MANAGEMENT OF ACUTE

DIABETIC EMERGENCIES-DFM
LECTURE
DR LONGMUT REMEN
DEPARTMENT OF FAMILY MEDICINE, JOS UNIVERSITY TEACHING
HOSPITAL
OUTLINE
• INTRODUCTION
• AETIOLOGICAL CLASSIFICATION OF DIABETES
• DIAGNOSIS
• MANAGEMENT OF THE ACUTE DIABETIC EMERGENCES
-DIABETIC KETOACIDOSIS
-HYPEROSMOLAR HYPERGLYCAEMIC
STATE (HHS)
-HYPOGLYCAEMIA
• CONCLUSION
INTRODUCTION
• A syndrome/group of diseases characterized by hyperglycaemia and
disturbances of carbohydrate, fat and protein metabolism due to
defects in insulin secretion, insulin action or both
• Globally, diabetes prevalence and its impact have increased
dramatically, particularly in sub-Saharan Africa.
• Consequently, diabetic emergencies continue to be a significant
health and socioeconomic problem among patients with diabetes
mellitus (DM)
AETIOLOGICAL CLASSIFICATION OF DIABETES
• Type 1 Diabetes due to beta cell destruction usually leading to absolute
insulin deficiency. often Immune mediated but could be Idiopathic as well
• Type 2 Diabetes (Insulin Resistance/ Insulin secretory defect)
• Other specific types of diabetes;
Genetic defects of beta cell function (MODY 1-5)
Genetic defects of insulin action
Diseases of the exocrine pancrease
Endocrinopathies
Drug or Chemical induced
• Gestational Diabetes Mellitus (GDM)
DIAGNOSIS
DIAGNOSTIC CRITERIA FOR DIABETES ARE:
• Fasting Plasma Glucose > 7.0mmol/L (126mg/dl)
• 2 Hours Post Prandial Plasma Glucose >11.1mmol/L (200mg/dl)
• Glycated HbA1C > 6.5%
ACUTE DIABETIC EMERGENCIES
• Also referred to as diabetes crises syndrome(DCS) or diabetic
emergencies
• It is associated with severe uncontrolled DM requiring
emergency treatment with insulin, intravenous fluids and other
medications
• It is a life-threatening situations
• The most common Acute Complications of Diabetes (Diabetic Emergencies) that
include;
-Diabetic ketoacidosis
-Hyperglycemic hyperosmolar syndrome
- Hypoglycemia
DIABETIC KETOACIDOSIS (DKA)
• Its define as an acute metabolic complication of DM with
uncontrolled catabolism associated with insulin deficiency
characterised by; hyperglycaemia, dehydration, and acidosis
EPIDEMIOLOGY OF DKA
• It is the most common endocrine emergency with few published
Nigerian data
• Data from Europeans and Americans quote 10 – 30 cases per 100,
000 population
• Commoner in females and non-whites
• With higher Mortality in the elderly
• Commonly seen in type 1 Diabetes, but may occur in type 2 Diabetes
• Mortality is around 2-5% in developed world, but as high as 20-30%
in the developing countries
PRECIPITATING FACTORS
• Being a newly diagnosed diabetic • Trauma , burns
(20-30%) especially type 1 • Drugs (glucocorticoids, thiazides,
• Failure to take insulin or faulty dobutamine, terbutaline)
insulin delivery system • Psychological stress
• Infections, UTI/respiratory (RTI) • Pulmonary embolism
(30-40% cases), gastroenteritis,
sepsis • Following Surgery
• Following Alcohol intake • Pancreatitis
• Acute vascular episodes (cerebral, • Ignorance about the disease
coronary or peripheral) • Unknown (20-25% cases)
• Acute MI
BACKGROUND PATHOPHYSIOLOGY OF DKA
• The pathogenesis of DKA begins with insulin deficiency
• Insulin deficiency makes it difficult for glucose to enter body cells to
be used for energy, this lead to high blood glucose in the plasma
(hyperglycaemia)
• In a state of deficient insulin, the body compensates by releasing
counter-regulatory hormones like glucagon, cortisol, growth
hormone, and catecholamines (epinephrine) which oppose the action
of insulin
• The increase in counter-regulatory hormones levels leads to the
following metabolic consequences:
BACKGROUND PATHOPHYSIOLOGY OF DKA
• Hyperglycaemia:
-due to increase glucose production by the liver through gluconeogenesis
and glycogenolysis ( from glycogen) .
• Ketosis
-Insulin deficiency also promotes lipolysis ( fat break down), releasing free
fatty acids into blood stream.
-These free fatty are converted into ketone bodies (acetoacetate, beta-
hydroxybutyrate and acetone) in the liver, a process known as ketogenesis
• Metabolic acidosis
- The accumulation of these ketone bodies which are strong acids in the
blood lowers the bloods PH, leading to metabolic acidosis
BACKGROUND PATHOPHYSIOLOGY OF DKA
• Osmotic diuresis:
-When the high blood glucose levels exceed the kidneys ability to
reabsorb glucose, the excess spill into the urine pulling water and
electrolytes along with it
• Dehydration:
- The loss of water and electrolytes through osmotic diuresis leads to
dehydration. The hypotension created leads to a decrease in the
glomerular filtration rate
• Electrolyte depletion:
-through osmotic diuresis particularly potassium
BACKGROUND PATHOPHYSIOLOGY OF DKA
• The Vicious cycle of worsening DKA
-As the body becomes more dehydrated and the kidney function
declines, ketones levels keep rising because they are filtered less
effectively by the kidneys
-Further volume depletion triggers the release of even more counter-
regulatory hormones creating a vicious cycle of worsening
hyperglycaemia and dehydration
BACKGROUND PATHOPHYSIOLOGY OF
DKA Insulin deficiency

Glucose uptake Lipolysis

Glycerol FFAs

Hyperglycaemia Gluconeogenesis
Ketogenesis
Glucosuria Ketonemia

Osmotic diuresis Electrolyte Ketonuria

depletion

Urinary water losses Dehydration

Acidosis

Adapted from Davidson 2001

CLINICAL FEATURES
• Onset is insidious occurring over hours or days
• The patient may be brought in a state of disturbed consciousness or
coma to the hospital
• Cases may developed spontaneously without any precipitating
illness/cause
• The triad of polyuria, polydipsia and polyphagia is characteristics due
to hyperglycaemia and osmotic diuresis
• Patient is often dehydrated in the presence of excessive thirst
• There could be non-specific symptoms of weakness, lethargy,
headache, myalgia etc
CLINICAL FEATURES
• GI symptoms of vomiting, abdominal distension and abdominal pain
could be mistaken for acute surgical abdomen
• The abdominal pain is related to metabolic acidosis and the ileus is
due to temporary autonomic neuropathy, electrolyte disturbance and
hyperglucagonaemia
• The respiratory symptoms could include; dyspnoea and deep
breathing
• CNS symptoms include; weakness, altered mental status, drowsiness
and eventually coma as a result of dehydration, hypotension and
increase plasma osmolarity
PHYSICAL SIGNS
• Signs of acidosis; tachypnoea, tachycardia and hypothermia
• Signs of dehydration; dry tongue, mucous membrane and skin.
Sunken eyes and cheeks
• Signs of hypotension; cold clammy skin, oliguria and obtunded
consciousness
• Kussmaul breathing; deep rapid respiration due to metabolic acidosis
• Acetone smell ( like pear drop or nail varnish) due to
hyperketonaemia
• There may be hypotonia, hyperreflexia and incoordinated ocular
movements
BIOCHEMICAL FEATURES

Increase Decrease or normal

• Blood glucose (250-600mg%) • Serum sodium (125-135 mEq/l)
• Plasma ketone
• Plasma osmolality (300-320mOsm/ml)
• Serum potassium
• Haematocrit • Serum magnesium
• WBC count > 20-25,000/cm (if > • Bicarbonate (<15 mEq/l)
25,000 it is suggestive of infection)
• Blood urea • PCO2 (20-30 mmHg)
• Serum FFA and triglycerides
• ketonuria
• Anion gap
LABORATORY 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
DIFFERENTIAL DIAGNOSIS
• CVA, hypoglycaemia and hyperosmolar coma due to altered mental
status (coma)
• Uraemia and alcohol poisoning due to presence of metabolic acidosis
• Gastroenteritis due to presence of nausea, vomiting and signs of
dehydration
• Starvation
• Salicylate poisoning
OBJECTIVES OR PRINCIPLES OF
MANAGEMENT
• Replacement of fluid loss to correct dehydration and hyperosmolality
• Correction of electrolytes (Na+ and K+) and acidosis
• Correction of hyperglycaemia with insulin
• Close monitoring of the patient by laboratory parameters ( eg plasma
glucose, urea, electrolytes, arterial PH and bicarbonate) at interval of
1-2 hours initially until the patient’s condition stabilizes
• Identification and treatment of the underlying cause/precipitants
MAGEMENT OF DKA-GENERAL MEASURES
• Admit patient
• Pass urethral catheter if patient is unconscious or when there is no
spontaneous urine production within 3 hours of admission.
• Pass Nasogastric tube for continuous stomach aspiration if
unconscious or semi unconscious (GCS<6/15)
• Give 60-100% oxygen 4-5L/min if the PaO2 is <11KPA (80mmHg)
• Pass central venous line in elderly (>65yrs) or in cardiac patients.
• Order strict input and output chart
MAGEMENT OF DKA-GENERAL MEASURES
• Do the following investigations
1. Urea, Electrolytes & creatinine-URGENT
2. Check plasma glucose hourly and electrolytes 8hrly at least in the 1st
24 Hours. Then daily E/U,Cr until stable
3. Do bedside urinalysis for glucose, ketones and proteins
4. Arterial blood gases- Urgent if possible.
5. Collect urine for microscopy culture and sensitivity
6. Full blood count
7. Arrange for ECG (to rule out MI or electrolyte abnormality)
8. Arrange for chest X-ray
MAGEMENT OF DKA-GENERAL MEASURES
• Give blood or plasma 1-2unis if Systolic Blood pressure remains
persistently below 80mmHg.
• Give prophylactic LMW heparin 5,000 u 12 hourly if the patient is
elderly, unconscious for >7hrs or the plasma osmolality is
>350mmosm/L
• Consider the use of diazepam in small i/v doses as a sedative if the
patient is very restless or convulsing.
• Use colloids if SBP remain <100mmHg after 3hrs or 3 litres of normal
saline.
MAGEMENT OF DKA-SPECIFIC MEASURES
• FLUID REPLACEMENT: (To correct dehydration and shock)
- Estimated fluid loss is approx. 6-8litres.
- Replace 6litres in the 1st 8hrs.
- Give 1litre of normal saline over 30minutes then
- Another 1litre of normal saline over 1 hour, then
- 1 litre normal saline over the next 2hrs,then
- 1 litre normal saline over the next 4hrs, then
- Continue rehydration at the rate of 1 litre over 4-6hrs depending on the patient’s
hydration status.
- Change normal saline to 5% dextrose when the blood glucose 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, hypernatraemia or a child.
MAGEMENT OF DKA-SPECIFIC MEASURES
• INSULIN REPLACEMENT (to stop ketogenesis and combat hyperglycaemia)
• Avoid subcutaneous route in dehydrated patients because of erratic
absorption
• Intravenous Route preferably.
• Use only soluble insulin initially.
• Start Soluble Insulin given IV – 0.1 IU/Kg/hr by infusion OR
• 10 IU IV and 10 IU IM as a loading dose
• Then 6 IU hourly till Plasma Glucose is < 14mmol/L
• Continue at 6 IU 2hourly or 12 IU 4 hourly until the patient is fully
conscious and can take food orally
MAGEMENT OF DKA-SPECIFIC MEASURES
• Once the patient starts feed orally, find the minimum effective units of
insulin which give the reasonable control and divide into three equal parts
and give TDS ( 8 hourly) giving each dose 30 minutes before meals
• After a few days on the TDS dose and with glucose satisfactorily controlled,
take 2/3 of the controlling dose and give it as intermediate/soluble e.g
Mixtard, Humulin 70/30 insulin in the a.m and p.m 30minutes before meal
• With continuous controlled the patient can be placed on his previous doses
of oral hypoglcaemic agents if a type 2 DM, if stress factors like infection
have been satisfactorily controlled
• If patient is being discharged on insulin, teach him to give himself insulin
injection
MAGEMENT OF DKA-SPECIFIC MEASURES
Correction of Electrolyte imbalance
• Potassium deficit is around 1-2mmol/L/kg in DKA
• Use KCL (13mmol/L of K = 1gm of KCl)
• Give potassium:
i. After the first litre of normal saline
ii. Patient is making adequate urine
Ii. When serum potassium is < 5mmol/L
iii. When there is ECG evidence of hypokalaemia (flat T wave, + U
wave)
MAGEMENT OF DKA-SPECIFIC MEASURES
• Potassium replacement guide in DKA based on serum E/U,Cr:
Plasma K (mmol/l) level = Amount of KCL (mmol) in 1L IVF
≥ 5.5 Observe. = No KCL
• 4.5 – 5.4 = 13
• 3.5 – 4.4 = 26
• < 3.5 = 39
• Continue with oral potassium supplementation for 5-7 days when the
patient can take orally.
• Aim to maintain serum potassium above 4mmol/L
MAGEMENT OF DKA-SPECIFIC MEASURES
• Do not give potassium if;
• Patient is Oliguric
• Potassium level is >5.5mmol/L
• There is ECG evidence of hyperkalaemia ( tall peaked T waves)
MAGEMENT OF DKA-SPECIFIC MEASURES
• RESTORATION OF ACID-BASE BALANCE - BICARBONATE
• The bicarbonate deficit is rapidly compensated for with well functional
kidneys.
• Replacement of bicarbonate is done only in the following situation;
pH < 7.0
Serum HCO < 10mmol/L
Serum K ≥ 6.5mmol/L
Respiratory rate > 30 cycles/min
• In these situations give 1.26% of NaHCO3 – 500mls over 1 hour OR
8.4% NaHCO3 – 50mls in 1 Litre of N/S over 2 hours
Phosphate is not routinely replaced.
MAGEMENT OF DKA-SPECIFIC MEASURES
• Treatment of precipitating causes; Start broad spectrum antibiotics
for suspected infection (UTI/Chest) after samples for microbiology
have been taken.
• Avoid complications of the disease; hypotension, ARF, coma,
aspiration pneumonia, orthostatic hypotension, cerebral oedema,
DVT, hypothermia, ARDS.
• Avoid Complications of treatment; hypoglycaemia, hypokalaemia,
pulmonary oedema, cerebral oedema
• Cerebral oedema is a common cause of mortality.it should be treated
with bolus infusion of 1 g mannitol/kg of body weight in the form of
20% or intravenous dexamethasone 8-12mg stat then 4mg 6 hourly
Monitoring of treatment
• Monitor Glucose at baseline, then hourly with insulin therapy
• Monitor E/U/C + HCO3 at Baseline and hourly for 3hours then 6
hourly
• Monitor ketones in urine through urinalysis
• Monitor blood Gases at baseline, 2hrs and 6hrs
• Monitor Vital signs closely including; Pulse, BP, RR, GCS.
• Ensure adequate Urine output – 0.5-1.0mls/Kg/hr
• If possible monitor the ECG changes
PREVENTION OF DKA
• Periodic check for DM especially in the presence of features
suggestive of the disease
• Use of insulin during stress
• Treat infection with adequate antibiotic and adjust the dose of the
insulin if the patient is on it
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)
• HHS demands urgent and faster rehydration than even DKA
Diagnostic criteria include:
• Severe hyperglycaemia ( plasma glucose >>35mmol/l)
• Altered mental status
• Serum osmolality > 320 mosm/L (normal 270- 290mosm/L)
HYPEROSMOLAR HYPERGLYCAEMIC
STATE (HHS)
Other features may include;
• Mild or absent ketonaemia/ketonuria
• Normal or slightly elevated Anion gap pH > 7.3
• Serum HCO3 > 18 mmol/L
• Patients is usually older, presenting in middle or later life
• The mortality may be as high as 35%
HHS PRECIPITATING FACTORS
• Newly diagnosed type 2 DM
• Consumption of glucose-rich fluids (eg Lucozade)
• Discontinuation of drugs
• Following Surgery
• Concurrent use of medications- thiazide diuretics or steroids
• Inter-current illness- CVD, MI, pancreatitis, UTI, respiratory tract
infection etc.
COMMON CLINICAL PRESENTATION
• Insidious onset with symptoms progressing over 1 week or more
• Polyuria
• Polydipsia
• Breathing is less laboured
• Severe dehydration (8 – 12litres)
• Confusion, seizures
• Stupor or coma in up to 20% of cases
• Evidence of underlying illness eg UTI, pneumonia etc
COMMON CLINICAL PRESENTATION OF HHS
• Stroke, MI, or peripheral arterial disease in the lower limbs due to
hyperosmolality
• No significant ketonuria
• Lab features include;
• Severe Hyperglycaemia; RBS > 35mmol/L (>600)
• PH> 7.3, HCO3 - >18mmol/L
• Anion gap – normal or mildly elevated
• Hyperosmolar plasma (Measure or Calculate Plasma Osmolality is higher
than Normal value of between 280 – 300mosm/Kg
{2(Na) + 2(K)+ (Glucose) + (Urea)} all in mmol/L
PRINCIPLES OF MANAGEMENT OF HHS
• Fluid Rehydration
• Correction of hyperglycaemia using insulin
• Correction of electrolyte imbalance especially potassium
• Treatment of underlying cause/precipitant
• Prevention of complication
• Monitor patient closely
MANAGEMENT OF HHS-GENERAL MEASURES
• The general management measures is the same as for DKA
• Take blood for glucose, ketone, UE/Cr etc
• Do ECG
• Do urinalysis
• Take samples blood and urine to look out for precipitating cause
• Do a chest x-ray if respiratory tract infection is suspected
• Calculate serum osmolality based on the formula: Serum osmolality =
[2(Na+ + K+) + plasma glucose + Urea] mosm/L.
MANAGEMENT OF HHS-GENERAL MEASURES
FLUID REPLACEMENT ;
-normal saline is the fluid of choice
• The fluid replacement regimen is as in DKA
INSULIN REPLACEMENT
Differs with DKA
Commence insulin only after rehydration has started
Intravenous insulin 3 IU/hr for the 1st 3 hours. May increase to 6 IU if rate
of glucose reduction is slow (<3mmol/hr)
OR ½ the dose of soluble insulin as in DKA. May double if rate of glucose
reduction . is slow
• Correction of electrolyte imbalance; As in DKA.
MANAGEMENT OF HHS-GENERAL MEASURES
TREATMENT OF PRECIPITATING CAUSE
• Broad spectrum antibiotics if infection is suspected
• Treat for MI, CVD, if indicated
PREVENTION OF COMPLICATIONS
Prophylactic anti-coagulant is Mandatory;
LMW Heparin 5000IU 12houly OR
Enoxaparin 40IU 12hourly
• Do baseline clotting profile and INR monitoring especially if using Heparin.
• Monitor vital signs and GCS
• Watch out for Cerebral oedema and treat if present
Differences between DKA & HHS
DKA HHS
PATIENT Younger( type1) older (type2)
Dehydration ++ ++++
Plasma Glucose 250-300 mg/dl >400 mg/dl
Blood Ketones >5 mmol/L < 5 mmol/L
Osmolality < 320 mosm/kg >320 mosm/kg
Bicarbonate < 15 Usually normal
PH <7.3 >7.3
Anion gap 14-15 meq/L < 12 meq/L
Ketonuria + + to + + + + 0 to + +
HYPOGLYCAEMIA
• Hypoglycaemia is defined as plasma glucose concentration ≤ 2.5mmol/l.
• It is a serious metabolic emergency and can potentially lead to irreversible
brain damage (neuroglycopaenia) if not recognized and treated
immediately.
• Hypoglycaemic crises are common among diabetics on insulin or on
sulfonyl ureas like diabenese and daonil
• It can be functional when its cause by over secretion of insulin by islet cells
in an excessive reaction to glucose or organic when it is due to
insulinomas,hypopituitarism,liver disease etc
• Occurs when drugs (Insulin or Oral drugs especially soluble insulin) are
taken without commensurate food.
 HYPOGLYCAEMIA
• If blood glucose falls, three primary physiological defense mechanisms
operate:
• Endogenous insulin release from the pancreatic B cells is suppressed.
• Release of glucagon from pancreatic alpha cells and stress hormones is
increased.
• Activation of Autonomic Nervous System with release of catecholamines
both systematically and within the tissues
• All these actions reduce whole body glucose uptake & increase glucose
production maintaining a glucose supply to the brain until when the
defense system fails leading to manifestation of features of hypoglycaemia
PHYSIOLOGICAL RESPONSE TO DECREASING
BLOOD GLUCOSE
PHYSIOLOGICAL RESPONSE TO DECREASING
BLOOD GLUCOSE
• 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.
PHYSIOLOGICAL RESPONSE TO DECREASING
BLOOD GLUCOSE
• 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.
PHYSIOLOGICAL RESPONSE TO DECREASING
BLOOD GLUCOSE
HYPOGLYCEMIC ASSOCIATED AUTONOMIC
FAILURE (HAAF)
• Is a concept in type 1 DM and long standing type 2 DM patients in
which the persistent hypoglycaemia 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 glucose
• Due to the shift, there's defective counter regulation by epinephrine.
• So at hypoglycemic levels, no sympathoadrenal outflow and hence no
warning symptoms (unawareness)
HYPOGLYCEMIC ASSOCIATED AUTONOMIC
FAILURE (HAAF)
EPIDEMIOLOGY
• Annually, ≈10% of pts with type 1 DM on twice daily insulin develop
severe hypoglycaemic episodes
• Patients attempting tight glucose control with either multiple daily
injections or continuous s.c insulin infusion has 3 X risk of developing
severe hypoglycemia
• There is less risk with type 2 DM: ≈ 0.5% per year in patients taking
sulphonylureas compared to a higher risk of ≈ 2–3% in patients
taking insulin
• The Critical glucose value for cerebral function to be become impaired
is ≈3 mmol/L which manifest as a lengthening of reaction time
CAUSES OF HYPOGLYCAEMIA
• The most common cause of hypoglycemia is medications used to
treat DM such as insulin, sulfonylureas, and biguanides.
• The 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 medications
• -Quinine medication
• -Renal failure
CAUSES OF HYPOGLYCAEMIA
• -Addison disease
• -Pituitary insufficiency
• -insulinoma
• -Sepsis
• -Gastric bye pass surgery
• - Hypothyroidism
SYMPTOMS OF HYPOGLYCEMIA
SIGNS OF HYPOGLYCAEMIA
• Diaphoresis (excessive sweating)
• Pallor
• Raised heart rate and BP
• Transient neurological deficit
• Rarely permanent neurological deficit
DIAGNOSIS
• History and examination
• History of clinical Features suggestive of hypoglycaemia
• History of risk factors and possible cause
• Diagnosis is mainly based on Whipple's triad:
i. Symptoms and signs consistent of hypoglycaemia
ii. Associated low blood glucose level
iii. Relief of symptoms with supplementation of glucose
• Investigation - laboratory diagnosis confirming hypoglycaemia and
possible cause
INVESTIGATIONS
• Random blood glucose
• Full blood count
• Insulin assay (Insulinoma)
• TFT (hypothyroidism)
• Drug screen - sulfonylurea, metformin
• Serum electrolyte/urea/creatinine( Renal Failure)
• Liver function test (Liver failure)
• Hormonal assay - GH, Cortisol
MANAGEMENT OF HYPOGLYCAEMIA
• Is done in three phases
• Acute management;
- To prevent and minimize neurological damage
• Maintenance therapy;
-To prevent recurrence of hypoglycaemia
• Subsequent measures;
- To search for and treat the underlying cause
ACUTE INTERVENTION
• Admit the patient because hypoglycemia is a medical emergency
• Institute ABC resuscitation measures
• Secure iv access using a wide bore cannula
• Give IV bolus 50mls of 50% Dextrose water (in double dilution)
• NOTE: In absence of 50% D/W, give, 250mls of 10% D/W, or 500mls of
5%D/S
• Re-assess the blood glucose in 30minute time then 1 hour time
MAINTENANCE THERAPY
• Continuous glucose administration of IV 10% Dextrose water infusion
1 L 6 hourly until patient can take orally
• Monitor hourly blood sugar until stable
• I.M. Glucagon a counter regulatory hormone to insulin that stimulate liver to
produce glucose through gluconeogenesis or glycogelolysis given at 0.5–1.0 mg
may be use in some situations
• Withhold all anti-diabetic medications including insulin until patient is
stable.
• If glucose infusion is not immediately available, give a bottle of soft
drink (Coca-cola, Fanta) or place a cube of sugar in patient’s mouth if
he/she can take orally.
MAINTENANCE THERAPY
• In the absence of a glucometer, any person with diabetes found to
have sudden onset of sweating, tremors, confusion and altered
consciousness should be investigated for urgent RBS in the lab.
• Then GIVE IV 50% dextrose 50ml bolus and maintain on 10% dextrose
until result of RBS is available.
• Counsel the patient on warning signs of hypoglycaemia, the relevance
of meals taken during or after medications, and importance of regular
follow-up visits.
SUBSEQUENT MEASURES
• For refractory cases and treatment of underlying cause including;
-Use of Glucagon injection periodically
Use of Diazoxide, a benzothiadiazine derivatives for symptomatic
management of hypoglycaemia
-Giving of Antibiotics for sepsis
-Hormone replacement therapy for hormone deficiencies
-Surgery
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
• Acute diabetic emergencies are common among diabetic patients
• The prevention of acute diabetic emergencies will go along way in
minimising the morbidities and mortalities associated with these
conditions
• The family physician as a frontline doctor should have the high index
of suspicion to identify early and mange these conditions which are
commonly seen in our emergency clinics
• THANK YOU FOR LISTENING
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