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.
