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Haemodynamic disorders

Hyperhydratio (water excess)

Dehydratio Oedema

Hyperaemia and congestion Haemorrhage

60 minutes

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Water excess

Conns syndrome: aldosterone producing adenoma hyperaldosteronism excessive reabsorption of sodiumand water. Fluid excess mostly in circulation:

hypervolemia hypertension.

SIAD: Syndrome of Inappropriate (high) ADH secretion:

fluid retention renin-angiotensin activity sodium and water loss. End result: euvolemia andmarked hyponatremia.

Iatrogenic water overload: excessive parenteral infusionin patients with impaired renal function.

Extensive edema: see later.

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Dehydration

Causes: Excessive water loss

Inadequate water intake

Combination of both

Water loss can be due to

Vomiting and diarrhoea Extensive burns

Excessive sweating

Diabetes insipidus (failure of proper ADH secretion) diuresis, e.g. osmotic loss accompanying glycosuriain DMInadequate water intake is common in drought and

famine areas.

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Clinical signs of dehydration

Dry mouth

Inelastic skin Sunken eyes( in extreme cases)

hematocrit blood viscosity sluggishcirculation function of many organs

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Oedema

Accumulation of protein-poor fluid in theinterstitial spaces and the body cavities.

Main ingredient: water, specific gravity

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Types of oedema

Venous Hypoalbuminaemic

Lymphatic Na retention-associated Inflammatory

(detailed later)

Physiology

Hydrostatic blood pressure forces water out ofcapillaries at the arterial end, but the plasma oncotic pressureattributable to albumin sucks it back into capillary beds at the

venous end.A small amount of water drains from the tissuesthrough lymphatic channels.

Yield protein-poortransssudates

Yields

protein-richexsudates

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Venous oedema

Increased hydrostatic pressure due to impairedvenous return forces fluid out the capillaries thatexceeds that of plasma oncotic pressure and sowater remains in the tissues.

Localisation follows gravity

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Venous oedema

Sudden onset of (acute) left-sided heart failure(reduced systolic output accompanied byinadequate emptying of the chamber) leads

to the elevation of hydrostatic pressure inlung capillarieslung oedema

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Lung oedema: the lungs 2 to 3 times exceed theirnormal weight; sectioning reveals a frothy, blood-tinged,

foamy mixture of air, oedema fluid, and RBCs

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Pulmonary oedema in acute left-HF

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Venous oedema

Chronic right-sided heart failure (reducedsystolic output accompanied by inadequateemptying of the chamber) leads to the elevation

of hydrostatic pressure in capillaries of thesystemic circulation, and in turn, systemicoedema and serous effusions:

- hydrothorax,- hydropericardium- ascites

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Hydrothorax in right-sided HF

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Venous oedema

Cirrhosis of liver causes increased hydrostaticpressure in the portal venous circulation (portalhypertension) ascites

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Venous oedema

Oedema of just one calf: due to thromboticobstruction of popliteal veins

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Hypoalbuminaemic oedema

Low albumin concentration reduces the plasmaoncotic pressure so that the water cannot be sucked

back into the capillary bed at the venous end.

Causes of hypoalbuminaemia:

Inadequate intake, as in protein-deficient diet(kwashiorkor)

Decreased synthesis in the liver, as seen in end-

stage liver disease Increased loss in the urine (e.g., nephrotic sy) or

stool (e.g., protein-losing enteropathy)

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Lymphatic oedema

Lymphatic obstruction prevents drainage of waterfrom the tissues. Typically, this is a localized form

of oedema involving certain parts of the body.

Elephantiasis - obstruction of inguinal lymph

nodes by filaria worms (filariasis) chronicoedema of lower extremities and externalgenitalia.

Oedema of the arm following surgical dissectionof axillary lymph nodes involved by breast cancer.

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Breast cancer. Severe lymphoedema of the arm followingmastectomy, surgical dissection of the axillary lymph nodes

and irradiation of the axillary region

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Sodium retention-associated oedema

Primary sodium retention, with obligatorilyassociated water retention, causes both increased

hydrostatic pressure (owing to hypervolaemia) andreduced osmotic pressure.

Sodium retention occurs in renal disease, e.g.,glomerulonephritis, acute tubular necrosis

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Hyperaemia and congestion

Both indicate increased volume of blood in aparticular tissue.

Active hyperaemia results from increased bloodinflow because of arteriolar dilatation

Skeletal muscle during exercise Sites of inflammation Facial skin during blushing

The affected tissue is redder than usual because ofthe engorgement happens with oxygenated blood.

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Congestion (passive hyperaemia)

Results from impaired venous outflow from atissue.

Systemic, as in cardiac failure Local, resulting from an isolated venousobstruction

The tissue has a blue-red color (cyanosis) becausestagnation of blood in the capillaries leads to

accumulation of deoxygenated haemoglobin.

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Congestion

Congestion of capillary beds is closely related tothe development of venous oedema, so that

congestion and oedema usually run together.

In long-standing congestion, the poorly

oxygenated blood causes chronic hypoxic injuryresulting parenchymal cell degeneration and evendeath, and induration (replacement of dead

parencymal cells by connective tissue; collagendeposition in extravascular spaces)

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Congestion

Capillary rupture at the sites of chronic congestioncauses small foci of haemorrhage. The

breakdown and phagocytosis of RBCs results inclusters of haemosiderin-laden macrophages.

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Morphology of congestion

Acute left ventricular failure acut pulmonarycongestion Alveolar capillaries engorged with blood

Alveolar septal oedema Intraalveolar oedema with focal haemorrhages

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Morphology of congestion

Chronic left ventricular failure chronicpulmonary congestion (brown induration of

lungs) Thickened and fibrotic septa Haemosiderin-laden macrophages in the alveoli

(heart failure cells) Intraalveolar oedema with focal haemorrhages

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Morphology of congestion

Liver manifestation of acute right ventricularfailure acute hepatic congestion Central veins and sinusoids are distended withblood

Hepatocyte degeneration around central veins

may occur + fatty change in periportal hepatocytes

CNS manifestation of acute right ventricularfailure brain oedema with cerebellar

herniation

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Morphology of congestion

Liver manifestations of prolonged rightventricular failure : Nutmeg liver

Gross: centrilobular areas are red-brown and areaccentuated against the surrounding zones ofuncongested hypoxic/fatty change-altered liver

zoneLM: centrilobular trabecular (compression)

atrophy widened sinusoids are filled by

RBCs, accompanied by peripherolobular fattychange

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Nutmeg liver: hypoxic/fatty hepatocytes at theperithery of the lobules are pale, central parts are red.

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Haemorrhage

Extravasation of blood.The source of bleeding may be

Rupture- Arterial or arteriolar aneurysm- Oesophageal varix

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Haemorrhage

Extravasation of blood. The source of bleeding maybe

Rupture- Arterial or arteriolar aneurysm- Oesophageal varix

Erosion- Artery by peptic ulcer of stomach or duodenum- Vessels by malignant tumor (e.g., cc of cervix)

Capillary bleeding- Chronic congestion- Haemorrhagic diatheses (

tendency to bleed

from insignificant injury)

Cl ifi ti f h h

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Classification of haemorrhage Surface- External, internal

Enclosed within a tissueHaematoma (3-dimensional); may be

- insignificant (bruise)- lethal (retroperitoneal, subarachnoidal)Suffusion (2-dimensional)

Subcutaneous suffusion due to trauma

S b h id l h t

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Subarachnoidal haematoma

i h d h id i

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Iatrogenic haematoma around the carotid arteriesas complication of catheterization

Petechiae i t 1 2 h h i t ki

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Petechiae: minute, 1-2 mm haemorrhages into skin,mucous membranes or serosal surfaces, seen in

thrombocytopenia, defective platelet function(uraemia) or clotting factor deficits

Purpura: slightly larger (>3 mm) haemorrhages

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Purpura: slightly larger (>3 mm) haemorrhages,may be associated with similar pathologies, as

well as trauma, vasculitis, or increased vascularfragility

Purpuras in small

vessel vasculitis

Sndor Husz, MD,SZTE Dermatology

Ecchymoses: 1 2 cm subcutaneous haematomas

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Ecchymoses: 1-2 cm subcutaneous haematomasafter trauma

The RBCs in these local haemorrhages aredegraded and phagocytosed by macrophages.

Color changes in haematoma: Haemoglobin (red-blue)

Bilirubin (red) Biliverdin (blue-green) Haemosiderin (gold-brown)

Accumulation of blood in cavities and the

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Accumulation of blood in cavities and theFallopian tube

Haemothorax Haemopericardium Haemoperitoneum (haemascos) Haemarthros

Haemocephalus Haemosalpinx

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Haemopericardium (lethal)

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C b l bl di ( l ) i t d ith

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Cerebral bleeding (apoplexy) associated withhaemocephalus

Other terms in association with haemorrhage

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Other terms in association with haemorrhage

Haematuria: appearance of blood in the urine;

microscopic or macroscopic Haematemesis: vomiting of blood; sign of

oesophageal and gastric haemorrhage Haematochezia: bleeding through the rectum Melaena: Sign of upper GI tract bleeding. Theblood is digested partly by HCl. The blackpigment haematein is passed in the faeces

Epistaxis: bleeding from the nose

Haemoptysis: bleeding from the lungs;literally it means spitting of blood Menorrhagia: heavy menstrual bleeding

Metrorrhagia: occurs any time and is not relatedto menstrual bleeding

Clinical significance of haemorrhage

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Clinical significance of haemorrhage

Depends on the volume and rate of blood loss. Rapid removal of up to 20% of the blood volume

may have little impact in healthy adults Greater and rapid losses result in haemorrhagic

shock

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Clinical significance of haemorrhage

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Clinical significance of haemorrhage

Recurrent external blood loss (peptic ulcer orsevere menstrual bleeding) iron deficiency

anaemia