MANAGEMENT OF DIABETES

EMERGENCIES

Dr. F. O. Finomo
 Diabetes mellitus
A syndrome/group of diseases
characterized by hyperglycemia and
disturbances of carbohydrate, fat and
protein metabolism due to defects in
insulin secretion, insulin action or both
 Acute Complications of Diabetes
(Diabetic Emergencies)

D ia b e te s

D ia b e tic K e to a c id o s is H y p e rg ly c e m ic H y p e ro s m o la r S ta te H y p o g ly c e m ia
H y p e rg ly c e m ia H y p e rg ly c e m ia
A c id o s is w ith a n io n g a p N o a c id o s is
E le c tro ly te D is tu rb a n c e s H y p e rn a tre m ia a n d o th e rs
 DIABETIC KETOACIDOSIS
• Definition
• Epidemiology
• Aetiopathogenesis/Pathophysiology
• Clinical features
• Investigations
• Treatment
• Prognosis
 Definition
• An acute metabolic complication of DM with
uncontrolled catabolism associated with insulin
deficiency aggravated by ensuing
hyperglycemia, dehydration, and acidosis-
producing derangements in intermediary
metabolism and characterized by:
– Hyperglycaemia (>200mg/dL, 11mm/L)
– Acidosis, blood pH <7.3 , HCO3- < 15mmol/L
– Increased total blood ketones, > 3mmol/L
– In clinical practice it is suspected when there is
ketonuria++ in the face of hyperglycaemia
 Epidemiology of DKA
• It is the most common endocrine emergency.
• Few published Nigerian data
• Europeans and Americans quote 10 – 30 cases per
100, 000 population.
• Commoner in females
• Commoner in non-whites
• Mortality higher in the elderly
• Commonly seen in type 1 Diabetes, but may occur
in type 2 Diabetes.
• Mortality is around 2-5% in developed world, it is as
high as 20-30% in the developing countries
 Precipitating factors
 Newly diagnosed diabetic (20-30%) especially type 1

 Failure to take insulin, faulty insulin delivery system

 Infections, UTI/respiratory (RTI) (30-40% cases)

 Unknown (20-25% cases)

 Miscellaneous- alcohol, infarction(CVD/myocardial), drugs

(glucocorticoids, thiazides, dobutamine, terbutaline),
trauma, psychological stress, pulmonary embolism, burns.
 Presentation

• Usually acute, within hours to a few days.

• Hyperglycaemia- polyuria,polydipsia,
weakness, abdominal pain.
• Dehydration
• Acidosis- nausea, vomiting, hypotension.
• Coma
• Rapid respiration with acetone breath
 Presentation (contd.)
• Hyperthermia/Hypothermia
• Raised urea, acidosis (HCO3 < 15mmol/L)
• Raised creatinine
• Ketonuria or/and ketonaemia
• Leucocytosis > 20-25,000/cm (if > 25,000 it is
suggestive of infection)
• Raised anion gap (90-95% of cases)
• Febrile/afebrile (even in the presence of infection)
• Symptoms of the precipitating illness e.g UTI,
pneumonia, MI.
 Aetiopathogenesis/Pathophysiology
• Insulin deficiency and glucagon excess leads to
excess acetyl-CoA
• Acetyl CoA is converted to acetoacetate
• Some acetoacetate is converted to other ketones
• These ketones require to be buffered and thus
bicarbonate is used up as pH drops
• The respiratory centre is stimulated and Kussmaul
breathing occurs
• Urine becomes acidic, osmotic diuresis occurs
• H and Na and K are lost in the urine together with
ketones
• Diagnosis of diabetic ketoacidosis (DKA) is
based on the biochemical triad of ketonaemia,
hyperglycaemia, and acidaemia.
 Pathophysiology
Hyperglycaemia :

-absolute insulin deficiency

-↑ hepatic glucose output

-↑ counter-regulatory hormones

-↑renal gluconeogenesis

-osmotic diuresis →dehydration

-dyselectrolytemia due to impaired renal sodium

reabsorption.
 Pathophysiology (contd.)
• Hyperketonaemia
- absolute insulin deficiency
- ↑NEFA
- ↑Ketone body formation
• Acidosis
-KBs are organic acids → H+
-Metabolic acidosis
-vomiting
-altered consciousness
-Kausmaul’s breathing
 Diagnosis
Hyperglycaemia;>200mg% (11mmol/L)

Metabolic Acidosis pH <7.3 (HCO3<15mmol/L)

Ketonuria++ and/or ketonaemia>3mmol/L

Anion gap >15 mmol/L

Anion gap = (Na++K+) – (HCO3-+Cl-).
Normal anion gap = 10–14 mmol/L
Interpreting Capillary Ketone Levels
• <0.6mmol/L - Normal blood ketone Value

• >0.6 to 1.5mmol/L - more ketones being

produced than normal; retest in a few hours

• 1.6 to3.0mmol/L - a high level of ketone; risk of

Ketoacidosis

• >3.0mmol/L - consistent with Diabetic

Ketoacidosis
 Management
Principles

Restore perfusion/rehydration

Stop ketogenesis by insulin replacement

Correct electrolytes imbalance

Avoid Complications

Treat the underlying cause/precipitants

• The most important initial therapeutic
intervention in DKA is appropriate fluid
replacement followed by insulin
administration.
• The main aims for fluid replacement are:
– restoration of circulatory volume > clearance of
ketones
– correction of electrolyte imbalance.
 General Measures
a) Draw blood for investigations
1. E/U, Cr-URGENT
2. Check plasma glucose hrly & electrolytes 8hrly in
1st 24 Hrs. Then daily E/U,Cr until stable- MUST
3. Do bedside urinalysis for sugar, ketones and
proteins- URGENT
4. ABGs- Urgent if possible.
5. Urine M/C/S
6. Full blood count
7. ECG (to r/o MI or dyselectrolytemia)
8. Arrange for chest X-ray
b. Catheterise if unconscious or when there is no
spontaneous urine in 3 hours.

c. Give 60-100% oxygen 4-5L/min if the PaO2 is <11KPA

(80mmHg)

d. NG Tube if unconscious or semi unconscious

(GCS<6/15)

e. Central venous line if elderly (>65yrs) or in cardiac

patients.

f. Give blood or plasma 1-2unis if Systolic BP remains

persistently below 80mmHg.
g. Give prophylactic heparin 5,000 u 12 hourly if
the patient is elderly, unconscious for >7hrs or
the plasma osmolality is >350mmosm/L

h. Consider the use of diazepam in small i/v

doses as a sedative if the patient is very
restless or convulsing.

i. Use colloids if SBP remain <100mmHg after

3hrs or 3litres of normal saline.
 Specific measures
a) Fluid Replacement:

 Estimated fluid loss is approx. 6-8L.

 Replace 6L in the 1st 8hrs.

 Give 1L normal saline over 30minutes, then

 1L over 1 hour, then

 1 L over the next 2hrs, then

 1 L over the next 4hrs, then

Continue rehydration at the rate of 1 L over 4-
6hrs depending on hydration status.

Change normal saline to 5% dextrose when the

blood sugar falls to <14mmol/L or use dextrose
saline when the patient’s BP remains
<100mmHg. 

NB - Use ½ strength normal saline as the initial

resuscitation fluid if the patient is in CCF,
hypertensive, hypernatraemic or a child. In the
absence of (CVP) monitoring, give ½ the initial
dose of intravenous fluids.
• Insulin should be administered intravenously and
given at a fixed rate using a weight-based formula:
0.1 units per kilogram body weight per hour. It may
be necessary to estimate the patient’s weight;
treatment should not be delayed waiting for an
accurate weight.
• Fixed rate intravenous insulin infusion (FRIII) not
only reduces blood glucose levels, but just as
importantly, suppresses further ketogenesis, as well
as correcting the electrolyte disturbance
METABOLIC TREATMENT TARGETS
• Reduction of the blood ketone concentration
by 0.5 mmol/L/hour.
• Increase the venous bicarbonate by 3.0
mmol/L/hour.
• Reduce capillary blood glucose by 3.0
mmol/L/hour.
• Maintain potassium between 4.0 and 5.5
mmol/L.
• If these targets not achieved, then the FRIII rate
should be increased.
• As clearing ketones is as important as normalising
blood glucose, it is often necessary to give
intravenous 10% dextrose, to avoid hypoglycaemia
and allow continued FRIII to suppress ketogenesis;
– start 10% dextrose when the blood glucose falls below
14.0 mmol/L.
• Continue 0.9% sodium chloride solution to correct
circulatory volume,
– often necessary to infuse these solutions concurrently.
 Resolution of DKA
• pH >7.3 units
• Bicarbonate >15.0 mmol/L
• Blood ketones level <0.6mmol/L
 More recent changes in diabetic
ketoacidosis management
• Measurement of capillary (not urinary) ketones
• Using capillary ketone level to guide treatment
rather than capillary glucose
• Measuring venous (not arterial) pH and
bicarbonate
• Using weight-based fixed rate intravenous insulin
infusion (FRIII) instead of ‘sliding scales’
• Monitoring of electrolytes on blood gas analyser
with intermittent laboratory confirmation
• Continuing long acting basal insulin analogues
alongside FRIII
 Troubleshooting
• If DKA is not resolving and the treatment targets
are not being achieved:
– check cannula patency and placement.
– Confirm the correct rate of intravenous infusions (FRIII
and fluids) has been administered.
– Look again for concomitant pathology, eg
intraabdominal sepsis, myocardial infarction.
– Consider if insulin resistance is likely, eg obesity,
concurrent steroid therapy;
– increase rate of FRIII.
– Reassess fluid status, and consider increasing rate of
intravenous (IV) fluids.
Continuing Long acting Subcut Insulin
• The patient’s basal (long acting) analogue insulin
should be continued alongside the FRIII to prevent
rebound hyperglycaemia when IV treatment is
stopped.
• Individuals with a new diagnosis of T1DM
presenting with DKA should be started on basal
insulin as soon as possible, and IV insulin
continued until there is some basal subcutaneous
(SC) insulin on board.
 Stopping FRIII
• may restart the pre-DKA SC insulin regimen. But if
pre-admission glycaemic control was suboptimal
(high HbA1c, recurrent hypoglycaemia) then a
medication review advisable.
• Once DKA has resolved & patient able to eat and
drink, SC insulin therapy can be restarted.
• Intravenous insulin infusion is not discontinued
until at least 30–60 minutes after the
administration of the SC insulin dose taken with a
meal. The patient’s basal insulin should have been
continued alongside the FRIII.
• If the basal insulin had been stopped in error, the
insulin infusion should not be stopped until some
form of background insulin has been given, eg a stat
dose of Insulatard at half the patient’s usual daily
dose of basal insulin.
• If the patient was on twice daily fixed-mix insulin (eg
NovoMix 30), restart their usual SC insulin either
before breakfast or before the evening meal.
Continue IV insulin infusion until 30–60 minutes after
the SC insulin was given.
• If DKA has resolved but patient is not yet ready to
eat and drink, then switch to a variable rate insulin
infusion and IV fluids according to fluid status.
 Markers of Severity in DKA
• Blood ketones over 6 mmol/L
• Bicarbonate level below 5 mmol/L
• Venous/arterial pH below 7.0
• Hypokalaemia on admission (under 3.5 mmol/L)
• Glasgow coma score less than 12 or abnormal alert,
verbal, pain, unresponsive (AVPU) scale
• Oxygen saturation below 92% on air (assuming
normal baseline respiratory function)
• Systolic blood pressure below 90 mmHg
• Pulse over 100 or below 60 bpm
• Anion gap above 16 [Anion gap = (Na+ + K+) − (Cl− + HCO 3− )]
Change to ‘TDS soluble insulin S/C & nocte
Intermediate Insulin S/C if hydration is
adequate,
Titrate dose of insulin until the plasma
glucose normalise, then convert the pt to
intermediate/soluble e.g Humulin 70/30,
Mixtard or the patient be placed on his
previous doses of oral hypoglcaemic agents, if
stress factors like infection have been
satisfactorily controlled.
c) Correction of Electrolyte imbalance 

I. Potassium (serum K+ may be low, normal or high)

Potassium deficit is around 1-2mmol/L/kg

Do not give potassium if

– Patient is Oliguric (urine < 1ml/min)
– Serum K+ > 5.5mmol/L
– ECG evidence of hyperkalaemia- Tall tented T waves
Give potassium

i. After the first litre of normal saline and the patient is

making urine

ii. When serum potassium is < 5.5 mmol/L

iii. When there is ECG evidence of hypokalaemia

iv. Double the amount of K+ if bicarbonate is being

administered

Give potassium chloride (KCL) based on serum E/U,Cr

as follows:
 Potassium replacement in DKA
Plasma Potassium Amount of KCL
(mmol/l) (mmol/l) in 1L IVF

>5.5 Observe. No KCL

4.5 – 5.4 13

3.5 – 4.4 26

<3.5 39
• Continue oral potassium supplementation for
5-7 days when the patient can take orally. 

• Aim to maintain serum potassium above

4mmol/L
NB: 13mmol/L of potassium = 1g KCL.
 Bicarbonate (HCO3)
There is no demonstrable clinical benefit from HCO 3
administration when the PH > 7.0
Give sodium bicarbonate if:
PH < 7.0Serum
HCO3 < 10mmol/l
Serum potassium ≥ 6.5 mmol/l
Hypotensive and unresponsive to fluid replacement
Late hypochloraemic acidosis
Respiratory rate > 30 cycles/min
If using 8.4% NaHCO3, give 50ml in 1litre of normal
saline over 2 hours
If using 1.26% NaHCO3, give 500ml over 1 hour.
• Phosphate: not routinely replaced
Treatment of precipitating causes
• Start broad spectrum antibiotics for suspected
infection (UTI/Chest) after samples for microbiology
have been taken. 

Avoid complications:
• Complications of the disease; hypotension, ARF, coma,
aspiration pneumonia, orthostatic hypotension,
cerebral oedema, DVT, hypothermia, ARDS.

• Complications of treatment; hypoglycaemia,

hypokalaemia, pulmonary oedema, cerebral oedema .
 HYPEROSMOLAR HYPERGLYCAEMIC
STATE (HHS)
This is a metabolic emergency in persons with
uncontrolled type 2 DM. It was previously called
hyperosmolar non-ketotic state (HONK).

Diagnosis: the following must be present

Severe hyperglycaemia ( plasma glucose >>35mmol/l)
Altered mental status
Serum osmolarlity > 320 mosm/L (normal 270-
290mosm/L)
Other findings which may be present include;
• ketonaemia/ketonuria – mild or absent.
• Anion gap – normal or slightly elevated.
• pH > 7.3
• serum HCO3 > 18 mmol/L 
• -patients are older, presenting in middle or
later life.
• -mortality may be as high as 35%
 Precipitating factors
-newly diagnosed type 2 DM
-consumption of glucose-rich fluids (eg Lucozade)
-discontinuation of drugs
-surgery
-concurrent medications- thiazide diuretics or
steroids
-intercurrent illness- CVD, MI, pancreatitis, UTI,
respiratory tract infection etc.
 Predisposing or precipitating factors
Acute illness
for HHS
Drugs/therapy
• Acute infection (32–60%)
• -Adrenergic blockers
– Pneumonia
– Urinary tract infection
• Calcium-channel blockers
– Sepsis • Chlorpromazine
• Cerebral vascular accident • Chlorthalidone
• Myocardial infarction • Cimetidine
• Acute pancreatitis • Diazoxide
• Acute pulmonary embolus • Diuretics
• Intestinal obstruction • Encainide
• Dialysis, peritoneal
• Ethacrynic acid
• Mesenteric thrombosis
• Immunosuppressive agents
• Renal failure
• L-asparaginase
• Heat stroke
• Loxapine
• Hypothermia
• Subdural hematoma • Phenytoin
• Severe burns • Propranolol
• Endocrine • Steroids
• Acromegaly • Total parenteral nutrition
• Thyrotoxicosis Previously undiagnosed diabetes
• Cushing’s syndrome
 Presentation
-insidious onset with symptoms progressing
over 1 week or more
-polyuria
-polydipsia
-severe dehydration (8 – 12litres)
-confusion, seizures
-stupor or coma in up to 20% of cases
-evidence of underlying illness eg UTI,
pneumonia etc
-stroke, MI, or peripheral arterial disease in the
lower limbs due to hyperosmolality
 Management
Principles
Rehydration
Correction of hyperglycaemia using
insulin
Correction of electrolyte imbalance
especially potassium.
Treatment of underlying
cause/precipitant
Prevention of complication
 Treatment
• Similar to DKA but less insulin required and
patient requires prophylactic anticoagulation
• Replacement of potassium often required
• Antibiotics
General measures
Same as for DKA
Calculate serum osmolality based on the
formular:
Serum osmolality = [2(Na+ + K+) + plasma
glucose + Urea] mosm/L.
Fluid replacement;
-normal saline is the fluid of choice
-fluid replacement regimen as in DKA.
Insulin replacement

-similar to DKA with the following exceptions:

1. use ½ the dose of soluble insulin as in DKA

2. double the dose of insulin if no appreciable fall in

plasma glucose at a rate of 3mmol/l/hr after 3
hours of starting treatment.

3. commence insulin therapy only after

rehydration has started.
Correction of electrolyte inbalance;
-As in DKA. 

Treatment of precipitating cause;

-broad spectrum antibiotics if infection is suspected
-treat for MI, CVD, if indicated.
 Prevention of complications;
 -prophylactic anticoagulant is compelling because of
the high tendency of thrombo-embolic events.
 -give subcut Heparin 5000 U 12Hourly (if no absolute
contra-indications). OR
 -subcut Enoxaparin 40mg 12Hourly. Do baseline
clotting profile and INR monitoring especially if using
Heparin.
Introduction
 Diagnosis

Whip ple 's Tr ia d

Sy m pt o ms c/w Hy p ogly c emia Low Ser u m Blo od Glu cos e Relie f of Sy m pt o ms wit h Nor m aliz a t io n of BG
Pathophysiology
• As plasma glucose decrease just below
the physiologic level, Glucagon increases
which in turn increases hepatic
glycogenolysis and hepatic and renal
gluconeogenesis. This is the 2nd
defense.
• With further reduction - epinephrine is
released from adrenal medulla which
acts like Glucagon as well as increase
delivery of gluconeogenic substrates
from fat cells and muscles. This is the
3rd defense.
• Beyond 4 hrs, Cortisol & growth hormone
also support glucose production and limit
utilization
.
• With persistent low levels, symptoms
prompt the behavioral defense against
hypoglycemia, including ingestion of food.

• Therefore a healthy liver, pancreas, kidneys,

adrenal glands are important for defense
against hypoglycemia.
Hypoglycemic associated autonomic
failure (HAAF)
• Is a concept in type 1 DM and long standing type 2
DM patients in which the persistent hypoglycemia
causes both defective counter regulation and
hypoglycemic unawareness which results in a
viscous cycle of hypoglycemia.
• There's a shift in the glycemic threshold for the
sympathoadrenal response to lower levels of
gluose
• Due to the shift, there's defective counter
regulation by epinephrine.
• So at hypoglycemic levels, no sympathoadrenal
outflow and hence no warning symptoms
(unawareness)
 Etiology
The most common cause of hypoglycemia is medications used to treat DM such
as insulin, sulfonylureas, and biguanides.
Risk is greater in diabetics who have eaten less than usual, exercised more than
usual or drunk alcohol.
Other cause of hypoglycemia include
-Aspirin poisoning
-ACEi inhibitor
-Quinine
-Renal failure
-Addison disease
-Pituitary insufficiency
-insulinoma
-Sepsis
-Gastric bye pass sugery
- Hypothyroidism
 Clinical Features
• Autonomic: Sweating, anxiety, hunger, tremor,
palpitations, dizziness.

• Neuroglycopenic: Confusion, drowsiness, visual

trouble, seizures, coma.

• Rarely focal symptoms, eg transient hemiplegia.

Mutism, personality change, restlessness, and
incoherence may lead to misdiagnosis of alcohol
intoxication or even psychosis
 Symptoms

Neuroglycopenic Neurogenic/Autonomic
• Altered mental status • Adrenergic
– Palpitations
• Confusion
– Tremor
• Fatigue – Anxiety
• Seizure
• Loss of consciousness • Cholinergic
• Death – Diaphoresis
– Hunger
– Paresthesias
 classification
Based on severity
-Mild: autonomic symptoms are present.
-Moderate : autonomic and neuroglycopenic symptoms are
present
-severe: autonomic and neuroglypenic symptoms are present,
may become unconscious, plasma glucose is usually < 2.8mmol/L .
 Diagnosis
• History and examination
• History of clinical presentation suggestive of
hypoglycemia
• Assess risk factors and identify etiology
• Diagnosis is mainly based on Whipple's triad
• A high index of suspicion, awareness of etiology
and obvious clinical manifestations should
prompt a quick bedside blood glucose
determination using a Glucometer.
• Investigation - laboratory diagnosis
 Investigation
• FBC
• Insulin assay
• C-peptide assay
• Drug screen - sulfonylurea, metformin
• Serum electrolyte/urea/creatinine
• Liver function test
• Hormonal assay - GH, Cortisol
Management
 Acute intervention
Hypoglycemia is a medical emergency.
•Admit patient
•Resuscitation: ABC
•Secure iv access
•IV bolus 50mls of 50% Dextrose water (in double
dilution)
•NOTE: In absence of 50% D/W, 250mls of 10% D/W, or
500mls of 5%D/S can be given.
•Re-assess the blood glucose in 30minute time then 1
hour time
 Maintenance therapy
- Continuous glucose administration and frequent
monitoring.

- IV 10% Dextrose water infusion 1mL 8 hourly for 24hours

- Monitoring blood glucose using a bedside Glucometer 4

hourly for a minimum of 24hrs.
Re-assess patient.
 Subsequent measures
For refractory cases and treatment of
underlying etiology
•Glucagon
•Diazoxide
•Stomatostain analogue
•Surgery
•Antibiotics for sepsis
•Hormone replacement therapy for hormone
deficiencies
 Prevention
• Education of patients and caregivers on
recognition of early warning signs & management
of mild to moderate cases.
• Adherence to prescribed medication and clinic
visits for diabetic patients
• Self monitoring of blood glucose(SMBG)
• Education on action to take in cases of emergency
• Glucagon emergency kit
 Differential diagnosis

• Sepsis
• Stroke
• Metabolic abnormalities - DKA
• Electrolyte derangement
• Congestive cardiac failure
• Liver failure
• Renal failure
 Conclusion

• Hypoglycemia is an acute medical

emergency mostly a complication of
diabetes and can cause severely disabling
features if taken for granted.
• Hypoglycemia is better prevented than
managed, hence a high index of suspicion is
required to anticipate and prevent it
especially in high risk group.
 Diabetes Associated Hypoglycemia
• Sulfonylurea (long acting)

• Insulin Excess
– Incorrect dosing/wrong timing/type
– ↓ PO intake: illness, fasting
– ↑ glucose utilization: exercise
– ↑ sensitivity peripherally to insulin: weight loss,
exercise
– ↓ endogenous production
– ↓ insulin clearance
 Management
 Urgent random blood sugar estimation is
mandatory.

• Availability of a glucometer is extremely useful

in getting an urgent blood sugar result.

• If a glucose meter is not available, send

samples in a fluoride-oxalate bottle to the
laboratory. Alert the laboratory at once.
Secure an intravenous access with a cannula
(preferably)

Give 50% glucose 50-100ml bolus IV in double dilution

using a large peripheral vein.

Maintain on 10% dextrose water IV 1Liter 6hourly until

patient can take orally.

Monitor hourly blood sugar until stable

Withhold all anti-diabetic medications including insulin

until patient is stable.
If glucose infusion is not immediately available,
give a bottle of soft drink or place a cube of sugar
in patient’s mouth if he/she can take orally.

In the absence of a glucometre, in any person

with diabetes if found to have sudden onset of
sweating, tremors, confusion and altered
consciousness, draw blood and send to the
laboratory for urgent RBS.

Then GIVE IV 50% dextrose 50ml bolus and

maintain on 10% dextrose until result of RBS is
available.