Endocrine emergencies

Published on 14/03/2015 by admin

Filed under Emergency Medicine

Last modified 22/04/2025

Print this page

This article have been viewed 1077 times

Chapter 26 Endocrine emergencies

Anna Holdgate, Glenn Arendts

EMERGENCIES IN PATIENTS WITH DIABETES

Diabetes is a disorder of glucose metabolism due to a relative (type 2) or absolute (type 1) insulin deficiency. With the rising rate of obesity in the community, diabetes is becoming increasingly common, and type 2 rather than type 1 diabetes is now often seen in young patients. Diabetic patients may present to the emergency department with acute life-threatening derangements of glucose metabolism, with complications related to long-standing diabetes, or with unrelated health problems which require concurrent management of their diabetes.

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is due to insulin deficiency resulting in acidosis with ketosis, hyperglycaemia and fluid and electrolyte losses. It occurs in patients with type 1 (insulin-dependent) diabetes and may be the presenting problem in patients with previously undiagnosed diabetes. The principles in assessment and management of DKA are identifying and treating the precipitating cause, assessing the severity of the illness, correcting fluid and electrolyte disturbances, and administering insulin.

Serum K⁺, mmol/L	Replacement therapy
> 5.5	Nil—repeat test in 1 h
3.5–5.5	KCl 5–10 mmol/h
< 3.5	KCl 20 mmol/h, cardiac monitoring and central line

Phosphate and magnesium levels are commonly low in DKA; however, there is no evidence to support the routine replacement of these electrolytes. Intravenous bicarbonate is of no proven benefit in patients with DKA as the acidosis usually improves with rehydration and insulin therapy. Bicarbonate should not be given without consulting a critical care specialist or endocrinologist. The measured sodium level should be corrected for the elevated glucose (true sodium = measured sodium + [glucose (mmol/L) ÷ 4]) as the high BSL will artefactually dilute the sodium.

Insulin therapy

Rehydration increases insulin sensitivity, and therefore insulin therapy should not precede fluid therapy. In the initial phase, insulin should be delivered via continuous intravenous infusion. A second intravenous line is usually required for this purpose. A common regimen is 50 units of Actrapid in 50 mL of normal saline via a syringe pump. The insulin infusion should commence at 0.05–0.1 units/kg/hour (2–8 units/hour), aiming for a fall in BSL of 2–4 mmol/hour. The BSL should be measured hourly initially, and the insulin infusion adjusted according to the rate of fall.

The insulin infusion should continue until the urine is clear of ketones or the serum bicarbonate is higher than 20 mmol/L, regardless of the blood sugar level. Once the BSL falls below 15 mmol/L, rehydration should continue with a dextrose-containing solution. Subcutaneous insulin can be commenced once the patient has adequate oral intake and is no longer acidotic. The first subcutaneous dose must be given before the insulin infusion is ceased.

Other therapy

• Treatment of associated infection with appropriate antibiotics.

• Subcutaneous heparin for thromboembolic prophylaxis.

• A nasogastric tube may be necessary if there is persistent vomiting.

• An indwelling catheter is often necessary to monitor urine output.

Ongoing management

The aim of treatment is to correct fluid and electrolyte disturbances, lower the blood sugar level to normal and control ketosis over 12–24 hours. Strict monitoring of BSL and serum K⁺ every 1–2 hours initially is vital. Other electrolytes, especially sodium, should be checked at least twice daily. Regular reassessment of the patient’s hydration status and acidosis is necessary to determine ongoing fluid management. The patient needs to remain closely monitored with hourly observations while the insulin infusion continues.

Cerebral oedema is a rare but life-threatening complication of DKA that is more common in children and usually occurs in the first 12 hours of therapy. Symptoms such as a falling level of consciousness, progressive headache, bradycardia and a rising blood pressure may indicate cerebral oedema and patients with any of these symptoms require urgent senior medical review.

Hyperosmolar hyperglycaemic non-ketotic state (HHNS)

This condition occurs primarily in older patients with non-insulin-dependent diabetes, although it has several clinical features in common with diabetic ketoacidosis. It is characterised by relative, rather than absolute, insulin deficiency leading to hyperglycaemia, hyperosmolarity and dehydration, with little or no acidosis or ketosis. The goals of therapy are identification and treatment of the precipitating event, controlled correction of fluid and electrolyte abnormalities, and correction of hyperglycaemia.

Assessment

HHNS is characterised by non-specific signs such as confusion, vomiting and weight loss, developing over days to weeks in elderly patients with undiagnosed or poorly controlled diabetes. Polyuria and polydipsia are not universally present. There are many possible precipitating events which are summarised in Box 26.2. These patients often have multiple comorbidities and may be on multiple medications.

Box 26.2 Precipitants of HHNS

Poor compliance

Newly diagnosed diabetes

Infection—urinary tract, respiratory, CNS, skin

Cardiovascular events—AMI, CVA/intracranial haemorrhage, mesenteric ischaemia

Other—gastrointestinal haemorrhage, pancreatitis, renal failure, diuretic therapy

Physical examination is focused on assessing the degree of dehydration and looking for evidence of a precipitating cause. The diagnosis is confirmed by the presence of severe hyperglycaemia (often > 50 mmol/L) and serum hyperosmolarity (> 350 mosm/L), with minimal acidosis (pH > 7.3).

Important early investigations include:

• UEC—severe dehydration may be associated with hypernatraemia; the sodium level should be corrected for the BSL (true sodium = measured sodium + [glucose (mmol/L) ÷ 4); potassium depletion and renal impairment are common

• septic screen—urine, blood, skin swabs ± CSF for culture

• chest X-ray—for evidence of infection and to evaluate heart size and presence of cardiac failure

• ECG—for evidence of myocardial infarction or atrial fibrillation

• CT head—for CVA or intracranial haemorrhage.

Management

These patients often have an altered level of consciousness and may have multiple comorbidities including heart and renal disease. Therefore they must be closely observed with full cardiorespiratory monitoring.

Fluid and electrolyte therapy

In the presence of shock (hypotension or poor tissue perfusion), fluid therapy should begin with 500 mL boluses of normal saline until blood pressure and tissue perfusion are restored. After correction of shock, fluid replacement should be performed relatively slowly. Although these patients are often profoundly dehydrated, this has usually occurred over a period of days to weeks and overly rapid replacement of fluid may lead to pulmonary or cerebral oedema. Most patients will have a fluid deficit of 8–12 litres and this should be replaced over a 24–48 hour period. Fluid therapy should begin with 1 litre of normal saline every 2–4 hours. If the corrected sodium is > 155 mmol/L or the sodium is rising, normal saline can be replaced by half saline/2.5% dextrose solution. The patient should be regularly assessed for clinical evidence of fluid overload, and may need central venous monitoring via a central line.

Potassium levels will fall rapidly once the patient is rehydrated and receiving insulin. Potassium replacement at 5–10 mmol/h should commence if the K⁺ is < 5.0 mmol/L and urine output has been established. In the presence of oliguria and renal failure, K⁺ replacement should be more cautious.

Insulin therapy

As for DKA, an intravenous insulin infusion should be commenced. Patients with HHNS are often insulin sensitive and usually require 0.03–0.05 units/kg/h to achieve a fall in BSL of 3–5 mmol/h. As hyperglycaemia has developed over a long time period, it is appropriate to correct the BSL slowly, aiming for normalisation over 24 hours. This minimises the risk of cerebral oedema.

Other therapy

Precipitating illnesses should be actively sought and treated. Serious diagnoses such as mesenteric ischaemia must be considered. Thromboembolic prophylaxis with subcutaneous heparin is particularly important in HHNS due to the thrombogenic effect of profound dehydration, and the presence of serious comorbidities.

Hypoglycaemia

Causes

Hypoglycaemia most commonly occurs in diabetic patients on insulin or oral hypoglycaemic therapy. It can also occur in non-diabetics secondary to diseases such as sepsis, alcoholism, hepatic failure, renal failure and insulin-producing tumours.

In diabetics, hypoglycaemia may be due to excess insulin or oral hypoglycaemic treatment, missed meals, physical exertion and alcohol. It may be the first presentation of renal impairment in patients on sulfonylureas.

Clinical features

Hypoglycaemia predominantly affects the brain and the autonomic nervous system. Neurological signs can vary widely and include agitation, aggressive or bizarre behaviour, coma, seizures, confusion, dysarthria and focal deficits such as hemiparesis (mimicking stroke). Autonomic features include sweating, tremor, blurred vision, vomiting and anxiety. The diagnosis is confirmed by BSL < 3 mmol/L on finger prick sampling. The diagnosis should be considered in all patients presenting with confusion, seizures or an altered level of consciousness.

Therapy

• Hypoglycaemia is easily reversed with oral or intravenous glucose. Prolonged, untreated hypoglycaemia can lead to permanent brain dysfunction so early diagnosis and treatment is essential.

• If the patient is still awake, oral glucose in the form of a sweet drink, biscuit or other sugary substances may be enough to restore BSL. If the patient is unable to swallow, 25 mL of 50% dextrose is given as an intravenous push through a large bore intravenous cannula, followed by a 20-mL saline flush (to prevent phlebitis). If the patient does not recover within 2–3 minutes, or the BSL remains < 3 mmol/L, the dose can be repeated.

• If intravenous access is not possible, 1 mg of intramuscular glucagon may temporarily reverse hypoglycaemia if the patient has normal hepatic function. This should be followed by oral or intravenous glucose.

• Hypoglycaemia secondary to oral hypoglycaemic agents may be recurrent and prolonged, particularly in the presence of renal impairment. These patients require a 5% dextrose infusion and observation in hospital until the BSL is stable.

• Once the BSL is restored, assessment and treatment of the precipitating cause is essential.

The ‘high risk’ diabetic patient

As well as the acute derangements of glucose metabolism outlined above, diabetic patients are at risk of other acute pathologies due to the long-term complications of their illness.

Infection

Diabetics are immunocompromised and thus are more prone to infection and are at greater risk of systemic sepsis than the general community. They may have significant infection in the absence of the usual clinical signs such as fever or elevated white cell count. Therefore, diabetic patients with actual or potential infection warrant more extensive work-up than other patients, with a lower threshold for tissue and blood cultures, soft tissue imaging and hospital admission. In particular, soft tissue infections are often poly-microbial and may invade into deeper structures such as muscle and bone. Specialist microbiology advice should be sought regarding antibiotic therapy.

Infarction

Macro- and microvascular disease seen in diabetic patients makes them more prone to acute vascular compromise in many organ systems including the heart, the brain, the kidneys, the gut and the peripheral vasculature. Acute myocardial ischaemia may present atypically with minimal or absent chest pain, unexplained acute heart failure or non-specific vomiting. Abdominal pain in a diabetic patient has many potentially serious causes including mesenteric ischaemia, myocardial infarction, leaking aortic aneurysm or renal infarction. Therefore these patients require thorough investigation which usually will include abdominal CT scanning.

Other

Most patients with long-standing diabetes will have some impairment of renal function and are at relatively high risk of acute renal impairment which may be precipitated by concurrent infection or any illness that leads to dehydration. Serum creatinine should be measured in any diabetic patient who presents with systemic illness.

Long-standing retinopathy may be acutely complicated by retinal haemorrhage, infarction or detachment and any diabetic patient with acute eye symptoms should have urgent ophthalmology review.

The diabetic patient with unrelated illness

In addition to the specific conditions for which they are at higher risk, diabetics are subject to the same spectrum of illness and injury as the general population. Admission to hospital requires concurrent management of their diabetes as well as their acute illness and this should begin in the emergency department. Poor glycaemic control in hospitalised diabetics increases the risk of death and infection and prolongs hospital stay. Acute illness will usually increase an individual’s basal insulin requirements and most diabetics will require upward adjustment of insulin therapy in the early part of their hospital admission.

The BSL should optimally be maintained in the region of 5–8 mmol/L and there are several methods available to achieve this. Many hospitals have well developed local protocols for managing diabetes and these should be followed closely. For critically ill patients, particularly those with acute stroke, myocardial infarction and sepsis, blood sugar control is best achieved by continuous insulin infusion with close monitoring of finger-prick BSLs.

All patients with type 1 (insulin-deficient) diabetes who are not critically ill should continue to receive regular subcutaneous therapy with intermediate- and short-acting insulin but will usually require higher doses. Many type 2 diabetics will require a period of insulin therapy during hospitalisation even if they are not usually managed with insulin. Basal insulin requirements should be provided with regular subcutaneous intermediate-acting insulin with additional short-acting insulin around meal times. This is preferable to ‘sliding-scale’ insulin therapy as it provides more stable glucose control.

ADRENAL EMERGENCIES

Hypoadrenal crisis (acute adrenocortical insufficiency)

Presentation and clinical features

Hypoadrenal crisis develops in two clinical settings. Occasionally, the patient presents with acute haemorrhagic destruction of the adrenal glands due to sepsis, burns, trauma or anticoagulant therapy. More commonly, the crisis develops as an acute deterioration in patients with Addison’s disease or other causes of chronic adrenal failure. This can be due to increased steroid requirements (infection, surgery, trauma), drug interactions that increase steroid metabolism (phenytoin, barbiturates) or noncompliance with maintenance steroid therapy.

The presenting symptoms are often non-specific and include malaise, lethargy, dizziness, nausea, diarrhoea and abdominal pain. However, in acute severe cases the patient presents with haemodynamic collapse—hypoadrenalism needs to be considered in any patient with unexplained shock.

Differential diagnosis

The differential diagnosis is very broad due to the non-specific presentations seen. Ascribing hypoadrenal symptoms to gastroenteritis or other intra-abdominal conditions is the most common misdiagnosis made.

Investigations

If acute hypoadrenalism is suspected the following initial investigations should be performed. Ideally these are done prior to starting treatment with steroids, but treatment should not be delayed waiting for results of any of these tests.

• UEC—the combination of a low bicarbonate, hyponatraemia and hyperkalaemia is highly suggestive of hypoadrenal crisis. Renal failure may occur.

• Random plasma cortisol level—a low level in the setting of acute stress is highly suggestive of adrenocortical insufficiency. ACTH, renin and aldosterone levels may be useful in diagnosing the cause of hypoadrenalism and should be collected at the same time as the cortisol level.

• Short corticotrophin test—this requires the administration of intravenous corticotrophin and then a repeat cortisol level 30 minutes later. This must occur prior to the administration of hydrocortisone. In most cases of suspected insufficiency testing is possible, but if the patient is moribund and treatment cannot be delayed, omit this test.

Other useful investigations include:

• BSL—hypoglycaemia

• ABG—non-anion gap metabolic acidosis

• Ca²⁺—hypercalcaemia

• ECG—arrhythmias or hyperkalaemic changes.

Management

The patient may present with haemodynamic collapse and require immediate resuscitation. High flow oxygen by mask should be applied. Hypotension should be treated initially with 1000 mL boluses of normal saline until BP or peripheral perfusion improve. Shock may be refractory to fluid resuscitation until hydrocortisone therapy is commenced. Even with adjuvant steroids, the patient may need inotrope support in decompensated shock. Hypoglycaemia, if present, should be treated initially with 25 mL of 50% dextrose IV.

After resuscitation, further fluid requirements should be determined by assessment of the patient’s hydration status. Normal saline should be used to replace any fluid deficit over the next 24–48 hours. If the patient has associated persistent hypoglycaemia, adding 50 g dextrose to each bag of normal saline given is preferable to using a dextrose-containing solution with a low sodium concentration. Blood glucose, Na⁺ and K⁺ levels should be measured every 2–3 hours initially.

IV hydrocortisone (100 mg every 6 hours) should be given promptly.

Other important acute management issues include the treatment of any underlying precipitant such as infection.

The majority of patients improve within 24 hours of commencing this treatment regimen. Oral combined glucocorticoid and mineralocorticoid therapy may then be commenced. Patient education after the acute treatment phase is over concerning increasing their maintenance steroid requirements at times of stress or illness is a vital part of management.

Pearls and pitfalls in the patient with chronic adrenal suppression

In emergency department practice, it is common to encounter cases of adrenal suppression due to chronic glucocorticoid therapy suppressing endogenous adrenocorticotrophic hormone (ACTH) production. When such patients become acutely unwell, they are at risk of developing a hypoadrenal syndrome as their steroid requirements increase but they are unable to match this with increased production. To prevent this, any patient on continuous maintenance glucocorticoid therapy for the previous 6 weeks or more should have their dose augmented when they present to emergency department with an acute stress. There is controversy about what constitutes an acute stress and by what magnitude the dose should change. As a general rule, for any severe potentially life-threatening illness, give an additional 100 mg hydrocortisone over and above the patient’s usual daily steroid dose. For less severe illness, give 25–50 mg of additional hydrocortisone.

THYROID EMERGENCIES

Thyrotoxic crisis (‘thyroid storm’)

Presentation and clinical features

Patients at risk of thyrotoxic crisis usually have either undiagnosed or poorly treated hyperthyroidism. The precipitants of thyrotoxic crisis that should be looked for are shown in Box 26.3.

Box 26.3 Precipitants of thyrotoxic crisis

Intercurrent illness or stress—infection, labour, major vascular events such as CVA

Drugs—thyroxine overdose, amiodarone, iodinated dyes, salicylates, cessation of antithyroid drug therapy

Trauma—multitrauma, thyroid gland surgery, vigorous palpation of thyroid gland

Thyrotoxic crisis represents the extreme of hyperthyroidism, and the diagnosis is a clinical one. Three signs in particular help distinguish thyrotoxic crisis from uncomplicated hyperthyroidism:

• hyperpyrexia (temperature > 38°C)

• extreme tachycardia (HR usually 130–200 bpm)

• CNS disturbance, ranging from restlessness and agitation to coma.

Vomiting and diarrhoea are common. Potentially life-threatening cardiac complications (arrhythmias, cardiac failure) occur in more than 50% of patients.

Investigations

No single test confirms the diagnosis of thyrotoxic crisis. Thyroid function tests (TFTs) confirm hyperthyroidism, but the levels of T₃ and T₄ in thyrotoxic crisis are usually no different from those in uncomplicated hyperthyroidism, and treatment should not be delayed for the TFT results. Hyperglycaemia, hypokalaemia, hypercalcaemia, abnormal liver function and leucocytosis occur commonly. CXR and ECG looking for specific cardiac complications should be performed.

Management

Patients with thyrotoxic crisis are usually extremely unwell and require continuous ECG, blood pressure and temperature monitoring. Unstable arrhythmias and profound cardiac failure may be evident at presentation and require urgent treatment. Early consultation with a critical care specialist or endocrinologist is important.

Good general supportive care is essential. These patients are hypermetabolic and have markedly increased oxygen, fluid, electrolyte and glucose requirements. High flow oxygen by mask should be started. The patient often requires 5–6 litres of normal saline in the first 24 hours, although less aggressive fluid resuscitation may be necessary in the elderly or those with heart failure. Hyperpyrexia should be treated with paracetamol and external cooling methods, for example axillary and groin cold packs. Thyrotoxic crisis patients have an increased risk of thromboembolism and should receive appropriate prophylaxis. The underlying cause should be sought for and managed appropriately.

Beta-adrenergic blockers antagonise the peripheral end organ effects of thyroid hormones and are the mainstay of emergency therapy. Oral (or nasogastric tube (NGT)) propranolol commenced at 40 mg every 6 hours is the treatment of choice, although much higher doses may be required. Intravenous propranolol is not currently commercially available in Australia and, if the patient requires intravenous beta blockade, esmolol is the best option due to its very short half-life. All beta-blockers can worsen cardiac failure and hypotension.

Oral or NGT propylthiouracil reduces the further synthesis of thyroid hormones and prevents the peripheral conversion of T₄ to the more active T₃. A loading dose of 400 mg followed by 200 mg every 6 hours should be given.

Corticosteroids improve survival in thyrotoxic crisis. Hydrocortisone 100 mg every 6 hours IV is an appropriate choice.

The majority of patients improve with this management regimen within 24 hours, although complete recovery may take many days. In patients not responding to these standard therapies other treatments are occasionally used. These include large doses of iodide or iodinated radiology contrast media, and plasma exchange techniques to reduce levels of circulating thyroid hormones.

Hypothyroid crisis (‘myxoedema coma’)

Presentation and clinical features

Myxoedema coma occurs most commonly following some precipitating event in a patient with unrecognised hypothyroidism (Box 26.4). The diagnosis is clinical and a high index of suspicion is required.

Box 26.4 Precipitants of myxoedema coma

Intercurrent illness—infection, GIT bleed, CVA, congestive cardiac failure (CCF)

Drugs—CNS depressants, anaesthetic agents, beta-blockers, lithium, amiodarone, cessation of thyroxine therapy

Environmental—extreme cold exposure

Myxoedema coma is the clinical extreme of hypothyroidism and is characterised by multiorgan failure due to reduced cellular metabolism. The cardinal features are:

• decreased conscious state

• hypoventilation progressing to hypercarbic respiratory failure

• bradycardia and hypotension

• hypothermia.

Increased total body water is common, leading to oedema, pleural and pericardial effusions, and hyponatraemia. Paralytic ileus and urinary retention may occur.

Differential diagnosis

• Environmental hypothermia

• Encephalopathies, e.g. hepatic, uraemic

• Cardiogenic shock

• Sepsis

Investigations

The diagnosis of myxoedema coma is clinical, although TFTs confirm hypothyroidism. A rapid T₄ assay is often available and, if normal, excludes the diagnosis. Other important investigation abnormalities include:

1. UEC—hyponatraemia, renal failure

2. BSL—hypoglycaemia

3. ABG—hypercapnia, hypoxia

4. FBC—anaemia, leukopenia

5. ECG—bradycardia, prolonged QT interval, low voltage complexes

6. CXR—pleural and pericardial effusions.

Hypothyroid crisis patients are commonly septic without exhibiting any of the usual clinical features of sepsis, and should have a septic screen as part of their initial work-up.

Management

Hypothyroid crisis patients are profoundly unwell and require management in an area with full monitoring and resuscitation equipment. Intubation and ventilation is often needed but requires special precautions due to hypothermia and gastric stasis. These patients, while oedematous, may have a reduced intravascular volume, and hypotension should initially be treated with 500 mL boluses of warmed intravenous normal saline. Hypoglycaemia, if present, should be immediately corrected with 25 mL of 50% dextrose IV.

Administration of thyroid hormones is the mainstay of therapy in myxoedema coma. If the diagnosis is clinically suspected early consultation with a critical care specialist or endocrinologist is essential so therapy is not delayed. Considerable controversy exists regarding the optimal dose, route and rate of thyroid hormone replacement. Initial intravenous therapy is preferred when ileus is suspected. Currently in Australia, only IV triiodothyronine (T₃) is readily available, and 10 μg can be given as a slow bolus every 4 hours initially. Oral T₃ or T₄ can be commenced once the ileus has resolved. As hypothyroid crisis usually develops slowly, rapid replacement of thyroid hormones may provoke serious complications such as cardiac ischaemia or arrhythmias. Providing supportive care is adequate, relatively low initial doses either IV or orally, titrated to clinical response, is prudent.

IV hydrocortisone 100 mg every 8 hours should be commenced as myxoedema coma is often associated with adrenal dysfunction.

Other important management issues include:

• Hypothermia—rewarming with warm blankets or a Bair Hugger is recommended provided it does not cause worsening hypotension from vasodilation.

• Hyponatraemia—usually corrects with water restriction but if severe and associated with altered conscious state may require hypertonic (3%) saline.

• Infection is common and should be covered with broad spectrum antibiotic therapy.

Recovery time with treatment is highly variable and improvement can occur anywhere from 24 hours to many days after commencing therapy.

Pearls and pitfalls in the emergency department

Up to 5% of female patients aged over 65 encountered in the emergency department have unrecognised hypothyroidism. Even though very few of these patients will ever develop a hypothyroid crisis, it may be appropriate in the correct clinical context to assess for symptoms, signs and laboratory evidence of hypothyroidism in this at-risk population.

Recent Posts

Meta

Categories

Search Engine

Endocrine emergencies

Share this:

Related

Related posts: