​
Clinical Procedures - Lumbar Puncture 
Indications
• In the diagnosis of meningitis, subarachnoid hemorrhage and other diseases including non-infective meningitis and Guillain- Barré syndrome
• Treatment (short term) of idiopathic intracranial hypertension:
• In this case, consider removing between 10-20mL of CSF.
Contraindications
• Infected skin or subcutis at the site of puncture
• Coagulopathy or thrombocytopenia
• Raised intracranial pressure, particularly where there is a differential pressure between the supra- and infratentorial compartments such as seen in space-occupying lesions. If in doubt, image first!
Risks
• Post-procedure headache
• Infection
• Haemorrhage (epidural, subdural, subarachnoid)
• Dysaesthesia of the lower limbs
• Cerebral herniation (always check local procedures regarding contraindication to lumbar puncture and whether to perform CT head first).
Procedure Tips
• Always use the smallest gauge spinal needle available:
• In some centres, 'pencil-point' needles are used which are associated with a much reduced incidence of post-procedure headache
• If the needle strikes bone and cannot be advanced, withdraw slightly, re-angle, and advance in a stepwise fashion until the gap is found
• Lumbar puncture can be performed with the patient sitting, leaning forwards. This is particularly useful if the patient is obese. However, pressure measurements will be erroneous if taken in this position.
Documentation
• Date, time, indication, and informed consent obtained
• Vertebral level needle inserted
• Number of passes before SF obtained
• Initial ('opening) pressure and final ('closing') pressure
• Amount and appearance of CSF
• Tests samples sent for
• Any immediate complications
• Signature, printed name and contact details.


Equipment
• Sterile gloves
• Sterile pack (containing drape, cotton balls, small bowl)
• Antiseptic solution (e.g. iodine)
• Sterile gauze dressing
• 1 × 25G (orange) needle
• 1 × 21G (green) needle
• Spinal needle (usually 22G)
• Lumbar-puncture manometer
• Three-way tap (may be included in a lumbar puncture kit)
• 5-10mL 1% lidocaine
• 2 × 10mL syringes
• 3 x sterile collection tubes and 1 biochemistry tube for glucose measurement.
​
Procedure
• Introduce yourself, confirm the identity of the patient, explain the procedure, and obtain verbal consent
• Position the patient lying on their left-hand side with the neck, knees, and hips flexed as much as possible:
Ensure that the patient can hold this position comfortably
• Place a pillow between the patient's knees to prevent the pelvis tilting
• Label the collections tubes *1, 2°, and '3"
• Identify the iliac crest. The disc space vertically below this (as you are looking) will be ~L3-L4
• Mark the space between the vertebral spines at this  point with a pen
• Wash hands and put on the sterile gloves
• Unwrap all equipment and ensure it fits together correctly:
• It is usually useful to give the 3-way tap a few twists as it can stick
• Apply the drapes around the area and sterilize with the antiseptic solution and cotton balls in outward-spiral motion
• Inject the lidocaine (using a 10mL syringe and the orange needle) at the marked site to raise a small wheal
• Swap the orange needle for the green one and infiltrate the lidocaine deeper. © Take care to aspirate before injecting to ensure blood vessels are avoided
• Wait for ~1 minute for the anaesthetic to take effect
• Introduce the spinal needle through the marked site at about 90° to the skin, heading slightly toward the umbilicus.
Keep the bevel facing cranially
• Gently advance the needle to ~5 cm depth
• At this point, a further slight push of the needle should produce a 'give as the needle enters the subarachnoid space (this takes a little practice to feel with confidence)
• Withdraw the stilette from the needle. CSF should begin to drip out
• Measure the CSF pressure: connect the manometer to the end of the needle via the 3-way tap (the CSF will rise up the manometer allowing you to read off the number)
• Turn the tap such that the CSF within the manometer pours out in a controlled manner and further CS can drip freely
• Collect about 5 or 6 drops into each collection tube in the order in which they have been labelled
• Collect a few more drops into the biochemistry tube for glucose measurement
• Close the tap so that the manometer will measure the pressure at the end of the collection ('closing pressure)
• Remove the needle, tap, and manometer in one action
• Apply a sterile dressing
• Send the fluid for analysis:
• Cell count (bottles 1 and 3)
• Microscopy, culture and sensitivities (bottles 1 and 3)
• Biochemistry: glucose (biochemistry tube), protein (bottle 2)
• Advise the patient to lie flat for ~1 hour and ask nursing staff to check CNS observations

​Clinical Procedures - Male Urethral Catheterization 
Indications
• Relief of acute urinary retention
• Accurate monitoring of urine output in the acutely unwell/those undergoing surgery
• Prevention of complications of chronic urinary retention (e.g. neurological; consider long-term alternatives)
• Urinary incontinence (consider alternatives e.g. convene/pad).
Contraindications
• Urethral/prostatic injury.
Risks
• Urinary tract infection
• Septicaemia
Pain
• Haematuria
• Creation of a 'false passage' through prostate
• Urethral trauma
• © Beware latex allergy.
Procedure Tips
• Difficulty passing an enlarged prostate is a common problem. Tricks to try to ease the catheter past include:
• Ensure the catheter is adequately lubricated
• Try moving the penis to a horizontal position between the patient's legs as prostatic resistance is reached
• Ask the patient to wiggle his toes
• Rotate the catheter back and forth as it advances
• If catheter fails to pass, consider using larger bore catheter (e.g. 16F
instead of 14F) as this may prevent coiling in the urethra
• If urine fails to drain despite the catheter being fully advanced:
•Palpate the bladder: if palpable, the catheter is inappropriately placed
• Manual pressure on the bladder may express enough urine from a near-empty bladder to show itself
• Aspirate with a bladder syringe, or flush with a little sterile saline
• D If it is impossible to pass the catheter, ask for help. If all else fails, it may be necessary to proceed to suprapubic catheterization.


Equipment
• Foley catheter (male) of appropriate French, usually 12-14
• 10mL syringe of sterile water
• Syringe of lidocaine gel 1% (e.g. Instilligel®
• Catheter bag
• Sterile gloves
• Catheter pack containing drape, kidney dish, swabs/cotton balls. and a small dish
• Sterile water/chlorhexidine sachet.
Procedure
• Introduce yourself, confirm the patient's identity, explain the procedure, and obtain informed consent
• Position the patient lying supine with the external genitalia uncovered:
• Uncover from umbilicus to knees
• Using aseptic technique, unwrap the equipment and pour the chlorhexidine or sterile water into the dish
• Wash your hands and put on the sterile gloves
• Tear a hole in the middle of the drape and place it over the genitals so as to allow access to the penis
• Use your non-dominant hand to hold the penis upright
• Withdraw the foreskin and clean around the urethral meatus using the water/chlorhexidine and a swab, moving from the centre outwards
• Instil local anaesthetic via urethral meatus, with the penis held vertically. Wait at least 1 minute for the anaesthetic to act
• Place the kidney bowl between the patient's this
• Remove the tip of the plastic sheath containing being careful not to touch the catheter itself
• Insert catheter into urethra, feeding it out of the plastic wrapper as it is advanced

• Insert the catheter to the 'hilt':
• If the catheter will not advance fully, don't force it.
Withdraw a little, extend the penis fully and carefully try again. See 'tips' for more advice
• At this point, urine may begin to drain:
• Let the end of the catheter rest in the kidney bowl to catch any spills
• Inflate the balloon using sterile water inserted into the catheter side-arm according to the balloon's capacity (written on the cuff of the balloon lumen)
• Watch the patient's face and ask them to warn you if they feel pain
• Once the balloon is inflated, remove the syringe and attach the catheter bag
• Gently pull the catheter until you feel resistance as the balloon rests against the bladder neck
• Replace the foreskin (this is essential to prevent paraphimosis)
• Re-dress the patient appropriately.
Documentation
• Date and time
• Indication, informed consent obtained
• Size of catheter inserted
• Aseptic technique used?
• Volume of water used to inflate the balloon
• Residual volume of urine obtained
• Foreskin replaced?
• Any immediate complications
• Signature, printed name, and contact details.

Clinical Procedures- Intravenous (via cannula)
Intravenous injections can be administered by puncturing the vein with a needle and syringe and injecting directly. The procedure below describes injecting via an intravenous cannula. If no cannula in place, cannulate first.
Ensure that you comply with the local policy regarding drug administration. In hospital, two healthcare professionals should usually check and administer medication.
Equipment
• Appropriate syringe (dependent upon quantity of drug to be administered)
• Prescribed drug
• Saline flush (10mL syringe with sterile saline)
• Prescription chart
• Antiseptic swab.
Procedure
• Assess patient for drugs required (i.e. for pain relief, vomiting etc.)
• Refer to prescription chart, double-checking the appropriate drugs and dosage to be given:
•Always ensure you are fully aware of any possible side effects of any drugs you are due to administer
•Double-check the prescription chart for date and appropriate route for administration
•Check administration of previous dose not tOn after last dose?
•Ensure that the drug to be given is within its use
•Check patient and chart for any evidence of allergie relevant drug reactions
• Always comply with the local hand-hygiene practices
Once checked by suitably qualified staff take drug and prescription chart to the patient
• Introduce yourself, confirm the patient's identity, explain the procedure, and obtain informed consent
• Check with patient: name and date of birth (if capable):
• If incapable, check name band with another healthcare professional
• © The patient may need to be assisted to change position, if unable to move themselves, and to enable access to an appropriate site
• Cleanse the cannula port with the antiseptic wipe
• Attach the saline flush to the syringe port and inject a few mL to check patency of the cannula:
• D Watch for a bleb forming as consequence of extravasation
• If no problems are encountered, swap the flush for the drug-containing syringe and inject drug slowly
• To finish, inject a few more mL of saline into the cannula port and re-attach the bung
• Once the procedure is completed without complication, withdraw needle and discard into a sharps bin
• Monitor patient for any negative effects of the drug.

​Clinical Procedures - Venous Sampling from a Central Venous Catheter
The following describes venous blood sampling from a line in the internal jugular vein. The principles are the same for a line at any site.
Equipment
• 3 × 10mL syringes
• 0.9% isotonic or heparinized saline
• Chlorhexidine or iodine solution
• Sterile gauze
• Sterile gloves and apron
• Sterile drape.
Procedure
• Introduce yourself, confirm the identity of the patient, explain the procedure, and obtain verbal consent
• Stop any infusions (if possible) for at least 1 minute before sampling
• Place the patient in a supine position
• Ask the patient to turn their head away from the line site during the procedure
• Drape the site and put on a pair of sterile gloves and apron
• Spray the line end with the chlorhexidine solution or wipe with gauze dipped in iodine
• Clamp the line port and remove the cap, if present
• Connect a 10mL syringe to the port and then unclamp
• Withdraw 5-10mL of blood, clamp the line and ren syringe
• Discard the blood
• Repeat the procedure with a new syringe, withdrawing tomL.
• Clamp the line, disconnect the syringe. Keep this sample!
• Fill the final syringe with saline and attach it to the port
• Unclamp the port and instil the saline. Clamp the port again before disconnecting the syringe
• Replace the port cap.
Risks
• Clot or infection in the line
• Air embolus
• Physical damage to the line: burst or torn port.
Central venous lines should only be used for blood sampling if it is not possible to obtain a sample via the peripheral route. Do not risk catheter sepsis or a clotted line unless there are no alternatives!
Procedure Tips
• Always be sure to clamp the port before removing the syringe and unclamp before withdrawing blood or instilling the saline
• Most central lines have several ports: which should I use?
• Blood should ideally be sampled from the port with its hole at the tip of the line this is often the brown port
• Check the ports: most will have the gauge printed on them, choose the largest gauge port available
• Be sure to remove any bubbles from the saline before instilling
• Infusions must be stopped: otherwise a significant portion of the sample obtained may be the solution that is entering via the other port giving inaccurate results at analysis!

​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 - 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 -  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 - 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 - 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 - 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.