Craniotabes is softening or thinning of the skull in infants and children, which may be normally present in newborns. It is seen mostly in the occipital and parietal bones. The bones are soft, and when pressure is applied they will collapse underneath it. When the pressure is relieved, the bones will usually snap back into place. Causes
Any condition that affects bone growth, most notably rickets (from vitamin D deficiency), marasmus,  syphilis, or thalassemia, can cause craniotabes if present during a time of rapid skull growth (most especially during gestation and infancy). It can be a "normal" feature in premature infants. It is the first sign in children and infants with rickets. Diagnosis
Physical examination

Management
Management of craniotabes depends on the cause. The majority of craniotabes occurs in term infants and can be a normal finding. Commonly, craniotabes results from the position of the head inside the uterus weeks prior to delivery. Calcium and Vitamin D levels should be obtained to rule out rickets, and in mothers who have prenatal labs concerning for T. pallidum infection, neonates should be evaluated for congenital syphilis. Etymology
The term (cranio- + tabes) is derived from the Latin words cranium for skull and tabes for wasting. References


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Rats survive indefinitely on extra salt alone, but in dogs and most humans, the amount of supplementary salt needed is so large that it is almost impossible to prevent eventual collapse and death unless mineralocorticoid treatment is also instituted. Diagnosis
Patients with a suspected diagnosis of hypoaldosteronism are often screened with simple blood tests. Potassium levels, plasma aldosterone concentration and plasma renin activity are the three most useful in the first instance. Low aldosterone levels in the presence of high renin activity, often with low sodium, high potassium, is associated with primary hypoaldosteronism. Secondary hypoaldersteronism may be suspected if renin activity is low with low aldosterone concentrations. The plasma aldosterone-to-renin ratio is calculated to determine if levels are sufficiently deranged to consider a diagnosis of hypoaldosteronism.If screening test is suggestive, a more definitive diagnosis is made by performing a saline suppression test, ambulatory salt loading test, or fludrocortisone suppression test. Imaging to detect an Adrenocortical adenoma may also be considered. Treatment
Aldosterone deficiency should be treated with a mineralocorticoid (such as fludrocortisone), as well as possibly a glucocorticoid for cortisol deficiency if present. Hyporeninemic hypoaldosteronism is amenable to fludrocortisone treatment, but the accompanying hypertension and edema can prove a problem in these patients, so often a diuretic (such as the thiazide diuretic, bendrofluazide, or a loop diuretic, such as furosemide) is used to control the hyperkalemia. See also
Addisons disease
Adrenal gland
Hyperaldosteronism
Pseudohypoaldosteronism

References


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