8 Penggunaan Insulin Pada Kasus Kedaruratan Medik

7/26/2019 8 Penggunaan Insulin Pada Kasus Kedaruratan Medik

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PB.PERKENI

Treatment Insulin

&Hyperglicemia

Crisis



DISCUSSION

HYPOGLYCEMIA

HYPERGLYCEMIC HYPEROSMOLAR STATE

DIABETIC KETOACIDOSIS



In 1552 BCDiabetes 1st Descibe! In "itin#

Ea$iest %n&'n ec&! &( !iabetes)enti&ne! &n *! D+nast+ E,+-tian

-a-+.s b+ -/+sician Hes+0Ra)enti&ns -&$+.ia as a s+)-t&)

253 BC4 A-&$$&ni.s &( Me)-/is c&ine!

t/e na)e !iabetes6 )eanin# t& #&t/&.#/ & si-/&n He .n!est&&! t/att/e !isease !aine! )&e 7.i! t/an a-es&n c&.$! c&ns.)e

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Ea$+ Diabetes

Disc&8eiesIn t/e 19:;4 Pa.$ Lan#e/ans4 a

Ge)an )e!ica$ st.!ent ann&.nce!

in a !issetati&n4 t/at t/e -anceas

c&ntains t'& s+ste)s &( ce$$s

199; Os%a Min%&'s%i an! <&se-/

8&n Mein# in =ance4 e)&8e! t/e-anceas (&) a !&# t& !ete)ine t/ee>ect &( an absent -anceas &n

!i#esti&n



Fred Banting (1891-1941) Charles H. Best (1899-1978) John J.R. McLeod (187-19!")Fred Banting (1891-1941) Charles H. Best (1899-1978) John J.R. McLeod (187-19!")

Ja#es B. Colli$Ja#es B. Colli$

(189%-19")(189%-19")Mar&orie ('-')Mar&orie ('-')

he isco*er+ o, nslin

(oronto 19%1)



Le&na! T/&)-s&n T/e ?st -atient t& ecei8e in@ecti&ns &(

-anceatic etact &n <an.a+ 114 1;22 He'as 1 T/e +&.n# T&&nt& esi!ent /a!

been !iabetic since 1;1; He 'ei#/e! &n$+:5 -&.n!s an! 'as ab&.t t& s$i- int& ac&)a an! !ie At ?st /e ecei8e! D4 =Bantin#s an! D C/a$es Bests etact

T'& 'ee%s $ate /e .se! t/e -.i?e!etact &( D <B C&$$i- an! T/&)-s&ns

s+)-t&)s be#an t& !isa--ea /is b$&&!s.#a et.ne! t& n&)a$ an! /e 'asbi#/te an! st&n#e T/&)-s&n $i8e!an&t/e 1* +eas 'it/ t/e ins.$in He !ie!at t/e a#e &( 2F !.e t& -ne.)&nia4 a

c&)-$icati&n &( /is !iabetes :



HYPOGLYCEMIA

H+-&#$+ce)ia is a b$&&! #$.c&se 8a$.e &($ess t/an 53 )#!$

C$inica$$+4 it is !e?ne! b+ "/i--$e tia! $&'

-$as)a #$.c&se $e8e$4 s+)-t&)s c&nsistent'it/ /+-&#$+ce)ia4 an! es&$.ti&n &(s+)-t&)s 'it/ c&ecti&n &( -$as)a#$.c&se



E-i!e)i&$&#+

*3 &( t+-e 1 & t+-e 2 !iabetic -atients &nins.$in t/ea-+

13 &( t+-e 2 !iabetic -atients

M&ta$it+ ate *0 es-ecia$$+ e$!e$+ ta%in#$&n# actin# &a$ /+-&#$+ce)ic a#ents



S+)-t&)s

A!ene#ic s+)-t&)s catec/&$a)ine )e!iate!J !ia-/&esis4 -a$-itati&ns4 -a$$&4 tac/+ca!ia a--e/ensi&n4 aniet+4 sensati&n &( /.n#e

/ea!ac/e4 'ea%ness4 est$essness

Ne.&#$+c&-enic s+)-t&)se!.ce! inte$$ect.a$ ca-acit+4 iitabi$it+4c&n(.si&n4 abn&)a$ be/a8i&4c&n8.$si&n4 c&)a



G$.c&e#.$at&+ (act&s

Blood-glucose-loweringfactor

Blood-glucose-raisingfactors

Insulin

Glucose-counterregulatoryfactors

Glucagon

Epinephrine

Growth hormoneCortisol

in minutes

In hours



P/+si&$&#ic es-&nse in /+-&#$+ce)ia

B$&&! #$.c&se 5:09 )#!$

a!ena$in seceti&n

!ia-/&esis4 te)&

e!.ce! (.ncti&n &( centa$ ne8&.s s+ste)

B$&&! #$.c&se 90*: )#!$

e!.ce! c&nsci&.sness

B$&&! #$.c&se *:019 )#!$

c&)a4 c&n8.$si&n B$&&! #$.c&se 19 )#!$

-e)anent bain !a)a#e





S+n!&)es &( c&)-&)ise! #$.c&sec&.ntee#.$ati&n in t+-e 1 !iabetes )e$$it.s

De(ecti8e #$.c&se c&.ntee#.$ati&n

I)-aie! a'aeness &( /+-&#$+ce)ia

E$e8ate! #$+ce)ic t/es/&$! !.in# intensi8e t/ea-+

E$e8ate! #$+ce)ic t/es/&$! (&$$&'in# ecent/+-&#$+ce)ia

E$e8ate! #$+ce)ic t/es/&$! !.in# ß-adrenergicblockade

The syndromes may occur in advanced type 2 diabetes mellitus(insulin-deficient

!utonomic failure



Sc/e)atic !ia#a) &( t/e c&nce-t &( /+-&#$+ce)ia0ass&ciate! a.t&n&)ic (ai$.e in T1DM

Ins.$in !e?cienc+ IDDM

N& #$.ca#&n es-&nses t& !ecease! #$.c&se $e8e$s

E-ine-/inees-&nses

I)-e(ect ins.$ines-&nses

E-is&!es &( /+-&#$+ce)ia

H+-&#$+ce)ia0ass&ciate! a.t&n&)ic (ai$.e

s+)-t&)atic es-&nses a'aenessJ a.t&n&)ic inc$.!in# e-ine-/ineJ es-&nses





Ris% (act&s

Ti#/t #$+ce)ic c&nt&$

A#e

D.ati&n &( !iabetes

Hist&+ &( /+-&#$+ce)ia S$ee-in#

A$c&/&$is)

=astin#

Incease! ins.$in sensiti8it+ ?tness4 b&!+ 'ei#/t

C$eaance)etab&$is) &( !.#s ena$ & /e-aticins.cienc+



Mec/anis)s b+ '/ic/ !.#s incease t/e/+-&#$+ce)ic e>ect &( s.$(&ni$.eas

Incease in /a$(0$i(e !.e t& in/ibiti&n &( )etab&$is)& eceti&n ate et/an&$4 -/en+$b.ta&ne4c&.)ain antic&a#.$ants4 c/$&a)-/enic&$4!&+c+c$ine4 s.$(&na)i!es4 a$$&-.in&$

C&)-etiti&n (& a$b.)in0bin!in# sites-/en+$b.ta&ne4 sa$ic+$ates4 s.$(&na)i!es

In/ibiti&n &( #$.c&ne&#enesis4 incease in #$.c&se&i!ati&n4 & sti).$ati&n &( ins.$in seceti&net/an&$4 ß-adrenergic drugs, monoamine oxidaseinhibitors, tranylcypromine, t



Mana#e)ent &( /+-&#$+ce)ia

Mi$! /+-&#$+ce)ia '/en se$( teat)ent'it/ &a$ cab&/+!ate s.ces

Se8e /+-&#$+ce)ia '/en etena$ /e$- is

e,.ie! t& e>ect ec&8e+



Mana#e)ent &( /+-&#$+ce)ia Pe8enti&n

1 Ea$+ (a)i$iaiati&n 'it/ t/e s+)-t&)s &(/+-&#$+ce)ia

2 D& e8ie'in# at inte8a$s

* E-$ain t/e e$ati&ns/i- bet'een ins.$ina!)inistati&n4 ti)in# &( )ea$s4 an! eecise

E-$ain )et/&!s &( se$(0teatin# /+-&#$+ce)ia

5 C/&&se a--&-iate ins.$in e#i)ens4 !&sesc/e!.$es 'it/ a--&-iate t/ea-e.tic #&a$s



Mana#e)ent &( /+-&#$+ce)ia Teat)ent

Mi$! /+-&#$+ce)ia &a$ #$.c&se 15023 #4 'ait 13015)in t/en c/ec% b$&&! #$.c&se I( #$.c&se $e8e$ !&esn&t incease 19 )#!$4 #i8e &a$ #$.c&se a#ain

Se8e /+-&#$+ce)ia s&$.ti&n 53 )$ &( !et&se 53

#i8en inta8en&.s$+4 c/ec% b$&&! #$.c&se in 23 )inI( it is sti$$ /+-&#$+ce)ia a!)inistate &nce a#ain

G$.ca#&n 13 )# sci)i8 a!8ese e>ects inc$.!ena.sea4 8&)itin#4 an! /ea!ac/e C&ntain!icate! t&s.$(&n+$.eas0in!.ce! /+-&#$+ce)ia Ine>ecti8e in

-atient '/& is an&ectic4 & 'it/ -&tacte!/+-&#$+ce)ia



DIABETIC KETOACIDOSIS

AND

HYPERGLYCEMIC HYPEROSMOLAR STATE

Pathogenesis of DKA



Pathogenesis of DKA

and HHS

"I!BETE# C!$E% &')*E 2+% ,)*BE$ 2% "ECE*BE$ 2.





DKADIABETIC KETOACIDOSISJ

Occ.s '/en ).sc$e ce$$s bec&)e s& sta8e! (&ene#+ t/at b&!+ ta%es e)e#enc+ )eas.es Qbea%s !&'n (at t&ic aci!s as %et&nes

M&st c&))&n t+-e 1 DM ins.cient ins.$in t&

[email protected] aise &( b$&&! s.#a Ca.se b+ ete)e stess & i$$ness In(ecti&n b&!+ -&!.ce a!ena$in '&%s

a#ainst ins.$in

=&#et t& ta%e ins.$in



DKA diagnostic criteria:

serum glucose 250 mg/dl,arterial pH 7.3,serum bicarbonate 18 mEq/l,

moderate ketonuria or ketonemia.

HHS diagnostic criteria:

serum glucose 00 mg/dl,arterial pH 7.3, serum

bicarbonate 15 mEq/l,minimal ketonuria and ketonemia

"I!BETE# C!$E% &')*E 2+% ,)*BE$ 2% "ECE*BE$ 2../



Si#ns Q s+)-t&)s &( DKA

Dee-4 a-i! beat/in# S'eet4 (.it+ s)e$$ &n beat/ L&ss &( a--etite Na.sea &)itin# =e8e

St&)ac/ -ain "ei#/t $&ss

• Fatigue• Weakness• Confusion• Drowsiness



C$inica$ -esentati&n

L&st )&e t/an 5 b&!+ 'ei#/t

M&e t/an *5 beat/s a )in.te

Cant c&nt&$ b$&&! s.#a Bec&)e c&n(.se!

Na.sea an! 8&)itin#



"/at s/&.$! +&. !&

C/ec% %et&nes i( (ee$in# es-ecia$$+stesse! & b$&&! s.#a -esistent$+ ab&8e23)#!L

Hi#/ %et&nes in b$&&! %et&nes ecete!in .ine

Hi#/ %et&nes in .ine s/&.$! be teate! Qn /&s-ita$ie!

DKA can $ea! int& c&)a an! -&ssib$+!eat/



Teat)ent

C&ectin# $&st 7.i!s t/&.#/ i8 $ine

G$.c&se in(.si&n 'it/ ins.$in )a+st&- %et&nes -&!.cti&n

Decease b$&&! s.#a $e8e$ #a!.a$$+4!eceasin# #$.c&se a-i!$+ )a+

-&!.ce bain s'e$$in#





HHS HYPERGLYCEMIC HYPEROSMOLAR STATEJ

A /i#/ $e8e$ &( b$&&! #$.c&se )a+ inte(ee b$&&!cic.$ati&n $e8e$ >:33 )#!$J

G$.c&se .-ta%e b+ t/e ce$$s !eceases4 t/e #$.c&se-asse! (&) b$&&! t& .ine !a's te)en!&.s

a)&.nts &( 7.i! (&) b&!+ an! -&!.ces !e/+!ati&n

C&))&n in t+-e 2 DM4 es-ecia$$+ '/& !&es n&t)&nit& b$&&! s.#a4 an! '/& !&es n&t %n&' /a8eDM

Ti##e (act&s /i#/0!&se ste&i!4 !i.etics4 in(ecti&n4i$$ness4 stess & !in%in# ecessi8e a$c&/&$



HHS si#ns Q s+)-t&)s

Ecessi8e t/ist Incease! .inati&n "ea%ness Le# ca)-s C&n(.si&n Ra-i! -.$se

C&n8.$si&ns C&)a



"/at s/&.$! +&. !&

C/ec% b$&&! #$.c&se $e8e$ > :33)#!LJ

E)e#enc+ teat)ent can c&ect t/e-&b$e) 'it/in /&.s

Gi8e inta8en&.s 7.i!s t& est&e 'ate t&t/e tiss.e

S/&t actin# ins.$in t& /e$- ce$$s can .-ta%e#$.c&se

"it/&.t -&)-t teat)ent can be (ata$







Conclsion /

0er+ lo dose inslin a$$lication and slo #otionre-e2ili3ration $ls #onitored s3stittion o,

electrol+tes are the 3asic strategies in the treat#ent

o, se*ere 5





GROUP I (Subcutant-1hour)• nitial dose 6C / ! nits:g

3od+ t ,olloed 3+• 6C as$art inslin at 1

nits:g e*er+ hor • ;hen 3lood glcose < %"

#gdl change 0 ,lids to"= 4"= saline and redce6C as$art inslin to ."nits:ghor to :ee$glcose at % #gdl ntilresoltion o, 5

La3orator+ chec: :a. Admission : Cell blood count with differential complete metabolic profile, venous p, and serum !"

h#dro$#but#rate

b. During treatment : %asic metabolic profile &glucose, bicarbonate, sodium, potassium, chloride, urea, andcreatine', venous p, phosporus, and !"h#dro$#but#rate at ( h, ) h and ever# ) h until resolution of D*A

c. +lucose b# finger stick : Check glucose ever# h in patients receiving -C" h and ever# ( h in patient /insulin or receiving -C"( h

GROUP II (Subcutant-2hour)• nitial dose 6C / ! nits:g

3od+ t ,olloed 3+• 6C as$art inslin at % nits 1

hor later and e*er+ % hor • ;hen 3lood glcose < %"

#gdl change 0 ,lids to"= 4"= saline and redce6C as$art inslin to .1nits:g e*er+ % hor to :ee$glcose at % #gdl ntilresoltion o, 5

GROUP III (Intravena RI)• nitial 0 3ols / .1 nits:g

3od+ t ,olloed 3+• Continos inslin in,sion

at .1 nits:ghor• ;hen 3lood glcose < %"

#gdl change 0 ,lids to"= 4"= saline and redceinslin in,sion rate to ."nits:g hor to :ee$glcose at % #gdl ntilresoltion o, 5

RESEARCH DESIGN & E!HODS

0mpierre1 +2, Diabetes Care (33) 4 (5 : 657"656



>#$ierre? @A ia3etes Care %4 %7 / 187!-1878

S"#"$ar Re%on%e o' e"ca$ treat#ent"th SC A%art "n co#ar"%on "th I* RI

ote / 6C-1h / 63ctaneos as$art e*er+ 1 hor 6C- %h / 63ctaneos as$art e*er+ % hor



S"#"$ar +$uco%e ro'"$e %ubcutaneou%In%u$"n A%art "n co#ar"%on "th

"ntravenou% Re+u$ar In%u$"n

333

33

(33

)33

833

633

6 ( 8 (3) ()

ration o, treat#ent (hors)

@ l . c o s e ( #

g 9 d l )


6C o*oRa$id D e*er+ 1 hr

6C o*oRa$id D e*er+ % hr

0 Reglar nslin



8

,8

,)

,(

,36

(,3

6

(,)

(,(

%11%4 8 %%

B i c a r 3 o n a t e ( # #

o l 9 L )

ration o, treat#ent (hors)


S"#"$ar ,"carbonate ro'"$e "th%ubcutaneou% In%u$"n A%art "n co#ar"%on

"th "ntravenou% Re+u$ar In%u$"n

6C o*oRa$id D e*er+ 1 hr

6C o*oRa$id D e*er+ % hr

0 Reglar nslin



S"#"$ar #etabo$"c ro'"$e "th%ubcutaneou% In%u$"n A%art

"n co#ar"%on "thIntravenou% Re+u$ar In%u$"n




Diabetes Care Publish Ahead of Print, published online April 1, !""#



Re%u$t

ia3etes Care E3lish 5head o, Erint $3lished online 5$ril 14 %9

5nalog nslin Reglar nslin



.earn"n+ 'ro# U#"erre/ Protoco$#ubcutaneous insulin !spart every 2 hour

9aborator# check :

a. Admission : Cell blood count with differential complete metabolic profile, venous p, and serum !"h#dro$#but#rate

b. During treatment : %asic metabolic profile &glucose, bicarbonate, sodium, potassium, chloride, urea, andcreatine', venous p, phosporus, and !"h#dro$#but#rate at ( h, ) h and ever# ) h until resolution of D*A

c. +lucose b# finger stick : Check glucose ever# ( h in patinet receiving -C"( h


Subcutaneou% "n%u$"n A%art ever0 2 hour

• nitial dose 6C / ! nits:g 3od+ t ,olloed 3+• 6C as$art inslin at % nits 1 hor later and e*er+ % hor • ;hen 3lood glcose < %" #gdl change 0 ,lids to "= 4"= saline and

redce 6C as$art inslin to .1 nits:g e*er+ % hor to :ee$ glcose at %#gdl ntil resoltion o, 5



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8 Penggunaan Insulin Pada Kasus Kedaruratan Medik