Introduction to the Slide (Overview) This slide is an educational tool designed to provide foundational knowledge about Diabetes Mellitus, a chronic metabolic disorder characterized by hyperglycemia (high blood sugar levels). The slide typically contains a title, a brief definition, types of diabetes, key statistics, and diagrams or visuals that illustrate the disease mechanism or complications. The aim of this slide is to educate viewers, whether medical students, healthcare professionals, or the general public, on the nature of diabetes, its classifications, pathophysiology, and importance in public health. In a classroom or clinical setting, this slide serves as an anchor for detailed discussion or lecture. 2. Slide Layout Description A typical diabetes slide would include: Header: “Diabetes Mellitus” Subtitle or objective: “Types, Causes, and Overview of Disease Mechanism” Visual: Image showing insulin function, or a diagram comparing Type 1 and Type 2 Diabetes Bullet points summarizing: Definition Types of diabetes Epidemiology Basic pathophysiology Clinical significance A chart or table for comparison (e.g., Type 1 vs Type 2 diabetes) Possibly a quote or statistical highlight (e.g., “1 in 10 adults globally has diabetes”) 3. Title and Definition The title “Diabetes Mellitus” is chosen because it is the umbrella term for a group of diseases characterized by prolonged elevated blood sugar. The word "diabetes" comes from the Greek "siphon", referencing excessive urination, while "mellitus" means "sweet" in Latin, indicating the presence of glucose in urine—a classical sign. Below the title, the slide typically includes a definition: “Diabetes mellitus is a chronic disorder characterized by either a lack of insulin production (Type 1) or insulin resistance (Type 2), leading to elevated levels of blood glucose.” This concise definition sets the tone for understanding the underlying dysfunctions in glucose metabolism that lead to diabetes. 4. Types of Diabetes The slide often divides diabetes into three main categories: Type 1 Diabetes Mellitus (T1DM): Autoimmune destruction of pancreatic beta cells. Typically presents in children and young adults. Patients are insulin-dependent for life. Accounts for 5–10% of all diabetes cases. Type 2 Diabetes Mellitus (T2DM): Caused by insulin resistance and relative insulin deficiency. Strongly associated with obesity, physical inactivity, and family history. Accounts for 90–95% of diabetes cases globally. Onset is usually in adults but increasingly seen in children due to rising obesity rates. Gestational Diabetes Mellitus (GDM): Occurs during pregnancy. Usually resolves postpartum but increases risk of T2DM later in life. Associated with fetal macrosomia and complications during delivery. Some slides may also include secondary diabetes (e.g., due to pancreatitis or steroid use) and monogenic forms like MODY (Maturity Onset Diabetes of the Young). 5. Epidemiology and Global

1. HYPERGLYCAEMIC AND
HYPOGLYCAEMIC
CRISES
A PRESENTATION BY DR. SOFOLA J.O.

2. OUTLINE
• Introduction
• Diabetic Ketoacidosis
• Hyperosmolar Hyperglycaemic state
 Hypogylcaemia

3. INTRODUCTION
• Diabetes mellitus is a group of metabolic disorders of multiple
aetiology characterized by chronic hyperglycaemia with
disturbances of carbohydrate, fat and protein metabolism
resulting from defects in insulin secretion, insulin action, or
both.
• Hyperglycaemic and hypoglycaemic crises are acute
complications of Diabetes mellitus.

4. HYPERGLYCAEMIC CRISIS
• Diabetic Ketoacidosis.
 Hyperosmolar Hyperglycaemic state.

5. DIABETIC KETOACIDOSIS
• DKA is one of the most serious acute complications of Diabetes
mellitus.
• It is typically associated type 1 DM.
• It may occur in type 2 DM under conditions of extreme stress such
as major infection or trauma or as a variant of type 2 DM( ketosis-
prone or flatbush diabetes).

6. EPIDEMIOLOGY
• It is commoner in females.
• Commoner in non-whites.
 Mortality is higher in the elderly

7. AETHIOPATHOGENESIS
• The three fundamental biochemical features of DKA include hyperglycemia,
ketosis, and acidosis.
• Results from the combined effects of deficient circulating insulin and counter-
regulatory hormone excess.
• Triglycerides and Aminoacids are metablized for energy
• Glycerol and Alanine are mobilized for hepatic gluconeogenesis.

8. CONTD.
• FFA are converted to ketones ( acetoacetic acid and
betahydroxybutyric acid)
• Glucose and ketones are thus released into the circulation
at greater rates than their utilization, resulting in severe
hyperglycemia (>300 mg/dL), ketoacidosis
(arterial pH <7.30 and total body ketones >5mmol/L)

9. CONTD.
• Hyperglycemia causes osmotic diuresis (loss of water and
electrolytes)
• Loss of ketones in the urine also leads to loss of sodium and
potassium.

10. CLINICAL FEATURES
• DKA can be the first presentation of a patient with type 1
DM
• Or it may present in a patient with established DM in the setting of a
coexisting illness or poor adherence
The clinical history of DKA typically involves deterioration during several
hours to days.

11. CONTD.
• SYMPTOMS
• Malaise
• Weight loss
• Polyuria, polydipsia,
• Nausea, vomiting, abdominal pain,

12. CONTD.
• Altered sensorium
• Shortness of breath
SIGNS
• Acetone breath, fever
• Confusion, lethargy, coma

13. CONTD.
Severe dehydration • Kussmaul respiration.
• Tachycardia, arrhythmias
Hypotension, tachypnoea,
• Abdominal tenderness
Glycosuria and ketonuria

14. INVESTIGATIONS
• Urine analysis
• Serum electrolytes and urea
• Blood PH and Ketones
• Plasma glucose
• FBC
• Urine and blood culture
• ECG

15. MANAGEMENT
Principles of treatment
 Replace the fluid losses
 Replace the electrolyte losses.
 Restore the acid-base balance.
 Replace the deficient insulin.
 Monitor blood glucose closely. Hourly
measurement is needed in the initial phases
of treatment.
 Seek the underlying cause.

16. TREATMENT
• Replace fluid ;Intravenous saline 6 – 8 litres in 24 hours in adults.
• 1 litre fast, then 1 litre in an hour, then 1 litre in 2hrs, then 1 litre 4
hourly.
• Replace insulin; Soluble insulin 10-20 units IM or IV stat, then give 5-10
units hourly by continuous IV infusion till RBS <200mg/dL.
replace electrolyte losses

17. CONTD.
• KCL: if pottasium less than 5.5mmol/l and patient is making
urine, give 10meq/h
• if pottasium less than 3.5mmol/l give 40-80meq/h end
ensure the pottasium and bicarbonate is measured every
4hours in the first 24hours.
If Ph is below 7, give HCO3 as 1.26% solution.

18. CONTD.
• Treat underlying cause.
• monitor vitals and hydration.
• When RBS <200mg/dL change the IV fluids to 5% dextrose to run 1 pint 4 hourly and add
KCl 20 – 40mmol per pint (depends on K level) with soluble insulin 4-6 units per pint
• When patient fully conscious and rehydrated then change insulin to subcutaneous tds
premeal and allow patient eat.
• Discharge patient home on insulin.

19. CONTD.
• FOLLOW UP
• After identifying cause of DKA put measures in place to
prevent recurrence.
Patient Education.

20. HYPEROSMOLAR
HYPERGLYCAEMIC STATE (HHS)
• Similar to DKA but:
• Blood sugars in range of 500 – 2000mg/dL
• No ketonuria or trace ketones
• No anion gap or mild anion gap
• Often have azotaemia, increased Na, K
• Normal blood PH

21. CONTD.
• hallmarks of the HHS are severe hyperosmolarity (>320 mOsm/L) and
hyperglycemia (>600 mg/dL).
• EPIDEMIOLOGY
• HHS is not as common as DKA
• Commoner in elderly patients who are often institutionalized or with
cognitive impairment

22. AETHIOPATHOGENESIS
• Patient is fairly insulin sensitive
• There is still some circulating insulin sufficient to suppress ketosis but
insufficient to suppress gluconeogenesis
• Renal impairment coupled with dehydration from reduced fluid intake over a
period
• Hyperosmolarity ensues with increased thrombogenicity

23. CLINICAL FEATURES
• Polyuria, polydyspia and oliguria.
• Altered sensorium (10% have frank coma)
• profound dehydration
• grand mal or focal seizures, extensor plantar reflexes, aphasia, hemisensory
or motor deficits, and worsening of a preexisting organic mental syndrome.
• No kussmaul respiration
• DVT or PE common

24. INVESTIGATIONS
• E/U/Cr
• Urinalysis
• Blood sugars
• Sepsis workup
• Plasma osmolarity, plasma pH
• ECG, CXR, D-dimer tests

25. TREATMENT
• Very similar to DKA treatment
• Admit, NPO
• Rehydrate with 6 – 10 litres of fluid preferably half normal
saline

26. CONTD.
• Hourly soluble insulin 4-6 units after a stat 10units IV.
• Use heparin or enoxaparin to anticoagulate
Watch out for fluid overload if CKD present

27. HYPOGLYCEMIA
• Defined as low blood sugar
• Blood sugars below 2.2mmol/L taken as hypoglycaemia in general population
• In DM patients the threshold for hypoglycaemia is lower so coma may occur
in blood sugars 50 – 80mg/dL and in those with rapid decline in blood sugars
• Thus, Whipple’s triad often used to identify and confirm hypoglycaemia in DM
patient

28. CONTD.
• Triad is made up of:
• hypoglycaemic symptoms
• biochemically proven low blood sugar
• relief of symptoms after administration of sugar or
carbohydrate containing drink/meals.

29. AETHIOPATHOGENESIS
• Excess insulin whether from injections or secretagogue
• Inadequate calorie intake
• Inadequate counterregulatory response

30. CLINICAL FEATURES
• Adrenergic symptoms: eg palpitations, tremors, sweating
• Neuroglycopenic symptoms: dizziness, headache, coma,
seizures, confusion, etc

31. INVESTIGATIONS
• Plasma glucose
• Insulin assays
• C-peptide
• Liver, renal function tests

32. MANAGEMENT
• Resuscitate with soft drink, sugar or glucose at home if
conscious
• Admit to hospital if unconscious or if first aid with sugar at
home not working
• Resuscitate and give IV 10% glucose or diluted 50%
glucose via wide bore access

33. CONTD.
• Give IM glucagon 1mg if available
• Continue to monitor blood sugars, omit insulin or OHAs
patient taking

34. CONCLUSION
It is imoprtant to recognise and diagnose the acute
complications of DM early as they are life threatening
emergencies.
Self glucose monitoring will be helpful to prevent these
conditions