Why shouldn't children benefit from oral rehydration solutions for calves?

BMJ 2005; 331 doi: (Published 24 November 2005) Cite this as: BMJ 2005;331:1267
  1. Bob Michell (bobmichell{at}, professor of comparative medicine
  1. Barts and The London School of Medicine and Dentistry, John Vane Science Centre, London

    When I was a veterinary student, in the early 1960s, diarrhoea was regarded entirely as an infection; antibiotics were the automatic remedy. During my final year, an exciting innovation was intravenous fluid therapy for calves with acute diarrhoea. Too expensive for widespread use, it never matched the success of similar treatment for human cholera, yet the practical problems of treating calf diarrhoea on farms were not much different from those of treating cholera in primitive surroundings. Indeed, as well as the general similarities in the pathophysiology of acute diarrhoea in any species, the then prevalent cause of calf diarrhoea, Escherichia coli enterotoxin, and cholera are similar.

    Oral rehydration for acute diarrhoea was first suggested by remarkable clinical research by W B O'Shaughnessy reported in the Lancet in 1831, within months of the arrival of a terrifying new disease from Asia—cholera. Sadly his wisdom was not appreciated until the 1970s, with the arrival of the World Health Organization's oral rehydration solution—described as the greatest lifesaving advance of the century. It converted cholera from a mostly fatal disease in the absence of intravenous rehydration, into one routinely and simply treated orally. Oral rehydration goes beyond symptomatic therapy; the fundamental cause of acute diarrhoea is impairment of net enteric sodium and water absorption sufficient to overwhelm the compensatory capacity of the colon.

    Veterinary oral rehydration solutions initially followed human formulations, but there are now three classes: type 1 solution (WHO formulation) corrects dehydration, hypovolaemia, and acidosis; type 2 solutions have the properties of type 1 solutions but avoid the energy deficits imposed by their low glucose content (2%), which is optimal for sodium absorption but inadequate for metabolism; and type 3 solution, which exploits the ability of glutamine to sustain villus structure and enterocyte function, and renal function, and can be helpful in conditions where reduced food intake imperils villus architecture.

    Principles validated in calves may not necessarily apply to children, but we should not simply assume that they won't. Calves are pre-ruminants; they are functionally simple-stomached until they are weaned onto solid food, well beyond the age at which oral rehydration is usually needed. Unlike children, calves can be studied in the laboratory to measure directly the parameters that matter in acute diarrhoea—such as hypovolaemia, acidosis, and prerenal failure.

    Paediatric research is necessarily restricted to indirect and fallible criteria such as faecal output or need for supplementary intravenous fluids; the dilemma for studies of human oral rehydration therapy is that the validity of systematic reviews and meta-analyses is undermined when the underlying data reflect crucial variables only indirectly and unreliably. It is therefore possible that the approaches currently used to treat calves, which are radically different from those used by paediatricians, could benefit children, especially those who are already cachectic before their diarrhoea. The necessary additional research should be started.

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