Complications of Diabetes Mellitus

Dr Omar Ahsan
• Short Term
• Long term
• Microvascular
• Macrovascular
Blood Glucose Levels
• NORMAL
• Before meals 4.0 to 5.4 mmol/L (72 to 99 mg/dL) fasting.
• After meals Up to 7.8 mmol/L (140 mg/dL) after2 hours.
Hypoglycemia
• Blood glucose 54 mg/dL (3 mmol/L),
• Sympathetic (tachycardia, palpitations, sweating,
tremulousness)
• Parasympathetic (nausea, hunger)
• Glucose <50 mg/dL (2.8 mmol/ L )then neuroglycopenic
symptoms appear, including irritability, confusion, blurred
vision, tiredness, headache, and difficulty speaking.
• Further decrease
• Loss of consciousness
• Seizures, brain death, coma
Causes
• Sulfonylureas , Repaglinide , and nateglinide
• Injecting too much insulin for the amount of carbohydrates
ingested.
• Drinking alcohol in excess, especially on an empty stomach
Management
• Oral glucose administration Toffees sweets Honey Refined sugars
• 50 mL of 50% glucose solution by rapid intravenous infusion.
• If intravenous access is not available, 1 mg of
glucagon can be injected intramuscularly.
• Unconscious patient should be turned on his or her
side to protect the airway
• The glucagon mobilizes glycogen from the liver,
raising the blood glucose by about 36 mg/dL (2
mmol/L) in about 15 minutes.
Hypoglycemic unawareness

• With repeated episodes of hypoglycemia, there is adaptation, and

autonomic symptoms do not occur until the blood glucose levels are
very low.
• Except for sweating, most of the sympathetic symptoms of
hypoglycemia are blunted in beta-blocking agents.
• Avoid NON SELECTIVE beta blockers eg nadolol, propranolol.
DIABETIC KETOACIDOSIS (DKA)
• Hyperglycemia greater than 250 mg /dL
• Acidosis with blood pH < 7.3.
• Serum bicarbonate less than 15 mEq/L
• Serum and urine positive for ketones
DKA
• Type I diabetics
• Infection , trauma, myocardial infarction, or surgery
• Life threatening medical emergency
• Quick onset
• DKA is usually preceded by a day or more of
polyuria and polydipsia associated with marked
fatigue, nausea, and vomiting.
• If untreated, mental stupor ensues that can
progress to coma
DKA
• Dehydration
• Stuporous or comatosed
• Rapid deep breathing
• "fruity“ breath odor of acetone
• Hypotension with tachycardia indicates profound
fluid and electrolyte depletion
• Mild hypothermia
• Abdominal pain and tenderness
DKA
• Plasma glucose of 350-900 mg/dL .
• Hyperkalemia (serum potassium level of 5-8 mEq/L)
• Hyponatremia
• Hyperphosphatemia
• Elevated blood urea nitrogen and serum creatinine
levels
ABGs
• Acidosis
• pH ranging from 6.9 to 7.2
• Serum bicarbonate 5 mEq/L to 15 mEq/L
• PC02 is low (15-20 mmHg) related to
hyperventilation.
Treatment
• Treat in ICU
• Restore plasma volume and tissue perfusion.
• Reduce blood glucose and osmolality
• Correct acidosis
• Replenish electrolytes losses
• Identify and treat precipitating factors.
Treatment
• NG tube
• Foley catheter
• CVP line and cardiac monitor
• The fluid deficit is 4-5 L.
• 0.9 %saline 1 L/h over the first 1 -2 hours.
• Then rate of 300-400 mL/h
• Keep an eye on CVP pressure and sodium.
• 3-4 L in 8 hours
Treatment
• Caution >5 L in 8 hours -Acute respiratory distress
syndrome or cerebral edema
• Blood glucose 250 mg/dL change to a 5% glucose
to maintain serum glucose in the range of 250-300
mg/dL
• Cerebral edema may occur if too rapid lowering of
blood glucose
Treatment
• Insulin 0.1 unit/kg as a bolus .
• Then 0.1 unit/kg/h are continuously infused.
• Replace potassium @ 10-30 mEq/h during the
second and third hours onwards
• Monitor ECG
• Give IV antibiotics
• Send cultures
• Find the precipitating cause
Hyperglycaemic Hyperosmolar Nonketotic
Coma (HONK)
• Hyperglycemia > 600 mg/dL
• Serum osmolality >310 mOsm/kg
• No acidosis; blood pH > 7.3
• Type II diabetics
• Middle or old age
• CKD IHD further bad prognosis
• Infection , MI, CVA, or recent surgery ppt
HONK

• Partial or relative insulin deficiency may initiate

the syndrome by reducing glucose utilization of
muscle, fat, and liver while inducing
hyperglucagonemia and increasing hepatic glucose
output.
• Glycosuria – water loss and dehydration.
• Severe hyperosmolality develops that causes
mental confusion and finally coma
HONK

• Insidious over a period of days or weeks,

• Weakness , polyuria, and polydipsia.
• The lack of features of ketoacidosis may retard
recognition of the syndrome
• Lethargy and confusion serum osmolality
>310mOsm/kg.
• Convulsions and coma when osmolality >320-330
mOsm/kg.
HONK Treatment
• 0.9% saline. Or 0.45% saline
• 4-6 L of fluid may be required in the first 8-10
hours.
• End point of fluid therapy is to restore urinary
output to 50 mL/h or more.
• Less insulin may be required to reduce the
hyperglycemia
• CORRECT FLUID LOSSES
Long Term Complications
• Long term diabetic complications
• Macrovascular disease
• Microvascular disease
• Neuropathy
• Infections
• Renal, Cardiovascular, Eye.
Macrovascular
• Large and medium-size blood vessels
• Occur with greater frequency and earlier onset in people
with diabetes
• Macrovascular diseases
• Cerebrovascular, coronary artery, and peripheral
vascular disease.
Macrovascular Changes
• Atherosclerotic changes
• Blood vessels thicken, sclerose & become thickened by plaque→adheres to
vessel wall
• Eventual blockage of blood vessel
• Changes occur at an earlier age and more often in the diabetic
Macroangiopathies
• Cerebrovascular Effects
• Glucose – stiffens the RBC’s, making platelet aggregation
easier
• Leads to TIA’s and causes CVA’s
• People with diabetes- 2x risk of CVA
Macroangiopathy
• Coronary artery disease (CAD)
• MI- 2x men & 3x women with diabetes
• ↑ likelihood of second MI
• Ischemic symptoms may be absent
• May be secondary to autonomic neuropathy
• Silent MI common in DM
Hypertension in Type 1 and 2
Diabetes

Type 1 Type 2

Develop after Mostly present at

several years of diagnosis
DM Affects at least
Ultimately affects 60% of patients
~30% of patients
Pathophysiology of hypertension
Type 1 DM Type 2 DM

Secondary to Hyperinsulinemia
nephropathy Secondary to
insulin resistance
Activation of the
sympathetic
nervous system
Dyslipidaemia in DM
• Most common abnormality is  s HDL and  s
Triglycerides
• A low HDL is the most constant predictor of CV
disease in DM
Peripheral Arterial Diseases

• Occurs 2-3x more frequently in diabetics

• Signs & symptoms
• Decreased pulses
• Intermittent claudication (pain in buttock, thigh or calf
when walking)
• Gangrene & amputation – result from severe form of
arterial occlusion
Peripheral arterial disease

• Good BS control- medication compliance

• Protect feet from heat and cold
• Foot care:
• No smoking (causes vasospasm)
• Check pulses; examine feet daily
Reduction of risk factors for Macroangiopathies

• Medical nutrition therapy & exercise

• Reduces obesity, HTN & hyperlipidemia
• Obesity increases insulin resistance
• BP control – meds and lifestyle changes
• Tight BS control
• ↓triglyceride concentrations
• ↓ complications
• No smoking
Microvascular Complications
• Result from thickening of the vessel membranes in
the capillaries and arterioles from chronic
hyperglycemia
• Clinical manifestations usually do not appear until
10 to 20 years after the onset of diabetes

• Areas most affected

– Eyes (retinopathy)
– Kidneys (nephropathy)
Diabetic Retinopathy
• Most common cause of new cases of blindness in
people ages 20 to 74 years
– Deterioration of small blood vessels that nourish the
retina

• Maintenance of blood glucose to near normal in

type 1 - decrease risk by 74%
Other eye problems in diabetes
• Glaucoma
• Cataracts
Diabetic Kidney
• Glomerular damage
• Ischaemia resulting from hypertrophy of afferent and
efferent arterioles
• Ascending infection
Diabetic Nephropathy
• A microvascular complication
• Damage to small blood vessels that supply the glomeruli
of the kidney
• Leading cause of end-stage renal disease ESRD
Management of Nephropathy
• Improvement of glycemic control
• Treatment of hypertension
• Treatment with ACEI
• Restriction of dietary intake of protein
• Refer to an Internist or Nephrologist
Management of Nephropathy
• Monitor urine for microalbuminuria, BUN, creatinine
annually
• Blood glucose control to prevent & delay
development of nephropathy
• Use of ACE-inhibitor drugs – delay progression of
nephropathy
• Aggressive control of BP- to slow progression of
nephropathy
Other interventions for nephropathy

• Decrease protein intake if indicated (renal diet)

• Low sodium diet
• Avoid nephrotoxic substances
• Dialysis or transplant
Diabetic Neuropathy
Sensorimotor neuropathy (acute/chronic)
Autonomic neuropathy
Mononeuropathy
Spontaneous
Entrapment
External pressure palsies
Proximal motor neuropathy
Screening for Neuropathy
• 128 Hz tuning fork for
testing of vibration
perception
The main purpose is to
identify patients at risk
for development of
diabetic foot
Management of Neuropathy
• Burning pain – TADs / Capsaicin
• Lancinating pain – Anticonvulsants / TAD /
Capsaicin
• Painful cramps – Quinidine sulphate
• Restless legs - Clonazepam
Do’s and Don'ts of foot care
Patient should
• check feet daily
• Wash feet daily
• Keep toenails short
• Protect feet
• Always wear shoes
• Look inside shoes before putting
them on
• Always wear socks
• Break in new shoes gradually
Sensorimotor Neuropathy
• Patients may be asymptomatic / complain of
numbness, paresthesias, allodynia or pain
• Feet are mostly affected, hands are seldom
affected
• In Diabetic patients sensory neuropathy usually
predominates
Complications of Sensorimotor
neuropathy
• Ulceration
(painless)
• Neuropathic
edema
• Charcot
arthropathy
• Callosities
Autonomic Neuropathy
Symptomatic Subclinical abnormalities
Postural hypotension Abnormal pupillary
reflexes
Gastroparesis
Esophageal dysfunction
Diabetic diarrhea Abnormal cardiovascular
Neuropathic bladder reflexes
Erectile dysfunction Blunted counter-
regulatory responses
Neuropathic edema to hypoglycemia
Charcot arthropathy Increased peripheral
Gustatatory sweating blood flow
Entrapment Neuropathies
• Carpal tunnel syndrome (median nerve)
• Ulnar compression syndrome
• Meralgia paresthetica (lat cut nerve to the thigh)
• Lat Popliteal nerve compression (drop foot)
Neuropathy: neurotrophic ulceration
Management -Peripheral Neuropathy

• Control of blood glucose -only treatment for diabetic neuropathy

• Medications:
• Analgesics, antidepressants, Neurontin
• Capsaicin- topical cream from chili peppers- depletes the accumulation of
pain-mediating chemicals in the peripheral sensory neurons
• TENS units
Infections
• Skin
• staphylococcal infections (boils, abscesses,
• carbuncles)
• mucocutaneous candidiasis
• Gastrointestinal tract
• rectal and ischiorectal abscess formation
• Periodontal disease
• Urinary tract
• – urinary tract infections (in women)
• – pyelonephritis
• – perinephric abscess
• Lungs
• – staphylococcal and pneumococcal pneumonia
• – Gram-negative bacterial pneumonia
• – tuberculosis
• Bone
• – spontaneous staphylococcal spinal osteomyelitis.
Pathophysiology
• Poor control leads to infection as chemotaxis and phagocytosis by
polymorphonuclear leucocytes are impaired because at high blood glucose
concentrations neutrophil superoxide generation is impaired