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    1

    INTRAABDOMINALHYPERTENTION &

    ABDOMINALCOMPARTMENTSYNDROME Aditya Bhayusakti, M.

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    important values

    Normal intra-abdominal pressure is 0 - 5mmHg. Pressures > 13mmHg may be sufficient to restrict perfusion

    to the organs of the gut. If the abdominal compartment pressures is beteen 1!-"5

    mmHg# hyper$olemic $olume e%pansion therapy can be usedto maintain the perfusion pressure gradient for the abdominalorgans.

    &hen compartment pressures e%ceed "5mmHg#decompression surgery should be considered to pre$ent

    organ damage. Pressure may rise rapidly ith acti$ebleeding. 'dema (hich occurs ith any ischemic insult) illgenerally result in a later rise in the pressure ("* hours ormore post insult).

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    Classiy IAH i!t" # $%"us'

    Hyperacute(sec,min):laughing,strain,coug-

    hing,sneez,physical activities)

    Acute(couple H):trauma,hge

    Subacute (couple days): most medicalcases.

    Chronic: morbid obesity,intraabdominal

    tumor,pregnancy.

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    Pati(!ts at %isk "% ACSi!)lud(' trauma (blunt or open),as a result of the

    accumulation of blood# fluid or edema.

    gastrointestinal hemorrhage can also lead to

    increased pressure in the abdominal compartment as

    ischemic cells sell or fluids collect.

    pancreatitis

    pneumoperitoneum

    neoplasm

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    syndrome may ollo! a rupturedabdominal aortic aneurysm

    intra-abdominal inection Coagulopathies !ith abdominal

    bleeding

    cirrhosis, or proound hypothermia

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    massive intra-abdominalretroperitoneal hemorrhage,

    severe gut edema

    intestinal obstruction

    ascites under pressure.

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    "atients !ho have undergone long surgical

    procedures !ith intraoperative hypotension andlarge luid re#uirements are at signiicant ris$,particularly i the abdomen has been closedunder pressure in the %&.

    'ternal pressure rom circumerential burnsabout the abdomen, application o military anti-shoc$ trousers (AS*), or even tight abdominalrestraint devices can cause tension !ithin theabdomen due to eternal orces and result inACS.+

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    &ecently, a!arenesso the ACS has increased or +

    primary reasons.

    irst, the increased use o laparoscopy among general

    surgeons has brought !ith it an appreciation o A" as a

    readily #uantiiable entity.

    Second, the more re#uent use o planned repeat

    laparotomy or trauma has allo!ed both surgeon andintensivist to appreciate the beneicial eects o

    abdominal decompression upon removal o pac$ing or

    evacuation o hematoma.

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    Th( Path"hysi"l"$y " IAH

    I+PASC/0A&

    C%"&'SS%1

    2&'C* %&3A1

    C%"&'SS%1

    2A"H&A3A*C

    '0'A*%1

    &" Clo!Cardiac

    compression ntrathoracicpressure

    Cardiac preloadCardiac contractility Systemic aterload

    ,+I+, /P&enal ascular

    &esistanceSplanchnic

    ascular &esistance

    &'1A0 A0/&' A42%1A0 5A00SCHA'A6%'2'A &'S"&A*%&7A0/&'

    C" S"0A1CH1CSCHA'A

    " pressure

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    Compartment syndrome occurs !hen

    the pressure !ithin a closedanatomic spaceincreases to the

    point !here vascular tissue is

    compromised !ith subse#uent losso tissue viability and unction. *his

    can occur !ithin any closedbody

    cavity.

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    ncreased A" leads to decreased

    4 and to 4acterial translocation

    (4*),!hich may contribute to laterseptic complications and organ

    ailure.

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    AH provo$es the release o pro-inlammatory cyto$ines !hich may

    serve as a second insult or the

    induction o %. production o interleu$in-8b (0-

    8beta), interleu$in-9 (0-9), tumor

    necrosis actor (*1-alpha)

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    Anaesthetic Implications ofACS:

    Renal implications

    PulmonaryImplications

    CardiovascularImplications

    Porto-systemicvisceral

    Implications

    Centralnervoussystem

    Implications

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    E*()ts "! C+S

    As intraabdominal pressure increases above 8mmHg, cardiac output declines, despite normalarterial pressures.

    Additionally, !hole body oygen consumption, pH,and "%+ decrease.

    ntraabdominal hypertension aects cardiac

    unction by pushing the hemidiaphragms up!ard,thus transmitting the abdominal pressure to theheart and its vessels.

    *his decreases preload and increases aterload onthe let ventricle and at the same time creates ahemodynamic picture o lo! cardiac output andhigh illing pressures.8,;

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    O! th( ul"!a%y syst(

    he most commonly noted effects of I+H on the

    pulmonary system are ele$ated pea2 inspiratory

    pressures# decreases in Pao" and increases in

    Paco" reuiring the use of complete $entilatory

    support to maintain adeuate o%ygenation and$entilation.

    Hypercarbia# hypo%emia# and acidosis are e$ident

    hen arterial blood gases are measured.!

    Positi$e end-e%piratory pressure has been shonto e%acerbate the cardiac and respiratory

    conseuences of I+H.

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    Pul"!a%y (*()ts " i!)%(as(di!t%a-ad"i!al %(ssu%( /0 mechanical ventilation

    oten necessary

    high pea$ air!ay

    pressures

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    Pul"!a%y (*()ts " i!)%(as(di!t%a-ad"i!al %(ssu%( /2

    "ressure on the C

    predisposes to venous

    stasis and increased

    ris$ o

    thromboembolism

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    R(!al (*()ts

    include decreased renal plasma flo# glomerular filtrationrate# and glucose reabsorption. /liguriaalso occurs# ithanuria noted in animal models hen I+P reaches 30mmHg.1 hese effects occur ithout significantdecreases in blood pressure(mechanical#4#compression of $ein6outflo obstuction64

    intraparenchymal pressure6shunting of blood from corte%) . Impro$ement of cardiac output does not impro$e renal

    function# nor do renal blood flo and glomerular filtrationrate impro$e.

    the placement of ureteral stents failed to impro$e renal

    function. Impro$ement in renal function occurred only after

    abdominal decompression.*

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    *hese indings suggest that the eects o AHon renal unction are related to compression o

    the renal parenchyma itsel and tocompression o renal vasculature and are notrelated to decreased cardiac output. %thermechanisms proposed include shunting oblood a!ay rom the renal corte into the

    medulla, decreased renal arterial lo! !ith aconcomitant increase in renal vascularresistance, and the presence o high levels orenin, aldosterone, and antidiuretic hormones.8

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    =

    8

    8=

    +

    = 8 8= + += luids

    A

    ldosterone

    level

    (ng6dl)

    A" (mmHg above baseline)

    'perimental

    Control

    'ect o increased intra-abdominal pressure on plasma

    aldosterone. *he increased levels are reduced by volume

    epansion (J Trauma8>>?@;+:>>?-8)

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    =

    8

    8=

    +

    +=

    = 8 8= + += luids

    "las

    mareninac

    tivity

    (ng6ml6hr)

    A" (mmHg above baseline)

    'perimental

    Control

    'ect o increased intra-abdominal pressure on plasma

    renin activity. *he increased levels are reduced by volume

    epansion (J Trauma8>>?@;+:>>?-8)

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    ncreases in A" have adverse

    eect on splanchnic lo!

    B8=mmHgSA blood lo!

    mar$ed reduction in hepaticartery and portal venous blood

    lo!

    leads to mucosal acidosis and

    oedema

    IAH a!d Sla!)h!i) 3l"4

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    Cy)l( " (5(!ts )%(at(d yIAH "! sla!)h!i) )i%)ulati"!

    AH

    Unrelieved

    ACS

    Splanchnic

    hypoperusion

    3ut mucosal acidosis

    4o!el oedema

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    hey measured mucosal and intestinal blood flo

    and intramucosal pH (pHi) and found that

    mesenteric and mucosal blood flo decreased henI+P reached "0mmHg# ith intestinal mucosal flo

    declining to !17of baseline.

    +t an I+P of 80mmHg# intestinal flo decreased to

    "97of baseline. he intestinal mucosa shoed signs of a se$ere

    degree of acidosis# measured by tonometer. hese

    changes in splanchnic blood flo occurred despite

    maintenance of baseline cardiac output ith $olumeloading.

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    pp

    + ; 9 8

    8

    =4o!el*"%+

    Aillary

    *"%+

    A" +=mmHg or

    9 min

    A" 8=mmHg or

    9 min

    4aseline

    'ects o increasing A" on bo!el mucosal oygen (tissue

    partial pressure, *"%+) compared !ith systemic tissue

    oygenation in the ailla (J Trauma 8>>=@>:=8>-=++)

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    blood lo! to virtually every abdominal organ

    decreased signiicantly. *he only eception

    !as the adrenal gland@ the reason this

    organ is not aected is un$no!n >>@;? :=>-=88

    Current opinion does

    not support liberal use

    of an open abdomen

    technique to preventACS

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    An alternative techni#ue is the vacuum-pac$techni#ue. Here the litre bag is opened and placed

    into the abdomen to protect the gut contents, underthe sheath. *his has been reerred to as the 4ogotabag, ater the city in Colombia, South America, o itsinception.>

    *!o large calibre suction drains are placed overthis, and a large adherent steridrape placed over the!hole abdomen. *he suction catheters areconnected to high-displacement suction to providecontrol o luid losses and create the vacuum-pac$

    eect

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    *he easiest method to control the open abdomen is

    to use a silo-bag closure. A litre plastic irrigationbag is emptied and cut open so it lies lat. *he

    edges are trimmed and sutured to the s$in, a!ay

    rom the s$in edges, using a continuous 8 sil$

    suture. t is useul to place a sterile absorbent drapeinside the abdomen to soa$ up some o the luid and

    ease control o the laparostomy.

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    Adverse Efects o Surgical

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    Adverse Efects o Surgical

    Decompression Sudden release o the abdominal compartment

    syndrome may lead to an ischaemia-reperusion inEury

    *he mechanism !as postulated to be related to !ashout

    o anaerobic metabolic products by reperusion o the

    previously underperused splanchnic bed causing

    acidosis, vasodilatation, cardiac dysunction and arrest.

    "rior to release the patient should be pre-loaded !ith

    crystalloid solution. annitol and vasodilators such as

    dobutamine or the phosphodiesterase inhibitors may

    have a place here.

    MEDICAL

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    MEDICALDECOMPRESSION

    *he adverse cardiovascular and

    pulmonary eects o intra-

    abdominal hypertension IAHJ!ere reversed !ith

    pharmacological neuromuscular

    bloc$ade (14(

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    Management

    Prevention

    Identicationof patients at ris!

    Monitoring

    Ade"uate resuscitationAde"uate ventilation

    #on-surgicalinterventions

    Paracentesis#euromuscular $loc!adeC#AP

    %ut emptying

    &ctreotide

    Prognosis

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    Prognosis

    he death rate in patients ith +,? is e%tremely high.

    ?e$eral small series ha$e reported death rates ranging from

    8"7 to *17.hese high rates must be considered in the

    conte%t of the patientsA underlying disease.

    he maority of these patients are critically ill and are

    admitted to the intensi$e care unit ith se$ere intra-abdominal sepsis# intra-abdominal inuries or after repair of

    a ruptured abdominal aortic aneurysm.

    '$en ith prompt recognition and abdominal

    decompression# the freuency of multiple organ dysfunction

    and death is high because of the se$erity of the initial

    physiologic insult.

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    Ho!ever, in the ace o elevated A"

    and a clinical picture consistent !ith

    ACS, the chance o survival isetremely lo! !ithout urgent

    abdominal decompression.8

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    THAN9 YO: