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By Melese A (mi)

Kalkidan A(mi)
Outline
Introduction
Pathophysiology
Precipitating factors
Work up
Management
Complications
Patient education
Our practice
References

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Objectives
At the end of this session every body should know
What DKA is
The pathophysiology of DKA and the precipitating factors
How to work up a patient with DKA
The management of DKA

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INTRODUCTION
Defn: DKA is one of acute complications of DM which is characterized
by the triad of hyperglycemia, anion gap metabolic acidosis, and
ketonemia.

The serum glucose concentration is usu. < 500 mg/dL (27.8 mmol/L)
and less than< 800 mg/dL (44.4 mmol/L)

may exceed 900 mg/dL (50 mmol/L) in patients with DKA who are
comatose

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Pathophysiology
DKA results from relative or absolute insulin deficiency combined
with counter regulatory hormone excess

The decreased ratio of insulin to glucagon promotes


fat gluconeogenesis,
glycogenolysis, and
 ketone body formation in the liver,
increases in substrate delivery from fat and muscle

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Cont’d
Glucagon excess ↓ the activity of pyruvate kinase,insulin
deficiency ↑ the activity of phosphoenolpyruvate
carboxykinase→pyruvate toward glucose synthesis and away
from glycolysis.

Insulin deficiency also ↓ levels of the GLUT4 glucose transporter


which impairs glucose uptake into skeletal muscle and fat

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Cont’d
Reduced insulin levels&↑catecholamines and growth hormone,
increase lipolysis and the release of free fatty acids.

 these free fatty acids are


normally converted to triglycerides or VLDL in the liver.
In DKA b\c of hyperglucagonemia → ketone body formation

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Precipitating factors
 Inadequate insulin administration
Infection (pneumonia, UTI, Gastroenteritis, sepsis)
Infarction (cerebral, coronary, mesentric, peripheral)
Drugs: glucocorticoids, higher dose thiazide diuretics, dobutamine and
terbutaline,cocaine
Pregnancy
Stress(trauma and surgery)
Burns,acute pancreatitis,PTE

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Clinical features
HISTORY
polydipsia, polyuria
anorexia,nausea, vomiting
Abdominal pain
SOB
Generalized weakness and fatiguability

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Cont’d
Altered consciousness...........coma(5-10%)
Symptoms of possible intercurent infections such as fever,
dysuria, coughing, acute chest pain, palpitation etc.
History of rapid weight loss
History of DM(unless first presentation)

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Cont’d
Physical examination
sign of dehydration
Tachycardia
Sunken eye ball
Reduced tissue turgor
Dry tongue and skin
Hypotension
Increase cap.refill time

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Cont’d

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ADA diagnostic criteria for DKA
&HHS
DIAGNOSTIIC Mild DKA Moderate DKA Severe DKA HHS
CRITERIA
Serum <250 <250 <250 <600
glucose(mg/dl)
Arterial Ph 7.25-7.3 7-7.24 <7 <7.3
Serum 15-18 10-15 <10 <18
bicarbonate
Serum variable variable variable .<330
osmolality
Anion gap <1o <12 <12 variable
Mental status Alert Alert/drowsy Stupor/coma Stupor/coma

Table 1.ADA dagnostic criteria for DKA &HHS

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Laboratory findings of
DKA
DKA is characterized by
hyperglycemia
ketosis
metabolic acidosis

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Work up
U/A- glucose&ketone
Blood glucose level
Serum ketones- beta hydroxybutyrate and acetoacetate
ABG
Serum electrolytes –K,Na,HCO3,Cl,Mg…
CBC
RFT
Plasma osmolality

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Cont’d
Based on indication
Urine culture
Blood culture
CXR
MRI
ECG

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DKA HHS
Glucose,mmol/L (mg/dL) 13.9–33.3 (250–600) 33.3–66.6 (600–1200)

Sodium, meq/L 125–135 135–145

Potassium Normal to Normal

Magnesium Normal Normal

Chloride Normal Normal

Phosphate decrease Normal

Creatinine Slightly increase Moderately increase

Osmolality (mOsm/mL) 300–320 330–380

Plasma ketones ++++ +/–

Serum bicarbonate,meq/L <15 meq/L Normal to slightly decrease


Arterial pH 6.8–7.3 <7.3

Arterial PCO2,mmHg 20–30 Normal


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DDx of DKA
Starvation ketoses
Alcoholic ketoacidosis(AKA)
HHS
MI
Appendicitis
Acute pneumonia
Drug toxicity eg. salicylate
Dehydration due to gastroenteritis
Shock
sepsis

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Management
Principles of management
Supportive therapy (ABC of life, NG tube and
catheterization.)
Fluid replacement
Correction of hyperglycemia
Correction of electrolytes and acid base disturbance
Treatment of precipitating cause

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1.Fluid replacement
Fluid deficit 3-5L
2-3L of 0.9% N/S over the 1st 1-3 hr(15-20ml/kg/hr)
If hemodynamic stability and adequate urine output is present
switch to 0.45% saline at a rate of 250 to 500 ml/hr.
Change to 5% glucose and 0.45 saline when the plasma glucose
reaches 200 mg/dl at a rate of 150-250ml/hr.

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2.Correction of
hyperglycemia
Administer short acting insulin IV(0.1u/kg) bolus then continue
with 0.1u/kg/hr continuous infusion
If no response after 2-4hr increase the infusion 2-3 fold
If the initial serum potassium level is <3.3meq/l hold insulin until
adequate urine out put(50ml/hr) and
the potassium level is corrected.
Hyperglycemia usually improves at a rate of (75–100 mg/dL)
per hour as a result of insulin-mediated glucose
disposal, reduced hepatic glucose release, and rehydration.

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Correction cont’d
Continue insulin & electrolyte administration until
Patient is stable
Glucose goal is 8.3-13.9meq/l(150-250mg/dl) and
Acidosis resolves
Insulin infusion may be reduced to 0.05-0.1U/kg/hr
Administer long acting insulin a soon as patient is eating allow for
over lap in infusion & SC insulin injection.

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3.Correction of electrolytes and acid
base disturbance

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Potassium
K+ deficit 3-5 meq/kg (350 meq 70kg)
Need K with initial IV fluid & insulin Rx unless:
Anuric
K < 5.5 meq/L or hyperkalemia ECG changes
Ketoacid Initial [K] Replacement
osis H+ H+
K+ K+ < 5.5 mEq/L nil (initially)
5.2-5.5 10 mEq/h
mEq/L
Insulin
4-5.2 mEq/L 20 mEq/h
3-4 mEq/L 30 mEq/h
< 3 mEq/L 40 mEq/h
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Other electrolytes
Bicarbonate
May exacerbate hypokalemia
Only give if pH < 6.9 AND evidence of cardiovascular
instability (arrythmia, CHF, hypotension)
50mmol/l NaHCO3 in 200ml of sterile water with 10mEq/l of
KCl given over 2h or until pH < 7.0
Phosphate
Routine IV not recommended
Rx symptomatic hypophosphatemia (rhabdo, unexplained
CHF or respiratory failure, severe confusion) or <0.32meq/l
10cc K Phos soln (3.0mEq Pi and 4.4 mEq K/cc) in 1L NS IV
over 8-12h

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4. Treatment of precipitating
cause

Asses patient what precipitate the episode


Non compliance
Infection
Trauma
Infarction
Cocaine

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Monitoring
Monitor BP,PR,RR,Mental status,fluid intake and out put every 1-4
hour.
Measure capillary glucose every 1-2 hour
Measure electrolyte( especially ,bicarbonate, phosphate) and
anion gap every 4 hr for the first 24hr

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Complications
Common complications Occasional complications
Hyperglycemia Venous thrombosis
Hypokalemia ARDS
Cerebral edema Upper GI bleeding

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Prognosis
With proper Mgt mortality rate of DKA is low (<1%)

May be Related to precipitating factor such as infection and MI

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Patient Education
During illness or when oral intake is compromised, patients
should
Frequently measure the capillary blood glucose;
 Measure urinary ketones when the serum glucose < 16.5
mmol/L (300 mg/dL);
 Drink fluids to maintain hydration;
 Continue or increase insulin; and
 Seek medical attention if dehydration, persistent vomiting, or
uncontrolled hyperglycemia develop.

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Our practice
Give 2-3 liters of N/S over 1-3 hr guided by the rehydration status of
the patient and the other 2 liters over 24 hour.

20 units of insulin(10 IM &10 IV)followed by 5iu IM every hour.

When the patient is completely out of ketosis we transfer the


patient on sliding scale. Regular inulin is given 4hourly according
to the following

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Cont’d
If RBG <350mg/dl...............16units
If RBG <250-350mg/dl......12units
If RBG <180-250mg/dl.......8units
If RBG <120-180mg/dl.........4units
If RBG <120mg/dl.................0 units of regular insulin is given.

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Cont’d
We can also use the modified sliding scale
That’s by calculating by 0.5iu/kg/24hr(NPH),2/3 in the morning
and 1/3 in the evening
We do Q6hrs RBS and give 5iu regular insulin if the RBS is
<250mg/dl

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cont’d
We add 1 ampule of KCL in each bag of N/S after adequate
urine out put.

Follow ; PR, RR, T, BP, Mental status ,urine output, RBS every
1hr, Urine ketone every 2hr.

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References
Harrison's™PRINCIPLES OF INTERNAL MEDICINE 18th
Edition
UpToDate® 20.3

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Comments/
Suggestion

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