HAEMORRHAGE

definition: Blood loss secondary to rupture of a blood vessel.

CAUSES

I. VASCULAR DEFECTS
A. Congenital- Berry aneurysms, cystic medionecrosis in Marfan syndrome
B. Acquired-these are usually complications of other disorders which cause a focal weakening and abnormal dilatation of the vessel wall (aneurysm) e.g.
1. Hypertension
2. Atherosclerosis
3. Infections~ aspergillosis, mucormycosis syphilis, salmonella bacteraemia

II. TRAUMA

III. INFLAMMATION i.e. Vasculitides e.g. PAN, Kawasaki syndrome

IV. NEOPLASTIC EROSION

V. HAEMORRHAGIC DIATHESES
A. Bleeding disorders caused by vessel wall abnormalities
B. Bleeding related to reduced platelet number: Thrombocytopaenia
C. Bleeding disorders related to defective platelet functions
D. Bleeding disorders related to abnormalities in clotting factors
E. Disseminated Intravascular Coagulation (DIC)

CLASSIFICATION

I. External & II. Internal

A. Within cavities
Haemothorax
haemopericardium
haemoperitoneum
haematocolpus

B. Within tissues
Haematoma
Ecchymoses~>1cm
Purpura ~3mm to 1cm
Petechiae~<3mm MORPHOLOGY Gross: Evidence of bleeding into tissues and cavities as described above i.e. dark red blood in tissues. May be dark brown following degradation of RBCs. May vary with respect to tissue type e.g. yellowish discolouration in the brain.

Microscopic: RBCs within the interstitium in fresh bleeds. Presence of golden brown haemosiderin pigments lying free in the interstitium and also within macrophages.

PATHOPHYSIOLOGY Blood loss -> reduced cardiac output (CO)-> fall in blood pressure -> pressure sensors relay to VMC -> vasoconstriction -> increased PR -> increased BP

Blood loss -> decreased GFR ->activation of Renin-Angiotensin System -> tubular reabsorption of Na & Water -> plasma volume

CLINICAL CORRELATION The consequences of haemorrhage depend on the quantity of blood loss. Mild bleeding that presents with petechiae and purpura may have negligible effects if they occur in the skin, for example. However if multiple petechiae occur in the brain they are likely to be accompanied by some cerebral oedema and clouding of the sensorium. Chronic loss of small amounts of blood can result in IDA External losses of <20% are usually well compensated for i.e. if the individual was not already compromised. Acute/sudden loss of up to 33% of the blood volume can be fatal. Losses of up to 50% of the blood volume can be tolerated if spread over 24hrs but the consequences are usually severe. Acute severe blood loss usually results in shock which may result in death if untreated. Haemorrhage, excessive discharge of blood from blood vessels, caused by pathological condition of the vessels or by traumatic rupture of one or more vessels. Haemorrhage is a complication of many diseases. Peptic ulcer, for example, may cause haemorrhage by eroding a blood vessel. Stroke is sometimes due to haemorrhage in the brain. Haemophilia, a hereditary blood disease, is characterized by failure of the blood to coagulate. Sudden loss of more than about 1 litre (1 qt) of blood may lead to shock; unless the blood is replaced by transfusion, this shock can be fatal.

HYPERAEMIA (AND CONGESTION) Definition: Increased volume of blood in an affected tissue or part. It could be an active or a passive process. Passive hyperaemia is otherwise referred to as congestion.

HYPERAEMIA (ACTIVE) Causes: Neurogenic/neurohumoral mechanisms, which help to dissipate heat during febrile states and physical exercise. Also responsible for blushing in Caucasians.

Mechanism: Arterial/arteriolar dilatation -> increased flow of blood to capillary beds -> opening of capillary beds -> increased redness of tissue.

CONGESTION (PASSIVE HYPERAEMIA) Causes: Impaired venous drainage e.g. in CCF (generalised), lymphatic obstruction (localised),venous obstruction (localised)

Mechanism: Impaired venous drainage -> congestion of capillary beds -> stasis -> hypoxia -> cyanosis -> bluish discolouration of affected tissue.

MORPHOLOGY: Gross: Affected organs are wet, heavy, red or bluish. Their cut surfaces are bloody and in chronic cases evidence of fibrosis may be present. The most obvious manifestation of chronic passive congestion is in the lungs, liver and spleen.

Microscopy: LUNGS: engorged septal capillaries -> rupture -> RBC and degradation product (haemosiderin) in septae -> haemosiderin laden macrophages in alveoli. In chronic congestion, fibrosis and focal deposition of calcium and haemosiderin occur- Gamma-Gandy Bodies

LIVER: congestion of centrilobular sinusoids -> atrophy of hepatocytes around the central vein and fatty change in the mid-zonal region (nutmeg appearance) In severe cases there is pericentral necrosis and mid-zonal haemorrhage (central haemorrhagic necrosis) Chronic severe congestion (as in CCF)----centrilobular fibrosis (cardiac sclerosis-not to be confused with liver cirrhosis). SPLEEN: the sinusoids in the red pulp are filled with red blood cells (congestion), sometimes encroaching on the white pulp (lymphoid follicles). In chronic congestion, the increased portal venous pressure causes deposition of collagen -> impairment of blood flow -> prolonged exposure of RBCs to phagocytes -> haemosiderin laden macrophages.
Haemorrhage -> fibrosis ->deposition of calcium and haemosiderin (Gamma-Gandy bodies).

CLINICAL CORRELATION Congestion and oedema commonly occur together because congestion of capillary beds is frequently followed by development of oedema. The clinical findings are therefore similar particularly in the lungs where pulmonary oedema tends to develop acutely. Chronically, pulmonary fibrosis and hypertension may develop. The clinical problems arising from congestion of the liver and the spleen are negligible compared to the clinical conditions causing them.