mias or severe hypokalemia are present. The rate of infu ­ sion should be no more than 20 mEq/hr, especially when the infusion is to run through a peripheral IV line. Pain

 

mias or severe hypokalemia are present. The rate of infu ­

sion should be no more than 20 mEq/hr, especially when

the infusion is to run through a peripheral IV line. Pain

and burning with peripheral IV potassium replacement

can be treated by slowing down the infusion rate. Avoid IV

potassium in patients in renal failure. Physicians should

treat concomitant hypomagnesemia, as potassium repletion is dependent of magnesium.

DISPOSITION

� Admission

Because of the potential for life-threatening arrhythmias, all

patients with moderate to severe hyperkalemia (K + level

>6.0 mEq/L) or severe hypokalemia (K+ level <2.5 mEq/L)

should be admitted to a hospital bed with a cardiac monitor.

� Discharge

Patients with mild to moderate hypokalemia (K+ 2.5-

3.4 mEq/L) and no clinical symptoms may be discharged

with appropriate oral repletion therapy. Mildly hyperkalemic (K+ level <6.0 mEq/L) who are asymptomatic, have

no ECG changes consistent with hyperkalemia, and have

an identifiable and correctable cause of their hyperkalemia

can be considered for discharge with early follow-up for a

repeat electrolyte panel.

SUGGESTED READING

Gennari FJ. Hypokalemia. N Engl ! Med. 1998;339:451-458.

Kelen GD, Hsu E. Fluids and electrolytes. ln: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th Ed. New York, NY: McGraw-Hill, 20 1 1, pp. 1 1 7-1 29.

Mahoney BA, Smith WAD, Lo DS, Tsoi K, Tonelli M, Clase CM.

Emergency interventions for hyperkalaemia Cochrane Database

Syst Rev. 2005;CD003235:1-28.

Thyroid Emergencies

Monika Pitzele, MD

Key Points

• In a critica lly ill patient with a goiter or history of

hyperthyroidism, consider and treat thyroid storm early.

• Thyroid storm and myxedema coma are clinical

diagnoses that do not depend on the absol ute levels

of thyroid-stimulating hormone and free thyroxine.

INTRODUCTION

Thyroid hormone (TH) is synthesized within the follicular

cells of the thyroid gland. Production begins with the uptake

of iodine into the follicular lumen. Thyroglobulin, produced within the follicular cell, is bound to iodine and then

coupled to produce the thyroid hormones, thyroxine (T 4

)

and triiodothyrinine (T3

). Release of thyroid hormone is

stimulated by one of the hormones secreted by the pituitary

gland, thyroid-stimulating hormone (TSH). In turn, TSH is

regulated by thyroid-releasing hormone (TRH) secreted by

the hypothalamus. High levels of T4 and T3 act to suppress

production of TSH and TRH via a negative feedback loop.

TH released from the thyroid gland is in its less active form,

T4

, which is converted in peripheral organs (kidney and

liver) into its 10 times more active derivative, T3

" The halflife of T 3 is significantly shorter, approximately a day,

compared with 1 week for T4

• In the serum, the majority of

TH is bound to thyroid-binding globulin (TBG), making it

inactive. The only active forms are free T3 and T4

• After TH

enters cells, it binds to its nuclear receptor and regulates

expression of genes involved in lipid and carbohydrates

metabolism and protein synthesis. As a net result of its

action, there is an increase in basal metabolic rate.

Emergencies related to the thyroid gland can be caused

by both excess and deficiency of TH. Excess of TH can

• Myxedema coma should be considered in elderly hypothyroid

patients who present with hypothermia and confusion.

• For successful treatment, it is important to try to identify a trigger that pushed the patient into the extreme

state of thyroid storm or myxedema coma.

cause a syndrome referred to as thyrotoxicosis and can be

caused either by excessive production of TH or its

exogenous administration. In its extreme state,

thyrotoxicosis can lead to a life-threatening condition

called thyroid storm, a state manifesting with fever,

tachycardia, and altered mental status.

Hyperthyroidism is the term used when excessive

production of TH by the thyroid is the cause of thyrotoxicosis. One of the most common causes of hyperthyroidism

is Graves disease (approximately 80% of cases), in which

autoimmune antibodies that bind to TSH receptors on the

surface of thyroid cells stimulate production and release of

TH. Other significant causes of hyperthyroidism include

toxic multinodular goiter, thyroiditis, pituitary adenoma,

and reaction to drugs ( eg, lithium, amiodarone and iodine).