DEHYDRATION

Dehydration denotes loss of TBWfrom extracellular and/or intracellular compartments, due to reduced intake or more likely, excessive losses via urine, stools, lungs or skin. As these losses are predominantly from ECF compartment, ECF dehydration dominates in early stages.

Etiology: Acute diarrhea and/or vomiting is the commo­nest cause of dehydration in children, apart from other causes, listed in Table 7.3.

Pathogenesis: As water loss is almost always associated with loss of other electrolytes, specially sodium, patho­physiological changes in dehydration can be broadly divided into three categories:

a. Isonatremic dehydration (50%), i.e. proportionate loss of water and sodium, e.g. in osmotic diarrhea, with normal serum osmolality. In established isotonic dehydration, usually 60% of fluid loss is from ECF and remaining 40% is from ICF.

b. Hyponatremic dehydration (30-40%), i.e. dis­proportionately higher loss of sodium than water, e.g. in secretory diarrhea. Serum osmolality falls with consequent movement of water from ECF to ICF,

TABLE 7.3: Common causes of dehydration

a. Excessive losses

- GIT: Diarrhea, vomiting, gastric aspiration

- Urine: Polyuria (e.g. diabetes insipidus)

- Lungs: Tachypnea (respiratory disorders)

- Skin: Fever, excessive sweating, burns

- Third-space losses: Paralytic ileus, gross ascites

b. Poor intake

- Unconscious/sick child

- Starvation

- Psychogenic

c. Re-distribution of fluids

- Edema (intravascular gt; interstitial fluid)

- Hyperosmolar states, e.g. DKA (ECF gt; ICF)

DKA: Diabetic ketoacidosis

leading to: (a) further depletion of ECF, and (b) cellular overhydration, e.g. cerebral edema. Clinical signs of dehydration in these cases are disproportionately more than the estimated fluid loss.

c. Hypernatremic dehydration is rare (lt;5%), usually attributed to erroneous fluid therapy with concentrated oral rehydration fluids or hypertonic parenteral fluids. In these cases, higher serum osmolality leads to movement of water from ICF to ECF with: (a) partial compensation of ECF loss by ICF fluids, and (b) cellular dehydration. Signs of dehydration in these cases are disproportionately less than estimated fluid loss.

Clinical features of dehydration depend on its severity and indicate:

• Compensatory mechanisms to restore/conserve body water, e.g. excessive thirst, oliguria, dry skin/mucus membranes, etc.;

• Circulatory decompensation, e.g. weak and thready pulse, hypotension and shock; and

• Cellular dehydration, e.g. loss of skin turgor and mental changes.

Important clinical indicators of the severity of dehydration are given in Table 7.4.

Severity of dehydration is likely to be overestimated in marasmic children due to severe wasting (confused with turgor) or underestimated in obese children or kwashiorkor. Urine output is the most reliable indicator in these cases. Severity may also be misinterpreted in cases with hyponatremic or hypernatremic dehydration, as discussed earlier.

Hypernatremic dehydration is characterized by: (a) typical doughy skin, and (b) excessive irritability, rather than drowsiness in iso-/hypo-natremic dehydration.

Laboratory evaluation: Although clinical signs are cornerstones to evaluate the presence and severity of dehydration, following investigations are essential at least in severe cases to assess co-existing electrolyte imbalance and renal dysfunction.

TABLE 7.4: Severity assessment of dehydration

*Irritable in hypernatremic dehydration **Doughy feel in hypernatremic dehydration.

• Serum electrolytes, e.g. Na⁺, K⁺, HCO₃^- and Cl^-,

• Renal parameters, e.g. blood urea, serum creatinine.

• Urinalysis, including specific gravity.

• Hemogram including hematocrit.

• Relevant etiological investigations.

Management of dehydration involves oral or parenteral fluid therapy. While oral fluid therapy is discussed in Ch 14.10, general principles of parenteral fluid therapy are discussed in Ch 7.7.

7.2