Hyperglicemic Emergency in Adults

YUDO PRABOWO
Canadian Diabetes Association Clinical Practice

Guidline Expert Committe 2013
Introduction
Diabetic ketoacidosis (DKA) and hyperosmolar
hyperglycemicstate (HHS) are diabetes emergencies
with overlapping features.
DKA :
Potassium is shifted out of cells, and ketoacidosis occurs
as a result of elevated glucagon levels and absolute
insulin deciency (DMTI)
high catecholamine levels suppressing insulin release
(DMTII)
Ketoacidosis prominent
Cont.
HHS :
the main features are ECFV depletion and
hyperosmolarity hyperglycemia causes urinary losses
of water and electrolytes (sodium, potassium, chloride)
Risk Factor
DKA HHS
new diagnosis of diabetes Same as DKA
mellitus also has been reported
insulin omission following cardiac surgery
Infection use of certain drugs,
myocardial infarction including diuretics,
glucocorticoids, lithium and
abdominal crisis atypical antipsychotics
trauma
treatment with insulin
infusion pumps
thyrotoxicosis
cocaine, atypical
antipsychotics and
interferon.
clinical presentation
DKA HHS
symptoms of often more profound
hyperglycemia ECFV contraction
Kussmaul respiration decreased level of
acetone-odoured breath consciousness
ECFV contraction
(proportional to the
elevation in plasma
nausea osmolality).
vomiting variety of neurological
abdominal pain presentations, including
decreased level of seizures and a stroke-like
consciousness state
resolve once osmolality
returns to normal
Diagnosis
DKA or HHS should be suspected whenever patients have
signicant hyperglycemia, especially if they are ill or highly
symptomatic.
to make the diagnosis and determine the severity of DKA or

HHS, the following should be assessed:
plasma levels of electrolytes (and anion gap)
glucose, creatinine, osmolality
beta-hydroxybutyric acid (beta-OHB) (if available)
Blood gases
Serum and urine ketones
uidbalance
level of consciousness, precipitating factors and
complications
Cont.
There are no denitive HHS:
criteria for the diagnosis higher glucose levels
of DKA. (typically 34.0
Typically, the arterial pH is mmol/L)( 612 mg/dl)
7.3 greater ECFV contraction
serum bicarbonate is 15 minimal acid-base
mmol/L disturbance
anion gap is >12 mmol/L
with positive serum and/or
urine ketones.
Plasma glucose is usually
14.0 mmol/L but can be
lower ( 252 mg/dl)
Management
Objectives of management of DKA and HHS
include restoration of normal ECFV
tissue perfusion;
resolution of ketoacidosis;
correction of electrolyte imbalances and
hyperglycemia; and the
diagnosis and treatment of coexistent illness.

Cont.
ECFV contraction
ECFV re-expansion, using a rapid rate of initial uid
administration, was associated with an increased risk
of cerebral edema (CE) in 1 study but not in another.
In adults, one should initially administer intravenous
(IV) normal saline 1 to 2 L/h to correct shock,
otherwise 500 mL/h for 4 hours, then 250 mL/h of IV
uids
Cont.
Potassium decit
Typical recommendations suggest that potassium
supplementation should be started for plasma
potassium <5.0 to 5.5 mmol/L once diuresis has been
established, usually with the second litre of saline.
If the patient at presentation is normo- or hypokalemic,
potassium should be given immediately, at
concentrations in the IV uid between 10 and 40
mmol/L, at a maximum rate of 40 mmol/h.
Cont.
Metabolic acidosis
Insulin is used to stop ketoacid production; IV uid
alone has no impact on parameters of ketoacidosis.
Shor acting insulin (0.1 U/kg/h) is recommended
initial bolus of IV insulin is recommended in some
reviews
Cont.
there has been only 1 randomized controlled trial (RCT) in
adults examining the effectiveness of this step. In this
study, there were 3 arms:
a bolus arm (0.07 units/kg, then 0.07 units/kg/h),
a low-dose infusion group (no bolus, 0.07 units/kg/h),
double-dose infusion group (no bolus, 0.14 units/kg/h).
Outcomes were identical in the 3 groups, except 5 of 12

patients needed extra insulin in the no-bolus/low-dose
infusion group, and the double dose group had the lowest
potassium .
Unfortunately, this study did not examine the standard dose
of insulin in DKA (0.1 units/kg/h).
Cont
The use of subcutaneous boluses of rapid-acting
insulin analogues at 1- to 2-hour intervals results in
similar duration of ketoacidosis with no more
frequent occurrence of hypoglycemia compared to
short-acting IV insulin 0.1 U/kg/h
Once plasma glucose reaches 14.0 mmol/L, IV

glucose should be started to prevent hypoglycemia,
targeting a plasma glucose of 12.0 to 14.0 mmol/L
Cont
Use of IV sodium bicarbonate to treat acidosis did
not affect outcome in RCTs. Sodium bicarbonate
therapy can be considered in adult patients in shock
or with arterial pH 7.0 1 amp sodium
bicarbonate added to 200ml D5W/ 1hour, repeat 1-
2 hours until ph 7.
Potential risks associated with the use of sodium

bicarbonate include hypokalemia and delayed
occurrence of metabolic alkalosis
Hyperosmolality
Hyperosmolality is due to hyperglycemia and a water
decit.
Because of the risk of CE with rapid reductions in
osmolality, it has been recommended that the plasma
osmolality be lowered no faster than 3 mmol/kg/h
adding glucose to the infusions when plasma glucose
reaches 14.0 mmol/L to maintain it at that level and by
selecting the correct concentration of IV saline
Phosphate deciency
Thereis currently no evidence to support the use of
phosphate therapy for DKA
thereis no evidence that hypophosphatemia causes

rhabdomyolysis in DKA
hypophosphatemia has been associated with rhabdo
myolysis in other states, administration of potassium
phosphate in cases of severe hypophosphatemia may be
considered for the purpose of trying to prevent
rhabdomyolysis
Complications
In Ontario, in-hospital mortality in patients hospitalized for
acute hyperglycemia ranged from<1% at ages 20 to 49
years to 16% in those over 75 years.
mortality in DKA ranges from 0.65% to 3.3%

HHS, recent studies found mortality rates to be 12% to
17%, but included patients with mixed DKA and
hyperosmolality
50% of deaths occur in the rst 48 to 72 hours
due to the precipitating cause, electrolyte imbalances
(especially hypo- and hyperkalemia) and CE
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YUDO PRABOWO

Canadian Diabetes Association Clinical Practice

to make the diagnosis and determine the severity of DKA or

correction of electrolyte imbalances and

hyperglycemia; and the

diagnosis and treatment of coexistent illness.

Outcomes were identical in the 3 groups, except 5 of 12

Once plasma glucose reaches 14.0 mmol/L, IV

Potential risks associated with the use of sodium

thereis no evidence that hypophosphatemia causes

mortality in DKA ranges from 0.65% to 3.3%

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