Chapter 40. Vascular Emergencies

Most vascular emergencies are due to either disruption of the blood vessel wall with bleeding (eg, from penetrating trauma) or to occlusion of the blood vessel lumen (eg, by an embolus or thrombus). The major consequences of these events are blood loss or acute distal ischemia. If vascular injury is untreated, hypotension or tissue necrosis may occur.

Immediate Management of Life-Threatening Vascular Injuries

Maintain Airway and Treat Associated Injuries

Treat associated life-threatening head, thoracic, and abdominal injuries (Chapters 12, 22, 24, and 25).

Stop Hemorrhage

1. Stop active bleeding from arterial or venous hemorrhage by gentle manual compression.

2. Avoid clamping the bleeding vessel because this will cause further injury.

3. Avoid the use of tourniquets.

4. Do not remove embedded objects because they may be preventing further bleeding.

Treat or Prevent Shock

(See also Chapter 11) Insert two or more large-bore (≥16-gauge) intravenous catheters. Two intravenous access sites are preferable if the patient is already in shock or is bleeding profusely.

While intravenous catheters are being inserted, draw blood for complete blood count (CBC), serum electrolytes, glucose and creatinine measurements, prothrombin time (PT), partial thromboplastin time (PTT), and typing and crossmatching (reserve 6–8 units of packed red blood cells or whole blood).

Begin intravenous infusion of crystalloid solutions (eg, normal saline or lactated Ringer's) to support blood pressure. Up to 2–3 L of crystalloid solution may be given before blood products are administered. Replace blood. The number of units administered depends on the severity of existing blood loss and on anticipated loss from projected surgery. Use fresh whole blood whenever possible.

Prevent Further Vascular and Nerve Injury

All fractures and joint dislocations associated with abnormal pulses should be carefully reduced and splinted to reduce further neurovascular damage. Control hemorrhage by pressure; avoid clamping vessels to stop hemorrhage. Consider adjunctive studies for further evaluation as appropriate (eg, computed tomography [CT] scan, angiography).

Minimize Ischemia

Keep ischemic limbs horizontal. Do not use tourniquets.

Relieve Pain

Provide adequate analgesia; if necessary, give narcotic analgesics.

Obtain Surgical Consultation

All documented or suspected vascular injuries should be examined promptly by a general or vascular surgeon before the patient is transferred from the emergency department.

Hospitalize Patients as Required

Hospitalize all patients with arterial or major venous injuries.

General Considerations

Acute vascular injury may result in either hemorrhage or tissue ischemia.

Arterial Injury

Hemorrhage

Obvious external hemorrhage is present in many patients. Occult bleeding into soft tissue, the retroperitoneum, the pelvis, or body cavities may also occur.

Ischemia

Ischemia from arterial injury must be recognized and treated promptly, because increased tissue pressure and swelling from ischemia further compromise arterial perfusion, and prolonged ischemia results in irreversible tissue damage.

Venous Injury

Hemorrhage

Obvious or occult bleeding usually occurs following venous injury. It is rarely life-threatening except in the case of injuries to central veins (eg, vena cava) or their immediate branches (eg, femoral vein).

Ischemia

Tissue ischemia from venous trauma alone is rare, although venous obstruction and resultant tissue congestion may worsen preexisting tissue ischemia resulting from arterial injury.

Causes of Vascular Injury

Penetrating Trauma

Penetrating trauma is the most common cause of peripheral vascular injury and ranges in severity from innocuous simple puncture wounds to extensive wounds caused by high-velocity missiles. Penetrating injuries to the central vessels may lead to massive hemorrhage and death.

Blunt Trauma

Blunt trauma may also cause vascular injury. Contusions or crushing injuries of an artery may cause either transmural disruption with hemorrhage, or partial disruption of the artery and elevation of the intima from an intramural hematoma (ie, dissection). Thrombosis of a segment of artery may also occur. Blunt trauma with dislocation of a joint may result in disruption of the arteries crossing that joint line, leading to ischemia distal to the site of injury (eg, disruption of the popliteal artery with posterior dislocation of the knee). Blunt trauma may also contribute indirectly to vascular occlusion by creating large hematomas near a blood vessel. Hematoma formation may lead to arterial spasm, distortion, or compartment syndromes, all of which may interfere with arterial flow.

Chemicals

Chemical injury to blood vessels is increasing in frequency. It is generally iatrogenic or associated with parenteral drug abuse. Intra-arterial injection of drugs that are chemically irritating to tissues (eg, barbiturates) causes occlusion of small peripheral vessels. If occlusion is severe, all or part of the limb may be lost. Extravasation of an intravenously administered chemical may also cause associated arterial spasm or tissue necrosis. Barbiturates, phenytoin, vasopressors, and chemotherapeutic agents (eg, doxorubicin) are notable examples. High doses of certain intravenously administered vasopressors (eg, dopamine) can cause intense peripheral vasoconstriction with ultimate digital ischemic necrosis.

Sequel

Late sequelae associated with major vascular injuries include the development of false aneurysms and arteriovenous fistulas.

False Aneurysms

False aneurysms do not contain all three layers of the vessel wall (intima, media, and adventitia). They result from walled-off disruptions of vessel walls. They enlarge over time, may compress adjacent veins or nerves, and may rupture without warning.

Fistulas

Fistulas may occur after adjacent arteries and veins are injured simultaneously, usually as a result of stab wounds or missile injury. The fistula may enlarge over time and cause increased cardiac output if a large left-to-right shunting of blood is present. If the fistula involves the blood supply to an extremity, dilated veins may be observed in that extremity. Turbulent blood flow through the fistula results in an obvious thrill or bruit. Fistulas may also compress adjacent nerves or impede collateral circulation, or they may rupture, causing a severe hemorrhage.

Principles of Diagnosis

Physical Examination

If there is a wound in the vicinity of a major blood vessel, assume that vascular injury has occurred. The findings listed below may not appear for hours to days following a significant vascular injury, and absence of these findings does not rule out the possibility of vascular injury.

Signs

Clinical manifestations of vascular injury include an expanding or pulsating hematoma, to-and-fro or continuous murmurs of arteriovenous fistulas, a false aneurysm, loss of pulses, progressive swelling of the injured part, unexplained ischemia or dysfunction, and unilateral cool or pale extremities.

Pulses

Perform a complete vascular examination unless treatment of other life-threatening injuries precludes it.

Palpation

Palpate all peripheral pulses: carotid, axillary, brachial, radial, femoral, popliteal, dorsalis pedis, and posterior tibial.

Doppler Ultrasound Examination

The presence of blood flow in a peripheral vessel can be detected using a standard pocket Doppler apparatus. Any assessment of the normality of this flow requires concomitant pressure measurements or waveform analysis.

Murmurs and Bruits

Auscultate over injured areas to detect bruits or murmurs.

Neurologic Function

Assess neurologic function. Paresthesia may be an early sign of developing vascular problems (eg, compartment syndrome).

Diagnostic Imaging

Arteriography and CT scan with contrast or CTA are the imaging modalities to evaluate vascular injury. In addition, ultrasonography may be useful in specific circumstances (discussed below).

Caution: Diagnostic imaging should not be performed in a patient whose condition is unstable and who needs emergency laparotomy or thoracotomy. The procedure should be delayed until after resuscitation and treatment of the life-threatening emergency, either in the emergency department or in the operating room.

Emergency Management of Specific Vascular Injuries

Neck Injuries

See also Chapter 23.

Essentials of Diagnosis

• History of blunt or penetrating trauma
• Consider concomitant injury to nonvascular structures
• CT scan and/or arteriography confirms diagnosis

General Considerations

Vascular injury to the neck is most often due to penetrating injuries; however, blunt trauma to the cervical vessels can result in intimal disruption, dissection, and thrombosis. Concomitant injury to nonvascular structures of the neck (eg, trachea, esophagus, and spinal cord) may also occur. The cervical spine must be protected until injury is excluded.

Penetrating Trauma

In penetrating trauma to the neck, two immediate concerns are massive hemorrhage and airway compromise secondary to a rapidly expanding hematoma.

Emergency Treatment

Control hemorrhage, preferably with direct pressure, along with ongoing fluid resuscitation; neither of these measures should delay transport to the operating room for definitive repair. If a rapidly expanding hematoma is suspected, tracheal intubation via direct laryngoscopy or intubating bronchoscope should be conducted before compression of the trachea makes this procedure more difficult or impossible. Transtracheal jet insufflation and cricothyrotomy are methods of last resort; in this setting, emergency tracheostomy in the operating room is preferable.

Further Treatment

Further management is a function of the patient's hemodynamic stability and the location of the wound. All actively bleeding, hemodynamically unstable patients are taken immediately to the operating room for surgical exploration. For stable patients with wounds that penetrate the platysma muscle, management is a function of the zone of the neck affected (Figure 40–1). Wounds should never be probed beyond the level of the platysma muscle in the emergency department.

Zone I Injuries

These wounds are frequently associated with injury to the great vessels and require imaging with CT or angiography to exclude major arterial injury.

Zone II Injuries

These injuries may be further evaluated by surgical exploration or imaging of the vessels and nonvascular structures with CT or angiography at the discretion of the attending surgeon.

Zone III Injuries

Because the relationship of the blood vessels to the base of the skull makes surgical exploration and distal control of hemorrhage difficult, preoperative imaging with CT or angiography should be conducted to define the injury and help plan the surgical approach.

Blunt Trauma

Blunt trauma to the carotid artery can result in intimal disruption, dissection, and thrombosis leading to acute cerebral ischemia manifest as a gross hemispheric neurologic deficit not explained by intracranial trauma. Conduct emergent imaging of the neck arteries with CTA or conventional angiography.

Diagnostic Imaging

The use of multiplanar CT scanning with arterial enhanced imaging allow the neck vessels to be evaluated for injuries to include complete or partial transaction, arteriovenous fistula, pseudoaneurysms or thrombosis. In addition, conventional arteriography may be required in addition to CT in zone I and III injuries.

Disposition

Asymptomatic patients with mild neck injuries due to blunt trauma or penetrating injuries that do not cross the platysma muscle may be discharged from the emergency department. Hospitalize all other patients with neck injuries, and consult with a general or vascular surgeon.

Chest Injuries

See also Chapter 24.

Essentials of Diagnosis

• Significant mechanism of thoracic trauma
• Tearing retrosternal or interscapular pain, dysphagia, hoarseness, or dyspnea
• In blunt trauma, less than half of patients will have visible signs of chest wall injury
• CT scan or TEE confirms diagnosis

General Considerations

Vascular injury to the chest occurs secondary to both penetrating and blunt trauma. If bleeding is not contained within fascial planes, these injuries can lead to exsanguination and death, often before the patient arrives in the emergency department. A high degree of suspicion for this type of injury must be maintained in any patient with a significant mechanism of thoracic trauma. CT with contrast has become the diagnostic study of choice in evaluating vascular injury in a hemodynamically stable patient with chest trauma.

Thoracic Aortic Injury

Penetrating and blunt trauma may cause thoracic aortic injury (TAI). Though penetrating TAI may be caused by any variety of objects or weapons, blunt TAI involves large, violent deceleration forces (eg, falls, motor vehicle collisions including occupant ejection or auto-pedestrian). The greatest risk of TAI in a motor vehicle collision exists when the impact occurs on the same side of the vehicle as the occupant, when there is greater than 15 in of intrusion into the passenger compartment, and when the overall change in velocity experienced by the vehicle and its occupants is greater than 20 miles/h. A significant mechanism of injury should heighten suspicion of blunt TAI, because less than half of these patients will have visible signs of chest wall injury.

Clinical Findings

Symptoms and Signs

Patients may complain of tearing retrosternal or inter-scapular pain. Less frequently, dysphagia, hoarseness, stridor, or shortness of breath is present. The physical examination often reveals no external evidence of chest wall injury. Classically, a difference in upper-extremity pulses and a harsh systolic murmur across the precordium and in the interscapular area are noted. Signs and symptoms of shock may be present.

Imaging

The chest X-ray is frequently the first imaging study obtained (Figure 40–2); the classic chest X-ray findings associated with TAI are listed in Table 40–1. However, 7% of patients with TAI can have a normal chest X-ray and further imaging studies may be warranted, based on clinical suspicion and mechanism of injury. In the past, aortography had been the study of choice in evaluating TAIs. However, CT scan has emerged as the study of choice after initial chest X-ray. It is more readily available than aortography and less invasive, and prospective clinical trials have shown spiral CT scan to be 100% sensitive and 99.7% specific in diagnosing TAI following blunt trauma. In centers where transesophageal echocardiography (TEE) is readily available, it is a highly sensitive (98%) and specific (100%) modality for diagnosing TAI. TEE can be done at the bedside, requires no contrast dye, and evaluates real-time cardiac function.

Treatment and Disposition

Patients with TAI will require emergency consultation with a vascular or thoracic surgeon. In the emergency department, it is important to maintain intravascular volume with crystalloid solutions and blood products. Systolic blood pressure should be lowered to less than 120 mm Hg. Exsanguinating hemorrhage may require emergency thoracotomy for the control of bleeding.

Pulmonary Vascular Injuries

Essentials of Diagnosis

• Usually due to penetrating thoracic or abdominal injury
• Rapidly expanding hemothorax on chest X-ray

Clinical Findings: General Considerations

Most patients present with penetrating chest or abdominal trauma and rapidly expanding hemothorax, visible on chest X-ray. Rarely, blunt chest trauma is associated with pulmonary vascular injury.

Treatment and Disposition

Most patients can be managed with a 36–42 F chest tube that uses suction and allows the lung to reexpand and tamponade the bleeding vessel. Continued massive bleeding requires prompt surgery. Consider the use of autotransfusion. Prompt consultation with a general, vascular, or thoracic surgeon is required, because exsanguination can occur rapidly. Hospitalization is indicated for all patients.

Abdominal Injuries

See also Chapter 25.

Essentials of Diagnosis

• History of abdominal trauma
• Signs and symptoms of shock that fail to respond to resuscitation efforts

Clinical Findings

Patients with injuries to major vessels within the abdominal cavity present mainly with hemorrhagic shock that fails to respond to resuscitative efforts. In hemodynamically stable patients, CT with contrast is used to evaluate intrabdominal vascular and solid organ injury.

Treatment and Disposition

Immediate operation is the only effective treatment for abdominal vascular injuries. Support blood pressure with infusion of intravenous fluids (colloid or crystalloid solutions) until surgery can be performed. Packed red blood cells or whole blood should be used as soon as available.

Injuries to the Extremities

Essentials of Diagnosis

• History of blunt or penetrating trauma
• Presence of a pulse does not rule out vessel injury
• Use CT or arteriography to evaluate

Clinical Findings

Penetrating Trauma

Vascular injuries are present in 25–35% of patients with penetrating trauma to the extremities. Occasionally vascular trauma is present without the usual physical findings, and the presence of a pulse does not rule out injury to the vessel. Imaging should be considered whenever the weapon's trajectory has passed close to major blood vessels.

Blunt Trauma

Vascular injury may also occur after blunt trauma, especially if fractures and joint dislocations are present. Even if the pulse is restored with splinting and traction, an arteriogram is necessary to rule out significant injury to the intima.

Posterior Dislocation of the Knee

Posterior dislocation of the knee is associated with popliteal artery injury in half of cases, and arteriography is therefore mandatory.

Treatment

Stabilize the patient, and stop hemorrhage as outlined above. Splint fractures. Do not clamp vessels or use a tourniquet.

Imaging and Disposition

All patients with suspected vascular injury should undego diagnostic imaging. CT angiography (CTA) in now the primary limaging modality for evaluating extremity arterial injuries in both blunt and penetratig extremity injuries. Obtain general or vascular surgical consultation for all penetrating extremity injuries.

Major Venous Trauma

Essentials of Diagnosis

• History of trauma
• Injuries to major venous structures manifested by progressive hemorrhagic shock (not ischemia)
• Venography may aid diagnosis

General Considerations

Trauma to peripheral veins without associated arterial injury usually does not require operative correction; however, disruption of the central large veins (vena cava or its immediate branches, subclavian or iliac veins)—especially where they are not enclosed by dense fascia or muscles—requires prompt operation.

Clinical Findings

Venous injury is usually manifested by hemorrhage, not ischemia. Patients with bleeding from the central veins present with progressive hemorrhagic shock (Chapter 9). Superior vena cava and subclavian vein hemorrhage is usually associated with hemothorax visible on chest X-ray.

In contrast, hemorrhage from the inferior vena cava and iliac vein is more difficult to detect. The only common finding is progressive hemorrhagic shock, and many of these injuries are not suspected before they are discovered at surgery.because most patients are too unstable to allow detailed radiologic evaluation.

Treatment and Disposition

Surgical correction in the operating room is indicated.

Acute Ischemia

Acute Peripheral Ischemia Due to Major Arterial Occlusion

Essentials of Diagnosis

• History of arrhythmia, myocardial infarction, valvular disease, or atherosclerosis may be presen
• Pain, paresthesias, and coolness of affectedextremity
• Pale, mottled, cyanotic limb with decreased or absent pulses
• Angiography confirms diagnosis

Clinical Findings

Acute arterial occlusion may be caused by an embolus, thrombosis, or trauma to an artery. Occlusion leads to distal ischemia, which if not corrected can progress to irreversible tissue damage and necrosis.

Embolic Occlusion

Embolic occlusion is caused by the dislodgment of an intravascular thrombus that travels distally and occludes a smaller artery. The majority of thrombi originate in the heart, but they may come from anywhere within the vascular system. A history of arrhythmia, myocardial infarction, or valvular heart disease suggests an embolic cause for acute peripheral ischemia.

Cardiac Emboli

Cardiac emboli generally originate in the left atrium in patients with atrial fibrillation or mitral valve disease and in the left ventricle in patients with recent myocardial infarction or ventricular aneurysm.

Vascular Emboli

Vascular emboli originate on irregular luminal surfaces of atherosclerotic vessels (eg, ulcerative plaques or aneurysms). These emboli may contain cholesterol in the clot.

Tumor Emboli

Tumor emboli are rare, the most common sources are atrial myxomas.

Thrombotic Occlusion

Thrombosis of an atherosclerotic artery resulting in acute ischemia is uncommon but may occur secondary to plaque disruption and resultant clot formation. A history of peripheral vascular disease, claudication, progressive rest pain, or nonhealing wounds of the distal extremities is suggestive of occlusion secondary to thrombosis, because these patients often lack sufficient collateral flow that can minimize ischemia.

Consequences of Occlusion

Acute occlusion of a previously patent major artery results in ischemia of the nerves, muscles, and skin distal to the occluded site. The severity of symptoms is a function of the adequacy of flow through collateral vascular channels. Within a few hours after persistent and severe occlusion, irreversible anesthesia, paralysis, and tissue infarction occur. During this time, the developing thrombus progressively occludes the distal vessels, reducing the likelihood of restoration of blood flow to distal parts. For these reasons, early recognition and appropriate treatment, before irreversible damage occurs, are critical.

Clinical Findings

Symptoms and Signs

Patients typically present with extremity pain but may also complain of paresthesias and even paralysis of the affected limb. Physical examination may reveal a pale, mottled, cool, or cyanotic limb. Pulses will be reduced or absent, and there may be tenderness to palpation of affected muscle groups.

Imaging Studies

Angiography of the affected limb confirms the diagnosis and is useful for planning surgical intervention. In addition, other imaging modalities such as CTA, MRA, and arterial duplex ultrasonography may be useful.

Treatment

Obtain an immediate general or vascular surgery consultation. Insert a large-bore (≥16-gauge) intravenous catheter. Obtain baseline laboratory studies, including CBC, PT, PTT, and blood chemistries. Also send a blood sample for typing and crossmatching. Begin intravenous heparin at full anticoagulation dosage as soon as possible.

Definitive treatment involves clot lysis through the use of localized intravascular thrombolytics, endovascular or open surgical treatment to avoid lim loss.

Disposition

All patients with acute arterial insufficiency should be hospitalized for management.

Acute Peripheral Ischemia Due to Small-Vessel Occlusion (“Blue Toe Syndrome”)

Essentials of Diagnosis

• Abrupt onset of small painful area on affected digit
• Affected area is tender, cool, and cyanotic
• Asymmetric distribution
• Livedo reticularis may be present

General Considerations

Acute occlusion of a digital artery by microemboli results in ischemia of the affected digit. The most common sources of these microemboli are proximal atherosclerotic plaques or aneurysms. Debris consisting of cholesterol, calcium, and platelet aggregates breaks off from these areas, travels distally through the vasculature, and lodges in the small digital arteries. Other sources of microemboli are clots on prosthetic heart valves and septic emboli from infected heart valves.

Clinical Findings

The diagnosis is based on clinical findings. Patients typically report the abrupt onset of a small painful area on the affected digit that is tender, cool, and cyanotic. If multiple areas are affected, the distribution of lesions is asymmetric. Pulses in the affected extremity are intact. A fine, lace-like rash (livedo reticularis) may be noted. If the patient presents late, gangrene may be present.

Treatment

Treatment is directed at identifying and treating the proximal source of the emboli because recurrence is likely if the source is not removed. Consult a vascular surgeon.

Disposition

Hospitalize the patient for evaluation and treatment of the source of the microemboli.

Acute Peripheral Ischemia Due to Venous Occlusion

Essentials of Diagnosis

• Massive acute swelling of affected leg
• Leg has doughy consistency
• Cyanosis and gangrene may occur
• Color-flow Doppler ultrasound or contrast venography confirms diagnosis

General Considerations

Phlegmasia cerulea dolens (venous gangrene) is a severe form of iliofemoral thrombosis characterized by massive venous occlusion. Rapidly progressive venous hypertension results in diffuse limb swelling to the level of the groin. Distal ischemia occurs secondary to increased venous and tissue pressure. Cyanosis develops and gangrene can occur.

Clinical Findings

Massive acute swelling of the entire leg and cutaneous cyanosis occur early. Distal pulses are diminished or absent. The leg has a doughy consistency, and bullae may be present. Gangrene is a late finding. The diagnosis is confirmed by color-flow Doppler ultrasound or contrast venography.

Treatment

Obtain immediate general or vascular surgery consultation. Begin intravenous heparin at full anticoagulant dosage. The first step in definitive treatment is catheter-directed intrathrombus thrombolysis. If this approach fails, or if the use of thrombolytics is contraindicated, the treatment is thrombectomy.

Disposition

Hospitalize all patients for definitive management.

Acute Visceral (Intestinal) Ischemia

Essentials of Diagnosis

• Severe, poorly localized abdominal pain
• May have history of intestinal angina
• Pain out of proportion to physical examination findings
• Gross or occult intestinal bleeding
• Mesenteric arteriography or CT confirms diagnosis

General Considerations

Significant arterial insufficiency can cause ischemia that results in necrosis of the bowel mucosa. This may progress to full-thickness involvement in 6–48 hours. The extent of necrosis depends on the vessel involved, the adequacy of collateral perfusion, and the degree of hypoperfusion. Untreated severe intestinal ischemia results in intestinal gangrene, diffuse peritonitis, cardiovascular collapse, and death.

Causes

Acute Mesenteric Vascular Occlusion

Acute mesenteric vascular occlusion is the cause of acute visceral ischemia in two-thirds of patients. Occlusion may be due to an embolus from a cardiac mural thrombus or to arterial thrombosis that is the end result of atherosclerotic stenosis of the involved vessel. Some patients give a history of intestinal angina (pain after eating, often relieved by vomiting). Rarely, arterial thrombosis is due to a dissecting aneurysm (aortic or mesenteric artery), connective tissue disease (eg, polyarteritis), or other conditions.

Venous thrombosis occurs occasionally and is associated with portal hypertension, abdominal sepsis, hypercoagulable state, trauma, or use of oral contraceptives.

Nonocclusive Arteriolar Intestinal Ischemia

Nonocclusive arteriolar intestinal ischemia is the cause of acute visceral ischemia in one-third of patients and can occur with cardiac arrhythmia, sepsis, or any prolonged hypotensive state. Splanchnic vasoconstriction causes ischemia secondary to a low-flow state.

Clinical Findings

Obscure abdominal pain and intestinal bleeding in elderly patients should suggest the diagnosis of intestinal ischemia.

Symptoms and Signs

Severe, poorly localized diffuse abdominal pain is invariable in intestinal ischemia. Classically the pain is out of proportion to that expected based on physical examination findings. See Chapter 15 for differential diagnosis of disorders causing acute abdominal pain. With major acute occlusion, the onset of pain is sudden. With nonocclusive ischemia, pain may develop more insidiously.

Usually, few abdominal findings occur early in the disease; later, abdominal distention and tenderness generally occur. Gross or occult intestinal bleeding may be present. Systemic toxicity may precede abdominal findings. Shock and generalized peritonitis occur late.

Laboratory and Other Findings

Laboratory Tests

Laboratory tests show leukocytosis, metabolic acidosis, and elevated serum lactate.

X-Ray Findings

Upright plain films show ileus, absence of intestinal gas, or diffuse distention with an air–fluid level. Ischemia and intestinal necrosis are late findings. Abdominal plain films are abnormal in only 20% of cases. A barium enema (not recommended if vascular disease is strongly suspected) may show “thumbprinting” of the colonic mucosa.

Mesenteric Arteriography

When performed early in the course of the disease, mesenteric arteriography is the definitive diagnostic procedure, because it demonstrates major vascular occlusion, if present. If it is done later, it merely delays necessary surgery and permits development of more extensive bowel necrosis and peritonitis. The catheter inserted in the superior mesenteric artery may be used to infuse vasodilating agents when the cause of disease is nonocclusive arteriolar intestinal ischemia and after the primary occlusive lesion is corrected.

CT Scan

CT scan is useful in evaluating acute visceral (intestinal) ischemia. In addition, it is useful to help exclude other causes of abdominal pain. CT angiography has a sensitivity ranging from 71 to 96% and a specificity ranging from 92 to 94%. CT angiography is noninvasive as well as being readily available compared to standard angiography and can be considered first line imaging modality.

Treatment

Treat hypotension and shock with infusion of intravenous crystalloid solutions and blood, if bleeding is present. Notify a vascular or general surgeon immediately to prepare for surgery. Prompt operation is required to resect necrotic bowel. In some cases, the embolus can be removed or the arterial obstruction bypassed.

Vasodilator drugs may be used as an adjunct to management of the vascular disease in selected cases of nonocclusive ischemia; however, operation is usually required to resect necrotic bowel. Begin parenteral administration of broad-spectrum antimicrobials.

Disposition

All patients with suspected or proved acute visceral ischemia should be hospitalized.

Arterial Aneurysms

Ruptured Abdominal Aortic Aneurysm

Essentials of Diagnosis

• Sudden onset of abdominal or flank pain, pulsatile abdominal mass, and hypotension
• Bedside ultrasound or CT scan with contrast confirms diagnosis

General Considerations

An artery is described as aneurysmal once it reaches more than twice its normal diameter. The exact mechanism behind the formation of an abdominal aortic aneurysm (AAA) is unknown and is likely multifactorial. The belief that aneurysms are due to atherosclerosis alone has undergone serious challenge in the past several years. Risk factors include a family history of AAA, male gender, age more than 70 years, long-term smoking, and systemic hypertension. Ninety-five percent of AAA's are infrarenal with a small amount extending proximally to involve the renal and splachnic vessels. This condition is fairly common, affecting 2–5% of the population over age 60 years. The primary complication of AAA is spontaneous rupture, which carries a high mortality rate of 80%. The chance of rupture increases exponentially as the diameter of the aneurysm increases (Table 40–2).

If the aneurysm ruptures into the peritoneal space, exsanguination and death occur rapidly, usually prior to arrival in the emergency department. When rupture occurs into the retroperitoneal space, a tamponade effect may temporarily control hemorrhage and allow time for diagnosis and treatment.

Clinical Findings

Symptoms and Signs

The classic symptoms of AAA rupture include sudden-onset abdominal or flank pain, pulsatile abdominal mass, and hypotension. However, because this triad is seen in only 50% of patients presenting with AAA rupture, a high level of suspicion must be maintained. The most common misdiagnosis given to patients with AAA is symptomatic nephrolithiasis. Consider the diagnosis of AAA in patients with hypotension and shock of uncertain cause and in patients presenting with myocardial ischemia or infarction. Additionally, patients who have undergone previous aortic bypass grafting can present with gastrointestinal bleeding caused by erosion of the graft into the duodenum and subsequent rupture.

Laboratory Findings

The hematocrit may be normal or low.

Electrocardiogram

The electrocardiogram (ECG) may show signs of myocardial ischemia.

Imaging

Bedside ultrasound is rapidly becoming the standard of care in the diagnosis of symptomatic AAA with reported sensitivities of 100%. Images of the aorta can be obtained by the emergency physician concurrently with the initial history and physical examinations and facilitate the early mobilization of surgeons and additional staff. Ultrasound is particularly useful in the hemodynamically unstable patient who presents with abdominal pain, allowing for rapid diagnosis without transfer to a distant radiology suite.

In the clinically stable patient, CT scanning allows for more detailed imaging and helps exclude other etiologies of abdominal pain. Abdominal X-ray may reveal the presence of an AAA due to calcification of the wall of the aneurysm (70% of AAAs). Aortography is used to investigate the vascular anatomy in the workup for elective (nonemergency) AAA repair.

Treatment

Act quickly. Even if the patient appears hemodynamically stable at the time of initial evaluation, the contained rupture may progress rapidly to exsanguinating hemorrhage at any time.

Treat hypotension and shock (see Chapter 9 for more detail):

1. Begin oxygen, 4 L/min, by nasal cannula or mask.

2. Insert two large-bore (≥16-gauge) peripheral intravenous catheters.

3. Obtain blood for CBC, electrolytes, and renal function tests; type and crossmatch for 10 units of packed red blood cells or whole blood. It is also imperative to replace other blood components such as platelets and FFP with massive transfusions. Measure the hematocrit immediately and at frequent intervals thereafter. Remember that the delay in equilibration of blood volume may keep the hematocrit falsely elevated for 12–18 hours.

4. Give 1–3 L of crystalloid solution intravenously to restore adequate blood pressure, and follow with crossmatched blood. If the initial hematocrit is below 20%, either “universal donor” blood or type-specific blood may be necessary.

5. Insert a urinary catheter, send urine for analysis, and monitor urine output.

Request urgent consultation with a general or vascular surgeon, since emergency surgery is the only definitive treatment.

Disposition

Hospitalize all patients with suspected or documented ruptured AAA.

Visceral and Hypogastric Artery Aneurysms

Essentials of Diagnosis

• Abrupt onset of diffuse abdominal pain
• Signs and symptoms of shock may be present
• CT scan with contrast or visceral angiography confirms diagnosis

General Considerations

Congenital aneurysm occurs in younger patients, whereas atherosclerotic aneurysm occurs more commonly in older patients. The splenic artery is the most commonly involved vessel. Bleeding may be confined to the lesser sac of the peritoneal cavity for the first 24–48 hours. However, free rupture into the general peritoneal cavity invariably causes exsanguination. Rupture is most common during pregnancy. Hypogastric artery aneurysms may rupture into the retroperitoneum or erode into contiguous organs, in which case gastrointestinal bleeding or hematuria occurs.

Clinical Findings

There is abrupt onset of diffuse abdominal pain. Hypotension occurs secondary to blood loss. The hematocrit is low if the bleeding is more than a few hours old. CT scan with contrast is an excellent tool for diagnosis in the hemodynamically stable patient. Peritoneal lavage may reveal gross blood. A plain film of the abdomen may show an aneurysm if it has calcified.

The only definitive diagnostic procedure is selective visceral angiography, which should be performed in the hemodynamically stable patient in whom an aneurysm is not present on a plain film.

Treatment

Start resuscitative measures, including insertion of a large-bore (≥16-gauge) intravenous catheter, nasogastric tube, Foley catheter, and the like (see Ruptured Abdominal Aortic Aneurysm section above and Chapter 9). Draw blood for CBC, and type and crossmatch for 8 units of packed red blood cells or whole blood.

Notify a vascular surgeon at once, because early operation is imperative.

Disposition

Immediately hospitalize all patients with suspected or documented visceral and hypogastric artery aneurysms.

Thoracic Aortic Aneurysm (Aortic Dissection)

Introduction

Essentials of Diagnosis

• Abrupt chest or abdominal pain, often radiating to the back, pulse differential, murmur of aortic regurgitation
• Chest CT with contrast or TEE are imaging studies of choice

General Considerations

Aortic dissection, a rare but deadly disease, is often misdiagnosed at first presentation. Sir William Osler, perhaps the most astute diagnostician of his day, suggested that no other disease could cause as much humility in a clinician. In one study of hospitalized patients with aortic dissection, the correct diagnosis was delayed over 24 hours in 31–53% of patients. An initial misdiagnosis rate of 85% in patients ultimately diagnosed with aortic dissection has been described.

Left untreated or misdiagnosed, aortic dissection is associated with a mortality rate of almost 1% per hour initially, 40–50% in the first 48 hours, and 90% at 1 year. Modern treatment has reduced the in-hospital mortality rate to 10–27% and the 10-year survival rate is now approximately 55%.

The annual incidence of aortic dissection is from 5 to 30 cases per million; incidence varies depending on risk factors of the population studied. Since this disease is often fatal prior to arrival at the hospital, the incidence may be underestimated.

Pathophysiology

Aortic dissection occurs when the intima (the innermost layer of the aorta) tears and allows blood to dissect between the intima and adventitia (the outermost layer of the aorta). Cystic medial necrosis, a weakening of the media (the central layer of the aorta) and hypertension contribute to this process although the exact mechanism is not known. The dissection may propagate either proximally or distally and a second tear often occurs, creating a false lumen through which blood flows freely. Approximately 90% of all dissections occur in the right lateral wall of the proximal ascending aorta, where shear forces are the highest. The next most common site of dissection is just distal to the origin of the left subclavian artery.

Risk factors for aortic dissection include hypertension, trauma, pregnancy, Marfan syndrome, Ehlers-Danlos syndrome, Turner syndrome, cocaine abuse, coarctation of the aorta, bicuspid aortic valve, previous aortic valve replacement, and intra-aortic catheterization.

Classification

The more commonly used Stanford Classification divides aortic dissections into type A dissections, which involve the ascending aorta, and type B dissections, which do not involve the same. The DeBakey system describes three categories (Table 40–3). Stanford type A and DeBakey types I and II usually require surgery, while Stanford type B and DeBakey III may be treated medically. Type A dissections managed medically have been demonstrated to have double the mortality (58% vs 26%) of surgically corrected cases. Type B dissections demonstrated a mortality of only 11% with medical management versus 31% of the surgically repaired patients. Beyond open surgical revision, endovascular repair has become an optimal alternative in selected patients with aortic dissection. Recent studies evaluating endovascular repair with medical management in acute Type B dissections have concluded medical management remains the gold standard in uncomplicated, asymptomatic Type B dissections.

History

The classic description of symptoms of aortic dissection is the abrupt onset of a tearing chest pain radiating to the back. The International Registry of Acute Aortic Dissection (IRAD) found that these classic symptoms are insensitive and nonspecific. Chest pain, for example, was found in only 72.7% of patients while back pain was found in only 53.2%. Only half of patients described the pain as “tearing or ripping,” and abdominal pain was the chief complaint in a third of the patients. The majority (84.8%) of patients described an abrupt onset of pain (when pain was present), and 9.4% of patients in the registry presented with syncope.

Physical Findings

Classic findings in aortic dissection include aortic regurgitation murmur and pulse deficit; however, these were present in only 31.6 and 15.1%, respectively, of patients in the IRAD study. Forty-nine percent of patients were hypertensive while 34.6% were normotensive, and 8.4% presented with a systolic blood pressure below 80 mm Hg. Neurological deficits were noted in 4.7% of IRAD patients, while congestive heart failure was described in 6.6%.

Physical findings are caused by ischemia due to the occlusion of thoracoabdominal aortic branch vessels, systolic failure due to severe aortic regurgitation, cardiac tamponade, or aortic rupture. Ascending dissections may cause cardiac tamponade and hemopericardium. Severe aortic regurgitation is the second most common cause of death after aortic rupture. Rupture of the aorta leads to sudden cardiovascular collapse and death.

Bruits may be auscultated in the carotid, subclavian, or femoral arteries. Painless bilateral lower extremity ischemia has been reported and bowel infarction may be the predominant presentation. Reports of aortic dissections rupturing into the esophagus or bowel and causing gastrointestinal hemorrhage are exceptionally rare.

Neurologic involvement occurs in 4.7–30% of aortic dissections and usually manifests as stroke, although a history of antecedent chest pain is usually elicited. Spinal cord ischemia may cause para- or quadriplegia or anterior spinal cord syndrome, or mimic transverse myelitis. Peripheral nerve involvement occurs rarely, leading to Horner's syndrome, hoarseness, or limb paresthesias.

Diagnosis

Aortic dissection is a life-threatening, time-dependent diagnosis. Patients may quickly become hemodynamically unstable. Clinical suspicion is paramount—if the diagnosis is not considered and pursued aggressively, valuable time will be lost. First line tests are unreliable; a widened mediastinum is present in 61.6%, abnormal aortic contour in 49.6%, and pleural effusion in 19.2% of initial chest radiographs. ECGs are normal 31.3% of the time, with 41.4% revealing nonspecific ST segment or T-wave changes. A critical misdiagnosis can occur in the 18.3% of patients who present with definite ischemic changes on ECG; anticoagulation or thrombolysis can be fatal in patients mistakenly believed to have ischemic coronary syndromes.

The classic gold-standard test for the diagnosis of aortic dissection was aortography. Because it is invasive, time-consuming, and usually requires transport of a potentially unstable patient to a distant angiogram suite, this modality is becoming less favored. MRI, TEE, and CT scanning are all sensitive for the diagnosis. Because of the difficulty in obtaining an MRI or TEE on an emergency basis, CT has become the test of choice for the initial diagnosis of aortic dissection with a sensitivity of 83–94% and specificity of 87–100%.

Difficulties with CT scanning include need for contrast dye administration and limited evaluation of branch vessel involvement and degree of aortic regurgitation.

Transthoracic echocardiography is an insensitive tool for the diagnosis of aortic dissection and is not considered a conclusive test. TEE, on the other hand, is exceptionally sensitive (98%) and specific (96%) for proximal dissections in the hands of an experienced echocardiographer. It can be performed at the bedside and requires no contrast administration. Distal segments of the abdominal aorta cannot be visualized by TEE.

Treatment

Goals of treatment are fourfold:

• Prevent extension of dissection.
• Control pain.
• Involve cardiothoracic or vascular surgeons early.
• Proper disposition of patient.

The primary goal in the normotensive or hypertensive patient is to reduce the shear forces caused by the rapid increase in arterial pressure (dP/dT). This is best achieved by both pulse rate and blood pressure reduction. Typically an esmolol infusion is begun, titrated to reduce pulse rate to 60 beats/min, followed by a nitroprusside infusion titrated to reduce the mean arterial pressure to 60–70 mm Hg. The β-blocker infusion is started first to blunt the reflex tachycardia often associated with nitroprusside infusions. Blood pressure should not be lowered to a level where end-organ perfusion is compromised. If these infusions are not immediately available, intravenous labetalol may be administered, 10–40 mg every 5 minutes until pressure and rate goals are achieved.

Pain control is achieved with intravenous opiates. Fentanyl is often used, 50–100 μg intravenously, due to its short half-life and few hemodynamic side effects.

The hemodynamically unstable patient should receive two large-bore peripheral intravenously; maintain ABCs and consult cardiothoracic or vascular surgeons on an emergency basis to discuss optimal management. The critically ill patient with persuasive indications of aortic dissection may best be managed with immediate surgery without further imaging.

All patients with acute aortic dissection must be admitted into the hospital, mostly to the intensive care unit setting where intravenous infusions and close monitoring may be administered. Surgical consultation is indicated for all dissections regardless of location and initial treatment choices.

Popliteal and Femoral Peripheral Aneurysms

Essentials of Diagnosis

• Symptoms are due to thrombus, embolization, or pressure from an expanding aneurysm
• Pulsatile mass on physical examination (if not thrombosed)
• Ultrasound confirms diagnosis
• Arteriography defines distal arterial circulation

General Considerations

Occlusion or distal embolization of the friable lining of peripheral aneurysms results in symptoms of distal ischemia. Unlike AAA or visceral aneurysm, rupture is rare. The most common locations of peripheral aneurysms are the popliteal artery and, secondarily, the femoral artery. Popliteal aneurysms are often bilateral and associated with AAAs.

Acute occlusion can result in severe distal ischemia. Distal embolization can also result in severe distal ischemia; however, it is often associated with episodes of moderate ischemia that decrease as collateral circulation improves.

Clinical Findings

Symptoms and Signs

Symptoms are due to thrombosis, embolization, pressure from an expanding aneurysm, or (rarely) rupture. There may be an arterial mass in the popliteal fossa or the groin. The aneurysm is pulsatile unless it is thrombosed. Signs of acute arterial occlusion often coexist.

Popliteal aneurysms can cause symptoms (eg, signs of venous obstruction, weakness, and sensory defects) when they compress the popliteal vein or tibial nerve. Rupture of the aneurysm is rare.

Imaging

Plain X-Ray

A rim of calcification may be apparent in the wall of the aneurysm.

Arteriography

Arteriography may not demonstrate the aneurysm if it is thrombosed, but this procedure is generally advised to define the status of the arterial circulation distal to the aneurysm.

Ultrasonography

Ultrasonography is helpful in identifying the presence of an aneurysm.

Treatment

Notify a vascular surgeon, because immediate operation is required when severe distal ischemia has occurred secondary either to acute thrombosis or to distal embolization. Elective operation is recommended for any aneurysm producing compression of adjacent structures as well as for most documented popliteal aneurysms, because the rate of complication is high if these are left untreated.

Disposition

All symptomatic patients should be hospitalized immediately.

Venous Disease

Lower-Extremity Deep Venous Thrombosis

Essentials of Diagnosis

• Unilateral swelling, warmth, and redness of affected limb
• Physical examination is unreliable in diagnosing deep venous thrombosis (DVT)
• Contrast venography or ultrasound confirms diagnosis

General Considerations

DVT results in 600,000 hospitalizations each year in the United States. If untreated, DVT commonly results in pulmonary embolism, thus making it a significant source of morbidity and mortality.

As described by Virchow in 1856, venous thrombosis is predisposed by stasis of blood flow, hypercoagulopathy, and vascular endothelial injury. Specific conditions associated with development of DVT are shown in Table 40–4.

Clinical Findings

Symptoms and Signs

Patients with symptomatic DVT typically complain of unilateral lower-extremity pain and swelling that begins gradually and progresses over days. The described sense of fullness may worsen with standing or walking. Physical examination is of little help in diagnosing DVT and should not be used to exclude diagnosis. Possible findings include unilateral lower-extremity edema, warmth, or erythema. There may be tenderness along the course of the affected vessel, and rarely the clot will be palpable. The time-honored Homans sign (pain in posterior calf with passive dorsiflexion of the foot) has been shown to be unreliable in diagnosing DVT. Because the DVT results in a systemic inflammatory response, the patient may be febrile. Adjunctive testing is required because physical examination is unreliable in diagnosing DVT.

Imaging and Laboratory Findings

Contrast Venography

Although contrast venography remains the gold standard for diagnosing DVT, it has been largely replaced by ultrasonography in most institutions. The advantages of contrast venography include a sensitivity and specificity of nearly 100% and the ability to detect DVTs of the calf, iliac vessels, and inferior vena cava that can be missed by ultra-sound. Its primary disadvantages include its invasive nature, use of contrast material, and availability. Additionally, 5–15% of studies performed are technically inadequate.

Ultrasonography

Ultrasonography is the most accurate noninvasive study for diagnosing lower-extremity DVT, with a sensitivity of 93–100% and a specificity of 97–100% in detecting proximal DVTs. The limitations of ultrasonography are its ability to detect pelvic and calf DVTs (20% of which will extend into the popliteal vein and thigh). The sensitivity for detecting distal (calf) DVT is only 70%.

D-Dimer Assay

D-dimer is formed when fibrin is degraded by plasmin. The testing for the presence of D-dimer is by latex agglutination (least sensitive), whole blood agglutination (bedside, qualitative), and enzyme-linked immunoassay (ELISA) (most accurate). When combined with ultrasound, the whole blood agglutination and ELISA have an almost 100% negative predictive value.

Treatment

For DVT of proximal veins of the thigh, put the patient on bed rest and elevate the limb. Start anticoagulation with intravenous heparin, subcutaneous low-molecular-weight heparin (enoxaparin or dalteparin) or fondaparinux (a factor Xa inhibitor). Alternatively, catheter-directed thrombolytic therapy with streptokinase or urokinase is effective in treating acute DVT less than 7 days old and may prevent postphlebitic complications. Obtain consultation with a vascular surgeon in cases of massive iliofemoral thrombosis. Surgery may be required for certain patients.

Management of calf DVT and the need for hospitalization are controversial. Isolated calf thrombi do not commonly produce pulmonary emboli, although they may propagate into proximal vessels. Traditional treatment has been low-dose heparin (eg, 5000 units subcutaneously twice a day), although some authors advocate serial noninvasive studies (eg, ultrasound) and treatment only if propagation occurs.

Disposition

All patients with proximal DVT should be hospitalized. Because of the association between DVT and malignancy, patients with a new diagnosis of DVT should be referred to a primary-care provider for further evaluation.

Superficial Thrombophlebitis

Essentials of Diagnosis

• Pain, tenderness, induration, and erythema along course of affected vein
• Affected extremity shows only slight to no edema (no other signs of impaired venous return)

General Considerations

Superficial venous thrombosis of the upper extremity is usually iatrogenic, occurring secondary to intravenous catheterization. Lower-extremity superficial venous thromboses may be associated with varicose veins, bacterial infection of surrounding tissues, trauma, or thromboangiitis obliterans. Trauma may play a part in the development of thrombi or may cause recurrences.

Clinical Findings

Pain, tenderness, induration, and erythema are noted along the course of the involved vein, which may feel like a cord. The extremity shows only slight or no swelling, and there are no other signs of impaired venous return.

Septic thrombophlebitis usually occurs following intravenous injections (especially among intravenous drug abusers) and at venous catheter sites. It should be suspected in the presence of the above symptoms or fluctuance along a superficial vein. Fever and rigors may be present. The diagnosis is confirmed if pus can be aspirated from the vein.

Treatment

Cases with No Complications

For uncomplicated superficial venous thrombosis, only symptomatic treatment is required. Neither bed rest nor anticoagulation is indicated. An elastic bandage at and above the level of thrombosis helps to speed remission. Elevation of the leg when the patient is sitting and nonsteroidal anti-inflammatory drugs are also helpful.

Cases with Complications

Obtain general or vascular surgical consultation for all complications. If clinical examination suggests that the thrombosis is approaching the saphenofemoral junction, ligation and division of the saphenous vein are indicated, because pulmonary embolization can result from deep venous involvement.

If septic thrombophlebitis occurs, parenteral antimicrobials are required and the involved segment of vein must be excised or ligated and drained to prevent persistent bacteremia.

Disposition

Patients with mild, localized superficial thrombosis may be discharged. Patients with more serious disease, including suspected or documented septic thrombophlebitis, should be hospitalized.

Upper-Extremity Venous Thrombosis

Essentials of Diagnosis

• Pain and swelling of affected limb
• Occurs in 3% of patients with a central venous catheter
• Examination reveals nonpitting edema, normal skin color, and intact distal pulses
• Contrast venography or ultrasonography confirms diagnosis

General Considerations

Upper-extremity DVT (UEDVT) is much less common (4% of all DVT cases) than lower-extremity DVT but remains an important cause of morbidity because of its association with pulmonary embolism and postphlebitic sequelae (persistent upper-extremity pain and swelling). Nearly 15–33% of cases of UEDVT will be complicated by pulmonary embolism. Mortality from UEDVT is approximately 1% overall, but one study was able to demonstrate that one third of UEDVT patients died within 3 months of a confirmed diagnosis.

The most common risk factor for UEDVT is central venous catheter placement, with clinically significant thrombus formation in 3% of patients with a central line. The second most common category of UEDVT is spontaneous (effort related) thrombosis. Risk factors include repetitive activities involving hyperabduction of the shoulder and aberrant anatomy of the costoclavicular space. Other causes include intravenous drug use, thoracic tumors, and radiation. The most commonly affected site of thrombosis is the axillary–subclavian venous system.

Clinical Findings

Symptoms and Signs

Patients typically present with pain and swelling of the affected limb. The risk factors discussed above may be present. Physical examination may reveal nonpitting edema of the affected side forearm (occasionally the whole arm), normal skin color, and intact distal pulses. Venous cords may be palpable.

Imaging

As with lower-extremity DVT, contrast venography remains the gold standard for diagnosis of UEDVT. However, it is slowly being replaced by ultrasonography, which has been shown to have a high degree of sensitivity and specificity for diagnosing UEDVT. Compression ultrasonography has been shown to have a sensitivity of 96% and a specificity of 94% for UEDVT found along the axillary and subclavian veins. As one moves more centrally in the exam towards the bony structures of the chest, the sensitivity and specificity decrease significantly.

Treatment

Initial treatment involves immobilization, elevation, and the application of heat to the affected limb. This is followed by systemic anticoagulation with intravenous heparin, subcutaneous low-molecular-weight heparin (enoxaparin or dalteparin) or fondaparinux (a factor Xa inhibitor). Other options include catheter-directed thrombolysis and surgical thrombectomy. Frequently surgery is required to correct underlying anatomic defects to prevent recurrence. Consult a vascular surgeon.

Disposition

Hospitalize all patients for definitive management.

Ruptured Venous Varicosities (Varicose Veins)

Essentials of Diagnosis

• Bleeding from varicose veins, usually due to minor trauma

General Considerations

Rupture is an uncommon complication of varicose veins. The skin overlying varices can become thin, and erosion can occur spontaneously or with minor trauma.

Clinical Findings

Bleeding from varicose veins is present and may be brisk.

Treatment

Gentle digital pressure over the bleeding site and elevation of the leg control the initial bleeding. Suture ligature of the ruptured vein may be necessary to definitively stop the bleeding. When the initial bleeding has been controlled, the leg should be wrapped in an elastic bandage or Unna's paste boot. Consult a vascular or general surgeon about elective stripping of varicose veins.

Disposition

Brief hospitalization may be advisable.

Pulmonary Embolism

Pulmonary embolism is an occasional complication of venous thrombosis. It is discussed in Chapter 33.

Arteriovenous Fistula

Essentials of Diagnosis

• Abnormal connection between arteries and veins
• Constant systolic and diastolic (to-and-fro) murmur and palpable thrill at site
• Arteriography confirms diagnosis

General Considerations

Arteriovenous fistulas are abnormal connections between arteries and veins. They may be congenital or acquired. Congenital lesions tend to have more diffuse connections and may involve an extremity. Acquired arteriovenous fistulas—other than those constructed to gain access for dialysis—generally occur secondary to trauma and result from erosion of the artery into a contiguous vein. Other causes include malignancy, infection, and arterial aneurysm. The physiologic effect depends on the size of the communication.

Clinical Findings

A constant systolic and diastolic (to-and-fro) murmur is heard, and a thrill is palpable over most arteriovenous fistulas. Cardiac output may be high if significant left-to-right shunting of blood exists. Patients with congenital arteriovenous fistulas may show increased muscle mass, increased bone length, clubbing, and cyanosis of the involved limb. Polycythemia may also be present.

Complications

Complications include cosmetic deformity due to limb disproportion, congestive heart failure, severe arterial insufficiency, expanding false aneurysm, and hemorrhage. Arteriography delineates the precise outlines of the lesion and may be used for therapeutic embolization.

Treatment and Disposition

Patients with pain, expanding mass, heart failure, or obvious high cardiac output require hospitalization. Others may be discharged from the emergency department and referred to a vascular surgeon or general surgeon.

Other Vascular Syndromes

Thoracic Outlet Syndrome

Essentials of Diagnosis

• Signs and symptoms caused by compression of the neural, arterial, or venous structures at the thoracic outlet
• Hand or arm fatigue with use, especially with abduction of the arm
• Elevated arm stress test may elicit symptoms

General Considerations

Thoracic outlet syndrome comprises a variety of disorders caused by abnormal compression of the neural, arterial, or venous structures at the superior aperture of the thorax (thoracic outlet); the most common is compression of nerve structures against the first rib. Symptoms of dysfunction of branches of the brachial plexus are far more common than symptoms secondary to compression of the axillary–subclavian artery or vein, accounting for approximately 95% of cases. Compression of the eighth cervical and first thoracic nerve roots (C8 and T1) is most common. The second most common pattern is involvement of the three uppermost nerve roots of the brachial plexus, the fifth through seventh cervical nerve roots (C5–C7). Thoracic outlet syndrome is rarely an emergency.

Clinical Findings

Symptoms

The diagnosis is typically made on clinical grounds with patients complaining of hand or arm fatigue with use, especially with activities involving abduction of the arm. More subtly, patients may note wasting of the muscles of the hand.

If symptoms are due to nerve compression, patients may complain of positional paresthesias in the distribution of one or more trunks of the brachial plexus. Compression of C8–T1 nerve roots results in paresthesias in the ulnar nerve distribution, whereas symptoms referable to C5–C7 compression may involve the ear, neck, upper thorax, or lateral aspect of the shoulder. Raynaud symptoms, secondary to compression of sympathetic nerve fibers may also be reported.

Symptoms of venous compression and thrombosis include pain and swelling of the affected limb. Patients with arterial thoracic outlet syndrome with resultant subclavian–axillary artery stenosis or aneurysm formation may present with symptoms of acute arterial occlusion or embolization.

Signs

Physical examination should include the elevated arm stress test (EAST) in an attempt to provoke symptoms. In this test, the patient externally rotates and abducts both arms to 90° with elbows flexed 90° and shoulders braced posteriorly. The patient then opens and closes both hands for a 3-minute period. Patients with thoracic outlet syndrome will complain of the rapid onset of fatigue and heaviness of the arms and are often unable to complete the entire test. Paresthesias may also be reproduced.

In neurologic thoracic outlet syndrome, wasting of the lateral thenar muscles of the hand, weakness of the intrinsic muscles of the hand, and patchy sensory deficits in the distribution of the involved nerve roots may be seen. Reproducible paresthesias during the EAST may be elicited.

Findings in arterial thoracic outlet syndrome include a blood pressure differential in the upper extremities, a bruit with auscultation over the subclavian or axillary artery, and radial pulse deficit on the affected side during the EAST. Findings of acute arterial occlusion or embolization may be found. Thoracic outlet syndrome secondary to venous occlusion or thrombosis may be associated with swelling of the affected extremity and normal pulses.

Imaging

X-Rays

Plain film radiographs of the cervical spine or chest may reveal skeletal abnormalities predisposing to thoracic outlet syndrome (cervical rib, first rib, or clavicle deformity).

Angiography

Angiography may be indicated for evaluation of acute arterial occlusion or embolization.

Ultrasonography

Ultrasonography may be indicated for evaluation of arterial aneurysms or venous thrombosis.

Venography

Venography may be indicated for evaluation of venous thrombosis.

Treatment and Disposition

Patients with neurologic thoracic outlet syndrome can be discharged with a referral to a neurologist or thoracic surgeon. Patients with evidence of a venous or arterial abnormality and stable symptoms should be referred to a vascular or thoracic surgeon. If venous thrombosis or arterial occlusion or embolization is present, the patient should be hospitalized with immediate surgical consultation.

Complications of Percutaneous Transluminal Angioplasty and Retrograde Angiography

Essentials of Diagnosis

• History of recent percutaneous procedure
• May see complications at puncture site or signs and symptoms due to thrombosis or embolization

Increasing number of patients are undergoing percutaneous transluminal angioplasty (balloon dilatation of the arteries) and angiography via the femoral artery. These patients are observed for the development of immediate complications but usually discharged from the hospital within 24–48 hours and may subsequently present to the emergency department with complications (Table 40–5).

Hospitalize the patient and obtain prompt vascular or cardiothoracic surgical consultation, because many of these complications require surgical treatment.

Intra-Arterial Injection of Drugs

Essentials of Diagnosis

• History of parenteral drug injection
• Severe burning pain distal to injection site

General Considerations

Inadvertent or intentional intra-arterial injection of drugs can cause intense vasospasm followed by arterial occlusion, with distal gangrene as a possible result. This is commonly known as a “hand trip” by intravenous drug abusers. Vasospasm may occur while the drug is being given, or the reaction may be delayed. Unfortunately, many patients with delayed reactions fail to seek medical attention until ischemia is advanced.

Clinical Findings

There is a history of therapeutic or illicit drug injection by the parenteral route. Severe burning pain in distal arterial distribution is followed by intense vasospasm. If the vasospasm has been prolonged, gangrene of the fingers or entire hand may occur even though the arterial vasoconstriction subsequently resolves.

Treatment and Disposition

Hospitalize the patient, and obtain vascular surgical consultation. If the needle is still in place, irrigate distally with heparinized saline. Start systemic anticoagulation with heparin. Systemic vasodilating agents may be necessary to treat the intense vasospasm. Intra-arterial injection of vasodilators (eg, reserpine) is not usually beneficial. If sympathetic nerve block is indicated because of persistent severe peripheral ischemia, consult an anesthesiologist or vascular surgeon.