Endocrine emergencies

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.



Assessment


Patients with DKA commonly present with vomiting, polydipsia, polyuria, shortness of breath and abdominal pain. History and examination should be directed at identifying the precipitating event and assessing the degree of dehydration. Most commonly, DKA is precipitated in patients with type 1 diabetes by intercurrent infection, although other causes should be considered (see Box 26.1). It occurs infrequently in patients with non-insulin-dependent diabetes.



Box 26.1 Precipitants of DKA


First presentation of insulin-dependent diabetes


Non-compliance/errors with insulin therapy


Infection—urinary tract, respiratory, gastrointestinal, skin


Other—steroid medication, myocardial infarction, pancreatitis, alcohol abuse, thyroid disease, surgery, pregnancy, trauma


A bedside venous blood sample will confirm the diagnosis by the presence of plasma ketones, acidosis (pH < 7.3 or bicarbonate < 15 mmol/L) and an elevated blood sugar level (BSL) > 12 mmol/L. Urinary ketones will also be present.


Other important investigations include:


• urea, electrolytes, creatinine (UEC)—potassium depletion is common and creatinine may be elevated

• FBE—elevated white cell count (WCC) suggests infection

• midstream urine for microscopy and culture

• blood culture if febrile

• liver function tests, amylase and lipase if abdominal pain

• ECG for silent myocardial infarction or arrhythmias

• chest X-ray (CXR) for respiratory infection.


Management


Patients with DKA are often extremely ill and should be initially managed in an area of the emergency department with continuous ECG and oximetry monitoring, and regular blood pressure measurements. If there is a depressed level of consciousness the patient requires supportive airway management and may need intubation. Ongoing regular measurement of BSL and serum K+ should continue throughout treatment.



Fluid and electrolyte therapy


All patients with DKA are volume depleted and require rehydration with intravenous fluids. Hypotension (systolic BP < 100 mmHg) should be treated with boluses of normal saline up to 2000 mL until blood pressure has improved. In the normotensive patient, 1 litre of normal saline should be given over the first hour, followed by a second litre over the next 2 hours. Subsequent fluid therapy will be guided by clinical assessment of pulse rate and hydration status, but most patients will require 5–8 litres of fluid over the first 24 hours. A dextrose-containing solution should be commenced once the BSL falls below 15 mmol/L, in addition to ongoing sodium requirements.


Potassium depletion is a feature of DKA, even in the presence of an initial elevated serum K+. Serum potassium should be measured as soon as possible and is often available on the initial blood gas. The administration of intravenous fluids and insulin will rapidly lower the measured K+. If the initial K+ is > 5.5 mmol/L, the level should be rechecked every 30–60 minutes as it will inevitably fall as a consequence of rehydration. Table 26.1 outlines the rate of potassium replacement. Monitoring of K+ levels every 1–2 hours is essential during the initial phase of treatment.


Table 26.1 Guide to potassium replacement in DKA















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.

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Jun 14, 2016 | Posted by in EMERGENCY MEDICINE | Comments Off on Endocrine emergencies

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