96.Hepatic Vascular abN Flashcards
percentage of congenital PSS that are single extrahepatic
66-75% of congenital PSS = single extra hepatic25-33% of congenital PSS = intrahepaticportocaval is most common singe EHPSS
causes of acquired PSS
20%older animalsmultiple, tortuous, extrahepaticnear kidneys, gonads, or internal thoracic veins1. cirrhosis/ hepatic fibrosis2. portal vein hypoplasia WITH PH (congenital noncirrhotic PH)–dobies over rep3. hepatic AV malformations
other name for PVH without PH
portal vein hypoplasia without portal hypertension=microvascular dysplasia (MVD)bc portal vein hypoplasia can occur with or without portal hypertension
percentage of dogs/cats with congenital PSS and MVD
PSS with MVD60% dogs90% cats
hepatic encephalopathy occurs when what percentage of the liver is dysfunctional
HE occurs with 70% liver function is lost
most important neurotoxin for HE
Ammonia (produced by GI flora)increases brain tryptophan (neurotoxic) and glutaminedecreases ATP increases neuronal excitability (excitotoxic)increases NMDA receptors w glutamatebrain edema, seizures
MOA of benzodiazipines and GABA for causing HE
neural inhibition through hyper polarization of neuronal membranecoma, stupor, depression
MOA bile acids for causing HE
membranocytolytic effects alter cell membrane permeability making BBB more permeable to other substances
causes of coagulopathy in liver failure
decreased factor synthesisincreased factor utilizationincreased fibrinolysissynthesis of anti coagulants decreased platelet function and numbervit K deficiencyincreased production of anticoagulants(TEG may suggest these patients are hyper coagulable)
odds ratio of Yorkshire Terriers for occurrence of congenital PSS
35.9 times greater than all other at risk breeds combined for occurrence of congenital PSS
other toy breeds affected with congenital PSS
suspect hereditary–yorkshire–maltese–cairn
breeds overrepresented with intrahepatic PSS
larger breeds–irish wolfhounds–retrievers–australian cattle dogs–australian shepherd
type of intrahepatic PSS in irish wolfhounds
left divisional intrahepatic PSShereditary in irish wolfhounds
type of intrahepatic PSS in australian shepherds
right divisional intrahepatic PSSoverrepresented in australian shepherds
MOA of PU/PD in PSS dogs
extremely common PU/PDMOA–medullary washout of BUN–increased renal blood flow–increased ACTH–psychogenic PD from HE
abdominal effusion in hepatic arteriovenous malformations in dogs
75%also seen with multiple acquired PSSand more common in intrahepatic vs extra hepatic PSSlikely cause–hypoalb (decr production liver, PLE from GI ulcers or IBD +/- lymphangiectasia)
preoperative GI hemorrhage reported in PSS patients
30% intrahepatic PSS—treat w gastroprotectants prepuncommon in extrahepatic PSS
ptyalism reported in cats as clinical sign of PSS
75%
causes of lower urinary tract signs in PSS patients
decreased ureaincreased renal ammonia excretiondecreased uric acid metabolismammonium urate calculi 30%+/- secondary bacT infection
clinicopathologic findings for hepatic vascular anomaly patients
microcytosis, normochromic nonregenerative anemia (iron sequestration)target cells–dogs; pokiolocytes–catsthrombocytopenialeukocytosis (associated with poor px)hypoalb, hypogly, decreased BUN, hypocholesterolmoderate incr liver enzymesbile acids incrUA–decr USG, crystalluria
protein C and ddx btwn PSS vs MVD
Protein C = antiinflm, antithrombotic, antiapoptotic (vit K dependent)PSS 88% patients had levels < 70%PVH–MVD 95% patients had levels > 70%cannot ddx normal vs PVH-MVD
flow of hepatic AV malformations vs extrahepatic PSS on doppler US
hepatic AV malformations–hepatofugalextrahepatic PSS–hepatopedal
diagnostic imaging for hepatic vascular anomalies
survey radsab USscintigraphy–transcolonic< transsplenic (technetium pertechnetate)CT angiographyCT transplenic portographyMR angiographyPorto(jejuno or spleno) venography–intra-operative, fluoro, 2-4 ml/kg iohexolother: percutanous US transsplenic venography, retrograde transjugular portography, cranial mesenteric angiography via femoral artery
normal scintigraphy shunt fractions
transcolonic shunt fraction < 15% normaltranssplenic shunt fraction «_space;15% normalmost congenital PSS >60-80% SFincreased in dogs with single congenital IHPSS/EHPSS, multiple acquired shunt, hepatic AV malformations
disadvantages of scintigraphy
cannot ddx intra vs extra hepatic PSScannot ddx normal vs PVH-MVD dogscannot ddx single vs multiple
dose for intra-operative portovenography
2-4 ml/kg iohexol (sterile, water soluble 240-360 mg I/ mL)jejunal or splenic vein catheterizationfluorocranial to 13th T IHPSScaudal to 13th T EHPSSlife threatening hemorrhage if splenic injection at AV malformations present
MOA and dose lactulose
0.5-1.0 ml/kg PO q6-8hr to effect5-10 ml/kg warm water enemapromotes acidification which traps luminal ammonium and decreases colonic bacT #also osmotic effect, reduces transit time
diuretic of choice to treat ascites from portal hypertension
spironolactone bc of potassium sparing effectsascites from decreased oncotic pressure however can be treated with colloidal therapy
epiploic foramen
dorsally—caudal vena cavaventrally–portal vein caudally–celiac artery/hepatic artery
most common area to find multiple acquired PSS
- near right kidney2. within intestines
normal portal pressures
measured through jejunal, splenic, or portal vnormal 8-13 cm H20 (6-10 mm Hg)patients with PSS have lower PP
ameroid constrictor material
inner casein–hygroscopic substance absorbs fluid decreasing inner diameter by 32%outter stainless steel
suture ligation of PSS
non absorbable synthetic monofilament2-0 silkpolpropylene to decrease risk of shunt recanalization
signs of portal hypertension
pallor or cyanosis of intestinesincreased intestinal peristalsiscyanosis/edema of pancreasincreased mesenteric pulsations
what percentage of dogs require partial shunt attenuation
86%
where is the ductus venous visible
ductus venosus is visible btwn left lateral lobe and papillary process of the caudate lobe before it enters the left hepatic veinmost dogs with left sided IHPSS have a patent ductus venousfunctional closure 2-6 daysstructure closure 3 weeks
what are portocaval windows
when portal vein and cava vascular walls fuse
list post operative complications PSS
hypoglycemia (44%)hemorrhage/anemiaportal hypertension (2-14% acute)hypothermiaseizures/HE (18% dog 22% cat day 5)recurrence of clinical signs
propofol CRI for PSS post op seizures
0.1-1.0 mg/kg/min
mortality rates for surgically treated EHPSS
2-32% suture ligation7% ameroid6-9% cellophane
mortality rates for surgically treated IHPSS
6-24% suture ligation9% ameroid27% cellophane(higher rates with intrahepatic attenuation)
portal vein tributaries
FROM CAUDAL TO CRANIAL–cranial mesenteric vein (largest)–caudal mesenteric vein–splenic vein–gastroduodenal vein (absent in cats)
three types of classifications of liver vascular disease
- congenital PSS2. primary hypoplasia of portal vein (abN hepatic blood flow or portal hypertension)3. disturbances in portal outflow
treatment for acute severe HE
–warm water enema–oral or rectal lactulose–dextrose administration–fix metabolic acidosis with IVF–antibiotics metro, neomycin, amoxiclav)–anticonvulsants
Greenhalgh et al 2010 JAVMA medical mgmt vs surgery for treatment of PSS and survival
long term survival in med tx alone 50%long term survival with surgery 90%age did not have a significant effect on survival time
prognosis for PVH-MVD (no portal hypertension)
excellent 90% long term survival
prognosis for PVH with portal hypertension
poor 40% long term survival
list 6 reasons for persistent post operative clinical signs
—ligated/device on wrong vessel–more than one shunt–placed too distal and missed a proximal branch–device didn’t occlude–acquired shunts develop–PVH-MVD in addition to PSS
list 6 methods to correct PSS
–ameroid–cellophane–silk ligation–hydraulic occluder–amplatzer intravascular plug–thrombogenic coil–cardio cyanoacrylate
methods to find IHPSS intraoperatively
—compression of parenchyma may lead to increase PP at site of IHPSS–intraop mesenteric/splenic portography–portal or transsplenic catheterization–intraoperative doppler ultrasonography
methods for IHPSS dissection/occlusion
intravascular–require temporary occlusion of portal vein/caudal vena cava; transcaval or portal venotomy approachesextravascular approach
T/Fin dogs undergoing ameroid occlusion for EHPSS, preop neuro status did not have affect on outcome
TRUEMehl et al 2005 JAVMA
complications in cats postoperative shunt occlusion
75%mostly neurologic dysfunction–seizures (30%) and blind in (45%)central blindness may resolve within 2 month
treatment for hepatic AV malformations
most often seen in Right and central divisionlobectomy/resection
T/Fage at the time of surgery for shunt occlusion had no effect on outcome
true
factors that may be negative predictors of outcome
NOT age at surgery, NOT preop neuro status, NOT post op bile acids, NOT liver biopsymaybe:leukocytosis, neutrophiliaanemiahypoalbuminemialarge breed dogs (have recurrence)
