The patient came to the clinic 27-February-2011 complaining of weak left upper limb with feeling of cold of this limb for 9 months. MRI cervical spine done 27-May-2010 showing bulge disc C4-5.  ECS done 26-December-2010 reporting demyelinating neuropathy both upper limbs. On examination at that time; the Romberg position was stable, but the left upper limb swaying down. There is hypalgesia of the left side of the face and the left upper limb with weak muscles left upper limb 3/5, except the left deltoid muscle. The patient was sent for investigations and MRI of the brain done 02-March-2011 showing malacia of the right parietal lobe with complete occlusion of the right ICA 10 mm above the bifurcation of the right CCA. MRI cervical spine showing the same data as before. Cardio consultation was uneventful. The patient underwent carotid angiography elsewhere and attempt to perform stenting 30-January-2012 failed. MRI of the brain with MRA repeated 31-December-2012 showed still complete occlusion of the right ICA. The patient 09-May-2013 was advised to undergo endarterectomy, but he escaped. The patient then came 25-December-2014 telling that he got another attack of infarction, and he was told that it was in another territory?

On examination, the patient is alert with the weak left hand extension and flexion -3/5 and weak dorsiflexion left foot.

The patient was sent for investigations and MRI of the brain and done 28-December-2014 showing the same data as before. He was another time advised to explore the right ICA territory.

Exposure of the right CCA, ECA with the branches arising from the last. The right hypoglossal nerve was dissected and preserved. There was a huge lymphnode in the area which was resected to obtain visual control in the field. The ICA was followed from distal to proximal to be sure that no abnormality could be present at the bifurcation. The right ICA is hypoplastic and its external diameter less than 3 mm. Direct angiography done demonstrating that the ICA is completely occluded 10 mm above the bifurcation and no pulsation is noted. After clamping of the right CCA and ECA arteriotomy was done. There was an atheroma completely occluding the right ICA. It was removed but no back flow was obtained. Using subclavian catheter No 20 three way with the brown canula connected to the end of the catheter, gradual dilatation and cleaning with saline and heparin was applied. Using the C-arm, the tip of the catheter was followed and continuous angiography and cleaning was performed until the right ophthalmic artery was seen. The segment above this level up to the bifurcation of ICA to A1 and M1 which usually 3-5 mm in length required 20 min and 10 passes to clean and dilate the area until proper angiography of the right circulation was established. The canula was removed and there was back flow from the ICA. Using Dacron patch the arteriotomy site was closed and control hemostasis was achieved after removing the clamps. The hypoplastic ICA regained good pulsation after that. Routine closure.

Smooth postoperative recovery. The power of the left upper limb became normal.

The patient underwent angiography elsewhere and attempt to introduce a stent failed.

The findings during surgery explain the cause of this failure. The hypoplastic right ICA not only completely occluded, but it became hypoplastic over the years. The subclavian canula with great difficulty could pass the artery lumen.

If the dilatation of the hypoplastic artery did not succeed and the angiography of the right A M was no seen and the back flow did not appear at the end of the procedure, than it was planned to make bypass from the CCA up to the supraclinoid part of the right ICA.

Of course the artery now is hypoplastic but it could dilate with time or return to the preoperative status. Time will tell the result.

Heparin was not used during surgery, because the flow to the right ICA was 0% and the artery was continuously dilated and irrigated all the time until back flow was seen. Aspirin was not topped preoperatively and Clexane 40 mg was administered 12 hours after surgery.

The cause of hypoplastic artery is the complete occlusion and long period of time elapsed since the occlusion with absent flow in the involved segment.