Hypochloraemic and hypokalaemic metabolic alkasosis was seen in both cases, which responded satisfactorily to water and electrolyte replacement. After ruling out vomiting, ingestion of drugs, tubular disease, and cystic fibrosis, the diagnosis was low intake, due to poor contribution of Na+ and Cl− provided by the “almond milk”.
Infant metabolic alkalosis of dietetic origin
 
  Keywords
 
 
  
   Almond milk
  
 
 
  
   Hypochloraemic metabolic alkalosis
  
 
 
  
   Hypokalaemia
  
 
 
  
   Hypothyroidism
  
 
 
  
   Optic neuritis
  
 
Abstract
 Cases of metabolic alkalosis are divided into susceptible or resistant to treatment with sodium chloride, depending on the response to it.
The resistant cases present with high urinary excretion of chloride, and are secondary to tubular disease or use of diuretics.
Included among the sensitive cases are, vomiting, cystic fibrosis and low intake.
Two infants were fed with “almond milk” and showed clinical symptoms of dehydration and failure to thrive.
Hypochloraemic and hypokalaemic metabolic alkasosis was seen in both cases, which responded satisfactorily to water and electrolyte replacement.
After ruling out vomiting, ingestion of drugs, tubular disease, and cystic fibrosis, the diagnosis was low intake, due to poor contribution of Na+ and Cl− provided by the “almond milk”.
This deficit induces an increase in proximal tubular reabsorption of H−CO3 and in parts of the distal nephron, an increase in reabsorption of Na+ and Cl− which are exchanged with K+ and H+, which can give rise to a hypochloraemic alkalosis and hypokalaemia.
Secondary hypothyroidism was found in one case, apparently due to the lack of iodine in the almond milk, and disorders of the myelination characterized by optic neuritis and <dis>hearing loss</dis>.
These disorders were resolved when feeding with human formula was established.
Abstract
 Cases of metabolic alkalosis are divided into susceptible or resistant to treatment with sodium chloride, depending on the response to it.
The resistant cases present with high urinary excretion of chloride, and are secondary to tubular disease or use of diuretics.
Included among the sensitive cases are, vomiting, cystic fibrosis and low intake.
Two infants were fed with “almond milk” and showed clinical symptoms of dehydration and failure to thrive.
Hypochloraemic and hypokalaemic metabolic alkasosis was seen in both cases, which responded satisfactorily to water and electrolyte replacement.
After ruling out vomiting, ingestion of drugs, tubular disease, and cystic fibrosis, the diagnosis was low intake, due to poor contribution of Na+ and Cl− provided by the “almond milk”.
This deficit induces an increase in proximal tubular reabsorption of H−CO3 and in parts of the distal nephron, an increase in reabsorption of Na+ and Cl− which are exchanged with K+ and H+, which can give rise to a hypochloraemic alkalosis and hypokalaemia.
Secondary hypothyroidism was found in one case, apparently due to the lack of iodine in the almond milk, and disorders of the myelination characterized by optic neuritis and hearing loss.
These disorders were resolved when feeding with human formula was established.
Hypochloraemic and hypokalaemic metabolic alkasosis was seen in both cases, which responded satisfactorily to water and electrolyte replacement. After ruling out vomiting, ingestion of drugs, tubular disease, and cystic fibrosis, the diagnosis was low intake, due to poor contribution of Na+ and Cl− provided by the “almond milk”.