Showing posts with label Pathology. Show all posts
Showing posts with label Pathology. Show all posts

Sunday, October 14, 2012

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Edema - Definition, pathophysiology, causes, clinical features

Edema is an abnormal presence of excessive fluid in the interstitial space.

The movement of water and low molecular weight solutes such as salts between the intravascular and interstitial spaces is controlled primarily by the opposing effect of vascular hydrostatic pressure and plasma colloid osmotic pressure. Normally the outflow of fluid from the arteriolar end of the microcirculation into the interstitium is nearly balanced by inflow at the venular end. A small residual amount of fluid may be left in the interstitium and is drained by the lymphatic vessels, ultimately returning to the bloodstream via the thoracic duct.

Either increased capillary pressure, diminished colloid osmotic pressure or inadequate lymphatic drainage can result in an abnormally increased interstitial fluid i.e. edema. An abnormal increase in interstitial fluid within tissues is called edema, while fluid collections in the different body cavities are variously designated hydrothorax (pleural cavity), hydropericardium (pericardial cavity) and hydroperitoneum (the last is more commonly called ascites). Anasarca is a severe and generalized edema with widespread subcutaneous tissue swelling.

The diagram above shows the actual change in pressure gradients at the capillary level. The numbers represent the pressure in the vessels in mmHg.
At the arteriolar end, the hydrostatic pressure (outward force) is 37 mmHg while the oncotic pressure and interstitial pressure (inward forces) are 25 and 1 mmHg respectively. Thus the net outward force is 37 – (25+1) = +11 mmHg. Since the net outward force is positive fluid moves from the capillary to the interstitial spaces.
At the venular end, the hydrostatic pressure is lower and has a value of 17 mmHg. The oncotic and interstitial pressure on the other hand remain the same i.e. a total of 26 mmHg (25+1). Thus the net outward force is 17 – (25+1) = -9 mmHg. Since the outward force is negative, it means fluid is not getting out of the capillary but instead it is moving into it.

The arrows in the diagram show the magnitude and direction of net fluid movement.

1) According to pathophysiological mechanism:
                a) Transudate (low protein content)
                b) Exudate (high protein content)
2) According to location:
                a) Localized
                b) Generalized
3) According to clinical finding:
                a) Pitting
                b) Non-pitting.

It means that the edema is localized to a specific region of the body. It is commonly due to venous/lymphatic causes, allergy and inflammation.

1) Venous edema: It is due to high venous pressure or venous constriction. Intravascular venous obstruction e.g. Deep vein thrombosis (DVT) or an external compression like a mass (tumour) or plaster are the common causes but there can also be failure of venous pumps due to paralysis of muscles (Cerebro-vascular accident), immobilization of parts of the body (Post-op, fractures) and failure of venous valves (Varicose veins). It is more frequent to see localized edema in the lower limbs but the upper limbs may also be affected.

2) Lymphatic edema: It is due to a blockage in the lymphatic return. It commonly occurs in conditions like cancer/ post-radiation, infections like elephantiasis (Filaria nematodes), surgery or congenital absence or abnormality of lymphatic vessels. The edema is persistent and non-pitting type. In case of elephantiasis, the affected limb may be dramatically enlarged.

3) Allergy/Angioedema (Quincke edema): During a case of allergy there is release of histamine and other mediators that lead to vasodilation. The swelling can involve the face, lips, tongue and even glottis. Edema of the glottis is a medical emergency as it can lead to asphyxia if not treated quickly. This type of edema is usually itchy but transitory. It resolves with antihistaminics and steroids.

4) Inflammation: Here also there is vasodilation because of the inflammatory mediators. Edema is seen with superficial (cellulitis) or deep infections (abscess).

In this case the edema involves more than 1 part of the body simultaneously. It is commonly due to cardiac, hepatic, renal or endocrine causes.

1) Cardiac edema: The initial pathology is because of increased venous pressure but as the condition becomes more severe, there is impairment of renal blood supply, activation of rennin-angiotensin-aldosterone system and finally hypoalbuminemia secondary to liver stasis. Left sided heart failure leads to pulmonary edema while right sided heart failure causes peripheral edema, ascites, hydrothorax and anasarca in severe and long standing cases. The edema is progressive. In ambulant individuals, it moves up with severity. The edema is usually of pitting type. In early stages of heart failure, there is improved renal circulation at night leading to nycturia. Thus the edema will be less in the morning and progressively increases towards the end of the day.

2) Hepatic edema: Liver pathology like cirrhosis leads to decreased synthesis of proteins. The hypoalbuminemia leads to decreased oncotic pressure. The scarred liver also causes a back pressure in the portal vein territory (portal vein hypertension) and increases the hydrostatic pressure there. These 2 factors combined lead to edema in the peritoneal cavity (ascites) and this in turn compresses the inferior vena cava and leads to edema in the lower limbs.

3) Renal edema: Kidney diseases like nephritic syndrome with decreased glomerular filtration rate and sodium/water retention or nephrotic syndrome where there is albumin loss in the urine lead to generalized edema. The edema frequently occurs in lax connective tissue like the face, periorbital area and genitalia. It is of pitting type. It occurs mostly during the morning and is associated with vasoconstriction. Thus it is called as ‘white’ edema.

4) Endocrine edema: Many endocrine problems can cause edema. In case of hyperaldosteronism (primary or secondary), there is retention of sodium and water. This leads to an increase in hydrostatic pressure. The edema is of pitting type. On the other hand, myxedema refers to a non-pitting type of edema seen in hypothyroidism. Finally, females experience edema as part of the pre menstrual syndrome due to hormonal changes.

  1. Increased capillary pressure (increased hydrostatic pressure)
    1. Excessive kidney retention of salt and water
      1. Acute or chronic kidney failure
      2. Mineralocorticoid excess
    2. High venous pressure and venous constriction
      1. Impaired heart functioning (Congestive heart failure, constrictive pericarditis)
      2. Venous obstruction (Deep vein thrombosis, External compression like a mass or plaster)
      3. Failure of venous pumps
        • (a) Paralysis of muscles (Cerebro-vascular accident)
        • (b) Immobilization of parts of the body (Post-op, fractures)
        • (c) Failure of venous valves (Varicose veins)
    3. Decreased arteriolar resistance
      1. Excessive body heat
      2. Insufficiency of sympathetic nervous system
      3. Drugs (vasodilators, calcium channel blockers)
  2. Decreased plasma proteins
    1. Loss of proteins in urine (Nephrotic syndrome) or G.I.T (Protein-losing gastroenteropathy)
    2. Loss of protein from denuded skin areas
      1. Burns
      2. Wounds
    3. Failure to produce proteins
      1. Liver disease (Cirrhosis)
      2. Serious protein or caloric malnutrition
  3. Increased capillary permeability
    1. Immune reactions that cause release of histamine and other immune products (Allergy)
    2. Toxins
    3. Bacterial infections (Cellulitis)
    4. Vitamin deficiency, especially vitamin C
    5. Prolonged ischemia
    6. Burns
  4. Blockage of lymph return
    1. Cancer
    2. Infections (Filaria nematodes)
    3. Surgery
    4. Congenital absence or abnormality of lymphatic vessels
    5. Post-radiation.
In dependent edema, which is typically present in congestive heart failure and in conditions associated with a low plasma protein level, the swelling first appears at the ankles and over the dorsum of the foot and only gradually involves the legs, thighs and trunk. The best place to check for slight degrees of edema in an ambulant patient is behind the malleoli at the ankles. In bed-bound patients edema often appears first over the sacrum. To recognize pitting edema it is important to press firmly and for a sustained period of 20-30s over a bony prominence (tibia, lateral malleoli or sacrum) to provide effective compression. The 'pit' will be as easily felt as seen. If the finger pressure is not maintained for an adequate period of time then slight degrees of edema may be overlooked.

Edema can be recognized by the pallid and glossy appearance of the skin over the swollen part, by its doughy feel and by the fact that it pits on finger pressure.
The edema of lymphatic obstruction does not pit on pressure or there may be minimal pitting. The skin is usually thickened and tough.

1) Without redness and scaling, bilateral periorbital edema may indicate acute nephritis, nephrosis or trichinosis. If there is irritation, contact dermatitis is the probable diagnosis.
2) In local venous obstruction the edema is confined to the parts from which the return of blood is impeded. Local edema is sometimes seen over inflamed joints.
3) Edema of the whole upper part of the body may result from intrathoracic tumours.

Last reviewed on: 1 September 2015

Thursday, July 5, 2012

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Centriacinar / Centrilobular emphysema

In a classical lesion, dilated and destroyed respiratory bronchioles coalesce in series and in parallel to produce sharply demarcated emphysematous spaces. They are separated from the acinar periphery (the  lobular septa) by intact alveolar ducts and sacs of normal size, as shown by the diagram below. 

The lesions vary in quality and quantity even within the same lung. There is striking irregularity of involvement of lobules, and even within the same lobule. The lesions are usually more common and become more severe in the upper than in the lower zones of the lung. Most affected are the upper lobe, particularly the posterior and apical segments, and the superior segment of the lower lobe as depicted below. 

This type of emphysema is commonly seen in chronic cigarette smokers. For classification of emphysema, follow this link: Emphysema

Saturday, March 17, 2012


Hypertrophic scars

In some cases, the scarring process remains in the remodelling phase for longer than usual. These hypertrophic scars are more cellular and more vascular than mature scars.  There is increased collagen production and collagen breakdown but the balance is such that excess collagen is produced. 

Clinical features:
The hypertrophic scars are red, raised, itchy and tender. They will eventually mature to become pale and flat, and it is this spontaneous resolution which distinguishes hypertrophic scars from keloid scars. 

Hypertrophic scars typically occur in wounds where healing was delayed, e.g. in cases where infection or dehiscence has occurred. 

They are more common in children and where skin tension is high such as the tip of the shoulder or any scar that runs across relaxed skin tension lines.

Prevention and treatment:
The risk of developing a hypertrophic scar can be minimised by ensuring quiet primary healing. Where hypertrophy does occur patience is usually rewarded by improvement with time. Massage of the scar with moisturising cream or the application of pressure to the remodelling scar can accelerate the natural process of maturation. Patients with hypertrophic bum scars are supplied with custom made Lycra pressure garments that promote acceleration of scar maturation. Revision of hypertrophic scars is appropriate where they cross skin tension lines or where a specific wound healing complication occurred. In the absence of these factors scar revision should be avoided as it will usually be met with recurrence.

Wednesday, February 15, 2012

Differences between hyperemia and congestion

Hyperemia and congestion both indicate a local increased volume of blood in a particular tissue.
Hyperemia is an active process that result from augmented blood flow due to arteriolar dilation (e.g. at sites of inflammation or in skeletal muscle during exercise). The affected tissue is redder than normal because of engorgement with oxygenated blood.
Congestion, on the other hand, is a passive process resulting from impaired venous return out of a tissue. It may occur due to systemic causes like cardiac failure or a local cause like isolated venous obstruction. The tissue is cyanosed because the worsening congestion leads to accumulation of deoxygenated hemoglobin in the affected tissues. 

Tuesday, January 3, 2012

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Abciximab - mechanism of action/ indication/ contraindication/ dose

It is a Fab fragment of a humanized monoclonal antibody directed against the glycoprotein IIb/IIIa. The latter is a platelet surface integrin. It is a receptor for fibrinogen which binds platelets to each other causing aggregation.

By inhibiting the receptor, abciximab acts as a potent antiplatelet agent. 

1) myocardial ischemia,
2) percutaneous coronary intervention.

1) For M.I - initially an I.V bolus of 0.25 mg/kg over 5 min followed by 0.125 µg/kg/min (to a maximum of 10 µg/min) for 12 hours.
2) For P.C.I - initially, 0.25 mg/kg I.V bolus over 5 min 20-60 min prior to angioplasty followed by 0.125 µg/kg/min (to a maximum of 10 µg/min) for next 12 hours.

1) bleeding disorder or use of anticoagulant within 7 days,
2) CVA within 2 years,
3) known allergy to this product,
4) major trauma or surgery within 6 weeks,
5) severe uncontrolled hypertension,
6) active internal bleeding,
7) thrombocytopenia i.e platelet count < 100,000/ µL.

Friday, December 23, 2011

Allergy symptoms more at start of season

Recent studies have found that allergic people tend to have more symptoms at the beginning of the season. This is regardless of the medications taken. The following are the proposed explanations:
1) Sufferers get used to the symptoms and are therefore not bothered by them. So they did not report the symptoms.
2) Allergen-specific regulatory T cells may down regulate the inflammatory response after high exposure to the pollen at the beginning of the season.
3) Pollen at the later part of the season are less allergenic.

Thursday, November 24, 2011

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Salmonella enterocolitis - food poisoning

It is a diarrheal disease and is commonly seen in cases of food poisoning.

Man acquires this infection by ingesting contaminated water or food. Water is usually infected by feaces from an infected animal or human. Poultry and eggs also comprise an important source of salmonella. The organisms may be present on the outer shell or even in the yolk.

The clinical syndromes that can occur in man includes gastroenteritis, enteric fever and septicaemia.

In the case of enterocolitis, the salmonella bacilli attach themselves to the microvilli of the ileal mucosa by means of adhesins and then invade the cells. They cause massive efflux of fluids and electrolytes.

Clinical presentaion:
There is large volume watery diarrhea, fever, headache, chills, abdominal pain and tenesmus. In simple uncomplicated cases, the diarrhea will last for 3-7 days.
Diagnosis is made by stool culture.

The disease is self limited. Treatment consists only of correcting any fluid and electrolyte imbalance. Antibiotics do not shorten the duration of symptoms.

Tuesday, July 19, 2011


Virchow's triad

Virchow's triad refers to the 3 primary influences for thrombus formation and it includes:
1) Endothelial injury
2) Stasis, turbulence or abnormal blood flow
3) Blood hypercoagulability.

Endothelial injury
Physical loss of endothelium leads to exposure of subendothelial extra-cellular matrix, adhesion of platelets, release of tissue factor, and local depletion of PGI2 and plasminogen activators.

Abnormal blood flow
Turbulence can cause endothelial injury which is in itself a major influence for thrombosis. Apart from that abnormal blood flow can:
1) Disrupt laminar flow and bring platelets into contact with the endothelium
2) Prevent dilution of activated clotting factors by fresh-flowing blood
3) Retard the inflow of clotting factor inhibitors and permit the buildup of thrombi
4) Promote endothelial cell activation, resulting in local thrombosis, leukocyte adhesion, etc. 

It can be primarily due to a genetic disorder and secondarily due to some acquired problems.

The primary causes are:
1) mutation of factor V gene a/k/a factor V Leiden
2) mutation of prothrombin gene
3) anti-thrombin III deficiency
4) protein C deficiency
5) protein S deficiency

The secondary causes are:
1) prolonged immobilization
2) myocardial infarction
3) atrial fibrillation
4) cancer
5) prosthetic cardiac valves
6) heparin induced thrombocytopenia
7) hyperestrogenic states e.g. pregnancy / OCP use
8) smoking
9) sickle cell anemia