Carmel Christy Christopher MM20605 MD Student

L14.2: Diabetes Mellitus (P2)

• Acute Complications of DM / Diabetic emergencies

o Diabetic Ketoacidosis (DKA)
o Hyper osmolar non-ketotic coma (HONC)
o Hypoglycaemia coma
o Lactic acidosis

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Diabetic Ketoacidosis (DKA)

• Definition
o Severe acute metabolic complication of type 1 diabetes, but may also occur in type 2 diabetes
o It is a major medical emergency serious cause of morbidity in people with type 2 diabetes
• Common precipitating factors
o Failure to take insulin
o Intercurrent infection
o Illnesses
o Trauma & any form of stress
• Pathogenesis of DKA
o Effect of insulin deficiency is activation of ketogenic machinery
o Insulin deficiency stimulate lipoprotein lipase → Breakdowm of adipose stores and increase in
level of free fatty acids
o Free fatty acids reach liver → They are esterified to fatty acyl coenzyme A
o Oxidation of fatty acyl coenzyme A molecule within mitochondria → Produce ketone bodies
(acetoacetic acid & β-hydroxybutyric acid)
o Rate of ketone body formation exceed rate of its utilization in peripheral tissues → Leads to
Ketonemia, Ketonuria
o If urinary excretion in compromised by dehydration → Result = Systemic metabolic ketoacidosis
Carmel Christy Christopher MM20605 MD Student

• Diagnosis of DKA
o Urinary and plasma ketone (positive +)
o Arterial pH ≤ 7.30
o Serum bicarbonate ≤ 15mmol/L
• Principle components of treatments
o Administration of short-acting (soluble) insulin
o Fluid replacement
o Potassium replacement
o Administration of antibiotics if infection is present

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Hyperosmolar hyperosmotic syndrome (HHS) / Hyper Osmolar Non Ketotic Coma (HONC)

• Definition
o This condition is characterized by severe hyperglycaemia (>50mmol/L or >900mg/dl) without
significant hyperketonaemia or acidosis
o Severe dehydration resulting from sustained osmotic diuresis.
• Character
o Elderly
o Mortality is high (40%)
o Insidious onset of polyuria, polydipsia
o Severe dehydration
o Pre-renal uraemia
o Impaired conscious, coma
o Respiration is usually normal
o Rarely present with CVA, seizure or MI
• Hypoglycaemic coma
Carmel Christy Christopher MM20605 MD Student

o Blood glucose < 3.5 mmol/L (63mg/dl)

o In diabetic pt, it is result of treatment
▪ With insulin
▪ With sulphonylurea drugs
▪ Rarely with metformin
o Missed, Delayed or inadequate meal
▪ When hypoglycaemia occurs in non-diabetic patient → Spontaneous hypoglycaemia
▪ Mortality → 2-4% in Insulin treated patient
Carmel Christy Christopher MM20605 MD Student

Lactic Acidosis

• Coma due to lactic acidosis

• Clinical features
o History of taking metformin for type 2 diabetes
o Very ill, over breathing
o Not dehydrated as in DKA
o Breath → No acetone smell
o Absent ketonuria
o Plasma bicarbonate & pH → Markedly reduced
o Confirmed by high lactic acid concentration (>5.0mmol/L)

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Chronic Complications of Diabetes mellitus

• Long-term (chronic) complications of DM

o Eyes → Retinopathy, Cataracts, Glaucoma
o Brain → Microangiopathy, Cerebral vascular infarcts, Haemorrhage
o Systemic → Hypertension
o Heart → Myocardial infects
o Blood vessels → Atherosclerosis
o Pancreas → Islet cell loss (Insulitis, type1 or Amyloid, type2)
o Kidney → Nephrosclerosis (Glomerulosclerosis, Arteriosclerosis, Pyelonephritis)
o Peripheral → Peripheral neuropathy, Peripheral vascular atherosclerosis, Gangrene
o Urinary → Autonomic neuropathy
o Infections
• Three major factors
o Susceptibility to infections
▪ Include → Tuberculosis, Pneumonia, Pyelonephritis, and Mucocutaneous candidiasis
▪ Caused by the hyperglycaemic environment that favours immune dysfunction (e.g.,
damage to the neutrophil function, depression of the antioxidant system, and humoral
immunity).
▪ Host susceptibility factors contributing to increased risk of infections in diabetes mellitus
will undoubtedly be
o Vascular disorder or Vasculopathy
▪ Vascular disorder → Diabetic macrovascular disease & Diabetic microvascular disease
• Diabetic macrovascular disease
Carmel Christy Christopher MM20605 MD Student

o Diabetes accelerated atherosclerosis involving the aorta and large and

medium sized arteries.
o Coronary atherosclerosis leads to Myocardial ischaemia and Myocardial
infarction.
o Cerebral atherosclerosis leads to stroke & TIA (Transient Ischaemic
Attack).
o Peripheral blood vessels involvement leads to claudication, ischaemia and
gangrene of lower extremities.
▪ Vasculopathy → Macroangiopathy & Microangiopathy
• Diabetic Microangiopathy
o Diabetes causes diffuse thickening of basement membranes in the
capillaries of the skin, skeletal muscle, retina, renal glomeruli, and renal
medulla.
o Despite the increase in the thickness of basement membranes, diabetic
capillaries are more leaky than normal to plasma proteins.
o Development of → Diabetic nephropathy, Retinopathy, and other
neuropathy
o Peripheral and autonomic neuropathy, manifesting as Sensory loss, Impotence, Postural
hypotension, Constipation, & Diarrhoea
▪ Diabetic nephropathy
• Glomerular lesions → Glomerular basement thickening, Diffuse mesangial
sclerosis, Nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
• Renal hyaline arteriolosclerosis
• Pyelonephritis or necrotising papillitis
▪ Diabetic nephropathy is a common cause of Peripheral neuropathy
Motor & Sensory neuropathy Autonomic neuropathy Diabetic neuropathy
Distal symmetric diabetic • Postural blood pressure↓ • Sudden footdrop
polyneuropathy affects both • Urinary retention • Wrist drops
motor & sensory function • Impotency (erectile dysfunction) • Isolated cranial nerve
(Symmetrical distal glove and • Nocturnal diarrhoea palsies
stocking type) • Gastroparesis

Diabetic foot disease (Neuropathy & vasculopathy) Clinical Features:

Neuropathy Vasculopathy
Symptoms None, Paraesthesiae, Pain, Numbness None, Claudication, Rest pain
Carmel Christy Christopher MM20605 MD Student

Structural dmg Ulcer, Sepsis, Abscess, Osteomyelitis, Ulcer, Sepsis, Gangrene

Digital gangrene, Charcot joints

Neuropathic Join (Charcot joint)

• Due to altered blood flow secondary to impaired sympathetic nervous system control
• Joint is swollen, with effusion, crepitus, marked instability & increased warmth

Management of Diabetes

In new cases of diabetes, adequate glycaemic control can be obtained by

1. Patient education, diet and lifestyle advice alone in approximately 50%

2. 20-30% will need oral anti diabetic medication
3. 20-30% will require insulin.

Regardless of aetiology, the choice of treatment is determined by the adequacy of residual β cell function.