​Surgery - Varicose Veins 
Introduction 
veins that have gotten longer, wider, and more twisted; these are typically the lower limbs' superficial veins. These smaller superficial venous telangiectasias and varicosities are referred to as thread veins, spider veins, or reticular veins.

Etiology 
Primary: As a result of decreased elasticity, gradual dilatation, and valvular incompetence brought on by a hereditary or developmental weakening of the vein wall.
Klippel-Trenaunay syndrome (port wine stains, varicose veins, and related hypertrophic limb tissue) and Parkes Weber syndrome (like KT, but with arteriovenous fistulas) are two congenital diseases linked to varicose veins.
Secondary: Obstacles to venous outflow include ascites, lymphadenopathy, ovarian cysts, pregnancy, pelvic cancer, and retroperitoneal fibrosis.
Damage to valves: After deep vein thrombosis (DVT). Arteriovenous fistula: high flow rate.

Epidemiology 
Common, rising with age; prevalence: 10-15% for men and 20-25% for women in adulthood.

History 
The patient may express dissatisfaction with their outward look or report experiencing symptoms like leg pain that worsens at the end of the day or after standing for extended periods of time; swelling, itching, or consequences including ulceration, bleeding, or infection. Ask about predisposing factors, vascular risk factors, and prior history of DVT.

Examination 
Examine the venous distribution, skin alterations (such as varicose eczema, lipodermatosclerosis, oedema, atrophie blanche, or ulceration) while the patient is standing.
Palpation: Incompetent perforators' sites, the facial deformities along the dilated veins, may be felt.One could feel a cough impulse across the SFJ. The tap test is a procedure whereby an impulse, which is typically absent due to competent valves, is felt distally along the vein after tapping over the SFJ. Foot pulses should be recorded if they are present. An AV fistula is indicated by the palpation of a thrill or the auscultation of a bruit.
Trendelenburg test: Capable of pinpointing valvular incompetence locations. The leg is lifted and the veins are emptied while the patient is supine. The SFJ is compressed using a hand or tourniquet. The leg is positioned dependently, and either before or after the tourniquet or hand is released, the veins are seen to be filling.
Hand Held  Doppler: Capable of displaying the valvular incompetence location.
Examining the pelvis or the rectum may be necessary if secondary reasons are thought to be present.

Pathogenesis 
Varicose vein etiology theories include primary valvular incompetence and the development of venous wall weakness as a result of anomalies in collagen and elastin, culminating in advanced stages of tunica media fibrosis. Hormonal fluctuations and venous hypertension are two more reasons that are implicated.

Investigations 
Visualization: Duplex ultrasound: Identifies reflux or incompetence locations. Moreover, to rule out DVT (essential if surgery is being considered). MR venography: reserved for complicated situations.

Management 
Conservative: Exercise recommendations (which enhance the calf muscle pump) and elevating the legs when at rest. Class II support stockings can help decrease edema and facilitate venous return.
Surgical procedures include SFJ ligation, lengthy saphenous vein stripping up to the knee, and varicosity avulsion using tiny stab incisions. To protect the sural nerve, the short saphenous vein is ligated rather than stripped.
Endovenous operations are becoming more and more common and can be carried out under local anesthesia. The long saphenous vein is ablateted using endovenous laser treatment (EVLT) after a tumescent local anesthetic is injected around the vein under ultrasound supervision. 
Thermal damage and ablation are also involved in radiofrequency ablation. With foam sclerotherapy, endothelial damage, inflammation, and subsequent vein fibrosis are caused by injecting sclerosing foam along the vein with the help of ultrasound guidance. The legs are wrapped following all treatments, and early mobilization is advised.
Using laser sclerotherapy or microinjection for reticular veins and venous telangiectasia.

Complications 
eczema, lipodermatosclerosis, venous ulcers, superficial thrombophlebitis, and venous pigmentation.
Treatment outcome: Recurrence. Intravenous therapy: Burns to the skin, nerve damage, bruises, emboli, and DVT. Surgical complications: bleeding, infection, nerve damage, or paraesthesia (up to 6%).

Prognosis 
generally progressing slowly. After surgery, recurrence rates can reach 40%.

Surgery - Chronic Lower Limb Ischemia 
Introduction 
Chronic vascular insufficiency of the lower extremities can cause ulcers or gangrene, as well as pain during exercise known as intermittent claudication.

Etiology 
Atherosclerosis in the leg arteries (femoral, iliac, and lower aorta).

Risk Factors 
Diabetes, high blood pressure, smoking, high cholesterol, and family history.

Epidemiology 
Common, occurrence 7–15% of senior citizens; male to female ratio is 2:1. In the UK, the yearly incidence of critical limb ischaemia is 50–100/100,000.

History 
La Fontaine's severity classification system:

I. Lack of symptoms.
II. Claudication that is intermittent. Calf cramps that occur during exercise after a continuous distance (claudication distance) and go away a few minutes after the exercise is stopped.
III. Pain while rest. severe aching pain in the foot or lower limb that usually goes away at night when the leg is draped over the edge of the bed.
IV. Gangrene or ulceration of the leg.

Critical ischaemia: Severe arterial insufficiency endangering the limb's survival when there is rest pain lasting more than two weeks, ulceration, or gangrene.
The Leriche syndrome: when lower aortoiliac blockage causes impotence and claudication in the buttocks and thighs.

Examination 
Check for evidence of hyperlipidemia, abdominal aortic aneurysm, carotid bruits, and signs of ischemic heart disease in the cardiovascular system.
Severe lower limb ischaemia is characterized by shining atrophic skin, atrophic nails, hair loss, and painful, punched-out ulcers (under toes, for example, or traditionally over the lateral malleolus). With weak or nonexistent pulses and a protracted capillary return time, the peripheries are chilly to the touch. 
Keep an ear out for bruits.
Buerger's examination: Pallor and venous guttering are the first signs of elevation of the leg, and dependent rubor follows.

The index of ankle-brachial pressure (ABPI): calculated by dividing the brachial pressure by the systolic ankle pressure, using a portable Doppler device. 0.8–0.6 for claudication; normal >0.9.
<0.5 or ankle systolic <50mmHg or toe systolic <30mmHg is considered critical ischaemia (numbers may be erroneously high in diabetics due to weakly compressible arteries).

Investigations 

Imaging: CT, MR, or arterial duplex angiography. Those receiving intervention can use digital subtraction angiography.
Bloods: FBC, lipids, glucose, coagulation, and preintervention group and save.

Management 
Medical: It has been demonstrated that supervised programs are beneficial; quit smoking and promote exercise. Treatment of other cardiovascular risk factors, such as aspirin, statins, and antihypertensives (avoid b-blockers). Patients with serious ischemia who are not responding to previous treatments may occasionally receive prostacyclin infusions.
Endovascular surgery includes arterial stenoses stenting and/or balloon angioplasty.
Surgical: For severe ischaemia or intermittent claudication that is incapacitating.
Revascularization: The technique varies according on the occlusion site.
Aortoiliac occlusive disease: unilateral iliac disease (femoro-femoral or ilio-femoral bypass), aorto-bifemoral bypass, or occasionally axillo-bifemoral bypass.

The term "femoropopliteal disease" refers to conditions involving the grafting of autogenous tissue, such as saphenous vein (either reversed or in situ with valves damaged with a valvulotome), or synthetic tissue, such as PTFE, for bypass purposes. In the case of the latter, longer-term patency rates are considerably increased by a vein patch (Millar cuff) at the distal anastomosis. 
observation of the graft with duplex scanning after surgery.
In cases of end-stage atherosclerotic disease, amputation is recommended if revascularization is not feasible, there is a substantial amount of necrosis, or sepsis is spreading. Revascularization may make it possible to amputate below the knee as opposed to above; the former is linked to improved mobility and the usage of prosthetic limbs after surgery.


Complications 
If wet, there is a danger of systemic sepsis, multiorgan failure, pain, ulceration, and gangrene.
3–4% risk with angioplasty, including thrombosis, embolism, dissection, flap, and failure.
From bypass grafting: . Early: Edema, infection, lymphocoele, hemorrhage, cardiac events, and graft thrombosis. Late: Graft stenosis, anastomotic false aneurysm, and thrombosis. Overall, patency rates above the knee (70–80% at 3 years) are higher than those below.

Prognosis 
Patients with lower limb ischaemia have an elevated risk of MI and stroke because it is a sign of atherosclerosis throughout the arterial tree. About 40% of people with intermittent claudication get better, 40% stay stable, and 20% worsen over the course of five years and need medical attention.

Surgery - Acute Ischemic Lower Limb 
Introduction 
abrupt blockage of the supplying artery resulting in limb ischaemia.

Etiology 
Pathophysiology: Abrupt stoppage of blood flow. Emboli typically settle in the locations where vessels split. Cell injury occurs in two stages: ischemic injury, which occurs when tissues are cut off from blood flow, and reperfusion injury, which occurs when blood flow is restored.
Thrombosis: Low flow conditions, such as hypovolemia, aneurysm, graft stenosis, atherosclerosis, and thrombotic states.
Heart: 90%, great vessels: 9%, and other: 1% are the sources of embolism. Atrial fibrillation, myxoma of the atrium, aneurysms, valvular heart disease, and recent MI.
Trauma or dissection are two examples of vascular damage.

Epidemiology 
14 cases out of 100,000 are estimated.
Pallor, pain, paraesthesia, pulselessness, paralysis, and a perishingly cold limb are the six Ps.The location of occlusion, length of ischaemia, and level of collateral circulation all affect the symptoms and signs.

Embolus is more likely to occur in cases of severe, abrupt onset, and recognizable possible cause, such as atrial fibrillation.
Thrombosis is typically less severe if collaterals are present, there is a history of peripheral vascular disease or claudication, and there isn't an identifiable embolus source.

Examination 
Pale limb with no pulse; capillary return is slow.
After a few hours, there is capillary rupture-related venous stagnation, which causes a mottled appearance and, in later stages, permanent staining. There are changes in sensation, and if the ischemia is severe, there may be muscle paralysis and anesthesia, indicating that the limb may not be viable.

Investigations 
Blood tests: thrombophilia screen, coagulation profile, G&S, FBC, and U&Es.
Imaging: CXR, Doppler or duplex blood flow scans, arteriography to show the occlusion site and, if the limb is still viable, to arrange an operation.
ECG: Checking for irregular heartbeat.

Management 

Immediate: Heparin anticoagulation, analgesics, and ABCs to stop the spread of thrombus.
Surgery: Revascularization in six hours to save the limb. When cardiac disease is present, there is frequently a substantial operational risk. Anticoagulation after surgery is crucial.

If an embolus is found, an embolectomy will be performed, which entails artery isolation, arteriotomy, and the insertion of a Fogarty balloon-tipped catheter that will be inserted past the embolus and then withdrawn to recover the embolus.

If the thrombosis is acute or chronic, collateral development may allow the limb to survive longer. In this case, percutaneous intervention such as suction, intraarterial thrombolysis with local infusion of t-PA, and angioplasty of underlying stenoses are viable options.


In the event that thrombosis is required for this treatment but the limb is not expected to survive for 12 to 24 hours: If physically feasible, urgent reconstructive surgery using synthetic (PTFE or Dacron) or autogenous (saphenous vein) bypass grafting is needed. 

Fasciotomy is necessary if compartment syndrome is a concern.

Amputation of the limb in question.

Complications 
From disease: death, limb loss, and gangrene.
From intra-arterial thrombolysis: severe bleeding, CVA, and mortality (1-2%).
Reperfusion syndrome, compartment syndrome, rhabdomyolysis, and rethrombosis are post-treatment complications.

Prognosis 
There is a 30% chance of losing a limb; 10% of people die from it, with heart disease being the main cause of death.

Surgery - Deep Vein Thrombosis 
Introduction 
thrombus formation in the deep veins, usually in the thigh or calf.

Etiology 
Virchow's triad: blood hypercoagulability, vascular wall damage, and venous stasis.

Risk Factors 
Factor V Leiden, deficits in Protein C or Protein S deficienceis  Prothrombin mutation, and insufficient Antithrombin III are all inherited.

Oral contraceptive pill, heparin-induced thrombocytopenia, immobility, obesity, pregnancy, polycythemia, anti-phospholipid syndrome, smoking, nephrotic syndrome, and aggressive cancer are among the acquired conditions.

Epidemiology 
Frequent, particularly in hospitalized patients; precise prevalence is unclear. Venous insufficiency and ulceration, long-term consequences of DVT, afflict 0.5 percent of the population. Around 145 per 100,000, around.

History 
asymptomatic or soreness or edema in the lower limbs. may exhibit pulmonary embolus signs and symptoms.

Examination 
Check for any swelling or soreness in the calf.
It is uncommon to have severe leg cyanosis and oedema (phlegmasia cerulea dolens).
checking the airways for indications of a pulmonary embolus.

Investigations 

Ultrasound Doppler: The gold standard. Less sensitive in calf veins, but good sensitivity in femoral veins.
Bloods: Only low-risk individuals can benefit from the sensitive but very non-specific D-dimers (fibrinogen degradation products) as a negative predictor. Before beginning anticoagulation, a thrombophilia screen should be sent if necessary (e.g., recurring occurrences).
FBC (platelet count before beginning heparin), coagulation, and U&E.
ABG, CXR, and ECG: If there is a possibility that PE may be present.

Management 

Anticoagulation: While waiting for a therapeutic INR from warfarin anticoagulation, patients should receive heparin treatment. Anticoagulation is prescribed for three months for DVTs that do not extend above the knee and for six months for those that do. Warfarin may be needed for a long time if DVTs recur. Interventional radiology should install an IVC filter, such as the Greenfield filter, if active anticoagulation is contraindicated or there is a high risk of embolization in order to prevent embolus to the lungs.
Using graded compression stockings is one way to prevent. mobilizing, if at all possible. Hospital patients who are considered to be at-risk should receive preventive heparin, such as low-molecular-weight heparin, provided there are no contraindications.

Complications 
Disease symptoms include pulmonary embolus, impaired vein valves, and persistent lower limb venous insufficiency (post-thrombotic syndrome). Venous infarction, or phlegmasia cereulea dolens, is uncommon.
Heparin-induced thrombocytopenia and bleeding are side effects of treatment.

Prognosis 
based on the severity of DVT. More proximal DVTs have a higher chance of propagation and embolization, which, if significant, may be deadly. Below-knee DVTs have a decreased risk of embolus.

Surgery -  Carotid Body Tumor 
A chemodectoma is a tumor that develops from chemoreceptor cells at the carotid bifurcation.

Etiology 
 connected to changes in the mitochondrial succinate dehydrogenase complex subunits. With autosomal dominant inheritance, one-third are family (more likely to be bilateral and numerous).
Shamblin has classified:. Type I: Carotid bifurcation-derived little tumors that are easily dissected. Type II: More expansive and sticky, involving but not encasing vessels. Type III: Encircling the carotid bifurcation, large in size.

Risk factors linked to von Hippel-Lindau syndrome, MEN II, and NF1.
People who spend extended periods of time living at high elevations have a "incidence."


The study of epidemiology 
uncommon. Present at any age; however, women are more likely than males to do so between the ages of 50 and 70.


History 
Most frequently manifests as a gradually expanding lump in the neck. Symptoms include dysphagia, choking, and hoarseness may be brought on by pressure on surrounding cranial nerves.

Examination 

A neck lump with transmitted pulse that is located in the carotid triangle of the neck. Horner syndrome with paresis or palsy of the cranial nerves VII, IX, X, and XI may be present.

Pathophysiology 

Paragangliomas, which include glomus jugulare tumors, pheochromocytomas, and vagal body tumors, are tumors produced from neural crest tissue. One type of paraganglioma is the carotid body tumor.
Vascular tumor with sustentacular cells encircling clusters of zellballen of epithelioid "chief cells" Although they have the capacity to release catecholamines, the cells are often nonsecretory.

Investigations 

Imaging: The link between the carotid bifurcation can be demonstrated by ultrasound and duplex scanning; angiography, which can be either CT or MR, verifies the typical splaying of the internal and external carotid arteries as well as the wine-glass-shaped tumor blush.
A CT or MRI scan is used to ascertain the tumor's extent. Metaiodobenzylguanidine (131I-MIBG) scintigraphy in functioning tumors.
Pharyngoscopy, both direct and indirect, can be used to evaluate pharyngeal invasion or involvement of cranial nerves.
Urine: VMA, metanephrine, and catecholamines.

Management 

Surgery: Risk based on tumor size and extent. Due to their high vascularity, big tumors may be embolized prior to surgery (a controversial procedure), and preoperative blood should be cross-matched. Excision of the tumor surgically: Tumor size and place determine the incision. cautious jugular vein dissection and control, detection of nerves, and carotid artery dissection. Following the ligation of the cancer feeding vessels, the tumour is meticulously removed from the carotid vessels. Internal carotid artery replacement or sacrifice is frequently necessary for type II tumors.
Radiotherapy: For individuals who are weak, have a lot of coexisting conditions, or have cancers that come back frequently.

Chemotherapy: Vincristine, dacarbazine, cyclophosphamide, and 131I-MIBG are among the agents utilized in systemic metastases.


Complications  
Tumor: Local invasion leading to distal metastases and cranial nerve palsies.
Bleeding, nerve injury (15 percent, mandibular branch of VII, IX, X, particularly the recurrent laryngeal nerves, XII), and stroke risk are associated with surgery.

Prognosis 
Young people with heritable tumors are most at risk; the majority are benign, with 5-7% malignant with the ability to spread to the lung, liver, and bones. Typically slow-growing; surgery can cure the majority of patients.

Surgery - Carotid Artery Disease  (Atherosclerosis)
Introduction 
Atherosclerosis-induced carotid artery narrowing is a common cause of stroke.

Etiology 
By causing distal embolization, thrombosis, or poor flow, atheromatous plaque at the common carotid bifurcation or any of the carotid branches might result in stroke or blindness. Atherosclerosis is widespread in the carotid artery bifurcation, a region of the vascular tree. Local hemodynamics, such as low shear stress and "turbulence affecting the outer walls opposite the flow divider," in conjunction with systemic risk factors, predispose to the formation of atheroma, luminal constriction, and the risk of plaque rupture, thrombosis, or embolism.

Epidemiology 
frequent, a major contributor to long-term impairment and the third greatest cause of death in the UK, frequency increases with age and is more frequent in men.

History 
frequently asymptomatic.
Amaurosis fugax: An embolism into the ophthalmic artery (an internal carotid artery branch) causes a transient unilateral vision loss that is described as "like a curtain coming down."
Temporary ischemic episodes (TIAs): Severe symptoms that persist less than a day could be a sign of an impending stroke. Following a TIA, people with an ABCD2 score of 4 (which requires immediate examination and treatment) are more likely to get a stroke.
Factor ABCD2  

Age over 59 years old: 1 point 
Presentation BP of 140/90 (1 point)
Clinical Characteristic :

Disturbance in speech but no weakness (1 point)
One-sided vulnerability (2 points)

Duration (minutes): 10–59  (1  point) 
>60   (2  points)
Diabetes (1 point)

Crescendo TIAs are TIAs that get longer, more severe, or happen more frequently. This is linked to a significant internal carotid artery stenosis.
Stroke: Long-lasting neurological impairment (based on the infarct-affected region).


Examination 

Examined normally shows no abnormalities if asymptomatic.
The degree of stenosis is not indicated by the presence of a carotid bruit.
symptoms of a TIA or CVA, such as limb weakness, dysphasia, or dysarthria.


Investigations 

This non-invasive imaging method uses duplex Doppler carotid ultrasound to measure the degree of stenosis.
Brain and carotid imaging using CT, CTA, MRI, and MRA (Fig. 35).
Angiography: Very accurate measurement of the severity of stenosis, invasive (stroke risk ∉1%).

Management 

The 90-day risk of recurrent stroke was found to be 80% lower with prompt assessment and treatment, according to the Early Usage of Existing Preventive Strategies for Stroke (EXPRESS) research. A TIA clinic should see everyone who has had a TIA or mild stroke (urgency evaluated by ABCD2 rating).

Medical treatment for: asymptomatic stenosis, <70% internal carotid artery stenosis (ECST criteria), <50% (NASCET criteria), or inoperable illness; low-dose aspirin; cessation of smoking; and treatment of additional risk factors, hypercholesterolemia, hypertension, and diabetes.

Surgical intervention: Carotid endarterectomy, however associated with a high perioperative risk, lowers the risk of further stroke in ECST and NASCET trials when performed within two weeks following a stroke or TIA.
May be taken into consideration in cases of crescendo TIAs that do not respond to therapy, symptomatic stenosis of 70–99% (ECST criteria), or 50–99% (NASCET criteria).
It is debatable whether surgery should be used to treat a disease that shows no symptoms.
Angioplasty, with or without stenting: A comparison with carotid endarterectomy for symptomatic illness is now being conducted.

Complications 
Disease-related complications: thromboembolic or watershed stroke.
Surgical complications: Cardiac ischaemia or infarction (3%), nerve injury (2–7%, mandibular branch of facial nerve, recurrent laryngeal or hypoglossal nerves), haematoma, hypertension, hypotension, perioperative stroke (1–5%). There is a 0.5-2.8% perioperative mortality rate.

Prognosis 
The annual stroke rate is 10–20% with carotid artery stenosis greater than 70%.
In patients with severe stenosis, surgical correction can result in a six- to eight-fold reduction in stroke risk when compared to the best medical therapy alone.

​Surgery - Arteriovenous Fistulae and Malformations 
Introduction 
An irregular link between an artery and vein that avoids the capillary bed is called an arteriovenous fistula.
vascular malformations: Deformity exhibiting typical endothelium.
Angioma/hemangioma: Deformity characterized by endothelial hyperplasia.

Etiology 
Congenital: categorized into malformations (AVMs) and haemangiomas (strawberry naevi, for example). The latter is separated into high flow and low flow types (such as pulmonary or hepatic AVM;

genetic: AVMs and haemangiomas are linked to a variety of genetic disorders, including hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) and Klippel–Trenaunay, Kasabach–Merritt, Sturge–Weber, and von Hippel–Lindau.

Aorto-venocaval fistula, glomus tumor, hypernephroma, sarcomas, infections, inflammations, or iatrogenic conditions (e.g., Brescia-Cimino fistula for hemodialysate or portocaval shunt in portal hypertension) are examples of acquired conditions.


Epidemiology 

The others are less prevalent than cutaneous haemangiomas.

History 

Depending on the location and extent of the AVM, symptoms might manifest differently and may result from either local or systemic effects (see Complications).
Congenital cutaneous haemangiomas frequently become apparent at birth or shortly thereafter.
Typically, malformations enlarge with aging, puberty, or pregnancy.
Internal organs may not exhibit symptoms until issues arise.
Other symptoms could be discomfort or swelling in the limbs, or varicose veins.

Examination 
Cutaneous haemangiomas, also known as Campbell de Morgan spots, are often firm, crimson in color, and blood-filled when compressed.
An overlaying bruit or palpable thrill, possibly accompanied by decreased distal pulses and increased pulse pressure, may indicate the presence of internal AVMs.


Investigational studies

AVM imaging: Depending on where the lesion is located. Among the modalities employed are invasive angiography, CT or MRI scanning, and duplex scanning.
SPECT scan: Radiolabelled microspheres that are too big to go through capillaries are injected into an artery to quantify AV shunting. Using a gamma camera, those going through AVMs are trapped in the lungs and measured.

Management 

Conservative: By the end of the first year of life, cutaneous haemangiomas typically spontaneously recede. Internal organ AVMs can be watched and may not require treatment.
Interventional radiology: Metal coils, tissue adhesive, or particles can be used to embolize internal AVMs or fistulae.
Surgery: Excision (following pre-operative embolization) is often challenging, although it is a possibility for small and easily accessible AVMs.

Useful for tiny AVMs, stereotactic radiosurgery may take years to fully manifest.

Complications 
Cutaneous: bleeding, ulcers, and cosmetic deformity.
Organ-specific: For example, lung AVMs might result in hemoptysis or paradoxical embolism; brain AVMs can induce localized neurological impairments, convulsions, or stroke.

Peripheral tissue ischemia is considered distal.
Systemic: When there are significant AVMs, high-output heart failure may occur.

Prognosis 
Depending on the aetiology and site. 90% of haemangiomas regress over a period of 5 to 10 years, while cerebral AVMs carry a 1-4 percent yearly risk of hemorrhage.

Surgery - Aortic Dissection 
Introduction 
A disorder where blood can enter the aorta wall through a rupture in the aortic intima, splitting the inner and outer tunica media and forming a false lumen.

Etiology 
The predisposing event is degenerative alterations in the aortic media's smooth muscle.
Aortic atherosclerosis, hypertension, connective tissue diseases (SLE, Marfan's, Ehlers-Danlos), congenital cardiac abnormalities (aortic coarctation, for example), aortitis (Takayasu's aortitis, tertiary syphilis), iatrogenic (during angiography or angioplasty, for example), trauma, and crack cocaine are common causes and predisposing factors.

Aortic Dissection is divided by Stanford categorization into:
Type A: Aorta tears that ascend (most common); Type B: Aorta tears that descend, extending away from the left subclavian artery.
False aneurysm expansion can block the renal, celiac, subclavian, or carotid arteries.

Epidemiology 

most typical in the age range of 40 to 60. Men outnumber women.

History 
An MI may seem like an abrupt core tearing pain that radiates to the back.
The aorta and its branches may become occluded as a result of aortic dissection.
Blackout, dysphasia, and hemiparesis due to carotid blockage.
Chest pain due to coronary artery blockage (angina or MI).
Ataxia and loss of consciousness due to subclavian blockage.
Paraplegia: anterior spinal artery.
Severe abdominal pain due to a celiac blockage (ischaemic bowel).
Renal failure and anuria due to renal artery blockage.

Examination 
A murmur on the back that descends to the belly below the left scapula.
Blood pressure: Wide pulse pressure, hypertension (BP difference between arms of >20 mmHg). In case hypotension indicates tamponade, make sure to look for pulsus paradoxus.
An insufficient aorta Early diastolic murmur across the aortic region, collapsing pulse.
Arm pulses that aren't equal.

Investigational studies

Blood: coagulation, U&E (renal function), FBC, and cross-match.
CXR: Localized aortic arch bulging and widened mediastinum.
ECG: Usually normal. indicators of inferior MI or left ventricular hypertrophy if the right coronary artery's ostia is compromised by dissection.
False lumen of dissection visible in CT thorax abdomen.
Trans-oesophageal echocardiography is quite specific.
Vascular angiography and cardiac catheterization.

Management 
Acute: In the event that resuscitation is suspected, an immediate CT scan should be carried out. Restart the heart and keep an eye on your blood pressure, pulse, and urine catheter. Idealized for ITU management.
Surgery is used to treat type A dissection. A surgical emergency due to the possibility of cardiac tamponade. A tube graft is used to repair the damaged aorta. Replaced aortic valves are another option.
Treatment options for type B dissection include medication, surgery, and endovascular stenting. take IV nitroprusside and/or IV labetalol to control blood pressure and stop additional dissection (take a calcium channel blocker if b-blockers are contraindicated). Patients with end-organ ischemia, aortic enlargement, intractable or recurrent pain, or dissection advancement may benefit from surgery. Some centers offer endovascular repair, a more recent procedure that uses endovascular stents (ADSORB trial results awaited).

Complications 
cardiac tamponade, syncope, cerebrovascular, renal, mesenteric, or spinal ischaemia; aortic rupture.

Prognosis 
30% in 24 hours and 75% at 2 weeks of untreated mortality.
5–10% operational mortality. 10% more suffer from neurological aftereffects.
Type B has a better prognosis than type A.

Surgery - Abdominal  Aortic Aneurysm
Defintion 
a deviation of >3 cm, or 50% over the normal diameter, in the abdominal aorta's localized dilatation. mostly affects the infrarenal aorta (95%) and the iliac arteries (30%).

Etiology 
Degeneration of collagen and elastin in the artery wall is most likely the cause. frequently connected to atherosclerosis. Other conditions include connective tissue illnesses including Marfan's syndrome and Ehlers-Danlos type IV, traumatic injuries, infectious (mycotic), inflammatory (chronic inflammatory infiltration in the artery wall), and arthritis.

Risk Factors 
Hypertension, smoking, coronary artery disease, popliteal artery aneurysms, smoking, and family history (10-fold "risk if first-degree relative affected). According to Laplace's law (tension as a radius, pressure), the diameter affects the likelihood of rupture. The risk for AAAs is 3.3% annually for 5–5.9 cm, 9.4% annually for 6–6.9 cm, and 24% annually for 7–7.9 cm.

Epidemiology 
15% of people over 80 years old and 5% of people over 60 will have a AAA. Four to six times more common in men; in England and Wales, there are 6000 deaths annually.

History 
Often asymptomatic, it can be discovered by accident during testing, imaging, or inspection.
Symptoms: The most typical presentation is collapse or epigastric or back pain due to the rupture of an unidentified AAA. Most patients who are admitted to the hospital have a retroperitoneal leak.
Perhaps mistaken as diverticulitis, muscular back pain, or renal colic. Because of distal embolization or vertebral erosion, intact aneurysms might result in lower limb ischaemia or back pain. Occasionally, exhibit severe gastrointestinal bleeding from erosion into the duodenum or high-output heart failure from an aortocaval fistula.

Examination 
One feels a pulsating mass over the umbilicus. If there is leakage or rupture, pallor in the abdomen and back, tachycardia, hypotension, hypovolaemic shock, sporadic bruises on the flanks, and indications of emboli to the feet.

Investigational studies
Sharp presentation Bloods: coagulation, ECG, CXR, U&Es, FBC, and urgent blood cross-matching.
Bedside ultrasonography: To verify the aneurysm's size and presence.
In stable or diagnostic uncertainty: If stable or diagnostic doubt.
CT scan: Not if unstable; instead, proceed directly to the operating room or endovascular suite for repair.
Numerous facilities provide emergency EVAR.
Examining: Research, like the Multicentre Aneurysm Screening Study (MASS), has demonstrated that screening males 65 years of age and older with ultrasound reduces the mortality associated with aneurysms, is economical, and will, over the course of 20 years, minimize the need for emergency surgery by more than two-thirds.
To determine the morphology of an aneurysm before therapy, use CT or MR angiography.

Conservative management of asymptomatic aneurysms (less than 5.5 cm) involves regular follow-up ultrasound scanning (every 3.4 cm annually, or every 6 months if enlargement exceeds 10% annually), as well as managing cardiovascular risk factors. This was shown by the UK Small Aneurysm Study.

Radiological: There are ongoing research comparing endovascular treatment with stent placement (EVAR) against open repairs. EVAR is becoming more common. Between 40 and 60 percent of AAAs are acceptable, meaning they have a neck and landing sites that are ideal for the endograft. When EVAR and open surgery were compared in individuals deemed surgically capable, EVAR1 had a 3% advantage in aneurysm-related survival after 4 years. When EVAR2 was applied to unfit patients, it did not find any differences in all-cause mortality between EVAR and no intervention.

Surgical: Using tube or bifurcation grafts (see to Procedures) is recommended for: asymptomatic aneurysms larger than 5.5 cm in diameter; symptomatic or quickly increasing aneurysms; emergency treatment (e.g., suspected leaking or ruptured aneurysm).


Complications 
The most common include rupture, distal embolus, abrupt total thrombosis, gram-negative or staphylococcal infection, persistent consumptive coagulopathy, ischaemia of the gut, aortic-intestinal fistula, and arteriovenous fistula resulting from aneurysm eroding into the inferior venous catheter.
following surgery: bleeding, thrombosis, embolism, colonic ischaemia, renal failure, problems related to the heart and lungs, and death.
Of EVAR: As mentioned before; also, migration, endoleak, kinking/distortion, fracture of the stent, renal infarction, and limb/pelvic ischaemia.

Prognosis 
Only roughly 50% of patients with a ruptured AAA survive once they get at the hospital, accounting for the remaining 80% of deaths.
Mortality from elective open surgery is less than 5% in specialized centers. EVAR has a 2% death rate, however re-intervention rates are greater and observation is necessary.

​Surgery - Urinary Tract Calculi 
Definition 

stone buildup in the urinary system. also referred to as renallithiasis.

Etiology 

Urine becomes supersaturated with chemicals that form stones, causing crystallization around a focal point and creating calculi.
Calculus type and description

80% calcium phosphate and calcium oxalate. 
Can be dotted, mulberry, or spiculated varieties

10%–20% of magnesium ammonium phosphate (struvite).
connected to microorganisms splitting urea, such as Proteus, Pseudomonas, and Klebsiella. may cause kidney stones known as staghorn stones.

5%  are urate,occurs in urine that is acidic and is linked to cell lysis, small bowel illness, and gout.

Cystine
Rare (<1%). forms in the uncommon autosomal recessive metabolic disease cystinuria


Etiology 
Hypercalciuria, hyperuricaemia, hypercystinuria, and hyperoxaluria are metabolic conditions.

Infection: Bacteria splitting urea, causing hyperuricemia.
Urinary stasis is caused by anatomic factors such as the horseshoe kidney and caliceal diverticulae.
Renal tubular acidosis type I, medullary sponge kidney, and adult polycystic kidney disease are examples of kidney diseases.
Medicines: indinavir, for instance.

Epidemiology 

Prevalence: 2-3%, common. Risk over lifetime is 5–15%. 15% of cases are bilateral. A 3:1 male to female ratio.

History 

be absent of symptoms. Severe discomfort extending from the loins to the groins caused by ureteric stones may be accompanied by nausea and vomiting.
urgency, regularity, infections, or retention of the urine.
Microscopic or frank haematuria (may not be present in up to 10% of cases).

Examination 

Tenderness in the lower abdomen or loins. The most crucial differential diagnosis for elderly people to take into account is a leaking AAA. indications of systemic sepsis in the event of infection and blockage.

Investigational studies

Blood: FBC, PO4 3-, urate, Ca2+, and U&E (to evaluate renal function).
Urine: 24-hour urine collection, dipstick, microscopy, culture, and sensitivity.
CT scan (KUB film): Ninety percent of stones appear on a plain radiograph because they are radio-opaque.
Intravenous urogram: At first, a delayed dense nephrogram is seen with an obstructed ureteric stone; later images reveal a dilated pelvicaliceal system and a standing column of contrast down to the stone's location.


Non-contrast CT: Higher radiation dose, most sensitive for detecting stones.
Ultrasound: Not sensitive for tiny stones, but can demonstrate hydronephrosis or ureteral dilatation due to obstructive uropathy. used in patients who shouldn't be exposed to radiation or contrast, such as those who are pregnant.

Isotope renography: Evaluation of renal function in complex stone disease (e.g., using DTPA or DMSA).

Management 
Analgesia and IV or oral hydration are the treatments for acute presentation. collecting urine to get the calculations that passed analysis. Ideal for stones that don't obstruct; most stones that are less than 5 mm can pass. Stones can be passed by ureteric relaxation with the aid of alpha-blockers, such as alfusozin. A kidney that has become infected and obstructed needs to be treated immediately. This can be done with a ureteroscopy and stent or a radiologically guided percutaneous nephrostomy along with supportive care and antibiotics.


Calculus removal: Suggested in cases of pyrexia, persistent discomfort, or blocking stones.

Ureteroscopy: A rigid or flexible ureteroscope is inserted into the bladder and up the ureter to visualize the stone, which can then be removed with a grasper, basket, or laser or ultrasonography. Urine drainage should be ensured by the placement of a JJ stent in the event that the stone is affected and cannot be removed.

Outside-the-body shock-wave lithotripsy: Non-intrusive. Calculus is subjected to an electromagnetic or piezoelectric shock wave in order to split it up into smaller pieces that can naturally pass. Fit for stones smaller than 2 cm, provided that there is no drainage blockage.

Nephrolithotomy via percutaneous means: Used for large, complicated stones, such as staghorn calculi. A nephroscope is inserted after the nephrostomy path is created, enabling the dissolution and removal of stones. During the first two days following surgery, a nephrostomy tube is left in place, and a nephrostogram is done to make sure the stone is gone and to verify ureteric drainage.


Seldom done open nephro-, pyelo-, or ureterolithotomies (for complicated cases).
Nephrectomy: in case of a non-functioning kidney, may be necessary.
Management of the cause: Based on the underlying reason, such as parathyroidectomy, dietary calcium or oxalate limitation, or allopurinol. Urate and cystine stones can be broken up by urine alkalinization with oral potassium citrate.
Suggestion: Promote a substantial intake of oral fluids.

Complications 
Of stones: Septicemia, urinary retention, and infections, including pyelonephritis.
False route, perforation in ureteroscopy.
Pain, haematuria, and steinstrasse—a ureteric blockage brought on by a column of broken stone—are symptoms of lithotripsy.

Prognosis 
Excellent, yet there is a 50% chance of recurrence during a five-year period, and infection may cause irreparable kidney scarring.