ACUTE DIABETIC

COMPLICATIONS
1- hypoglycemia(COMMON)
2-DKA(COMMON)
3-hyperosmolar hyperglycemia(LESS COMMON)
4-lactic acidosis(VERY RARE)
HYPOGLYCEMIA
GLODEN RULES
1- NO CHART=NO TREATMENT
2-D=DIRECT OBSERVATION BY YOURSELF
3-K=KIND REDUCTION OF GLUCOSE
4-A=ALWAYS RECHEK
5-ADMITION IS MUST
6-I.V N/S IS THE MOST IMPORTANT
7-ANTIBIOTIC COVER IF INFECTION SUSPECTED
8-I.V SOD.BICRAB RARELY NEEDED ONLY IF SEVER
ACIDOSIS
9-K REPLACEMENT DONE ONLY IF=GOOD
U.O.P+URINE CATHETER PLACED +SLOW I.V
INFUSION +EVIDENCE OF HYPOK.BY ECG OR LAB
10-DON’T DISCHAGE BEFOR 48H
11-HHS DIFFER FROM DKA IN=NO SIGNIFICANT
KETONEURIAOR ACIDOSIS +SEVER
HYPERGLYCEMIA+MORE DEHYDRATION+MORE
THROMBOSIS+MORE SENSITIVE TO
INSULIN+0,45N/S IS NEEDED
12-DKA PATIENT MAY WALK TO THE E,R
13-DKA OCCURE MAINLY IN TYPE 1 RARELY IN
TYPE2…HHS ONLY IN TYPE 2
14-MORTALITY OF DKA=5-10%...HHS=40%
DEFINITION

Exact definition is variable

Most consistent is:

Blood glucose level greater than 250 mg/dL
Bicarbonate less than 15 mEq/L
Arterial pH less than 7.3
Moderate ketonemia

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Acetone presents with odor in some patients

Absence of fever does not exclude infection as a

source of the ketoacidosis

Hypothermia may occur due to peripheral

vasodilatation

Abdominal pain and tenderness may occur with

gastric distension, ileus or pancreatitis
Abdominal pain and elevated amylase in those with
DKA or pancreatitis may make differentiation difficult
Lipase is more specific to pancreatitis
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ECG CHANGES
Underlying rhythm is sinus tachycardia

Changes of hypo/hyperkalemia

Transient changes due to rapidly changing metabolic

status

Evaluate for ischemia because MI may precipitate DKA

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TREATMENT
Order of therapeutic priorities is volume first, then insulin and/or
potassium, magnesium and bicarbonate

Monitor glucose, potassium and anion gap, vital signs, level of

consciousness, volume input/output until recovery is well
established

Need frequent monitoring of electrolytes (every 1-2 hours) to meet

goals of safely replacing deficits and supplying missing insulin

Resolving hyperglycemia alone is not the end point of therapy

Need resolution of the metabolic acidosis or inhibition of ketoacid
production to signify resolution of DKA
Normalization of anion gap requires 8-16 hours and reflects clearance of
ketoacids

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 FLUID ADMINISTRATION
Rapid administration is single most important step in treatment

Restores:
Intravascular volume
Normal tonicity
Perfusion of vital organs

Improve glomerular filtration rate

Lower serum glucose and ketone levels

Average adult patient has a 100 ml/Kg (5-10 L) water deficit and a
sodium deficit of 7-10 mEq/kg

Normal saline is most frequently recommended fluid for initial

volume repletion 34
Recommended regimen:
First L of NS within first 30 minutes of presentation
First 2 L of NS within first 2 hours
Second 2 L of NS at 2-6 hours
Third 2 L of NS at 6-12 hours

Above replaces 50% of water deficit within first 12

hours with remaining 50% over next 12 hours

Glucose and ketone concentrations begin to fall

with fluids alone

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Add D5 to solution when glucose level is
between 250-300 mg/dL

Change to hypotonic ½ NS or D5 ½ NS if
glucose below 300 mg/dL after initially
using NS

If no extreme volume depletion, may

manage with 500 ml/hr for 4 hours
May need to monitor CVP or wedge pressure in
the elderly or those with heart disease and may
risk ARDS and cerebral edema

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INSULIN

Recommended dose is 0.1 unit/kg/hr

Effect begins almost immediately after initiation

of infusion

Loading dose not necessary and not

recommended in children

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 POTASSIUM
Patients usually with profound total body hypokalemia

3-5 mEq/kg deficient

Created by insulin deficiency, metabolic acidosis, osmotic diuresis,

vomiting

2% of total body potassium is intravascular

Initial serum level is normal or high due to:

Intracellular exchange of potassium for hydrogen ions during acidosis
Total body fluid deficit
Diminished renal function
Initial hypokalemia indicates severe total-body potassium depletion and
requires large amounts of potassium within first 24-36 hours
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During initial therapy the serum potassium
concentration may fall rapidly due to:
Action of insulin promoting reentry into cells
Dilution of extracellular fluid
Correction of acidosis
Increased urinary loss of potassium

Early potassium replacement is a standard modality

of care
Not given in first L of NS as severe hyperkalemia may
precipitate fatal ventricular tachycardia and ventricular
fibrillation

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Fluid and insulin therapy alone usually lowers the
potassium level rapidly
For each 0.1 change in pH, serum potassium
concentration changes by 0.5 mEq/L inversely

Goal is to maintain potassium level within 4-5

mEq/L and avoid life threatening
hyper/hypokalemia

Oral potassium is safe and effective and should be

used as soon as patient can tolerate po fluids

During first 24 hours, KCl 100-200 mEq usually is

required 40
COMPLICATIONS AND MORTALITY

Complications related to acute disease

Main contributors to mortality are MI and infection
Old age, severe hypotension, prolonged and severe
coma and underlying renal and cardiovascular
disease
Severe volume depletion leaves elderly at risk for
vascular stasis and DVT
Airway protection for critically ill and lethargic patients
at risk for aspiration

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COMPLICATIONS RELATED TO THERAPY

Hypoglycemia

Hypophosphatemia

ARDS

Cerebral edema

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COMPLICATIONS RELATED TO THERAPY
Cerebral edema
Occurs between 4 and 12 hours after onset of therapy but
may occur as late as 48 hours after start treatment
Estimated incidence is 0.7 to 1.0 per 100 episodes of DKA in
children
Mortality rate of 70%
No specific presentation or treatment variables predict
development of edema
Young age and new-onset diabetes are only identified potential
risk factors

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CEREBRAL EDEMA
Symptoms include:
Severe headache
Incontinence
Change in arousal or behavior
Pupillary changes
Blood pressure changes
Seizures
Bradycardia
Disturbed temperature regulation

Treat with Mannitol

Any change in neurologic function early in therapy should
prompt immediate infusion of mannitol at 1-2 g/kg
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