Academic discussion/ Lecture class for 5th year MBBS students on Diabetic Emergencies, types, their sign-symptoms and managements. Most of the Data was taken from Davidson's Principles and Practice of Medicine.

1. Diabetic Emergencies
Dr Md Mamunul Abedin
Medical Officer
General Hospital, Jamalpur

2. Diabetic Emergencies
Diabetic ketoacidosis (DKA)
Hyperglycaemic hyperosmolar state
Hypoglycemia

3. DKA
 Diabetic ketoacidosis (DKA) is a medical emergency,
principally occurring in people with type 1 diabetes.
 Mortality is higher in developing countries and among non-
hospitalized patients.
 May be the presenting feature of diabetes
 May be precipitated by stress, particularly infection, in those
with established diabetes. Sometimes, DKA develops
because of errors in self-management.

4. DKA- Cardinal Features
The cardinal biochemical features of DKA are:
Hyperketonaemia (≥ 3.0 mmol/L) or ketonuria
Hyperglycaemia (blood glucose ≥ 11mmol/L)
Metabolic acidosis (venous bicarbonate < 15
mmol/L and/or venous pH < 7.3 (H+ > 50 nmol/L))

5. DKA- Pathophysiology
Hyperglycaemia causes an osmotic diuresis,
leading to dehydration and electrolyte loss.
Ketosis is caused by insulin deficiency, exacerbated
by stress hormones (e.g. catecholamines), resulting
in unrestrained lipolysis and supplying FFAs for
hepatic ketogenesis.

6. DKA- Pathophysiology
When ketosis exceeds the capacity to metabolise acidic
ketones, these accumulate in blood. The resulting
acidosis forces H+ ions into cells, displacing K+ ions,
which are lost in urine or through vomiting.
Patients with DKA have a total body K+ deficit but this is
not reflected by plasma K+ levels, which may initially be
raised due to disproportionate water loss.
Once insulin is started, however, plasma K+ can fall
precipitously due to dilution by IV fluids, K+ movement
into cells, and continuing renal loss of K+.

7. DKA- Water & Electrolyte Loss

8. DKA- Clinical Features

9. DKA- Clinical Features

10. DKA- Investigations
The followings are important but should not delay IV fluid
and insulin replacement:
Urea &Electrolytes,
Blood glucose,
Plasma bicarbonate (< 12 mmol/L indicates severe acidosis).
Urine and Plasma for Ketones.
ECG.
Infection screen: FBC, blood/urine culture, CRP, CXR.

11. DKA- Emergency management
 Establish IV access, assess patient and perform initial investigations
Commence 0.9% Sodium Chloride:
-If systolic BP > 90 mmHg, give 1 L over 60 mins
-If systolic BP < 90 mmHg, give 500 mL over 10–15 mins,
then re-assess; if BP remains < 90 mmHg, repeat and seek
senior review.
Commence insulin treatment:
50 U human soluble insulin in 50 mL 0.9% NaCl infused
intravenously at 0.1 U/kg body weight/hour
-Continue with SC basal insulin analogue if usually taken by
patient.
0 – 60
min

12. DKA- Emergency management
Perform further investigations.
Establish monitoring schedule:
-Hourly capillary blood glucose and ketone testing
-Venous bicarbonate and potassium after 1 and 2 hrs,
then every 2 hrs for first 6 hrs
-Plasma electrolytes every 4 hrs
-Clinical monitoring of O2 saturation, pulse, BP,
respiratory rate and urine output every hour
Treat any precipitating cause
0 – 60
min

13. DKA- Emergency management
IV infusion of 0.9% sodium chloride with potassium
chloride added as indicated below:
1L over 2 hrs
1L over 2 hrs
1L over 4 hrs
1L over 4 hrs
1L over 6 hrs
Add 10% glucose 125 mL/hr IV, when glucose < 14
mmol/L (252 mg/dL)
60 mins
to
06 hours

14. DKA- Emergency management
Be more cautious with fluid replacement in
-older or young people,
-pregnant patients and
-those with renal or heart failure;
if plasma sodium is > 155 mmol/L, 0.45% sodium
chloride may be used
60 mins
to
06 hours

15. DKA- Emergency management
Adjust potassium chloride infusion:60 mins
to
06 hours

16. DKA- Emergency management
Clinical status, glucose, ketonaemia and
acidosis should be improving; request senior
review if not
Continue IV fluid replacement
Continue insulin administration
Assess for complications of treatment (fluid
overload, cerebral oedema)
Avoid hypoglycaemia
06 to 12
hours

17. DKA- Emergency management
By 24 hrs, ketonaemia and acidosis should have
resolved (blood ketones < 0.3 mmol/L, venous
bicarbonate > 18 mmol/L)
If patient is not eating and drinking:
-Continue IV insulin infusion at lower rate of 2–3
U/hr
-Continue IV fluid replacement and biochemical
monitoring
12 to 24
hours

18. DKA- Emergency management
If ketoacidosis has resolved and patient is
able to eat and drink:
-Re-initiate SC insulin with advice from
diabetes team; do not discontinue IV insulin until
30 mins after SC short-acting insulin injection
12 to 24
hours

19. DKA- Emergency management
 Consider urinary catheterisation if anuric after 3 hrs or
incontinent
 Insert NG tube if obtunded or there is persistent vomiting
 Insert CV line if cardiovascular system is compromised, to allow
fluid replacement to be adjusted accurately; also consider in older
patients, pregnant women, renal or cardiac failure, other serious
comorbidities and severe DKA
 Measure ABG; repeat chest X-ray if O2 saturation < 92%
 Institute ECG monitoring in severe cases
 Give thromboprophylaxis with LMWH
Additional
Procedures

20. HHS
 Hyperglycaemic hyperosmolar state (HHS) is characterised by
-Severe hyperglycaemia (> 30 mmol/L (600 mg/ dL)),
-Hyperosmolality (serum osmolality > 320 mOsm/ kg)
-Dehydration in the absence of significant hyperketonaemia
(< 3 mmol/L) or acidosis (pH > 7.3, HCO3 > 15 mmol/L).
 It was previously referred to as hyperosmolar non-ketotic (HONK)
coma but, as in DKA, coma is not invariable.

21. HHS
 Typically occurring in the elderly, HHS is increasingly seen in
younger adults.
 Common precipitating factors include
infection, myocardial infarction, cerebrovascular events or
drug therapy (e.g. corticosteroids).
 Poor prognostic signs include
hypothermia, hypotension (systolic blood pressure < 90
mmHg), tachy- or bradycardia, severe hypernatraemia (sodium >
160 mmol/L), serum osmolality > 360 mOsm/kg, and the presence of
other serious comorbidities.

22. HHS Principles of management
Measure or calculate serum osmolality frequently
Give fluid replacement with 0.9% sodium chloride (IV).
Use 0.45% sodium chloride only if osmolality is
increasing, despite positive fluid balance. Target fall in
plasma sodium is ≤ 10 mmol/L at 24 hrs
Aim for positive fluid balance of 3–6 L by 12 hrs, and
replacement of remaining estimated loss over next 12
hrs

23. HHS Principles of management
Initiate insulin IV infusion (0.05 U/kg body weight/hr)
only when blood glucose is not falling with 0.9% sodium
chloride alone OR if there is significant ketonaemia (3β-
hydroxybutyrate > 1 mmol/L or urine ketones > 2+).
Reduce blood glucose by no more than 5 mmol/L/hr
Treat coexisting conditions
Give prophylactic anticoagulation
Assume high risk of foot ulceration

24. HHS Key Recommendation
0.9% sodium chloride solution alone is used for initial
treatment,
and
Insulin is introduced only when the rate of fall in blood
glucose has plateaued.

25. HHS
Osmolarity can be calculated as follows
Plasma osmolarity = 2[Na+ ]+[glucose]+[urea]
The normal value is 280–290 mmol/L and consciousness
is impaired when it is high (> 340 mmol/L), as commonly
occurs in HHS.

26. Hypoglycaemia
 Hypoglycemia is called, if blood glucose is < 3.5 mmol/L (63
mg/dL)
 in most circumstances it is due to
insulin therapy,
less frequently from use of oral insulin secretagogues such as
sulphonylurea drugs, and rarely with other anti-diabetic drugs.

27. Hypoglycaemia
If blood glucose falls, three primary physiological defence
mechanisms operate:
1. Endogenous insulin release from pancreatic β cells is
suppressed;
2. Release of glucagon from pancreatic α cells is increased;
and
3. Activation of ANS, with release of catecholamines both
systemically and within the tissues.
In addition, stress hormones, such as cortisol and GH, are
increased in the blood.
These actions reduce whole-body glucose uptake and increase
hepatic glucose production, maintaining a glucose supply to the
brain.

28. Hypoglycaemia
 People with type 1 diabetes cannot regulate insulin once it is
injected subcutaneously, and so it continues to act, despite
developing hypoglycaemia.
 In addition, within 5 years of diagnosis, most patients will have
lost their ability to release glucagon specifically during
hypoglycaemia. This is thought to result mainly from loss of -cell
regulation by β cells.
 These two primary defects mean that hypoglycaemia occurs
much more frequently in people with type 1 and longer
duration type 2 diabetes.

29. Hypoglycaemia Causes
 Missed, delayed or inadequate meal
 Unexpected or unusual exercise
 Alcohol
 Errors in oral anti-diabetic agent(s) or insulin dose/schedule/ administration
 Poorly designed insulin regimen, particularly if predisposing to nocturnal
hyperinsulinaemia
 Lipohypertrophy at injection sites causing variable insulin absorption
 Gastroparesis due to autonomic neuropathy causing variable carbohydrate
absorption
 Malabsorption, e.g. coeliac disease
 Unrecognised other endocrine disorder, e.g. Addison’s disease
 Factitious (deliberately induced)
 Breastfeeding

30. Hypoglycaemia Risk Factors
 Strict glycaemic control
 Impaired awareness of hypoglycaemia
 Age (very young and elderly)
 Long duration of diabetes
 Sleep
 C-peptide negativity (indicating complete insulin deficiency)
 History of previous severe hypoglycaemia
 Renal impairment
 Genetic, e.g. angiotensin-converting enzyme (ACE) genotype

31. Hypoglycaemia Symptoms
Neuroglycopenic
 Confusion
 Drowsiness
 Speech difficulty
 Inability to concentrate
 Incoordination
 Irritability, anger
Autonomic
 Sweating
 Trembling
 Pounding heart
 Hunger
 Anxiety
Non-specific
 Nausea
 Tiredness
 Headache

32. Hypoglycaemia
Emergency treatment of hypoglycaemia
 Mild (self-treated)
• Oral fast-acting carbohydrate (10–15 g) is taken as glucose
drink or tablets or confectionery
• This should be followed with a snack containing complex
carbohydrate

33. Hypoglycaemia
Emergency treatment of hypoglycaemia
 Severe (external help required)
• If patient is semiconscious or unconscious, parenteral
treatment is required:
IV 75 mL 20% dextrose (= 15 g; give 0.2 g/kg in children)*
Or
IM glucagon (1 mg; 0.5 mg in children)
• If patient is conscious and able to swallow:
Give oral refined glucose as drink or sweets (= 25 g) Or Apply
glucose gel or jam or honey to buccal mucosa.

34. Hypoglycaemia
Avoidance and treatment of hypoglycaemia during travel
 Carry a supply of fast-acting carbohydrate (non-perishable,
in suitable containers)
 Screwtop plastic bottles for glucose drinks, Packets of
powdered glucose (for use in hot, humid climates),
Confectionery (foil-wrapped in hot climates)
 Companions should carry additional oral carbohydrate,
and glucagon
 Perform frequent blood glucose testing (carry spare meter
and/or visually read strips)
 Use fast-acting insulin analogues for long-distance air travel