OEDEMA

 Excessive accumulation of fluid in the extra vascular compartment (intersttitial tissues). This includes ascites (peritoneal sac), hydrothorax (pleural cavity) hydropericardium (pericardial space) and anasarca (generalised)

Factors which tend to accumulate interstitial fluid are:

- Intravascular hydrostatic pressure

- Interstitial osmotic pressure.

- Defective lymphatic drainage.

- Increased capillary permeability.

Factors that draw fluid into circulation are:

- Tissue hydrostatic-pressure (tissue tension).

- Plasma osmotic pressure,

Oedema fluid can be of 2 types:

A. Exudate.

It is formed due to increased capillary permeability as in inflammation.

B. Transudate

Caused by alterations of hydrostatic and osmotic pressures.

Local Oedema

1. Inflammatory oedema. Mechanisms are.

- Increased capillary permeability.

- Increased vascular hydrostatic pressure.

- Increased tissue osmotic pressure.

2.Hypersensitivity reactions especially types I and III

3. Venous obstruction :

- Thrombosis.

- Pressure from outside as in pregnancy, tourniquets.

4. Lymphatic obstruction:

- Elephantiasis in fillariasis

- Malignancies (Peau de orange in breast cancer).

Generalized Oedema

1.         Cardiac oedema

Factors :Venous pressure increased.

2. Renal oedema

- Acute glomerulonephritis

- Nephrotic syndrome

3. Nutritional (hypoproteinaemic) oedema. it is seen in

- Starvation and Kwashiorkor

- Protein losing enteropathy

4.  Hepatic oedema (predominantly ascites)

Factors:

- Fall in plasma protein synthesis

- Raised regional lymphatic and portal venous pressure

5. Oedema due to adrenal corticoids

As in Cushing's Syndrome

Pulmonary oedema

- Left heart failure and mitral stenosis.

- Rapid flv infusion specially in a patient of heart failure.

THROMBOPHLEBITIS AND  PHLEBOTHROMBOSIS 
- The deep leg veins account for more than 90% of cases (DVT) 
- the most important clinical predispositions are: congestive heart failure, neoplasia, pregnancy, obesity, the postoperative state, and prolonged bed rest or immobilization 
- local manifestations: distal edema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling, and pain 
- migratory thrombophlebitis (Trousseau sign): hypercoagulability occurs as a paraneoplastic syndrome related to tumor elaboration of procoagulant factors 

Clinical & biologic death

Clinical death

Clinical death is the reversible transmission between life and biologic death. Clinical death is defined as the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery.

Signs indicating clinical death are

• The patient is without pulse or blood pressure and is completely unresponsive to the most painful stimulus.

• The pupils are widely dilated

• Some reflex reactions to external stimulation are preserved. For example, during intubations, respiration may be restored in response to stimulation of the receptors of the superior laryngeal nerve, the nucleus of which is located in the medulla oblongata near the respiratory center.

• Recovery can occur with resuscitation. 

Biological Death

Biological death (sure sign of death), which sets in after clinical death, is an irreversible state

of cellular destruction. It manifests with irreversible cessation of circulatory and respiratory

functions, or irreversible cessation of all functions of the entire brain, including brain stem.

Eosinophilia:
Causes

-Allergic disorders.
-Parasitic infection.
-Skin diseases.
-Pulmonary eosinophilia.
-Myeloproliferative lesions and Hodgkin's disease.