Ischemia of the Liver Secondary to Portal Vein Thrombosis
A 59-year-old woman complainsof progressively worsening bloatingand right upper quadrant pain thatbegan 1 day earlier. She denies feverand trauma. Her medical history includescholecystectomy for cholelithiasisand several emergency departmentvisits for treatment of woundssustained in falls. She has a history ofalcohol abuse, for which she now receivescounseling. However, she admitsthat she occasionally has boutsof heavy drinking.
Case 1:
Bloating and Abdominal Painin a Woman With aHistory of Alcohol Abuse
A 59-year-old woman complainsof progressively worsening bloatingand right upper quadrant pain thatbegan 1 day earlier. She denies feverand trauma. Her medical history includescholecystectomy for cholelithiasisand several emergency departmentvisits for treatment of woundssustained in falls. She has a history ofalcohol abuse, for which she now receivescounseling. However, she admitsthat she occasionally has boutsof heavy drinking.This markedly obese woman isin moderate distress because ofher abdominal pain. Temperature is36.6C (98F); heart rate, 88 beatsper minute, with normal rhythm; respirationrate, 18 breaths per minute;and blood pressure, 113/82 mm Hg.Head and neck are normal. Lungs areclear, but air excursion is diminished.The patient's obesity makes examinationof the abdomen difficult. However,tenderness is elicited in the rightupper quadrant. The abdomen is softand bowel sounds are normal. Extremitiesare also normal. Liver functionenzyme levels are elevated.A conventional radiograph of theabdomen shows centralization of thebowel loops, which is consistent withascites; the bowel gas pattern is unremarkable.You order an abdominal ultrasonographicexamination. What dothe scans reveal about the cause ofthe ascites, and what further investigationis warranted?
Case 1:
Bloating and abdominal pain in awoman with a history of alcoholabuse:
A large amount of ascites iseasily identified in the right lowerquadrant (
A
, arrow), which is mostlikely the cause of this woman's complaintof "fullness." During the examination,a thrombus in the portal veinis questionably visualized. However, itis difficult to obtain an image that isdiagnostic of portal vein thrombosis;moreover, flow is identified withinthat vessel (
B
, arrows).You order a CT scan to investigatefurther. An image through thepelvis confirms the presence of alarge volume of ascites (
C
, arrow).Two images through the upper abdomen(
D
and
E
) reveal a thrombusin the portal vein (red arrows) and alow central density within the liver(yellow arrows); by contrast, theliver capsule appears to have beenspared. Mesenteric venous collateralscan be seen (
D
and
E
, whitearrows). There is no evidence of gastroesophagealvarices, and thespleen is normal in size (probablybecause of decompression caused by the mesenteric venous collaterals).
Ischemia of the central part of the liversecondary to portal vein thrombosis isdiagnosed.
The many possible causes ofportal vein thrombosis include:
- Blood dyscrasia
- Chronic heart failure.
- Constrictive pericarditis.
- Cirrhosis.
- Cholangitis.
- Pancreatitis.
- Inflammation/infection of the liver.
- Catheterization (in newborns).
However, in more than half ofpatients with portal vein thrombosis,no cause is found. No cause wasfound in this woman.This case illustrates several interestingpoints. First, abdominal ultrasonographyis difficult to performin very obese patients; moreover, resultscan be compromised by thisbody habitus. Ultrasonography maybe useful in the investigation of vessels,but it can fail to identify partialthrombosis--particularly in deep vesselsin obese patients. Here, althoughthe ultrasound scan did correctlyidentify blood flow in the normal directionin the portal vein, it was un-able to definitively reveal the thrombusin that vein.Second, although injury to theportal vein or hepatic artery doesnot usually result in liver ischemia,this may occur--as it did here.These 2 vessels both supply blood tothe liver. The portal vein carries 75%of the flow, and the hepatic arterycarries 25%. Typically, if either of thetwo is injured, flow through theother increases to meet the requirementsof the liver and preserve function.However, do not assume thatthe "other vessel" will compensateuntil its status is clearly known. Herea preexisting hepatic artery abnormality--perhaps atherosclerosis--prevented that vessel from compensatingwhen the portal vein thrombosisoccurred; consequently, liverischemia developed.Finally, the typical presentingfeatures of portal vein thrombosis--GI bleeding and/or splenomegaly--were not evident in this patient becausenumerous mesenteric venouscollaterals had developed. Instead,she presented with ascites. She mostlikely had underlying cirrhosis (relatedto her alcohol abuse), which hadgiven rise to chronic portal hypertension;the development of mesentericvenous collaterals was secondary tothe portal hypertension, which theyat least partially decompressed.
Outcome of this case.
The patientwas treated with heparin followedby warfarin. A subsequent CTscan demonstrated resolution of thethrombus in the portal vein, dramaticimprovement in the ascites, and reductionin the size of the mesentericvenous collaterals. The ischemicchanges in the liver were reversed,and results of liver function tests returnedto normal. Warfarin was prescribedat discharge, and the patientdid well.
