Tuesday, February 23, 2016

Hyperthyroidism

Today's case involved a middle-aged woman who presented with one week of palpitations, anxiety, and tremors.  The patient had a number of physical examination signs of hyperthyroidism, and confirmatory biochemical evidence.  She was treated with beta blockade and investigated on the internal medicine service.

Learning points:

We spoke about the physical examination findings of hyperthyroidism and hypothyroidism (outside the thyroid gland itself).  The easiest way is to break them down by body system:


Hyperthyroidism
Hypothyroidism
Vital Signs
Systolic hypertension, tachycardia, hyperthermia, elevated RR
Diastolic Hypertension, bradycardia, hypothermia, reduced RR
Skin
Velvety, moist, warm, pretibial myxedema
Cool, dry, non-pitting myxedema
Hands
Palmar erythema, thyroid acropatchy (clubbing), onycholysis
Yellow discoloration (carotinemia)
Hair
Thin, soft
Coarse
Eyes
Grave (exophthalmos, proptosis, chemosis, visual loss, restricted EOM), lid lag, stare
Queen Anne sign (lateral 1/3 of eyebrow missing), periorbital edema
Mentation
Slow, low mood
Irritable, disinhibited
Cardiovascular
Tachydysrhythmias, flow murmurs from increased output, Heart failure
Bradycardia
Respiratory
Increased respiratory rate
Hypoventilation
Neurologic
Proximal muscle weakness, brisk reflexes
Proximal muscle weakness, delayed relaxation of reflexes, proximal muscle weakness


The diagnosis of hyperthyroidism can usually be made be examining the serum TSH and free thyroid hormones.  Central hyperthyroidism from something like a TSH-producing pituitary adenoma is very rare, most causes will give you a low TSH.  Grave disease patients will often have positive Thyroid Receptor Anitbodies while patients with Hashimoto thyroiditis will often have positive thyroid peroxidase antibodies.  Thyroglobulin antibodies can also be useful.

If someone has hyperthyroidism clinically and biochemically, the next step is to consider the differential diagnosis:
·      Central causes – TSH-secreting tumours or hypothalamic causes
·      Primary Thyroid Causes
o   Thyroid destruction
§  Hashimoto thyroiditis
§  Subacute (viral) thyroiditis
§  Post-partum thyroditis
§  Other thyroid infections
§  Medication-induced thyroiditis (amiodarone)
o   Excessive Thyroid Hormone production
§  Toxic adenoma
§  Toxic multinodular goitre
§  Jodd-Basedow effect of iodine ingestion
§  Medication-induced J-B effect (amiodarone)
§  Grave disease
§  Cross-stimulation by beta-HCG in molar pregnancy
§  Resistance to feedback of T4/T3 resulting in inappropriate overproduction
§  Surreptitious thyroxine ingestion

The best way to differentiate among these etiologies is to do a Radioactive Iodine Uptake and Scan of the thyroid.  The result of such as can is the percentage of iodine that is taken up.

If it is very low (cold thyroid, less than 1%) then you can assume that some form of thyroiditis is occurring.  If it is very high diffusely, then depending on whether there is a toxic multinodular goiter or Grave disease, you may see very high uptakes (>6%).  The intermediate range of uptake usually occurs with adenomas or Jodd-Basedow effect.

Treatment of hyperthyroidism can be divided into symptomatic management and long-term management.  The first question to talk is regarding stability as thyrotoxicosis or thyroid storm requires different treatment.

Thyroid storm has a mortality of around 20%, and patients presenting with this should be looked after in a critical care setting.  There are no accepted diagnostic criteria for thyroid storm.  Physicians grade patients with hyperthyroidism based on the degree of thermoregulatory dysfunction, central nervous system effects, hepatic/gastrointestinal dysfunction, cardiovascular dysfunction, and presence or absence of heart failure or a precipitant history such as parturition or thyroid surgery.  Treatment of thyroid storm involves several facets: non-selective beta-blockade (propranolol), thionamides such as methimazole or PTU to block hormone synthesis, steroids to block peripheral hormone conversion, and an iodine load (Lugol solution) to prevent release of thyroid hormone.  Long term management usually involves radioactive iodine ablation of the thyroid gland, thyroid surgery, or long-term use of thionamide antithyroid drugs.
In milder cases of hyperthyroidism like the one presented, beta blockade is usually used for symptom control.  If a subacute thyroiditis is the likely precipitant, then prednisone at 0.5-1mg/kg for 2-8 weeks is usually required.  Depending on the reason for the hyperthyroidism, thionamides, radioactive iodine, or surgical removal may be the long-term treatment modality of choice.

Further Reading:

Burch, H. B., & Wartofsky, L. (1993). Life-threatening thyrotoxicosis. Thyroid storm. Endocrinology and metabolism clinics of North America, 22(2), 263-277.

Chiha, M., Samarasinghe, S., & Kabaker, A. S. (2013). Thyroid Storm An Updated Review. Journal of intensive care medicine, 0885066613498053.


Franklyn, J. A. (1994). The management of hyperthyroidism. New England Journal of Medicine, 330(24), 1731-1738.

Image Credit: Alive.com

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