Emergency care and nursing in case

Emergency care and nursing in case

of nondiabetic coma and crises in endocrinology

 

 

 

Thyroid storm.

Thyroid storm is a life- threatening emergency requiring prompt and specific treatment.

Thyroid storm results from:

– untreated or inadequately treated thyrotoxicosis

It may be precipitated by:

–         infection;

–         trauma

–         surgery;

–         embolism;

–         diabetic acidosis;

–         fright;

–         toxemia of pregnancy;

–         labor;

–         discontinuance of antithyroid medication;

–         radiation thyroiditis.

         It is characterized by abrupt onset of more severe symptoms of thyrotoxicosis, with some exacerbated symptoms and signs atypical of uncomplicated Graves disease:

–         fever;

–         marked weakness and muscle wasting;

–         extreme restlessness with wide emotional swings;

–         confusion;

–         psychosis or even coma;

–         hepatomegaly with mild jaundice;

–         the patient may present with cardiovascular collapse or shock.

 

Treatment of thyroid storm;

Iodine-30 drops Lugol’s solution/day orally in 30g 4 divided doses; or 1 to 2 gr. sodium iodide slowly by i/v drip.

Iodine in pharmacological doses inhibits the release of T3 to T4 within hours and inhibits the organification of iodine, a transitory effect lasting  from a few days to a week (”escape phenomenon”.)

         Indications it is used for

–         the emergency management of thyroid storm;

–         thyrotoxic patients undergoing emergency surgery;

–         preoperative preparation of thyrotoxic patients selected for subtotal thyroidectomy /since it also decreases the vascularity of the thyroid gland.

 It is not used for routine treatment of hyperthyroidism. The usual dosage is 2 to 3 drops of satured potassium iodide solution orally tid or dig 1300 to 600 mg/day; or 0,5gr sodium iodide in 0,9% sodium chloride solution given i/v slowly g 12h.

         Complication of iodine therapy include:

–         inflammation of the salivary glands;

–         conjunctivitis;

–         skin rashes;

–         a transient hyperthyroidism (iod-BASEDOW phenomenon) (it can be observed in patients with nontoxic goiters after administration of iodine-contrast agents).

Antithyroid drugs

 Propylthiouracil (merkazolil) – 900 to 1200 mg/day orally or by gastric tube.

Doses of PPU of 450-600 mg/day or greater 800 to 1200mg/day are generally reserved for the patient with thyroid storm, because such doses block the peripheral conversation of T₄ to T₃.

β-adrenergic blocking drugs

 Propranolol – 160mg/day orally in 4 divided doses; or 1mg slowly i/v g 4h under careful monitoring; a rate of administration should not exceed 1mg/min; a repeat 1mg dose may be given after 2 min i/v glucose solutions.

Propranolol rapidly decreases heart rate, usually within 2 to 3 h when given orally and within minutes when given i/v.

Correction of dehydration and electrolyte imbalance cooling blanket for hypertermia.

Digitalis if necessary.

Treatment of underlying disease such as infection.

Corticosteroids-100 to 300mg hydrocortisone/day i/v.

It is very important to:

•         Maintain a patent airway and adequate ventilation.

•         Monitor continually for cardiac dysrhythmias.

•         Monitor vital signs every 30 minutes.

•         Provide comfort measures, including a cooling blanket.

•         Give medicament treatment (antithyroid drug, propranolol, glucocorticoids, nonsalicylate antipyretics) as ordered.

Even with treatment, thyroid storm has a mortality rate of 25%

 

Myxedema coma

Definition

It is a life-threatening complication of hypothyroidism, which is extremely rare in warm climates but not uncommon in cold areas.

Predisposing factors

·        exposure to cold;

·        acute infection;

·        trauma;

·        myocardial infarction;

·        sedatives.

Diagnostic criteria

Myxedema coma characteristics include a background of long-standing hypothyroidism with

сlinical signs of extreme hypothermia (temperatures 24 to 32⁰C), areflexia, seizures, CO₂ retention, and respiratory depression caused by decreased cerebral blood flow. Severe hypothermia may be missed unless special low reading thermometers are used. Rapid diagnosis (based on clinical judgement, history, and physical examination) is imperative because early death is likely.

Laboratory investigations show hyponatraemia, anaemia, hypoglycemia, hypercholesterolemia, elevated LDH and creatinine kinase. If secondary hypothyroidism is suspected, hydrocortisone should also be taken. However, to establish the diagnosis determination of TSH and free T4 are essential; in this respect it is important to be aware that TSH levels can be only slightly elevated as a result of nonthyroidal illness.

Treatment of myxedema coma

Treatment should take place in an intensive care unit. Thyroid hormone substitution should not be delayed until results of thyroid function tests are known.

It is treated with large doses of T₄ (200-250 µg I/v followed by 100 µg after 24 hours and thereafter 50 µg daily (preferably oral otherwise intravenously) or T₃ if available (10 µg I/v bolus 3 times a day until normalization of vital function), because TBG must be saturated before any free hormone is available for response. The maintenance dose for T4 is 50 µg day I/v and for T3 10 20 mkg/day I/v until the hormone can be given orally.

The patient should not be rewarmed rapidly because of the threat of cardiac arrhythmia.

Hypoxemia is common, so PaO₂ should be measured at the outset of treatment. If alveolar ventilation is compromised, immediate mechanical ventilatory assistance is required.

 

Adrenal glands

Historical perspectives

•         1563: Eustachius first described adrenal glands

•         1855: Thomas Addisooted real importance of adrenal glands

•         1856: Brown Sequard demonstrated that adrenals are very necessary for life (without adrenal glands animals could not survive)

Schematic showing the cellular zonation of the adrenal cortex and blood flow through the cortex to the collecting veins in the medulla

Adrenal crisis –

is a medical emergency caused by sudden marked insufficiency of adrenocortical hormones.

Precipitating factors.

1)     stress (infection (especially with septicemia, trauma, surgery, prolonged fasting, salt loss due to excessive sweating during hot weather);

2)    sudden withdrawal of adrenocortical hormone therapy in patients with chronic insufficiency.

Clinical features.

An adrenal crisis is characterized by:

–         profound asthenia,

–         severe pains in the abdomen, lower back or legs;

–         nausea, vomiting diarrhea;

–         peripheral vascular collapse;

–         renal shutdown with azotemia.

–         Body temperature may be subnormal, through severe hyperthermia due to infection is often seen.

Hyperpigmentation

Treatment

The main principles of adrenal crise treatment:

1) substitutional gluco– and mineralocorticoid therapy;

2) liquidation of electrolyte disturbances;

3) treatment of hypoglycemia, dehydration;

4) prevention and treatment of recurrent infection.

Therapy should be instituted immediately once a provisional diagnosis of adrenocortical failure has been made.

1)     hydrocortisone 100 – 150 mg as a water – soluble ester (usually the succinate or phosphate) is injected IV over 30 seconds, followed by infusion of 1 L of 5 % glucose – in – saline solution containing 100 mg hydrocortisone ester given over 2 h.

2)     Additional saline is given until dehydration and hyponatremia have been corrected. Hydrocortisone therapy is given continuously to a total dosage in 24 h of 400 – 600 – 800 mg. Mineralocorticoids are not required when high – dose hydrocortisone is given. Restoration of BP and general improvement may be expected within 1h or less after the initial dose of hydrocortisone. Vasopressors may be needed until the full effect of hydrocortisone is apparent (a delay in instituting corticosteroid therapy may result in the patient’s death, particularly if hypoglycemia and hypotension are present). A total dose of hydrocortisone 150 mg is usually given over the second 24-h period if the patient is markedly improved, and 75 mg is given on the third day. Maintenance oral doses of hydrocortisone (30 mg) and fludrocortisone acetate (0.1 mg) are given daily there – after. Recovery depends upon treatment of the underlying cause and adequate hydrocortisone therapy.

3)     Total infusion of saline and 5 % glucose  – 2,5 – 3,5 l during first day

4)     Treatment of complications (hyperpyrexia, psychotic reactions).

Prognosis.

With a substitution therapy, the prognosis is excellent and a patient with Addison’s disease should be able to lead a full life.

 

ACUTE SEVERE HYPOCALCEMIC TETANY

1.     It is treated initially with IV infusion of Ca salts. 10 – 50 ml of 10% solution of Ca gluconate or Ca chloride may be given IV over 15 – 30 min, but the effect lasts for only a few hours. (side effects: thrombophlebitis, IM injection can cause local necrosis).

2.     Magnesium repletion.

3.     Parathyroidin 1 – 2 ml IM 2 times a day.

4.     Sedative preparations and spasmolitics.

 

In patients with HYPERCACEMIC CRISIS, which is medical emergency and characterized by dehydration, hypotension, abdominal pain, vomiting, fever and altered consciousness:

–         rehydration 2 – 6 l of sodium chloride solution and furosemid 40 – 160 mg;

–         calcitonine 1 – 4 units/kg;

–         prednisolone 40 – 60 mg/day.