Individuals with arterial thrombosis or embolism often develop collateral circulation to compensate for the loss of arterial flow. However, it takes time for sufficient collateral circulation to develop, making affected areas more vulnerable for sudden occlusion by embolisation than for e.g. gradual occlusion as in atherosclerosis. Materials
Arterial embolisms can consist of various materials, including:

Thromboembolism – embolism of thrombus or blood clot. Cholesterol embolism - embolism of cholesterol, often from atherosclerotic plaque inside a vessel. Fat embolism – embolism of bone fracture or fat droplets. Air embolism (also known as a gas embolism) – embolism of air bubbles. Septic embolism – embolism of pus containing bacteria. Cancer embolismIn contrast, amniotic fluid embolism almost exclusively affects the venous side. Diagnosis
In addition to evaluating the symptoms above, the health care provider may find decreased or no blood pressure in the arm or leg.Tests to determine any underlying cause for thrombosis or embolism and to confirm presence of the obstruction may include:

Doppler ultrasound, especially duplex ultrasonography. It may also involve transcranial doppler exam of arteries to the brain
Echocardiography, sometimes involving more specialized techniques such as Transesophageal echocardiography (TEE) or myocardial contrast echocardiography (MCE) to diagnose myocardial infarction
Arteriography of the affected extremity or organ Digital subtraction angiography is useful in individuals where administration of radiopaque contrast material must be kept to a minimum. Magnetic resonance imaging (MRI)
Blood tests for measuring elevated enzymes in the blood, including cardiac-specific troponin T and/or troponin I, myoglobins, and creatine kinase isoenzymes. These indicate embolisation to the heart that has caused myocardial infarction.
Higher plasma concentrations also lead to cardiovascular effects, though cardiovascular collapse may also occur with low concentrations. Adverse effects on the central nervous system may indicate impending cardiotoxicity and should be carefully monitored. Central nervous system: circumoral numbness, facial tingling, vertigo, tinnitus, restlessness, anxiety, dizziness, seizure, coma
Cardiovascular: hypotension, arrhythmia, bradycardia, heart block, cardiac arrestToxicity can also occur in the setting of subarachnoid injection during high spinal anesthesia. These effects include: paresthesia, paralysis, apnea, hypoventilation, fecal incontinence, and urinary incontinence. Additionally, bupivacaine can cause chondrolysis after continuous infusion into a joint space.Bupivacaine has caused several deaths when the epidural anaesthetic has been administered intravenously accidentally. Treatment of overdose
Animal evidence indicates intralipid, a commonly available intravenous lipid emulsion, can be effective in treating severe cardiotoxicity secondary to local anaesthetic overdose, and human case reports of successful use in this way. Plans to publicize this treatment more widely have been published. Pregnancy and lactation
Bupivacaine crosses the placenta and is a pregnancy category C drug. However, it is approved for use at term in obstetrical anesthesia. Bupivacaine is excreted in breast milk. Risks of stopping breast feeding versus stopping bupivacaine should be discussed with the patient. Postarthroscopic glenohumeral chondrolysis
Bupivacaine is toxic to cartilage and its intra-articular infusions may lead to postarthroscopic glenohumeral chondrolysis. Pharmacology
Pharmacodynamics
Bupivacaine binds to the intracellular portion of voltage-gated sodium channels and blocks sodium influx into nerve cells, which prevents depolarization. Without depolarization, no initiation or conduction of a pain signal can occur.