Surgical Anatomy of the Adrenal Glands, Indications, and Principles of Adrenalectomy

1. Surgical Anatomy

General Features

Relations

Blood Supply - Arterial

• Superior adrenal arteries - branches of the inferior phrenic arteries
• Middle adrenal arteries - direct visceral branches from the aorta
• Inferior adrenal arteries - branches of the ipsilateral renal artery

Venous Drainage - The Critical Surgical Landmark

• Right adrenal vein: Short (5-10 mm), drains directly and posteriorly into the IVC. This brevity makes it susceptible to avulsion injury during dissection - the most feared intraoperative complication.
• Left adrenal vein: Longer, joins the inferior phrenic vein before draining into the left renal vein. Identified by tracing superiorly along the left renal vein.

Lymphatics and Innervation

Embryology

• Cortex: Intermediate mesoderm of the urogenital ridge (mesenchymal origin) - develops from week 5 of gestation
• Medulla: Neural crest cells that migrate centrally by week 9 and achieve their central position surrounding the adrenal vein by week 18

2. Indications for Adrenalectomy

• Cortisol hypersecretion (Cushing syndrome - adrenal adenoma, carcinoma, or bilateral hyperplasia)
• Pheochromocytoma (including hereditary forms in MEN IIA, VHL, NF1)
• Aldosterone hypersecretion (Conn syndrome - unilateral adenoma confirmed by adrenal vein sampling)
• Sex steroid-secreting tumors

• Mass >4 cm (exception: myelolipoma, which may be managed conservatively unless very large/symptomatic)
• Mass with imaging features suspicious for malignancy: lipid-poor, heterogeneous, irregular borders, invasion of surrounding structures
• Adrenal incidentaloma that grows >1 cm on follow-up imaging

• Adrenocortical carcinoma (ACC) - requires open approach with oncologic principles
• Isolated adrenal metastasis from another primary (multidisciplinary decision required)
• Adrenalectomy during renal surgery for RCC when: adrenal is abnormal on imaging, large upper-pole tumor, or venous thrombus extends to the adrenal vein level

• Failed neurosurgical treatment of Cushing disease - bilateral adrenalectomy
• Select ectopic ACTH syndrome
• ACTH-independent macronodular adrenal hyperplasia (AIMAH)
• Primary pigmented nodular adrenocortical disease (PPNAD)

3. Principles of Surgical Technique

Universal Surgical Principles (Regardless of Approach)

1. Confirm the correct operative site during preoperative and intraoperative timeouts
2. Minimal handling of the tumor - the gland is friable; manipulate via surrounding adventitia only
3. Early isolation and ligation of the adrenal vein before mobilizing the gland (prevents catecholamine surges in pheochromocytoma and reduces bleeding)
4. Strict avoidance of capsular rupture - even for benign tumors, rupture can lead to tumor spread and recurrence
5. Specimen extraction in a bag
6. Surgeon volume matters: surgeons performing at least 6 adrenalectomies per year have demonstrably better outcomes

Preoperative Preparation

• Pheochromocytoma: Mandatory alpha-blockade (phenoxybenzamine or doxazosin) for 10-14 days preoperatively, then beta-blockade if needed. Adequate volume expansion.
• Cushing syndrome: Preoperative cardiopulmonary and anesthetic consultation; optimize fluid status, blood pressure, and glucose; correct electrolytes; prophylactic antithrombotic therapy; consider ketoconazole or metyrapone; plan perioperative steroid replacement.
• Conn syndrome: Correct hypokalemia; spironolactone preoperatively.

4. Surgical Approaches

A. Minimally Invasive Adrenalectomy (Gold Standard)

1. Patient in full or modified lateral decubitus position, affected side up; table minimally flexed
2. 3-4 trocar ports placed from the lateral rectus edge to mid-axillary line
3. Mobilization of the splenic flexure of the colon along the line of Toldt (inferiorly)
4. Division of splenocolic and lienorenal ligaments to achieve medial rotation of the spleen; tail of pancreas dissected off
5. Left adrenal gland comes into view; trace the left renal vein superiorly to find the left adrenal vein
6. Ligate the left adrenal vein with at least 2 clips on the stay side before dividing
7. Mobilize gland from surrounding fat; arterial branches controlled with cautery or clips
8. Specimen extraction in a bag

1. The right triangular ligament of the liver is divided to allow hepatic retraction
2. Peritoneal layer over the vena cava is opened along the medial border of the gland
3. Plane between adrenal and lateral IVC is bluntly developed to expose the short right adrenal vein
4. Right adrenal vein isolated with a right-angle (Mixter) clamp - ligated between clips or ties
5. Gland dissected superiorly, with care at inferomedial attachments to the kidney

B. Posterior Retroperitoneoscopic Adrenalectomy

• Patient prone; table flexed at the 12th rib level
• Most direct route; no intraperitoneal organ mobilization; ideal for bilateral adrenalectomy without repositioning and for morbidly obese patients (panniculus falls forward)
• Limited field; not for large tumors or ACC

C. Open Adrenalectomy

• Anterior transabdominal: Excellent exposure, access to great vessels and hilar structures; higher risk of ileus and visceral injury
• Thoracoabdominal approach (8th/9th intercostal incision curving over costal margin into abdomen): Reserved for very large tumors or ACC requiring en bloc resection; divides diaphragm circumferentially (spare the central phrenic nerve); requires chest tube

• Flank approach (11th rib excision, lateral decubitus): The anterior periosteum is stripped, the rib excised, and the retroperitoneum entered. Adrenal vein is the first step in dissection.
• Posterior lumbodorsal approach (prone, 11th or 12th rib or hockey-stick incision): Most direct, least ileus, but limited exposure

• No-touch technique
• Preserve intact peritoneum over the anterior surface if no invasion
• En bloc resection with wide margin outside tumor capsule
• Strict preservation of intact tumor capsule
• Exclude remaining peritoneal cavity with laparotomy pads or drapes
• Minimize bleeding and fluid spillage
• Extract specimen in a bag
• Change gloves, gowns, and instruments after tumor removal
• Lymphadenectomy including periadrenal fat, perirenal fat, and renal hilum (at least 5 nodes)

D. Robot-Assisted Adrenalectomy

• 3D magnification of the operative field
• Tremor filtering
• Enhanced wrist degrees of freedom (EndoWrist)
• Superior ergonomics in a deep narrow retroperitoneal space

5. Partial Adrenalectomy

• Bilateral hereditary pheochromocytoma (MEN IIA, VHL, NF1, PGL syndromes)
• Unilateral pheochromocytoma in documented genetic cases
• Primary aldosteronism from unilateral adenoma (contralateral gland normal)
• Unilateral adenoma in Cushing syndrome
• Pseudocyst or endothelial cyst

6. Postoperative Considerations

• Steroid replacement must begin at the time of tumor resection and continue until recovery of the contralateral gland (unilateral) or permanently (bilateral)
• Pheochromocytoma patients: monitor for hemodynamic instability and hypoglycemia
• Cushing patients: early breathing exercises, epidural analgesia preferred, monitor for respiratory depression
• Bilateral adrenalectomy patients: lifelong replacement; risk of Addisonian crisis; significantly reduced quality of life

Acute Mesenteric Ischemia (AMI)

1. Types (Pathophysiologic Classification)

A. Superior Mesenteric Artery (SMA) Embolism - Most Common (40-50%)

• Atrial fibrillation/flutter (most common)
• Left ventricular mural thrombi (post-MI, low ejection fraction, heart failure)
• Valvular disease, endocarditis
• Aortic aneurysms with mural thrombi
• Up to 68% of patients have simultaneous embolic events in other vascular beds (cerebrovascular, peripheral)

B. Arterial Thrombosis - Second Most Common (20-35%)

C. Nonocclusive Mesenteric Ischemia (NOMI) - ~20% of cases

• Post-cardiac surgery patients
• Critically ill on vasopressors (epinephrine, norepinephrine, vasopressin)
• Hemodialysis patients
• Severe congestive heart failure

D. Mesenteric Venous Thrombosis (MVT) - 5-15% of cases

• Primary MVT: No identifiable cause (~20%)
• Secondary MVT: Identified etiology - hypercoagulable states (factor V Leiden, antiphospholipid antibodies, protein C/S deficiency), portal hypertension, intraabdominal infection or inflammation (appendicitis, diverticulitis, pancreatitis), abdominal malignancy, oral contraceptive use, abdominal trauma, prior splenectomy

2. Clinical Features

The Cardinal Symptom

Pain out of proportion to physical examination - This is the hallmark of AMI regardless of the underlying mechanism.

Temporal Evolution by Type

Early vs. Late Signs

• Severe diffuse abdominal pain with minimal tenderness (classic discordance)
• Nausea, vomiting
• Diarrhea (sometimes bloody - "currant jelly" stool in late stages)
• Urge to defecate
• Tachycardia

• Guarding and rebound tenderness
• Board-like abdomen
• Septic shock: tachycardia, hypotension, fever, altered mental status
• Rapid clinical deterioration

Key Risk Factors Raising Clinical Suspicion

3. Investigations

Temporal Principles

Laboratory Findings (Adjuncts - Not Diagnostic Alone)

Imaging

CT Angiography (CTA) - Gold Standard

• Arterial phase: evaluates visceral vessel filling defects, emboli, thrombus
• Venous phase: evaluates portal/SMV system and bowel wall perfusion

• Filling defect in SMA or celiac artery (embolus or thrombus)
• Pneumatosis intestinalis (gas within bowel wall) - late, ominous sign
• Portal venous gas - very late, very poor prognostic sign
• Focal bowel wall non-enhancement
• SMV/portal thrombosis
• Bowel wall thickening with mucosal enhancement (early ischemia)
• "Thumbprinting" - submucosal hemorrhage and edema

Plain Abdominal Radiograph

• Ileus and dilated loops
• Thumbprinting
• Pneumatosis linearis
• Portal venous gas

Duplex Ultrasound

Conventional (Digital Subtraction) Angiography

MR Angiography

4. Treatment

The "Four R's" Framework (Olson & Teixeira, 2021)

A. Initial Medical Management (All Types)

1. IV access, resuscitation - crystalloid fluid resuscitation; correct electrolyte abnormalities
2. Systemic anticoagulation (IV heparin) - prevents thrombus propagation; begin promptly upon diagnosis
3. Broad-spectrum IV antibiotics - to cover bacterial translocation from ischemic bowel
4. Nasogastric decompression
5. Vasopressors - avoid if possible; if mandatory for refractory hypotension, use agents with less splanchnic vasoconstriction: dobutamine, milrinone, or low-dose dopamine; avoid vasopressin and high-dose norepinephrine
6. Peritonitis = emergent laparotomy; do not delay for imaging

B. Embolic AMI - Surgical Revascularization

1. Midline laparotomy; omentum and transverse colon reflected cephalad; small bowel moved to patient's right
2. Horizontal incision at the transverse mesocolon base to expose the SMA anterior surface
3. Superior mesenteric vein identified (lies to the left of the SMA) and protected
4. SMA controlled proximal to the middle colic artery; systemic heparinization
5. Transverse or longitudinal arteriotomy proximal to the embolus
6. Fogarty balloon catheter (3-4 Fr antegrade, 2-3 Fr for distal branches) passed to extract embolus and showered distal clot; repeated until free of thrombus
7. Direct infusion of 0.5-1 mg tPA into the vessel may be considered if distal thrombus persists
8. Arteriotomy closed primarily with 5-0 or 6-0 monofilament suture; vein or bovine patch if vessel is diminutive or heavily calcified
9. Temporary abdominal closure placed; second-look laparotomy in 24-48 hours

• Catheter-directed thrombolysis (CDT) or percutaneous aspiration thrombectomy
• May be appropriate in patients with early diagnosis and no peritonitis
• No high-quality RCT evidence to mandate one approach over another

C. Thrombotic AMI - Bypass Revascularization

• Inflow from the right (or left) common iliac artery or infrarenal aorta
• "Lazy C" configuration using 6-8 mm externally enforced PTFE or Dacron
• Anastomosed end-to-side to the lateral SMA distal to the occlusion
• Autologous vein preferred if gross contamination present

• Inflow from distal descending thoracic or supraceliac aorta
• Associated with greater hemodynamic shifts; reserved for younger/more robust patients
• Bifurcated graft (e.g., 12×6 Dacron) for combined celiac + SMA revascularization

• SMA exposed via laparotomy; retrograde access gained via micropuncture distal to the lesion
• Guidewire and sheath placed; lesion traversed; balloon-expandable bare metal or covered stent deployed
• Avoids aortic clamping; allows simultaneous bowel inspection
• Comparable outcomes to open bypass with shorter operative times

D. NOMI - Medical and Minimally Invasive Management

• Improve cardiac output
• Wean vasopressors
• Treat sepsis/infection
• Supportive critical care

• Papaverine (30-60 mg/h) or nitroglycerin or prostaglandin analogues
• Selectively increases splanchnic blood flow
• Evidence limited to small case series; no large controlled trials
• Continued for 12-24 hours or until clinical improvement

E. Mesenteric Venous Thrombosis - Anticoagulation First

• Anticoagulation reduces thrombus propagation, promotes recanalization, and reduces recurrence
• Duration: typically 3-6 months minimum; lifelong if underlying hypercoagulable state identified
• Thrombolysis (catheter-directed or systemic) may be considered in extensive thrombosis failing anticoagulation
• Surgery (bowel resection ± superior mesenteric venous thrombectomy) reserved for peritonitis, bowel perforation, or failure of anticoagulation with clinical deterioration

F. Bowel Viability Assessment and Second-Look Laparotomy

• Clinical criteria: color (pink vs. dusky/black), peristalsis, mesenteric pulse
• Intraoperative Doppler: loss of signal confirms non-viable segments
• Fluorescein dye + Wood's lamp: viable bowel fluoresces uniformly; ischemic bowel does not
• Frankly necrotic or perforated bowel is resected; marginally ischemic bowel is preserved pending second-look

• Re-assess bowel viability when microcirculation has recovered after reperfusion
• Resect any bowel that has not recovered
• Perform definitive abdominal closure

G. Postoperative and Long-Term Management

• Ongoing heparin infusion in the acute postoperative period
• Broad-spectrum antibiotics continued
• After endovascular stenting: dual antiplatelet therapy for 1-3 months, then aspirin for life
• After bypass grafting: aspirin at minimum; vitamin K antagonists or DOACs for comorbid conditions
• Surveillance imaging: duplex ultrasound or CTA at 1, 6, and 12 months, then annually for patients with stents or grafts
• Lifestyle modification and medical optimization to prevent recurrence

Summary Table

Superior Mesenteric Artery (SMA) Syndrome

Anatomy and Pathophysiology

Predisposing Conditions and Risk Factors

• Anorexia nervosa and other eating disorders (most common in young women)
• Malignancy, severe burns, major trauma
• Prolonged illness with cachexia
• Post-bariatric surgery (e.g., Roux-en-Y gastric bypass)

• Immobilization in a body cast (spica cast, hip spica) - increases lumbar lordosis, acutely angulating the SMA
• Scoliosis correction surgery - spinal lengthening reduces the aortomesenteric angle (presents 1-2 weeks postoperatively); thin habitus and significant spinal lengthening are risk factors
• Prolonged bed rest
• Loss of abdominal muscle tone

• Adolescent growth spurts (the spine elongates faster than mesenteric fat accumulates)

• Abnormally high ligament of Treitz (fixing the duodenum too high)
• Unusually low origin of the SMA from the aorta
• Abdominal adhesions fixing the bowel in a compromised position

• Inflammatory diseases of the abdomen
• Abdominal surgery with peritoneal adhesions

Clinical Features

Symptoms

• Epigastric pain and fullness - postprandial, often described as pressure or cramping
• Nausea and vomiting - characteristically bilious, as the obstruction is distal to the ampulla of Vater; may be projectile
• Early satiety
• Weight loss - may worsen the underlying aortomesenteric angle in a vicious cycle
• Abdominal distension - due to gastric and duodenal dilatation

Characteristic Postural Relief

Acute vs. Chronic Presentation

Investigations

Laboratory Tests

• No specific laboratory marker exists
• May reveal hypokalemia, hypochloraemia, metabolic alkalosis (from vomiting)
• Hypoalbuminaemia and malnutrition markers in chronic cases
• Exclude other causes of obstruction

Plain Abdominal Radiograph

• Usually unremarkable in adults
• In children: a double-bubble sign (dilated stomach + dilated proximal duodenum) may be seen
• Dilated loops of bowel, gastric dilatation in severe cases

Upper Gastrointestinal (UGI) Contrast Series - Key Diagnostic Test

• Abrupt, vertical linear cutoff in the third portion of the duodenum at the site of SMA compression
• Marked proximal dilation of the first and second portions of the duodenum and stomach
• Prolonged retention of contrast proximal to the obstruction
• Relief of obstruction and passage of contrast in the prone or left lateral decubitus position - this is a classic diagnostic manoeuvre
• The appearance may be misleading - duodenal dilatation can result from atony (dysmotility) rather than mechanical obstruction, so proximal stasis must be confirmed

CT Angiography (CTA) / MR Angiography (MRA)

• Currently the preferred imaging modality - provides noninvasive, detailed anatomic information
• Directly measures the aortomesenteric angle (normally 25-60°; <25° diagnostic) and aortomesenteric distance (<8-10 mm supportive)
• Identifies compression of the third part of the duodenum between the SMA and aorta
• Useful for surgical planning (identifies duodenal position, ligament of Treitz, and vascular anatomy)
• Biphasic contrast-enhanced CTA provides both vascular and bowel detail

Conventional Angiography (Lateral View)

• Lateral aortogram shows the narrowed aortomesenteric angle
• Largely superseded by CTA/MRA

Antroduodenal Manometry

• Can distinguish mechanical obstruction from functional motility disorder - an important distinction before surgery
• Mechanical obstruction produces characteristic pressure patterns distinct from those in motility disorders
• Particularly useful when imaging findings are equivocal

Functional Test: Post-Pyloric Feeding

• Placement of an enteric catheter across the obstruction into the proximal jejunum with relief of vomiting is strong supportive evidence for mechanical SMA syndrome (vs. functional disorder)

Differential Diagnosis

• Functional vomiting / cyclic vomiting syndrome
• Gastroparesis
• Peptic ulcer disease with duodenal obstruction
• Annular pancreas
• Duodenal web or stricture
• Malignant duodenal obstruction (periampullary, pancreatic cancer)
• Crohn's disease of the duodenum
• Chronic intestinal pseudo-obstruction

Treatment

1. Correct Precipitating Factors

• Remove the body cast if present - symptoms often resolve
• Nutritional rehabilitation and weight gain in eating disorders or malnutrition - restoration of mesenteric fat re-establishes the aortomesenteric angle
• Treat the underlying malignancy or systemic illness

2. Conservative / Medical Management (First-line)

• Nasogastric decompression (or long intestinal tube) to relieve proximal obstruction
• IV fluid resuscitation and electrolyte correction
• Parenteral nutrition (TPN) if oral feeding is not tolerated - promotes weight gain and fat deposition to restore the mesenteric angle

• Frequent small meals (reduces distension)
• Postural manoeuvres after eating: prone or left lateral decubitus positioning to mechanically displace the SMA off the duodenum
• Post-pyloric enteral feeding via a nasojejunal tube placed beyond the obstruction (supports weight gain while bypassing the obstruction)

3. Surgical Management (Reserved for Refractory Cases)

• Chronic, relapsing SMA syndrome confirmed objectively
• Failed adequate conservative management (nutritional rehabilitation, positional measures)
• Irreversible predisposing condition

• Gastrojejunostomy alone is not effective - it does not decompress the proximal duodenum, and stasis in the first and second portions of the duodenum persists
• Open duodenojejunostomy remains an alternative when laparoscopic access is not feasible

• Division of the ligament of Treitz to mobilise the duodenojejunal flexure inferiorly, relieving traction on the duodenum
• Reported as beneficial in selected cases
• Less commonly performed than duodenojejunostomy

• The original described approach - mobilisation and freeing of the duodenum at the ligament of Treitz
• Largely replaced by laparoscopic approaches

Prognosis

• Patients with a reversible precipitating cause (body cast, scoliosis surgery, eating disorder) generally respond well to conservative management
• Weight gain is curative in most nutritional cases
• Surgical outcomes with laparoscopic duodenojejunostomy are generally favourable with a low recurrence rate
• Prognosis in malignancy-associated cases is determined by the underlying disease
• A vicious cycle can develop in eating disorders: SMA syndrome causes vomiting → further weight loss → worsening aortomesenteric angle → more obstruction and vomiting → even more weight loss. Breaking this cycle requires aggressive nutritional support

Clinical Case Analysis: Dry Gangrene of Right Great Toe with Absent Femoral and Distal Pulses Bilaterally

Probable Diagnosis

Diagnostic Reasoning

Leriche Syndrome - Classic Triad

1. Buttock/thigh/calf claudication (pain on walking - present)
2. Absent or diminished femoral pulses bilaterally (present)
3. Impotence (due to internal iliac artery insufficiency) - should be asked about

Fontaine / Rutherford Classification of PAD

Evaluation

History

• Duration and severity of claudication - distance walked before onset, which muscle groups
• History of rest pain (worse at night, relieved by hanging leg dependent)
• Progression of gangrene - whether wet or dry, spread, pain
• Impotence (internal iliac insufficiency - part of Leriche triad)
• Prior vascular interventions or aortic surgery
• Cardiac history: angina, MI, heart failure, arrhythmias
• History of stroke/TIA (systemic atherosclerosis)
• Smoking history (most strongly associated with severe aortoiliac disease)
• Diabetes mellitus - poor wound healing, neuropathy confounding pain assessment
• Medications

Physical Examination

• Signs of chronic ischaemia in both legs: hair loss, thickened nails, shiny atrophic skin, muscle wasting
• Skin temperature - cool bilaterally
• Colour changes: pallor on elevation, dependent rubor (reactive hyperaemia when legs hang down)
• Capillary refill time
• The gangrene: confirm it is dry (demarcated, shrunken, black/mummified, no odour) vs. wet (infected)

• Aorta (midline abdominal): pulsatile mass?
• Bilateral femoral - absent bilaterally (established)
• Bilateral popliteal, dorsalis pedis, posterior tibial - absent bilaterally
• Radial/brachial pulses - to assess upper limb circulation and obtain brachial BP for ABI calculation

• Aortic/iliac/femoral bruits (may be absent in complete occlusion)

• Elevate legs to 45° - note time to pallor (normally >2 min; in severe ischaemia, pallor in <30 seconds)
• Lower legs - note time to rubor (normally <15 sec; delayed in ischaemia)

• Sensation (ischaemic neuropathy may produce numbness, hyporeflexia)

• Blood pressure both arms (significant difference suggests subclavian stenosis)
• Carotid bruits
• Cardiac examination (arrhythmia - AF as embolic source)
• BMI, waist circumference

Investigations

Laboratory Tests

Vascular Noninvasive Tests

• Systolic BP at the ankle (posterior tibial or dorsalis pedis) divided by brachial systolic BP
• Normal: 0.9-1.3
• Claudication: 0.5-0.9
• Critical/CLTI: <0.4 (expect very low or unrecordable in this patient)
• >1.3: abnormally high (vessel calcification/non-compressible vessels) - common in diabetes; use toe-brachial index instead
• Toe-brachial index (TBI): normal >0.7; CLTI <0.3

• Pressure cuffs at thigh, above knee, below knee, ankle
• Locates the level and severity of obstruction
• A pressure drop >20 mmHg between segments indicates significant stenosis at that level
• The marked pressure drop at the thigh level bilaterally confirms aortoiliac disease

• Non-invasive, no radiation, no contrast
• Assesses aorta and iliac arteries - detects occlusion, stenosis, calcification
• Limited by bowel gas and obesity in the abdomen

Imaging for Anatomy and Revascularisation Planning

• Sensitivity and specificity >95% for detecting arterial stenosis/occlusion
• Maps entire aortoiliac-femoral-popliteal-tibial tree in one study
• Identifies extent and level of occlusion, calcification, collateral vessels
• Guides endovascular vs. open surgical planning
• Renal function must be checked first (contrast nephropathy risk)

• Alternative to CTA; no radiation, no iodinated contrast (safer in renal impairment)
• Slightly longer acquisition time; overestimates stenosis at times
• Cannot be used in patients with pacemakers or certain metallic implants

• Gold standard for arterial anatomy
• Reserved for cases with equivocal non-invasive imaging or when therapeutic intervention is planned simultaneously
• Invasive, requires access site (femoral or brachial), contrast, radiation
• Lateral views of the aorta demonstrate the aortic bifurcation and iliac origins

Cardiac Assessment

• Resting ECG: mandatory
• Echocardiography: assess LV function, wall motion, valvular disease
• Stress testing (pharmacological if exercise limited): if angina or poor functional capacity
• Preoperative cardiac risk assessment is essential before any revascularisation

Management

1. Limb salvage - revascularisation
2. Local wound care - management of gangrene
3. Cardiovascular risk reduction - prevent MI, stroke, and death

A. Immediate General Measures

• Hospital admission; nursing in a dependent position (legs down or at 20-30° below horizontal to maximise perfusion pressure)
• Avoid elevation of ischaemic limbs (worsens perfusion)
• Protect the gangrenous toe: dry dressings, no occlusive dressings, avoid pressure
• Do NOT aggressively debride dry gangrene until revascularisation is achieved - converting dry to wet gangrene risks infection and amputation
• IV fluids if dehydrated; maintain good renal perfusion especially pre-contrast
• Analgesia: opioids may be required for rest pain
• Strict glycaemic control if diabetic
• Low-molecular-weight heparin (LMWH) prophylaxis (venous thromboembolism)
• Wound swab culture if any signs of infection

B. Medical / Risk Factor Modification

• Aspirin 75-100 mg/day or Clopidogrel 75 mg/day (preferred in PAD)
• Clopidogrel reduces adverse cardiovascular events more than aspirin in PAD
• Rivaroxaban 2.5 mg twice daily + aspirin 100 mg/day: the COMPASS trial showed significant reduction in cardiovascular events and adverse limb outcomes in established PAD, including amputation reduction

• High-intensity statin: e.g., atorvastatin 40-80 mg or rosuvastatin 20-40 mg
• Target: ≥50% LDL reduction
• Statins reduce MI, stroke, death, and adverse limb events including amputation in PAD
• Associated with decreased risk of adverse limb events

• ACE inhibitors (e.g., ramipril) or ARBs preferred - reduce cardiovascular events in PAD
• Beta-blockers do not worsen claudication and may be used if coexistent CAD
• Target BP <130/80 mmHg

• Severe aortoiliac disease is most strongly associated with smoking
• Pharmacotherapy: nicotine replacement, bupropion, or varenicline
• Reduces disease progression and cardiovascular mortality

• Intensive glucose lowering reduces amputation risk
• GLP-1 agonists and SGLT2 inhibitors have additional cardiovascular benefit

C. Revascularisation (Primary Treatment for CLTI)

TASC Classification of Aortoiliac Lesions

Endovascular Options

• First-line for suitable lesions (TASC A and B)
• Balloon-expandable stents preferred for ostial iliac lesions
• Self-expanding stents or stent grafts for mid and distal iliac disease
• "Kissing stents" technique: bilateral iliac stents extending into the distal aorta simultaneously to treat aortic bifurcation disease
• Less invasive, shorter recovery, suitable for higher operative risk patients
• Primary patency at 5 years: ~70-75% for iliac stenting

Open Surgical Options

• Most durable long-term option: 10-year patency ~70-80%; perioperative mortality ~2-3%
• Indicated for: TASC C-D lesions, total aortic occlusion, failed endovascular approach
• Technique:
  • Both femoral arteries exposed at the groin bilaterally
  • Midline laparotomy (or retroperitoneal approach - left flank - especially in re-do surgery or cardiopulmonary risk)
  • Aorta exposed below renal arteries; in complete aortic occlusion, suprarenal or supraceliac clamping may be needed
  • Thrombus removed from occluded aorta
  • Bifurcated Dacron or PTFE graft anastomosed end-to-end (or end-to-side) to the infrarenal aorta, tunnelled retroperitoneally to both femoral arteries
  • Distal anastomoses to common femoral or profunda femoris arteries

• Less commonly performed; reserved for localised disease without extensive tibial involvement
• Removes plaque from within the lumen without graft
• Good for localised aortic disease with good distal runoff

• When open aortic surgery is prohibitively high risk (severe cardiopulmonary disease, hostile abdomen, prior aortic surgery)
• Inflow from axillary artery; subcutaneous tunnel to both femoral arteries
• Avoids laparotomy, aortic cross-clamping, visceral ischaemia
• Lower long-term patency (~50-60% at 5 years) vs. aortobifemoral bypass
• Reserved for patients unfit for direct aortic reconstruction

• Only when disease is unilateral (not applicable here - bilateral absent femorals)

Second-Look and Multi-level Revascularisation

D. Management of Gangrene

1. Revascularise first - restore circulation to allow healing
2. Allow auto-amputation of the gangrenous toe if possible
3. If the line of demarcation is clear and the toe is fully mummified after revascularisation - minor amputation (ray amputation of the great toe or transmetatarsal amputation)
4. Wound care: dry, non-adherent dressings; keep clean and protected

• Urgent surgical debridement/amputation cannot wait for revascularisation
• Broad-spectrum IV antibiotics (gram-positive cocci coverage + anaerobes)
• Revascularise as soon as possible post-debridement

E. Amputation (Last Resort)

• Revascularisation is not technically feasible or has failed
• Extensive non-viable limb with unsalvageable tissue loss
• Overwhelming sepsis from a gangrenous limb threatening life
• Patient unfit for any revascularisation procedure

F. Postoperative Care and Follow-Up

• Surveillance imaging (duplex USS or CTA) at 1, 6, 12 months then annually
• Continued antiplatelet therapy for life
• Lifelong statin and antihypertensive therapy
• Wound care and podiatry for foot protection
• Supervised exercise rehabilitation post-revascularisation
• Cardiology follow-up (high cardiovascular event risk)

Summary Algorithm

76M, HTN, absent bilateral femoral + distal pulses, claudication, dry gangrene right great toe

                    ↓
     DIAGNOSIS: Leriche syndrome (aortoiliac occlusive disease)
                     + CLTI (Fontaine IV / Rutherford 5-6)
                    ↓
     EVALUATE: ABI, segmental pressures → CTA aortogram
               Cardiac risk assessment
               Lab: lipids, glucose, HbA1c, renal function, FBC
                    ↓
     MANAGE:
     Medical: statin, antiplatelet, ACE-I/ARB, smoking cessation
     Protect gangrenous toe (dry dressings, no debridement yet)
                    ↓
     REVASCULARISE:
     TASC A-B → Endovascular (PTA ± stenting, kissing stents)
     TASC C-D → Aortobifemoral bypass (open)
     Poor operative risk → Axillobifemoral bypass
                    ↓
     POST-REVASCULARISATION:
     Reassess distal perfusion → distal bypass if needed
     Minor amputation of gangrenous toe after healing
     Lifelong surveillance and risk factor modification