Hypocalcaemic fit in an adolescent boy with undiagnosed rickets
- Correspondence to I Seerat,
- Published 31 January 2010
Rickets in early childhood has been well documented in the literature. We present the case of a teenage Somalian boy who had a generalised tonic-clonic fit (an unusual presentation of rickets in late childhood) and was diagnosed with vitamin D deficient rickets.
It is important to highlight that rickets can present not only in early childhood but also in late childhood with various clinical manifestations such as musculoskeletal pain, muscle weakness, bone pains and atypically in adolescence with seizures as in our case.
A 15-year-old Somalian boy presented to our emergency department having had a 5 min generalised tonic-clonic fit at school. He reported seeing a white patch in his temporal field of vision and then he felt dizzy, collapsed and started fitting. There was no history of fever, vomiting or diarrhoea.
His clinical examination was normal. His blood results showed a corrected calcium of 1.51 mmol/l with phosphate of 1.29 mmol/l and alkaline phosphate (ALP) of 751 units. He had a normal diet. There were no symptoms, signs, or laboratory evidence of malabsorption, hepatic or renal disease. His vitamin D and parathyroid hormone values were 14.4 nmol/l (normal range 19–106 nmol/l) and 53.3 pmol/l (normal range 1.6–6.9 pmol/l), respectively. He was diagnosed with vitamin D deficient rickets. His right wrist x-ray showed sclerotic and widened end plates of the radius and ulna. These appearances are consistent with previous healed rickets as shown in fig 1. His electrocardiogram (ECG) and electroencephalogram (EEG) were normal. He was started on oral vitamin D and calcium supplement (Calcichew, one tablet twice daily). After 3 months his calcium (2.24 mmol/l), phosphate (1.73 mmol/l), ALP (328 units), vitamin D (27.5 nmol/l) and parathyroid hormone values (6.1 pmol/l) had returned to normal. The repeat x-ray showed normal bony appearances (fig 2).
Outcome and follow-up
The patient responded very well to vitamin D and calcium for 3 months and since then he has been completely asymptomatic.
There are many cases which have been reported in the literature regarding rickets in early childhood, as it is more common in this age group. The most common presentations are bony deformities such as bow legs and fractures, stridor1 or fits2 due to hypocalcaemia. There are some case reports about adolescent patients who were diagnosed with vitamin D deficiency rickets, and they are usually asymptomatic3 or present initially with bone pains,4 musculoskeletal pain, muscle weakness and hypocalcaemic tetany.
It is important to recognise that rickets can present not only in early childhood but also in late childhood with various clinical manifestations. Rickets may present atypically in adolescence with seizures. Screening of at risk immigrant families should be implemented through public health policies, and paediatricians should be aware that rickets is not just a disease of early childhood.
Nutritional rickets is re-emerging in western societies, particularly in young children and in adolescents of African or Asian descent. Hypocalcaemic fits resulting from vitamin D deficiency are rare in adolescents. It is likely that low dietary calcium led to rickets in the patient described here. This responds well to treatment with oral vitamin D.
Hypocalcaemia can cause generalised tonic-clonic seizures.
Vitamin D deficiency and dietary calcium deficiency are important causes of hypocalcaemia.
Rickets can present with seizures secondary to hypocalcaemia.
This article has been adapted with permission from I Seerat, M Greenberg. Hypocalcaemic fit in an adolescent boy with undiagnosed rickets. Emerg Med J 2007;24:778–9.