Hematoma

A localized hematoma remains the most common complication in any endovascular procedure. The adverse consequences range from minimal to life threatening if retroperitoneal space is involved. A high puncture level above the inguinal ligament is an important risk factor for the development of retroperitoneal hematoma.

A hematoma will cause pain and swelling, while a retroperitoneal hematoma may result in flank/abdominal pain, a painful/cold limb, loss of peripheral pulses, acute anemia, and hemorrhagic shock in extreme cases. Management with local compression, serial groin/flank checks marking hematoma growth, and frequent follow-up of hemoglobin is the first line of treatment. There should be a low threshold to get CT of the abdomen and pelvis in patients with falling hematocrit and physical signs consistent with shock. Progressive blood loss and hypovolemic shock necessitate reversal of anticoagulation, blood transfusion, and aggressive management of shock. Continued bleeding with evidence of retroperitoneal bleeding requiring multiple transfusions may necessitate surgical/endovascular management to explore the arteriotomy site for active bleeding and repair.

Long-term complications of these hematomas include compressive femoral neuropathy/lumbar plexopathy causing weakness, numbness, and pain.

Pseudoaneurysm

A pseudoaneurysm is a contained vascular rupture (hematoma) within the elements of the surrounding tissue at the arteriotomy site that creates turbulent flow between the vessel and soft tissue space. Diagnosis is suspected based on a groin examination that shows ecchymosis, a pulsatile palpable mass, and/or bruit. If left untreated, the pseudoaneurysm can serve as a source of emboli, infection, or rupture [10]. Duplex ultrasound shows a hypoechoic region, either lobulated or cystic, adjacent to the artery with color flow map that demonstrates turbulent, swirling flow (“yin-yang sign”) [11]. Obese patients may need CT or MR angiography for diagnosis. Retroperitoneal extension may be investigated using a CT of the abdomen to identify the arterial injuries.

Management and treatment of a pseudoaneurysm depends on the size, location, and progression of the lesion. Smaller pseudoaneurysms (<2 cm) can be observed with frequent Doppler exams. Larger pseudoaneurysms are treated using ultrasound-guided compression (USGC), ultrasound-guided thrombin injection (USGTI), or less commonly open surgical repair.

Arteriovenous fistula (AVF)

Iatrogenic fistulas (communication between femoral artery and vein) are a rare VAS complication. Most cases resolve spontaneously, but rarely long-standing fistula may give rise to cardiac failure, limb edema, or degeneration of the artery. Treatment should be pursued using USGC or endovascular or open surgical repair.

Infection

Infection is a low-frequency complication in percutaneous interventions (including diagnostics, angioplasty, stenting, and/or embolization procedures). There is no need to use prophylactic antibiotics [12].

Blood pressure management

Blood pressure (BP) should be frequently monitored along with the neurologic examination for the first 24 h in patients receiving mechanical thrombectomy. BP parameters are similar to management following IV thrombolysis, although experts suggest different titration strategies based on the extent of recanalization [18, 19]. Sudden changes in BP with worsening of neurological examination should immediately be investigated for spontaneous intracranial hemorrhage. In the event of full recanalization, BP should be kept in the systolic 120–140 mmHg range to minimize the risk of reperfusion hemorrhage. Those receiving mechanical thrombectomy alone with only partial recanalization may benefit from a higher BP target—up to 180/105 mmHg.

Intracranial hemorrhage

Small volume intracranial hemorrhage (ICH) after thrombolysis is frequently seen on follow-up imaging studies (Fig. 3.1). This may be a marker of early successful recanalization that has been shown to be associated with reduced infarct size and improved clinical outcome [20]. On the other hand, deterioration in neurological examination with ICH or symptomatic ICH (sICH) is a feared complication that results in worsened outcomes and increased mortality. This risk may increase with longer onset-to-reperfusion times (>270 min) [21]. In addition, more severe deficits at presentation (NIHSS > 20), the presence of cerebral edema on initial imaging, involvement of >1/3 of the MCA territory, as well as deviation from thrombolysis protocols may increase the risk of sICH. Guidelines regarding management of sICH following thrombolysis/thrombectomy are currently lacking, and empirical treatment is done based on the clinician’s judgment. Some strategies are based on fibrinogen levels—if <100 mg/dl, cryoprecipitate is administered at 0.15 U/kg. Alternatively, fresh frozen plasma along with platelets (6–8 U, if platelet dysfunction is suspected) is relied upon at some centers [22]. A neurosurgical consultation should be obtained for potential decompression or clot evacuation in the event of a life-threatening decline, while remaining vigilant for secondary cardiorespiratory failure. Seizure prophylaxis in the event of sICH is not generally recommended, although this area also is lacking in high-level evidence.

Intracranial Pressure (ICP) management

Large hemispheric infarcts complicated by hemorrhagic conversion or cerebral edema can result in elevated ICP. There is no benefit in routine ICP monitoring as patients may develop pupillary abnormalities and signs of brainstem compression even with normal ICP values [23]. Patients with high NIHSS (>15) on presentation and large territorial involvement due to a large vessel occlusion are at risk for developing malignant MCA infarction.

While sICH generally occurs in the first 24 h after presentation, cytotoxic edema and ICP elevation often peak 3–4 days after the initial injury. Patients with large hemispheric infarcts that involve >50 % MCA territory with greater than 66 % perfusion deficit are at risk of developing life-threatening malignant brain edema within 24 h [24]. Hemicraniectomy provides definitive treatment for malignant brain edema while medical management is at best temporizing in such situations.

Antithrombotic use post-thrombectomy

Initiation of anticoagulation and/or antiplatelet agents is an individualized decision post-thrombectomy given the absence of formal guidelines. Initial studies and clinical trials (NINDS and PROACT II) excluded patients with infarct volume >1/3 MCA territory due to concerns of hemorrhagic reperfusion injury. In general if reperfusion hemorrhage has occurred, antithrombotic therapy should be held for 1–4 weeks.

BP management

Aneurysmal rupture is associated with a sympathetic surge and resultant increase in blood pressure. The incidence of rebleeding is 5–10 % in the first 72 h. The exact blood pressure beyond which the risk of rebleeding significantly rises is not clear; however, systolic blood pressures up to 160 mmHg or mean blood pressure up to 110 mmHg is generally acceptable. Short-acting BP medications (e.g., labetalol or hydralazine) may be used intermittently or continuously (e.g., nicardipine). Premorbid blood pressure should be taken into consideration while hypotension should be avoided. Hypertension that is accompanied by bradycardia should raise concern for increased intracranial pressure and may require osmotic therapy to treat cerebral edema or extraventricular diversion of cerebrospinal fluid if hydrocephalus is diagnosed.

BP is commonly elevated in the acute phase following aSAH. After the aneurysm is secured, strict BP control is not required. BP goals should be relaxed to allow for cerebral perfusion. Strict BP control may mask the early warning signs of vasospasm during which BP typically increases. BP should be titrated in the event of signs and symptoms of end-organ damage.

Vasospasm

Arterial narrowing or vasospasm as evidenced on angiography is seen between 3 and 21 days post-aneurysmal rupture with the peak being around 7–10 days. It is seen in two-thirds of patients presenting with aSAH, and in approximately 30 % of such cases, arterial vasospasm results in focal neurological deficits also known as delayed cerebral ischemia (DCI). If not treated appropriately, DCI can result in cerebral infarction—a feared complication that can greatly affect the long-term outcome. Vasospasm risk increases with the thickness of SAH as measured by the modified Fisher scale [30]. Nimodipine (60 mg every 4 h), a dihydropyridine calcium channel antagonist, is the only agent shown to reduce cerebral ischemia and mortality when used prophylactically. It is used for 21 days in aSAH. Sometimes due to its hypotensive effect, it may need to be given at a reduced dose but greater frequency (30 mg every 2 h).

In the event of neurological worsening, potential confounders (fever, hypotension, hyponatremia, seizures, etc.) should be ruled out. In parallel, vasospasm should be investigated using catheter angiography. While catheter angiography is the preferred modality in cases at high risk for vasospasm where intra-arterial intervention may be required, CT/MR angiograms with/without perfusion maybe reasonable alternatives in select situations. CT/MR angiograms are less sensitive in detecting mild–moderate vasospasm compared to catheter angiography. While planning for a catheter angiogram, hemodynamic augmentation should be attempted using a fluid bolus with/without a vasopressor (Neo-Synephrine or norepinephrine) in order to up-titrate mean arterial pressure by 15–20 %. Occasionally, an inotropic agent may be useful in this setting. If vasospasm on angiogram is diagnosed, it may require treatment with intra-arterial vasodilator agents or angioplasty. Only the induced hypertension component of the conventional “triple H” therapy should be used as hypervolemia and hemodilution do not improve cerebral blood flow or oxygen delivery and may even cause cardiopulmonary complications.