(1)
Nuffield Department of Surgical Sciences, Oxford University, Oxford, UK
Preamble
Out of a clear blue sky, when least expected, they come. You set sentries against them and do not send invitations, but still they come. We all have to accept that complications are an inevitable component of what we do. This fact does not exonerate us from the duty to maintain all possible preventative precautions and to instigate a process of objective analysis of any adverse event. For all concerned, patients and medical staff, understanding the mechanism of a medical accident is important. Discussion and peer review of the circumstances surrounding a complication is needed to correct any system failures, plan any appropriate changes in practice and alert others of the danger.
For the novice, complications are disturbing, and it is the role of seniors to protect them as much as possible by ensuring that they work within their capabilities and with appropriate supervision and guidance. In my department, we review all procedures at a weekly meeting of practitioners, trainees, nurses and radiographers. This ensures that everyone in the department knows if something has gone wrong, we are all alerted to any equipment or system failure as quickly as possible. Decisions are taken concerning immediate remedies and how far the lessons learnt need to be escalated, i.e. to the rest of the hospital, to specialist network groups or to the wider medical community through statutory agencies and/or publications. It gives the junior members a chance to hear the views of colleagues not directly involved in a particular complication and has proved enormously beneficial. In the event of a complication resulting in serious morbidity to a patient, it is my practice to meet with all the involved staff, as soon as the situation permits, to talk about what happened. This is to ensure that young people do not leave the hospital with a sense of culpability for what was an accident or the result of several contributing factors whose combined effect could not be anticipated.
In the last few years, an objective reality has emerged about this subject with doctors now expected to audit their practice in terms of the efficacy and safety of the treatments they perform. This is a relatively simple process, particularly when it becomes routine, and benchmark data are now published against which a practitioner can compare their personal audit figures. Appraisal and revalidation processes give us a chance to ensure that we are working to the highest possible standards of safety; we need that knowledge to face the consequences of complications.
20.1 Generic and Specific Complications
Complications can be divided into generic groups, which are common to endovascular treatments in general and those that are specific to treatments of a particular condition. In addition, some complications are caused, or more likely to occur in a particular patient because of medications they are taking or a pre-existing condition, e.g. dissection in Ehlers–Danlos syndrome. Some complications are specific to the technology used. For example, embolisation with particles may cause alopecia, retinal blindness or cranial nerve damage, angioplasty vessel dissection, sclerotherapy systemic toxic and adhesive liquid embolic agents stuck catheters.
When formulating a list of possible complications, it is helpful to separate complications due to endovascular navigation and those associated with treatments for specific conditions, as set out in Table 20.1. The purpose of the table is to provide a framework for thinking through the things that can go wrong prior to a procedure so that a checklist of precautions can be generated, and the operator and assistants start each operation prepared. This process is second nature to most interventionalists but tends to concentrate on complications associated with the specific techniques they plan to use to treat a particular patient. Generic complications associated with angiography and endovascular navigation are often forgotten.
Table 20.1
Examples of generic and specific complications
Generic | Specific conditions |
|---|---|
Complications due to vascular access | Aneurysms |
Haematoma/Bleeding | Thromboembolic events |
Nerve damage | Rupture |
Pseudoaneurysm | Implant misplacement or migration |
Acute artery thrombosis | Vasospasm |
AV fistula | Hydrocephalus |
Infection | Aneurysm regrowth |
Manipulation of catheters and guidewires | AVM and AVFs |
Dissection | Collateral embolisation |
Embolism | Procedural bleeding |
Perforation | Delayed haemorrhage |
Haemoptysis | |
Complications due to drugs | Angioplasty and stenting |
Nephropathy | Ischaemic events |
Allergic reactions | Dissection |
Anaphylaxis | Early thrombosis |
Thrombocytopenia | In-stent stenosis |
Complications due to ionising radiation | Tumour embolisation |
Erythema | Swelling |
Alopecia | Skin necrosis |
Teratogenicity effects | Nerve damage |
Secondary haemorrhage |
Enquiry about patient-specific factors and the likely effects of known comorbidities, e.g. allergies, anticoagulants, etc., is part of the standard pretreatment work-up. Its purpose is primarily to ensure that the appropriate treatment is given, but a major component of this process is the prevention of iatrogenic disease. One final point is that we do not usually include intracranial infections on our checklist because they are so rare (except at puncture sites). The low incidence of serious infection in interventional neuroradiology occurs despite the fact that we often deploy intracerebral foreign bodies in sterile but not class 1 or 2 theatre conditions [1]. However, rarity is not a reason for complacency when planning and using facilities, and infection control is a duty of all medical professionals.
20.1.1 Severity of Complications
Complication can also be separated according to their effect on the patient and whether their consequences are transient or permanent. The Society of Interventional Radiology clinical practice guidelines recognise two classes and six categories of outcomes after a complication [2]. These are:
- 1.
Minor Complications:
- (a)
No therapy, no consequence
- (b)
Nominal therapy, no consequence; includes overnight admission for observation only
- (a)
- 2.
Major Complications:
- (c)
Require therapy, minor hospitalisation (<48 h)
- (d)
Require major therapy, increased level of care, prolonged hospitalisation (>48 h)
- (e)
Permanent adverse sequelae
- (f)
Death
- (c)
This is useful shorthand for service audits and highlights that the clinical effect of a complication is an unpredictable spectrum of severity and thus difficult to present in pretreatment discussions with patients.
20.2 Complications Caused by Catheter Angiography
20.2.1 Complications at the Puncture Site
The femoral artery is the more common site of endovascular access, and the following section concentrates on complications at this location, but similar adverse events can be expected when other arteries are punctured. Venipuncture is less likely to cause more than minimal local bleeding, but needle puncture and injections can cause local trauma including nerve damage.
20.2.1.1 Groin Haematoma
This is the commonest of all complications associated with catheter angiography by femoral artery puncture. A minor haematoma with bruising and moderately severe discomfort occurs after about 5% of studies and probably some degree of periarterial haematoma in 100%. A major haematoma can be defined as one requiring transfusion, surgical evacuation or delay in discharge from hospital. These are rare after diagnostic angiograms, i.e. 0.5% but occur after about 3% of interventional procedures [3].
Causes and prevention: Anticoagulation, large catheters or sheaths (>6 F) and increasing patient weight are risk factors. Larger catheters are associated with small haematomas and high patient weight with large haematomas, the latter presumably because detection and compression are more difficult [4].
Femoral artery puncture should be performed below the inguinal ligament. After higher punctures, it is more difficult to control the bleeding point and retroperitoneal bleeding is more likely. If the puncture is too low, it is more likely to be complicated by an arteriovenous fistula (this is because of the relative position of the femoral artery and vein). Adequate time for compression prevents these complications.
The use of closure devices is associated with an increase in complications at the puncture site. Despite this, they are widely used because of their convenience, especially after procedures using anticoagulation [5]. The incidence of minor complication is 2–8% and major complications 1–5% for the range of device in current use [6].
Clinical signs: Symptoms due to haematoma vary from mild groin discomfort to considerable pain, swelling and skin necrosis. Haemorrhage may be severe enough to reduce plasma haemoglobin levels, and if retroperitoneal extension is suspected, a CT scan should be performed.
Treatment: Manual compression concentrated as accurately as possible at the puncture site is best instigated early. Once overt bleeding has stopped, the margins of the haematoma should be marked and monitored every 15 min for 2 h and then hourly to detect any continued deep bleeding. If the haematoma is very large, surgical exploration of the groin should be considered and may be required to evacuate the haematoma. Limiting the degree of swelling is important to reduce the risk of secondary infection and prevent skin necrosis and ulceration.
20.2.1.2 Retroperitoneal Haematoma
This is a rare but potentially fatal complication (incidence of 0.15%) that carries a significant morbidity. The risk factors are the same as groin haematoma, i.e. anticoagulation or antiplatelet drugs and a high double wall femoral artery puncture.
There are two patterns of haematoma spread, either along iliopsoas (which may cause a compression neuropathy) or true retroperitoneal spread (which can lead to haemodynamic instability and compression of the ipsilateral kidney).
Clinical findings: Patients complain of lower abdominal or thigh pain. The groin and lower abdomen are tender, and there may be quadriceps weakness and numbness over the thigh. Tachycardia, systemic hypertension and other signs of active bleeding may progress to cardiac instability.
Treatment: Emergency CT is indicated as soon as this complication is suspected and a high-intensity observation regime instigated. Any anticoagulation or antiplatelet prophylactics treatments should be stopped and appropriate antidotes to reverse their effects given. Blood haematocrit, haemoglobin, bleeding time and platelet function should be assessed. Consider giving haemostatic drugs such as tranexamic acid and fresh platelet or whole blood transfusions. Surgical decompression and arterial repair are indicated if the patient develops neurological signs or becomes haemodynamically unstable.
20.2.1.3 Pseudoaneurysms and Arteriovenous Fistulas
The incidence of these complications after femoral artery puncture is 1% and 0.3% respectively. The cause is a failure of compression to close the puncture site so that a circulation is established within a haematoma or to the femoral vein. Pseudoaneurysms usually develop early (24–48 h) and the rare arteriovenous fistulas later (1–2 weeks) [7].
Clinical findings: Failure of a haematoma to resolve, a pulsatile mass and persistent local swelling are present. A thrill or bruit suggests the diagnosis, which should be confirmed by ultrasonography. A characteristic sound due to the circulation within the sac of a pseudoaneurysm is described as ‘yin/yang’.
Treatments:
- (a)
Pseudoaneurysms: Intervention is usually required because once established, the sac is unlikely to thrombose spontaneously. They are effectively treated by ultrasound-guided compression or thrombin injections [8]. Ultrasound-guided compression is the first-line treatment. It is performed using the ultrasound probe to compress the aneurysm neck, but it may take 20–120 min of firm compression and is not as reliable as percutaneous injection of thrombin (500–1000 units), which is made into the sac (under ultrasound imaging control) [9].
- (b)
Arteriovenous fistulas: Usually require surgical repair but a covered stent is an endovascular treatment option.
20.2.1.4 Femoral Artery Thrombosis
This is a serious but fortunately rare complication leading to acute arterial ischaemia in the lower limb. It is usually caused by pre-existing atherosclerosis of the femoral artery, use of occlusion devices, dissection or hypercoagulability states.
Clinical signs: Symptoms may be minimal, but the limb may be cold and pulseless. Early diagnosis is important, and a regime of observations that includes assessing the distal arterial pulses should be part of routine postangiography patient care.
Treatment: Emergency thrombolytic therapy and/or mechanical thrombectomy, angioplasty and, if these measures fail to restore the circulation, surgical bypass should be considered.
20.2.1.5 Infections of the Percutaneous Puncture Site
Puncture site infections are rare and associated with comorbidities such as diabetes, obesity and impaired immunity. Other risk factors are early repeat arterial punctures and the use of closure devices, which involve residual implants.
Treatment: Antibiotics initially and, if an abscess develops, surgical drainage or debridement may be required.
20.2.1.6 Entrapped Closure Devices
This complication occurs when a closure device fails to operate properly and becomes entrapped. Management usually requires surgical exploration, arteriotomy and retrieval.
20.2.1.7 Complications at Other Access Sites
A haematoma in the neck following carotid or jugular puncture is a potentially life-threatening complication because it can obstruct the upper airway. Special care should be taken to ensure adequate haemostasis when common carotid artery punctures are performed, especially for procedures involving anticoagulation. This complication may require emergency intubation or tracheostomy.
20.2.2 Complications Caused by Catheters and Guidewires
20.2.2.1 Dissection
This is caused by intramural contrast injections or by guidewire or catheter tip penetration of the vessel intima. It is more likely in patients with pre-existing arterial diseases, e.g. atherosclerosis, Ehlers–Danlos syndrome (particularly type IV) and Marfan syndrome. Though minor arterial wall damage is probably common, dissection causing arterial occlusion is rare (about 0.1–0.4% of angiograms) and symptoms as a result, even rarer [10]. It should be suspected when contrast fails to clear from the site of a test injection.
Prevention: Since the operator causes this adverse event, it is less likely if catheter and wire manipulations are performed carefully and gently. The operator must ensure good backflow into catheters before injecting contrast media and observe a small test injection after catheters are positioned and prior to fast injections for angiograms.
Treatment: Once dissection is detected, its management is to retrieve the catheter or wire, assess the extent of any flow reduction and, if this is compromised or there is evidence of an extending flap, place a stent [11].
20.2.2.2 Thromboembolism
This is the most common cause of a new neurological deficit after catheter angiography. It occurs during about 1.0–2.6% of cerebral angiograms and results in permanent neurological deficits in 0.1–0.5% of patients [12]. The risk is greater in patients over 60 years, those with a history of cerebral vascular disease (the frequency in angiograms for TIAs or previous stroke is about 4.5%) or sickle cell disease and during long and complex procedures [13]. Emboli include blood clots, atheromatous plaque, cholesterol, air or foreign materials.
Prevention: A meticulous technique will prevent this complication. The commonest preventable cause is blood clot forming in catheters and delivery devices (the brain is surprisingly tolerant to injected air). Flush saline solutions should therefore contain heparin (500–2500 units per litre), and closed systems are used to draw up and inject all liquids. In high-risk procedures, pre-treatment with antiplatelet agents and higher levels of periprocedural anticoagulation should be considered and blood tests performed to confirm effective anticoagulation (i.e. activated clotting time (ACT) estimation) and antiplatelet activity.
Treatment: When thromboembolism is identified (e.g. new occlusion of a cerebral artery), the first step is to establish the extent of collateral support by angiography and, if not contraindicated, give a thrombolytic or antiplatelet agent. The initial priority is to establish the effect of any identified embolus on cerebral perfusion; this may require additional imaging (see below, complications during aneurysm treatments). The next steps will depend on the response to these measures.
20.2.2.3 Vessel Perforation or Rupture
Can be caused by guidewires and catheters, but this is extremely rare during diagnostic angiography and is usually associated with interventions such as angioplasty, balloon-assisted coiling and distal catheterisation during treatments of arteriovenous malformations. It will be discussed in the circumstances of specific treatments.
20.2.3 Reactions to Radiographic Contrast Medium and Periprocedural Drugs
20.2.3.1 Allergic Reactions
In the past, radiographic contrast was a frequent cause of allergic reactions during angiography. They occur less often after intraarterial than intravenous injection, and the incidence has been substantially reduced by the introduction of nonionic contrast media. Mild reactions (tachycardia, hypertension, nausea or vomiting) occur in 3/100 and severe reactions (skin rash, oedema, bronchospasm, hypotension) in 1/2500 intravenous injections and are fatal in about 1/170,000 patients.
Reactions to other procedural drugs are now more common, and adverse reactions have been reported to almost all the drugs we commonly use. These include lignocaine, heparin, aspirin, atropine, papaverine, nimodipine, abciximab, protamine sulphate and chymopapain. An important reaction to diagnose is thrombocytopenia that may occur after heparin administration. A transient fall in the platelet count 1–4 days after initiation of treatment in common but a more serious autoimmune-mediated response occurs in 3–5% of patients exposed to heparin and was discussed in Tutorial 5. Heparin-induced thrombocytopenia (HIT) is caused by antibodies against the heparin platelet factor-4 complex and occurs between days 5 and 10 after starting heparin [14].
Prevention: Pretreatment of patients with allergic histories may be given using prednisolone (e.g. 40–50 mg given 12 and 2 h before the procedure).
Treatment: Minor reaction should be treated with antihistamine drugs and IV fluids, and more severe reactions with adrenalin, oxygen, high-dose corticosteroids and ventilation support.
20.2.3.2 Toxic Effects
Toxic effects are dose related, but an individual’s response to a drug varies. Two agents will be considered for their potential toxicity during catheter angiography.
- (a)
Local anaesthetic agents: Lignocaine, like other amide local anaesthetic agents (prilocaine, mepivacaine and bupivacaine), can cause dose-related side effects as well as hypersensitivity or idiosyncratic reactions. These involve the central nervous system (excitation, confusion, blurred or double vision, convulsions and respiratory depression) and the cardiovascular system (bradycardia, hypotension and cardiac arrest).Related posts:
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