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| Acute arterial ischemic disorder |
| Classification and external resources |
Vascular ischemia of the toes with characteristic cyanosis.
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In medicine, ischemia, also spelled as ischaemia or ischæmia, (//;[1][2][a]) is a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissue alive).[3] Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, thrombosis or embolism).
Contents
- 1 Signs and symptoms
- 1.1 Cardiac ischemia
- 1.2 Bowel
- 1.3 Brain
- 1.4 Limb
- 1.5 Cutaneous
- 2 Causes
- 2.1 Occlusion
- 2.2 Trauma
- 2.3 Other
- 3 Pathophysiology
- 4 Treatment
- 5 See also
- 6 Notes
- 7 References
- 8 Bibliography
Signs and symptoms
Since oxygen is carried to tissues in the blood, insufficient blood supply causes tissue to become starved of oxygen. In the highly aerobic tissues of the heart and brain, irreversible damage to tissues can occur in as little as 3–4 minutes at body temperature. The kidneys are also quickly damaged by loss of blood flow. Tissues with slower metabolic rates may undergo irreversible damage after 20 minutes.
Clinical manifestations of acute arterial ischemia include pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia (the "six Ps")[citation needed]
Without immediate intervention, ischemia may progress quickly to tissue necrosis and gangrene within a few hours. Paralysis is a very late sign of acute arterial ischemia and signals the death of nerves supplying the extremity. Foot drop may occur as a result of nerve damage. Because nerves are extremely sensitive to hypoxia, limb paralysis or ischemic neuropathy may persist after revascularization and may be permanent.[4]
Cardiac ischemia
See also: Myocardial infarction
Cardiac ischemia may be asymptomatic or may cause chest pain, known as angina pectoris. It occurs when the heart muscle, or myocardium, receives insufficient blood flow. This most frequently results from atherosclerosis, which is the long-term accumulation of cholesterol-rich plaques in the coronary arteries. Ischemic heart disease is the most common cause of death in most Western countries and a major cause of hospital admissions.[5]
Bowel
Both large and small bowel can be affected by ischemia. Ischemia of the large intestine may result in an inflammatory process known as ischemic colitis. Ischemia of the small bowel is called mesenteric ischemia.
Brain
Main article: Stroke
Brain ischemia is insufficient blood flow to the brain, and can be acute (i.e., rapid) or chronic (i.e., long-lasting). Acute ischemic stroke is a neurologic emergency that may be reversible if treated rapidly. Chronic ischemia of the brain may result in a form of dementia called vascular dementia. A brief episode of ischemia affecting the brain is called a transient ischemic attack (TIA), frequently referred to as a mini-stroke.
Limb
Main article: Acute limb ischaemia
Lack of blood flow to a limb results in acute limb ischemia.
Cutaneous
See also: Cyanosis and Gangrene
Reduced blood flow to the skin layers may result in mottling or uneven, patchy discoloration of the skin
Causes
Ischemia is a vascular disease involving an interruption in the arterial blood supply to a tissue, organ, or extremity that, if untreated, can lead to tissue death. It can be caused by embolism, thrombosis of an atherosclerosis artery, or trauma. Venous problems like venous outflow obstruction and low-flow states can cause acute arterial ischemia. An aneurysm is one of the most frequent causes of acute arterial ischemia. Other causes are heart conditions including myocardial infarction, mitral valve disease, chronic atrial fibrillation, cardiomyopathies, and prosthesis, in all of which thrombi are prone to develop.[4]
Occlusion
The thrombi may dislodge and may travel anywhere in the circulatory system, where they may lead to pulmonary embolus, an acute arterial occlusion causing the oxygen and blood supply distal to the embolus to decrease suddenly. The degree and extent of symptoms depend on the size and location of the obstruction, the occurrence of clot fragmentation with embolism to smaller vessels, and the degree of peripheral arterial disease (PAD).[4]
- Thromboembolism (blood clots)
- Embolism (foreign bodies in the circulation, e.g. amniotic fluid embolism)
Trauma
Traumatic injury to an extremity may produce partial or total occlusion of a vessel from compression, shearing or laceration. Acute arterial occlusion may develop as a result of arterial dissection in the carotid artery or aorta or as a result of iatrogenic arterial injury (e.g., after angiography).[4]
Other
An inadequate flow of blood to a part of the body may be caused by any of the following:
- Thoracic outlet syndrome (compression of the brachial plexus)
- Atherosclerosis (lipid-laden plaques obstructing the lumen of arteries)
- Hypoglycemia (lower than normal level of glucose)
- Tachycardia (abnormally rapid beating of the heart)
- Hypotension (low blood pressure, e.g. in septic shock, heart failure)
- Outside compression of a blood vessel, e.g. by a tumor or in the case of superior mesenteric artery syndrome
- Sickle cell disease (abnormally shaped red blood cells)
- Induced g-forces which restrict the blood flow and force the blood to the extremities of the body, as in acrobatics and military flying
- Localized extreme cold, such as by frostbite or improper cold compression therapy
- Tourniquet application
- An increased level of glutamate receptor stimulation
- Arteriovenous malformations, and peripheral artery occlusive disease
- rupture of significant blood vessels supplying a tissue or organ.
- Anemia vasoconstricts the periphery so that red blood cells can work internally on vital organs such as the heart, brain, etc., thus causing lack of oxygen to the periphery.
Pathophysiology
Main article: Ischemic cascade
Ischemia results in tissue damage in a process known as ischemic cascade. The damage is the result of the build-up of metabolic waste products, inability to maintain cell membranes, mitochondrial damage, and eventual leakage of autolyzing proteolytic enzymes into the cell and surrounding tissues.
Restoration of blood supply to ischemic tissues can cause additional damage known as reperfusion injury that can be more damaging than the initial ischemia. Reintroduction of blood flow brings oxygen back to the tissues, causing a greater production of free radicals and reactive oxygen species that damage cells. It also brings more calcium ions to the tissues causing further calcium overloading and can result in potentially fatal cardiac arrhythmias and also accelerates cellular self-destruction. The restored blood flow also exaggerates the inflammation response of damaged tissues, causing white blood cells to destroy damaged cells that may otherwise still be viable.[6]
Treatment
Early treatment is essential to keep the affected limb viable. The treatment options include injection of an anticoagulant, thrombolysis, embolectomy, surgical revascularisation, or amputation. Anticoagulant therapy is initiated to prevent further enlargement of the thrombus. Continuous IV unfractionated heparin has been the traditional agent of choice.[4]
If the condition of the ischemic limb is stabilized with anticoagulation, recently-formed emboli may be treated with catheter-directed thrombolysis using intraarterial infusion of a thrombolytic agent (e.g., recombinant tissue plasminogen activator (tPA), streptokinase, or urokinase). A percutaneous catheter inserted into the femoral artery and threaded to the site of the clot is used to infuse the drug. Unlike anticoagulants, thrombolytic agents work directly to resolve the clot over a period of 24 to 48 hours.[4]
Direct arteriotomy may be necessary to remove the clot. Surgical revascularization may be used in the setting of trauma (e.g., laceration of the artery). Amputation is reserved for cases where limb salvage is not possible. If the patient continues to have a risk of further embolization from some persistent source, such as chronic atrial fibrillation, treatment includes long-term oral anticoagulation to prevent further acute arterial ischemic episodes.[4]
Decrease in body temperature reduces the aerobic metabolic rate of the affected cells, reducing the immediate effects of hypoxia. Reduction of body temperature also reduces the inflammation response and reperfusion injury. For frostbite injuries, limiting thawing and warming of tissues until warmer temperatures can be sustained may reduce reperfusion injury.
See also
- Cerebral ischemia
- Infarction
- Inhibitor protein
- Ischemic cascade
- Organ donation
- Reperfusion injury
- Trauma triad of death
Notes
- ^ From Greek language ισχαιμία, iskhaimía; iskh- root denoting a restriction or thinning or to make or grow thin/lean, (h)aima blood
References
- ^ OED 2nd edition, 1989.
- ^ Entry "ischemia" in Merriam-Webster Online Dictionary.
- ^ Merck & Co. Occlusive Peripheral Arterial Disease, The Merck Manual Home Health Handbook website, revised and updated March 2010. Retrieved March 4, 2012.
- ^ a b c d e f g Lewis. S.L (2008). Medical-Surgical Nursing (7th ed.) Vascular disorder. pp. 907-908.
- ^ World Health Organization Department of Health Statistics and Informatics in the Information, Evidence and Research Cluster (2004). The global burden of disease 2004 update. Geneva: WHO. ISBN 92-4-156371-0.
- ^ Sims, N.R.; Muyderman, H. Mitochondria, oxidative metabolism and cell death in stroke, Biochimica et Biophysica Acta, January 2010, 1802(1):80-91. Epub September 12, 2009. PubMed PMID 19751827.
Bibliography
- Elizabeth (editor). Oxford Reference: Concise Medical Dictionary (1990, 3rd ed.). Oxford University Press: Market House Books, 1987, 2nd ed., pg. 107, ISBN 0-19-281991-7, ISBN 978-0-19-281991-8
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Medicine: Pathology
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| Principles of pathology |
- Disease
- Hemodynamics
- Inflammation
- Wound healing
- Cell death
- Necrosis
- Liquefactive necrosis
- Coagulative necrosis
- Caseous necrosis
- Fat necrosis
- Apoptosis
- Pyknosis
- Karyorrhexis
- Karyolysis
- Cellular adaptation
- Atrophy
- Hypertrophy
- Hyperplasia
- Dysplasia
- Metaplasia
- Squamous
- Glandular
- Accumulations:
- pigment
- Hemosiderin
- Lipochrome/Lipofuscin
- Melanin
- Steatosis
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| Anatomical pathology |
- Surgical pathology
- Cytopathology
- Autopsy
- Molecular pathology
- Forensic pathology
- Oral and maxillofacial pathology
- Gross examination
- Histopathology
- Immunohistochemistry
- Electron microscopy
- Immunofluorescence
- Fluorescence in situ hybridization
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| Clinical pathology |
- Clinical chemistry
- Hematopathology
- Transfusion medicine
- Medical microbiology
- Diagnostic immunology
- Immunopathology
- Enzyme assay
- Mass spectrometry
- Chromatography
- Flow cytometry
- Blood bank
- Microbiological culture
- Serology
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| Specific conditions |
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Pathology: hemodynamics
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| Decreases |
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Thrombus/thrombosis
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Renal vein thrombosis
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Ischemia
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- Brain ischemia
- Ischaemic heart disease
- large intestine: Ischemic colitis
- small intestine: Mesenteric ischemia
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Infarction
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general:
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- Anemic infarct
- Hemorrhagic infarct
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regional:
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- Myocardial infarction
- Cerebral infarction
- Splenic infarction
- Limb infarction
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| Increases |
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Hemorrhage
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general
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- Bruise/Hematoma
- Petechia
- Purpura
- Ecchymosis
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regional
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- head
- Epistaxis
- Hemoptysis
- Intracranial hemorrhage
- Hyphema
- Subconjunctival hemorrhage
- torso
- Hemothorax
- Hemopericardium
- Pulmonary hematoma
- abdomen
- Gastrointestinal bleeding
- Haemobilia
- Hemoperitoneum
- Hematocele
- Hematosalpinx
- joint
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Edema
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general
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- Anasarca
- Angioedema/Lymphedema
- Exudate/Transudate
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regional
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- Cerebral edema
- Pulmonary edema
- Hydrothorax
- Ascites/hydroperitoneum
- Hydrosalpinx
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Other
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