Hawkins Group I fracture of neck of talus and Salter Harris Type III tibial epiphyseal injury of medial malleolus.

We are reporting an unusual combination of Hawkins Group I fracture of the neck of left talus in association with Salter Harris Type III distal tibial epiphyseal injury of medial malleolus in a child with cerebral palsy and hemiplegia of contralateral limbs and discussed the possible mechanism as well as management. Fractures of medial malleolus usually occur in Hawkins Group III fracture-dislocations in adults. Forced dorsiflexion of talus against the anterior edge of tibia appears to be the accepted common mechanism, despite limited experimental and clinical evidence incriminating axial compression. Fracture of medial malleolus implicates supination. We managed this unusual pattern of injury conservatively. At 15 months, the child was asymptomatic with no radiological evidence of avascular necrosis of body of talus or growth disturbance of distal tibial epiphysis.

Myxedema coma in a patient with subclinical hypothyroidism.

BACKGROUND: Myxedema coma is the extreme manifestation of hypothyroidism, typically seen in patients with severe biochemical hypothyroidism. Its occurrence in association with subclinical hypothyroidism is extremely unusual. We describe a patient with subclinical hypothyroidism who developed clinical manifestations of myxedema coma. SUMMARY: A 47-year-old woman presented to our endocrine clinic with complaints of fatigue and biochemical findings of subclinical hypothyroidism. She was started on treatment with thyroxine (T4) but remained unwell and was later admitted to hospital with hormone profile showing persisting subclinical hypothyroidism (elevated thyrotropin and normal free T4 [FT4] and free triiodothyronine [FT3]): FT4 10.7 pmol/L (reference range 10.3-24.5), FT3 2.7 pmol/L (reference range 2.67-7.03), and thyrotropin 6.09 mU/L (reference range 0.4-4.0). She subsequently developed hypothermia (temperature 33.2°C), circulatory collapse, and coma. Biochemical profile showed hyponatremia, elevated creatinine phosphokinase, metabolic acidosis, and renal failure. An echocardiogram revealed a moderate-sized pericardial effusion. We diagnosed myxedema coma and started treatment with intravenous T3. She responded dramatically with improvement in level of consciousness and normalization of metabolic parameters. We found no explanation other than hypothyroidism to account for the presentation. Adrenocorticotrophic hormone (ACTH) stimulation tests excluded adrenal insufficiency, and serum gonadotrophins were within the normal reference range. FT4 estimation by equilibrium dialysis excluded analytical interference, and molecular analysis for the thyroid hormone receptor ß gene associated with thyroid hormone resistance was negative. CONCLUSIONS: To the best of our knowledge this is the first report of myxedema coma in a patient with subclinical hypothyroidism. The reason for normal thyroid hormone levels is unclear but may reflect deviation from a higher pre-morbid set-point. The case highlights the importance of careful clinical evaluation in patients with disparate clinical and laboratory findings.