Hallinan, Brigid, DO

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Lehigh Valley Health NetworkLVHN Scholarly WorksAdministration & LeadershipAbdominal Compartment Syndrome Presenting asDiuretic-Refractory Cardiorenal SyndromeBrigid Hallinan DOLehigh Valley Health NetworkFollow this and additional works at: https://scholarlyworks.lvhn.org/administration-leadershipPart of the Business Administration, Management, and Operations Commons, EmergencyMedicine Commons, Health and Medical Administration Commons, and the Management Sciencesand Quantitative Methods CommonsThis Poster is brought to you for free and open access by LVHN Scholarly Works. It has been accepted for inclusion in LVHN Scholarly Works by anauthorized administrator. For more information, please contact LibraryServices@lvhn.org.Published In/Presented AtHallinan, B. (2012). Abdominal Compartment Syndrome Presenting as Diuretic-Refractory Cardiorenal Syndrome. LVHN ScholarlyWorks. Retrieved from https://scholarlyworks.lvhn.org/administration-leadership/52 Lehigh Valley Health Network, Allentown, PennsylvaniaAbdominal Compartment Syndrome Presenting as Diuretic-Refractory Cardiorenal SyndromeBrigid Hallinan, DOReferences:1.	 	Cheatham	ML,	Malbrain	ML,	Kirkpatrick	A,	et	al.	Results	from	the	International	Conference	of	Experts	on	Intra-Abdominal	Hypertension	and	Abdominal	Compartment	Syndrome.	II.	Recommendations.	Intensive	Care	Med	2007:951-62.2.	 	Gestring	M.	(2012).	Abdominal	compartment	syndrome.	UpToDate.	Retrieved	from	http://www.uptodate.com/contents/abdominal-compartment-syndrome.3.	 	Mullens	W,	Abrahams	Z,	Francis	GS,	et	al.	Importance	of	venous	congestion	for	worsening	of	renal	function	in	advanced	decompensated	heart	failure.	J	Am	Coll	Cardiol	2009:589-96.4.	 	Mullens	W,	Abrahams	Z,	Skouri	HN,	et	al.	Elevated	intra-abdominal	pressure	in	acute	decompensated	heart	failure.	J	Am	Coll	Cardiol	2008:300-6.5.	 	Cheatham	ML.	Nonoperative	management	of	intraabdominal	hypertension	and	abdominal	compartment	syndrome.	World	J	Surg	2009:1116-22.6.	 	Ronco	C,	Haapio	M,	House	AA,	et	al.	Cardiorenal	syndrome.	J	Am	Coll	Cardiol	2008:1527-39.7.	 	Mullens	W,	Abrahams	Z,	Francis	GS,	et	al.	Prompt	reduction	in	intra-abdominal	pressure	following	large-volume	mechanical	fluid	removal	improves	renal	insufficiency	in	refractory	decompensated	heart	failure.	J	Card	Fail	2008:508-14.	Introduction:Abdominal	compartment	syndrome	(ACS)	is	an	increasingly	recognized	condition,	defined	as	sustained	intra-abdominal	pressure	≥	20	mmHg	with	resultant	organ	dysfunction.1	Most	often	associated	with	critically	ill	patients	in	the	setting	of	trauma,	abdominal	surgery,	sepsis,	pancreatitis,	massive	fluid	resuscitation,	or	intra-abdominal	hemorrhage,	ACS	can	also	result	from	third-spacing	of	fluid	into	the	abdomen	in	patients	with	acute	decompensated	heart	failure	(ADHF).	Here,	I	present	a	case	of	ACS	in	the	setting	of	diuretic-refractory	cardiorenal	syndrome	(CRS).Conclusion:Elevated	intra-abdominal	pressure	(IAP)	is	common	among	patients	admitted	with	acute	decompensated	heart	failure	(ADHF)	due	to	third-spacing	of	fluid	into	the	abdominal	compartment.	As	IAP	rises,	hemodynamics	become	further	impaired	and	renal	compression	ensues,	causing	poor	response	to	diuretic	therapy	and	clinical	deterioration.	The	diagnosis	of	intra-abdominal	hypertension	(IAH)	or	abdominal	compartment	syndrome	(ACS)	should	be	considered—and	IAP	measurement	obtained—in	any	patient	with	oligoanuric	AKI	in	the	setting	of	volume	overload,	such	as	in	ADHF.	If	IAH	or	ACS	is	diagnosed,	the	aggressiveness	of	the	therapy	warranted	depends	primarily	on	the	patient’s	clinical	condition	rather	than	the	actual	measured	pressure	of	the	abdominal	compartment.	In	patients	with	significantly	elevated	intra-abdominal	pressure	and	resultant	acute	organ	failure,	as	described	in	this	case,	rapid	abdominal	decompression	is	indicated	to	prevent	hemodynamic	collapse	and	even	death.	Figure	1.	IABP	Transducer	SetupHistory: An	85-year-old	Caucasian	female	presented	to	the	emergency	department	with	progressively	worsening	shortness	of	breath,	abdominal	distention,	decreased	urine	output,	and	lower	extremity	edema.	She	had	a	history	of	chronic	systolic	congestive	heart	failure	(CHF)	with	a	left	ventricular	ejection	fraction	(LVEF)	of	25%	and	CKD	III	with	a	baseline	creatinine	of	1.2	mg/dL.Physical Exam: At	the	time	of	presentation,	vital	signs	were	T	97.6°F,	HR	65	bpm,	BP	123/67	mmHg,	RR	20	bpm,	and	SpO2	97%	on	2	L	nasal	cannula.	She	appeared	to	be	comfortable	and	in	no	acute	distress.	Scattered	inspiratory	wheezes	and	bibasilar	rales	were	auscultated.	Cardiac	rhythm	was	regular,	with	a	3/6	blowing	systolic	ejection	murmur	over	the	left	upper	sternal	border.	Jugular	venous	distention	was	noted	to	the	level	of	the	earlobe.	The	abdomen	was	mildly	distended	and	firm	but	nontender	and	with	normoactive	bowel	sounds.	Venous	stasis	changes	and	3+	pitting	edema	were	present	in	the	lower	extremities	bilaterally.Diagnostic Studies:	Diagnostic	studies	revealed	BUN	54,	Cr	1.6	(baseline	Cr	1.2),	K+	5.6,	Na+	136	and	HCO3-	29.	Troponin	I	was	mildly	elevated,	peaking	at	0.29	ng/mL.	B-type	natriuretic	peptide	(BNP)	was	elevated	at	1644	pg/mL.	The	EKG	showed	no	acute	change	as	compared	with	prior	studies.	A	chest	X-ray	showed	pulmonary	vascular	congestion	and	new	bilateral	pleural	effusions.Hospital Course:	The	patient	was	admitted	for	acute	systolic	CHF	exacerbation	and	IV	furosemide	therapy	was	initiated.	Despite	an	escalation	of	diuretic	dosing,	the	addition	of	metolazone,	and	the	administration	of	a	constant	furosemide	infusion,	she	failed	to	diurese	and	remained	oliguric	throughout	her	first	hospital	day.	On	the	second	hospital	day,	her	blood	pressure	dropped	to	a	nadir	of	72/37	and	her	O2	requirements	increased.	Labs	revealed	an	increase	in	Cr	from	1.6	to	2.0	mg/dL	and	she	remained	dyspneic	and	oliguric.	A	renal	ultrasound	was	obtained,	which	demonstrated	normal	kidneys	along	with	mild	to	moderate	ascites.	Given	her	worsening	renal	function,	poor	response	to	diuretics,	hypotension,	and	evidence	of	ascites	on	the	ultrasound,	intra-abdominal	pressure	was	measured	using	the	transvesical	technique	(Figure	1).2	The	intra-abdominal	pressure	was	found	to	be	significantly	elevated	at	35	mmHg,	suggesting	a	diagnosis	of	abdominal	compartment	syndrome.	The	patient	promptly	underwent	therapeutic	paracentesis,	which	yielded	1.5	L	of	clear	ascitic	fluid.	Repeat	bladder	pressure	obtained	post-paracentesis	was	still	elevated	but	improved	to	22	mmHg.	Within	four	hours	of	paracentesis,	urine	output	increased	to	100	cc/hr	with	intermittent	IV	furosemide	dosing.	The	following	day,	she	had	significant	symptomatic	improvement	and	was	successfully	transitioned	to	oral	furosemide	with	continued	diuresis.		Within	three	days	of	the	procedure,	her	weight	decreased	by	5	kg,	creatinine	had	returned	to	her	baseline	of	1.2	mg/dL	and	blood	pressure	and	oxygenation	were	improved.	She	remained	stable	and	did	not	require	repeat	paracentesis	or	other	invasive	intervention	during	her	hospitalization.	With	some	medication	changes,	her	heart	failure	regimen	was	optimized	and	she	was	discharged	home	in	good	condition.Case Presentation:Background: Traditionally,	cardiorenal	syndrome	(CRS)	type	I—acute	decompensated	congestive	heart	failure	leading	to	acute	kidney	injury—was	thought	to	be	the	result	of	a	low	cardiac	output	state	causing	poor	renal	perfusion.3	Recent	data,	however,	highlight	the	significant	contribution	of	elevated	intra-abdominal	pressure	(IAP)	to	worsening	renal	function	in	acute	decompensated	heart	failure	(ADHF).	In	fact,	elevations	in	IAP	may	play	a	larger	role	in	the	development	of	acute	kidney	injury	(AKI)	in	this	setting	than	decreased	cardiac	index.3-4		Epidemiology: Elevated	IAP	(IAP	≥	8	mmHg)	is	likely	common	and	under-recognized	in	patients	hospitalized	with	ADHF.		A	single-center	study	reported	a	60%	prevalence	of	elevated	IAP	in	a	study	group	of	40	consecutive	patients	admitted	to	a	heart	failure	unit	with	ADHF,	with	10%	of	these	total	patients	meeting	the	criteria	for	intra-abdominal	hypertension	(IAP	≥	12	mmHg).4Pathophysiology: The	mechanisms	by	which	elevated	IAP	causes	worsening	renal	function	include	the	following:	reduction	in	the	glomerular	filtration	gradient,	renal	vein	and	ureter	compression,	impaired	venous	return	leading	to	decreased	cardiac	output,	and	induction	of	inflammatory	mediators.4Diagnosis: Measurement	of	IAP	by	the	transvesical	technique	(Figure	1)2	should	be	performed	in	CRS	patients	who	are	not	responding	to	diuretic	therapy.	A	normal	abdominal	examination	and	lack	of	patient	discomfort	should	not	delay	IAP	measurement	in	CRS	patients.	Physical	examination	findings	and	patient	symptomatology	have	been	found	to	correlate	poorly	with	measured	IAP,	possibly	owing	to	the	slow	increase	in	IAP	in	ADHF,	as	opposed	to	the	rapid	IAP	increase	classically	seen	in	trauma	or	surgical	patients	with	ACS.4		Management: If	intra-abdominal	hypertension	(IAP	≥	12	mmHg)	is	detected	in	a	hemodynamically	stable	patient,	conservative	management	is	initially	recommended	to	attempt	IAP	reduction.	Potentially	useful	techniques	include	evacuation	of	intraluminal	contents	via	nasogastric	or	rectal	tube,	administration	of	prokinetic	agents,	and	decreasing	or	holding	enteral	feedings.		In	the	case	of	refractory	ileus	or	colonic	pseudo-obstruction,	however,	colonoscopic	decompression	may	be	necessary.	Abdominal	imaging	with	CT	or	ultrasound	may	reveal	ascites	amenable	to	percutaneous	drainage.	Abdominal	wall	compliance	may	be	improved	with	adequate	analgesia,	removal	of	constrictive	dressings,	placing	the	patient	in	the	reverse	Trendelenburg	position,	or	raising	the	head	of	the	bed	to	≥	20	degrees.	In	mechanically	ventilated	patients,	neuromuscular	blockade	can	be	highly	effective	in	decreasing	IAP.5	If	the	patient	is	agreeable	to	acute	renal	replacement	therapy,	isotonic	fluid	removal	with	slow	continuous	ultrafiltration	(SCUF)	may	be	a	viable	option.6In	ADHF	patients	meeting	criteria	for	ACS	(sustained	IAP	≥	20	mmHg	with	resultant	organ	dysfunction)	more	urgent	and	definitive	treatment	is	warranted.	Standard	measures	for	treating	intra-abdominal	hypertension,	as	previously	described,	should	still	be	considered.		In	particular,	the	presence	of	ascites	should	be	sought	and	fluid	promptly	removed	if	present,	as	decreasing	the	IAP	in	this	manner	can	lead	to	rapid	improvement	in	hemodynamics	and	renal	perfusion.7	If	paracentesis	is	not	an	option	or	the	patient	is	hemodynamically	unstable,	surgical	evaluation	for	decompressive	laparotomy	should	be	sought	without	delay.1Discussion:Contact Information: Brigid	K.	Hallinan,	DO1240	S.	Cedar	Crest	Blvd.Suite	410Allentown,	PA	18103(610)	402-5200brigid.hallinan@gmail.com1.		Clamp	the	drainage	tube	of	the	Foley	(bladder)	catheter.2.		Instill	up	to	60	cc	sterile	saline	into	the	bladder	via	the	aspiration	port	of	the	Foley	catheter.	Be	certain	the	catheter	is	filled	with	fluid.3.		Attach	a	pressure	transducer	to	an	18-gauge	needle,	and	insert	into	the	aspiration	port.	With	some	newer	style	Foley	catheters,	a	needle-less	connection	system		can	be	used.4.		Zero	the	transducer	at	the	level	of	the	midaxillary	line.5.		With	the	patient	in	the	supine	position,	ensure	that	abdominal	muscle	contractions	are	absent,	and	measure	the	bladder	pressure	at	end-expiration.Reproduced	with	permission	from:	Gestring	M.	Abdominal	compartment	syndrome.	In:	UpToDate,	Basow,	DS	(Ed),	UpToDate,	Waltham,	MA,	2012.Copyright	©	2012	UpToDate,	Inc.	For	more	information	visit	www.uptodate.com.

Abdominal Compartment Syndrome Presenting as Diuretic-Refractory Cardiorenal Syndrome

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Abdominal Compartment Syndrome Presenting as Diuretic-Refractory Cardiorenal Syndrome

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