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Renovascular Hypertension 233
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B. Clinical investigation with blood pressure control.
C. Angiography.
D. Duplex ultrasonography.
E. Captopril scintigraphy.
Commentary
Renovascular disease is responsible for hypertension in around 1 per cent of all
patients with high blood pressure. The definition of renovascular hypertension is,
however, complicated by the complex and sometimes unclear relation between
morphological alterations in the renal artery and the physiological effect of the
stenosis. Hypertension is seen in 10–15 per cent of the adult population, and a renovascular cause varies between 0.2 and 5 per cent of those with hypertension; most
often, a figure of around 1 per cent is given [1]. The most common cause is arteriosclerosis, which is the probable aetiology in our case (age, sex, smoking, previous
hypertension). With the potent antihypertensive drugs of today, it is possible to
obtain fairly good blood pressure control in patients with renovascular hypertension. Patients therefore are often not evaluated until there is ischaemic nephropathy
with increasing creatinine [2]. As every patient with hypertension cannot be
screened for renal artery stenosis, there are some criteria that may raise suspicion:
• Rapid onset of hypertension in young people.
• Rapid deterioration of previously well-controlled essential hypertension.
• Malignant hypertension or hypertensive crises.
• Three-drug-resistant hypertension.
• Hypertension and deteriorated renal function.
• Impaired renal function when starting ACE inhibitors.
• Abdominal, flank or back bruit.
Our patient had had essential hypertension for more than 10 years, there was
difficulty in controlling the blood pressure with three drugs, and there was an
increase in serum creatinine when starting ACE inhibitor treatment. The
absence of bruit is of no value; its presence would have given further support.
[Q1: A, B, C]
Diagnosis is difficult and the low prevalence contributes to the problem. If there
is a clinical suspicion of renovascular hypertension, as in our patient, then renin in
serum is of little if any value [3]. Angiography is not indicated to decide whether
there is renovascular hypertension: it gives a morphological picture but there are
many patients even with advanced renal artery stenosis in whom it is not of functional importance [4–6]. Although hypertension is prevalent in patients with renal
artery stenosis, this does not mean it is a causal relationship [7]. To further
strengthen the diagnosis a trans-stenotic pressure gradient of >15 mm Hg indicates
that stenosis is of functional importance. The only absolutely certain way to define
the relationship of renal artery stenosis in hypertension or ischaemic nephropathy
234 Vascular Surgery
is to observe the beneficial effect of an intervention. MRA and CT angiography are
increasingly used to verify the diagnosis. The alternatives, isotope renography,
preferably with captopril provocation [8], and duplex ultrasonography [9], both
give some functional information but none has sufficiently high sensitivity and
specificity to be truly diagnostic. [Q2: C, E]
The first treatment choice in an uncomplicated case of renal artery stenosis is
PTA [10], which was performed in this patient. Because of an irregular lumen with
dissection, the procedure was completed with a stent with good morphological
result. Stent placement in renal arteries was first used to correct suboptimal balloon
dilations (recoil or plaque resistance), and complications such as dissection or
restenosis [11–13]. Some authors recommend primary stenting [11, 14]. [Q3: D]
Acute serious complications are infrequent. In a recent overview, the total rate
was 17 per cent, with 2 per cent leading to surgery [15]. The most common serious
acute complication is acute occlusion. [Q4: B]
PTA of the renal artery stenosis is a convenient procedure for the patient, with
few complications and short hospitalisation time. However, restenosis is not
uncommon [10, 16, 17], and it therefore seems reasonable to have a surveillance
programme, although the value of such a programme has not been established in
any scientific study. The risk for restenosis is highest during the first year [10].
When there has been adequate preinterventional duplex investigation, as in this
patient, it seems logical to continue with this investigation every 3 months during
the first year and biannually thereafter. If this is not possible, then clinical investigation with blood pressure control will be the choice. It must be noted, however, that
the evidence basis for follow-up routines after renal artery angioplasty has yet to be
defined. [Q5: B, D]
References
1. Berglund G, Andersson O, Wilhelmsson L. Prevalence of primary and secondary hypertension. BMJ
1976;2:554–6.
2. Bergentz S-E, Bergqvist D, Weibull H. Changing concepts in renovascular surgery. Br J Surg
1989;76:429–30.
3. Pohl MA. Renal artery stenosis, renal vascular hypertension and ischemic nephropathy. In: Schrier
RW, Gottschalk CW, editors. Diseases of the kidney, 6th edn. Boston: Little, Brown, 1997;1367–423.
4. Dustan HP, Humphries AW, De Wolf VG, Page IH. Normal arterial pressure in patients with renal
arterial stenosis. JAMA 1964;187:1028–9.
5. Schwartz CJ, White TA. Stenosis of renal artery: an unselected necropsy study. BMJ 1964;2:1415–21.
6. Missouris CG, Buckenham T, Cappucio FP, Mac Gregor GA. Renal artery stenosis: a common and
important problem in patients with peripheral vascular disease. Am J Med 1994;96:10–14.
7. P, Thorvinger B, Pärsson H, Norgren L. Renal artery stenosis in patients with peripheral vascular
disease and its correlation to hypertension. A retrospective study. Int Angiol 1992;11:195–9.
8. Nolly JV, Chen C, Fire E. Diagnostic criteria of renovascular hypertension with captopril renography
– a consensus statement. Am J Hypertens 1991;4:7495–525.
9. Hansen KJ, Tribble RW, Reavis SW. Renal duplex sonography: evaluation of clinical utility. Vasc
Surg 1990;12:227–36.
10. Weibull H, Bergqvist D, Bergentz S-E. Percutaneous transluminal renal angioplasty versus surgical
reconstruction of atherosclerotic renal artery stenosis: a prospective randomized study. J Vasc Surg
1993;18:841–50.
11. Dorros G, Prince C, Mathiak L. Stenting of a renal artery stenosis achieves better relief of the
obstructive lesion than balloon angioplasty. Catheter Cardiovasc Diagn 1993;29:191–8.
12. Raynaud AC, Beyssen BM, Turmel-Rodriques LE. Renal artery stent placement: immediate and midterm technical and clinical results. J Vasc Intervent Radiol 1994;5:849–58.
Renovascular Hypertension 235
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13. Van de Ven PJ, Bentler JJ, Kaatee R. Transluminal vascular stent for ostial atherosclerotic renal
artery stenosis. Lancet 1995;346:672–4.
14. Bush R, Najibi S, MacDonald J, Lin P, Chaikol E, Martin L, Lumsden A. Endovascular revascularization of renal artery stenosis: technical and clinical results. J Vasc Surg 2001;33:1041–9.
15. Slonim S, Dake M. Radiographic evaluation and treatment of renovascular disease. In: Rutherford R,
editor. Vascular surgery, 5th edn. Philadelphia: WB Saunders, 2000;1611–39.
16. Jensen G, Zackrisson BF, Delin K. Treatment of renovascular hypertension: one year results of renal
angioplasty. Kidney Int 1995;48:1936–45.
17. Tullis M, Zierker R, Glickerman D, Bergelin R, Cantwell-Gab K, Strandness E. Results of percutaneous transluminal angioplasty for atherosclerotic renal artery stenosis: a follow-up study with
duplex ultrasonography. J Vasc Surg 1997;25:46–51.
27. Management of Portal Hypertension
Yolanda Y. L. Yang and J. Michael Henderson
A 37-year-old woman with a history of hepatitis C, cirrhosis, and esophageal
varices presented with hematemesis and melena. The patient had a history of a
prior esophageal variceal bleeding episode 7 years ago, which required transfusion of 4 units of packed red blood cells (PRBC) and had been treated with endoscopic sclerotherapy. She was placed on nadolol at that time.
Question 1
If the patient had been found to have varices before any bleeding episode, she would
benefit from which of the following?
A. Endoscopic treatment: sclerotherapy or band ligation.
B. Transjugular intrahepatic portal systemic shunt (TIPS).
C. Non-cardioselective beta-blocker.
D. A surgical shunt.
The patient re-presents one year prior to her current admission with a further
variceal bleed documented at endoscopy, which required 5 units of PRBC. The acute
episode of bleeding was managed with variceal banding, and the patient underwent
a course of banding on an outpatient basis. She had no encephalopathy at that time,
but did develop some ascites for a short period that responded to salt restriction,
Aldactone, and Lasix. Over this past year, her liver function tests have been stable
with her bilirubin at 1.0, albumin at 3.5, and a normal prothrombin time.
Question 2
An episode of acute variceal bleeding usually requires which of the following?
239
240 Vascular Surgery
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A. ICU admission with hemodynamic monitoring, blood, blood products, and fluid
resuscitation.
B. An emergency portacaval shunt.
C. A transjugular intrahepatic portal systemic shunt.
D. Endoscopic therapy with sclerosis and/or band ligation.
E. Pharmacologic therapy.
At the present admission the patient is alert and oriented with no evidence of
encephalopathy. She has well-preserved muscle mass on examination and is not
clinically jaundiced. Her abdomen shows minimal ascites, with no hepatomegaly,
but evidence of splenomegaly. Her laboratory studies showed a hemoglobin of
7 g/dl, AST 24, alkaline phosphatase 84, albumin 2.6, bilirubin 3.4, and international
normalized ratio (INR) 1.6. She was receiving blood transfusion when examined
and octreotide infusion at 50 µg/h. Esophagogastroduodenoscopy showed clot over
an esophageal varix with evidence of other non-bleeding varices in both the distal
esophagus and gastric fundus.
Question 3
Which of the following studies are important in evaluation and management
decisions?
A. Calculation of Child’s score.
B. Calculation of MELD score.
C. Endoscopy.
D. Doppler ultrasound.
E. Angiography.
Question 4
Which of the following statements are accurate in prevention of recurrent variceal
bleeding?
A. All patients require portal decompression.
B. First-line treatment is with endoscopic band ligation and a beta-blocker.
C. Variceal decompression can only be achieved with a surgical shunt.
D. Liver transplant is good treatment for variceal bleeding in patients with end-
stage liver disease.
Question 5
Decompression of gastroesophageal varices:
Management of Portal Hypertension 241
Fig. 27.1. Splenic artery injection. The catheter is in the splenic artery and is injected with contrast.
A. Can be achieved equally well with surgical shunt or TIPS.
B. Should only be used for patients who have failed endoscopic and pharmacologic
therapy for bleeding varices.
C. Improves survival in patients with bleeding varices when compared to endo-
scopic therapy.
D. Is best achieved by liver transplant for all patients with variceal bleeding.
The patient presented in this case had recurring bleeding episodes through firstline treatment and was therefore a candidate for decompression. Evaluation with
angiography and ultrasound showed patent splenic and portal veins and a normal
left renal vein (Figs 27.1–27.4). The patient had an elective distal splenorenal shunt
for variceal decompression. She was in hospital for 7 days, and was discharged following shunt catheterization (Fig. 27.5) and documentation of patency. Follow-up
over the next 4 years showed some progression of her hepatitis C, but no further
episodes of variceal bleeding.
Commentary
The case presented illustrates several important points:
• Prophylactic management of gastroesophageal varices, strictly speaking, is prior
to the first bleeding episode. The risk of bleeding in a patient with cirrhosis is
242 Vascular Surgery
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Fig. 27.2. Splenic vein. The contrast is followed as it flows out of the splenic vein and then cephalad in the
portal vein. There is a significant umbilical vein (double shadow with the portal vein) and a small left gastric vein
(off the splenic vein) filling on this study. The second, more caudal catheter is positioned within the left renal
vein to aid preoperative determination of the spatial relationship between the splenic and left renal veins.
Fig. 27.3. Normal left renal vein. This study has been performed via the right jugular vein, and demonstrates
the left renal vein as it heads cephalad towards the inferior vena cava.
Management of Portal Hypertension 243
Fig. 27.4. Circumaortic left renal vein. A circumaortic left renal vein, present in 20 percent of the population,
does not prevent construction of a distal splenorenal shunt. The superior and anterior component is always
larger and can be used for the shunt. More problematic is a totally retroaortic vein, found in 4 percent of the
population, which runs transversely and is more fixed in the retroperitoneum, making exposure of the anastomosis more difficult. These patients are better served with a splenocaval shunt.
Fig. 27.5. Postoperative catheterization of the distal splenorenal shunt. The tip of the catheter lies within the
mobilized splenic vein, and the first bend marks the splenorenal anastomosis. The skin staples mark the
extended left subcostal incision.
244 Vascular Surgery
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approximately 30 percent. Once they have had one bleeding episode, the risk of
rebleeding rises to 75 percent without active therapy. Non-cardioseclective betablockade with propranolol or nadolol is the preferred treatment for true prophylaxis for medium or large size varices.
• Acute variceal bleeding is an emergency situation with a high mortality if not
appropriately managed. Appropriate monitoring, pharmacologic therapy, and
endoscopic diagnosis and treatment are the mainstays of treatment of an acute
bleeding episode. It is a very small percentage of patients who do not have their
bleeding controlled with the above measures and come to an emergency decompression.
• The evaluation of the patient after an acute bleeding episode should assess the
varices (endoscopy), the vascular anatomy (ultrasound and angiography) (Figs
27.1–27.4), and the liver disease (Child’s class and MELD score). [Q3: A, B, C, D, E]
• When a patient has had an acute bleeding episode, their risk of rebleeding is
over 70 percent if they have no specific treatment. The initial approach to treatment is to reduce the portal hypertension with a non-cardioselective betablocker, and to deal with the bleeding varices directly with endoscopic therapy.
The majority of patients do not need variceal decompression at this stage. If the
patient obviously has advanced to end-stage liver disease, a transplant evaluation is in order, and appropriate candidates should move forward with that
treatment [Q4: B, D]
• When patients have recurrent bleeding through first-line treatment they may
need decompression of their gastroesophageal varices. Surgical therapy will do
this well in 95 percent of patients, while the success rates of radiologic shunts in
the literature are not this high. Decompression of varices does not improve the
survival of patients compared to other first-line treatment options. Liver transplant provides excellent variceal decompression, but its use is dictated by endstage disease rather than variceal bleeding. [Q2: A ,D, E]
General Considerations
The major complications of portal hypertension are variceal bleeding, ascites, and
progressive hepatic dysfunction. Ascites and encephalopathy are signs of decompensation, and as a general guideline, are only effectively managed by liver transplant. Not all patients with these clinical endpoints may be suitable candidates for
transplant. In contrast, variceal bleeding can occur in patients who have wellpreserved liver function and therefore have a wider range of treatment options
available.
The etiology of portal hypertension may be presinusoidal, as in portal vein
thrombosis; sinusoidal, as in cirrhosis; and rarely, post sinusoidal, as in
Budd–Chiari syndrome. Much the most common etiology in the USA and Europe is
cirrhosis, with approximately 90 percent of patients having this etiology. The evaluation of the patient with suspected portal hypertension includes an endoscopy to
assess size and extent of varices with risk factors for bleeding. Larger varices with
red color signs are at increased risk of bleeding or of rebleeding. Laboratory tests
should assess liver function, and overall disease status. Non-specific tests include
bilirubin, prothrombin time, albumin, and liver enzymes. Recently documented is
the importance of serum creatinine in assessing overall severity of disease and prog-
Management of Portal Hypertension 245
Table 27.1. Child–Pugh classification
Parameter 1 point 2 points 3 points
Serum bilirubin (mg/dl) <2 2–3 >3
Albumin (g/dl) >3.5 2.8–3.5 <2.8
Prothrombin time (↑s) 1–3 4–6 >6
(INR) <1.7 1.71–2.24 >2.25
Ascites None controlled medically controlled poorly or
Encephalopathy None 1–2 3–4
Classification: A, 5–6 points; B, 7–9 points; C, 10–15 points.
Table 27.2. MELD score for stratification of liver disease severity
Score = 0.957 × logecreatinine (mg/dl)
+ 0.378 × log
+ 1.120 × logeINR
bilirubin (mg/dl)
e
uncontrolled
nosis. The two standard methods for assessing this are the Child–Pugh score (Table
27.1), and the Model for Endstage Liver Disease (MELD score – Table 27.2). Other
laboratory studies that are important relate to the etiology with hepatitis panels,
alpha-fetoprotein as a marker for hepatocellular carcinoma, and specific markers
for metabolic diseases such as hemochromatosis and Wilson’s disease.
Imaging studies are important in evaluation, with ultrasound used to assess the
liver morphology, and Doppler evaluation for liver vasculature. Patency of the main
vessels and direction of flow can be assessed well with Doppler ultrasound.
Angiography is still indicated for patients being considered for surgery. Accurate
assessment of the splenic, portal, and left renal veins is important for distal
splenorenal shunt, and may further elucidate details that are not seen on ultrasound. Liver biopsy is occasionally indicated in some patients for clarification of
etiology and to delineate the activity of the liver disease process.
Management of portal hypertension falls in to three broad groups:
• Prophylactic treatment.
• Management of an acute variceal bleed.
• Prevention of recurrent variceal bleeding.
Prophylactic treatment is indicated for moderate or large size varices to reduce
the risk of an initial bleed. Varices are present in 30–60 percent of patients with cirrhosis. Thirty percent of patients with varices will bleed from them. After an initial
bleed, 20–50 percent will rebleed in the first week, and 75–80 percent will rebleed
within a year. The mortality of an acute bleeding episode is approximately
25 percent. To reduce the risk of this initial bleed, the goal is to reduce portal pressure to <12 mm Hg or by 20 percent from the baseline. This is best achieved with a
non-cardioselective beta-blocker (propranolol, nadolol) [1]. Other treatments,
such as endoscopic therapy, TIPS, or surgical shunt are not indicated for prophylaxis. There are currently further ongoing trials looking at band ligation for
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