Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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instituted as early as possible because thrombi older than 3–5

days are less likely to respond. Bleeding, both superficial and

internal, is the most common complication. When a severe

coagulopathy develops, transfusion with fresh-frozen plasma

may be necessary to correct the deficit.

The use of thrombolytic agents in the treatment of

venous thromboembolism continues to be highly individual-

ized. In general, patients with hemodynamically unstable

pulmonary embolus or massive iliofemoral thrombosis, who

are at low risk to bleed, are the most appropriate candidates.

Endovascular placement of stents for residual iliac stenosis

after venous thrombolysis also has been reported. In a small

group of patients, patency was shown to be superior than

with conventional heparin and warfarin. Survival rates on

Kaplan-Meier life-table analysis, however, were equivalent.

D. Vena Caval Interruption—Historically, ligation of the

vena cava was performed to prevent thrombi arising in the

lower extremities and pelvis from reaching the pulmonary

bed. Plication with a clip also has been attempted. Avoidance

of complete occlusion maintained circulatory stability and

resulted in a lower frequency of recurrent pulmonary emboli

than complete ligation. In the latter, dilation of collateral ves-

sels in the retroperitoneum became a potential route for pul-

monary emboli.

Placement of a stainless steel filter, such as the Greenfield

filter, is now the preferred procedure. Absolute indications

for filter placement include recurrent thromboembolism

despite adequate anticoagulation and deep venous thrombo-

sis in patients at risk for hemorrhage. Relative indications

include the presence of a propagating iliac or femoral vein

thrombus despite adequate anticoagulation and a high-risk

patient with a large, free-floating iliac or femoral vein throm-

bus demonstrated on venography. Sepsis is not a contraindi-

cation to filter placement.

Filters usually are placed percutaneously through the

uninvolved femoral vein or through a jugular vein and posi-

tioned below the renal veins. The long-term patency rate of

the device is 98%, with a recurrent embolism rate of 4%. Up

to 80% of the filter may become filled with thrombus before

it loses its efficacy. Recurrent embolism is an indication for

inferior venacavography to evaluate the filter for the presence

of proximal thrombus. The most common complication is

displacement, which occurs in 7% of patients.

E. Operative Embolectomy—Operative removal of a deep

venous thrombus is usually reserved for cases of phlegmasia

cerulea dolens with limb threat. The highest success rate is

achieved when the procedure is performed within 24 hours

after onset of symptoms. Although early postoperative

results may be encouraging, subsequent venograms usually

show rethrombosis. This is often due to incomplete throm-

bus removal and injury to the venous endothelium.

Reocclusion is often well tolerated as long as it occurs after

the formation of sufficient venous collaterals. Mechanical

thrombectomy with creation of a temporary arteriovenous

fistula can improve early patency and allow collaterals to

develop. A recent study that examined long-term results after

embolectomy found fewer instances of venous hypertension,

valvular incompetency, and restrictions in activity among

patients who had embolectomy performed for deep venous

thrombosis of less than 3 days duration.

Postthrombotic Syndrome

Venous thrombosis is often accompanied by symptoms of

pain, swelling, and skin ulceration occurring immediately or

years after an episode of deep venous thrombosis. It is pres-

ent in over 50% of patients with proximal thrombosis and

has been reported in a third of patients with calf thrombosis.

The symptoms are thought to stem from the development of

venous hypertension caused by valvular dysfunction.

Residual venous obstruction also may contribute to the syn-

drome to a lesser extent. Thrombolytic therapy preserves

valvular function and potentially can reduce the incidence of

this phenomenon. Early results are promising. Standard

treatment involves the use of graduated compression stock-

ings and sequential compression devices.

Venous Thromboembolism in Pregnancy

Care of the pregnant patient focuses on avoiding teratogenic

injury to the fetus. Patients can be treated with continuous

UFH and gradually switched over to multiple daily subcuta-

neous doses of LMWH until delivery. Warfarin, reportedly

safe for infants of nursing mothers, is continued for 4–6

weeks postpartum. Supplemental calcium should be given in

cases of prolonged heparinization (>1 month) to prevent

heparin-induced osteoporosis. In the event of a bleeding con-

traindication or a documented pulmonary embolus, a vena

caval filter can be placed. The procedure should be performed

in the third trimester through an internal jugular approach.

The site of deployment—contrary to what is done for a non-

pregnant patient—is above the renal veins. This avoids kink-

ing and displacement of the device by a gravid uterus.

AbuRahma AF et al: Iliofemoral deep vein thrombosis:

Conventional therapy versus lysis and percutaneous translumi-

nal angioplasty and stenting. Ann Surg 2001;233:752–60.

[PMID: 11371733]

Anaya DA, Nathens AB: Thrombosis and coagulation: Deep vein

thrombosis and pulmonary embolism prophylaxis. Surg Clin

North Am 2005;85:1163–77. [PMID: 16326200]

Andersen JC: Advances in anticoagulation therapy: The role of

selective inhibitors of factor Xa and thrombin in thrombopro-

phylaxis after major orthopedic surgery. Semin Thromb

Hemost 2004;30:609–18. [PMID: 15630666]

Decousus H et al: A clinical trial of vena caval filters in the preven-

tion of pulmonary embolism in patients with proximal deep-vein

thrombosis. N Engl J Med 1998;338:409–15. [PMID: 9459643]

Erdman WA et al: Deep venous thrombosis of extremities: Role of

MR imaging in the diagnosis. Radiology 1990;174:425–31.

[PMID: 2404315]

Geerts WH et al: Prevention of venous thromboembolism. Chest

2001;119:132–75S.

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CHAPTER 29

648

Gutt CN et al: Prophylaxis and treatment of deep vein thrombosis in

general surgery. Am J Surg 2005;189:14–22. [PMID: 15701484]

Hyers TM et al: Antithrombotic therapy for venous thromboem-

bolic disease. Chest 2001;119:176–93S.

Kerr TM: Analysis of 1084 consecutive lower extremities involved

with acute venous thrombosis diagnosed by duplex scanning.

Surgery 1990;108:520–7.

Lensing AWA et al: Detection of deep-vein thrombosis by real-time

B mode ultrasonography. N Engl J Med 1989;320:342–5.

[PMID: 2643771]

Levine M et al: A comparison of low-molecular-weight heparin

administered primarily at home with unfractionated heparin

administered in the hospital for proximal deep-vein thrombo-

sis. N Engl J Med 1996;334:677–81.

Levine MN et al: Hemorrhagic complications of anticoagulant

treatment. Chest 1995;108:276–90S.

Levine MN et al: Optimal duration of oral anticoagulant therapy:

A randomized trial comparing four weeks with three months of

warfarin in patients with proximal deep vein thrombosis.

Thromb Haemost 1995;74:606–11. [PMID: 8584992]

Markel A, Manzo RA, Strandness DE Jr: The potential role of

thrombolytic therapy in venous thrombosis. Arch Intern Med

1992;152:1265–7. [PMID: 1599356]

Martinelli I et al: Risk factors for deep venous thrombosis of the upper

extremities. Ann Intern Med 1997;126:707–11. [PMID: 9139557]

McRae SJ, Ginsberg JS: Initial treatment of venous thromboem-

bolism. Circulation 2004;110;I3–I9.

Plate G et al: Venous thrombectomy for iliofemoral vein thrombo-

sis: 10-year results of a prospective randomized study. Eur J Vasc

Endovasc Surg 1997;14:367–74. [PMID: 9413377]

Porteous MJ et al: Thigh length versus knee length stockings in the

prevention of deep vein thrombosis. Br J Surg 1989;76:296–7.

[PMID: 2720328]

Schulman S et al: The duration of oral anticoagulant therapy after

a second episode of venous thromboembolism. N Engl J Med

1997;336:393–8. [PMID: 9010144]

Wakefield TW: Treatment options for venous thrombosis. J Vasc

Surg 2000;31:613–20. [PMID: 10709079]

Weitz JI: New anticoagulants for treatment of venous thromboem-

bolism. Circulation 2004;110:I9-I26.

Wells PS et al: Accuracy of clinical assessment of deep-vein throm-

bosis. Lancet 1995;345:1326–30. [PMID: 7752753]



Acute Mesenteric Ischemia

ESSENTIALS OF DIAGNOSIS



Severe acute abdominal pain out of proportion to the

physical examination.



GI symptoms: nausea, emesis, forceful evacuation.

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Abdominal distention and GI hemorrhage.

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Leukocytosis, acidosis, and hyperamylasemia.

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Mesenteric arterial occlusion with minimal collateraliza-

tion on angiography.

General Considerations

Acute mesenteric ischemia of the bowel is an uncommon but

dramatic occurrence among ICU patients, with an estimated

overall incidence of 0.1% of all hospital admissions.

Predisposing factors include age, cardiovascular disease, ath-

erosclerosis, systemic disorders (eg, collagen-vascular dis-

ease), hypercoagulable states, malignancy, portal

hypertension, inflammation, and trauma. Semiacute and

chronic syndromes have been described, but they are rare

among ICU patients admitted for other reasons.

The consequences of vascular occlusion depend on the

vessel involved, the extent of collateral flow, and the time

period over which the occlusion took place. Acute occlusion

of vascular inflow or outflow quickly causes ischemia and

leads to transmural necrosis within 6–12 hours. The sero-

muscular layer is particularly sensitive and begins to slough

within 4 hours. Xanthine oxidase, found in high concentra-

tions within the villi, is responsible for the production of

superoxides that mediate many of the toxic reactions.

Ulceration and bacterial overgrowth follow ischemic slough-

ing. Bacterial proliferation leads to increased edema and fur-

ther thrombosis of small vessels. Increased capillary

permeability and the absorption of toxic products across the

compromised mucosa cause remote complications such as

respiratory distress syndrome. Continued ischemia leads to

intraluminal sequestration of fluid, which ultimately results

in hypovolemia and hypotension. Four general categories of

acute mesenteric ischemia are recognized.

A. Acute Embolic Occlusion—Emboli to the superior

mesenteric artery account for 40–50% of all cases. Because

these are almost always mural thrombi of cardiac origin, up to

20% of patients have synchronous emboli to other arteries. In

the majority of cases, the embolus lodges just distal to the ori-

gin of the superior mesenteric artery. Occasionally, the emboli

fracture and travel into the distal arcades of the artery before

they become lodged. Initially, collateral flow is adequate to

maintain viability of the intestine. However, after a period of

partial occlusion, vasoconstriction develops both proximal

and distal to the embolus and produces profound ischemia.

B. Mesenteric Thrombosis—Progressive atherosclerotic

narrowing of the origin of the superior mesenteric artery is

responsible for mesenteric thrombosis. Conditions that com-

promise flow through the stenotic orifice can lead to throm-

botic occlusion. Between 20% and 50% of patients with

mesenteric thrombosis will give a history of postprandial

pain and weight loss within the 6 months prior to admission.

Many have severe and diffuse atherosclerosis, with a history

of coronary, cardiac, or peripheral vascular arterial insuffi-

ciency. Mesenteric thrombosis occurs in 10–15% of all cases

of acute mesenteric ischemia.

C. Venous Thrombosis—Once thought to be the major

cause of acute mesenteric ischemia, venous thrombosis is

diagnosed in 8–10% of patients. Hypercoagulable states

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CRITICAL CARE OF VASCULAR DISEASE & EMERGENCIES

649

including neoplasms, cirrhosis and portal hypertension, pan-

creatitis, peritonitis, diverticular disease, trauma, and

splenectomy are precipitating factors. Presentation can be

either acute or protracted, developing over a period of sev-

eral weeks. Up to 60% of patients have a history of deep

venous thrombosis in an extremity.

D. Nonocclusive Intestinal Ischemia—Hypoperfusion or a

low-flow state is the inciting event of acute mesenteric

ischemia in 25% of cases. Coexisting conditions—predomi-

nantly cardiac pump failure—lead to prolonged visceral arte-

rial spasm and subsequent tissue infarct. Shunting of arterial

blood away from the seromuscular layer and villi causes acti-

vation of toxic intermediates. The vasoconstriction may per-

sist long after the inciting cause or agent has been removed.

Pharmacologic agents such as ergotamine derivatives, digi-

talis, cocaine, and peripheral vasocontrictors administered for

sepsis or after cardiovascular surgery are also associated with

acute mesenteric ischemia. In 4% of patients undergoing

repair of an aortic coarctation, postoperative hypertension

may lead to a necrotizing vasculitis from reperfusion injury.

Clinical Features

A. Symptoms and Signs—Acute abdominal pain is the

most common finding. Peritoneal signs are often absent on

physical examination despite the complaint of sharp excruci-

ating pain—thus the sine qua non of “pain out of propor-

tion.” Shortly thereafter, many patients experience rapid and

forceful evacuation of the bowels. Nausea and vomiting—

seen in 50% of patients—hematochezia, hematemesis,

abdominal distention, back pain, and shock are late signs

that usually accompany progression of intestinal necrosis.

The presence of peritoneal signs often heralds the onset of

systemic toxicity. Up to 30% of elderly patients develop men-

tal confusion. The duration of symptoms, however, does not

correlate with the reversibility of injury. A history of weight

loss and an acute exacerbation of chronic abdominal pain are

suggestive of acute thrombosis owing to underlying chronic

occlusive disease.

Mesenteric venous thrombosis also presents with pain as

the initial finding, but only two-thirds of patients manifest

clear signs of peritonitis. Occult blood is often present,

although frank hematochezia or hematemesis is found in

15% of patients, usually from bleeding esophageal varices.

The most common findings are abdominal pain (90%),

vomiting (77%), nausea (54%), diarrhea (36%), and consti-

pation (14%). Most patients have temperatures higher than

38°C. Hemorrhage resulting from gastric varices owing to

isolated splenic vein thrombosis is termed sinistral portal

hypertension. In this case, intestinal ischemia is not expected.

A variant of splanchnic venous disease has been described

recently. Mesenteric inflammatory veno-occlusive disease

results in unexplained acute mesenteric ischemia. Diagnosis

is based on the presence of venulitis or phlebitis with a lym-

phocytic, necrotizing, granulomatous mural infiltrate on

pathologic specimen examination.

B. Laboratory Findings—A marked leukocytosis, often

greater than 15,000/mm

, is usually present, although 10% of

patients have a normal white blood cell count. The smooth

muscle fraction (BB) of creatine kinase (CK) is elevated in

the presence of intestinal infarction. Elevations of lactate

dehydrogenase (LDH) also may be seen. Serum inorganic

phosphate is often elevated owing to either spillage from

phosphate-rich intestinal cells or degradation of intracellular

ATP. Approximately 80% of patients with intestinal infarc-

tion have high serum levels of inorganic phosphate, and 50%

demonstrate hyperamylasemia. Fluid sequestration results in

hemoconcentration and oliguria. Increased base deficit may

occur but was found in only 18 of 43 patients in a retrospec-

tive study. Peritoneal fluid analysis typically reveals leukocy-

tosis and bacteria proportionate to the extent of necrosis. It

may not be helpful in the early stages.

C. Imaging Studies—Plain films of the abdomen should be

obtained as an initial screening procedure. Nonspecific find-

ings consistent with the diagnosis include air-fluid levels,

dilated and thickened bowel wall, blunted plicae circulares,

and distention of the bowel to the level of the splenic flexure.

Specific findings of bowel necrosis include transmural air,

pneumatosis intestinalis, or gas in the portal system. Barium

contrast studies may reveal decreased motility and

thumbprinting owing to necrosis.

Angiography is the mainstay of the diagnosis and should

be individualized. The presence of peritoneal signs and sys-

temic toxicity requires immediate operative treatment to

remove devitalized tissue. Mesenteric angiography can be per-

formed early in hemodynamically stable patients suspected of

having the disease with a sole complaint of abdominal pain.

Radiographic findings will vary depending on the cause.

When an embolus is present, early truncation of the superior

mesenteric artery is observed. With acute thrombosis, com-

plete obliteration of the trunk of the artery is common. The

findings of nonocclusive ischemia are (1) tapered narrowing

of the origins of multiple branches of the superior mesenteric

artery, (2) segmental irregularities of the intestinal branches,

(3) spasm of the arcades, and (4) impaired filling of the intra-

mural branches. Findings consistent with mesenteric venous

thrombosis include (1) demonstration of a thrombus in the

superior mesenteric vein with partial or complete occlusion,

(2) failure to visualize the superior mesenteric vein or portal

vein, (3) slow or absent filling of the mesenteric veins, (4) arterial

spasm, (5) failure of the arterial arcades to empty, (6) reflux of

contrast material into the artery, and (7) a prolonged blush

phase. Abdominal CT scanning can establish the diagnosis in

more than 90% of patients with venous occlusion. Thrombus

with enhanced venous wall opacification is a highly indicative

finding. Hypodensity of the superior mesenteric vein, thick-

ening of the bowel wall, and the presence of peritoneal fluid

are a diagnostic triad seen on CT suggesting probable bowel

infarction. Scintiangiography with

99m

Tc sulfur colloid–labeled

leukocytes has been described but is too unreliable for general

use. Recently, the use of duplex scanning has been proposed

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650

as a bedside screening test, although the technique is limited

by intestinal gas overlying the vessels of interest and the

need for a skilled technician.

D. Special Studies—Laparoscopy can be useful in diagnosis,

although complete exploration of the abdomen with the

laparoscope is difficult. Furthermore, abdominal insufflation

to more than 20 mm Hg reduces mesenteric blood flow and

may exacerbate the condition. Preliminary evidence indicates

that if CO

is used for insufflation at lower pressures, it may

provide some mesenteric vasodilation. Colonoscopy may be

useful if the large intestine is involved, although nonspecific

colitis may be the only finding. Esophagograstroduodenoscopy

can be used to detect and sclerose bleeding varices but does not

treat the underlying venous thrombosis. Both modalities avail

little in small bowel ischemia, the most common location of

acute mesenteric ischemia. Bowel tonometry using an inflat-

able balloon to provide information about intramucosal pH

(pH

) may be helpful, although decreased motility may prevent

proper peroral placement.

Differential Diagnosis

Other conditions associated with abdominal pain in the ICU

such as a perforated ulcer, pancreatitis, acalculous cholecys-

titis, appendicitis, and gynecologic pathology in women

must be investigated. These often can be identified by ultra-

sound and specific serum tests. Renal calculi produce colicky

pain radiating to the groin. Aortic dissection and rupture of

an abdominal aortic aneurysm are rare occurrences in

patients admitted to the ICU for other reasons.

Treatment

Optimal outcome depends on rapid recognition and treat-

ment. Initial therapy consists of fluid resuscitation, correction

of electrolyte and acid-base abnormalities, and management

of cardiac arrhythmias. Systemic heparinization is instituted

in patients with suspected superior mesenteric artery throm-

bosis or venous occlusion. If time permits, demonstration of

the offending lesion by angiography is ideal. When arterial

spasm is present, 25 mg tolazoline may be injected, followed

by repeat angiography. If an embolus is the cause, an infusion

of papaverine into the superior mesenteric artery orifice

should be instituted immediately. The dose customarily used

is 30–60 mg/h. Some also use papaverine in the face of mesen-

teric thrombosis, although catheter placement is difficult

owing to the occluded arterial orifice. Papaverine infusion

should be continued while the patient is readied for surgery.

Because arterial spasm and the hypercoagulable state may

persist even after successful surgery, papaverine and heparin

infusions should be continued following operation. Broad-

spectrum antibiotics are indicated both before and after sur-

gery. Nonoperative therapy is appropriate (1) if there are

significant contraindications to surgery, (2) if there are no

peritoneal signs, and (3) if there is adequate perfusion of the

vascular beds distal to the site of partial obstruction.

Infusion of thrombolytic agents has been successful anecdo-

tally in both venous and arterial thromboses. Gastroesophageal

varices—once thought to be a contraindication to this prac-

tice—were seen to resolve with successful venous clot lysis.

Problems with access to the splanchnic venous system have lim-

ited this approach. In arterial thrombosis, lytic therapy should

be instituted only in the most stable patients because of the time

required for clot lysis. When patients are treated without opera-

tion, repeat angiography at 6–8-hour intervals is required to

monitor the progress of therapy. Any worsening in the patient’s

condition is an indication for immediate operation.

Surgical management is aimed at restoration of flow and

resection of nonviable bowel. Arterial inflow may be restored

either by bypass, endarterectomy, or embolectomy. When venous

thrombosis is present, extensive bowel resections may be

required. Assessment of intestinal viability is often difficult, and

adjuncts such as Doppler flow probes and tissue fluorescence are

often used, although no method is always reliable in separating

viable from ischemic bowel. A wide resection is usually under-

taken as long as more than 6 feet of normal bowel remains. Sixty

percent of recurrent infarcts occur in the area adjacent to the

anastomosis. If the majority of the intestine is compromised,

resection is more conservative, and “second look” procedure to

determine the viability of unresected bowel commonly is per-

formed within 12–24 hours of the initial procedure.

Nonocclusive ischemia is best managed through treat-

ment of the underlying disorder causing the low-flow state.

Resuscitation and optimization of the patient’s hemodynamic

status are essential. Vasopressors should be discontinued if

possible. An alternative to digoxin should be sought, espe-

cially in patients with portal hypertension. Digitalis deriva-

tives promote mesenteric vasoconstriction in patients with

hepatic congestion from congestive heart failure. Ergotamine

poisoning is treated with selective infusion of vasodilators

(eg, papaverine), sympatholytics, and anticoagulants.

Angiotensin-converting enzyme (ACE) inhibitors (eg, capto-

pril) also serve to assuage the vasoconstrictive effects of the

renin-angiotensinogen axis in hypovolemic patients. Surgery

is reserved for resection of nonviable intestine. In addition to

careful hemodynamic support, perioperative anticoagulation

has been shown to improve survival in patients with mesen-

teric venous thrombosis. In one study, half of patients receiv-

ing no postoperative anticoagulation died. Without

anticoagulation, one-third of patients also will experience a

recurrence. Most centers recommend continuing anticoagu-

lation indefinitely unless there is a contraindication or the

factor responsible for the venous thrombosis has been cor-

rected. Recently, intravenous glucagon administered during

the early phase of reperfusion of ischemic intestinal segments

has been shown experimentally to improve mucosal recovery,

suggesting possible adjunctive use in the clinical setting.

Prognosis

Acute mesenteric ischemia carries a high mortality rate—in

some series approaching 70%. When more than half the small

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CRITICAL CARE OF VASCULAR DISEASE & EMERGENCIES

651

bowel must be resected, the death rate increases to as high as

85%. The cause of death in most cases is irreversible shock or

advanced intestinal necrosis. Reconstruction is attempted in

less than 10% of patients because findings at laparotomy often

show advanced disease. Patients diagnosed with superior

mesenteric artery thrombosis have an overall worse prognosis

than those in whom distal embolization has occurred. Acute

venous thrombosis has a 30% mortality rate, whereas nonoc-

clusive intestinal ischemia has been associated with death rates

as high as 90%. Early recognition of low-flow states, resuscita-

tion, and aggressive therapy have lowered mortality.

Abd RA, Achor BG, Dallies DJ: Mesenteric venous thrombosis

1911 to 1984. Surgery 1987;101:383–8.

Bakau CW, Sprayregen S, Wolf EL: Radiology in intestinal

ischemia: Angiographic diagnosis and management. Surg Clin

North Am 1992;72:125–41. [PMID: 1731380]

Boley JS, Alyea RN, Brandt LDI: Mesenteric venous thrombosis.

Surg Clin North Am 1992;72:183–201. [PMID: 1731383]

Gangadharan SP, Wagner RJ, Cronenwett JL: Effect of intravenous

glucagon on intestinal viability after segmental mesenteric

ischemia. J Vasc Surg 1995;21:900–7. [PMID: 7776469]

Geelkerken RH, van Bockel JH: Mesenteric vascular disease: A

review of diagnostic methods and therapies. Cardiovasc Surg

1995;3:247–60. [PMID: 7655837]

Greene FL, Ariyan S, Stansel HC Jr: Mesenteric and peripheral vas-

cular ischemia secondary to ergotism. Surgery 1977;81:176–9.

Harward TR et al: Mesenteric venous thrombosis. J Vasc Surg

1989;9:328–33. [PMID: 2918628]

Jona J et al: Recurrent primary mesenteric venous thrombosis.

JAMA 1974;227:1033–5. [PMID: 4405930]

Kaleya RN, Sammartano RJ, Boley SJ: Aggressive approach to acute

mesenteric ischemia. Surg Clin North Am 1992;72:157–82.

[PMID: 1731382]

Kazmers A: Operative management of acute mesenteric ischemia.

Ann Vasc Surg 1998;12:299–308. [PMID: 9514240]

Kurland B, Brandt LJ, Delaney HM: Diagnostic tests for intestinal

ischemia. Surg Clin North Am 1992;72:85–105. [PMID: 1731391]

Leo PJ, Simonian HG: The role of serum phosphate level and acute

ischemic bowel disease. Am J Emerg Med 1996;14:377–9.

[PMID: 8768159]

Lilly MP et al: Duplex ultrasound measurements of changes in

mesenteric blood flow. J Vasc Surg 1989;9:18–25.

Moneta GL et al: Mesenteric artery duplex scanning: A blinded,

prospective study. J Vasc Surg 1993;17:79–84. [PMID: 8421345]

Myers SI et al: Chronic intestinal ischemia caused by intravenous

cocaine use: Report of two cases and review of the literature. J

Vasc Surg 1996;23:724–9. [PMID: 8627913]

Rhee RY, Gloviczki P: Mesenteric venous thrombosis. Surg Clin

North Am 1997;77:327–38. [PMID: 9146716]

Robin P et al: Complete thrombolysis of mesenteric vein occlusion

with recombinant tissue-type plasminogen activator. Lancet

1988;1:1391. [PMID: 2898060]

Sachs SM, Morton JH, Schwartz SI: Acute mesenteric ischemia.

Surgery 1982;92:646–53. [PMID: 7123485]

Serreyn RF et al: Laparoscopic diagnosis of mesenteric venous

thrombosis. Endoscopy 1986;18:249–50. [PMID: 2947800]

Wilson C et al: Acute superior mesenteric ischaemia. Br J Surg

1987;74:279–81. [PMID: 3580801]

CRITICAL CARE OF THE VASCULAR SURGERY

PATIENT

Atherosclerosis affects one in four Americans and constitutes

a major international health problem. There are over

600,000 episodes of stroke and 1.5 million myocardial

infarctions each year in the United States alone. Medical care

of these patients is complicated by advanced age and addi-

tional medical comorbidities that create a challenge in pre-

and postoperative management. This section will address

specific problems encountered when caring for vascular

surgery patients.



Respiratory Management

Vascular surgery patients often have an extensive smoking

history. Chronic obstructive pulmonary disease (COPD),

bronchitis, and asthma therefore are not unexpected. A

room-air arterial gas measurement often determines

whether more extensive pulmonary workup is necessary.

Formal pulmonary function tests are useful to determine

the nature and extent of respiratory compromise.

Encouragement in cessation of smoking for a minimum of

2 weeks prior to elective surgery and maximization of pul-

monary reserve with adequate pharmacologic support for

patients with obstructive or restrictive airway disease are

ideal. Instruction in the use of incentive spirometry and

deep breathing exercises is also helpful in restoring postop-

erative lung function. Mechanical ventilator support is the

rule in patients undergoing intracavitary aortic operations.

An aggressive attempt at weaning should be instituted once

the patient is sufficiently awake to cooperate and maintain

airway patency. This should be followed by aggressive incen-

tive spirometry, adequate pain control, and early ambula-

tion. The details of ventilator management are presented in

Chapter 12.



Nutritional Management

Nutritional support is a mandatory but frequently neglected

aspect of postoperative care. The catabolic response follow-

ing aortic surgery is pronounced. Because most vascular sur-

gery patients are well nourished prior to surgery, immediate

institution of nutritional support is not necessary. However,

if resumption of oral intake is not anticipated within

5–7 days after surgery, enteral nutrition should be started

through a nasoenteric feeding tube. Extensive manipulation

of the small bowel may cause mechanical ileus, although

absorptive capacity is maintained. Transient pancreatitis

also can be encountered in aortic surgery from retractor

blade pancreatic irritation. Feeding with an elemental for-

mula can be instituted at low rates (30 mL/h) and increased

in volume as tolerated. Enteral feedings reduce the risk of

septicemia associated with hyperalimentation catheters. This

is of particular importance in vascular disease patients who

have unincorporated graft surfaces exposed to the circulation.

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652

If nutritional support is required for more than 1 week, a

nitrogen balance study should be completed to ensure that

protein needs are being met.



Management of Ischemic Heart Disease

Atherosclerosis is a systemic disease that affects both the

peripheral vasculature and the coronary arteries. An analysis

of pooled data from 50 studies with more than 10,000

patients demonstrated the presence of coronary artery dis-

ease in 50% of patients who had operations for aortic

aneurysms, carotid artery disease, and lower extremity

ischemia. In another series of patients with known coronary

artery disease undergoing vascular surgery, 63% were found

to have ischemic cardiac events. In the Cleveland Clinic

series, fatal myocardial infarction accounted for a 3.3% mor-

tality rate after lower extremity procedures and a 6% mortal-

ity rate after aortic aneurysm resection. A study from the

same institution using routine coronary angiography before

aortic surgery found that 85% of patients had some degree of

coronary artery disease, whereas 31% had severe disease con-

sisting of either two- or three-vessel involvement or stenosis

of the left anterior descending artery. In a study of 1000

patients undergoing routine coronary angiography, 14–22%

of patients without any prior clinical history of coronary

artery disease had severe coronary artery disease on angiog-

raphy. It should be remembered, however, that demonstra-

tion of an anatomic lesion does not necessarily equate with

physiologic compromise.

The pathophysiology of acute perioperative infarction is

not completely understood, although multiple factors are

certainly involved. These include catechol release, increased

myocardial sensitivity to catechols, fluid sequestration, alter-

ations in oxygen transport, hypercoagulable states, and

tachycardia. Because elevations in heart rate and blood pres-

sure increase the tension-time index, they result in increased

oxygen consumption. Tachycardia further limits oxygen

delivery by decreasing the diastolic filling time, during which

the myocardium receives its perfusion.

Valvular heart disease also increases morbidity after vas-

cular procedures. In the presence of aortic stenosis, up to

20% mortality may be expected for abdominal or thoracic

operations and up to 10% for peripheral procedures.

Preoperative Assessment of Risk Owing

to Coronary Artery Disease

The high incidence of cardiac ischemia after vascular surgery

frequently occasions preoperative admission of these

patients to the ICU for hemodynamic evaluation and

optimization of cardiac status. Several scales have been

devised to predict surgical risk based on clinical assessment.

The American Association of Anesthesiologists score is based

on assessment of overall health and chronic disease. While

generally useful, it is not sufficiently specific for use in

patients with critical illnesses. An evaluation developed by

Goldman employs nine variables to predict cardiac risk.

Unfortunately, it underestimates cardiac complications in

vascular patients and is able to predict cardiac mortality in

only 50% of cases. An alternative scale includes a history of

previous myocardial infarction, congestive heart failure,

unstable angina, diabetes, and age over 70. Patients classified

as intermediate or high risk were expected to have an event

rate of 10–15%. Those in the low-risk group had a less than

5% incidence of cardiac ischemia.

A. Ambulatory Electrocardiographic (Holter) Monitoring—

Continuous ambulatory monitoring of the ECG is used to

detect clinically silent ischemia. A positive finding consists of

six or more episodes in a 24-hour period of ST-segment

depression of more than 2 mm. A significantly greater inci-

dence of perioperative cardiac morbidity and mortality

occurs in those with abnormal results. A recent study found

that 38% of patients with preoperative ischemia had postop-

erative cardiac events, whereas fewer than 1% of patients

without ischemia suffered cardiac morbidity. Continuous

preoperative monitoring identifies patients with clinically

silent ischemia who might benefit from therapy. Although

this method is simple, noninvasive, and inexpensive, it suf-

fers from low sensitivity and has a positive predictive value of

only 38%.

B. Exercise Electrocardiographic Testing—Exercise stress–

induced alterations in the ECG have been used extensively

to assess cardiac risk. Because they typically require walk-

ing or running, they are not suitable for use in dysvascu-

lar patients whose exercise tolerance is limited by

claudication. Submaximal effort may yield false-negative

results.

C. Dipyridamole-Thallium Scintigraphy—In this test, a phar-

macologic agent is substituted for exercise to increase coro-

nary artery blood flow. Intravenously administered

dipyridamole promotes coronary artery blood flow without

increasing myocardial oxygen consumption by increasing the

intracellular concentration of adenosine. Blood flow

increases through normal arteries that dilate maximally.

Stenotic arteries do not respond because of fixed anatomic

lesions. Prior to administration of dipyridamole, thallium-

201 is injected to demonstrate areas of myocardial ischemia.

Because thallium-201 is preferentially taken up by the nor-

mal myocardium, areas of hypoperfusion appear as “cold”

spots. If homogeneity improves after dipyridamole is given,

thallium redistribution is said to have occurred, and the scan

is considered positive. Redistributed areas consist of viable

but ischemic myocardium that are at risk for infarction.

Areas that fail to improve after dipyridamole infusion

probably consist of previously infarcted muscle that is not at

risk for a future ischemic event. Thallium redistribution is

associated with a 30–50% risk of some postoperative cardiac

event. The positive predictive value of the test is only 22%.

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CRITICAL CARE OF VASCULAR DISEASE & EMERGENCIES

653

A negative scan indicates a low likelihood of perioperative

infarction, but a positive scan is of ambiguous import. The

specificity of thallium scans can be increased by combining

them with other risk factors for myocardial ischemia, includ-

ing age, a history of angina, the presence of Q waves on ECG,

the presence of type 1 diabetes, and a history of therapy-

dependent ventricular ectopy. The risk of a cardiac event in

intermediate-risk patients (one or two predictors) is as high

as 30%. This finding has since been challenged by reports

from several centers finding little use for dipyridamole-

thallium scanning in moderate-risk patients and suggesting

that a new procedure be investigated.

D. Radionuclide Ventriculography—Multiple-gated acquisi-

tion (MUGA) blood pool scans provide quantitative infor-

mation about the left ventricular ejection fraction (LVEF)

and ventricular wall motion. The normal LVEF is 55% or

greater. Those with a normal LVEF are at low risk for postop-

erative cardiac events. Those with LVEF values between 36%

and 55% are at intermediate risk, with a perioperative infarc-

tion risk of 20%. High-risk patients have LVEF values of less

than 35% and had an 80% risk of myocardial infarction.

Unfortunately, the test has a low sensitivity (44%), which

means that a negative study does not necessarily eliminate

the risk of myocardial infarction.

E. Dobutamine Stress Echocardiography—Dobutamine

stimulates myocardial contractility and increases heart

rate through β

activity. Administration of this pharmaco-

logic agent results in higher oxygen demand. Two-

dimensional echocardiography then is used to visualize

regional wall dysfunction from myocardial ischemia.

Compared with dipyridamole-thallium scanning, this test

also was initially more successful in predicting periopera-

tive cardiac events. However, ensuing studies reported

inconsistent results with a sensitivity ranging from

54–96% and specificity in the range of 57–95% in com-

parison with cardiac catheterization.

F. Coronary Angiography—Coronary angiography should

be used only in selected patients whose noninvasive studies

place them at high risk for coronary events. The results of

angiography can be used to plan further procedures such as

angioplasty or coronary artery bypass.

Postoperative Cardiac Management

Postoperative cardiac ischemia and myocardial infarction are

caused by an increased myocardial oxygen requirement in

the face of inadequate supply. Myocardial oxygen consump-

tion is related to the tension-time index, which is the prod-

uct of systolic blood pressure and heart rate. Animal studies

have shown that cardiac work and myocardial oxygen con-

sumption both increase when the heart pumps against

elevated diastolic pressures. Prolonged work against

increased afterload results in myocardial hypertrophy, which

also increases oxygen consumption. Tachycardia has two

adverse effects on myocardial oxygen balance. First, it

directly increases oxygen demand by increasing the time-

tension index, and second, it reduces the diastolic filling

time, thereby limiting the period during which myocardial

blood flow occurs. Pharmacologic management is frequently

necessary to improve myocardial oxygenation by decreasing

the heart rate and lowering blood pressure.

Antihypertensive Therapy

Postoperative hypertension occurs in up to 50% of patients

after aortic or carotid surgery. Pain is one of the most com-

mon causes and should be addressed initially. Small intra-

venous doses of morphine sulfate should be titrated to effect.

Hypotension and respiratory depression are the major com-

plications of opioid administration. Opioids should be

given to carotid surgery patients only after they have recov-

ered from their anesthetic and a postoperative neurologic

examination has been completed. Lorazepam is a relatively

short-acting benzodiazepine that provides sedation. It may

be used as an adjunct to the analgesic effect of morphine.

Lorazepam is particularly useful in aortic surgery patients

who require mechanical ventilation after operation. The initial

intravenous dose is usually 2–3 mg titrated to effect at inter-

vals of 4–6 hours.

Excessive intraoperative volume administration may

cause postoperative hypertension. This is particularly true

among patients who have received epidural anesthetics that

cause vasodilation. Resolution of the block and return of

normal vascular tone may result in hypertension.

Hypervolemia also may follow mannitol administration and

excessive volume loading instituted prior to removal of the

aortic cross-clamp. Postoperative volume status should be

evaluated and optimized with the aid of a pulmonary artery

flotation catheter. Careful administration of diuretics is

required to avoid inadvertent iatrogenic hypervolemia.

Once remediable causes of hypertension have been elimi-

nated, persistent hypertension should be treated to reduce

myocardial oxygen demand owing to increased wall stress.

The threshold for treatment will vary with the patient, the

type of procedure performed, the duration of hypertension,

and preoperative risk factors. Elevation of systolic blood pres-

sure above 120% of baseline is a reasonable point at which

therapy should be instituted. Agents with shorter half-lives

allow more precise titration of blood pressure, whereas

longer-acting agents have the advantage of decreased dosing

requirements. Nitroprusside and nitroglycerin are both fast-

acting agents that can be given intravenously. Nitroprusside

has a balanced effect because it dilates both arterioles and

veins. As an arterial vasodilator, it lowers blood pressure by

decreasing arteriolar vascular resistance without increasing

venous capacity. The decreased afterload reflexively

increases cardiac sympathetic stimulation that may result in

undesirable tachycardia. Nitroglycerin is preferred because

it produces coronary artery vasodilation in addition to



CHAPTER 29

654

decreasing preload. Because nitroglycerin can precipitously

decrease filling pressures, it is imperative to ensure normal

pulmonary capillary wedge pressure (PCWP) prior to the

institution of therapy. Intravenous doses are started near 5 μg/min

and increased by this amount every 5–10 minutes until the

desired effect is reached. The normal vasodilatory dose is

between 50 and 100 μg/min, although some patients require

doses as high as 400 μg/min. High doses can be tolerated for

several days, although methemoglobin concentration should

be monitored.

Agents that provide β-adrenergic blockade also may be

used to treat postoperative hypertension. Labetalol is partic-

ularly useful because it provides not only nonspecific beta

blockade but prevents reflex increases in vasoconstriction by

its α-adrenergic blocking activity. Labetalol has a relatively

long half-life of 6–8 hours and should be used with caution

in patients with hepatic and renal insufficiency because of its

route of elimination. The initial intravenous dose is 10–25 mg,

supplemented every half-hour to desired effect. ACE

inhibitors, initially used to decrease afterload in heart failure,

were demonstrated recently to significantly reduce mortality,

myocardial infarction, stroke, cardiac arrest, and heart fail-

ure. The Heart Outcomes Prevention Evaluation Study inves-

tigators found that treating 1000 patients with ramipril

(a long-acting ACE inhibitor) for 4 years prevented approxi-

mately 150 events in 70 patients.

Tachycardia

Fever, pain, and hypovolemia are the most common causes of

tachycardia (heart rate >100 beats/min) in postoperative

patients. Hypovolemia may be caused by inadequate volume

replacement or by continued volume loss such as hemorrhage

or osmotic diuresis. Unrecognized causes of obligatory

osmotic diuresis include hyperglycemia and intravenous

contrast material administered prior to or during surgery.

Pulmonary artery flotation catheters facilitate the evaluation

of tachycardia by providing information on relative volume

status. After inciting causes have been addressed, primary

tachycardia should be treated if the heart rate remains ele-

vated. Esmolol is an agent that is relatively β

-selective and has

a half-life of only 9–10 minutes. A loading dose of 500 μg/kg is

administered over 1 minute, followed by a continuous infu-

sion of 50 μg/kg per minute. The infusion rate is decreased as

tachycardia resolves.

Renal Failure

The incidence and prognosis of acute renal failure occurring

after vascular surgery depend on the overall preoperative sta-

tus of the patient, the nature of the surgery performed, and

associated complications such as cardiac failure or sepsis.

The reported incidence of acute renal failure after elective

aortic surgery ranges from 1–15%. Following surgery for

ruptured aortic aneurysms, it is between 21% and 100%,

with associated mortality rates between 50% and 95%.

Despite improved intra- and postoperative management, the

incidence of acute renal failure after vascular surgery has not

changed appreciably in the past 20 years. Several factors con-

tribute to the development of renal failure, including

suprarenal aortic cross-clamping, renal artery occlusion,

declamping hypotension, and embolization of atheroscle-

rotic debris to the kidneys. Autopsy studies of patients with

postischemic acute renal failure have found minimal alter-

ations of glomerular architecture in the face of profound dis-

ruption of tubular morphology. Acute tubular necrosis or

luminal obstruction caused by sloughing of tubular cells is

thought to be the inciting event.

Intraoperative maneuvers aimed at protecting renal func-

tion are directed mainly at reducing the severity and dura-

tion of renal ischemia. Circulating blood volume and cardiac

output should be optimized prior to interruption of renal

blood flow. The intravenous infusion of 12.5–25 g mannitol

prior to aortic occlusion is common practice. Mannitol offers

a protective effect by (1) expanding circulating blood vol-

ume, (2) acting as an osmotic diuretic to promote urine flow

and prevent stasis, (3) attenuating the reduction in cortical

blood flow, and (4) serving as a free-radical scavenger.

Intraoperative contrast angiography produces a postopera-

tive osmotic diuresis and makes absolute urine output an

unreliable indicator of renal perfusion. When dye has been

used, sufficient fluid should be administered to reduce urine

specific gravity below 1.015. In the postoperative period,

maintenance of adequate blood volume and cardiac output

are the best defenses against renal failure. A pulmonary

artery catheter should be used to assess venous return and

cardiac function in patients who have had intraabdominal

surgery. Sufficient maintenance and replacement fluid must

be given to ensure adequate cardiac preload. Inotropic agents

such as dopamine or dobutamine also may be required.

Dopamine in doses below 5 μg/kg per minute promotes

diuresis by dilating renal afferent arterioles. Recently, the

administration of oral acetylcysteine along with hydration

has been shown to prevent the reduction in renal function

caused by low-osmolarity contrast agents in patients with

chronic renal insufficiency. Its vasodilatory and antioxidant

properties are speculated to be the mechanisms of action.

Acetylcysteine is given in a dosage of 600 mg twice on the day

prior to and on the day of contrast material administration.

Reperfusion of severely ischemic muscle beds may cause

the release of myoglobin into the circulation. A positive dip-

stick reaction for urine hemoglobin without the presence of

red blood cells on microscopic analysis is evidence of myo-

globinuria. Sodium bicarbonate (100 meq/L) admixed with

maintenance intravenous solutions should be administered

to alkalinize the urine. Urine volume must be maintained

above 1–2 mL/kg per hour. The myonephrotic syndrome of

renal failure in the face of progressive rhabdomyolysis carries

a mortality rate of more than 50%.

Other causes of oliguria include aminoglycoside toxicity

and postrenal obstruction. The latter may be caused by a

kinked urinary catheter or by inadvertent intraoperative

ureteral ligation. After other causes of oliguria have been

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CRITICAL CARE OF VASCULAR DISEASE & EMERGENCIES

655

excluded, radionuclide imaging is reasonable to assess renal

blood flow and urinary excretion. If concern about postrenal

obstruction exists, bedside ultrasound can be used to identify

hydronephrosis.



Complications of Vascular Surgery

Infection

Prosthetic graft infection is a devastating complication that

occurs in 1–6% of patients depending on comorbid factors,

location, and type of graft. The organism usually responsi-

ble is Staphylococcus aureus, although others, including

yeasts, anaerobic bacteria, and mycobacteria, have been

identified. Most graft infections are diagnosed after discharge

(>4 months) rather than in the early postoperative period.

Perioperative antibiotic prophylaxis usually consists of a

first-generation cephalosporin with good activity against

S. aureus and S. epidermidis. It should be noted that compa-

rable rates of graft infection have been reported both with

and without the use of perioperative antibiotics.

Antibiotic administration should be continued until all

indwelling intravenous and urinary catheters have been

removed. Patients who have undergone reconstruction fol-

lowing vascular trauma should be observed closely for evi-

dence of necrosis at wound sites. Devitalized tissue is an

excellent culture source for bacteria. Early debridement and

sufficient autologous coverage can prevent the late sequelae

of graft infections—namely, thrombosis, rupture, and the

development of paraanastomotic pseudoaneurysms.

Gastrointestinal Complications

Ischemic colitis and mesenteric ischemia are feared compli-

cations following resection of an abdominal aortic

aneurysm. Interruption of the blood supply to the left colon

following ligation of the inferior mesenteric artery is the

usual cause, especially after repair of a ruptured aneurysm. In

patients with severe chronic occlusive disease or those who

have had previous abdominal procedures, interruption of

vital visceral collaterals also can contribute to bowel

ischemia. Early nonspecific harbingers of this complication

include an acute fever spike with increased white blood cell

count, lactic acidosis, and bloody diarrhea. Antibiotics, intra-

venous fluid administration, and immediate sigmoidoscopy

and colonoscopy are undertaken. Once the diagnosis is veri-

fied, a transmural infarct requires operative resection.

Expectant management is justified in patients in whom

ischemia does not involve the full thickness of the bowel wall.

Acalculous cholecystitis occurs in 1% of all patients

undergoing aortic surgery. Right upper quadrant abdominal

pain, fever, leukocytosis, and hyperbilirubinemia are com-

mon. Bedside ultrasonography is preferred over

99m

Tc-HIDA

scanning to establish the diagnosis. Immediate cholecystec-

tomy or cholecystostomy is usually required. Ischemic

pancreatitis may be confused with cholecystitis. Elevations of

the serum amylase and lipase allow separation of the two. A

mild pancreatitis is caused by exposure of the aorta and

retractor injury. It is usually self-limiting.



Complications of Common Vascular

Procedures

Carotid Endarterectomy

Either hypotension or hypertension may occur early in the

postoperative course. Hypertension may lead to the forma-

tion of neck hematomas and hemorrhagic stroke.

Hypotension can lower the cerebral perfusion pressure that a

hypertensive patient is normally accustomed to and thus

results in cerebral infarct. Judicious use of fast-acting

vasodilators (eg, nitroglycerin or nitroprusside), β-blockers

(eg, esmolol), or vasoconstrictors (eg, dopamine) in the

immediate perioperative period to maintain a constant and

stable blood pressure is a sound management stratagem.

Effective weaning from these agents is accomplished once

sufficient volume is infused.

The incidence of postoperative strokes ranges from

1–3%. Although the majority result from intraoperative

embolization or cerebral ischemia, up to 19% may be due to

acute thrombosis of the carotid artery. Transient ischemic

attacks within the first week have been reported to be as high

as 8%. When a patient is first noted to have a neurologic

deficit, determining internal carotid artery patency is impor-

tant because prospects for neurologic recovery are directly

related to the speed with which flow is restored. If no intra-

operative completion studies were performed, initial diag-

nostic evaluation should be via noninvasive bedside imaging

such as Doppler ultrasound or duplex scanning. Patients

with abnormal or equivocal findings require immediate

reexploration. If noninvasive studies are normal, emergency

carotid angiography is indicated to identify small defects that

can be repaired. If the patient had a normal intraoperative

completion arteriogram or duplex scan, the source of deficit

is embolic, and reoperation offers little benefit.

Headaches after carotid surgery are not uncommon.

Severe headaches in the face of hypertension should be mon-

itored carefully and the blood pressure expeditiously con-

trolled. A CT scan of the brain is obtained, and a diagnosis of

cerebral hyperperfusion syndrome is then entertained. This

can happen in patients undergoing endarterectomy for

chronic severe occlusive disease or in patients with an acute

cerebrovascular accident. The common denominator is reac-

tive hyperemia or cerebral reperfusion injury. Lesser forms of

this condition result in symptoms consistent with mild cere-

bral edema, headache, and seizures. A more severe presenta-

tion results in catastrophic intracerebral hemorrhage from

vessel rupture. Prompt recognition and treatment with anti-

hypertensives, osmotic diuretics, and anticonvulsants can be

lifesaving. If intracerebral hemorrhage has occurred, the

prognosis is poor.



CHAPTER 29

656

Aortic Operations

Abdominal aortic aneurysm repair in the elective setting

has a mortality rate of 1–3%. Repaired emergently, mortal-

ity is often greater than 50%. Predictors that herald poor

survival include the duration and severity of perioperative

shock, hypothermia, and cardiac reserve. Postoperatively,

myocardial infarction, coagulopathy, renal failure, respira-

tory insufficiency, ischemic bowel, poor nutrition, and

infection often contribute to morbidity. Meticulous ICU

monitoring with a pulmonary catheter and aggressive treat-

ment are mandatory. Adequate intravascular volume

replacement is necessary to maintain organ perfusion.

Patients often require a significant amount of volume for

the first 24–48 hours owing to shifts of intravascular fluid

into the interstitium. On the third or fourth day, reentry

into the vascular system occurs, and a brisk diuresis ensues.

At this stage, electrolytes are replaced carefully and urine

output maintained, with diuretics if necessary. Prolonged

mechanical ventilation is required for respiratory failure

and hemodialysis for renal compromise. Mesenteric

ischemia and ischemic colitis may result, and the first sign

is often an uncorrectable metabolic acidosis, fever, and

rapid leukocytosis. Melena and hematochezia are late signs

and portend bowel necrosis. Prolonged shock and ischemia

of the spinal cord result in paraplegia in 2% of patients.

Corticosteroids may be used once other causes of spinal

shock have been eliminated.

Peripheral Operations

The most common cause of morbidity in lower extremity

bypass operations is cardiac insufficiency. Preoperative opti-

mization and dosing with β-blockers have been shown to

decrease postoperative events. Prolonged hypotension or

hypovolemia may lead not only to myocardial ischemia but

also to thrombosis of the bypass graft. Careful hemodynamic

monitoring and support can prevent these complications. If

a palpable pulse is present distal to the graft, it should be

monitored regularly for any change in strength or character.

An abrupt decline in or absence of the pulse is highly sugges-

tive of graft occlusion. In patients who are admitted to the

ICU without palpable pulses, a Doppler probe or piezoelec-

tric pulse monitor can be used to evaluate graft patency.

A pulse oximeter probe placed on a finger or toe distal to the

bypass site is another convenient technique for monitoring

graft patency. Revascularization for traumatic injury or

chronic ischemia may cause limb swelling that resolves with

elevation. The development of a compartment syndrome

should be recognized immediately and treated promptly

with fasciotomies. In patients with prolonged ischemia, myo-

globinuria may occur after revascularization and may lead to

renal failure unless recognized and treated with adequate

hydration and diuresis.

Angevine PD et al: Significant reductions in length of stay after

carotid endarterectomy can be safely accomplished without

modifying either anesthetic technique or postoperative ICU

monitoring. Stroke 1999;30:2341–6. [PMID: 10548668]

Bjorek M, Bergqvist D, Troeng T: Incidence and clinical presenta-

tion of bowel ischemia after aortoiliac surgery: 2930 operations

from a population-based registry in Sweden. Eur J Endovasc

Surg 1996;12:139.

Davila-Roman VG et al: Dobutamine stress echocardiography pre-

dictors of surgical outcome in patients with an aortic aneurysm

and peripheral vascular disease. J Am Coll Cardiol 1993;

21:957–63. [PMID: 8450165]

Eagle KA et al: Combining clinical and thallium data optimize pre-

operative assessment of cardiac risk before major vascular sur-

gery. Ann Intern Med 1989;110:859–66. [PMID: 2655519]

Eagle KA et al: Guidelines for perioperative cardiovascular evalua-

tion for noncardiac surgery. Report of the American College of

Cardiology/American Heart Association Task Force on Practice

Guidelines, Committee on Perioperative Cardiovascular

Evaluation for Noncardiac Surgery. Circulation 1996;93:

1278–317.

Farkas JC et al: Acute colorectal ischemia after aortic surgery:

Pathophysiology and prognostic criteria. Ann Vasc Surg

1992;6:111–8. [PMID: 1599829]

Frishman WH et al: Beta-adrenergic blockade and calcium chan-

nel blockade in myocardial infarction. Med Clin North Am

1989;73:409–36. [PMID: 2563784]

Goldman L et al: Multifactorial index of cardiac risk in noncardiac

surgical procedures. N Engl J Med 1977;297:845–50. [PMID:

904659]

Hertzer NR et al: Coronary artery disease in peripheral vascular

patients: A classification of 1000 coronary angiograms and

results of surgical management. Ann Surg 1984;199:223–33.

[PMID: 6696538]

Jamieson WR et al: Influence of ischemic heart disease on early

and late mortality after surgery for peripheral occlusive vascular

disease. Circulation 1982;66:I92–7.

Jayr C et al: Preoperative and interoperative factors associated with

prolonged mechanical ventilation: A study in patients following

major vascular surgery. Chest 1993;103:1231–6.

Mangano DT et al: Dipyridamole thallium-201 scintigraphy as a

preoperative screening test: A reexamination of its predictive

potential. Circulation 1991;84:493–502.

Miller DC, Myers BD: Pathophysiology and prevention of acute

renal failure associated with thoracoabdominal or abdominal

aortic surgery. J Vasc Surg 1987;5:518–23. [PMID: 3334683]

Nicholson ML et al: Randomised controlled trial of the effect of

mannitol on renal reperfusion injury during aortic aneurysm

surgery. Br J Surg 1996;83:1230–3. [PMID: 8983613]

O’Donnell D, Clarke G, Hurst P: Acute renal failure following sur-

gery for abdominal aortic aneurysm. Aust NZ J Surg

1989;59:405–8.

Pasternack PF et al: The value of radionuclide angiography as a

predictor of perioperative myocardial infarction in patients

undergoing abdominal aortic aneurysm resection. J Vasc Surg

1984;1:320–5.

Perry MO, Fantini G: Ischemia: Profile of an enemy. Reperfusion

injury of skeletal muscle. J Vasc Surg 1987;6:231–4. [PMID:

2442426]