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Thyroid and adrenal emergencies


Essentials

  • 1

    The thyroid and adrenal emergencies that pose an acute threat to life are thyroid storm, myxoedema coma and acute adrenal insufficiency. Diagnosis of these conditions requires a high index of suspicion and treatment frequently must be initiated on clinical rather than laboratory diagnosis.

  • 2

    Common features of thyroid storm are fever, alteration in mental state, cardiovascular complications, such as tachyarrhythmias and cardiac failure, and signs of hyperthyroidism. Treatment is with β-blockers, drugs that block thyroid hormone synthesis and release, and corticosteroids.

  • 3

    Common clinical signs of myxoedema coma are an alteration in conscious state, hypothermia and features of hypothyroidism. Treatment is with intravenous tri-iodothyronine and corticosteroids.

  • 4

    The most important clinical feature of acute adrenal insufficiency is hypotension unresponsive to fluid therapy. Although hyponatraemia and hyperkalaemia are usual in acute adrenal insufficiency, serum electrolytes may be normal. Treatment is with intravenous corticosteroid replacement on suspicion of the diagnosis.

  • 5

    General supportive measures and treatment of the precipitating event must parallel the specific treatment regimen in all of these conditions.

Introduction

Four conditions are covered in this chapter: thyrotoxicosis, hypothyroidism, hypoadrenal states and hyper adrenal states. Patients with the first three present relatively infrequently to emergency departments (EDs), but all four conditions are potentially fatal if they go unrecognized and untreated. The most common cause of Cushing syndrome is exogenous steroid administration. An inability to produce endogenous steroids in times of physiological stress and therefore the potential for adrenal insufficiency occurring with insufficient replacement therapy must be considered in such patients.

Thyrotoxicosis

Aetiology, genetics, pathogenesis and pathology

Normal secretion of thyroid hormone relies on an intact feedback loop involving the hypothalamus, pituitary gland and thyroid gland. Thyrotropin-releasing hormone (TRH) released from the hypothalamus stimulates thyroid-stimulating hormone (TSH) production in the anterior pituitary, which stimulates thyroid hormone release from thyroid follicular cells. Thyroid hormones suppress TRH and TSH production, and act at a cellular level, binding with nuclear receptors to enable gene expression and protein synthesis. Thyroid hormone may also have an effect on modulating cellular metabolism.

There are a number of pathological causes of thyrotoxicosis ( Table 11.3.1 ). Graves disease is an autoimmune condition related to a combination of genetic and environmental factors, including iodine intake, stress and smoking. The thyrotoxicosis of Graves disease is caused by autoantibodies, which stimulate the thyroid resulting in excess thyroid hormone production.

Table 11.3.1
Causes of thyrotoxicosis
Primary hyperthyroidism Graves disease
Toxic multinodular goitre
Toxic adenoma
Thyroiditis de Quervain syndrome (subacute)
Postpartum
Radiation
Central hyperthyroidism Pituitary adenoma
Ectopic thyroid tissue
Metastatic thyroid tissue
Drug-induced Lithium
Iodine (including radiographic contrast)
Amiodarone
Excess thyroid hormone ingestion (‘factitious thyrotoxicosis’)

Thyroiditis may be acute (rare), subacute or chronic. Inflammation of the thyroid is associated with damage to follicles with the release of thyroid hormone. Subacute thyroiditis (de Quervain syndrome, also known as subacute granulomatous) may follow a viral infection and is typically painful, with localized tenderness and neck pain, sometimes with odynophagia.

Multinodular goitre occurs in areas of both iodine deficiency and sufficiency, indicating that a multiplicity of genetic and environmental factors is at play. Fibrosis, hypercellularity and colloid cysts are the main pathological findings.

Epidemiology

Graves disease accounts for at least 80% of cases of thyrotoxicosis. The prevalence increases in areas with high iodine intake. Graves disease has a strong female predominance, affecting up to 2% of all women. Thyrotoxicosis due to Graves disease usually occurs in the second to fourth decades of life, whereas the prevalence of a toxic nodular goitre increases with age.

Clinical features

The signs and symptoms of hyperthyroidism are secondary to the effects of excess thyroid hormone in the circulation. The severity of the signs and symptoms is related to the duration of the illness, the magnitude of the hormone excess and the age of the patient. These symptoms and signs are summarized in Box 11.3.1 , which illustrates the wide spectrum of possible clinical features.

Box 11.3.1
Clinical features of thyrotoxicosis

  • Nervousness, irritability

  • Heat intolerance and increased sweating

  • Tremor

  • Weight loss and alteration in appetite

  • Palpitations and tachycardia, particularly atrial fibrillation

  • Widened pulse pressure

  • Exertional intolerance and dyspnoea

  • Frequent bowel movements

  • Fatigue and muscle weakness

  • Thyroid enlargement (depending on cause)

  • Pretibial myxoedema (with Graves disease)

  • Menstrual disturbance and impaired fertility

  • Mental changes

  • Sleep disturbances

  • Changes in vision, photophobia, eye irritation, diplopia, lid lag or exophthalmos

  • Dependent lower extremity oedema

  • Sudden paralysis, with or without hypokalaemia

A comprehensive history and physical examination should be performed, with particular attention to weight, blood pressure, pulse rate and rhythm, looking specifically for cardiac failure, palpation and auscultation of the thyroid to determine thyroid size, nodularity and vascularity, neuromuscular examination and an eye examination for evidence of exophthalmos or ophthalmoplegia.

Clinical investigations and criteria for diagnosis

The TSH level is the single best screening test for hyperthyroidism. Hyperthyroidism of any cause (except excess TSH production from the anterior pituitary) results in a lower than normal TSH. The reference range is 0.4 to 5.0 mIU/L depending on the method.

Other laboratory and isotope tests may include:

  • Free thyroxine (T4) or free tri-iodothyronine (T3) assay, when there is strong clinical suspicion of hyperthyroidism but the TSH is high or high normal.

  • Thyroid autoantibodies, including TSH receptor antibody. These are not routine but may be helpful in selected cases.

  • Radioactive iodine uptake and/or thyroid scan. These tests are helpful in establishing the cause of the hyperthyroidism, but are not part of the ED assessment.

Treatment

Mild hyperthyroidism does not require any treatment in the ED and the patient may simply be referred to an appropriate outpatient clinic. Any features of thyroid storm (discussed later) mandate admission, as does any significant intercurrent illness. Atrial arrhythmias should be controlled by the use of β-blockers, aiming to achieve a rate of less than 100 beats/min.

Ensure that all bloods have been collected first if thyroid-blocking drugs are to be commenced in the ED. High doses of thyroid-blocking drugs are often required to gain an initial response, after which the dose can be tapered.

Commence carbimazole 10 to 45 mg daily or propylthiouracil 200 to 600 mg daily in two or three divided doses initially, using the larger doses for more severe cases. Ideally, discuss the initiation of these agents with the physician who will continue managing the patient after his or her discharge from the ED.

Thyroid storm

Aetiology

Thyroid storm occurs in about 1% of patients with hyperthyroidism. It usually occurs as an acute deterioration in a patient with poorly controlled or undiagnosed hyperthyroidism, precipitated by factors such as surgery, trauma, infection, radioiodine treatment, use of iodinated contrast, exogenous thyroxine ingestion or any other significant stressor.

The diagnosis is entirely clinical, as there is no test to differentiate a thyroid storm from thyrotoxicosis. The mortality rate, if untreated or if the diagnosis is missed, is over 90%. Death is usually due to cardiovascular collapse.

Clinical features of a thyroid storm

The symptoms and signs of thyrotoxicosis are present and significantly exaggerated, with the abrupt onset of a combination of the following:

  • fever >37.6°C up to 41°C

  • cardiovascular complications:

    • tachycardia with pulse rates up to 200 to 300/min, including rapid atrial fibrillation

    • wide pulse pressure

    • high output cardiac failure

  • alteration in mental state, varying from agitation and restlessness to delirium, coma and seizures

  • abdominal pain with vomiting and diarrhoea.

Differential diagnosis

The following differential diagnoses of a thyroid storm need to be considered:

  • sepsis

  • heat stroke

  • malignant hyperthermia

  • neuroleptic syndrome

  • sympathomimetic ingestion

  • drug withdrawal (including alcohol)

  • phaeochromocytoma crisis.

Treatment

The treatment of thyroid storm is directed to blocking thyroid hormone synthesis and release, the peripheral effects of the thyroid hormones, and corticosteroids.

β-Blockers

β-Blockade is the most important factor in decreasing morbidity and mortality. Many of the peripheral manifestations of hyperthyroidism, in particular the cardiovascular effects, are reduced by the use of propranolol. Propranolol also inhibits the peripheral conversion of T4 to T3 as well as antagonizing the effects of thyroid hormones and the hypersensitivity to catecholamines.

Give intravenous increments of 0.5 mg initially up to 10 mg total with continuous cardiovascular monitoring. Subsequent doses of 40 to 120 mg 6-hourly orally can be given.

β-Blockers should treat the cardiac failure secondary to the tachyarrhythmia or high cardiac output, but may cause complications in patients with pre-existing heart disease or asthma.

In this situation, use the short-acting β-blocker esmolol, as any adverse effects will be of brief duration. Give a 250 to 500 μg/kg bolus followed by an infusion starting at 50 to 100 μg/kg/min titrated to effect. Another option is to use the combination of a β-blocker and digoxin.

Thyroid-blocking drugs

Give propylthiouracil 900 to 1200 mg loading dose orally or via a nasogastric tube if necessary. This is followed by 200 to 300 mg 4- to 6-hourly. Propylthiouracil acts by preventing hormone synthesis by blocking the iodination of tyrosine and also inhibits the peripheral conversion of T4 to T3.

Iodine in large doses inhibits the synthesis and release of thyroid hormones and may be given either orally as Lugol’s iodine, 30 to 60 drops daily in divided doses, or intravenously as sodium iodide 1 g 12-hourly. Iodine should not be given until at least 1 hour after anti-thyroid medication has been commenced as otherwise it will provide substrate for the production of more thyroid hormone. Lithium carbonate may be used in patients allergic to iodine or be added when there is difficulty with control.

Cholestyramine also can be considered, which acts by binding with thyroxine after biliary excretion and hence increases elimination.

Corticosteroids

Corticosteroids are given to inhibit the peripheral conversion of T4 to T3 and as a relative deficiency may also be present. Hydrocortisone 100 mg IV 6-hourly or dexamethasone 4 mg IV 12-hourly are used.

General supportive measures

Dehydration and electrolyte disturbances need correction. Aggressive treatment of hyperthermia with cooling measures and paracetamol are necessary, but induction of shivering should be avoided. Salicylates are contraindicated as they displace T4 from binding proteins. In addition, it is essential to look for and treat any precipitating cause, which will improve the prognosis.

Prognosis

Mortality rates are high, at 10% to 30%, despite treatment.

Apathetic hyperthyroidism

Patients with this condition are generally older, although it has been recorded in all age groups. The clinical picture is of a depressed mental state with cardiac complications, in particular cardiac failure. Weight loss is usually not significant and eye signs are rare. Most of the usual hyperkinetic manifestations of hyperthyroidism are absent. Treatment is as for standard hyperthyroidism.

Hypothyroidism

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