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Medico Macha
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00:00Complications following amputation. So, early complications, there can be hemorrhage,
00:14infection, flap necrosis and DBT. So, if properly the flap is not raised, if the blood supply is
00:22not proper, then flap can become necrosis as well. The late complications can be pain and
00:29a phantom limb syndrome. Phantom limb syndrome can occur when neuromas form. If the nerves are not
00:35sharply cut, neuromas can form there and these patients can perceive as if the limb is still
00:42there and they are still having pain in that limb. So, this was briefly about amputation,
00:48what has been written in Bailey. For more details, please refer to Dr. Abbas's video as well where he
00:55discussed amputations in detail. Now, moving on from arterial occlusion, let's move on to the next
01:02topic in the arterial system and that is regarding aneurysms. Aneurysm is a dilatation of the vessel
01:10and the most common type of aneurysm is a fusiform aneurysm. Fusiform is when there is
01:18uniform dilatation. When there is uniform dilatation of the vessel, that is a fusiform aneurysm. The most
01:27common vessels involved are the vessels of the circle of villus, are the vessels of the circle
01:32of villus and this I've covered in the neurosurgery modules where I've spoken about intracranial
01:38aneurysms and subarachnoid hemorrhage. Most common extracranial vessel involved is the
01:46infrarrenal abdominal aorta, is the infrarrenal abdominal aorta. Most common peripheral vessel
01:55involved is the popletial vessel. Most common visceral vessel is splenic artery and splenic
02:03artery aneurysms I've covered in the module on spleen in detail and the most common vessel involved
02:09in mycotic aneurysm is also the aorta. Now, the term mycotic is a misnomer. It does not mean
02:16it is a fungal aneurysm. This is bacterial aneurysm and the organism which is involved
02:23is staph aureus. Pseudoaneurysm formation. Pseudoaneurysm formation is commonly seen in
02:33the femoral artery. Most commonly seen in the femoral artery and this is secondary to cannulation
02:40or trauma. This can form a pseudoaneurysm. So, these were some one-liners which I wanted you to
02:46know regarding aneurysms. Let's talk about abdominal aortic aneurysms, something from which questions
02:53have been asked a lot of times in the AIMS exam and in the future they can be asked in the INICET or the
02:59SS exam as well. Now, I just told you that infrarenal abdominal aorta is the most common
03:10extracranial vessel to be involved with aneurysm formation. The most important risk factor for
03:18aneurysm formation is atherosclerosis. So, this also you should remember atherosclerosis is the most
03:27important risk factor and screening in UK for abdominal aortic aneurysm starts from 65 years of
03:34age and this is done using an ultrasound abdomen. It is done using an ultrasound abdomen. Now, why are
03:42we screening for abdominal aortic aneurysms? So, the reason why we screen is because it is a very common
03:50in that population set and b everyone has figured out there is a critical diameter of the aneurysm.
03:57And if that critical diameter is reached, then the chances of rupture of the aneurysm go up
04:04exponentially. So, what are these critical diameters for all the aneurysms? For abdominal aortic aneurysm,
04:11the critical diameter is 5.5 centimeters. That means if an abdominal aortic aneurysm reaches the
04:21diameter of 5.5 centimeters, then the chances of rupture go up. And even in asymptomatic patients,
04:28then we need to surgically manage this patient. Also, you should remember that the chances of
04:35rupture are higher in females. So, the critical diameter in females is going to be 5 centimeters.
04:41It is 0.5 centimeters less. So, this is the critical diameter for abdominal aortic aneurysms.
04:49So, let me just cover the critical diameters of other aneurysms as well here only so that you can
04:54have all this information in one particular page. Ascending thoracic aortic aneurysms,
05:00also the critical diameter is 5.5 centimeters. And it has been seen that if there is more than 0.5
05:08centimeter per year increase in size, that is also considered significant. And in these patients
05:16also then surgery is recommended. For descending thoracic aortic aneurysms, the values were changing,
05:22but the final value given in the latest Bailey is 6 centimeters. And if there is more than 1 centimeter
05:29per year increase in size, then again, it is a significant finding in these patients.
05:36Marfan's patients are also more predisposed to thoracic aortic aneurysms. And in patients with
05:40Marfan's syndrome, the critical diameter is 4.5 to 5 centimeters. So, these are the values which you
05:47should remember regarding critical diameters for various aneurysms. Now, abdominal aortic aneurysms,
05:53what are the clinical features? These patients can be asymptomatic and they can just be picked up on
05:58routine screening. Or these patients can come with abdominal pain. They can come with a mass in the
06:06abdomen. And this mass is pulsatile in nature. This mass is pulsatile in nature. Sometimes this aneurysm
06:15acts as a source of embolus. It acts as a source of embolus. And this can give rise to blue toe
06:21syndrome. So, they can be emboli which can get showered from this aneurysm and they can cause
06:29gangrene in the toes. And that is known as blue toe syndrome. These patients can also come with
06:33rupture of the aneurysm. And rupture, I will talk about later, is associated with high mortality and it
06:40is usually in the retroperitoneum. So, this I will cover slightly later as well. So, these are the clinical
06:46features with which patients can present with an abdominal aortic aneurysm. The investigation of
06:53choice in a patient with abdominal aortic aneurysm is CT angiography. So, CT angiography is the
07:00investigation of choice in these patients. Now, again, I don't want any confusion. I told you the
07:07screening modality is ultrasound abdomen. But the investigation of choice is CT angiography,
07:14right? So, no confusion at all. CT angio is the investigation of choice. And you can see here,
07:22you can see the diameter of the aneurysm in the CT angio and then take a call. The management of
07:28abdominal aortic aneurysms, if so, intervention is required. The indications for intervention are
07:36in all symptomatic aneurysms in all symptomatic patients and in asymptomatic patients, in asymptomatic
07:49patients where it is more than 5.5 centimeters in size. These are the patients who require
07:56intervention. Now, intervention in abdominal aortic aneurysms can be of two types. You can either
08:03have EVAR, which has become the first line of treatment now, or you can have open surgery.
08:11EVAR stands for endovascular. EVAR stands for endovascular aneurysm repair, stands for endovascular
08:22aneurysm repair. And more than 75 to 80 percent patients are candidates for EVAR or endovascular
08:30aneurysm repair. Now, in EVAR, we have to use a graft and this graft has to get hooked onto the
08:37vessel, right? Because we are going by the endovascular route, this graft has to get hooked
08:43onto the vessel. So, the graft has a body and the graft has limbs as well. So, that this portion will
08:52remain in the iota, this portion will remain in the iota and this portion goes in the iliac vessels.
08:58This will go in the iliac vessels so that the graft stays in place. Now, what are the places where
09:07EVAR is contraindicated? So, EVAR is contraindicated when you have difficult iliac access.
09:16When you have difficult iliac access, that is where it is contraindicated. If there is increased
09:21angulation, if there is increased angulation, these are the places where doing EVAR is extremely
09:29difficult and it is contraindicated. One thing which you need to remember that if EVAR is done,
09:35if EVAR is done, then these patients have to be kept under lifelong monitoring.
09:41These patients have to be kept under lifelong monitoring and the reason why lifelong monitoring
09:47is required is because these patients can develop endoleaks. They can develop endoleaks. These
09:53grafts can leak. So, you can see in the CT angio here, this is what an EVAR looks like. This is what
09:59EVAR looks like in the iota. You can see the hooks there where the graft is in place. This is EVAR.
10:06And I told you that endoleaks can occur in these patients. So, we have to monitor them lifelong.
10:14Type 1 endoleak is, type 1 is proximal or distal to the graft attachment site, right? It is an improper
10:22seal which can give rise to type 1 leak and this is the most common type of leak in thoracic
10:28aortic aneurysm repair. This has been asked in the INI-SS exam as well. So, type 1 is most common
10:37for thoracic aortic aneurysm leaks. Type 2 is retrograde flow from the sac through the lumber
10:44vessels and type 2 is most common in abdominal aortic. So, type 2 is retrograde leak from the
10:51lumbar vessels and this is the most common in abdominal aortic aneurysm repair. This has been
10:58asked multiple times in the CTVS part of the super speciality exam as well. Type 3 is caused by a
11:05defect in the graft due to fabric tear or disconnection. That is type 3. So, type 3 is leak from the graft.
11:13Type 4 is when there is a porous graft and there is leak and type 5 is when there is increased tension
11:20in the graft and because of increased tension there are leaks, endoleaks which develop. So, mainly I
11:29want you to remember about type 1 and type 2. I want you to know type 1 is most common in thoracic
11:34aortic aneurysm repair and type 2 is most common in abdominal aortic aneurysm repair. So, these two
11:42points I want you to remember for the exam. Now, if we cannot do EVAR then we carry out open surgery
11:49and in open surgery we have to carry out a graft repair. We have to carry out a graft repair and
11:57this graft is usually a Dacron graft. This is usually a Dacron graft repair which is done. So,
12:07to access the iota I first have to carry out certain maneuvers to access the iota and then only I can do this
12:14grafting. So, we know that the iota is slightly on the left hand side, right? Slightly on the left
12:20side in the retroperitoneum. So, to expose the iota we have to carry out a Mattox procedure. Now,
12:27what is a Mattox maneuver or Mattox procedure? Mattox procedure is left medial visceral rotation.
12:35is left medial visceral rotation. What does this mean? This means that we are going to mobilize,
12:45we will mobilize the descending colon, we will mobilize the descending colon medially and when
12:54we mobilize the descending colon medially that will expose the iota behind it. So, to expose the iota,
13:01we do a Mattox procedure. This Mattox procedure has been asked in the exam. It is left medial
13:07visceral rotation and it is when we mobilize the descending colon medially. Now, you should also
13:13know the opposite of Mattox is known as cattle brash, right? The opposite of Mattox is known as
13:20cattle brash maneuver, is known as cattle brash maneuver and this is right medial visceral rotation.
13:29This is right medial visceral rotation. So, here we are going to mobilize the ascending colon medially
13:37and this when we mobilize the ascending colon medially, this is going to expose the IVC, right? This exposes
13:44the IVC. So, where will this be used? No, not for IVC aneurysms. This will be used when you have,
13:53supposing you have a renal cell carcinoma. Remember we discussed RCC and we discussed that RCCs can
13:59spread along the renal vein and can go into the IVC as well. So, to expose the IVC in such situations,
14:06we will carry out a cattle brash maneuver. Another thing, another term which I want you to remember,
14:12I have covered this in the abdominal modules is cockerization. Cockerization is when we mobilize the,
14:18when we mobilize the duodenum, that is known as cockerization. So, coming back to abdominal aortic
14:28aneurysm repair, we will have to carry out a Mattox procedure to expose the aorta and once we've done
14:33that, we will use a graft like this to bridge the aneurysm gap. We will use a graft, a Dacron graft.
14:42Okay. So, this you can see is how we deploy the EVAR graft. We go via the iliac route and then we
14:50deploy the graft. Now, you should know about the complications of abdominal aortic aneurysm surgery.
14:58Abdominal aortic aneurysm surgery, these have been asked multiple times in the AIMS exam.
15:06The leading cause of death following abdominal aortic aneurysm surgery are cardiovascular causes,
15:12are cardiovascular causes. This is the most common cause of death following abdominal aortic aneurysm
15:20repair. Renal failure can also occur in patients and an iotodiodinal fistula can occur. So,
15:27iotodiodal fistula is the graft which we've done that can get stuck to the duodenum, right? That can get
15:34stuck to the duodenum and a fistula can from and this can present as upper GI hemorrhage.
15:41This is a rare cause of upper GI hemorrhage. The patient can also come with melina. So,
15:47the typical history which you will see in the question is going to be that few years back,
15:54abdominal aortic aneurysm repair was done and now the patient comes with upper GI hemorrhage and
15:59melina. What is the most likely cause? It is an iotodiodinal fistula, okay? Colonic ischemia can
16:08occur. This colonic ischemia is commonly seen in the left side of the colon. It is commonly seen in
16:14the left side of the colon and the inferior mesentric artery is the one which is involved
16:20and patients who develop colonic ischemia in the postoperative period are going to come with bloody
16:26stools. They come with bloody stools and you can diagnose it using colonoscopy or angiography can
16:33tell you about this ischemia. These patients can also develop paraparesis and this was asked in the
16:38AIMS exam that why does paraparesis develop in patients following abdominal aortic aneurysm
16:44and this develops because of the involvement of
16:47artery of Adam Kiwis. This is the artery of Adam Kiwis which is involved and this artery of Adam Kiwis
16:59supplies the anterior spinal artery supplies the anterior spinal artery and this can give rise to
17:06paraparesis following surgery as well. There can be mortality also following abdominal aortic aneurysm
17:13surgery and mortality following abdominal aortic aneurysm surgery if it is an elective repair
17:21if it is an elective repair then it is two to three percent is the elective mortality risk but if
17:27it is an emergency repair and emergency repair would usually be done when there is a rupture
17:36then in these patients there is more than 50 percent mortality rate. This question has also been asked twice
17:42in the AIMS exam. Now if you talk about a ruptured aortic aneurysm this rupture will usually occur in
17:47the left retroperitoneum this rupture will occur in the left retroperitoneum and these patients the
17:54clinical features when a rupture occurs these patients are going to come with shock they will come with a
18:01pulsatile swelling a pulsatile swelling shock and flank pain. So these patients are going to come with shock
18:11a pulsatile swelling and pain in the abdomen that is how these patients are going to present. If the
18:17patient has stable vitals we can do a CT angio you can see this is a CT angio which is showing us that
18:25this is the rupture which has occurred in the left retroperitoneum and the management of these patients
18:31is again we have to carry out a Dacron graft repair. A Dacron graft repair has to be done and when we are
18:38operating such patients I told you there is more than 50 percent mortality rate in such cases.
18:46So this was regarding abdominal aortic aneurysms. Let's now move on to thoracoabdominal
18:52aortic aneurysm. So sometimes these aneurysms can be more extensive and you can get thoracoabdominal
18:58aortic aneurysms and this classification is known as the Crawford's classification.
19:03This is the Crawford's classification for thoracoabdominal aortic aneurysms and what you need to remember
19:09for your exam is that type 2 Crawford's is the most extensive thoracoabdominal aortic aneurysm.
19:18Type 2 Crawford is the most extensive thoracoabdominal aortic aneurysm. Type 1 extends from left
19:24subclavian to renal artery. Type 2 I told you is from left subclavian to aortic bifurcation
19:30and this is the most extensive aneurysm which is present. Type 3 is mid-descending aorta to aortic
19:40bifurcation and type 4 is upper abdominal aorta to infrarenal. So these are the four types and type 2
19:48is the most extensive. Again we have to carry out a graft repair in these patients. Moving on to
19:54thoracic aortic aneurysms. So thoracic aortic aneurysms can be secondary to atherosclerosis.
20:02They can be secondary to atherosclerosis and they can be seen in Marfan syndrome like I pointed out
20:09earlier as well. They can even be seen in Marfan syndrome. So they can also be seen in Ehlers-Danlos
20:15syndrome. Can also be seen in Ehlers-Danlos syndrome. Now these thoracic aortic aneurysms,
20:22the clinical features how the patient can present, they can either be asymptomatic. So the patients
20:27can be asymptomatic or these patients can come with hoarseness and this is very important for your
20:34exam. This is given in the latest submission. So hoarseness can be due to pressure from,
20:39this can be due because of pressure of descending aneurysm, descending thoracic aneurysm on left
20:50recurrent laryngeal nerve can give rise to progressive hoarseness and this is known as
20:55Ortner's syndrome. So this I want you to remember for the exam. This is Ortner's syndrome which can be
21:02because of pressure over the left recurrent laryngeal nerve. These patients can also present with
21:08dysphagia. They can come with dysphagia or they can come with dyspnea as well. Now if the aneurysm
21:17ruptures, if the aneurysm ruptures then these patients will come with sudden onset dyspnea and
21:25these patients can also develop left-sided pleural effusion. They can develop left-sided pleural
21:32effusion. The investigation of choice again in these patients is CT angiography and management of
21:40these patients. We've discussed, we've discussed the critical diameters for ascending and descending
21:45thoracic aortic aneurysms. We know the management will be done in all symptomatic patients, in all
21:54symptomatic patients, in asymptomatic patients, in asymptomatic patients, ascending aneurysms 5.5
22:07centimeters is the critical diameter, descending 6 centimeter is the critical diameter and in Marfan
22:13Marfan syndrome, in Marfan syndrome, 4.5 to 5 centimeters is the critical diameter. So all
22:22symptomatic patients and symptomatic can also be those who have aortic valve insufficiency,
22:29those who are developing aortic valve insufficiency which can be picked up on echocardiogram and these
22:38asymptomatic patients, these are the ones who require intervention. Again the intervention can either
22:44be EVAR or it can be open graft repair or it can be open graft repair. The complications are also
22:54similar to what we've discussed for abdominal aortic aneurysm surgery. Now another very interesting
23:00complication here is aortic dissection. So very important for the exam, aortic dissection. Now what
23:06exactly do we mean by dissection? So what do we mean by dissection? So normally we know that this is our
23:14externa, this is the media of the vessel and this is the intima, right? So intima media externa
23:21and we know blood is flowing within the intima, which is flowing within the intima. But now if there
23:27is a tear in the intima, if there is a tear in the intima, tear in the intima, now blood is going to flow
23:34between the intima and the media and that is dissection. That is called dissection. So what is
23:41the thing which triggers the tear? So the most important risk factor, the most important risk
23:47factor which triggers this tear is hypertension. So because of hypertension the intima splits and now
23:54blood is flowing between the intima and the media. The most common site for aortic dissection is the lateral wall
24:04is the lateral wall of ascending thoracic aorta. Lateral wall of ascending thoracic aorta is the most common
24:12site of aortic dissection and the clinical features. So chest pain is the most common clinical feature
24:20with which these patients present and this pain radiates to the back. It radiates to the back
24:27back in the interscapular region. Now aortic dissection is also more common in males as compared to females
24:40and it is usually seen between the fifth to the seventh decade of life. Now if this tear extends, if the
24:48tear keeps on extending, it can give rise to aortic insufficiency as well.
24:53Aortic insufficiency and coronary insufficiency can also be there if the tear extends.
25:05Aortic and coronary insufficiency can also be there in these patients. Now these are the clinical
25:11features. What are the investigations in these patients with aortic dissection? So the investigation
25:17of choice has been asked in the exam. In a stable patient with aortic dissection,
25:22the investigation of choice is a CT angiography. And you can see here in the CT angio very clearly
25:32that this is the aorta and you can see the dissection which is occurring. So a parallel
25:38lumen is being formed. A parallel lumen is being formed. That is aortic dissection.
25:43If the patient is unstable, this has also been asked in the exam. If the patient is unstable,
25:48then transesophageal echo is done. Then the investigation of choice is transesophageal
25:57echocardiogram. That is the investigation of choice.
26:00If you do a chest x-ray in these patients, you can see widening of the mediastinum.
26:04There is widening of the mediastinum which is seen, which can be seen in thoracic aneurysms,
26:13aortic aneurysms. Otherwise as well, there will be widening of the mediastinum. And there can be
26:17left pleural effusion also which can be seen in these patients. Now based on the CT angio findings,
26:24there are two types of classifications for aortic dissections. You have the DeBakey classification and
26:31you have the Stanford's classification. So according to the DeBakey classification, there are three types
26:37of aortic dissections. Type 1 is one which involves the ascending plus descending thoracic aorta and type
26:441 is the most common. So type 1 involves ascending and descending thoracic aortic
26:48aorta. Dissection is there and it is the most common type. Type 2 is only ascending thoracic aorta is
26:58involved and this is type 2. Type 1 and type 2 combined are known as Stanford's A. So the other
27:06classification is the Stanford's classification and type 1 and type 2 DeBakey combined are Stanford's A.
27:12And type 3 is the one which involves the descending thoracic aorta which involves the descending thoracic
27:23aorta. And in the latest submission, this has also been further divided into 3A and 3B. This has been
27:30divided into 3A and 3B. 3A is when only the descending thoracic aorta is involved.
27:38Descending thoracic aorta is involved. And 3B is when the tear is below the diaphragm.
27:45When the tear is below the diaphragm, we call it 3B. And Stanford's B includes DeBakey type 3.
27:55So DeBakey type 1 and 2 is Stanford's A and DeBakey type 3 is Stanford's B. These are the two
28:02classifications for aortic dissection which you should know about. Now, like I told you,
28:09that hypertension is the one which triggers the tear. But once the tear occurs, there is hypotension,
28:16right? Because a parallel lumen has formed and there is hypotension. So the management of these
28:22patients, you should know, the management is very important. First, we have to aim towards permissive
28:28hypotension. What is permissive hypotension is something which I want you to understand here.
28:34This I have also covered in the trauma modules. So like I told you, that hypertension is the one
28:40which triggers the tear. But once the tear occurs, there is hypotension. Now when the patient comes with
28:46hypotension to the emergency, it is a reflex mechanism to give a lot of fluids. Because there is hypotension,
28:53we want the BP to increase. Now, if you give a lot of fluids in this patient, BP will suddenly
29:00increase. And when BP increases, the tear will also increase. So a sudden increase in BP in these
29:07patients can be counterproductive, can be counterproductive, which is why BP should be
29:13kept, systolic BP should be kept at the lower limit of normal. And that is called permissive
29:20hypotension. Which is why all patients with aortic dissection, we first give esmolol. Esmolol is a
29:28short acting beta blocker. This has been asked many times in the exam. So first treatment is we give esmolol,
29:35which is a short acting beta blocker. And we will stabilize the patient. If it is a
29:45type 1 and 2, Debeki type 1 and 2, once we have given esmolol, then we have to carry out a graft repair.
29:57Then we have to carry out surgery and we have to carry out a graft repair in this patient.
30:01Type 3 patients, type 3 patients are monitored. Type 3 patients are monitored. If progressive symptoms are
30:10there, if progressive symptoms are present, then we have to carry out surgery. Otherwise, in these
30:18patients, for chronic type 3, conservative management can also be done. But type 1 and type 2, after esmolol,
30:24we have to take up the patient for a graft repair. So this covers entirely about aneurysms. I've spoken
30:31about abdominal, thoracic and thoracoabdominal aortic aneurysms. Two more aneurysms which we'll
30:38quickly cover. One is popliteal aneurysm. Popliteal, I told you, is the most common
30:42peripheral vessel to be involved with aneurysm formation. And 50% popliteal aneurysms are
30:48bilateral. Patient will come with a pulsatile swelling behind the knee and there is loss of
30:53contour of the knee behind. There can be pain and distal emboli as well. The investigation of choice
31:00in these patients is CT angio, which will tell us about the size of the aneurysm. And the indications
31:07for intervention are 2 centimetres is the critical diameter. So asymptomatic aneurysms more than 2
31:14centimetres. And all symptomatic aneurysms, we need to carry out surgery in these patients.
31:21Otherwise, we can manage them conservatively. Femoral artery aneurysms are caused by puncture.
31:27So if you are puncturing it for cannulating it or puncturing it for some procedure, that can give rise
31:33to femoral artery aneurysms. And the critical diameter for femoral artery aneurysms is 3 centimetres.
31:39If it is less than 3 centimetres, the treatment is thrombin injection under ultrasound guidance.
31:45If it is more than 3 centimetres, then we have to carry out surgical repair in these patients.
31:51Now, there are certain brief topics in arterial system which we need to know. And from these topics,
31:58invariably one question is usually asked in the MCQ exam. The first one is Reynolds phenomena. This is
32:03a hot favourite of the FMG exam and also the NEAT exam. So Reynolds phenomena is when there is
32:09vasospasm. And when there is vasospasm, there are three typical changes which take place.
32:16So in the first phase, in phase one of Reynolds, what happens that the artery and vein are both in
32:23spasm. So when the artery and vein both are in spasm, then the hand is going to become white or there's
32:29going to be pallor, right? You can see here there's pallor, artery and vein both are in spasm.
32:34In phase two, what happens? In phase two, what happens that the venous spasm is still there,
32:42right? So the vein is still in spasm, but the artery dilates, the artery dilates. So what is
32:48going to happen? There's going to be deoxygenated blood which is already here
32:52since before and new oxygenated blood will come in mixed with it, right? So artery relaxes,
32:59but vein is in spasm, vein is still in spasm. So when oxygenated and deoxygenated blood mix,
33:07the hand is going to become blue and it is going to be extremely painful, right? So hand is going to
33:12become cyanose and it will be extremely painful, you can see here. And the final phase, phase three is,
33:18phase three is when artery and vein both relax. And when artery and vein both relax,
33:26then oxygenated blood is going to come in and the hand will become red again. So white, blue, red,
33:32that is the sequence of event which is seen in Reynolds phenomena. Now, there are two types of
33:37Reynolds, primary and secondary Reynolds. And this was also asked in the FMG exam. So primary Reynolds is
33:44more common than secondary Reynolds. And primary Reynolds is not associated with
33:52collagen vascular diseases, is not associated with collagen vascular diseases. And there can be a
33:58family history of Reynolds phenomena in these patients, okay? Pharmacological treatment is not
34:05usually required and complications are rarely seen in primary Reynolds, are rarely seen in primary Reynolds.
34:12secondary Reynolds. Secondary Reynolds is commonly seen in patients with collagen vascular diseases
34:20like SLE, rheumatoid arthritis. So collagen vascular diseases are usually associated. It is
34:26rare as compared to primary Reynolds. But pharmacological treatment is frequently required
34:31and complications can also occur. It has also been seen that Reynolds phenomena can be seen in
34:38patients who use drills, right? Drill workers. So constant vibrating tools if they are using.
34:44So that can also give rise to Reynolds phenomena. So drill workers, vibrating tools, that can also
34:50predispose to Reynolds. Now the management of Reynolds, the drug of choice for Reynolds is calcium channel.
34:58Our calcium channel blockers, this you should know for the exam. This has also been asked.
35:02So you should know the sequence of change of colour and you should know the differences between primary
35:09and secondary Reynolds. Another term mentioned in Bailey and Sebastian is acrocinosis. This is
35:14predominantly seen in females. It is painless, right? And it is non-episodic. It is non-episodic,
35:21unlike Reynolds. And there is mottled sinosis followed by paresthesias. So this is a differential
35:28diagnosis of Reynolds phenomena. But I have told you the differences. It is painless and it is non-episodic.
35:38Another very interesting condition is subclavian steel syndrome. So subclavian steel syndrome occurs
35:44when there is stenosis in the first part, when there is stenosis or block in first part of subclavian
35:54artery, in first part of subclavian artery. And when there is block in the first part of subclavian artery,
36:04so flow to that arm will not occur through the subclavian artery. But what happens when the patient
36:10starts exercising, when the patient is exercising, when the patient is exercising with subclavian stenosis,
36:20there is retrograde flow, there is retrograde flow which occurs from the vertebral vessels,
36:28from the vertebral artery. Okay? So this side was the stenosis. Now, when the patient is moving his left
36:36arm, where the stenosis was in the subclavian vessel, there is going to be retrograde flow from the vertebral
36:44artery. There is going to be retrograde flow preferentially into the left arm. So less blood
36:49is going to go into the brain. So when these patients exercise, retrograde flow occurs and these patients
36:56can have syncopal attacks. They can have syncopal attacks and they can have dizziness. They can have
37:04syncopal attacks and dizziness and this is how patients with subclavian steel syndrome present.
37:10The investigation of choice is CT angio and CT angio will be able to localize the site of block and the
37:17management is angioplasty. The management is angioplasty and stenting in these patients.
37:26Carotid artery stenosis is another very common problem which is encountered and the most common
37:33site is bifurcation of the carotid vessels and the most common cause is that it is secondary to
37:40atherosclerosis. It is secondary to atherosclerosis. Now, clinical features, these patients can be
37:48asymptomatic and it can be detected when a Doppler is done for the neck or they can have transient
37:54ischemic attacks. This is the most common presentation how they present. They can come with transient
37:59ischemic attacks. They can be transient ischemic attacks which resolve within 24 hours or they can
38:09have episodic blindness. This is amorosis, amorosis fugax where they will have momentary blindness and
38:18that resolves after some time. They can also have dysphagia also can be seen in these patients.
38:25So, again, the investigation of choice here is a duplex scan that will tell us what is the amount
38:32of block which is there. The indications for surgery, right? Indication for surgery when there is
38:39carotid artery stenosis, there should be 70% or greater stenosis and there should be ipsilateral amorosis,
38:48fugax or monoocular blindness. This is one of the features. Facial paralysis, arm or leg paralysis,
38:56hemianopia or dysphagia. These are all clinical features which can be seen with carotid artery
39:01stenosis. So, if there is a greater than 70% stenosis and any of these findings are there,
39:08then we have to intervene and we have to carry out an angioplasty or we have to do grafting for these
39:14patients with carotid artery stenosis. So, these indications for surgery have been asked in the
39:18INICET exam and in the superspeciality exam as well. The next condition which we need to discuss
39:25is thoracic outlet syndrome. So, this is the diagram of thoracic outlet. So, you can see here
39:31through the thoracic outlet is what you will get the subclavian vessels. So, you have the subclavian
39:36vessels coming out. This is the subclavian artery, this is the subclavian vein and you have the brachial
39:42plexus also which comes out through the thoracic outlet. Now, thoracic outlet syndrome can occur
39:53get blocked that can give rise to thoracic outlet syndrome and you can have either arterial blockade,
40:01they can either be arterial block or they can be venous symptoms or the patient can come with neural
40:08symptoms or nerve related symptoms. The causes of block, why does this block occur? So, this can occur
40:17because of cervical rib. This can occur because of cervical rib. It can also occur because of poor tone
40:25of muscles. So, that is why physiotherapy seems to help in these patients. Cervical rib can cause this
40:31problem. Arthritis can give rise to this problem and there can be tumors which can also predispose to
40:39thoracic outlet syndrome. Now, arterial there will be subclavian artery which will be compressed,
40:46subclavian artery which is compressed and there can be a thrombus which can be which can form here
40:52and there can be embolic phenomena. So, emboli can also break off from this thrombus
40:58and it can cause distal gangrene or there can be clodigation as well which can occur.
41:05In the vein, there can be venous thrombosis. There can be thrombosis of the subclavian
41:10vein which can occur or axillary vein thrombosis can also occur in these patients.
41:15And the neural symptoms, there can be brachial plexus. The brachial plexus can get compressed and
41:23that can give rise to symptoms mainly on the ulnar side. So, mainly most commonly this is on the ulnar
41:29distribution. They are seen in the ulnar distribution. So, this is how these patients
41:37are going to present to us and the investigation of choice to diagnose thoracic outlet syndrome
41:43is a CT angiography. This CT angio will tell us the cause of block and where exactly is the block
41:50located. Even a simple x-ray can tell us about cervical rib as well. In thoracic outlet syndrome,
41:58there are certain clinical tests which are also done in these patients and in the last three years,
42:03lots of times these clinical tests have been asked in the exam. In fact, in one of the INICAT exam,
42:08they had shown a GIF image as well where they had shown a particular clinical test and they had asked
42:14you to diagnose which test was it. So, I have made a video of all these tests but quickly let me just
42:21tell you the theory and then I will show you that video as well so that it becomes clear to you for
42:26your exams. Adson's test is when the affected arm is abducted at 30 degrees and at the shoulder
42:34while extending the neck and turning the head towards the same side, we ask the patient to
42:40breathe. So, you will see in the video, patient's neck is turned towards the same side, 30 degree
42:44abduction and deep breath and when we do this, we will keep on feeling the pulsation. If we see decreased
42:51radial pulsation, then this test is positive. The elevated arm test or the ruse test is when they
42:57abducted at 90 degrees and they keep on compressing their opening and closing their fists and this
43:04is going to precipitate pain, then the test is considered as positive. Then upper limb tension
43:11test also I have demonstrated in the video as well as well as the rights test also has been
43:17demonstrated. So, let's see that video of the test and then let's talk about the management of
43:22thoracic outlet syndrome. So, in this video, I will demonstrate the elevated arm stress test or
43:28also known popularly as the ruse test. So, this is done for thoracic outlet syndrome and you can
43:34see that the patient is asked to first flex the elbows and first abduct the arm at 90 degrees,
43:40flex the elbows and then open and close the palm and make a fist. He does that for two or three
43:48minutes and if there is thoracic outlet obstruction, then the patient will start feeling pain. There will
43:54be pain and fatigue which is going to set in. So, in this video, I am going to demonstrate the rights
43:58test for thoracic outlet obstruction. To carry out the rights test, we first abduct the shoulder of
44:04the patient, then we flex the elbow and we do external rotation. We ask the patient to clench his
44:13fist and this test would be done in two parts. In the first part when the patient does this,
44:19this stretches the pectoralis minor tendon and you can see that I am feeling for the radial pulse.
44:24Now, if there is thoracic outlet obstruction, then the radial pulse would be affected and I won't be
44:31able to feel the radial pulse. The second step is when I carry out hyperabduction of the shoulder
44:38and when I do hyperabduction of the shoulder, this is going to cause compression of the costoclavicular
44:43ligament and I keep on feeling for the radial pulsation. If the radial pulsation goes away, that means
44:49that there is thoracic outlet obstruction. So, in this video, I will be demonstrating the
44:54absence test for thoracic outlet obstruction. Now, the absence test is also one of the provocative
45:00tests with which we can know whether there is thoracic outlet obstruction present or not. So,
45:05in this test, we ask the patient to look towards the side which is affected. This is also called the
45:12testing position. Then, we ask the patient to take a deep breath inside. Deep breath.
45:17And then, we ask the patient to hold his breath for 30 seconds and at the same time, we are feeling for
45:24the radial pulsation. The modification is that the arm can be extended by 15 degrees and a positive test
45:31is when we can't feel the radial pulsation. That is known as a positive absence test. So, the management of
45:38thoracic outlet syndrome, if the patient is symptomatic, if the patient is symptomatic,
45:46if there is a cervical rib, if there is a cervical rib, that should be resected. Cervical rib needs to
45:52be resected. A lot of patients benefit from physiotherapy especially if it is secondary to
45:57arthritis. Physiotherapy is also very beneficial in these patients. If there is an arterial blockade,
46:05if there is an arterial block, then we have to do angioplasty in these patients. Angioplasty and
46:12stenting needs to be done. And if there is venous thrombosis, then anticoagulants need to be started
46:17in patients with thoracic outlet syndrome. Now, another condition which you should know and the
46:22image of this was asked in the NEAT exam and the INICET exam. This is a chrysoid aneurysm. So,
46:28a chrysoid aneurysm is an AV malformation. This is an AV malformation which is seen usually in the
46:36region of the scalp or in the extremities. And if it is seen in the region of the scalp,
46:43it is commonly associated with the superficial temporal vessels. The superficial temporal vessels
46:49are the ones which are commonly involved. And you can see, you will see a vascular swelling like this.
46:53And this vascular swelling will be pulsatile. It will be a pulsatile swelling. And it is partly
47:00compressible as well. Right? I have already told you in the hernia module, the difference between
47:06compressibility and reducibility. Compressibility means when you press it, as soon as you leave it,
47:12the swelling will bulge out again. Right? Without a counterforce also, it will bulge out again.
47:17So, it is a partly compressible swelling. And the clinical features, patients can have cosmetic
47:23problems. So, cosmetic problems. And because of the pressure, there can be functional problems where
47:29there can be pain as well in these patients. And the management of these aneurysms, if the patient
47:35is symptomatic, then we have to surgically manage these aneurysms or embolization can also be carried out
47:42in these patients. The next condition is AV fistulae. Arteriovenous fistulae. And
47:46arteriovenous fistulae, the causes can be traumatic. So, they can be traumatic arteriovenous fistulae.
47:52Like, you know, you can get after liver trauma. I covered in the abdominal trauma module.
47:57You can get after renal trauma also, AV fistulae can form.
48:02Iatrogenic AV fistulae are the most common. And these are created for dialysis purposes. For renal dialysis,
48:11iatrogenic fistulae are created. This is a simino fistula, which is a radiocephalic fistula.
48:18A radiocephalic fistula between the radial artery and the kephalic vein. This is the most common type
48:25of arteriovenous fistula. There can be congenital AV fistulae as well. Congenital AV fistulae can be
48:31seen in Park-Weber syndrome. I covered Park-Weber syndrome in the varicose vein module.
48:37They can be seen in Beckwith-Weedman syndrome. Beckwith-Weedman syndrome also,
48:45you can see congenital AV fistulae. And you can even see them in Sturge-Weber syndrome.
48:50Now, the clinical features of arteriovenous fistulae, so the clinical features of arteriovenous
48:56fistulae, these patients are going to come with a pulsatile swelling. There is going to be a pulsatile
49:01swelling, right? There is a palpable thrill, which you can, there is a palpable thrill,
49:09which you can feel over the swelling. And you can auscultate,
49:13you can auscultate a bruit as well in these patients. Now, if it is a congenital fistula over
49:23the limb, if it is a congenital fistula in a limb, then it can give rise to hypertrophy of the limb as
49:32well. It can give rise to hypertrophy of the limb. And these patients can also develop high output
49:41cardiac failure, right? Because it acts as a low resistance channel, there can be high output
49:48cardiac failure, which can occur in these patients as well. There is one clinical sign,
49:55which has been asked many times in the exam. This is known as the Nicoladoni. This is the Nicoladoni
50:02or the Branham sign. So, the Nicoladoni or the Branham sign is when we press the feeding vessel.
50:12So, when we press the feeding vessel of the AV fistula, what is going to happen? So, when you
50:18press the feeding vessel, the size of the fistula will reduce, okay? The size of the fistula is going
50:26to reduce. Pulse rate is going to reduce. Thrill and bruit are going to reduce. Thrill and bruit are
50:36going to reduce. But the systolic BP is going to increase. So, bradycardia and hypertension, right?
50:45Braddy and hypertension. So, systolic BP will increase in these patients and pulse rate is going to
50:52decrease. This is the Nicoladoni or the Branham sign, which you should know about. The investigation
50:59of choice for AV fistula is MR angio because MR gives better soft tissue resolution to us. And
51:07digital subtraction angiography, DSA's digital subtraction angiography can also be done. But MR angio
51:14will be the best answer here. The management of AV fistula if symptomatic, if the patient is
51:23symptomatic, then the first line of treatment is embolization. The first line of treatment is
51:31embolization. But if it is seen, if it is in drug abusers, if you have a fistula which is
51:39an infected fistula, infected fistula, if it is in drug abusers, if there is hypertrophy of the limb,
51:49if there is hypertrophy of the limb, then in these patients, we have to carry out surgical ligation
51:56of the fistula. We have to do surgical ligation of the AV fistula. So, that is how we manage patients
52:05with arteriovenous fistula. First, we do embolization. Otherwise, in these situations,
52:09surgical ligation is carried out. The final thing I want you to know is an arterial ulcer.
52:16I have covered this in great detail in the common ulcer module where I have described of what all
52:22points you should note in an arterial ulcer. And if you are given a case of peripheral arterial disease,
52:28what are the points which you should look out in the history and examination.
52:32So, that brings us to the end of this module on arterial disorders. For final year students,
52:38short notes regarding this module. Reynolds phenomena, difference between atherosclerosis,
52:47difference between atherosclerosis versus Burgers.
52:53AV fistula has been asked as a short note in your college exam.
52:57Subclavian steel syndrome has also been asked as a short note in the college exams.
53:02Okay. Now, before we end this module, let's talk about some MCQs which have been asked in various
53:09exams. All of the indications, all our indications for carotid end arterectomy, right? So, that is the
53:15surgery which is done. Carotid end arterectomy, that means you have to remove that thrombus.
53:20Carotid end arterectomy is to be done. All of the following are indications except
53:26hemianopia is an indication, monocular blindness is, dysphagia is, persistent hypertension is not an
53:33indication, right? So, persistent hypertension is not an indication. This question was asked in the
53:39INICT exam. 70 year old female presents with pain in the thigh during walking. Investigation reveals the
53:46following findings. What will be the best surgical treatment? So, you can see here, this is the iota
53:53and the block is in the iliac vessels. Now, if there is an iliac block, I told you,
53:58for iliac blocks, endovascular procedures work well. So, the first line of treatment will be
54:04angioplasty with stenting. If angioplasty with stenting fails, then we will carry out a bypass in
54:11these patients. But first would be angioplasty and stenting. Which of the following is false regarding
54:17investigations for peripheral arterial disease? Duplex scanning is a non-invasive technique. True.
54:23On Doppler, normal artery shows biphasic flow. This is false. I told you this is triphasic flow.
54:30Digital subtraction angiography is a standard technique. Yes. Computed tomography is not used
54:36routinely to diagnose peripheral arterial disease. This is also true for peripheral arterial disease.
54:42We use duplex scanning only. DSA will also be used when we are planning an intervention to know
54:48more details regarding the anatomy. That's where we use digital subtraction angiography. So, I told you
54:53that it is not routinely used. Only if we are planning a revascularization procedure, then computed
54:59angiography, CT angio, is going to be used in these patients. We have to match the following
55:03ABPI value less than 0.3 is value for critical limb ischemia. Less than 0.9 is intermittent
55:11claudication. 0.9 to 1.3 is normal and more than 1.3 is seen in chronic kidney disease or calcified
55:20vessels. Critical limb ischemia is characterized by all of the following except ulceration, rest pain,
55:27gangrene, intermittent claudication, no. Critical limb ischemia means already rest pain has started.
55:33So, no intermittent claudication here. A 30-year-old man with a history of smoking presents with
55:39cramping gluteal pain after walking 500 meters. So, he walks 500 meters and there is cramping gluteal
55:46pain. So, gluteal pain, I told you, iotoiliac involvement. Which syndrome did I tell you?
55:53Leric syndrome. This is known as Leric syndrome. Male patient presents to the hospital with abdominal
55:59pain and is incidentally detected with an abdominal aortic aneurysm. What is the appropriate management
56:05for this patient? Okay. So, incidentally detected abdominal aortic aneurysm is there. Ultrasound,
56:13we monitor the size till it is 5.5 centimeters. That is the treatment. We monitor the size till it
56:19is 5.5 centimeters. Which of the following is false regarding abdominal aortic aneurysms?
56:27Abdominal aneurysms are more suitable to endovascular repair. This is true. Most abdominal
56:32aortic aneurysms rupture in the retroperitoneal space. True. Systolic BP should be maintained less
56:38than 100 in rupture. This is permissive hypertension. This is true. And ultrasound is used to diagnose
56:45ultrasound. Abdominal aortic aneurysm rupture. This is a false statement. This is a false statement.
56:52Aortic dissection true and false. Chest pain radiating to the back is the most common symptom.
56:57Hypertension is the most common risk factor. Transesophageal echo is the investigation of
57:03choice in unstable patient. Not stable. Unstable patient. And first line of treatment is
57:09esmolol administration. This is also correct. This was the question which I told you. This is a
57:14chrysoid aneurysm. I showed you the image as well. This is a chrysoid aneurysm. Patient presents with
57:19bluish discoloration of the toe. Intermittent claudication. What will be the next appropriate
57:24investigation? It is going to be a duplex scan which we've discussed previously. 45 year old lady
57:31presents to the emergency with severe pain in her hand. This was asked in the FMG exam. You can see
57:36these are findings of Reynolds. They have not mentioned any association with collagen vascular diseases.
57:44So the answer is going to be primary Reynolds phenomena. That is the answer primary Reynolds
57:49phenomena. So these were some questions regarding the arterial system. This is a very very important
57:55module from the point of view of both your college exams and MCQ exams. Thank you.