Severe dehydration in a young woman

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Problem 48 Severe dehydration in a young woman

Sanghamitra Guha

An 18-year-old girl is brought into the emergency department by ambulance from a youth hostel. She is a backpacker and has been travelling around the country. She is drowsy and unable to give any history. Her airway is clear and her breathing is unhindered. She reacts purposefully to painful stimuli, moving all limbs, and grunts but does not speak. She opens her eyes briefly in response to you shouting her name.

Q.1

What is her Glasgow coma score?

She is of normal build and is well kept. Her temperature is 37.5°C, her pulse rate is 135 bpm and her supine blood pressure is 95/60 mmHg. She has deep sighing respirations with a respiratory rate of 25 breaths/minute. Her mouth is extremely dry and her tissue turgor is reduced. She has no other abnormalities on cardiac and respiratory examination, and she has no focal neurological signs. Her abdomen is not distended but appears guarded and she reacts as if in pain when palpated. Bowel sounds cannot be heard.

Another girl appears who says she is a companion from the hostel. The two have only known each other for 2 weeks and agreed to travel together. The girl claims her friend became unwell over the last week, particularly over the last 2 days. She complained of being very tired. The patient had become lethargic and listless. She had not wanted to eat, but had complained of being very thirsty and had been drinking large amounts of water. Today she stayed on her bunk and was unable to get up. She complained of abdominal pain and vomited three times. The friend had gone out for a few hours and on her return found the patient looking very unwell and an ambulance had been called. The patient is not known to have any major medical problems or to take medications or drugs of any kind.

Q.2

Provide a differential diagnosis.

There are a number of possible causes for this woman’s comatose state.

Q.3

What should be done immediately?

A finger-prick blood glucose measurement has been obtained using a bedside glucose meter and reads ‘high’. A urinary catheter drains 50 mL urine which, when tested with a strip, registers ketones as ++++. After initial resuscitation, results of the preliminary blood tests come back as follows:

Investigation 48.1 Summary of results

Q.4

What are the abnormalities? How do they help in clarifying your differential diagnosis?

You have a working diagnosis for this patient who is critically ill.

Q.5

What is your acute management plan?

You institute emergency management. An intravenous line is inserted, and she is managed in the high dependency ward with close nursing care to monitor all vital signs and to keep the airway clear. The patient’s urine output is regularly charted to establish that renal function is normal and urine production is taking place. An insulin infusion is commenced.

In addition to your fluid replacements, the electrolytes are checked after 2 hours to measure the potassium concentration. It is now 3.6 mmol/L and you begin to add potassium supplementation to the intravenous infusion at 13.6 mmol and later to 27.2 mmol (1–2 g KCl) per hour. You check her potassium level again at 4 hours and 8 hours. A chest X-ray is performed and urine microscopy sent off to look for any intercurrent infection. After 12 hours the patient’s blood glucose is down to 15 mmol/L. The intravenous fluid is changed to 5% dextrose 1 L over 6 hours with 2 g KCl added to each litre of fluid.

Twenty-four hours later your patient’s condition has significantly improved. She is fully conscious, no longer vomiting or nauseated and is allowed to start eating. The urine shows only a trace of ketones.

Q.6

How will you change her insulin therapy now?

She responds well to your insulin regimen, and is stable for discharge. Further history establishes that she has previously been healthy: now she has a diagnosis of diabetes. She is frightened by what has happened, and anxious about her diabetes management.

Q.7

Describe your ongoing management plan for this patient while she is in hospital and prior to discharge.

The patient decides to curtail her backpacking holiday and return home.

Answers

A.1 Her Glasgow coma score is 11 (E4, V2, M5).

A.2 Given her young age, history of polydipsia and clinical evidence of dehydration and hyperventilation, the most likely diagnosis is diabetic ketoacidosis. Abdominal pain is quite common in this condition and does not indicate any acute abdominal problem (although intra-abdominal problems must be considered in the differential diagnosis). Other diagnoses to consider include poisoning (alcohol, food or drug-related, particularly street drugs) and infection (e.g. meningitis).

A.3 As part of the immediate management, the following must be undertaken:

• Protect the airway.

• Insert an intravenous cannula and take blood for electrolytes, urea and creatinine, blood glucose, complete blood picture, lipase.

• Collect a finger-prick blood sample for glucose estimation and, if available, ketone measurement.

• Perform an arterial blood gas assay to obtain the pH and ascertain if patient is acidotic.

• Insert a urinary catheter and check for urinary ketones and measure the urine output.

• Commence emergency resuscitation with intravenous infusion of isotonic saline. At least 1–1.5 litres should be given over the first hour.

A.4 The patient has a severe metabolic acidosis as characterized by the low serum pH and low bicarbonate level. The low pCO₂ is due to respiratory compensation for the metabolic acidosis. This explains the hyperventilation.

The increased anion gap is due to the presence of anions not measured in the calculated anion gap. This ‘hidden’ anion here is ketone bodies.

Metabolic acidosis can be divided into:

• High anion gap acidosis (addition of anions to the blood, e.g. ketoacidosis, lactic acidosis and salicylate or alcohol poisoning).

• Normal anion gap acidosis with a high chloride level, usually as a result of loss of alkali (bicarbonate), for example from the gut with severe diarrhoea or in renal tubular acidosis.

The apparent hyperkalaemia is due to the shift of potassium from the intracellular space to the extracellular space caused by the acidosis (potassium in exchange for hydrogen ions). In spite of the elevated serum potassium, these patients are usually depleted of total body potassium. This is an important point to grasp. Large amounts of potassium are lost via the kidneys as a result of the glucose diuresis and also through vomiting. The serum potassium level will need careful monitoring as it will drop rapidly when treatment with insulin is commenced and the acidosis starts to correct, placing the patient at risk of hypokalaemia and arrhythmias.

Hyperglycaemia is consistent with the diagnosis of diabetes and is a marker of insulin deficiency. The glucose level, though usually elevated in patients with ketoacidosis, may not be particularly high nor at the levels generally seen in patients with hyperosmolar non-ketotic coma.

Leucocytosis is seen quite commonly in association with ketoacidosis and does not necessarily indicate infection. Infections are common triggers for ketoacidosis, and patients should be checked for septic foci once their resuscitation has started.

The combination of the clinical picture, hyperglycaemia, metabolic acidosis with high anion gap and ketones in the urine confirms the diagnosis of diabetic ketoacidosis.

A.5 Diabetic ketoacidosis is an acute medical emergency, requiring rapid diagnosis and treatment. These patients are critically ill and need specialized care and close monitoring. The patient’s vital signs must be observed regularly, and recorded along with fluid input and output and bedside blood glucose monitoring. If the patient’s potassium concentrations are significantly abnormal cardiac monitoring may be needed. Ketoacidosis may induce gastroparesis and the patient should be kept fasted to minimize the risk from gastric aspiration.

Fluid and Sodium Replacement

• Severe dehydration is common. This is secondary to the osmotic diuresis (hyperglycaemia and ketonuria) compounded by vomiting and hyperventilation. The degree of dehydration needs to be assessed both clinically and biochemically.

• Sodium depletion is common. This is consequent on the diuresis (although the serum sodium level may appear normal).

• Rehydration is started with isotonic saline. For example, give 1 L/hour for 2 hours then a third litre over the following 4 hours. The severely dehydrated patient may need up to 6 litres of fluid in the first 24 hours.

After 12 hours (or once the blood glucose has dropped to 13 mmol/L), fluid replacement can be changed to 5% dextrose.

Urine output should be monitored (an indwelling bladder catheter can be placed as part of the initial resuscitation). Hypovolaemia and the risk of acute renal tubular necrosis must be minimized. During the osmotic diuresis, the urine output must be matched on a regular basis with intravenous fluid replacement. Once the dehydration has been corrected, an output of at least 30 mL/hour must be maintained.

Correction of Acidosis and Hyperglycaemia with Insulin

Insulin therapy will correct both the acidosis and hyperglycaemia.

Continuous intravenous infusion of insulin using an insulin pump at 4–8 units per hour is the best method of delivering insulin. Rapid changes in pH, glucose and potassium are thus avoided, thereby preventing complications such as cardiac arrhythmias and cerebral oedema.

If infusion is not possible hourly intramuscular doses may be used; subcutaneous insulin therapy should not be used in the acute treatment of diabetic ketoacidosis particularly in significantly dehydrated patients because of the unreliable rate of insulin absorption.

Blood glucose must be monitored hourly using a bedside glucose meter while patient is receiving intravenous insulin infusion.

The use of bicarbonate is generally not required in the treatment of diabetic ketoacidosis. The metabolic acidosis is corrected by rehydration and by cessation of ketogenesis with the use of insulin.

Potassium Replacement

Rapid shifts in potassium will occur once treatment for ketoacidosis is started. Use of insulin and correction of the acidosis will cause shift of potassium back from the extracellular to the intracellular space. As the patient is depleted of total body potassium, the drop in serum potassium can be potentially life threatening.

• Replacement potassium can commence with the second litre of saline – provided the initial serum potassium was in the normal range.

• If the initial potassium level is high, recheck the potassium after 2 hours of intravenous saline infusion and commence potassium replacement as soon as the serum potassium is in the normal range (do not wait till hypokalaemia has occurred to start potassium replacement).

• Potassium replacement in range of 10–20 mmol/L/hour (1 g KCl = 13.6 mmol). This rate is likely to be required for the first 12 hours. Be prepared to increase this rate if serum potassium is not being maintained in the desirable range.

• Check serum electrolytes every 2–4 hours for the first 24 hours. Insertion of a central line allows repeated drawing of blood without venepuncture as well as monitoring of central venous filling.

• Ensure adequate urine output has been established. If the patient is not producing urine they may be in acute renal failure, and potassium replacement may need to be modified.

Diagnosis and Treatment of Precipitating Events

Once resuscitation of the acute metabolic state is underway it is important to look for any precipitating event that may have triggered the onset of ketoacidosis. In this patient’s age group the commonest causes are either infection or omission of insulin. Investigations should be performed for chest, urinary tract, skin and gastrointestinal infections.

Prevention of the Complications of Ketoacidosis

• Cerebral oedema is a rare but dangerous complication; it can be prevented by careful fluid balance and avoiding dramatic drops in blood glucose levels.

• Aspiration of gastric contents can be prevented by careful nursing and keeping the patient fasting until she is fully conscious and has bowel sounds.

• Thrombosis is a relatively common complication; anticoagulation until the patient is mobile may need to be considered.

A.6 You are now able to change the patient to subcutaneous insulin using a bolus of short-acting insulin with each main meal and a long-acting insulin to provide basal cover. (Some patients may wish to consider a subcutaneous insulin infusion pump.)

Insulin infusion is ceased 1 hour after the first dose of subcutaneous insulin is given.

A.7 Once the acute event of the ketoacidosis is over a long-term management plan for the ongoing treatment of the patient will need to be developed. In this patient ketoacidosis was the mode of first presentation of her diabetes. During hospitalization she might not be able to fully comprehend the diagnosis and its implications. She would not be reasonably expected to assimilate all the information that she needs to manage her diabetes. Therefore she should be given the necessary information to enable her to manage her diabetes in the immediate future with further education to occur as an outpatient. Diabetes nurse educators should be contacted to assist with her education.

In Hospital:

• She needs to be commenced on a basal/bolus insulin regimen using short-acting insulin before each main meal and basal insulin at bedtime. She should be taught the action of the different insulins that she will be using. (A starting dose of insulin may be estimated using the calculation of 0.3–0.5 unit insulin per kg of body weight per 24 hours split half into basal and half to be divided into the three bolus doses.)

• She needs to be taught to recognize the symptoms of hypoglycaemia and instructed on how to prevent and treat hypoglycaemia.

• She needs to understand that she should not omit her insulin therapy.

• She should be taught how to self-administer insulin using syringes or an insulin pen device. Diabetes nurse educators will be important in helping her cope with these and other issues.

• She should be taught how to use a personal blood glucose monitor and how to interpret the readings that she obtains. She needs to understand what factors affect blood glucose levels, e.g. food, exercise, insulin dose. She should learn to keep a record of her blood glucose.

As an Outpatient

• A diet plan is important with basic knowledge on the appropriate food types. A balanced diet with complex carbohydrates should be encouraged and simple sugars avoided. The diet should have less than 30% as fat. Most importantly she should understand the necessity to eat regularly with an even spread of carbohydrates over the day and not to miss meals. Between-meal snacks and supper will need to be taken.

• She should be advised to be very moderate with alcohol consumption and to ensure that she eats adequate carbohydrate-type food when she drinks alcohol.

• She should be taught how to recognize the symptoms of hypoglycaemia and what the appropriate treatment is.

• She should be given information on how travelling can affect diabetes and what steps she needs to take.

• The patient needs to understand that diabetes is a lifelong disease that needs to be managed well to prevent long-term complications. However, details of long-term treatment and prevention and monitoring of long-term complications can be given at a later date when she is getting used to her condition.

• She should be strongly advised to seek referral to a specialist diabetes centre on her return to her home country to continue her diabetes management and education.

• If she drives a car, her licence may be affected and she will need to contact the appropriate authority.

Revision Points

Diabetic Ketoacidosis

Diabetic ketoacidosis is an acute medical emergency that is potentially life threatening but completely reversible if diagnosed and treated rapidly.

With aggressive and early management of ketoacidosis in recent years the mortality rate from ketoacidosis has been markedly reduced to less than 5%.

Ketoacidosis can occur as the first presentation of a patient with type 1 diabetes or as a complication in a patient known to have the condition. It occurs in type 1 diabetics when there is absence or insufficiency of insulin due to:

• Failure to administer insulin; or

• An increased need for insulin at times of physical stress (e.g. an intercurrent infection, trauma, surgery, etc.).

Aetiology

Insufficient insulin leads to uncontrolled gluconeogenesis and impaired peripheral glucose utilization, both of which result in hyperglycaemia and glucosuria. A severe osmotic diuresis results leading to loss of fluid and electrolytes. Insulin deficiency also leads to the formation of ketone bodies which are strong acids leading to a metabolic acidosis.

Clinical Features

• Polydipsia.

• Anorexia, nausea and vomiting.

• Long sighing respiration (Kussmaul breathing).

• Sweet-smelling ketotic breath.

• Clinical signs of dehydration.

• Coma (in severe cases).

Treatment

Intravenous insulin infusion allows a gradual and steady correction of the metabolic abnormalities.

Complications

• Electrolyte disturbances as indicated above (particularly hypokalaemia).

• Hypoglycaemia.

• Infections such as aspiration or stasis pneumonia and urinary tract infection from indwelling catheters.

• Thrombosis risk may require short-term anticoagulation.

• Gastric dilatation and haemorrhage.

• Ominous but fortunately rare complications include adult respiratory distress syndrome and the cerebral dysequilibrium syndrome from cerebral oedema.

Follow-up

Patients must be encouraged to learn and perform regular home blood glucose monitoring for day-to-day adjustment of their insulin regimen, while their longer-term glycaemic control can be monitored by measuring the glycosylated haemoglobin (HBA1c).

Macrovascular complications leading to ischaemic heart disease, cerebrovascular disease and peripheral vascular disease can also be significantly reduced by concomitantly treating hypertension and hyperlipidaemia and urging patients to stop smoking.

Patients with type 1 diabetes should be followed in specialized diabetes centres if possible, where multidisciplinary care is available from endocrinologists, diabetes nurse educators, dieticians and podiatrists.

The achievement of optimal control of diabetes is especially important in young patients with type 1 diabetes such as this patient as there are now impressive data to show that the long-term microvascular complications (retinopathy, nephropathy and neuropathy) are significantly reduced with good blood glucose levels.

Young women such this patient should be counselled in avoiding unplanned pregnancy as it is important for the diabetes to be optimally controlled prior to conception to achieve the best outcome for both mother and baby. Contraception should be encouraged if the patient is sexually active and not planning pregnancy. Patients with diabetes may face restrictions with their driving licences and need to apply annually for licence renewal.

Future developments in the management of diabetes range from glucose-monitoring devices which do not require finger punctures, new insulin analogues, new insulin delivery methods such as inhaled insulin, pancreas transplantation, in islet cell transplantation and possible gene therapy to replace insulin-producing cells in patients with type 1 diabetes. However, the current imperatives remain to assist patients in achieving the best control of diabetes to prevent both short-term problems such as ketoacidosis and long-term complications such as blindness, renal failure, etc.

Issues to Consider

• How do you manage a type 2 diabetic patient in hyperosmolar non-ketotic state?

• What new drugs are becoming available for the treatment of type 1 and type 2 diabetes?

Further Information

www http://emedicine.medscape.com/article/766275-overview. A tutorial on the emergency management of diabetic ketoacidosis

www www.diabetesnet.com. A patient-focused website dealing with many of the practical aspects of living with diabetes, including information on the newer insulins

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