2. These are -
Diabetic ketoacidosis( DKA)
Hyperglycaemic hyperosmolar state(HHS)
Hypoglycaemia.
ACUTE COMPLICATIONS OF DIABETES
MELLITUS
3. DKA is the end result of the metabolic abnormalities
resulting from a severe deficiency of insulin or
insulin effectiveness.
Diabetic ketoacidosis (DKA) is a medical emergency
and remains a serious cause of morbidity, principally
in people with type 1 diabetes.
DKA
4. Diabetes/hyperglycemia Glucose ≥200 mg/dL (11.1 mmol/L)
or prior history of diabetes
Ketosis -Hydroxybutyrate concentration
ẞ
≥3.0 mmol/L or urine ketone strip 2+
or greater
Metabolic acidosis pH <7.3 and/or bicarbonate
concentration <18 mmol/L
Diagnostic Criteria Of DKA
5. DKA most commonly occurs in people with type 1 diabetes and
can be the first presentation of the condition . It can also occur in
type 2 diabetes, particularly if it has been longstanding or in
individuals who are ketosis-prone (i.e. have significant β-cell
dysfunction) or who have been misclassifed as type 2 rather than
type 1 diabetes.
In established diabetes, DKA may be precipitated by an
underlying illness or physiological stress.
Infection is the most common of these: pneumonia and urinary tract
infection.
Acute myocardial infarction, cerebrovascular disease and pancreatitis are
other common examples of a precipitating illness.
Physiological stress such as surgery, trauma and pregnancy can also be
implicated.
6. The second most common cause of DKA is insulin defciency
due to discontinuation (accidental or deliberate) or inadequate
delivery (error in administration, insulin pump failure, pen
malfunction, out of date or inadequate storage) of insulin.
Drug and social history may reveal glucocorticoid, sodium-
glucose co-transporter 2 (SGLT2) inhibitors or cocaine use, all
of which have been associated with DKA.
In young people with recurrent episodes of DKA, psychological
or personality factors are frequent causes of insulin omission and
infrequent or absent monitoring of glucose levels.
12. DKA is a medical emergency that should be treated in hospital,
preferably in a high-dependency area.
The aims of DKA management
Are to correct circulating volume and electrolyte imbalance
while halting lipolysis and suppressing ketogenesis.
It is important to identify and treat precipitating causes as well as to
prevent complications.
The central tenets of the management of DKA
Include intravenous insulin,
Intravenous fluid
Potassium replacement.
A referral to the diabetes specialist team should be made as early as
possible with review within 24 hours. Regular clinical and
biochemical review is essential, particularly during the first 24
hours of treatment
13. Monitoring for complications is paramount during management.
Vital signs including
Cardiac monitoring should be regularly assessed per protocol:
low oxygen saturations may suggest the development of
pulmonary oedema and acute respiratory distress syndrome
(ARDS).
In children and adolescents, the Glasgow Coma Scale (GCS)
should be monitored hourly for cerebral oedema.
Supportive measures may include nasogastric tube insertion for
persistent vomiting or reduced level of consciousness and urinary
catheter insertion to assess urine output and monitor treatment of
oliguria (<0.5 ml urine/kg/hr).
16. Adequate fluid and insulin replacement should resolve the
acidosis. The use of intravenous bicarbonate therapy is not
generaly recommended (due to lack of evidence of benefit), but
may be considered in the context of a pH of <6.9 folowing
discussion with a senior specialist clinician. Acidosis may
reflect an adaptive response, improving oxygen delivery to the
tissues, and so excessive bicarbonate may induce a paradoxical
fall in cerebrospinal fluid pH; this has been implicated in the
pathogenesis of cerebral oedema in children and young adults.
There is little evidence for intravenous phosphate replacement,
but levels of <0.6 mmol/L are often corrected, particularly in the
presence of respiratory or muscle weakness.
Intravenous bicarbonate and phosphate
17. Ongoing management
Restoration of the usual insulin regimen, by subcutaneous
injection, should not be instituted until the patient is:
(i) biochemically stable and
(ii) able to eat and drink normally.
The fixed rate insulin infusion should be continued for 30
minutes after short-acting (or premixed) insulin is
given at a mealtime. If using an insulin pump, then the
infusion should be started during the daytime at the usual
basal rate (commencement overnight is not recommended
as ward staff may be unfamiliar with this method of insulin
delivery) and the fixed insulin rate infusion should be
continued until the next meal bolus is given.
18. It is important to review the precipitating factors that led to DKA.
Glycaemic control, glucose monitoring, insulin injection technique
and injection sites should all be considered. If insulin pump therapy
is used then it is important to ensure that there is an adequate supply
of equipment, the insulin pump is working (for example not out of
warranty) and that there is access to ‘back up’ insulin within expiry
date via pen injector devices.
DKA prevention should be discussed and written guidance on ‘sick
day rules’ provided or reinforced. A blood ketone meter should be
provided. A telephone number for the diabetes specialist team
should be made available at the point of discharge from hospital.
Given the mortality rates associated with DKA, early educational
assessment and the provision of a personalised management plan
are critical. Specialist psychological support may also be necessary.
19. DKA Complications
Important complications including
Hypoglycaemia
Hypokalaemia
Pulmonary oedema
Acute respiratory distress syndrome
Cerebral oedema
A single episode of DKA is associated with an approximate 5%
risk of death, rising to almost 25% in those with recurrent DKA,
particularly in low- and middle-income countries. Death most
commonly relates to the underlying precipitating illness rather
than direct metabolic complications.
21. HHS is a medical emergency that is a consequence of
prolonged relative insulin deficiency an so requires a
different management approach from DKA.
22. Pathophysiology
I. Relative insulin deficiency and inadequate fluid intake.
II. Insulin deficiency increase hepatic glucose production
through glycogenolysis and gluconeogenesis and impairs
glucose utilization in skeletal muscle.
III. Hyperglycemia induces an osmotic diuresis that leads to
intravascular volume depletion which is exacerbated by
inadequate fluid replacement.
IV. Lower levels of counter regulatory hormones and free fatty
acids have been found in HHS than in DKA.
24. Risk factors for hyperglycemic crises
Type 1 diabetes/absolute insulin deficiency
Younger age
Prior history of hyperglycemic crises
Prior history of hypoglycemic crises
Presence of other diabetes complications
Presence of other chronic health conditions
(particularly in people with type 2 diabetes)
Presence of behavioral health conditions (e.g.,
depression, bipolar disorder, and eating disorders)
Alcohol and/or substance use
High A1C level
Social determinants of health
28. Hypothermia
Hypotension ( systolic BP less than 90 mmHg)
Tachy/ bradycardia
Severe hypernatraemia ( if plasma Na more than 160
mmol/ L.
Plasma osmolarity more than 360 mOsmol/Kg)
Presence of other co-morbidities.
POOR PROGNOSTIC FACTORS OF HHS
29. Arterial thrombosis
Ischemic stroke,
Renal failure , heart failure, multiple organ failure.
Cerebral edema,
Malignant dysrhythmias (due to volume deficiency, which
prompts poor end-organ perfusion),
And Gram negative sepsis (from infection that may have caused
the problem to ensue).
COMPLICATIONS
32. Hypoglaycaemia has been defined by the ADA in 3 distinct levels
Level 1 Glucose <70 mg/dL (<3.9 mmol/L) and ≥54 mg/dL
(≥3.0 mmol/L)
Level 2 Glucose <54 mg/dL (<3.0 mmol/L)
Level 3 A severe event characterized by altered mental
and/or physical status requiring assistance for
treatment of hypoglycemia, irrespective of glucose
level
33. If blood glucose falls , three important primary physiological defense
mechanisms operate :
1. Endogenous insulin release from pancreatic β- cell is suppresed.
2. Release of glucagon from pancreatic α- cell increased.
3. The autonomic nervous system is activated , with release of
cathecholamine both in systemically and in the tissues.
In addition , stress hormone like cortisol and growth hormone are
increased in blood .these action reduced whole body glucose uptake and
increased hepatic glucose production ,maintaining a glucose supply to
brain.
BODY RESPONSE TO HYPOGLYCEMIA
36. Severe hypoglycemia may cause convulsion,coma ,
focal neurological deficit and have a mortality rate of
4% in insulin treated patient .
Sudden death may occurs during sleep due to
hypoglycemia induced cardiac arrhythmia ( dead -in-
bed –syndrome)
CIRCUMSTANCES OF HYPOGLECEMIA
38. For most individuals, the glucose level at which they
first become aware of hypoglycemia is not constant
but varies according to the circumstances in which
hypoglycemia arises (e.g. during the night or during
exercise).
In addition, with longer duration of disease, and
particularly in response to frequent hypoglycaemia,
the threshold for generation of symptom responses to
hypoglycaemia shifts to a lower glucose
concentration.
AWARENESS OF HYPOGLECEMIA
39. This cerebral adaptation has a similar effect on the counter-
regulatory hormonal response to hypoglycaemia. Taken
together, this means that individuals with type1 diabetes may
have reduced (impaired) awareness of hypoglycaemia.
Symptoms can be experienced less intensely,or even be absent
despite blood glucose concentrations below 3.0mmol/L(55
mg/dL). Such individuals are at an especially high risk of
severe hypoglycaemia.
The prevalence of impaired awareness of hypoglycaemia
increases with time; overall, it affects around 20–25%of
people with type 1 diabetes and under 10% with insulin treated
type 2 DM.
