The most likely diagnosis is median arcuate ligament syndrome (MALS).

MALS, also known as coeliac artery compression syndrome, is a condition characterized by abdominal pain attributed to compression of the coeliac artery and the coeliac ganglia by the median arcuate ligament. The pain may be related to meals, may be accompanied by weight loss, and may be associated with an abdominal bruit.

The diagnosis of MALS is one of exclusion, as many healthy patients demonstrate some degree of coeliac artery compression in the absence of symptoms. Consequently, a diagnosis of MALS is typically only entertained after more common conditions have been ruled out. Once suspected, screening for MALS can be done with USS and confirmed with CT or MRI scan.

Treatment is generally surgical, the mainstay being open or laparoscopic division or separation of the median arcuate ligament combined with removal of the celiac ganglia. The majority of patients benefit from surgical intervention. Poorer responses to treatment tend to occur in patients of older age, those with a psychiatric condition or who use alcohol, have abdominal pain unrelated to meals, or who have not experienced weight loss.

Lymphovenous anastomosis – Identifiable lymphatics are anastomosed to sub dermal venules. Usually indicated in 2% of patients with proximal lymphatic obstruction and normal distal lymphatics.

Causes of lymphoedema:
Primary:
Sporadic, Milroy’s disease, Meige’s disease
Secondary:
Bacterial/fungal/parasitic infection (filariasis)
Lymphatic malignancy
Radiotherapy to lymph nodes
Surgical resection of lymph nodes
DVT
Thrombophlebitis

Other options given:
Homans operation – Reduction procedure with preservation of overlying skin (which must be in good condition). Skin flaps are raised and the underlying tissue excised. Limb circumference typically reduced by a third.

Charles operation – All skin and subcutaneous tissue around the calf are excised down to the deep fascia. Split skin grafts are placed over the site. May be performed if overlying skin is not in good condition. Larger reduction in size than with Homans procedure.

This patient has an axillary vein thrombosis. It classically presents with pain and swelling of the affected limb. Venous duplex scan is needed to exclude a thrombus.

Primary proximal upper-extremity deep vein thrombosis (UEDVT) is less common than its secondary forms. The most common primary form is effort-related thrombosis, also called Paget-Schroetter syndrome. It usually occurs in, otherwise, healthy young men who report, before the onset of thrombosis, vigorous arm exercise such as lifting weights, playing badminton/tennis, pitching a baseball, or performing repetitive overhead activities, such as painting or car repair. Most patients with effort-related UEDVT have an underlying venous thoracic outlet syndrome (VTOS). Secondary causes of UEDVT include central line insertion, malignancy, or pacemakers.

Patients with UEDVT typically present with heaviness, discomfort, pain, paraesthesia, and swelling of the affected arm. Physical examination may reveal pitting oedema, redness, or cyanosis of the involved extremity; visible collateral veins at the shoulder or upper arm; and fever.

Diagnosis is made by:
1. FBC: platelet function
2. Coagulation profile
3. Liver function tests
4. Venous duplex scan: investigation of choice, provides information relating to flow and characteristics of the vessels.
5. D-dimer testing
6. CT scan: for VTOS

Treatment options for primary UEDVT are as follows:
1. Anticoagulation therapy should be undertaken with a once-daily regimen of LMWH or fondaparinux for at least five days, followed by vitamin K antagonists for at least three months. Unfractionated heparin instead of LMWH is recommended for patients with renal failure or for those treated with CDT.

2. Early thrombus removal and restoration of venous patency aim should be done immediately after starting the patient on heparin. Catheter-based therapy is recommended for patients with proximal UEDVT of recent onset and severe symptoms, low risk for bleeding complications, and good functional status.

The presence of a necrotic and infected forefoot with necrosis of the heel and a boggy indurated swelling anterior to the ankle joint in a patient with sepsis secondary to diabetic foot ulcer indicates that a below knee amputation is the best option.

Based on Wagner’s Classification of Diabetic Foot Ulcers, this patient has a grade of 5 where there is gangrene or necrosis of large portion of the foot
requiring major limb amputation.

Infection in a diabetic foot is usually secondary to ulceration. Rarely, infection itself causes ulceration. It can either be local or systemic. Treatment requires early incision and drainage or debridement and empirical broad-spectrum antibiotic therapy. If there is co-exiting gangrene or extensive tissue loss, early amputation at the appropriate level should be considered to remove the focus of infection.

Klippel-Trenaunay syndrome is a condition that affects the development of blood vessels, soft tissues (such as skin and muscles), and bones. The disorder has three characteristic features: a red birthmark called a port-wine stain, abnormal overgrowth of soft tissues and bones, and vein malformations.

Most people with Klippel-Trenaunay syndrome are born with a port-wine stain. This type of birthmark is caused by swelling of small blood vessels near the surface of the skin. Port-wine stains are typically flat and can vary from pale pink to deep maroon in colour.

Klippel-Trenaunay syndrome is also associated with overgrowth of bones and soft tissues beginning in infancy. Usually this abnormal growth is limited to one limb, most often one leg. However, overgrowth can also affect the arms or, rarely, the torso.

Malformations of veins are the third major feature of Klippel-Trenaunay syndrome. These abnormalities include varicose veins and deep veins in the limbs. Malformations of deep veins increase the risk of a deep vein thrombosis (DVT).

Other complications of Klippel-Trenaunay syndrome can include cellulitis, lymphedema, and internal bleeding from abnormal blood vessels. Less commonly, this condition is also associated with fusion of certain fingers or toes (syndactyly) or the presence of extra digits (polydactyly).

Adductor canal compression syndrome most commonly presents in young males, and it is important to differentiate it from acute limb ischaemia on exertion. Of the listed options, popliteal fossa entrapment is the main differential diagnosis. However, the popliteal pulse disappears when the knee is fully extended in popliteal fossa entrapment.

Adductor canal compression syndrome is caused by compression of the femoral artery by the musculotendinous band of adductor magnus muscle. The treatment consists of division of the abnormal band and restoration of the arterial circulation.

Catheter-directed thrombolysis (CDT) is recommended as the next step of management for patients with proximal upper-extremity deep vein thrombosis (UEDVT) of recent onset or severe symptoms.

Primary UEDVT is less common than secondary forms. The most common primary form is effort-related thrombosis, also called Paget-Schroetter syndrome. It usually occurs in otherwise healthy young men who report, before the onset of thrombosis, vigorous arm exercise such as lifting weights, playing badminton, pitching a baseball, or performing repetitive overhead activities, such as painting or car repair. Most patients with effort-related UEDVT have an underlying venous thoracic outlet syndrome (VTOS). Secondary causes of UEDVT include central line insertion, malignancy, or pacemakers.

Patients with UEDVT typically present with heaviness, discomfort, pain, paraesthesia, and swelling of the affected arm. Physical examination may reveal pitting oedema, redness, or cyanosis of the involved extremity; visible collateral veins at the shoulder or upper arm; and fever.

Diagnosis is made by:
1. FBC: platelet function
2. Coagulation profile
3. Liver function tests
4. Duplex scan: investigation of choice
5. D-dimer testing
6. CT scan: for VTOS

Treatment options for primary UEDVT are as follows:
1. Anticoagulation therapy should be undertaken with a once-daily regimen of LMWH or fondaparinux for at least five days, followed by vitamin K antagonists for at least three months. Unfractionated heparin instead of LMWH is recommended for patients with renal failure or for those treated with CDT.

2. Early thrombus removal and restoration of venous patency should be done immediately after starting the patient on heparin. Catheter-based therapy is recommended for patients with proximal UEDVT of recent onset and severe symptoms, low risk for bleeding complications, and good functional status.

A cervical rib in humans is an extra rib which arises from the C7 vertebra. Its presence is a congenital abnormality located above the normal first rib, and it consists of an anomalous fibrous band that often originates from C7 and may arc towards but rarely reaches the sternum. It is estimated to occur in 0.2% to 0.5% of the population. People may have a cervical rib on the right, left, or both sides.

Most cases of cervical ribs are not clinically relevant and do not have symptoms; cervical ribs are generally discovered incidentally. However, they vary widely in size and shape, and in rare cases, they may cause problems such as contributing to thoracic outlet syndrome due to compression of the lower trunk of the brachial plexus or subclavian artery.

Compression of the brachial plexus may be identified by weakness of the muscles near the base of the thumb. Compression of the subclavian artery is often diagnosed by finding a positive Adson’s sign on examination, where the radial pulse in the arm is lost during abduction and external rotation of the shoulder.

Treatment is most commonly undertaken when there is evidence of neurovascular compromise. A transaxillary approach is the traditional operative method for excision of the cervical rib.

Mesenteric venous thrombosis (MVT) is a blood clot in one or more of the major veins that drain blood from the intestine. The superior mesenteric vein is most commonly involved. The exact cause of MVT is unknown. However, there are many diseases that can lead to MVT. Many of the diseases cause swelling (inflammation) of the tissues surrounding the veins, and include:
Appendicitis
Cancer of the abdomen
Diverticulitis
Liver disease with cirrhosis
High blood pressure in the blood vessels of the liver
Abdominal surgery or trauma
Pancreatitis
Inflammatory bowel disorders
Heart failure
Protein C or S deficiencies
Polycythaemia vera
Essential thrombocythemia
People who have disorders that make the blood more likely to stick together (clot) have a higher risk for MVT. Birth control pills and oestrogen medicines also increase risk.

MVT is more common in men than women. It mainly affects middle aged or older adults. Symptoms may include any of the following:
Abdominal pain, which may get worse after eating and over time; Bloating; Constipation; Bloody diarrhoea; Fever; Septic shock; Lower gastrointestinal bleeding; Vomiting and nausea.
Blood thinners (most commonly heparin or related medicines) are used to treat MVT when there is no associated bleeding. In some cases, medicine can be delivered directly into the clot to dissolve it. This procedure is called thrombolysis. Less often, the clot is removed by thrombectomy.

Deep vein thrombosis (DVT) is the formation of a blood clot in a deep vein of the legs, thigh, or pelvis. Thrombosis is most often seen in individuals with a history of immobilization, obesity, malignancy, or hereditary thrombophilia. Vascular endothelial damage, venous stasis, and hypercoagulability, collectively referred to as the Virchow triad, are the main factors contributing to the development of DVT.
Symptoms usually occur unilaterally and include swelling, tenderness, and redness or discoloration. Pulmonary embolism (PE), a severe complication of DVT, should be suspected in patients with dizziness, dyspnoea, and fever. The diagnostic test of choice for DVT is compression ultrasound. In most cases, a negative D-dimer test allows thrombosis or PE to be ruled out, but a positive test is nonspecific.
Initial acute treatment of DVT consists of anticoagulation with heparin and, if the thrombus is large or unresponsive to anticoagulation, may also include thrombolysis or thrombectomy. Secondary prophylaxis is achieved with oral warfarin or direct factor Xa inhibitors and supportive measures such as regular exercise and compression stockings.