1. OBJETO DE LA CONTRATACIÓN
1.4. Caracterización del Área de Servicio
tissue associated with neovascularisation. Both closed- and open-angle glaucoma are more common in people with diabetes. Measurement of intraocular pressure along with visual acuity and fundoscopy should therefore be part of the assessment in people with diabetes presenting with visual complaints.1,2
3. Answer: B
In the Somogyi effect, nocturnal insulin may reduce blood glucose levels overnight. If prolonged, this can stimulate the release of glucagon and catecholamines, resulting in hyperglycaemia.
Strict glycaemic control has been shown to slow the development of long-term diabetic complications such as neuropathy, nephropathy and vascular problems. It is also important in the short term because of the more obvious risks of immediate complications. It has not, however, been shown to reverse vascular disease.
Acarbose is effective in reducing post-prandial blood glucose rise by selectively inhibiting
disaccharidases, therefore decreasing carbohydrate absorption from the gut.
The most common cause of unstable blood sugar levels is underlying infection, which should be carefully sought because the site may appear relatively minor. Other precipitants include changes in oral hypoglycaemic drugs, and poor compliance. Recurrent episodes of hypoglycaemia or DKA should prompt a careful drug history and review to detect patterns such as diurnal variations.
Medication use should be reviewed with the patient for their education. Considerations of safety should ensure the patient is not only euglycaemic but is returning to a stable environment before planning discharge.1
4. Answer: C
Oral glucose preparations will raise blood glucose to normal in minutes but require subsequent slower release carbohydrates to maintain the rise. Glucagon functions by increasing glycogenolysis and
gluconeogenesis, and peak effect is of slower onset. Glucagon usually takes 7–10 minutes for
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normalisation when a patient has an altered mental status due to hypoglycaemia. Due to its mechanism of action, it is less effective in patients with low glycogen stores such as chronic
alcoholics or children.
The critical level for a patient to develop symptomatic hypoglycaemia varies between individuals, but symptoms start usually below
5 mmol/L. The adrenergic response to hypoglycaemia may be prevented by the use of β-receptor
antagonists, but not by calcium channel blockers.1
5. Answer: B
Sulfonylurea-induced hypoglycaemia in a patient with type 2 diabetes is more challenging to manage in the ED than insulin-induced hypoglycaemia. Often hypoglycaemia persists and recurs despite initial treatment, and therefore requires admission for treatment and close monitoring of blood glucose levels. In a previously stable patient with diabetes who has been on a regular dose of sulfonylurea, sudden development of hypoglycaemia is usually associated with an underlying precipitating factor. This may include an increased drug level due to interactions, reduced metabolism and excretion. Vigilance is also required to detect underlying precipitating factors such as sepsis or acute adrenal insufficiency.
In the management, the initial treatment would be oral or intravenous glucose as for any other type of hypoglycaemia; however, blood glucose maintenance is more important in this situation. Generally this may be achieved with intravenous infusion of 10% glucose titrated against the blood glucose level. If the blood glucose is difficult to be maintained with the above, octreotide should be considered. Octreotide is a potent inhibitor of pancreatic insulin release, and has been shown to be effective in preventing recurrences in sulfonylurea- induced hypoglycaemia. Dose recommendations vary but octreotide can be give as an intravenous infusion.2
6. Answer: B
The standard urine ward test using test strips detects only acetoacetate as ketones but not beta-hydroxybutyrate. Blood or serum should be tested to detect both types of ketones. This can be performed at the bedside using special test strips or
in the laboratory. Measuring both types of ketones is important for monitoring the response to insulin therapy in DKA. Insulin infusion should be continued until ketones are completely cleared from blood and the AG is normalised. The majority of DKA patients present with metabolic acidosis with a wide AG due to ketonaemia. However, some patients may present with compensatory metabolic alkalosis with normal or high HCO3 levels. In these patients a wide AG is still present due to ketonaemia.
Kussmaul hyperventilation is a compensatory respiratory reflex induced by severe metabolic acidosis. In DKA, there are increased renal losses of important electrolytes (sodium, chloride, potassium, calcium, magnesium and phosphate) due to the high osmotic load provided by hyperglycaemia. Acidaemia increases renal losses of potassium ion (K+), further depleting the total body K+. However, acidaemia pushes intracellular potassium to the extracellular space, which can result in initial normal or high serum K+ level. When volume depletion is
corrected and acidaemia improved with treatment, hypokalaemia develops unless potassium is adequately replaced.1,3
7. Answer: B
The main priority in the treatment of DKA is to replace the total body water deficit, which averages 5–10 L (100 mL/kg) in an average adult. It is recommended that 50% of this volume is replaced within the first 12 hours and the rest during the next 12 hours.
A loading dose of insulin is not recommended for use in children and is optional in adults. In the majority of patients, initial serum K+ level is either normal or elevated despite the gross depletion of total body potassium. This is mainly due to total body water depletion and movement of potassium ions to the extracellular space secondary to acidosis.
Consequently, initial hypokalaemia means there is a severe depletion of total body potassium, and acidosis and water depletion have not been able to increase the serum K+ concentration. Initial
hypokalaemia < 3.5–4.0 mmol/l should be aggressively corrected before commencement of insulin therapy. Initial hypokalaemia does not indicate less severe disease process.
Correction of the metabolic problem will normally correct the associated acid–base disorder. Sodium
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bicarbonate is not recommended to correct acidosis except in a limited subset of patients including patients who are critically unwell with arterial pH < 6.9 (severe acidaemia).1,3
8. Answer: C
Cerebral oedema is a serious complication that occurs (especially in children) during treatment of DKA. It has a mortality risk of 70% once developed, with 10% of survivors having
permanent neurological sequelae. Cerebral oedema usually develops when it appears to be having clinical and biochemical improvement in the child. However, at that point the child develops mainly neurological signs and symptoms. These include:
• altered level of consciousness
• headache
• seizures
• focal deficits.
Cerebral oedema is a clinical diagnosis. Immediate treatment with intravenous mannitol is indicated to prevent potential serious
consequences.
Intubation and ventilation are required to control rising intracerebral pressure. A head CT can be performed once mannitol is given. Specific risk factors associated with the development of cerebral oedema include:
• young age (more common in <5 years)
• severe hyperosmolarity
• persistent hyponatraemia
• severe acidosis.
There is no evidence to suggest increased volume replacement, sodium-containing fluids, or rate of fall of blood glucose cause cerebral oedema.
Rapid volume expansion during treatment improves glomerular filtration rate (GFR) and urine output. In the kidneys, this increases ketone excretion with an increase in chloride reabsorption (as HCO3 is low). This may cause hyperchloraemic acidosis with a normal AG, and hypophosphataemia. As described in answer 7, correction of fluid depletion and acidaemia without adequate supplementation may also cause rapid development of severe hypokalaemia.1,3,4
9. Answer: A
HHS presents most commonly in elderly, poorly controlled or undiagnosed type 2 diabetes patients. It
often develops insidiously over days or weeks after a variety of serious illnesses. These patients often have multiple comorbidities and lack capacity to communicate. They may have limited ability to access water intake freely. All these factors may contribute to the higher mortality seen in HHS. In HHS, blood glucose levels are often much higher than seen in DKA, often >60 mmol/L.
There is severe total body water (TBW) contraction secondary to losses caused by osmotic diuresis due to severe hyperglycaemia in the face of severely restricted access to free water intake. TBW loss may reach 8–10 L in an average adult (compared with 5–6 L in DKA). Therefore calculated serum osmolality is often >315 mmol/L. Arterial pH usually remains >7.3, although wide AG metabolic acidosis may develop during the course of disease. This is mainly due to hypoperfusion of tissues and may be contributed by starvation ketosis. The ketone bodies remain small in amount and do not significantly contribute to acidosis.1,5
10. Answer: D
HHS patients are significantly dehydrated and poorly mobile, and may develop disseminated intravascular coagulation. Thromboembolic risk is therefore high, and so heparin prophylaxis should be initiated at an early point.
These patients are usually sensitive to insulin, with insulin resistance being quite uncommon. Higher doses are usually not required. Insulin therapy should be started only after adequate volume repletion and correction of hypokalaemia. Adequate volume replacement prior to administration of insulin in HHS prevents cardiovascular collapse, caused by a sudden intracellular fluid shift that accompanies the
intracellular glucose movement induced by insulin. Insulin should therefore be administered cautiously to produce a slow fall in blood glucose. While total body potassium deficits are significant, the initial serum level may be normal in the face of severe volume contraction. Insulin therapy will result in the intracellular movement of potassium causing hypokalaemia, so replacement will generally be required at an early stage.
In HHS there is a total body sodium deficit. However, initial corrected serum sodium may be low, normal or high, depending on the degree of volume
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depletion. Hypernatraemia along with very high serum osmolality, are poor prognostic factors and correspond to severe volume depletion. Fluid replacement, guided by central venous pressure (CVP) monitoring if necessary, should aim first to correct hypotension, then to slowly replace water deficit over a period of several days.1,5
11. Answer: D
The diagnosis of underlying osteomyelitis associated with a diabetic foot ulcer can be difficult. A diabetic foot ulcer extending deep down to the bone is highly likely to be associated with underlying osteomyelitis. This can be determined with sterile surgical probing of the ulcer, if necessary under an appropriate anaesthetic.
Wound swabs taken from diabetic foot ulcers usually grow colonising organisms only. It may not be possible to identify deep-seated infection purely from wound swabs, and collection of purulent material from the depth of the ulcer is usually required. It has also been found that there is a relatively high positive likelihood ratio for the diagnosis of osteomyelitis when the foot ulcer is >2 cm.2
There is no direct association between Charcot’s arthropathy and osteomyelitis.2
12. Answer: D
Lower extremity infections in diabetics often start as an ulcer, due either to skin breakdown in pressure areas of the foot, or to minor injury. They have the potential to spread rapidly to limb-threatening or life-threatening infections, and therefore demand careful assessment and initiation of appropriate treatment.
Any ulcer with the following features should be considered as limb-threatening:
• a deep ulcer
• ulcer associated with >2 cm of surrounding cellulitis
• ulcer associated with lymphangitis
• presence of purulent or malodorous discharge
• presence of necrotic or gangrenous tissue
• associated limb ischaemia with no palpable pulses.
If not treated promptly and aggressively these infections often become life threatening with sepsis and septic shock. Intravenous antibiotics should be given without delay on presentation.
Broad-spectrum antibiotics should be used to cover staphylococci and streptococci, gram-negative and anaerobic bacteria.
Uncomplicated ulcers are not limb-threatening, and can be managed in the community. If the ulcer is longstanding and is not infected (no surrounding cellulitis or discharge), it does not require antibiotic treatment. When peripheral pulses are not palpable, urgent vascular assessment is needed and
revascularisation should be considered.2
13. Answer: C
Alcoholic ketoacidosis typically presents in patients with a history of chronic alcohol abuse. These patients usually present with vomiting and abdominal pain 1–3 days after termination of an alcoholic binge. Prolonged vomiting results in severe dehydration and contraction of the extracellular fluid compartment. This is associated with depletion of carbohydrate stores. While ethanol may have initially functioned as a carbohydrate source for gluconeogenesis, the patient is likely to have been abstinent for several days by the time of the presentation, and most chronic alcoholics have poor glycogen stores.
Unlike in DKA, Glasgow Coma Scale (GCS) is usually normal despite metabolic disturbance; confusion or altered level of consciousness should prompt investigation for other pathology. In severe acidosis, ketone bodies exist largely as beta- hydoxybutyrate, which is not detected by Ketostix testing.6
14. Answer: B
While the patient is significantly fluid depleted due to prolonged vomiting, intravenous glucose provides a metabolic substrate, halting ketogenesis and returning the patient to normal.
In contrast, while intravenous saline reduces lactate levels, it may result in elevated beta-hydroxybutyrate levels, paradoxically worsening acidosis. Insulin does not affect resolution. Thiamine (vitamin B1) prevents Wernicke’s encephalopathy and is a cofactor in pyruvate metabolism to glucose.6
15. Answer: B
Vitiligo is an autoimmune disorder, commonly associated with other organ-specific autoimmune
176 CHAPTER 5 EndoCRinE EmERgEnCiEs
disorders including primary adrenal insufficiency (Addison’s disease).
Hyperpigmentation occurs in the presence of primary adrenal failure when adrenocorticotropic hormone (ACTH) levels are elevated in the absence of negative feedback. Elevated ACTH levels stimulate melanin production in skin and mucosa. The most common cause of secondary adrenal insufficiency is chronic glucocorticoid therapy inhibiting ACTH production, and so suppressing primary adrenal function. A careful drug history should be taken, and any recent illness or stress noted. Other sources of hypothalamic–pituitary dysfunction – including pituitary or hypothalamic tumours, infiltrative disorders, severe head trauma and pituitary necrosis or bleeding – may cause secondary adrenal insufficiency. Cushingoid features are usually not found in a patient with Addison’s disease but may be present in a patient who has been on long-term glucocorticoid therapy.7,8
16. Answer: C
Adrenal crisis is a life-threatening emergency that occurs in patients with primary as well as secondary adrenal insufficiency. Features include:
• unexplained hypotension
• circulatory shock (which can be refractory to treatment including vasopressors)
• weakness
• lethargy
• delirium
• hyponatraemia
• hyperkalaemia.
In adrenal crisis there is a severe exacerbation of adrenal insufficiency due to increased physiological demand or decreased supply of cortisol. In vulnerable patients any major stress such as intercurrent illness, sepsis, surgery, major trauma, acute myocardial infarction or acute complete/partial withdrawal of long-term steroids may provoke the crisis. Profound hypoglycaemia is not normally a significant issue in this condition.7,8
17. Answer: A
In suspected adrenal crisis, intravenous fluid
resuscitation should be commenced rapidly to correct fluid loss and hypotension. Both intravenous hydrocortisone and dexamethasone will provide effective steroid replacement, and hydrocortisone
is considered the drug of choice because it has both glucocorticoid and mineralocorticoid actions.
However, hydrocortisone interferes with cortisol assay in the ACTH stimulation test (short
synacthen test) and therefore intravenous dexamethasone may be used for initial treatment if diagnostic testing is planned. Fluid resuscitation should be commenced immediately. Crystalloid containing both normal saline and 5% dextrose is recommended to treat associated hyponatraemia and hypoglycaemia. Specific mineralocorticoid (fludrocortisone) therapy is not usually required if adequate fluid and sodium replacement is delivered, and the patient receives hydrocortisone. Patients unresponsive to fluid resuscitation may require vasopressor treatment to normalise their haemodynamic status.7,8
18. Answer: D
This patient has been treated with long-term steroids and hence there is a high risk of developing adrenal crisis as a result of stress caused by sepsis. As the patient is in septic shock with hypotension, intravenous hydrocortisone may not be adequate to provide adequate mineralocorticoid activity, although it provides adequate glucocorticoid activity. Until shock resolves, both hydrocortisone and fludrocortisone is recommended to prevent adrenal crisis. If the patient is not in shock, intravenous hydrocortisone alone is adequate to provide both glucocorticoid and mineralocorticoid cover. In non-shock situations, intravenous dexamethasone, which mainly provides glucocorticoid cover, can also be used.8
19. Answer: C
Lid lag, lid retraction and proptosis
(exophthalmos) are part of thyroid ophthalmopathy and all seen in Graves’ autoimmune thyroid disease. Lid lag (von Graefe’s sign) is a delay in downward movement of the upper eyelid following the downward-moving iris on directing gaze inferiorly, exposing the sclera above the iris. It may resolve with treatment of the underlying endocrine disorder. Lid retraction (hyperthyroid stare or Dalrymple’s sign) is due to retraction of the upper eyelid more than normal, exposing the globe above the iris. Proptosis due to chronic inflammation and swelling of retro- orbital tissues may precede or succeed the
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proptosis may both continue to deteriorate despite correcting the hormone imbalance. Tarsorrhaphy may be indicated in thyroid ophthalmopathy to protect the cornea from drying and ulceration.7
20. Answer: B
Patients may present acutely with thyrotoxic periodic paralysis. Hypokalaemia is generally present during these attacks, which may be recurrent. The condition is distinct from familial periodic paralysis, a group of inherited disorders.
Graves’ disease is due to a type 2 hypersensitivity reaction, in which IgG antibodies stimulate thyroid cells to produce and release thyroxine. Thyroid ophthalmopathy is due to IgG antibodies provoking a chronic inflammatory cell infiltrate of extraocular muscles. It may predate the onset of clinical hyperthyroidism by several years, or may develop or deteriorate despite successful treatment of the thyroid disorder itself. The development of pretibial
myxoedema (pinkish-brown plaques on the shins) is likewise independent of thyroid status.7
21. Answers: B
Beta-blockers (IV propranolol or esmolol) reduce cardiovascular effects by antagonising effects of thyroid hormones, reducing sensitivity to
catecholamines, and inhibiting peripheral conversion of T4 to T3.
In thyrotoxic crisis, propylthiouracil is given to reduce the synthesis of new hormone in the thyroid gland. It also inhibits the peripheral conversion of T4 to T3, but does not inhibit the release of stored hormone from the thyroid. At least 1 hour after PTU is given, iodine (e.g. Lugol’s iodine, potassium iodide) can be given to stop the release of stored hormone. It decreases iodide transport and oxidation in the follicular cells.
Glucocorticoids (hydrocortisone or dexamethasone) should be given to prevent the peripheral conversion of T4 to T3, and also to manage the risk of relative adrenal insufficiency.
Salicylates are contraindicated because they displace T4 peripherally, exacerbating the crisis.7,10
22. Answer: C
In a patient with previously diagnosed
hyperthyroidism, thyroid storm is a clinical diagnosis. A patient presenting to the ED without this
background diagnosis but with highly suspicious clinical features of thyroid storm should be given careful consideration for a number of important differential diagnoses. These include:
• sepsis
• sympathomimetic abuse such as amphetamine or cocaine
• malignant neuroleptic syndrome
• alcohol withdrawal – delirium tremens
• heat stroke
• hypothalamic stroke
• malignant hyperthermia.
In acute salicylate overdose, the clinical features depend mainly on the dose of ingestion. The typical presentation is with tinnitus, hearing loss, sweating, nausea and vomiting and these occur with mild toxicity. In severe toxicity, altered level of consciousness, tachypnoea, hyperpyrexia and seizures may occur but the overall clinical picture may be different to thyroid storm.5,10
23. Answer: A
Myxoedema crisis is a clinical diagnosis and is precipitated mainly in elderly patients with previously untreated hypothyroidism. Precipitating conditions include underlying infection or sepsis, acute myocardial infarction, heart failure,
cerebrovascular accident (CVA), seasonal exposure to cold environments, post-surgery or multitrauma. Sedative and anaesthetic use may precipitate the condition as well. The main clinical features are due to reduced metabolic rate:
• hypothermia