnia interaction any indication.
dehydration
 FINDINGS:
 The patient has objective evidence of pain in
the right hypochondrium.
 Additionaly laboratory diagnosis revealed
ketoacidosis
 ASSESMENT OF PROBLEM:
 Therapy is given for treatment of pain in right
hypochondrium.
 No therapy is given for the management of
diabetic ketoacidosis
 PROBLEM RESOLUTION:
 Patient should be given electrolyte
replacement therapy for the management of
diabetic ketoacidosis.
 MONITORING:
 Blood sugar level and urine ketone bodies
level should be monitored in the patient.
SAMPLE TEST RANGE PHYSILOGIC INTERPRETAT COMMENTS
COLLECTION NORMAL BASIS ION
$ VALUES
PROCESSING
URINE NORMAL; Ketones which Ketouria occur Urine ketones
KETONES o.o5 –o.3mg/dl results from in following gives an
PATIENT the conditions; indication of
VALUE; metabolism of 1METABOLIC diabetic
0.5mg/dl fatty acids $ fat CONDITIONS2 ketoacidosis
consist of 3 .DIETARY
substances… CONDITIONS
ACETONE, β- 3.HIGH
HYDROXY METABOLISM
BUTYRIC ACID
$
ACETOACETIC
ACID
 The disease of the patient was not properly
treated and she was given incomplete
treatment of the disease.
 Patient should be properly managed about
the treatment.
 Pharmacist intervention is strictly required.