A case of critical ischemia presenting with pain and finger gangrene in the right hand of a patient on hemodialysis is presented. The multifactorial origin of ischemia and its pathophysiology are discussed, together with the most appropriate diagnostic approach. Innovative endovascular treatment of such conditions is also described.
Nephrol @ point care 2015; 1(1): e35 - e38
Article Type: PATIENTS @ POINT OF CARE
- • Accepted on 18/03/2015
- • Available online on 28/04/2015
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Mr. M is a 58-year-old man. He developed type 1 diabetes mellitus when he was 20 years old, and started hemodialysis at the age of 52. The last 3 years have been a real ordeal: angina pectoris resolved with a triple coronary bypass graft, an isolate episode of transitory brain ischemic attack, multiple laser treatments of retinopathy, gangrene and repeated infections of the feet that, after several unsuccessful attempts at revascularization and removal of necrotic tissue, led to a bilateral below-the-knee amputation of the legs.
Now Mr. M is in a wheelchair and hopes to get a limb prosthesis soon, to be able to drive and to go back to work in his company. He does not give up and wants to live.
In September 2010, during the dialysis sessions, he began to feel pain in his right hand. Mr. M had dialysis through a proximal radiocephalic fistula. The fistula flow was estimated to be approximately 275 ml/min, therefore a steal effect was excluded, and the symptoms were underestimated. In October, due to an accidental trauma, an ulcerated lesion appeared on the fourth finger of his right hand (
The first lesion: an ischemic ulcer of the fourth finger with surrounding infection.
Evolution of gangrene of the distal phalanx.
Angiographic study of the forearm showing a normally functioning fistula, obstruction of the distal radial and ulnar arteries, diffuse disease of the blood vessels of the hand. AVF = arteriovenous fistula.
Despite these treatments, in the following weeks, the situation did not improve: The pain persisted, surgical wounds did not heal but were reinfected and showed dehiscence (
Dorsal view of the hand after amputation of the fourth finger, showing dehiscence of the wound.
Palmar view of the hand after amputation of the fourth finger.
The presence of an arteriovenous fistula that steals blood from the natural antegrade flow
The presence of disease of the great vessels of the upper limb, which prevents the blood to reach the hand directly, diverting the flow onto small collateral branches with high hydraulic resistance.
The presence of obstructive disease of the small vessels of the hand (arches, metacarpal and digital vessels) which is a further obstacle to the final distribution of blood flow to the tissues.
In our experience (over 130 ischemic hands), only rarely have we found a single cause of critical hand ischemia; in most cases there is a combination of several factors that determine the poverty of the blood supply to the distal tissues.
The pathophysiology of ischemia in Mr. M’s hand was complex, because he presented simultaneously with all of the possible causes. The proximal radiocephalic fistula was a standard hemodialysis fistula, its flow was not pathological and, by itself, it would not have been sufficient to cause hand ischemia. However, we must consider that at the level of the fistula, the blood flow is roughly distributed on the basis of the ratio of the resistances offered by the 2 circuits, the venous retrograde and arterial antegrade, as described in detail by various mathematical models (4). In the case of Mr. M, retrograde venous flow was meeting a standard resistance, because the anastomotic mouth and the vein circuit were of the proper size. In contrast, the antegrade arterial circuit offered a high resistance, because it presented 2 sequential barriers: at the level of the great vessels of the forearm and of the small vessels of the hand. Beyond refined functional or angiographic investigations, a simple radiography of the hands of Mr. M pointed out that every vessel was encased in a shell of calcium, spreading, fiercely and ubiquitously, up to the extreme arteries of the fingertips (
X-ray of the hands showing vessel calcification extending to the fingertip arteries.
On March 23rd, the patient underwent an angiography of the right forearm by a humeral antegrade approach carried out with a small caliber (4 French) sheath. In the same session, radial and ulnar arteries were reopened by percutaneous angioplasty (
Angiographic study after closure of the arteriovenous fistula and after angioplasty of the radial and ulnar arteries.
In the following days, we proceeded to the debridement of the tissue lesions. The surgical treatment was carried out with particular delicacy, due to the persistence of the intractable disease of the small vessels of the hand (
Final angiogram of the hand, showing diffuse disease of the metacarpal and finger vessels.
In the following week, we revascularized also the left forearm, because it mirrored the right, presenting small digital lesions.
After 2 months, Mr. M had healed (
Dorsal view of the hand after healing.
Palmar view of the hand after healing.
Patients with critical hand ischemia and diffuse calcifications present a mortality of almost 40% per year; despite this, Mr. M is still alive after 3 years. The hand lesions never returned, and he is fully autonomous, driving a car and working every day in his company. Walking with the leg prostheses is very tiring; Mr. M prefers to move in a wheelchair. The central venous catheter, fortunately, still works well.