Is it important to differentiate whether the vascular malformation is arteriovenous, venous, or lymphatic? Are there comorbidities to expect?

How does this diagnosis influence the anesthetic technique? What if it is characterized as a “slow-flow” lesion?

What are the anesthetic issues if alcohol embolization is planned? Is there a difference between the use of alcohol and Sotradecol (sodium tetradecyl sulfate) as a sclerosing agent? What are the risks of using platinum coils? How does it affect your anesthetic management?

How painful will this procedure be in the perioperative period, and how will it influence your postoperative management in the PACU?

The various kinds of vascular malformations arise from different vascular tissues and therefore have different characteristics that are important for the anesthetic technique chosen and the success of the radiologist’s intervention. The broad categories from a blood flow perspective are either fast-flow or slow-flow lesions. Arteriovenous malformations are fast flow, and venous, lymphatic, capillary, and mixed lesions are typically slow flow. The flow characteristics are particularly important because they affect how volume, ventilation, and hemodynamics are managed and may contribute to patient comorbidity, e.g., high-output cardiac failure, which is also relevant to the anesthetic technique chosen. Specifically for lymphatic malformations, accumulated, static lymph in the malformation typically results in bleeding and infection as well as enlargement, disfigurement, and distortion of adjacent structures [1].

As a result of increased volume and pressure within the malformed lymphatics, leakage and fluid accumulation can occur in contiguous areas or areas of upstream impaired drainage. Ascites and pleural and pericardial effusions can be of significance. Peripheral edema and hypoproteinemia are of anesthetic significance because they affect volume of distribution and drug binding. Infection commonly accompanies areas of skin breakdown with oozing of proteinaceous fluid. Pulmonary consequences such as restrictive and obstructive lung disease can occur with large lesions.

Very often, high-flow lesions are not autoregulated, and therefore hyperventilation, while acting to vasoconstrict blood vessels in general, may actually enhance imaging of non-autoregulated vessels. Adequate intravascular volume and depth of anesthesia as well as preservation of cardiac output is necessary in order to provide sufficient perfusion pressure and transit time to the intended area of embolization. Lymphatic malformations are typically slow-flow lesions, and therefore the anesthetic technique influences the transit time less.

The embolization material is important as well. Absolute alcohol has the locally desirable effects of sclerosis, but the undesirable effects locally of skin blistering and nerve injury. In addition, constitutional effects of nausea and intoxication are significant considerations in younger age groups. Sodium tetradecyl sulfate, or Sotradecol, has the advantage of less severe tissue necrosis, hence less severe postoperative swelling and pain and much less nausea than ethanol. Because of tissue destruction, it is still a significant concern for hemoglobinuria and skin blistering. There is no intoxication because it is a detergent. Ethanol may also cause pulmonary arterial hypertension [2–4]. While various types of coils and glues [5] have been used (which may result in paradoxical or misplaced embolization), alcohol or Sotradecol is now more commonly utilized.

The goal of sclerotherapy is to produce endothelial necrosis; therefore, pain typically accompanies successful treatment in the perioperative period. The pain is more marked with ethanol than with Sotradecol. This may be superimposed on the chronic pain that these patients often have [1]. Ethanol causes more tissue swelling and edema than Sotradecol. Therefore, patients may require increased doses of opioids for adequate analgesia. Regional techniques are often relatively contraindicated because of the risk of vascular proliferation in treatment areas.

What anesthetic technique will you choose? Does this patient need invasive monitoring or are standard noninvasive monitors acceptable?

What ventilation management strategy will you choose? Will ventilation affect the radiologist’s treatment? What if this was a venous malformation? An arteriovenous malformation with high flow?

How will you plan for IV fluid management with regard to the quality of imaging? Effects of contrast/sclerosing agents on the kidneys? What will you do if the urine, which previously had been clear and yellow, is now rose color? Anything you can do diagnostically? Therapeutically? Recommendations for perioperative monitoring?

What perioperative concerns do you have about the method(s) chosen to embolize this patient (alcohol, Sotradecol, foreign bodies, e.g., platinum coils; cyanoacrylate glue)?