Difference between revisions of "Oedema"
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+ | {{review}} | ||
+ | |||
+ | {{toplink | ||
+ | |linkpage =General Pathology | ||
+ | |linktext =General Pathology | ||
+ | |maplink = General Pathology (Content Map) | ||
+ | |pagetype =Pathology | ||
+ | |sublink1=Circulatory Disorders - Pathology | ||
+ | |subtext1=CIRCULATORY DISORDERS | ||
+ | }} | ||
+ | <br> | ||
==Introduction== | ==Introduction== | ||
− | 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."''' | + | * Oedema is NOT a disease. |
+ | **Is the sign of a disease state. | ||
+ | * 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. | ||
Line 14: | Line 29: | ||
** '''Lungs'''. | ** '''Lungs'''. | ||
− | ==[[Local | + | ==Local oedema== |
+ | |||
+ | * Local oedema is the local accumulation of excess interstitial fluid. | ||
+ | * Caused by disturbance of the balance betwen fluid extravasation and resorption at the level of the capillaries. | ||
+ | ** '''Outwards Forces''' - arteriolar | ||
+ | *** Vasuclar hydrostatic pressure - 35 mmHg | ||
+ | *** Interstitial osmotic pressure - 3 mmHg | ||
+ | ** '''Inwards forces''' - venular | ||
+ | *** Plasma protein osmotic pressure - 25 mmHg | ||
+ | *** Interstitial hydrostatic pressure - 4 mmHg | ||
+ | * May be of inflammatory or non-inflammatory origin. | ||
+ | |||
+ | ===Types of Local Oedema=== | ||
+ | |||
+ | ====Inflammatory oedema==== | ||
+ | |||
+ | * Generated by one or more of the following: | ||
+ | *# Increased vascular permeability | ||
+ | *# Increased arteriolar blood pressure | ||
+ | *# Breakdown of tissue protein or transfer of plasma proteins into ECF. | ||
+ | *#* Results in raised osmotic pressure of tissue fluid. | ||
+ | *# Obstruction to lymphatic drainage. | ||
+ | *#* Usually by fibrin. | ||
+ | |||
+ | ====Lymphatic oedema==== | ||
+ | |||
+ | * Results in accumulation of high protein fluid. | ||
+ | * May provoke a [[Chronic Inflammation - Pathology#Granulation Tissue|granulation]] or fibrous tissue response. | ||
+ | * Due to: | ||
+ | *# '''Lymphangitis/ lymphadenitis ''' | ||
+ | *#* [[Acute Inflammation - Pathology|Acute inflammation]] of lymphatics/ lymph nodes. R | ||
+ | *#* Caused by stasis in lymphatics and/or bacterial infection. | ||
+ | *#* E.g. “Monday Morning leg” in horses. | ||
+ | *# '''Chronic inflammation''' caused by persistent or granuloma-producing bacterial infection. | ||
+ | *#* E.g. [[Intestines Proliferative Enteritis - Pathology#Paratuberculosis (Johnes disease)|Johne's disease]], [[:Category:Actinobacillus species|actinobacillosis]]. | ||
+ | *# '''Tumour spread'''. | ||
+ | *#* [[Neoplasia - Pathology#Dissemination of Malignant Neoplasia|Metastasis]] of tumour cell plugs lymphatics and nodes | ||
+ | *#* e.g. mammary carcinoma. | ||
+ | *# '''Parasitic migration''' | ||
+ | *#* Larvae may be following their normal pathway (e.g. Schistosomiasis), or may be aberrant. | ||
+ | |||
+ | ====Local venous obstruction==== | ||
+ | |||
+ | * Obstruction to venous drainage may be mechanical or inflammatory-mediated. | ||
+ | ** Causes raised hydrostatic pressure. | ||
+ | ** Endothelial permeability increases due to hypoxia. | ||
+ | ** There may be inflammatory damage. | ||
+ | * '''Mechanical obstruction''', e.g. | ||
+ | ** [[Intestine Physical Disturbances - Pathology#Positional Changes/ Displacements|Torsions of bowel]] | ||
+ | ** Misplaced organs. | ||
+ | ** Pressure from outside vein from adjacent structures. | ||
+ | *** [[Neoplasia - Pathology|Tumours]]. | ||
+ | * '''Venous inflammation (phlebitis)''' | ||
+ | ** May be associated with [[Thrombosis - Pathology#Introduction|thrombosis]] (thrombophlebitis). | ||
+ | |||
+ | ===="Allergic" oedema==== | ||
+ | |||
+ | * Results from immediate (Type I ) or delayed (Type IV) hypersensitivity. | ||
+ | * Vasular permeability is increased due to release of histamine and vaso-dilating substances. | ||
+ | * E.g. | ||
+ | ** Insect stings (immmediate). | ||
+ | ** Vaccination (delayed). | ||
+ | ** Food reaction (delayed). | ||
+ | |||
+ | ====[[Lungs Circulatory - Pathology#Pulmonary oedema|Pulmonary oedema]]==== | ||
+ | |||
+ | * In the normal state, pulmonary alveoli are kept dry by three mechanisms: | ||
+ | *# Normal "push-pull" mechanism at capillary level. | ||
+ | *# Efficient lymphatic drainage by rhythmic pumping action near airways. | ||
+ | *# Integrity of the alveolar epithelial basement membrane is relatively impermeable. | ||
+ | *#* Unlike the capillary basement membrane, which is relatively permeable. | ||
+ | |||
+ | =====Pathogenesis===== | ||
+ | |||
+ | # The pumping efficiency of the lymphatics is exceeded. | ||
+ | # Fluid accumulates in connective tissue adjacent to airways. | ||
+ | # The alveolar walls fill with fluid. | ||
+ | # The alveoli abruptly and severely fill with fluid. | ||
+ | #* Associated with the disintegration of alveolar epithelial junctional complexes. | ||
+ | |||
+ | |||
+ | =====Haemodynamic type===== | ||
+ | |||
+ | * Fluid leaks into alveoli via junctional complexes BUT the alveolar basement membrane remains intact. | ||
+ | ** I.e. is due to elevated pulmonary venous pressure. | ||
+ | * Potentially reversible. | ||
+ | * Causes: | ||
+ | *# '''Cardiogenic''' | ||
+ | *#* Usually left ventricular failure. | ||
+ | *#* Also occurs with cardiac overload due to valvular disease. | ||
+ | *# '''Mechanical''' | ||
+ | *#* Large primary pulmonary tumours. | ||
+ | *#* Severe metastatic disease. | ||
+ | *#* Granulomatous infections may raise pulmonary venous pressure. | ||
+ | *# '''Neurogenic''' | ||
+ | *#* Seizures or CNS disorder. | ||
+ | *#* Rare in domestic species. | ||
+ | |||
+ | =====Permeability type===== | ||
+ | |||
+ | * Fluid fills the alveoli following damage to cells or junctional complexes, or permanent ionic alteration of the alveolar basement membrane. | ||
+ | * Irreversible. | ||
+ | * Causes: | ||
+ | *# '''Toxins''' | ||
+ | *#* Bacterial | ||
+ | *#** [[:Category:Pseudomonas and Burkholderia species|''Pseudomonas'']] | ||
+ | *#** [[:Category:Pasteurella and Mannheimia species|''Pasteurella'']] | ||
+ | *#** [[:Category:Staphylococcus species|''Staphylococcus'']] | ||
+ | *#* Chemical | ||
+ | *#** Paraquat. | ||
+ | *# '''Aspiration/inhalation''' | ||
+ | *#* Gastric contents (low pH) | ||
+ | *#* Smoke. | ||
+ | *#* Excess ozone. | ||
+ | *#* Oxygen. | ||
+ | |||
+ | * There may be a combination of haemodynamic and permeability types in electrocution syndromes and "shock" lung. | ||
+ | ** E.g. in Adult Respiratory Distress Syndrome (ARDS). | ||
+ | |||
+ | ==General oedema== | ||
+ | |||
+ | * General oedema involves subcutaneous and tissue spaces/body cavities. | ||
+ | * Indicative of severe upset of overall body fluid balance. | ||
+ | ** Usually one or more vital organ system is abnormal. | ||
+ | * Requires one or more of the following conditions: | ||
+ | *# General increase in arteriolar hydrostatic pressure. | ||
+ | *# Decrease in osmotic pressure of blood. | ||
+ | *# Increase in tissue fluid osmotic pressure. | ||
+ | *#* E.g. sodium retention in renal disease. | ||
+ | *# Increased capillary permeability. | ||
+ | *#* E.g. due to hypoxic damage. | ||
+ | ===Types of General Oedema=== | ||
− | ==[[ | + | ====Cardiac oedema==== |
+ | |||
+ | * Seen in heart failure. | ||
+ | ** Shows that cardiac output fails to meet the demands of the tissues throughout the body. | ||
+ | ** Left-side failure gives pulmonary congestion. | ||
+ | *** Leads to pulmonary oedema. | ||
+ | ** Right-side failure gives systemic congestion. | ||
+ | *** Leads to generalised oedema. | ||
+ | * Chronic venous congestion develops when cardiac output fails to keep pace with venous return to the heart. | ||
+ | * Fluid balance is further complicated by secondary renal impairment. | ||
+ | ** Sodium is retained, triggering the renin-aldosterone loop with further sodium retention. | ||
+ | |||
+ | ====Renal oedema==== | ||
+ | |||
+ | * Kidney malfunction induces oedema as a consequence of deranged sodium and water handling. | ||
+ | ** There is often secondary cardiac involvement. | ||
+ | *** Due to via renin effect on heart and myocardial depressant factor. | ||
+ | * Causes: | ||
+ | *# '''Acute glomerulonephritis''' | ||
+ | *#* Reduction in glomerular filtration rate results in systemic hypertension and retention of excess sodium and water. | ||
+ | *# '''Nephrotic syndrome''' | ||
+ | *#* A glomerular filtration defect gives selective heavy loss of plasma proteins (especially albumin) | ||
+ | *#** Reduction of plasma osmotic potential results in oedema. | ||
+ | *# '''Acute renal tubular necrosis''' | ||
+ | *#* Tubules can no longer selectively reabsorb sodium and other electrolytes. | ||
+ | *#** Water retention with the sodium and urea produces oedema. | ||
+ | *# '''Fibrosing glomerulonephritis''' | ||
+ | *#* Causes systemic hypertension and secondary cardiac failure with oedema. | ||
+ | |||
+ | ====Protein-losing enteropathies==== | ||
+ | |||
+ | * Mucosal damage leads to loss of ability to absorb and retain proteins. | ||
+ | ** Plasma proteins, especially albumin are lost. | ||
+ | *** Circulating plasma proteins area therefore reduced, leading to oedema. | ||
+ | * E.g. | ||
+ | ** Johne's disease in cattle and sheep. | ||
+ | ** Ulcerative colitis or regional enteritis in dogs. | ||
+ | * For more on protein-losing enteropathies, see [[Intestines Protein-Losing Diseases - Pathology|Protein-Losing Diseases]]. | ||
+ | |||
+ | ====Hepatic oedema==== | ||
+ | |||
+ | * Associated with severe [[Liver - Anatomy & Physiology|liver]] damage. | ||
+ | ** Liver damage may be: | ||
+ | *** '''Actue''' | ||
+ | **** E.g. due to acute fascioliasis or canine viral hepatitis. | ||
+ | **** Lymphatics and blood vessels of the [[Liver - Anatomy & Physiology|liver]] and [[Peritoneal cavity - Anatomy & Physiology|peritoneal caivity]] are damaged. | ||
+ | ***** Results in "overflow" of fluid into the [[Peritoneal cavity - Anatomy & Physiology|peritoneal cavity]]. | ||
+ | **** Additionally, hepatocyte damage may result in inadequate inactivation of aldosterone. | ||
+ | ***** Increases sodium retention giving further water accumulation in the abdomen | ||
+ | *** '''Chronic''' | ||
+ | **** E.g. metastatic neoplasia or fibrosing hepatopathy (cirrhosis). | ||
+ | **** Failure to produce plasma proteins leads to osmotic imbalance in the peripheral circulation. | ||
+ | **** This is seen as subcutaneous oedema. | ||
+ | ***** E.g. "bottle jaw". | ||
==Composition of oedema fluid== | ==Composition of oedema fluid== | ||
+ | |||
* 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]]. | + | | Very low. mesothelial cells, some macropahges and lymphocytes/[[Monocytes - WikiBlood]]. |
− | | High. Often macrophages, [[Neutrophils|neutrophils]], lymphocyes etc. Depends on cause and chronicity | + | | High. Often macrophages, [[Neutrophils - WikiBlood|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. | ||
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Revision as of 23:19, 14 May 2010
This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing. |
|
Introduction
- Oedema is NOT a disease.
- Is the sign of a disease state.
- 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.
- Excess fluid may accumulate in:
- Subcutaneous tissue and between muscle.
- Serous cavities.
- Depending on the cavity, this has different terms.
- Thorax - hydrothorax.
- Pericardium - hydropericardium
- Abdomen - hydroperitoneum (ascites).
- Anasarca is when there is generalised body cavity accumulation plus subcutaneous involvement.
- Depending on the cavity, this has different terms.
- Lungs.
Local oedema
- Local oedema is the local accumulation of excess interstitial fluid.
- Caused by disturbance of the balance betwen fluid extravasation and resorption at the level of the capillaries.
- Outwards Forces - arteriolar
- Vasuclar hydrostatic pressure - 35 mmHg
- Interstitial osmotic pressure - 3 mmHg
- Inwards forces - venular
- Plasma protein osmotic pressure - 25 mmHg
- Interstitial hydrostatic pressure - 4 mmHg
- Outwards Forces - arteriolar
- May be of inflammatory or non-inflammatory origin.
Types of Local Oedema
Inflammatory oedema
- Generated by one or more of the following:
- Increased vascular permeability
- Increased arteriolar blood pressure
- Breakdown of tissue protein or transfer of plasma proteins into ECF.
- Results in raised osmotic pressure of tissue fluid.
- Obstruction to lymphatic drainage.
- Usually by fibrin.
Lymphatic oedema
- Results in accumulation of high protein fluid.
- May provoke a granulation or fibrous tissue response.
- Due to:
- Lymphangitis/ lymphadenitis
- Acute inflammation of lymphatics/ lymph nodes. R
- Caused by stasis in lymphatics and/or bacterial infection.
- E.g. “Monday Morning leg” in horses.
- Chronic inflammation caused by persistent or granuloma-producing bacterial infection.
- E.g. Johne's disease, actinobacillosis.
- Tumour spread.
- Metastasis of tumour cell plugs lymphatics and nodes
- e.g. mammary carcinoma.
- Parasitic migration
- Larvae may be following their normal pathway (e.g. Schistosomiasis), or may be aberrant.
- Lymphangitis/ lymphadenitis
Local venous obstruction
- Obstruction to venous drainage may be mechanical or inflammatory-mediated.
- Causes raised hydrostatic pressure.
- Endothelial permeability increases due to hypoxia.
- There may be inflammatory damage.
- Mechanical obstruction, e.g.
- Torsions of bowel
- Misplaced organs.
- Pressure from outside vein from adjacent structures.
- Venous inflammation (phlebitis)
- May be associated with thrombosis (thrombophlebitis).
"Allergic" oedema
- Results from immediate (Type I ) or delayed (Type IV) hypersensitivity.
- Vasular permeability is increased due to release of histamine and vaso-dilating substances.
- E.g.
- Insect stings (immmediate).
- Vaccination (delayed).
- Food reaction (delayed).
Pulmonary oedema
- In the normal state, pulmonary alveoli are kept dry by three mechanisms:
- Normal "push-pull" mechanism at capillary level.
- Efficient lymphatic drainage by rhythmic pumping action near airways.
- Integrity of the alveolar epithelial basement membrane is relatively impermeable.
- Unlike the capillary basement membrane, which is relatively permeable.
Pathogenesis
- The pumping efficiency of the lymphatics is exceeded.
- Fluid accumulates in connective tissue adjacent to airways.
- The alveolar walls fill with fluid.
- The alveoli abruptly and severely fill with fluid.
- Associated with the disintegration of alveolar epithelial junctional complexes.
Haemodynamic type
- Fluid leaks into alveoli via junctional complexes BUT the alveolar basement membrane remains intact.
- I.e. is due to elevated pulmonary venous pressure.
- Potentially reversible.
- Causes:
- Cardiogenic
- Usually left ventricular failure.
- Also occurs with cardiac overload due to valvular disease.
- Mechanical
- Large primary pulmonary tumours.
- Severe metastatic disease.
- Granulomatous infections may raise pulmonary venous pressure.
- Neurogenic
- Seizures or CNS disorder.
- Rare in domestic species.
- Cardiogenic
Permeability type
- Fluid fills the alveoli following damage to cells or junctional complexes, or permanent ionic alteration of the alveolar basement membrane.
- Irreversible.
- Causes:
- Toxins
- Bacterial
- Chemical
- Paraquat.
- Aspiration/inhalation
- Gastric contents (low pH)
- Smoke.
- Excess ozone.
- Oxygen.
- Toxins
- There may be a combination of haemodynamic and permeability types in electrocution syndromes and "shock" lung.
- E.g. in Adult Respiratory Distress Syndrome (ARDS).
General oedema
- General oedema involves subcutaneous and tissue spaces/body cavities.
- Indicative of severe upset of overall body fluid balance.
- Usually one or more vital organ system is abnormal.
- Requires one or more of the following conditions:
- General increase in arteriolar hydrostatic pressure.
- Decrease in osmotic pressure of blood.
- Increase in tissue fluid osmotic pressure.
- E.g. sodium retention in renal disease.
- Increased capillary permeability.
- E.g. due to hypoxic damage.
Types of General Oedema
Cardiac oedema
- Seen in heart failure.
- Shows that cardiac output fails to meet the demands of the tissues throughout the body.
- Left-side failure gives pulmonary congestion.
- Leads to pulmonary oedema.
- Right-side failure gives systemic congestion.
- Leads to generalised oedema.
- Chronic venous congestion develops when cardiac output fails to keep pace with venous return to the heart.
- Fluid balance is further complicated by secondary renal impairment.
- Sodium is retained, triggering the renin-aldosterone loop with further sodium retention.
Renal oedema
- Kidney malfunction induces oedema as a consequence of deranged sodium and water handling.
- There is often secondary cardiac involvement.
- Due to via renin effect on heart and myocardial depressant factor.
- There is often secondary cardiac involvement.
- Causes:
- Acute glomerulonephritis
- Reduction in glomerular filtration rate results in systemic hypertension and retention of excess sodium and water.
- Nephrotic syndrome
- A glomerular filtration defect gives selective heavy loss of plasma proteins (especially albumin)
- Reduction of plasma osmotic potential results in oedema.
- A glomerular filtration defect gives selective heavy loss of plasma proteins (especially albumin)
- Acute renal tubular necrosis
- Tubules can no longer selectively reabsorb sodium and other electrolytes.
- Water retention with the sodium and urea produces oedema.
- Tubules can no longer selectively reabsorb sodium and other electrolytes.
- Fibrosing glomerulonephritis
- Causes systemic hypertension and secondary cardiac failure with oedema.
- Acute glomerulonephritis
Protein-losing enteropathies
- Mucosal damage leads to loss of ability to absorb and retain proteins.
- Plasma proteins, especially albumin are lost.
- Circulating plasma proteins area therefore reduced, leading to oedema.
- Plasma proteins, especially albumin are lost.
- E.g.
- Johne's disease in cattle and sheep.
- Ulcerative colitis or regional enteritis in dogs.
- For more on protein-losing enteropathies, see Protein-Losing Diseases.
Hepatic oedema
- Associated with severe liver damage.
- Liver damage may be:
- Actue
- E.g. due to acute fascioliasis or canine viral hepatitis.
- Lymphatics and blood vessels of the liver and peritoneal caivity are damaged.
- Results in "overflow" of fluid into the peritoneal cavity.
- Additionally, hepatocyte damage may result in inadequate inactivation of aldosterone.
- Increases sodium retention giving further water accumulation in the abdomen
- Chronic
- E.g. metastatic neoplasia or fibrosing hepatopathy (cirrhosis).
- Failure to produce plasma proteins leads to osmotic imbalance in the peripheral circulation.
- This is seen as subcutaneous oedema.
- E.g. "bottle jaw".
- Actue
- Liver damage may be:
Composition of oedema fluid
- Inflammatory oedema which produces an exudate.
- This is a protein rich fluid containing many inflammatory cells.
- Non inflammatory oedema which produces a transudate.
- This fluid is low in protein and cells.
- Transudates and exudates are distinguished by the following criteria:
Criteria | Transudate | Exudate |
---|---|---|
Appearance | Clear/ pale yellow ("straw coloured") | Dark yellow, red or brown. Often cloudy or opaque. |
Consistency | Thin, serous | Viscous |
Protein content | 0.05 - 0.5%, mainly albumin | Usually 2 - 4% |
Coagulability | No fibrinogen, no coagulation | Contains fibrinogen, coagulates |
Specific gravity | Low (< 1.012) | High (1.012 - 1.020) + |
Cell content | Very low. mesothelial cells, some macropahges and lymphocytes/Monocytes - WikiBlood. | High. Often macrophages, neutrophils, lymphocyes etc. Depends on cause and chronicity |
- Examples of transudates:
- Ascites
- Excessive fluid in abdominal cavity.
- Hydrothorax
- Excessive fluid in the thorax.
- Hydropericardium
- Excessive fluid in the pericardium.
- Anasarca
- Generalised tissue oedema most noticeable in subcutaneous tissues.
- Ventral subcutaneous oedema
- Ascites
- Seen in heart failure in horses and cattle.