Diabetic ketoacidosis

Course of events

Intercurrent infection
Lose their appetite
Drastically stop or reduce insulin intake

Pathogenesis
Insulin deficiency

Enhanced lipolysis (lipoprotein lipase)

Increased free fatty acids delivery to the

liver.

Increased fatty acylCo! entry into hepatic

"itochondria (acetone)

!nd #lucagon e$cess

!ltered hepatic "etabolis"

Increased activity of carnitine pal"itoyl

transferase.

%ree fatty acid conversion to ketoacids&

')acetoacetic acid
()betahydro$ybutyric acid

Cardinal bioche"ical features

)yperglycae"ia

)yperketonae"ia

*etabolic acidosis

Clinical features
+y"pto"s

Polyuria,thirst

-ausea ,vo"iting

!bdo"inal pain

+y"pto"s

Leg cra"ps

.lurred vision

/eakness

+igns

Dehydration

)ypotension (postural or supine)

Cold e$tre"ities0peripheral cyanosis

1achycardia

+igns

!ir hunger (kuss"aul breathing)

+"ell of acetone

)ypother"ia

Confusion


Investigation

.lood glucose

2rea and electrolytes

!rterial blood gases

2rinanalysis ketones

EC#

Infection screen (%.C and .lood culture)

*anage"ent

*edical e"ergency.

3egular clinical and bioche"ical revie4.

Particularly the first (5 hours of treat"ent.

*onitoring
Laboratory baseline ' hr (hr 6hr 7hr '(hr (5hr
#lucose 8 8 8 8 8 8 8
2rea,
Electrolyte
8 8 8 8 8 8 8
Creatinine 8 8 8 8
.icarbonate 8 8 8 8 8 8 8
.lood gases (8) 8 8

Prevention

Carefully track blood sugar levels .

.e infor"ed and 4atchful for early signs of

dehydration and infection

9no4 4hat to do should blood glucose

levels rise too high i.e. eating less,
e$ercising, or taking "edication

+tay in control of type ( diabetes

Principles of "$

!d"inistration of short acting insulin

%luid replace"ent

Potassiu" replace"ent

!d"inistration of antibiotics if infection is

present.

Insulin

:; units soluble insulin in :; "l ;.<=

saline i.v. via infusion pu"p.

7 units 0hr initially

6 units0hr 4hen blood glucose > ': ""ol0l

( units0hr if blood glucose declines> ';

""ol0l.

Check blood glucose hourly,if no reduction

in first hour, increase the dose.

1he blood glucose level should fall by 67

""ol0l per hour.

! "ore rapid fall should be avoided.

/hen the blood glucose has fallen ';':

""ol0l the dose should be reduced to '5
units hourly.

+liding scales of insulin should not be

used.

%luid replace"ent

E$tracellular fluid deficit should be

replenished by intravenous isotonic
saline(;.<= -a Cl)

Early and rapid rehydration for insulin to

reach the poorly perfused tissues.

1he intracellular deficit "ust be replaced

by := or ';= de$trose and not by "ore
saline.

%luid replace"ent

?.<= -aCl i.v.

' litre over 6; "in
' litre over ' hr
' litre over ( hrs
' litre over ne$t (5 hrs.

/hen blood glucose > ': ""ol0l,give de$trose

:= ,' litre @ hourly.

1ypical reAuire"ent is 7 litres over first (5 hrs.

!void fluid overload in elderly patients.

*onitor urine output.

Potassiu"

+tart 4hen > 6 ""o0l.

!t presentation,potassiu" is usually
high,start infusion cautiouslyB

If C 6.: ""ol0l,give 5; ""ol in ' litre of

fluid.

!void infusion rate of C (; ""ol0hr.

If potassiu",6.::.;""ol0l ,give (; ""ol0l

added potassiu".

If "ore than :.; ""ol0l ,or patient is

anuric,give no potassiu".

Carefully "onitor the level and cardiac

rhyth" "onitoring.

.icarbonate

In patients 4ho are severely acidotic

(D)EFC ';; n"ol0l,p) > G.;),infusion of
sodiu" bicarbonate should be considered.

/ith si"ultaneous potassiu" infusion.

Co"plete correction should not be

atte"pted.

!ntibiotics

Higorously treat infection to control

ketosis.

Co"plications

Cerebral oede"a

!cute respiratory distress syndro"e.

1hro"boe"bolis"

!cute circulatory failure.

))+

Plas"a os"olality I( J-aEK E ( J9EKE

JglucoseKEJureaK
(all in ""ol0l)

-or"al valueI (@; 6;; ""ol0kg

1he patient should be given ;.5:= saline

until os"olality approaches nor"al.

1hen ;.<= saline substituted.