The rise in the availability of free thyroid hormone may be the result of manipulating the thyroid gland. In the setting of an individual receiving radioactive iodine therapy, free thyroid hormone levels may acutely increase due to the release of hormone from ablated thyroid tissue. Decrease in thyroid hormone binding protein
A decrease in thyroid hormone binding protein in the setting of various stressors or medications may also cause a rise in free thyroid hormone. Increased sensitivity to thyroid hormone
Along with increases in thyroid hormone availability, it is also suggested that thyroid storm is characterized by the bodys heightened sensitivity to thyroid hormone, which may be related to sympathetic activation (see below). Sympathetic activation
Sympathetic nervous system activation during times of stress may also play a significant role in thyroid storm. Sympathetic activation increases production of thyroid hormone by the thyroid gland. In the setting of elevated thyroid hormone, the density of thyroid hormone receptors (esp. beta-receptors) also increases, which enhances the response to catecholamines. This is likely responsible for several of the cardiovascular symptoms (increased cardiac output, heart rate, stroke volume) seen in thyroid storm. Thyroid storm as allostatic failure
According to newer theories, thyroid storm results from allostatic failure in a situation where thyrotoxicosis hampers the development of non-thyroidal illness syndrome, which would help to save energy in critical illness and other situations of high metabolic demand.Usually, in critical illness (e.g.
Causes
The issue is thought of as representing any of the following:

An acute loss of blood of a substantial volume;
a decreased production of normal-sized red blood cells (e.g., anemia of chronic disease, aplastic anemia);
an increased production of HbS as seen in sickle cell disease (not sickle cell trait);
an increased destruction or loss of red blood cells (e.g., hemolysis, posthemorrhagic anemia, hypersplenism);
an uncompensated increase in plasma volume (e.g., pregnancy, fluid overload);
a B2 (riboflavin) deficiency
a B6 (pyridoxine) deficiency
or a mixture of conditions producing microcytic and macrocytic anemia.Blood loss, suppressed production of RBCs or hemolysis represent most cases of normocytic anemia. In blood loss, morphologic findings are generally unremarkable, except after 12 to 24 hrs where polychromasia appears. For reduced production of RBCs, like with low erythropoietin, the RBC morphology is unremarkable. Patients with disordered RBC production, e.g. myelodysplastic syndrome, may have a dual population of elliptocytes, teardrop cells, or other poikilocytes as well as a nucleated RBCs. Hemolysis will often demonstrate poikilocytes specific to a cause or mechanism, e.g. bite cells and/or blister cells for oxidative hemolysis, acanthocytes for pyruvate kinase deficiency or McLeod phenotype, sickle cells for sickle cell anemia, spherocytes for immune-mediated hemolysis or hereditary spherocytosis, elliptocytosis for iron deficiency or hereditary elliptocytosis and schistocytes for intravascular hemolysis. Many hemolytic anemias show multiple poikilocytes such as G6PD deficiency, which may show blister and bites cells as well as shistocytes. Neonatal hemolysis may not follow the classic patterns as in adults. Treatment
Treatment will depend on the cause of the normocytic anemia.