Predictors of insufficient recanalization and portal hypertensive complications after treatment of non-cirrhotic, non-malignant portal vein thrombosis – a population-based study

Figures & data

Figure 1. Flowchart of patient selection. HUS: Helsinki University Hospital.

Table 1. Basic demographics and onset.

	N (%) n = 145
Age, median (IQR)	52.8 (41.9–63.7)
Sex, Female n (%)	47 (32%)
Comorbidity, n (%)
Diabetes	15 (10%)
Previous deep vein thrombosis	12 (8%)
Other comorbidity^a	36 (25%)
No comorbidity	83 (57%)
Medication at diagnosis, n(%)
Anticoagulation medication^b jj	7 (5%)
Antithrombotic medication^c	15 (10%)
Hormone therapy
Indication: contraception	12 (8%)
Indication: menopause	3 (2%)
Incidental^d	12 (8%)
Laboratory results at diagnosis, n (%)
Thrombophilia investigations performed	97 (67%)
Hemoglobin
Anemia^g	60 (41%)
Erythrocytosis^h	8 (6%)
Platelets
Thrombocytopenia^i	29 (20%)
Thrombocytosis^j	33 (23%)
D-dimer (n = 40)^e
Normal (<0.5 mg/l)	3 (7%)
Elevated (>0.5 mg/l)	37 (93%)
Elevated liver enzymes^f^,k	65 (45%)
eGFR < 90 ml/min/1.73m^2	48 (33%)

eGFR: estimated glomerular filtration rate; IQR: interquartile range.

^ahypertension (n = 26), atrial fibrillation (n = 10), coronary artery disease (n = 6), previous stroke (n = 4), previous acute myocardial infarction (n = 1), congestive heart failure (n = 3), atherosclerosis (n = 2), chronic obstructive pulmonary disease (n = 2), kidney failure (n = 1), previous pulmonary embolism (n = 2), Alzheimer (n = 2).

^bIndication for anticoagulation: atrial fibrillation (n = 5), previous thromboembolism (n = 1), postoperative thrombosis prophylaxis (n = 1).

^cIndication for antithrombotic medication: myeloproliferative disease (n = 3), coronary artery disease (n = 4), not known (n = 8).

^dPortal vein thrombosis found incidentally during imaging for other purposes.

^eD-dimer determined in 40 patients.

^fAspartate aminotransferase and/or alanine aminotransferase determined in 138 patients.

^gwomen < 117g/l, men < 134g/l.

^hwomen > 155g/l, men > 167g/l.

ⁱ<1,50,109/l.

^j>3,60,109/l.

^kwomen: aspartate aminotransferase >35 U/l, men: aspartate aminotransferase >45 U/l and/or women: alanine aminotransferase >35 U/l, men: alanine aminotransferase >50 U/l.

Table 2. Prevalence of etiological factors.

	N (%)
	n = 145
Number of etiological factors
No etiological factors found	13 (9%)
1 etiological factor	69 (48%)
2 etiological factors	57 (39%)
3 etiological factors	5 (3%)
4 or more etiological factors	1 (1%)
Hematological disease	18 (12%)
JAK V617F	2 (1%)
Polysytemia vera	1 (1%)
Essential thrombocytosis	1 (1%)
JAK V617F + polysytemia vera	9 (6%)
JAK V617F + Essential thrombocytosis	5 (3%)
Genetic mutation	12 (7%)
Factor V Leiden mutation	7 (5%)
Factor II mutation	3 (2%)
Both mutations	2 (1%)
Thrombophilia	86 (59%)
Factor VIII > 160%	38 (26%)
Protein S < 65%	34 (23%)
Protein C < 74%	24 (17%)
Antithrombin 3 < 85%	29 (20%)
Cardiolipin antibodies positive	20 (14%)
Beta-2 glycoprotein 1 antibodies positive	5 (3%)
More than one pro-coagulative finding	42 (29%)
No pro-coagulative finding	59 (41%)
Inflammatory disease alone	66 (46%)
Acute pancreatitis^d	20 (14%)
Cholecystitis^e	12 (8%)
Acute-on-chronic pancreatitis	11 (8%)
Intra-abdominal abscess	8 (6%)
Diverticulitis	2 (1%)
Other ^a	13 (9%)
Traumatic	2 (1%)
Postoperative	8 (6%)
Splenectomy	3 (2%)
Cholecystectomy	2 (1%)
Other^b	3 (2%)
Other possible reasons^c	13 (9%)
No etiologic factor found	13 (9%)

JAK V617F: Janus kinase 2 gene mutation; GI: gastrointestinal.

^aCholangitis (n = 2), appendicitis (n = 2), sepsis (n = 2), pouchitis (n = 1), ischaemic colitis (n = 2), ileitis (n = 1) Crohn’s disease (n = 1), infection NAS (n = 1), postoperative infection of anal fistula (n = 1).

^bPancreatic resection for necrotizing pancreatitis, no vascular reconstruction (n = 1), appendicectomy (n = 1), proctocholectomy (n = 1).

^cSepsis (n = 2), obesity (n = 3), secondary polysytemia (n = 1), Osler-Weber-Rendu syndrome (n = 1), Klippel-Trenaunay syndrome (n = 1), hereditary spherocytosis (n = 2), hepatitis (n = 1), AIDS (n = 1), acute liver failure (n = 1).

^dAtlanta classification: mild (n = 1), moderately severe (n = 12), severe (n = 7).

^eChronic (n = 7), acute (n = 5).

Table 3. Characteristics of thrombosis at the time of diagnosis and treatment.

	N (%)
Completeness of PV thrombosis, n (%)	n = 145
Partial	73 (50%)
Total	67 (46%)
Unknown	4 (3%)
Extent of thrombosis, n (%)
PV alone	56 (39%)
PV + SMV	32 (36%)
PV + SV	16 (22%)
PV + SMV + SV	41 (28%)
Age of thrombosis^a, n (%)
Acute	91 (63%)
Sub-acute	40 (28%)
Chronic	14 (10%)
Varices at baseline	1 (0.7%)
Ascites at baseline imaging	42 (29%)
First treatment modality, n(%)	138 (95%)
Anticoagulation (other than unfractionated heparin)^b	111 (77%)
Unfractionated heparin	21 (15%)
Thrombolysis	2 (1%)
Surgery^c	4 (3%)
Second treatment modality, n(%)	14 (10%)
Unfractionated heparin	12 (8%)
Endovascular thrombectomy	2 (1%)
Third treatment modality, n(%)	2 (1%)
Unfractionated heparin	2 (1%)
Fourth treatment modality, n(%)	1 (1%)
Thrombolysis	1 (1%)

PV: portal vein; SMV: superior mesenteric vein; SV: splenic vein.

^aAcute = first-time detected portal vein thrombosis in previously patent portal vein, the presence of hyperdense thrombus on imaging, absent, or limited collateral circulation, dilated portal vein at the site of occlusion, symptomatic. Sub-acute = first-time detected portal vein thrombosis in previously patent portal vein, the presence of hyperdense thrombus on imaging, absent, or limited collateral circulation, dilated portal vein at the site of occlusion, asymptomatic. Chronic = no hyperdense thrombus; previously diagnosed PVT on follow-up, portal cavernoma, and clinical features of portal hypertension.

^bLow-molecular-weight heparin (n = 104), Warfarin (with low-molecular-weight heparin used a bridge) (n = 7).

^cThrombectomy via laparotomy (n = 4).

Table 4. Outcomes and complications.

	N (%) n = 145
Follow-up results of treatment
Portal vein thrombosis at baseline
Partial	73 (50%)
Complete	67 (46%)
Unknown	5 (4%)
Thrombosis at 4–8 months (n = 84)
No thrombosis	21 (15%)
Partial thrombosis	36 (25%)
Complete thrombosis	16 (11%)
Cavernoma	11 (8%)
No imaging at this time	61 (42%)
Thrombosis at 10–14 months (n = 72)
No thrombosis	27 (19%)
Partial thrombosis	24 (17%)
Complete thrombosis	6 (4%)
Cavernoma	15 (10%)
No imaging at this time	73 (50%)
Thrombosis at last imaging control (n = 127)
No thrombosis	49 (34%)
Partial thrombosis	23 (16%)
Complete thrombosis	15 (10%)
Cavernoma	40 (28%)
No follow-up imaging or died	18 (12%)
Last imaging modality	7 (7%)
CT, no contrast	9 (6%)
CT with contrast	52 (36%)
MRI	7 (5%)
Ultrasound, no Doppler	37 (26%)
Ultrasound with Doppler	22 (15%)
Imaging done for follow-up of PVT	69 (48%)
Clinical follow-up, median (IQR)	6.9 (5.3 − 9.4) years
Radiologic follow-up, median (IQR)	1.3 (0.4 − 4.6) years
New-onset portal hypertensive complications	40 (28%)
Ascites	11 (8%)
Only visible on imaging	6 (4%)
Requiring treatment	5 (3%)
Varices	30 (21%)
Varices without bleeding	22 (15%)
Variceal bleeding	8 (6%)
Symptomatic portal biliopathy	2 (1%)
Recurrence of portal vein thrombosis^a	6 (4%)
Other thromboembolic condition during follow-up	8 (6%)
Stroke	2 (1%)
PE	1 (1%)
DVT	1 (1%)
Upper limb thrombosis	2 (1%)
Deep vein thrombosis + PE	2 (1%)
Complications^c	25 (17%)
GI bleeding	13 (9%)
Other bleed^b	12 (8%)
More than one bleed	5 (3%)

PE: pulmonary embolism; DVT: deep-vein thrombosis; GI: gastrointestinal.

^aTreatment: UFH (n = 2), LMWH dose raised (n = 1), argatroban infusion (n = 1).

^bIntramuscular hematoma (n = 5), epistaxis (n = 7).

^cAll bleedings were considered to be related to anticoagulation treatment.

Figure 2. Predictors of insufficient recanalization divided by (a) age of thrombosis and (b) etiology (acute pancreatitis).

Lang SA, Loss M, Wohlgemuth WA, et al. Clinical management of acute portal/mesenteric vein thrombosis. Viszeralmedizin. 2014;30(6):394–400.

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