Atlas of General Surgical Techniques (Courtney M. Townsend Jr., B. Mark Evers)

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The right renal artery is exposed posterior to the vena cava by retracting the right renal vein cephalad and the vena cava to the left (Figure 88-6, D).

A 10-cm segment of saphenous vein is harvested and gently distended with a papaverine solution (see Figure 88-2, B). After systemic heparinization and the administration of mannitol, the hepatic artery is occluded between clamps and the saphenous vein graft is anastomosed end-to-side to the hepatic artery distal to the takeoff of the gastroduodenal artery with running 6-0 polypropylene suture (Figure 88-6, E).

The renal artery is similarly divided close to its origin from the aorta, and the proximal end is suture ligated with 5-0 polypropylene suture. An end-to-end spatulated anastomosis between the saphenous vein graft and the distal end of the renal artery is constructed with interrupted 6-0 polypropylene suture (Figure 88-6, F-G). The patency of the anastomosis is evaluated with duplex ultrasound.

After the renal anastomosis is completed, heparin is reversed with protamine sulfate (1 mg/100 U heparin), and 40 mg furosemide is administered intravenously.

Hepatic arteriotomy

Right renal vein retracted cephalad

Right kidney

Right renal artery

Inferior vena cava

retracted medially

D

FIGURE 88–6, cont’d

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3. CLOSING

Both of the inner two layers of the right and left subcostal incisions are closed in a similar fashion with running absorbable suture (2-0 Vicryl), and the outer layers (external oblique and anterior rectus fascia) are closed with running monofilament (2-0 PDS or Maxon) suture.

STEP 4: POSTOPERATIVE CARE

The patient is returned to the ICU with arterial line and Swan-Ganz pulmonary artery catheter in place. IV fluids are administered to control fluid volume and blood pressure. Nicardipine or sodium nitroprusside is used to control blood pressure. Beta blockade begun in the preoperative period is continued to control heart rate and blood pressure. Urine output is carefully monitored, and IV fluid administration is adjusted accordingly.

There are often significant fluid shifts in the immediate postoperative period. A combination of fluid administration, vasopressors, and antihypertensive medications may be required to ensure adequate perfusion pressures and to prevent hypertensive crises.

STEP 5: PEARLS AND PITFALLS

The renal artery should be carefully palpated to determine the distal extent of the plaque before an aortorenal bypass or endarterectomy is performed. This maneuver is especially important if endarterectomy is contemplated if difficulties with the end point are to be avoided.

Each renal anastomosis should be completed in 15 to 20 minutes. If prolonged renal ischemic times are anticipated, cold electrolyte solution can be infused into the renal artery and the kidney packed in ice.

Immediate evaluation of the patency of the repair with duplex ultrasound or renal isotope flow studies is indicated if anuria develops in the postoperative period. Prompt return to the operating room is indicated if the vessels are occluded.

Atheroembolism is an uncommon but serious complication of renal revascularization. Careful preoperative assessment of the aorta to determine the presence and location of atheromatous debris or thrombus on a CT scan and the correct sequential application and removal of clamps is imperative if this complication is to be avoided. Oliguria or anuria that does not resolve, eosinophilia, and cholesterol crystalluria are clues to the diagnosis.

In patients with oliguric acute renal failure dialysis, enteral or parenteral nutrition should be undertaken early to avoid the rapid loss of muscle mass encountered in these patients.

SELECTED REFERENCES

1. Hansen KJ, Tribble RW, Reavis SW, et al: Renal duplex sonography: Evaluation of clinical utility. J Vasc Surg 1990;12:227-236.

2. Wylie EJ, Perloff DL, Stoney RJ: Autogenous tissue revascularization techniques in surgery for renovascular hypertension. Ann Surg 1969;170:416-428.

3. Moncure AC, Brewster DC, Darling RC, et al: Use of the splenic and hepatic arteries for renal revascularization. J Vasc Surg 1986;3:196-203.

4. Benjamin ME, Dean RH: Techniques in renal artery reconstruction: Part I. Ann Vasc Surg 1996;10: 306-314.

5. Benjamin ME, Dean RH: Techniques in renal artery reconstruction: Part II. Ann Vasc Surg 1996;10: 409-414.

C H A P T E R 89

MESENTERIC ISCHEMIA

Glenn C. Hunter

INTRODUCTION

Despite recent advances in the diagnosis and treatment of mesenteric ischemia, the mortality rate remains between 59% and 93%. The low incidence of mesenteric ischemia, as well as the difficulties and delays encountered in establishing the diagnosis, contributes to

the high morbidity and mortality rates. Acute mesenteric ischemia may either be caused by thromboembolic occlusive disease (80%) or result from nonocclusive ischemia (20%). The thromboembolic causes of mesenteric ischemia include mesenteric embolism (50%), thrombosis of a pre-existing atherosclerotic orificial stenosis (20%), and mesenteric venous thrombosis (10%). Nonocclusive mesenteric ischemia occurs in the absence of anatomic arterial or venous obstruction and is the result of hypoperfusion-induced vasoconstriction throughout the entire mesenteric circulation. Chronic mesenteric ischemia is due to atherosclerotic occlusive disease in most patients. Less common causes include aortic coarctation, aortic dissection, mid-aortic stenosis, vasculitides, fibromuscular dysplasia, neurofibromatosis, and celiac artery compression syndrome.

STEP 1: SURGICAL ANATOMY

The blood supply to the abdominal viscera arises from the celiac, superior mesenteric, inferior mesenteric, and hypogastric arteries. The celiac artery arises from the aorta at the level of the T12 and L1 vertebral bodies and is 1.5 to 2.0 cm in length. The artery divides into the left gastric, splenic, and common hepatic arteries. At its origin, the artery is surrounded by the ganglia and fibers of the celiac autonomic nerve plexus.

The superior mesenteric artery (SMA) arises 1 cm below the celiac trunk at the L1-L2 intervertebral disc. It lies posterior to the splenic vein and pancreas and is separated from the aorta by the left renal vein.

The inferior mesenteric artery (IMA), the smaller of the three vessels, arises from the anterior lateral aspect of the aorta at the level of the third lumbar vertebra, approximately 3 to 4 cm above the aortic bifurcation.

The abdominal viscera have a rich collateral blood supply formed by the interconnections between the three major vessels: the celiac artery and SMA communicate via the superior and inferior pancreaticoduodenal arteries and the SMA and IMA communicate via the arc of

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Riolan (middle and left colic arteries). The marginal artery of Drummond formed by anastomoses between the main trunks and the arcades arising from the ileocolic, right colic, middle colic, left colic, and sigmoid arteries, augmented by the superior, middle, and inferior rectal arteries—branches of the hypogastric arteries.

STEP 2: PREOPERATIVE CONSIDERATIONS

EVALUATION

The modes of presentation of patients with acute mesenteric ischemia are quite varied. The acute onset of severe abdominal pain, nausea, and vomiting in a patient with cardiac arrhythmias suggests mesenteric embolism. The exacerbation of symptoms in a patient with the symptom triad of abdominal pain, fear of eating, and severe weight loss is suggestive of thrombotic occlusion of a high-grade celiac artery or SMA stenosis. The symptom complex of diffuse abdominal pain, hypotension, and severe lactic acidosis in the setting of cardiogenic, septicemic, or hypovolemic shock is suggestive of nonocclusive mesenteric ischemia. The clinical presentation of mesenteric venous thrombosis is often more insidious and the physical findings more subtle than those of acute arterial ischemia. However, severe abdominal pain out of proportion to the physical findings is present in more than 80% of patients.

A history of pre-existing congestive heart failure, use of digoxin or -adrenergic agents, cardiac arrhythmias, valvular heart disease, recent myocardial infarction, cardiopulmonary bypass, hypercoagulable states, vasculitides, and malignancy should be elicited.

In patients with chronic mesenteric ischemia, severe abdominal pain, fear of food, and weight loss in patients with atherosclerotic peripheral vascular disease (PVD) or underlying thrombotic or coagulation disorders should be elicited.

PHYSICAL EXAMINATION

Careful assessment of the abdomen for the presence of distention, tenderness, signs of peritoneal irritation, bruits, and presence or absence of femoral pulses should be undertaken.

In the early phases, signs of peritoneal irritation such as guarding and rebound tenderness are usually absent. As the bowel becomes more ischemic, abdominal distention, absent bowel sounds, excruciating tenderness, feculent vomiting, and occult bleeding become evident.

DIAGNOSTIC TESTS

An electrocardiogram should be performed in all patients and an echocardiogram in selected patients with poor cardiac output. A complete blood count and routine laboratory chemistries for electrolytes, blood urea nitrogen, creatinine, troponin levels, liver function tests, and arterial blood gases should be performed. In patients with suspected

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hypercoagulable states, blood should be drawn for the prothrombotic work-up before the administration of heparin. Blood and blood products are typed and crossmatched.

In patients suspected of having acute mesenteric ischemia, a plain abdominal radiograph may demonstrate “thumbprinting,” ileus, or pneumatosis. A contrast-enhanced computed tomography (CT) scan with CT angiography provides the definitive diagnosis but does not allow treatment with intra-arterial vasodilators.

Angiography with anterior posterior and lateral views of the aorta is indicated in patients with acute and chronic mesenteric ischemia and in whom diagnostic uncertainty exists. If nonocclusive mesenteric ischemia is present, the angiographic catheter is left in place for the infusion of vasodilators, such as papaverine, nitroglycerin, tolazoline, or verapamil. In patients with exacerbation or recent onset of symptoms (less than 3 hours) found to have a high-grade celiac artery or SMA stenosis, angioplasty and stenting should be considered.

Resuscitation with intravenous fluid is begun while the investigation is ongoing. Broadspectrum antibiotics are administered, and any potential underlying mechanism such as arrhythmias or congestive heart failure is corrected. A heparin infusion is begun to prevent extension of thrombus into the microvessels.

STEP 3: OPERATIVE STEPS

1.INCISION

The abdomen is opened via an upper midline incision, and the extent of the ischemia is assessed (Figure 89-1). Perfusion of the proximal 10 to 15 cm of jejunum is indicative of embolic occlusion, whereas bowel ischemia including this segment suggests arterial thrombosis. Both the small and large bowel appears dusky if nonocclusive mesenteric ischemia is present. Segmental ischemic changes with edema of the adjacent mesentery are indicative of mesenteric venous thrombosis. If the entire bowel is necrotic, the abdomen should be closed and comfort measures instituted.

Midline incision

MC

FIGURE 89–1

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2. DISSECTION

Mesenteric Embolism

The transverse colon is elevated superiorly, and the fourth part of the duodenum is mobilized. The small bowel is retracted to the right, and a self-retaining retractor is placed. The SMA is isolated at the root of the mesentery and mobilized, taking care to preserve all its branches (Figure 89-2).

Jejunum

Middle colic artery

Embolus

Superior mesenteric artery

FIGURE 89–2