Fluid volume deficit, excess and water intoxication DEPARTMENT OF PHYSIOLOGY DR.TAYYABA AZHAR.

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Presentation transcript:

Fluid volume deficit, excess and water intoxication DEPARTMENT OF PHYSIOLOGY DR.TAYYABA AZHAR

Fluid Volume Disturbances Fluid Volume Deficit (Hypovolemia)

Fluid Volume Deficit Mild – 2% of body weight loss Moderate – 5% of body weight loss Severe – 8% or more of body weight loss

THREE TYPES OF deficit Hyperosmolar fluid volume deficit- water loss is greater than the electrolyte loss Isosmolar fluid volume deficit – equal proportion of fluid and electrolyte loss Hyposmolar –Water loss is less than the electrolyte loss

Fluid Volume Deficit Pathophysiology – results from loss of body fluids and occurs more rapidly when coupled with decreased fluid intake

Fluid Volume Deficit Clinical manifestations -Acute weight loss -Decreased skin turgor

Fluid Volume Deficit - Oliguria - Concentrated urine - Postural hypotension - Weak, rapid, heart rate - Flattened neck veins - Increased temperature - Decreased central venous pressure

ETIOLOGY AND RISK FACTORS Severe vomiting Traumatic injuries Burns Use of diuretics

LABORATORY FINDINGS Increased osmolality(> 295 mOsm/ kg) Elevated hematocrit (> 55%) Increased specific gravity of urine ( > 1.030)

MANAGEMENT Management of fluid in patient with fluid deficit should aim at Replacing deficit Correcting ongoing losses Maintenance

Management of mild deficit Mild fluid volume loss can be corrected with oral fluid replacement

Management of moderate/severe volume deficit IV fluids needed

Fluid Volume Excess (Hypervolemia)

Fluid Volume Excess Pathophysiology – may be related to fluid overload or diminished function of the homeostatic mechinisms responsible for regulating fluid balance

ETIOLOGY AND RISK FACTORS Heart failure Renal disorders Increased ingestion of high sodium foods Excessive amount of IV fluids containing sodium Electrolyte free IV fluids decreased colloid osmotic pressure lymphatic and venous obstruction Cushing’s syndrome & glucocorticoids

Why does heart failure leads to oedema Reduced renal perfusion--- activates renin angiotensin aldosterone mechanism---- results in fluid retention

CLINICAL MANIFESTATION Dyspnea & crackles in lungs pleural effusion Neck veins prominant Bounding pulse &elevated BP Pitting & sacral edema Weight gain Increased CVP Change in level of consciousness

Fluid Volume Excess

LAB INVESTIGATION serum osmolality <275mOsm/ kg Decreased hematocrit [ < 45%]

MANAGEMENT Diuretics Restrict fluids In people with HF, ACE inhibitors A low sodium diet

Water intoxication At the onset of this condition fluid outside the cells has an excessively low amount of solutes in comparison to inside the cells, the fluid shifts through osmosis into the cells in order to balance its concentration. This causes the cells to swell. In the brain, this swelling increases ICP

features headache personality changes changes in behavior, confusion, irritability difficulty breathing during exertion cramping, nausea, vomiting, seizures, brain damage, coma or death due to cerebral oedema

Risk factors Psychiatric conditions-polydipsia Over replacement of IV fluids Heat stress

management Restriction of fluids is sufficient in mild cases If severe diuretics needed