DIABETIC EMERGENCIES –
UPDATE AND CONTROVERSIES
Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu), Dip. Diab.
DCA, Dip. Software statistics PhD
(physio)
Mahatma Gandhi Medical college and
research institute , puducherry India
When ever there are updates ,
there will be controversies
Diabetic emergencies
 Diabetic keto acidosis
 Hyper osmolar hyperglycemic
non ketotic coma
 Hypoglycemia
 Lactic acidosis - ?? nonexistent
Definition – clinical and
biochemical
 DKA is defined clinically as an acute state of
severe uncontrolled diabetes associated with
ketoacidosis that requires emergency
treatment with insulin and intravenous fluids
 RBS = > 250 mg %
 Ketones > 5 meq/l
 pH < 7.3
bicarb < 18 meq / l
Insulin Deficiency
(Absolute or Relative)
Glucose uptake
Hepatic glucose
Production
Hyperglycemia
Osmotic diuresis
Hypotonic losses
Lipolysis
Protein catabolism
Nitrogen
loss
Amino
acids
Gluconeogenesis
Glycerol
Free
Fatty acids
Ketogenesis
Ketonemia
ELECTROLYTE
DEPLETION
DEHYDRATION
Pathophysiology of DKA
ACIDOSIS
Ketonuria
Mind boggling slide !!
Looks like
As simple as this
 Uncontrolled DM
 Trigger factor
 Severe hyperglycemia
 Glycosuria , loss of water,
electrolytes
 Protein breakdown
 Lipid breakdown and
Ketogenesis
What happens in DKA ??
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Hyperglycemia
Glycosuria
Water ( 6 litres)
Electrolytes ( K+ 300, Cl- 400 Na 500 meq)
Beta oxidation of fatty acids –
Keto acids
-acetone, beta-hydroxy butyrate, aceto
acetate.
 Fruity odour, nausea
The “I” problem
 I am the professor !!
 I am rich !!
 I am well qualified !!
 I am the best doctor !!
 I am the best husband !!
The precipitating factors
 Infection.
 Infarction (heart or cerebrum)
 Insulin lack.
 Indiscrete drugs.
 Infant (pregnancy)
 Injuries
 And as usual unidentified ??
Update
 avoid DKA
 self-testing for urinary ketones and adjusting
their insulin regimens on sick days.
Symptoms
Anorexia, Nausea, vomiting, Acute abdomen
Lethargy, Myalgia, Dyspnea
Hypothermia, Hyporeflexia, Hypotonia,
Seizures , Stupor, coma
Headache, chest pain, pleurisy
Signs
Air hunger – acidotic (kussmaul) respiration
Dehydration,Confusion, drowsiness, coma (=
10%).
Hypotension,Tachycardia
Acetone odour on breath
Any system
We know medicine !!
 symptom spectrum is a clinical collection but
a patient may present with uncontrolled
diabetes, an UTI and vomiting.
 Beware don’t treat as gastritis.
 It may be DKA
 Uncontrolled diabetes ,
 Discomfort,vomiting
 ECG – MI , Ketones + ve
Diagnostic Criteria For DKA
Features
Mild
Moderate
Severe
Plasma glucose (mg/dl)
> 250
> 250
> 250
Arterial pH
7.25-7.30
7.00-7.24
<7.00
Serum bicarbonate (mEq/L)
15-18
10 to <15
< 10
Urine ketones
Positive
Positive
Positive
Serum ketones
Positive
Positive
Positive
Effective serum osmolality
Variable
Variable
Variable
(mOsm/kg)
> 10
> 12
> 12
Anion gap
Alert
Alert/drowsy
Stupor/coma
Alteration in sensoria
Take history !!
Investigate
 Blood – sugar , urea , creatinine, electrolytes
 ABG, (venous BG)
 ketones , TC, DC, blood cultures ,amylase, Serum
lipase
 CVP , X ray,
 CT , MRI sos
 ECG every 6 hours if doubted
 Urine ketones, deposits and culture
Plasma osmolarity
 2 (Na + K) + BUN/3 + glucose/18
 2( 135 +5) + 15/3 + 300/18
 280 + 5 + 16.6 = 301.6
 Around 290 in DKA
 Around 310 in HHS
Don’t believe lab fully
 Test
false
 High glucose
hyponatremia
 High triglycerides
low glucose
 Ketones
high creatinine
Treat patients – not labs
 Urine tests acetoacetate
 But betahydroxy butyrate is predominant
 Next day urine positive but patient better
Treatment of DKA in Adults
 Fluid replacement
 Insulin replacement
 Potassium replacement
 Phosphate replacement
 Bicarbonate replacement
 Management of precipitating factor
 General Medical Care (ICU).
The average fluid deficit is
3–5 liters
 In young, otherwise healthy patients
 begin with bolus of 1 liter of normal
saline
 followed by an infusion of normal
saline at 500 ml/hour for several hours.
1 +1
2
in medicine
 IV fluids - Vary in infarct patients ,
 Appropriate monitoring and infusion √
 mild DKA should be given normal saline at
250 ml/hour;
 those with elevated corrected serum sodium
should be given half-normal saline at 250
ml/hour. (150 meq 0r osm 330 )
 Glucose NS at 250 mg or 180 mg
 If sure of the electrolytes, Ringer lactate
infusion is acceptable
Insulin
 loading dose of regular insulin at 0.1
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units/kg
60 kg means 6 units regular insulin IV
Followed by 6 units / hour
RBS comes down by 50 – 75 mg/ hour
RBS does not fall – double the dose
Mild cases no loading dose
Actre
Actress jayamala
sabarimala controversy
 Insulin 0.14 units / kg start – no loading
dose
 IM regular insulin (0.3 units/kg), – some
centers
 Oral intake - SC insulin 6 hours prior to
stopping IV
 Extended insulin- better results
Electrolyte replacement:

Serum potassium (mEq/L)
 > 5.3
Action
No additional potassium;
recheck in 1 hr
 4.0–5.3
Add KCl 10
 3.5 to < 4.0
Add KCl 20
 < 3.5
Hold insulin Add KCl 20–60
 Continuous cardiac monitoring
Critically ill patients with DKA manifest
hypophosphatemia during resuscitation
 avoid
potential
muscle
cardiac
weakness
and
and
skeletal
respiratory
depression from hypophosphatemia,
a serum phosphate of < 1.5 mg/dl
should be repleted with K2PO4 at 0.5
ml/hour.
Usually rare
NO ROUTINE bicarbonate
 SIX’ indications of sodium bicarbonate after
ABG
 Arterial pH ≤

7.0
Serum HCO3 ≤ 5 mmol/L
 Imminent cardiovascular collapse /shock
 Coma
 Life threatening hyperkalemia
 Severe lactic acidosis complicating DKA
Laboratory tests follow up
 Blood tests for glucose every 1-2 h
until patient is stable, then every 6 h
 Serum
electrolyte
determinations
every 1-2 h until patient is stable, then
every 4-6 h
 Initial blood urea nitrogen (BUN)
 Initial arterial blood gas (ABG)
measurements,
followed
with
bicarbonate as necessary
Complications of DKA
 The recovery pattern may be slow to come
but complications like
 cerebral
oedema,
arrhythmias
stroke,
infarction, aspiration, infection and sepsis
may hinder the recovery to cause death in
some patients.
 Mortality (5-10%)
Remember clinical clues
 Monitor blood pressure,
 pulse, respirations,
 mental status,
 fluid intake and output every 1–4 h.
Update
 DKA is a thrombotic state
 DKA can precipitate stroke
 Stroke can precipitate DKA
DKA in pregnancy- points to
note
 with pregestational, insulin dependent
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diabetes
Foetal loss – 50 %
Maternal loss - 1 %
Proper antibiotic choice
Labour may precipitate DKA
Paediatric DKA
 0.05 units /kg insulin
 ideal to rehydrate in 36 hours than 24 fours
 initial resuscitation with 20 ml/kg of 0.9 % NS
 0.45% saline avoids cerebral edema
 SC lispro suggested
Hyperglycemic hyperosmolar
syndrome
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Some insulin – no ketosis, no acidosis
Less common
Coma
Hyper osmolarity ,
RBS 500- 600
10 liters or more
Its is ideal to switch to half normal saline if
either the osmolality or sodium is high.
 No urgent insulin
Hypoglycemia:
 In practice, hypoglycemia is generally defined
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as a blood glucose level < 60 mg/dl. A
definitive diagnosis
Whipple’s triad:
1. Symptoms compatible with
hypoglycaemia
2. A low plasma glucose concentration
3. Relief of symptoms after plasma glucose
is raised.
Why important
 Brain needs glucose
 It cant synthesize glucose
 We cant let it starved of
glucose for even a few minutes
40 or 50 or 60 or 70???
 Arterial plasma 10 % higher than venous.
 Fasting ok but pp no good.
 Whole blood (finger pricks) 10% lower!!
 High hematocrit – venous-arterial gap is
more.
Incidence of hypo
 Type 2 without insulin :
4-10 /patient/year
 Type 2 on insulin : 16 /patient/year
 Type 1 : 40 episodes /patient/year
What happens if sugar
decreases ??
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approx 80 mg
Decreased insulin secretion
Approx 70 mg
Increased glucagon
Approx 65 mg
Increased epinephrine
Approx 55-65 –
Cortisol & growth hormone (Noncritical)
Less than 55 - cognition affected
Symptoms
 Autonomic
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neuroglycopenic
Palpitation
headache
Sweats
fatigue
Anxiety
mental dullness
Tremors
vision blurring
Tachycardia
confusion
Hypertension
amnesia
Nausea ,hunger
seizure,coma
Risk factors
 Use of insulin secretagogues ( sulphonyl
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ureas)
insulin therapy
Missed or irregular meals
Advanced age
Duration of diabetes, strict control
Impaired awareness of hypoglycemia
 Autonomic failure, beta blockers
DPP 4 inhibitors – less incidence
In insulin patients !!
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The depth of needle
Exercising limb
Hot bath after injection
Bigger size needle
Type of insulin
 Glargine and detemir - less
hypoglycemia
Potentially hypoglycemic
combines
 Aspirin - dec. insulin resistance
 Quinine – inc. insulin secretion.
 Tetracyclics - inc. insulin secretion
 Gatifloxacin - inc. insulin secretion
 Beta blockers- interact hepatic gluconeo
 Fibrates – sensitivity to insulin
 Fluoxetine -stimulate beta cells
 And a few others.
Other diseases – prone for
hypos
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Adrenal
Gastrointestinal
Hepatic
Renal
Dementia
sepsis
Categories of hypoglyemia
 Mild :
 55-70 mg pallor,sweats,palpitation
 Moderate :
 45-55 mg- headache,vertigo,mood changes
 Severe :
 < 45 mg. Conscious status?
Treatment
 Mild : 15 grams glucose =
 increase 18 mg- 18 min
 4 cubes sugar
 2 spoons honey
 150 ml fruit juice
Chocolate ,milk ,cereal bars
– some sweets are not good
Moderate: 20 -25 grams
 Sulphonyl ureas induced
 hypos – prolonged ,
 Observe and give snacks
Severe – what is it??
 Patient needs someone’s help
 50 ml of 25 % dextrose IV –------- 2cc/kg-10% - infants
 2cc/kg – 25% - adolescents
 2cc/kg - 50% - adults
 See that the vein is free flowing –
 other wise risk of necrosis
Some antidiabetics
 Acarbose - alpha glucosidase inhibitor
 So only glucose should be given
 Miglitol -- sometimes even glucose may be
refractory
Treatment continuum
 Measure blood sugar ,Assess conscious status
 Maintain vitals, Start 10 % dextrose solution
 1 mg glucagon IM or SC
 Look for precipitating factors-alcohol
 Assess for liver status,renal status,
 Serum insulin, c peptide, epinephrine, cortisol
 TSH, growth hormones etc,etc…..
Sulfonyl urea overdose
 Inj. Octretide 50 µgm SC can be repeated 8
hrly
 Refractory unconscious state –
 can be cerebral edema
 IV mannitol and dexa 10 mg to be considered
Summary
 I hope the lecture was pushed into your brains

 Diabetic emergencies –update and
controversies
 Or atleast the picture
Thank you all