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| − | {{review}}
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| − | {{toplink
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| − | |linkpage =General Pathology
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| − | |linktext =General Pathology
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| − | |maplink = General Pathology (Content Map)
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| − | |pagetype =Pathology
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| − | |sublink1=Circulatory Disorders - Pathology
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| − | |subtext1=CIRCULATORY DISORDERS
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| − | }}
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| − | <br>
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| | ==Introduction== | | ==Introduction== |
| − | | + | Oedema is NOT a disease; it is the sign of a disease state. |
| − | * Oedema is NOT a disease.
| + | * Oedema is defined as :'''"The swelling of tissues resulting from accumulation of excess fluid in the intercellular tissue spaces and serous cavities."''' |
| − | **Is the sign of a disease state.
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| − | * Oedema is defined as : | |
| − | | |
| − | '''"The swelling of tissues resulting from accumulation of excess fluid in the intercellular tissue spaces and serous cavities."''' | |
| | | | |
| | * Small amounts of fluid are normally present to lubricate cavities and viscera - this is not oedema. | | * Small amounts of fluid are normally present to lubricate cavities and viscera - this is not oedema. |
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| | ** '''Lungs'''. | | ** '''Lungs'''. |
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| − | ==Local oedema== | + | ==[[Local Oedema|Local oedema]]== |
| − | | |
| − | * Local oedema is the local accumulation of excess interstitial fluid.
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| − | * Caused by disturbance of the balance betwen fluid extravasation and resorption at the level of the capillaries.
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| − | ** '''Outwards Forces''' - arteriolar
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| − | *** Vasuclar hydrostatic pressure - 35 mmHg
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| − | *** Interstitial osmotic pressure - 3 mmHg
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| − | ** '''Inwards forces''' - venular
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| − | *** Plasma protein osmotic pressure - 25 mmHg
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| − | *** Interstitial hydrostatic pressure - 4 mmHg
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| − | * May be of inflammatory or non-inflammatory origin.
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| − | | |
| − | ===Types of Local Oedema===
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| − | | |
| − | ====Inflammatory oedema====
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| − | | |
| − | * Generated by one or more of the following:
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| − | *# Increased vascular permeability
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| − | *# Increased arteriolar blood pressure
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| − | *# Breakdown of tissue protein or transfer of plasma proteins into ECF.
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| − | *#* Results in raised osmotic pressure of tissue fluid.
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| − | *# Obstruction to lymphatic drainage.
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| − | *#* Usually by fibrin.
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| − | | |
| − | ====Lymphatic oedema====
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| − | | |
| − | * Results in accumulation of high protein fluid.
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| − | * May provoke a [[Chronic Inflammation - Pathology#Granulation Tissue|granulation]] or fibrous tissue response.
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| − | * Due to:
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| − | *# '''Lymphangitis/ lymphadenitis '''
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| − | *#* [[Acute Inflammation - Pathology|Acute inflammation]] of lymphatics/ lymph nodes. R
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| − | *#* Caused by stasis in lymphatics and/or bacterial infection.
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| − | *#* E.g. “Monday Morning leg” in horses.
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| − | *# '''Chronic inflammation''' caused by persistent or granuloma-producing bacterial infection.
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| − | *#* E.g. [[Intestines Proliferative Enteritis - Pathology#Paratuberculosis (Johnes disease)|Johne's disease]], [[:Category:Actinobacillus species|actinobacillosis]].
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| − | *# '''Tumour spread'''.
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| − | *#* [[Neoplasia - Pathology#Dissemination of Malignant Neoplasia|Metastasis]] of tumour cell plugs lymphatics and nodes
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| − | *#* e.g. mammary carcinoma.
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| − | *# '''Parasitic migration'''
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| − | *#* Larvae may be following their normal pathway (e.g. Schistosomiasis), or may be aberrant.
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| − | | |
| − | ====Local venous obstruction====
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| − | | |
| − | * Obstruction to venous drainage may be mechanical or inflammatory-mediated.
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| − | ** Causes raised hydrostatic pressure.
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| − | ** Endothelial permeability increases due to hypoxia.
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| − | ** There may be inflammatory damage.
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| − | * '''Mechanical obstruction''', e.g.
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| − | ** [[Intestine Physical Disturbances - Pathology#Positional Changes/ Displacements|Torsions of bowel]]
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| − | ** Misplaced organs.
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| − | ** Pressure from outside vein from adjacent structures.
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| − | *** [[Neoplasia - Pathology|Tumours]].
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| − | * '''Venous inflammation (phlebitis)'''
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| − | ** May be associated with [[Thrombosis - Pathology#Introduction|thrombosis]] (thrombophlebitis).
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| − | | |
| − | ===="Allergic" oedema====
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| − | | |
| − | * Results from immediate (Type I ) or delayed (Type IV) hypersensitivity.
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| − | * Vasular permeability is increased due to release of histamine and vaso-dilating substances.
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| − | * E.g.
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| − | ** Insect stings (immmediate).
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| − | ** Vaccination (delayed).
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| − | ** Food reaction (delayed).
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| − | | |
| − | ====[[Lungs Circulatory - Pathology#Pulmonary oedema|Pulmonary oedema]]====
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| − | | |
| − | * In the normal state, pulmonary alveoli are kept dry by three mechanisms:
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| − | *# Normal "push-pull" mechanism at capillary level.
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| − | *# Efficient lymphatic drainage by rhythmic pumping action near airways.
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| − | *# Integrity of the alveolar epithelial basement membrane is relatively impermeable.
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| − | *#* Unlike the capillary basement membrane, which is relatively permeable.
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| − | | |
| − | =====Pathogenesis=====
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| − | | |
| − | # The pumping efficiency of the lymphatics is exceeded.
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| − | # Fluid accumulates in connective tissue adjacent to airways.
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| − | # The alveolar walls fill with fluid.
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| − | # The alveoli abruptly and severely fill with fluid.
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| − | #* Associated with the disintegration of alveolar epithelial junctional complexes.
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| − | | |
| − | | |
| − | =====Haemodynamic type=====
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| − | | |
| − | * Fluid leaks into alveoli via junctional complexes BUT the alveolar basement membrane remains intact.
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| − | ** I.e. is due to elevated pulmonary venous pressure.
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| − | * Potentially reversible.
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| − | * Causes:
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| − | *# '''Cardiogenic'''
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| − | *#* Usually left ventricular failure.
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| − | *#* Also occurs with cardiac overload due to valvular disease.
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| − | *# '''Mechanical'''
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| − | *#* Large primary pulmonary tumours.
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| − | *#* Severe metastatic disease.
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| − | *#* Granulomatous infections may raise pulmonary venous pressure.
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| − | *# '''Neurogenic'''
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| − | *#* Seizures or CNS disorder.
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| − | *#* Rare in domestic species.
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| − | | |
| − | =====Permeability type=====
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| − | | |
| − | * Fluid fills the alveoli following damage to cells or junctional complexes, or permanent ionic alteration of the alveolar basement membrane.
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| − | * Irreversible.
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| − | * Causes:
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| − | *# '''Toxins'''
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| − | *#* Bacterial
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| − | *#** [[:Category:Pseudomonas and Burkholderia species|''Pseudomonas'']]
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| − | *#** [[:Category:Pasteurella and Mannheimia species|''Pasteurella'']]
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| − | *#** [[:Category:Staphylococcus species|''Staphylococcus'']]
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| − | *#* Chemical
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| − | *#** Paraquat.
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| − | *# '''Aspiration/inhalation'''
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| − | *#* Gastric contents (low pH)
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| − | *#* Smoke.
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| − | *#* Excess ozone.
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| − | *#* Oxygen.
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| − | | |
| − | * There may be a combination of haemodynamic and permeability types in electrocution syndromes and "shock" lung.
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| − | ** E.g. in Adult Respiratory Distress Syndrome (ARDS).
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| − | | |
| − | ==General oedema== | |
| − | | |
| − | * General oedema involves subcutaneous and tissue spaces/body cavities.
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| − | * Indicative of severe upset of overall body fluid balance.
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| − | ** Usually one or more vital organ system is abnormal.
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| − | * Requires one or more of the following conditions:
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| − | *# General increase in arteriolar hydrostatic pressure.
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| − | *# Decrease in osmotic pressure of blood.
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| − | *# Increase in tissue fluid osmotic pressure.
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| − | *#* E.g. sodium retention in renal disease.
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| − | *# Increased capillary permeability.
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| − | *#* E.g. due to hypoxic damage.
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| | | | |
| − | ===Types of General Oedema===
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| | | | |
| − | ====Cardiac oedema==== | + | ==[[General Oedema|General oedema]]== |
| − | | |
| − | * Seen in heart failure.
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| − | ** Shows that cardiac output fails to meet the demands of the tissues throughout the body.
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| − | ** Left-side failure gives pulmonary congestion.
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| − | *** Leads to pulmonary oedema.
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| − | ** Right-side failure gives systemic congestion.
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| − | *** Leads to generalised oedema.
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| − | * Chronic venous congestion develops when cardiac output fails to keep pace with venous return to the heart.
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| − | * Fluid balance is further complicated by secondary renal impairment.
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| − | ** Sodium is retained, triggering the renin-aldosterone loop with further sodium retention.
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| − | | |
| − | ====Renal oedema====
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| − | | |
| − | * Kidney malfunction induces oedema as a consequence of deranged sodium and water handling.
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| − | ** There is often secondary cardiac involvement.
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| − | *** Due to via renin effect on heart and myocardial depressant factor.
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| − | * Causes:
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| − | *# '''Acute glomerulonephritis'''
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| − | *#* Reduction in glomerular filtration rate results in systemic hypertension and retention of excess sodium and water.
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| − | *# '''Nephrotic syndrome'''
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| − | *#* A glomerular filtration defect gives selective heavy loss of plasma proteins (especially albumin)
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| − | *#** Reduction of plasma osmotic potential results in oedema.
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| − | *# '''Acute renal tubular necrosis'''
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| − | *#* Tubules can no longer selectively reabsorb sodium and other electrolytes.
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| − | *#** Water retention with the sodium and urea produces oedema.
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| − | *# '''Fibrosing glomerulonephritis'''
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| − | *#* Causes systemic hypertension and secondary cardiac failure with oedema.
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| − | | |
| − | ====Protein-losing enteropathies====
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| − | | |
| − | * Mucosal damage leads to loss of ability to absorb and retain proteins.
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| − | ** Plasma proteins, especially albumin are lost.
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| − | *** Circulating plasma proteins area therefore reduced, leading to oedema.
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| − | * E.g.
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| − | ** Johne's disease in cattle and sheep.
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| − | ** Ulcerative colitis or regional enteritis in dogs.
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| − | * For more on protein-losing enteropathies, see [[Intestines Protein-Losing Diseases - Pathology|Protein-Losing Diseases]].
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| − | | |
| − | ====Hepatic oedema====
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| − | | |
| − | * Associated with severe [[Liver - Anatomy & Physiology|liver]] damage.
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| − | ** Liver damage may be:
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| − | *** '''Actue'''
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| − | **** E.g. due to acute fascioliasis or canine viral hepatitis.
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| − | **** Lymphatics and blood vessels of the [[Liver - Anatomy & Physiology|liver]] and [[Peritoneal cavity - Anatomy & Physiology|peritoneal caivity]] are damaged.
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| − | ***** Results in "overflow" of fluid into the [[Peritoneal cavity - Anatomy & Physiology|peritoneal cavity]].
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| − | **** Additionally, hepatocyte damage may result in inadequate inactivation of aldosterone.
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| − | ***** Increases sodium retention giving further water accumulation in the abdomen
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| − | *** '''Chronic'''
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| − | **** E.g. metastatic neoplasia or fibrosing hepatopathy (cirrhosis).
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| − | **** Failure to produce plasma proteins leads to osmotic imbalance in the peripheral circulation.
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| − | **** This is seen as subcutaneous oedema.
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| − | ***** E.g. "bottle jaw".
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| | | | |
| | ==Composition of oedema fluid== | | ==Composition of oedema fluid== |
| − |
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| | * Inflammatory oedema which produces an exudate. | | * Inflammatory oedema which produces an exudate. |
| | ** This is a protein rich fluid containing many inflammatory cells. | | ** This is a protein rich fluid containing many inflammatory cells. |
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| | |- | | |- |
| | | '''Cell content''' | | | '''Cell content''' |
| − | | Very low. mesothelial cells, some macropahges and lymphocytes/[[Monocytes - WikiBlood]]. | + | | Very low. mesothelial cells, some macropahges and lymphocytes/[[Monocytes]]. |
| − | | High. Often macrophages, [[Neutrophils - WikiBlood|neutrophils]], lymphocyes etc. Depends on cause and chronicity | + | | High. Often macrophages, [[Neutrophils|neutrophils]], lymphocyes etc. Depends on cause and chronicity |
| | |} | | |} |
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| | ** '''Ventral subcutaneous oedema''' | | ** '''Ventral subcutaneous oedema''' |
| | * Seen in heart failure in horses and cattle. | | * Seen in heart failure in horses and cattle. |
| | + | |
| | + | |
| | + | |
| | + | [[Pulmonary Oedema]] |
| | + | |
| | + | |
| | + | [[Category:Circulatory Disorders - Pathology]] |
| | + | [[Category:Cardiology Section]] |