Professional Documents
Culture Documents
Diabetic complications
Review
This article has been double-blind
Diabetes peer reviewed
Management of diabetic
ketoacidosis in adults
In this article... 5 key
pidemiology and pathophysiology of diabetic ketoacidosis
E
points
Guidance on diagnosis, management and complications 1 The majority of
patients
presenting with
The nurses role in caring for patients with DKA
diabetic
ketoacidosis have
Authors Georgia Noble-Bell and Alison of the pathophysiology of DKA and type 1 diabetes
Cox are diabetes specialist nurses at Kings
College Hospital, London.
Abstract Noble-Bell G, Cox A (2014)
advances in the clinical management.
Many cases could be prevented by better
access to medical care, education and
2 Patients with
type 2 diabetes
can develop DKA,
Management of diabetic ketoacidosis in effective communication between patients especially during
adults. Nursing Times; 110: 10, 14-17. and health professionals during concur- acute illness
Ketoacidosis is a serious complication of
diabetes. It is commonly precipitated by
poor adherence to medication, stress and
rent illness (Kitabchi et al, 2004).
Pathophysiology
3 Infection is the
most common
precipitating factor
concurrent illness; it can be life threatening DKA results from a dysregulation of carbo- for DKA
if it is not addressed quickly and
effectively. This article discusses the
pathophysiology, diagnosis and
hydrates, protein and lipid metabolism
(Yehia et al, 2008) and usually occurs as a
consequence of absolute or relative insulin
4 Clinical signs
of DKA include
polyuria,
management of the condition, and deficiency accompanied by an increase in polydipsia,
highlights the nurses role in this. counter-regulatory hormones (glucagon, weakness, fatigue,
D
catecholamine, cortisol, growth hormones weight loss,
iabetic ketoacidosis (DKA) is a and epinephrine), which contribute to vomiting and
serious and potentially life- increased blood glucose levels and insulin abdominal pain
threatening complication of
diabetes (Joint British Diabetes
Societies, 2013). It is a complex disordered
resistance.
The combination of insulin deficiency
and increased counter-regulatory hor-
5 DKA is a
medical
emergency
metabolic state characterised by hypergly- mones leads to alteration in glucose pro-
caemia (elevated blood glucose), acidosis duction and use, increased lipolysis
(pH imbalance) and ketonaemia (excess (breakdown of fatty acids to form alternate
ketones in the blood). source of energy) and production of ketone
Although the majority of patients pre- bodies (Umpierrez et al, 2002). An increase
senting with DKA have type 1 diabetes, in hepatic gluconeogenesis (production
those with type 2 diabetes can also develop of glucose from non-carbohydrate
the condition, especially during acute ill- sources) and glycogenolysis (breakdown
ness (Umpierrez et al, 2002). People from of glycogen to glucose), renal glucose pro-
non-Caucasian ethnic groups are more duction and impaired glucose use in
likely to develop DKA in the presence of peripheral tissues leads to severe hypergly-
type 2 diabetes (Yehia et al, 2008). caemia (JBDS, 2010). An increase in free
While the incidence of DKA is difficult fatty acids in circulation as a result of
to establish, population-based studies lipolysis enhances hepatic production
suggest an annual incidence of 4.6-8.0 epi- of ketone bodies, which result in keto-
sodes per 1,000 patients with diabetes naemia and metabolic acidosis (Kitabachi
(Faich et al, 1983); the worldwide mortality et al, 2004).
rate is 2-10% (Yehia et al, 2008). Over the Dehydration and electrolyte imbal-
past 20 years, mortality rates in developed ances occur in DKA as a result of several
countries have fallen from 7.96% to 0.67% mechanisms. Hyperglycaemia causes fluid Signs of dehydration, including decreased
Alamy
(Lin, 2005) due to a better understanding and electrolytes to shift from the skin turgor, are often seen in DKA
Box 1. Criteria for state can vary from full alertness to pro-
Box 2. Criteria for found lethargy (Umpierrez et al, 2002).
diagnosing DKA high dependency care
Ketonaemia 3mmol/L (normal Patients exhibiting one or more of these Laboratory investigations
values: <0.6) or significant ketonuria signs should be assessed by a Although DKA can be suspected on clin-
(>2+ on standard urine dipstick) consultant physician and considered for ical observations, confirmation of the
Blood glucose >11mmol/L (normal referral to a high dependency unit: diagnosis is based on laboratory findings.
values: 3.5-7.8mmol/L) or known Blood ketones >6mmol/L The syndrome of DKA consists of the
diabetes Bicarbonate level <5mmol/L biomedical triad of hyperglycaemia, keto-
Bicarbonate blood levels (HCO3) Venous/arterial blood gas <7.0 naemia and metabolic acidosis (JBDS, 2013;
<15 mmol/L (normal values: Hypokalaemia (low potassium) on Umpierrez et al, 2002). The laboratory
22-26mmol/L) and/or venous pH <7.3 admission (3.5mmol/L) investigation in DKA includes measure-
(normal values: 7.35-7.45) Glasgow Coma Scale <12 or abnormal ment of:
AVPU assessment scale Venous blood glucose;
Source: JBDS (2013) Oxygen saturation <92% on air Electrolytes, urea, creatinine, osmo-
(assuming normal baseline respiratory larity and ketones;
function) Urinalysis for ketones;
Systolic BP <90mmHg Blood tests for infection markers;
intracellular to the extracellular space, Pulse rate >100 or <60bpm Venous blood gas values.
leading to cellular dehydration and elec- Further investigations may be carried
trolyte imbalance. Both hyperglycaemia Source: JBDS (2013) out to identify potential infection or myo-
and high ketone levels also cause osmotic cardial infarction as precipitating factors
diuresis, resulting in further dehydration; for DKA; these tests may include complete
vomiting is commonly associated with 24 hours), but the signs and symptoms of blood count, blood cultures, cardiac
DKA and contributes to fluid depletion poor glycaemic control may be evident for enzymes and ECG (Kitabchi et al, 2004).
and electrolyte imbalances (JBDS, 2013). several days before this (Kitabchi et al, Clinical presentation and laboratory
2006). These include polyuria, polydipsia, investigations usually provide the infor-
Precipitating factors weakness, fatigue and weight loss. Vom- mation needed to diagnose DKA. It is
About one in five adults with type 1 dia- iting and abdominal pain are frequently important to remember that not all
betes initially present with DKA (Ump- the presenting symptoms in DKA (Kearney patients who present with ketoacidosis
ierrez et al, 2002). Common precipitating and Dang, 2007). have DKA (Umpierrez et al, 2002) so when
factors for DKA in those with established On physical examination, signs of diagnosing DKA, other causes of ketosis
diabetes are infection, poor adherence to dehydration are often present, including should be considered, including starva-
medication, psychological stress and con- dry mucus membranes, decreased skin tion ketosis and alcohol ketoacidosis
current illnesses (Umpierrez et al, 2002; turgor, tachycardia and hypotension. In (Yehia et al, 2008; Umpierrez et al, 2002).
Delaney et al, 2000). addition the smell of acetone on the breath Other differential diagnoses include lactic
Infection is the most common precipi- and deep and laboured breathing (Kuss- acidosis, renal failure and drug intoxica-
tating factor for DKA and occurs in about maul breathing) may be observed, particu- tion (Yehia et al, 2008). Box 1 outlines the
30-50% of adult cases; other acute condi- larly in patients with severe acidosis. This JBDS (2013) criteria for diagnosing DKA.
tions that may precipitate DKA include change in breathing is an attempt by the DKA is a medical emergency and should
cerebral vascular accident, alcohol/drug body to correct the metabolic acidosis and be managed promptly (JBDS, 2013). It is
misuse, pancreatitis, myocardial infarc- compensatory respiratory alkalosis (Yehia important to assess for severity to deter-
tion and trauma (Umpierrez et al, 2002). et al, 2008; Umpierrez et al, 2002). Mental mine the clinical setting in which the
Recent studies have identified the sig- patient is to be managed; criteria are out-
nificance of medication non-adherence lined in Box2.
and psychological factors in DKA (Ump- Box 3. Key management
ierrez et al, 2002). High incidences of DKA points Management
related to medication non-adherence have The management of patients presenting
been identified in subgroups with type 1 Fluid resuscitation with 0.9% sodium with DKA includes a full clinical assess-
diabetes, including young women with chloride ment, while regular monitoring of vital
psychological problems such as eating dis- Insulin infusion (fixed-rate intravenous signs and consciousness levels using the
orders (Umpierrez et al,2002). insulin infusion) at 0.1 unit/kg/hr Glasgow Coma Scale is essential (JBDS,
Other risk factors include poor gly- Close monitoring of vital signs, blood 2013). Key areas in the management of DKA
caemic control, clinic non-attendance and glucose, ketones, electrolytes and blood include:
lower socioeconomic status (Wright et al, gases Restoring circulatory volume;
2009). The JBDS (2010) has also highlighted Continue FRIII until DKA has resolved Insulin therapy (fixed-rate intravenous
a lack of self-management skills as another before converting to subcutaneous insulin infusion);
risk factor associated with recurrent DKA. insulin Correcting metabolic acidosis and
Give background insulin alongside IV electrolyte imbalances;
Clinical presentation and to prevent rebound hyperglycaemia Identifying and treating precipitating
diagnosis Involve the diabetes specialist team as factors;
The metabolic abnormalities associated soon as possible Early involvement of the diabetes
with DKA develop rapidly (usually within specialist team (JBDS, 2013).
Key management points are summa- along with the IV insulin infusion to cerebral oedema and fluid overload is vital
rised in Box 3. reduce the risk of rebound hyperglycaemia (JBDS, 2013).
when the IV insulin infusion is discon-
Restoring circulatory volume tinued. If background insulin is discon- The diabetes specialist team
Fluid replacement is one of the most tinued, a subcutaneous dose must be given The JBDS (2010) stipulates that the diabetes
important initial therapeutic interven- before the IV insulin infusion is discon- specialist team must be involved in the
tions in the management of DKA. Patients tinued (JBDS, 2013). The conversion to the management of every patient admitted
are usually dehydrated and correcting this subcutaneous insulin regimen should be with DKA, and referral should be made as
deficit will result in significant metabolic planned around a mealtime; subcutaneous soon as possible during the acute phase.
improvement (Kitabchi et al, 2004). The short-acting insulin should be given at the The teams involvement is necessary to
aims of fluid resuscitation are to: meal and then IV insulin discontinued one improve safety and reduce length of stay
Restore circulatory volume; hour later (JBDS, 2013). (Sampson et al, 2006). Team members play
Clear ketones; an important role in assessing the precipi-
Correct electrolyte imbalance (JBDS, Correcting metabolic acidosis and tating cause of DKA, acute management,
2010). electrolyte imbalance discharge planning, education and follow-
Pulse and blood pressure should be The JBDS (2010) recommends the fol- up care including psychological support
used to assess the severity of dehydration, lowing metabolic treatment targets for (JBDS, 2010).
as hypotension (systolic BP<90mmHg) is DKA: The best-practice tariffs stipulate that
likely to be due to low circulatory volume. Reduction in blood ketones of at least people admitted with DKA must be
Other causes such as heart failure, sepsis 0.5mmol/L/hr; referred to the diabetes team and be seen
and factors such as age, sex and medica- Increase in venous bicarbonate by by a member of the team within one
tion history should also be taken into con- 3mmol/L/hr; working day of admission (Price et al, 2013).
sideration (JBDS, 2013). Reduction in capillary blood glucose by
Normal saline (0.9% sodium chloride) is 3mmol/L/hr; The nurses role
recommended for fluid resuscitation Maintenance of serum potassium at All health professionals involved in caring
(JBDS, 2013). Rapid fluid replacement is 4-5.5 mmol/L. for patients with DKA have a responsi-
usually required in the first few hours of Blood glucose, ketones, electrolytes, bility to ensure safe delivery of patient care
treatment; most patients require between including bicarbonate, and venous pH, in accordance with local and national clin-
500ml and 1L to be given rapidly (JBDS, should be monitored closely at or near the ical guidelines.
2013). However, the rate of fluid replace- bedside. If the above targets for blood Some of the roles and responsibilities
ment must be tailored to patients clinical ketones and/or bicarbonate are not reached, for nurses include:
situation. Special attention must be paid the rate of the IV insulin infusion should Ongoing clinical assessment of the
to fluid balance in patients at high risk of be increased by 1 unit every hour until met- patient: this involves regular (at least
complications these include older abolic targets are achieved (JBDS, 2013). hourly) monitoring of vital signs and
people, pregnant women, children and level of consciousness during the acute
young people (18-25 years), and those with Potassium phase (JBDS, 2013).The early warning
heart and kidney failure (JBDS, 2010). Maintaining normal serum potassium and score system should be used as a guide
prevention of hypoglycaemia are impor- to determine the patients clinical
Insulin therapy tant in the management of DKA as hypoka- condition and response to treatment,
The aim of insulin therapy in DKA man- laemia (low potassium level) and hyper- and escalated to senior or specialist
agement is to suppress ketogenesis, kalaemia (high potassium level) are both colleagues or medical team as
reduce blood glucose and correct electro- life-threatening conditions and common appropriate;
lyte imbalance. Insulin therapy increases complications. Accurate monitoring of fluid balance:
peripheral glucose use and decreases Serum potassium is often high on this includes accurate intake and
hepatic glucose production, thereby low- admission but falls rapidly with insulin output charts (JBDS, 2013). Prescribed
ering blood glucose concentration. It treatment, so regular monitoring is essen- fluids should be administered and
inhibits the release of free fatty acids from tial and potassium should be added to IV patients monitored for signs of
adipose tissues and decreases ketogenesis infusions if serum potassium is complications related to fluid overload,
(Umpierrez et al, 2002). <5.5mmol/L (JBDS, 2013). dehydration and electrolyte imbalance;
A continuous fixed-rate intravenous Insulin therapy: this should be
insulin infusion (FRIII) of 0.1 units/kg/hr is Capillary blood glucose administered as prescribed;
recommended (JBDS, 2013). The recom- Prevention of hypoglycaemia is vital, so Regular monitoring of capillary blood
mendation for preparation of insulin infu- bedside blood glucose monitoring should glucose and ketones: this is required at
sion is 50 units of human soluble insulin be performed every 1-2 hours (JBDS, 2010). least hourly (JBDS, 2013) during the
made up with 50ml normal saline (0.9% It is sometimes necessary to give dextrose acute phase. Nurses should liaise with
sodium chloride) (JBDS, 2013). FRIII should infusions to stabilise blood glucose levels; the medical team for appropriate
continue until DKA is resolved. When the this should be given concurrently with the adjustment to insulin doses as
blood ketones are <0.6mmol/L, pH >7.3 and sodium chloride infusions used to correct required;
the patient is able to eat and drink, an circulatory volume (JBDS, 2010). Monitoring of metabolic acidosis and
appropriate subcutaneous insulin reg- To avoid complications related to rapid electrolytes: this involves liaising with
imen should be recommenced (JBDS, infusion it is important to monitor fluid the medical team to ensure blood gases
2013). The JBDS (2013) recommends that balance and electrolytes closely. Regular and appropriate blood tests are carried
background insulin should be continued assessment for complications such as out regularly, results interpreted and
Times.net
go to nursingtimes.net/criticalcare